ORAL AND

MAXILLOFACIAL
SURGERY
SECOND EDITION
VOLUME I
Anesthesia and Pain Control
Dentoalveolar Surgery
Practice Management
Implant Surgery

VOLUME EDITOR
Raymond J. Fonseca, DMD
Private Practice
Oral and Maxillofacial Surgery
Asheville, North Carolina
Clinical Professor, Department of Oral and Maxillofacial Surgery
University of North Carolina
Chapel Hill, North Carolina

SECTION EDITORS
H. Dexter Barber, DDS
John D. Matheson, DDS, FACD, FICD
11830 Westline Industrial Drive
St. Louis, Missouri 63146

ORAL AND MAXILLOFACIAL SURGERY, VOLUME I ISBN-13: 978-1-4160-6657-6

ISBN-10: 1-416066578
Copyright © 2009, 2000 by Saunders, an imprint of Elsevier Inc.

All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any
means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval
system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s
Rights Department: phone: (+1) 215 239 3804 (US) or (+44) 1865 843830 (UK); fax: (+44) 1865 853333;
e-mail: healthpermissions@elsevier.com. You may also complete your request on-line via the Elsevier website
at http://www.elsevier.com/permissions.

Notice

Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or
appropriate. Readers are advised to check the most current information provided (i) on procedures
featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose
or formula, the method and duration of administration, and contraindications. It is the responsibility of
the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to
determine dosages and the best treatment for each individual patient, and to take all appropriate safety
precautions. To the fullest extent of the law, neither the Publisher nor the Editors/Authors assumes any
liability for any injury and/or damage to persons or property arising out of or related to any use of the
material contained in this book.
The Publisher

ISBN-13: 978-1-4160-6657-6
ISBN-10: 1-416066578

Vice President and Publisher: Linda Duncan

Acquisitions Editor: John J. Dolan
Developmental Editor: Brian S. Loehr
Publishing Services Manager: Julie Eddy
Project Manager: Marquita Parker
Designer: Kim Denando
Medical Illustrator: William M. Winn

Working together to grow

libraries in developing countries
Printed in the United States www.elsevier.com | www.bookaid.org | www.sabre.org

Last digit is the print number: 9 8 7 6 5 4 3 2 1

 DEDICATION

I would like to dedicate this book to Dr. Robert Moore and Dr. Donald Obson. These two
oral and maxillofacial surgeons were friends and role models and their death at an early
age was a loss not only to those who knew and loved them, but also to our specialty.
Raymond J. Fonseca

To Kymberly, Taylor, David, and Noah with much love and appreciation for your love
and support. To Mom and Dad for your love and the dedication you have provided for
your children.
H. Dexter Barber

To Lynne; our children John Jr., Marion, and Kate; and to Denny Hillenbrand,
surgeon, teacher, and friend.
John D. Matheson
 SECTION EDITORS

H. Dexter Barber, DDS

Vice-Chairman, Department of Oral and Maxillofacial Surgery
Temple University Hospitals
Philadelphia, Pennsylvania
Private Practice
Oral and Maxillofacial Surgery
Elkins Park, Pennsylvania and Sewell, New Jersey

John D. Matheson, DDS, FACD, FICD

Private Practice
Oral and Maxillofacial Surgery
Asheville, North Carolina

Raymond J. Fonseca, DMD

Private Practice
Oral and Maxillofacial Surgery
Asheville, North Carolina
Clinical Professor, Department of Oral and Maxillofacial Surgery
University of North Carolina
Chapel Hill, North Carolina
 CONTRIBUTORS

John O. Akers, DDS Jeffrey D. Bennett, DMD

Oral and Maxillofacial Surgery Professor and Chair, Department of Oral Surgery and Hospital Dentistry
Contributing Faculty, Student Oral Surgery Clinic Indiana University School of Dentistry
University of Florida Indianapolis, Indiana
Gainesville, Florida Chapter 5 Anesthetic Concepts and Techniques
Chapter 17 Accreditation of Surgicenters
Russel S. Bleiler III, DMD
Pamela L. Alberto, DMD Assistant Clinical Professor, Temple University Hospital and Dental School
Clinical Associate Professor Private Practice
Director of Predoctoral Surgery Langhorne, Pennsylvania
Department of Oral and Maxillofacial Surgery Chapter 35 Miniimplants and Transitional Implants
University of Medicine and Dentistry of New Jersey
Newark, New Jersey Per-Ingvar Brånemark, MD, PhD
Chapter 12 Complications of Dentoalveolar Surgery P-I Brånemark Institute Bauru
Bauru S.P. Brazil
H. Dexter Barber, DDS Chapter 29 Zygomatic Implant: A Graftless Approach for Treatment of the
Vice-Chairman, Department of Oral and Maxillofacial Surgery Edentulous Maxilla
Temple University Hospitals
Philadelphia, Pennsylvania Kasey E. Call, DMD
Private Practice Resident, Department of Oral and Maxillofacial Surgery
Oral and Maxillofacial Surgery Temple University Hospitals
Elkins Park, Pennsylvania and Sewell, New Jersey Philadelphia, Pennsylvania
Chapter 30 Platelet-Rich Plasma and Bone Grafting in Implant Surgery Chapter 35 Miniimplants and Transitional Implants
Chapter 33 Implant Placement Immediately Following Tooth Extraction
Louis F. Clarizio, DDS, PA
Barry Kyle Bartee, DDS, MD Private Practice
Private Practice Oral and Maxillofacial Surgery
Lubbock, Texas Portsmouth, New Hampshire
Assistant Clinical Professor, Department of Surgery, Texas Tech Health Chapter 31 Immediate Implant Loading
Sciences Center School of Medicine Lubbock, Texas
Adjunct Clinical Professor, Baylor College of Dentistry Bernard J. Costello, DMD, MD, FACS
Texas A&M University Associate Professor, Program Director, and Chief
Dallas, Texas Division of Craniofacial and Cleft Surgery
Clinical Consultant, Osteogenics Biomedical, Inc. Department of Oral and Maxillofacial Surgery
Lubbock, Texas Chief, Pediatric Oral and Maxillofacial Surgery
Chapter 25 Guided Tissue Regeneration in Implant Dentistry: Techniques Children’s Hospital of Pittsburgh
for Management of Localized Bone Defects Pittsburgh, Pennsylvania
Chapter 13 Skeletal Anchorage for Orthodontics
Edmond Bedrossian, DDS, FACD, FACOMS
Private Practice Charles Lynum Cuttino III, DDS
San Francisco, California Oral and Maxillofacial Surgery
Director, Implant Training Private Practice
University of the Pacific, OMFS Residency Program Commonwealth Oral and Facial Surgery
San Francisco, California Richmond, Virginia
Chapter 29 Zygomatic Implant: A Graftless Approach for Treatment of the Chapter 21 Coding, Insurance, and Third-Party Payers
Edentulous Maxilla
Jeffrey Dembo, DDS, MS
Gregory S. Bell, DDS Professor, Division of Oral and Maxillofacial Surgery
Resident, Department of Oral and Maxillofacial Surgery University of Kentucky College of Dentistry
David Grant Medical Center Lexington, Kentucky
Travis AFB, California Chapter 2 Monitoring for the Oral and Maxillofacial Surgery Patient
Chapter 7 Pediatric Pharmacosedation and General Anesthesia Chapter 4 Pharmacology of Drugs in Ambulatory Anesthesia

ix
x CONTRIBUTORS

Sean W. Digman, DDS Chapter 6 Management of Acute Postoperative Pain

Program Director, Oral and Maxillofacial Surgery Residency
Department of Oral and Maxillofacial Surgery Steven M. Holmes
David Grant USAF Medical Center Private Practice
Travis AFB, California Oral and Maxillofacial Surgery
Chapter 10 Pediatric Dentoalveolar Surgery Miami, Florida
Director, Oral and Maxillofacial Surgery National Insurance Company
Harry Dym, DDS (OMSNIC)
Chairman, Department of Dentistry and Oral and Maxillofacial Surgery Chairman, Risk Management
Director, Oral and Maxillofacial Surgery Training Program Rosemont, Illinois
The Brooklyn Hospital Center Chapter 22 Risk Management in Oral and Maxillofacial Surgery
Clinical Professor Oral and Maxillofacial Surgery
Columbia University College of Dental Medicine Howard A. Israel, DDS
Brooklyn, New York Professor of Clinical Surgery
Chapter 11 Basic and Complex Exodontia and Surgical Management of Division of Oral and Maxillofacial Surgery
Impacted Teeth Cornell University
Weill Cornell Medical College
Raymond J. Fonseca, DMD New York, New York
Private Practice Private Practive
Oral and Maxillofacial Surgery Great Neck, New York
Asheville, North Carolina Chapter 8 The Essential Role of the Oral and Maxillofacial Surgeon in the
Clinical Professor, Department of Oral and Maxillofacial Surgery Diagnosis, Management, Causation, and Prevention of Chronic
University of North Carolina Orofacial Pain: Clinical Perspectives
Chapel Hill, North Carolina
Brandon Iverson, DDS
David E. Frost, DDS, MS Chief Resident, Temple University Hospitals
Private Practice Department of Oral and Maxillofacial Surgery
Oral and Maxillofacial Surgery Philadelphia, Pennsylvania
Chapel Hill, North Carolina Cooper Medical Center
Adjunct Clinical Assistant Professor Division of Oral and Maxillofacial Surgery
University of North Carolina at Chapel Hill Camden, New Jersey
Chapter 16 Oral and Maxillofacial Surgery—Office Management Chapter 30 Platelet-Rich Plasma and Bone Grafting in Implant Surgery

Michael A. Gentile, DMD Ole T. Jensen, DDS, MS

Oral and Maxillofacial Surgery Private Practice
United States Navy Oral and Maxillofacial Surgery
Lemoore, California Denver, Colorado
Chapter 6 Management of Acute Postoperative Pain Chapter 27 Dentoalveolar Modification by Osteoperiosteal Flaps

Michelle Soltan Ghostine, MD Glenn Jividen Jr., DDS

Resident, Department of Otolaryngology/Head and Neck Surgery Private Practice
Loma Linda University Periodontics
Loma Linda, California Dayton, Ohio
Chapter 26 Contemporary Sinus-Lift Subantral Surgery and Graft Chapter 28 Soft Tissue Procedures Around Implants

John M. Gregg, DDS, MS, PhD David A. Johnson, PhD

Adjunct Professor, Virginia Tech University Associate Professor of Pharmacology and Toxicology
Department of Human Nutrition, Foods and Exercise Director of Graduate Studies
Virginia-Maryland College of Veterinary Medicine Graduate School of Pharmaceutical Sciences
Blacksburg, Virginia Duquesne University
Chapter 9 Chronic Maxillomandibular, Head and Neck Pain Pittsburgh, Pennsylvania
Chapter 15 Treatment of Trigeminal Nerve Injuries Chapter 23 Pharmacology for Implant Dentistry

Samuel L. Hayes, DDS Amin Kazemi, DMD, MD

Resident, Department of Oral and Maxillofacial Surgery Private Practice
David Grant USAF Medical Center Chester County Hospital
Travis AFB, California West Chester, Pennsylvania
Chapter 10 Pediatric Dentoalveolar Surgery Chapter 1 Preoperative Evaluation

David Lee Hill Jr., DDS

Resident, University of North Carolina
Department of Oral and Maxillofacial Surgery
Chapel Hill, North Carolina
 CONTRIBUTORS xi

Jack T. Krauser, DMD Roger L. Myers, DMD

Private Practice Private Practice
Periodontics Oral and Maxillofacial Surgery
Boca Raton, Florida Hinesville, Georgia
Treasurer, International Congress of Oral Implantologists Chapter 30 Platelet-Rich Plasma and Bone Grafting in Implant Surgery
Faculty, Division of Oral and Maxillofacial Surgery
University of Miami School of Medicine Talib A. Najjar, DMD, MDS, PhD
Miami, Florida Professor, Oral and Maxillofacial Surgery
Chapter 32 Impressions at Surgical Placement and Provisionalization of New Jersey Dental School
Implants University of Medicine and Dentistry of New Jersey
Newark, New Jersey
David P. Kretzschmar, DDS, MS Chapter 35 Miniimplants and Transitional Implants
Chief, Oral and Maxillofacial Surgery
Wake Forest University Baptist Medical Center Joseph Niamtu III, DMD
Associate Professor, Oral and Maxillofacial Surgery Private Practice
Wake Forest University School of Medicine Cosmetic Facial Surgery
Winston-Salem, North Carolina Richmond, Virginia
Chapter 18 Credentialing and Hospital Privileging Chapter 19 Marketing the Oral and Maxillofacial Surgery Practice

John L. Lignelli II, DMD Jean-Luc G. Niel, DMD

Private Practice Resident, Department of Oral and Maxillofacial Surgery
Pottstown, Pennsylvania David Grant Medical Center, USAF
Chapter 25 Guided Tissue Regeneration in Implant Dentistry: Techniques Travis AFB, California
for Management of Localized Bone Defects Chapter 10 Pediatric Dentoalveolar Surgery

Trent W. Listello, DDS Orrett E. Ogle, DDS

Resident, Department of Oral and Maxillofacial Surgery Director, Residency Training Program
David Grant Medical Center Chief, Oral and Maxillofacial Surgery
Travis AFB, California Woodhull Medical and Mental Health Center
Chapter 7 Pediatric Pharmacosedation and General Anesthesia Brooklyn, New York
Chapter 11 Basic and Complex Exodontia and Surgical Management of
Nima S. Massoomi, DMD, MEd, MD Impacted Teeth
Fellow, Facial Cosmetic Surgery
T. W. Evans Maxillofacial and Facial Aesthetic Surgery Center Larry P. Parworth, DDS, MS
Columbus, Ohio Private Practice
Chapter 3 Local Anesthetics Oral and Maxillofacial Surgery
Asheville, North Carolina
John D. Matheson, DDS, FACD, FICD Chapter 7 Pediatric Pharmacosedation and General Anesthesia
Private Practice
Oral and Maxillofacial Surgery Joseph FA Petrone, DDS, MSD, MPH
Asheville, North Carolina Interim Chair and Program Director, Department of Orthodontics and
Chapter 6 Management of Acute Postoperative Pain Dentofacial Orthopedics
University of Pittsburgh School of Dental Medicine
Craig M. Misch, DDS, MDS Pittsburgh, Pennsylvania
Private Practice Chapter 13 Skeletal Anchorage for Orthodontics
Prosthodontics and Oral and Maxillofacial Surgery
Sarasota, Florida Joel Rosenlicht, DMD
Chapter 24 Autogenous Bone Grafting for Dental Implants Private Practice
Oral and Maxillofacial Surgery
Joseph P. Mulligan, DMD Manchester, Connecticut
Associate Clinical Professor, Department of Oral and Maxillofacial Surgery Chapter 32 Impressions at Surgical Placement and Provisionalization
Cooper Medical Center of Implants
Camden, New Jersey
Temple University Hospital
Philadelphia, Pennsylvania
Private Practice
Oral and Maxillofacial Surgery
Elkins Park, Pennsylvania
Sewell, New Jersey
Chapter 34 Radiography for Dental Implantology
xii CONTRIBUTORS

Ramon L. Ruiz, DMD, MD Muna Soltan, DDS, FAGD

Director, Pediatric Craniomaxillofacial Surgery General Practitioner
Pediatric Oral and Maxillofacial Surgery Riverside, California
Arnold Palmer Hospital for Children Chapter 26 Contemporary Sinus-Lift Subantral Surgery and Graft
Orlando, Florida
Clinical Assistant Professor, Oral and Maxillofacial Surgery Mark F. Sosovicka, DMD
University of North Carolina at Chapel Hill Assistant Professor, Department of Oral and Maxillofacial Surgery
Chapel Hill, North Carolina University of Pittsburgh School of Dental Medicine
Adjunct Instructor, Oral and Maxillofacial Surgery Pittsburgh, Pennsylvania
University of Florida Chapter 14 Lasers in Oral and Maxillofacial Surgery
Gainesville, Florida
Chapter 13 Skeletal Anchorage for Orthodontics Gaetano G. Spinnato, DMD, MD
Clinical Associate Professor, Department of Oral and Maxillofacial Surgery
James L. Rutkowski, DMD, PhD University of Medicine and Dentistry of New Jersey
Graduate School of Pharmaceutical Sciences New Jersey Dental School
Duquesne University Newark, New Jersey
Pittsburgh, Pennsylvania Chapter 12 Complications of Dentoalveolar Surgery
Private Practice
Clarion, Pennsylvania James Spivey, DMD, MS
Chapter 23 Pharmacology for Implant Dentistry Private Practice
Periodontics
Manaf Saker, DMD Portsmouth, New Hampshire
Director, Department of Oral and Maxillofacial Surgery Chapter 33 Implant Placement Immediately Following Tooth Extraction
The Valley Hospital
Ridgewood, New Jersey Joseph M. Thomas, MS
Chapter 11 Basic and Complex Exodontia and Surgical Management Department of Biology
of Impacted Teeth Clarion University of Pennsylvania
Clarion, Pennsylvania
Richard F. Scott, DDS, MS Chapter 23 Pharmacology for Implant Dentistry
Private Practice
Ann Arbor, Michigan Debra K. Udey
Chapter 20 Office Design and Ergonomics Vice President, Risk Management
Oral and Maxillofacial Surgery National Insurance Company (OMSNIC)
Bethany L. Serafin, DMD Rosemont, Illinois
Assistant Professor, Division of Oral and Maxillofacial Surgery Chapter 22 Risk Management in Oral and Maxillofacial Surgery
University of Kentucky College of Dentistry
Lexington, Kentucky Franklin T. Walker, MBA
Chapter 2 Monitoring for the Oral and Maxillofacial Surgery Patient Chief Executive Officer, Oral and Maxillofacial Surgery Associates
Chapter 4 Pharmacology of Drugs in Ambulatory Anesthesia Adjunct Instructor, University of North Carolina
School of Public Health
Dennis G. Smiler, DDS, MScD Chapel Hill, North Carolina
Private Practice Chapter 16 Oral and Maxillofacial Surgery—Office Management
Oral and Maxillofacial Surgeon
Encino, California James Ward, DMD
Chapter 26 Contemporary Sinus-Lift Subantral Surgery and Graft Chief Resident, Temple University Hospitals
Department of Oral and Maxillofacial Surgery
Brian M. Smith, DMD, MD Philadelphia, Pennsylvania
Chair, Department of Oral and Maxillofacial Surgery Cooper Medical Center
Temple University Hospitals Division of Oral and Maxillofacial Surgery
Philadelphia, Pennsylvania Camden, New Jersey
Division Chief, Division of Oral and Maxillofacial Surgery Chapter 32 Impressions at Surgical Placement and Provisionalization
Cooper Medical Center of Implants
Camden, New Jersey Chapter 34 Radiography for Dental Implantology
Chapter 30 Platelet-Rich Plasma and Bone Grafting in Implant Surgery

Jerry L. Soderstrom, DDS

Clinical Instructor, Department of Restorative Dentistry
State University of New York
Buffalo School of Dentistry
Buffalo, New York
Private Practice
Rapid City, South Dakota
Chapter 34 Radiography for Dental Implantology
 FOREWORD
The breadth and scope of this book in three volumes evokes
wonderful memories of another era for me. When I first
became head of the oral surgery residency program at our
institution in 1956, there were no guidelines, as we have
today, for the educational content or range of surgical proce-
dures to be included in the curriculum. Knowledge and pro-
cedures were usually taught at the level of practice in the
community. The most worthy surgeon and author at the time
was Kurt Thoma whose two volume second edition of Oral
Surgery, 1952,1 comprised of 10 parts that included 47 chapters
on contemporary and leading-edge oral surgery, was in every
respectable practitioner’s library. The book included fresh
information relative to everyday office needs and just enough
edgy, bold surgery, such as open reductions of fractures and
condyles, to make for engrossing reading. There was nothing
in that age to even closely rival his monumental and inspira-
tional work. I kept the table of contents of Thoma’s book
before me at all times. If a surgical procedure or treatment
method was included in the book, it became a part of the
training of our residents. It became our curriculum. And here
we have the same attractiveness in Fonseca’s, Marciani’s, and
Turvey’s book, which is eerily the same—but, contemporary,
with more authors and a far wider scope. There is no merit in
comparing the books, which are two generations apart. But
the point is, if there were a need to start a new education
program in the specialty today with nothing more than this
book as a guideline for a curriculum, and the program could
deliver education at the level and reach described in the book,
the program would be flooded with applicants.
The ambition and organization of this book—covering the
full scope of oral and maxillofacial surgery—is remarkable not
only for its huge content, but because it introduces a new
generation of knowledgeable contributors to the specialty.
The book has many known and authoritative colleagues with
respected academic affiliations who are at their best in their
writings. However, it is the new breed largely still in training
or private practice with adjunct university positions bringing
front-line experience to the pages that is exciting. We are
accustomed to thinking that new advances and scholarship
are the provenance of seasoned workers in universities and
hospitals. But it is the growing underground of dedicated,
amateur scholars still in residency or fellowship training or
early in private practice or academia who have discovered that
the joy of learning and writing is a big reward for the revela-
tions of their exciting, young work. Even though Fonseca,
Barber, Costello, Dembo, Gregg, Jensen, Smith, Marciani,
Carlson, Braun, Alpert, Dierks, Ghali, Hudson, Helman,
1
Thoma K: Oral Surgery, ed. 2, St. Louis, 1952, The C.V. Mosby Co.
Indresano, McCoy, Mercuri, Ochs, Swift, Williams, Turvey,
Waites, Epker, Frost, Guerrero, O’Ryan, Posnick, Prescious,
Reyneke, Schendel, Van Sickels, and Wolford are rightfully
big attractions of the book, be prepared for fulfillment in
reading the work of a host of fresh names, which will soon be
well known to you. The editor is commended for bringing this
nascent talent to the book.
Beyond surgery, there is a valuable and needed section of
the book devoted to practice management with expert cover-
age of the aggravations, which are a part of current practice.
These partially include office management, accreditation of
surgicenters, credentialing and hospital privileging, office
design, coding, insurance, and third party payers and risk
management. There is much to appreciate in this solid address
to the business of the specialty.
There is always more to learn in the world of oral and
maxillofacial surgery than any of us has time to achieve or do.
Today’s immense, expanding frontier of knowledge, proce-
dures, and technology pertinent to the specialty is so vast that
we now need a lifetime even to penetrate the body of scholar-
ship and skills at hand. These are reasons why an encyclopedia
of the kind compiled by Fonseca, with assistance from
Marciani and Turvey, is so comforting as an immediate all
embracing resource to what is current and important to every-
one captivated by oral and maxillofacial surgery—or even as
an emergency curriculum.
This is a big book with an ambitious scope that will appeal
to a large readership engaged in oral and maxillofacial surgery.
It is not for the person described by Beecher:
“If a man has come to that point where he is so
content that he says,
‘I do not want to know any more,
or do any more or be any more,’
he is in a state in which he ought to be changed
into a mummy.”2
No one will remotely suggest that the editor of this marvelous
book be relegated to that state. He does things—and he does
them well. He has an amazing and enviable record in the
production of excellent, multiple-authored, surgical tomes. He
has outdone himself with this one.
Robert V. Walker, DDS, FFDRSC(I), FDSRCS(E)
Professor Emeritus and Past Chairman
Division of Oral and Maxillofacial Surgery
University of Texas Southwestern Medical Center
Dallas, Texas
2
Beecher HW: in Thoughts on Leadership, The Forbes Leadership Library,
Chicago, 1995, Triumph Books, p.17.
xiii
 PREFACE
It is our privilege to present the second edition of Oral and
Maxillofacial Surgery. This multiauthored, comprehensive text
will be presented in three volumes. The first edition, published
in 2000, was well received; but 8 years later, with all the
extensive changes in techniques and technology, we felt that
a second edition was overdue. Drs. Marciani and Turvey have
been brought on board to bring together the best minds to
create a contemporary and comprehensive text. They have
recruited section editors who have worked tirelessly to ensure
that the authors submitted chapters that reflected the state of
the art in their area of responsibility.
This book is a comprehensive resource on oral and maxil-
lofacial surgery, examining the full scope of the field, includ-
ing dentoalveolar surgery, orthognathic surgery, trauma
surgery, surgical pathology, temporomandibular joint surgery,
dental implantology, cosmetic surgery, cleft and craniofacial
surgery, and reconstructive surgery. Every surgical procedure
performed by oral and maxillofacial surgeons today is covered
in detail. The set’s greatest strength is its comprehensive grasp
of the subject. This multivolume text provides solid coverage
of a wide range of issues related to surgical care, such as anes-
thesia, diagnostic imaging, treatment planning, rehabilitation,
physical therapy, and psychological considerations. We have
included additional content in diagnosis, treatment planning,
and surgical decision making. There are more than 80 new
chapters in three volumes.
Volume I covers anesthesia, dentoalveolar and implant
surgery, and office management. Although all sections have
new material, the area of implant surgery has undergone the
greatest change since the first edition was published. Dr. H.
Dexter Barber has recruited an outstanding group of contribu-
tors who present current techniques and technology related
to this discipline. Drs. John Matheson and Raymond J. Fonseca
also elicited contributions from authorities in the other sec-
tions of this volume.
Dr. Robert Marciani was in charge of editing Volume II.
He recruited Dr. Eric Carlson to oversee the section on surgi-
cal pathology and Dr. Thomas Braun to edit the section on
the temporomandibular joint. These three individuals
recruited top-notch authors who have covered their area of
responsibility comprehensively. The chapter on bisphospho-
nate related osteonecrosis of the jaws is not only timely but
informative. The diagnosis and management of facial pain is
presented in this section and complements Dr. John M.
Gregg’s chapter in Volume I on chronic maxillomandibular
pain, head and neck pain, and TMJ pain. Dr. Marciani has
assembled a variety of specialists to cover the complete gamut
of maxillofacial and head and neck trauma.
Volume III has been organized by Dr. Timothy Turvey. He
recruited Drs. Bernard J. Costello and Ramon L. Ruiz to
oversee the cleft and craniofacial sections, and Dr. Peter D.
Waite oversee the esthetic surgery section. Dr. J. Robert Scully
assisted Dr. Turvey in editing the orthognathic surgery section.
Perhaps the greatest improvement in this volume is an added
emphasis on diagnostic and treatment planning. The esthetic
surgery and cleft and craniofacial surgery sections have been
expanded in scope and depth.
After an analysis of the changing field of oral and maxillo-
facial surgery, we strove to present a comprehensive, current
book that defined the present scope of our specialty. We hope
that the reader appreciates and agrees with our efforts. We
stated in the preface of the first edition that we hoped that
our future attempts will present an even broader scope of oral
and maxillofacial surgery. The fact that this edition has suc-
ceeded in that regard is a testament to the individuals who
are constantly expanding the envelope.
xv
 ACKNOWLEDGMENTS
The second edition of Oral and Maxillofacial Surgery is a team
effort. Drs. Robert Marciani and Timothy Turvey were tire-
less in their efforts to improve on the first edition. They
brought numerous authors on board who added depth and
breadth to this edition. The section editors were equally
invaluable contributors to the success of this effort. Drs. H.
Dexter Barber, Thomas W. Braun, Eric R. Carlson, Bernard
J. Costello, John Matheson, Ramon L. Ruiz, J. Robert Scully,
and Peter D. Waite diligently pestered authors so that dead-
lines could be almost met. This edition attempts to compre-
hensively define the scope of oral and maxillofacial surgery
and could not have come to fruition without these
contributors.
Residents are the lifeblood of our specialty. Many have
contributed portions of chapters in this book. They also have
provided us with friendship, dedication, intellectual stimula-
tion, and humility, without which this book would not have
been written.
Last, we would like to thank all the staff who helped prepare
these manuscripts and the editorial staff at Elsevier, who were
so patient with our procrastination, and meticulous in their
development and editing of this book.
xvii
 SECTION I •
PREOPERATIVE EVALUATION
Amin Kazemi
To provide the ultimate in surgical care, the surgeon must be
intricately intoned with the complex risks wrought by anes-
thesia and surgery in concurrence with the patients preexist-
ing medical conditions. It is the surgeon’s responsibility to
investigate each patient’s unique risk factors and assemble the
appropriate plan to maximize surgical outcome.
Oral and maxillofacial surgeons have the unique privilege
of providing an array of various anesthetic methods. As such
we must be dually prepared to identify and deal with the risks
associated with performing the surgery and anesthesia in
concert. Therefore given this task, one must be keenly aware
of the tools available to fully evaluate the patient before a
surgical procedure. Complete and detailed history and physi-
cal examination, previous anesthetic and surgical history,
appropriate family and social history, laboratory and radio-
graphic tests, proper involvement of a specialist, prophylactic
measures, and behavioral modification each provide an invalu-
able method to prepare the patient for successful surgery.1 In
combination with complete mastery of the anesthesia and
surgical techniques, the practitioner is well prepared to deliver
a custom designed and well-planned surgical treatment.
The course of preoperative evaluation provides an oppor-
tunity for the practitioner to declare a genuine care and inter-
est for the patient, which in turn allows for further global
success and satisfaction. It allows for involvement of the
patient and their support team, thus gaining tangible insight
into the surgical procedure and obtaining realistic expecta-
tions. This can be invaluable for the patient because the
amount of satisfaction with the surgical treatment is maxi-
mized when the patient’s expectations are close to reality.
A complete immersion into the preoperative evaluation
process is conducted in this chapter to provide the reader with
a clear understanding of current methods and the reason for
their use.
■ HISTORY AND PHYSICAL
EXAMINATION
A complete history and physical examination is an integral
part of the preoperative evaluation. It is the practitioner’s first
Anesthesia and Pain Control
CHAPTER 1
opportunity to identify any abnormalities or dysfunctions that
could require further evaluation or planning before the
operative procedure. To streamline this process and allow
the patient adequate anonymity to disclose important health
information that one can then further explore, a health ques-
tionnaire is valuable. This form and also any history and
physical examinations performed by other admitting house
staff, should not in any way become the preoperative history
and physical examination required. The form should only be
used as an aid to identify the most critical risk factors and
guide one to further scrutinize them. For example, if the form
identifies a patient as an asthmatic, one needs to further
understand the extent of this dysfunction by conducting a
detailed interview with the patient regarding their disease.
(When was the diagnosis made? How often do the attacks
occur and under what circumstances? How do they control
their asthma? How often are medication(s) used? How often
do they visit the emergency department for their asthma?,
etc.)
A patient’s medication(s) can have a large effect on anes-
thesia and surgical planning. The general rule is to continue
most medications as prior; however, there are unique situa-
tions that require altered dosing, change to shorter acting
preparations, and even discontinuing the medication tempo-
rarily2 (Table 1-1). Furthermore, the patient’s current
medication(s) can require the modification of postoperative
medications used for the treatment of pain, swelling, infec-
tion, and so forth.
Allergies and reactions to medication(s) are important to
identify. It is of further importance to explore the circum-
stances and extent of such reaction (from a mild rash to an
anaphylactic reaction). The offending drugs are obviously
avoided, unless formal immunologic treatment has been per-
formed or pretreatment with antihistamines or steroids is
conducted.
A complete list of previous surgical procedures along with
the mode of anesthesia used should be obtained. Moreover,
detailed exploration of each surgical and anesthesia experi-
ence to identify any complications, effective pain control, and
1
2 SECTION I ■ Anesthesia and Pain Control

TABLE 1-1 Medications, Anesthetic Implications, and Recommendations for Preoperative Management
Medications Anesthetic Implications Recommended Management
Aminoglycosides Can potentiate nondepolarizing relaxants Monitor neuromuscular relaxants carefully
Aspirin Platelet dysfunction, bleeding potential Consider preoperative discontinuation for at least 10-14 days;
discuss with prescribing physician regarding risk of stroke,
myocardial infarction (MI), or thrombosis with discontinuation
Clonidine Acute withdrawal can cause hypertensive Continue therapy the day of surgery; can use dermal delivery
crisis; decrease anesthetic requirements perioperatively; decrease anesthetic requirements intraoperatively
Insulin Hypoglycemia if not monitored Depends on time of surgery and serum glucose range; recommend
to continue partial dose (one-half or one-third) of long-acting insulin
and delete short-acting insulin the day of surgery; monitor serum
glucose closely perioperatively; watch for combined long- and short-
acting preparations
Lithium Potentiate neuromuscular blockers, induce Monitor neuromuscular blockade carefully; obtain thyroid function
hypothyroidism in some patients; lithium tests preoperatively if indicated; monitor serum sodium and avoid
concentrations increase with decreased sodium wasting diuretics
serum sodium
Monoamine oxidase inhibitors Increased catecholamine stores; Avoid indirect-acting sympathomimetics and use reduced doses of
(isocarboxazid, pargyline, phenelzine, hepatotoxicity; rare but potentially fatal direct-acting agents; serum liver function tests if not done; avoid
tranylcypromine) reactions with opioids, especially opioids, especially meperidine; for elective surgery, request
meperidine psychiatrist to discontinue for 14-21 days unless suicide risk; less
time needed for pargyline and tranylcypromine because reversibly
bound
Warfarin Excessive intraoperative bleeding Manage with prescribing physician; withdrawal in advance;
substitute with heparin; heparin may be stopped immediately
preoperatively and restarted postoperatively
From Longnecker DE, Murphy FL: Introduction to anesthesia, vol 1, ed 9, 1997, Philadelphia WB Saunders, p 13.

patient’s social and emotional experience is invaluable. The
anesthetic plan can be fine-tuned based on such previous
experience. For example, ease or difficulty of airway intuba-
tion, reaction to anesthetic(s) used, and other detailed history
are vastly important to reduce anesthetic risks. Past surgical
dictations pertinent to the surgical procedure planned should
also be obtained and reviewed to gain insight into pitfalls and
success of previous techniques.
Identifying a family history of malignant hyperthermia,
pseudocholinesterase abnormalities, or glucose-6-phosphate
dehydrogenase (G6PD) deficiency can be lifesaving for the
patient.3 History of smoking, drug use, and alcohol abuse
should be further explored with detailed cardiovascular, pul-
monary, and hepatic evaluation. Women of child-bearing age
should be questioned in regards to the possibility of being
pregnant, and if any doubt proper testing should be
conducted.
The physical exam should both be global and targeted. An
organized evaluation including vital signs, height, weight,
airway evaluation, head and neck, cardiac, pulmonary, gastro-
intestinal (GI), renal, neurologic, musculoskeletal, and other
physical markers pertinent to the history is essential. A more
scrupulous examination of the surgical site is immensely valu-
able, to identify possible complicating factors and plan for
them.
With the above complete, the practitioner can further sub-
merge into the specific review of systems to uncover any dys-
functions that would require possible laboratory or radiographic
testing along with proper specialist consultation. Once all the
above information has been amassed, the practitioner can use
a risk stratification scheme to more globally expose the level
of risk and allow for better communication of such risks
amongst the medical staff. The American Society of Anesthe-
siologists Physical Status Classification System (ASA) has
provided a simple and effective means of communicating the
severity of patient’s illness since 1940. However, there has
been no proven direct correlation between the ASA classifica-
tion and surgical and anesthesia risk.4 Therefore certain modi-
fications have been implemented to safeguard the simplicity
of this design and yet add more true risk stratification. Such
modifications have been put forth by Natalie F. Holt et al at
the Yale University Department of Anesthesiology that take
into account the physical status modified for individual system,
surgical invasiveness and risk, anesthetic risk and complexity,
and other special “risk indicators.” This information is then
communicated in a simple integrated system to facilitate cat-
egorization and communication of large amounts of informa-
tion, highlight potentially high-risk situations, guide
perioperative planning, and provide a means by which to
analyze outcomes.5
■ SYSTEM APPROACH TO
PREOPERATIVE SURGERY
CARDIOVASCULAR
It is widespread knowledge that cardiovascular disease is
extremely common in the industrialized world. As such, car-
diovascular complications are the most common cause of
 CHAPTER 1 • Preoperative Evaluation 3

Goldman’s Criteria (Computation of the The American College of Cardiology and the American
TABLE 1-2 Heart Association (ACC/AHA) guidelines first introduced in
Cardiac Risk Index)
Criteria Points 1996, and then updated in 2002 and 2006, further enhance
HISTORY the assessment and cardiac risk evaluation of patients under-
Age >70 yr 5 going noncardiac surgery. The ACC/AHA guidelines further
Myocardial infarction <6 mo 10 take into account patients’ functional capacity and surgery
PHYSICAL EXAMINATION types to determine risk and then counsel properly based on an
S3 gallop or jugular venous distention 11 easy-to-follow flowchart10 (Figure 1-1).
Aortic valvular stenosis 3 Once the risk assessment process is complete, the practi-
ELECTROCARDIOGRAM (ECG) tioners, along with consultants (if appropriate), need to
Rhythm other than sinus or premature atrial 7 consider perioperative interventions, which can include coro-
contraction nary revascularization (bypass, percutaneous transluminal
>5 Premature ventricular contractions/min 7 coronary angioplasty), modification of anesthetic technique,
GENERAL STATUS and use of invasive monitoring.11
PO2 <60 or PCO2 >50 3
Current general recommendations regarding the optimal
K <3.0 or HCO3 <20 mEq/L 3
timing of elective surgery after a myocardial infarction (MI) is
BUN >50 or creatinine >3.0 mg/dL 3
4 to 6 weeks.12 This is mildly different than the 3-month delay
Abnormal SGOT or chronic liver disease 3
previously recommended through the evidence presented by
Bedridden 3
Tarhan et al and Steen et al.13,14 Today this decision is based
OPERATION
Intraperitoneal, intrathoracic, or aortic operation 3
on assessment of ischemic risk either by clinical or noninvasive
Emergency operation 4
studies. The infarction event is considered a major clinical
TOTAL
predictor in the context of ongoing ischemic risk.15
Possible 53 points
Recent ACC/AHA update (2006) focuses on the periop-
BUN, blood urea nitrogen; SGOT, serum glutamic-oxaloacetic transaminase. erative use of beta-blockers to reduce cardiovascular morbidity
From Goldman L et al: Multifactorial index of cardiac risk in noncardiac surgical
procedures, N Engl J Med 297:26, 1977.
and mortality in the noncardiac surgery patient. The periop-
erative risk of cardiovascular morbidity and mortality was
decreased by 67% and 55%, respectively, in patients receiving
beta-blockade in the perioperative period versus those receiv-
ing placebo.16 The general philosophy behind beta-blockade
perioperative mortality. Of the 27 million patients undergoing and aspirin use perioperatively is to reduce the effects of
surgery in the United States every year, 8 million have signifi- adrenergic surge and halt platelet activation and microvascu-
cant coronary artery disease or other cardiac comorbidities.6 lar thrombosis. The specific perioperative beta-blocker recom-
One million of these patients will go on to have perioperative mendations for each patient class (based on size of treatment
cardiac complications with substantial morbidity, mortality, effect and estimate of certainty of treatment effect) are well
and cost.6 Given these facts, meticulous assessment of the illustrated in the 2006 update and are beyond the scope of this
cardiovascular system is intensely important in determining a chapter.16
patient’s surgical candidacy, preoperative planning, and anes- Prevention of endocarditis through appropriate prophylac-
thesia planning. tic measures is a vital part of the preoperative evaluation of a
As mentioned earlier, one of the early risk stratification cardiac patient. The American Heart Association recommen-
methods was the ASA classification, which lacked accuracy dations have been illustrated in Tables 1-3, 1-4, and 1-5.17
in predicting risk and was not easily reproducible among phy- In summary, it is extremely important to have a consistent
sicians. Recent methods rely more on easily defined and mea- and reliable way to stratify cardiac risk in a noncardiac surgical
sured parameters and were enhanced by multivariate statistical patient. Furthermore the practitioner needs to be completely
methodology.7 An exemplary example is the Goldman’s cri- clear on the steps required for each patient to decrease cardiac
teria, which is reliant on multivariate analysis and assigns risk and to safely plan a surgical and anesthetic treatment.
points to easily reproducible characteristics.8 Once tallied the Appropriate and clear communication with the anesthesia
point total correlates well with the cardiac risk (Table 1-2). and cardiac specialists regarding the patient’s cardiovascular
Class I (0 to 5 points) has a 0.9% risk of serious risk will also increase the patient’s confidence before an inva-
cardiac event or death sive procedure.
Class II (6 to 12 points) has a 7.1% risk
Class III (13 to 25 points) has a 16.0% risk ■ PULMONARY
Class IV (greater than 26 points) has a 63.6% risk Postoperative lung complications are a significant source of
A major advancement in the above method of risk stratifi- overall perioperative morbidity and mortality.18 In some
cation is the inclusion of the patient’s functional capacity, review articles, pulmonary complications have proven to be
clinical signs and symptoms, and operative risk assessment to as common as or more common than cardiac complications.19
estimate overall risk and plan preoperative intervention.9 Some of the most common pulmonary problems, such as
4 SECTION I ■ Anesthesia and Pain Control

Emergency
Need for noncardiac surgery

Coronary revascularization Yes, no symptoms

OR
within 5 years

No
Yes, with
favorable results
Recent coronary evaluation

Major Clinical Predictors Intermediate Clinical Minor or No Clinical Predictors

Unstable angina, Predictors Abnormal age, abnormal
decompensated CHF, Mild angina, prior MI, ECG, rhythm other than
significant arrhythmia, compensated CHF, diabetes, sinus, HTN, stroke history,
severe valvular disease renal insufficiency poor functional capacity

Delay noncardiac Poor Moderate or good Poor Moderate or good

surgery ⱕ4 METs ⱖ4 METs ⱕ4 METs ⱖ4 METs

Medical management High risk Intermediate Low risk High risk Intermediate
risk factor modification procedure risk procedure procedure procedure risk procedure

Coronary Noninvasive OR OR Noninvasive OR

angiograph testing testing

Subsequent care Coronary Coronary

depends on treatment Angiography Angiography
results and findings

Subsequent care Subsequent care

depends on treatment depends on treatment
results and findings results and findings

FIGURE 1-1. Stepwise approach to preoperative cardiac assessment. An abbreviated list of metabolic equivalents
(METs) includes the following: 1-Take care of yourself, eat, dress, and so forth; 4-Light housework; 5-Climb a flight of
stairs or walk up a hill; 10-Strenous sports. “Procedure risks” are defined as the following: High-emergent major opera-
tions, aortic surgery, other vascular surgery, large blood loss; Intermediate-carotid, head and neck, intraperitoneal,
intrathoracic, orthopedic, or prostate surgery; Low-all others. OR, operating room; CHF, congestive heart failure; MI,
myocardial infarction; ECG, electrocardiogram.

chronic obstructive pulmonary diseases (asthma, bronchitis,
emphysema, bronchiectasis), pulmonary infections, and cystic
fibrosis, should be easily identifiable through a thorough pre-
operative history and physical examination (Table 1-6). Once
identified, the extent of the disease process needs to be revealed
through further testing and consultation with the pulmonary
specialist. Amongst the tools available to extract further tan-
gible evidence of the severity of the pulmonary disease, chest
radiograph, arterial blood gas analysis, and pulmonary func-
tion test are worth mentioning.
By obtaining such detailed information regarding the
patient’s pulmonary dysfunction, one can then properly strat-
ify the risk of perioperative pulmonary complication and make
the necessary actions to optimize results.
The pulmonary risk factors can be best illustrated by divid-
ing them into two categories: patient-related risk factors and
surgery-related risk factors.
■ PATIENT-RELATED RISK FACTORS
SMOKING
Smoking is a well-established risk factor as proven by numer-
ous studies since Morton’s pioneering work in 1944.20 Regard-
less of other pulmonary dysfunction, smoking will increase
 CHAPTER 1 • Preoperative Evaluation 5

T Cardiac Conditions Associated with the
Highest Risk of Adverse Outcome from
TABLE 1-3
Endocarditis for Which Prophylaxis with
Dental Procedures Is Recommended
Prosthetic cardiac valve
Previous IE
Congenital heart disease (CHD)*
Unrepaired cyanotic CHD, including palliative shunts and conduits
Completely repaired congenital heart defect with prosthetic material or
device, whether placed by surgery or by catheter intervention, during the
first 6 mo after the procedure†
Repaired CHD with residual defects at the site or adjacent to the site of
a prosthetic patch or prosthetic device (which inhibit endothelialization)
Cardiac transplantation recipients who develop cardiac valvulopathy
*Except for the conditions listed above, antibiotic prophylaxis is no longer
recommended for any other form of CHD.
† tract infections. One thing is clear, that enough time needs
Prophylaxis is recommended because endothelialization of prosthetic
material occurs within 6 mo after the procedure.
From Wilson W et al: Prevention of infective endocarditis. Guidelines from the
American Heart Association, 116 (15):1736-1754, 2007.
Dental Procedures for Which Endocarditis
TABLE 1-4 Prophylaxis Is Recommended for Patients in
Table 1-3
All dental procedures that involve manipulation of gingival tissue or the
periapical region of teeth or perforation of the oral mucosa*
*The following procedures and events do not need prophylaxis: routine anesthetic
injections through noninfected tissue, taking dental radiographs, placement of
removable prosthodontic or orthodontic appliances, adjustment of orthodontic
appliances, placement of orthodontic brackets, shedding of deciduous teeth, and
bleeding from trauma to the lips or oral mucosa.
From Wilson W et al: Prevention of infective endocarditis. Guidelines from the
American Heart Association, Circulation 2007.
the risk of perioperative pulmonary complications.21 The
relative risk of perioperative pulmonary complication in
smokers compared with nonsmokers range from 1.4 to 4.3.21
According to Warner et al, the previously mentioned relative
risk decreases only after 8 weeks of smoking cessation.22 It is
surprising to note that those who stopped smoking less than
8 weeks had a higher risk compared with those who continued
smoking.21 Significant effort should be made by the practitio-
ner and staff to relay such risk to the patients during the pre-
operative course and equip them with practical measures to
achieve smoking cessation.
ACUTE RESPIRATORY TRACT INFECTIONS
Different general advice has been provided regarding the post-
ponement of elective surgery in the face of acute respiratory
to be permitted to allow for the acute treatment of the infec-
tion and symptoms followed by a period of recovery of the
tracheobronchial mucosa. In general this can range from 2
weeks to 6 weeks. One must be cautious to further evaluate
the patient following respiratory tract infection recuperation
to ensure complete recovery, thus avoiding undue risk. In
cases of mild viral upper respiratory infections in adults who
are undergoing planned elective surgery of a site besides the
chest or abdomen, it is acceptable to proceed because there is
little evidence of increased risk.23
TABLE 1-6 Physical Exam Signs of Pulmonary Disease
Dyspnea Tachypnea
Decrease breath sounds Rhonchi
Wheezing Prolonged expiratory phase
Cyanosis Barrel chest

TABLE 1-5 Regimens for a Dental Procedure

Regimen: Single Dose 30 to 60 Min before Procedure
Situation Agent Adults Children
Oral Amoxicillin 2g 50 mg/kg
Unable to take oral medication Ampicillin 2 g IM or IV 50 mg/kg IM or IV
OR
Cefazolin or ceftriaxone 1 g IM or IV 50 mg/kg IM or IV
Allergic to penicillins or ampicillin—oral Cephalexin*† 2g 50 mg/kg
OR
Clindamycin 600 mg 20 mg/kg
OR
Azithromycin or clarithromycin 500 mg 15 mg/kg
Allergic to penicillins or ampicillin and unable Cefazolin or ceftriaxone† 1 g IM or IV 50 mg/kg IM or IV
to take oral medication OR
Clindamycin 600 mg IM or IV 20 mg/kg IM or IV
IM, intramuscular; IV, intravenous.
*Or other first- or second-generation oral cephalosporin in equivalent adult or pediatric dosage.
†
Cephalosporins should not be used in an individual with a history of anaphylaxis, angioedema, or urticaria with penicillins or ampicillin.
From Wilson W et al: Prevention of infective endocarditis. Guidelines from the American Heart Association, Circulation 2007.
6 SECTION I ■ Anesthesia and Pain Control

TABLE 1-7 Influence of Surgical Site on Rates of Postoperative Pulmonary Complications

Type of Surgery % of Cases with Complications (Total No. of Cases)
Study Yr Upper Abdominal Lower Abdominal Laparoscopic Cholecystectomy Thoracic All Others
Pooler 1949 19 (331) 11 (1334) 0.7 (4204)
Wightman 1968 19 (130) 6 (323) 0.6 (330)
Tarhan et al* 1973 13 (75) 7 (45) 10 (112) 3 (396)
Gracey et al† 1979 25 (57) 0 (7) 19 (21) 17 (72)
Garibaldi et al‡ 1981 17 (201) 5 (208) 40 (102)
Pedersen et al 1990 33 (419) 16 (200) 3 (6687)
Southern surgeons club 1991 0.3 (1518)
Phillips et al 1994 0.4 (841)
Brooks-Brunn 1997 28 (238) 15 (162)
*Patients had moderate-to-severe chronic obstructive pulmonary disease. Complication was defined as postoperative death.
†
Patient had chronic obstructive pulmonary disease.
‡
Complication was defined as pneumonia.

ASTHMA
Having a complete understanding of the extent and severity
of asthma in a patient is critical in their operative and anes-
thesia planning. Information, such as number of hospitaliza-
tions and emergency department visits secondary to asthma
attacks in the past 2 years, amount of inhaler usage in a day,
history of steroid and other medications used, and scenarios
that may aggravate symptoms, is vital in planning for an asth-
matic patient. It is known that well-controlled asthmatics
with peak flow greater than 80% of that predicted can proceed
to surgery with an average risk.24 Continued use of inhalers as
per patient routine (well-controlled asthmatic) all the way up
to the surgical procedure is advisable. Poorly controlled asth-
matics require immediate and aggressive treatment before
elective surgery. Such measures as stress dose steroids, avoid-
ance of anesthetics with bronchospastic potential, use of bron-
chodilating anesthetics (ketamine), and meticulous intubation
technique and planning (airway management) are important
for the practitioner to consider during the planning of surgery
and anesthetic technique.
CHRONIC OBSTRUCTIVE PULMONARY
DISEASE (COPD)
Relative risk of pulmonary complication in this disease group
ranges from 2.7 to 4.7.25 This variation is explained by the
degree of severity of the disease state in each individual. As
previously discussed, the preoperative evaluation should reveal
the extent of the dysfunction through an excellent history and
physical examination along with information obtained from
appropriate laboratory and radiographic tests and consultants.
Those with poor symptomatology, significant airflow obstruc-
tion, and poor exercise capacity require aggressive treatment
before any consideration of elective surgery. Treatment modal-
ities, such as bronchodilators, steroids, and antibiotics, along
with smoking cessation and aggressive physical therapy can
significantly reduce perioperative risk in this patient population.
OBESITY
Recent evidence suggests that there is absolutely no difference
in the risk of pulmonary complications between obese and
nonobese patients.26
AGE
Age alone, based on numerous studies, is not a factor in
increasing risk of pulmonary complications. Such complica-
tions are very much dependant on coexisting conditions rather
than age.
SURGERY-RELATED FACTORS
The most important factor in determining the risk of pulmo-
nary complication is the site of surgery27 (Table 1-7). The risk
increases as the incision site approaches the diaphragm.
Therefore thoracic and upper abdominal surgery ranks highest
in postoperative pulmonary complications. Complications are
rare in operations outside the thoracic and abdominal
cavities.
Another surgical factor is the duration of surgery. Opera-
tions greater than 4 hours are associated with increased risk
of pulmonary complications.
Even though the evidence is not conclusive, it is well
appreciated that general anesthesia carries a higher risk
than epidural or regional anesthesia when considering
pulmonary complications. Within the general anesthesia
group, the use of long-acting muscle relaxants (pancuronium)
should be avoided when possible in those with risk of
pulmonary complication. The use of short-acting muscle
relaxants will allow for decreased hypoventilation
postoperatively.28
In summary, pulmonary complications are a significant
hazard that require careful attention during the preoperative
evaluation. Certain well-known risk-reduction strategies
should be used during the perioperative course to maximize
outcome (Table 1-8).

TABLE 1-8 Risk-Reduction Strategies
PREOPERATIVE
Encourage cessation of cigarette smoking for at least 8 wk.
Treat airflow obstruction in patients with COPD and asthma.
Administer antibiotics and delay surgery if respiratory infection is present.
Begin patient education regarding lung-expansion maneuvers.
INTRAOPERATIVE
Limit duration of surgery to less than 3 hr.
Use spinal or regional anesthesia.
Avoid use of pancuronium.
POSTOPERATIVE
Use deep-breathing exercises or incentive spirometry.
Use continuous positive airway pressure.
Avoid excessive analgesia (opioids).
Etiology and Signs/Symptoms of Renal
TABLE 1-9
Dysfunction
Etiology Signs/Symptoms
Hypertension, diabetes mellitus, Polyuria, polydipsia, fatigue, dyspnea,
nephrolithiasis, glomerulonephritis dysuria, hematuria, oliguria or anuria
polycystic disease, lupus, peripheral edema, easy bruising
polyarteritis nodosa, Goodpasture’s
disease, trauma, previous surgical or
anesthetic insult
■ RENAL
The preoperative identification of renal disease, which affects
approximately 5% of the adult population, is imperative.
Renal dysfunction has very important multiorgan ramifica-
tions that should not be ignored. The goal of one’s evaluation
should be to identify the dysfunction, its severity, and the
extent to which it compromises the cardiovascular, circula-
tory, hematologic, and metabolic systems.
In this process, it is essential to be familiar with the main
causes of renal dysfunction and to have clear knowledge of its
signs and symptoms (Table 1-9).
Avoidance of elective surgery in a patient with acute geni-
tourinary tract infection is essential because the potential for
urosepsis becomes very viable with transient immunosuppres-
sion associated with general anesthesia.29 If such a situation
arises, the procedure is deferred while the patient is treated
with appropriate antibiotics with a possible urology consulta-
tion based on the severity of the infection.
Appropriate laboratory testing of the patient with renal
dysfunction to identify the extent of the disease along with
other end-organ damage could include ECG, chest radio-
graph, electrolyte panel, complete blood count, coagulation
studies, bleeding time, and urinalysis.
Nephrology, anesthesia, and cardiology consults should be
reserved for more severe renal dysfunctions with end-organ
effects.
CHAPTER 1 • Preoperative Evaluation 7
END-STAGE RENAL FAILURE
As eluded to previously, these patients provide a unique chal-
lenge secondary to multiorgan compromise caused by their
renal failure. Such problems as anemia, coagulopathy, cardio-
vascular insufficiency and arrhythmias, altered drug clearance,
increased potential for infection, demineralization of bone,
blunted sympathetic response, and chronic metabolic acidosis
are part of the immense challenge of preoperative planning
for an end-stage renal disease patient.30
Having a clear understanding of the effects of renal failure
on other organ systems allows one to effectively evaluate these
systems to gain a better understanding of the extent of their
compromise31 (Table 1-10). Once this comprehension is
achieved, proper planning to maximize operative outcome can
be instituted32 (Table 1-11).
It is of value to mention that this patient population is at
increased risk of carrying blood-borne pathogens; thus, the
usual strict universal precautions should be observed.
In summary those with renal dysfunction present a very
unique and exigent dilemma that requires meticulous work-up
and planning. The multitude of variables that enter the picture
with end-stage renal failure patients may necessitates cohesive
collaboration with nephrology and anesthesia specialists for
appropriate and careful perioperative management.
■ GASTROINTESTINAL
Identification of certain specific signs and symptoms during a
thorough history and physical examination is our first insight
into the GI dysfunction. Noteworthy among such signs and
symptoms are dyspepsia, abdominal pain, nausea, vomiting,
diarrhea, hematochezia, steatorrhea, pruritus, fatigue, and
melena. As important are the significant indicators of hepatic
disease, such as history of hepatotoxic treatment, jaundice,
history of blood transfusion, hepatomegaly, splenomegaly,
ascites, asterixis, encephalopathy, icterus, spider angioma, and
delirium.
Recognition of these signs and symptoms warrants further
investigation to determine the specific disease process and the
extent of such process. This can be accomplished through
further testing (Table 1-12) and possible involvement of a GI
specialist (endoscopy, liver biopsy, and radiographic
examination).
Careful integration of the above information along with
the input of the consultants allows the patient to have a
comprehensive preoperative plan in place to maximize the
patient’s surgical outcome. Ignoring such GI dysfunction can
lead to many generalized complications: poor wound healing,
excessive bleeding, cardiovascular demise secondary to
decreased peripheral vascular resistance, fluid and electrolyte
imbalance, severe anemia, medication toxicity, and possible
aspiration pneumonia with possible adult respiratory distress
syndrome.15
GASTROINTESTINAL REFLUX DISEASE (GERD)
GERD is an extremely common disease process confronted by
surgeons on a daily basis. Those with well-controlled GERD
8 SECTION I ■ Anesthesia and Pain Control

TABLE 1-10 Physiologic Disorders of Renal Failure That Affect Preoperative Management
Disorder Consequence
CARDIOVASCULAR
Increased rennin secretion Hypertension
Increased cardiac output, as a result of anemia High-output failure
Left ventricular hypertrophy Myocardial Infarction
AV shunt for dialysis High-output renal failure
Volume overload or deficiencies following dialysis CHF or hypovolemic hypotension
Associated diabetes > accelerated atherosclerosis Myocardial infarction, stroke
Renal: Failure to excrete potassium Progressive hyperkalemia
7 mEq/L: Tall peaked T waves
8 mEq/L: Prolonged PR interval, QRS widening
9 mEq/L: P wave disappears, QRS widens further
Renal: Failure to excrete fixed acid Progressive acidemia
Renal: Water excretion
Failure to excrete water (oliguria or anuria) Volume overload, pulmonary edema
Failure to concentrate urine Fasting dehydration, hypotension, salt wasting
PULMONARY
Pulmonary calcification Decreased diffusing capacity
Diaphragmatic elevation with peritoneal dialysis Decreased functional residual capacity, restriction
NERVOUS SYSTEM
Uremic toxemia Mental slowing, fatigue, seizures, myoclonus, coma
Sensory peripheral neuropathy Lower extremity numbness
Dysautonomia Orthostatic hypotension, gastroparesis
GASTROINTESTINAL
Increased volume and acidity of gastric contents Increased risk of aspiration pneumonia
Ulcers Gastrointestinal bleeding
Anorexia, nausea, vomiting
HEMATOLOGIC
Erythropoietin secretion decreased Anemia
Decreased red cell life span Anemia
Dialyzable toxins impair platelet aggregation Platelet dysfunction
IMMUNE SYSTEM
Uremia impairs leukocyte chemotaxis Infection, sepsis
Steroid treatment
Loss of immunoglobulin
PHARMACOKINETICS
Diminished excretion of water-soluble drugs and metabolites Accumulation of active metabolites of morphine, Demerol, benzodiazepines
Hypoalbuminemia Increased free fraction of drugs bound to albumin
Acidosis Drugs with acid pKa are less ionized, have greater volumes of distribution and longer
Impaired function of blood-brain barrier half-lives
Accentuated effects of drugs with central nervous system effects
From Longnecker DE, Murphy FL: Introduction to anesthesia, vol 1, ed 9, 1997, WB Saunders, p 316.

require continuation of medications preoperatively, preopera- PEPTIC ULCER DISEASE

tive fasting (nothing by mouth (NPO) 6 to 8 hours before
surgery), and careful anesthesia planning to prevent aspira-
tion. However, their preoperative evaluation is not signifi-
cantly different than those without the disease. In a poorly
controlled GERD patient, elective procedures should be
avoided until the disease is under control. However, if the
need for emergent surgery arises, the following precautions are
of great value to prevent significant risk:
1. Preanesthesia H2 blockers
2. Rapid sequence intubation with cricoid pressure
3. Postoperative/preextubation gastric suction with naso-
gastric tube
Peptic ulcer disease is characterized with periodic exacerbation
and remission caused by an imbalance between the digestive
(acids, pepsin) and protective factors.32 The symptomatology
of affected patients is extremely variable, ranging from clear-cut
symptoms to those with vague symptoms with significant ulcers.
Pain is the main clinical identifier of peptic ulcer disease.
As mentioned above, however, asymptomatic ulcers can also
unfortunately develop (from nonsteroidal antiinflammatory
treatment usually).33 Therefore conclusive diagnosis can be
reached with direct inspection of the mucosa using an endo-
scope (gold standard—allows for biopsy) or via radiographic
means with contrast agents.32

TABLE 1-11 Preoperative Management of Renal Failure
Considerations
ANEMIA
Hgb ≥8 g/dL chronic
Hgb <8 g/dL (physiologic changes)
COAGULOPATHY
Uremic platelet dysfunction
HYPERKALEMIA
>5.5-6.0 mEq/L
INFECTION
Malnutrition
Functional abnormality of neutrophils, monocytes, and
macrophages
Symptomatic hypocalcemia
Hyperphosphatemia
Anesthetic and medication clearance
Hypervolemia or hypovolemia
Avoid nephrotic agents
Common Laboratory Testing for GI
TABLE 1-12
Dysfunction
Hematocrit Bilirubin
Platelet count Serum proteins
Electrolytes Serum aminotransferase
Creatinine/blood urea nitrogen Alkaline phosphatase
Partial thromboplastin time/prothrombin time Lactate dehydrogenase
Viral hepatitis screen
Those undergoing nonrelated surgery who suffer from
peptic ulcer disease can be categorized into four groups and
treated appropriately before surgery.32
1. Acute ulcer, requiring emergent surgery:
a. Immediate administration of antiulcer regimen (H2
blockers, proton pump inhibitors).
b. Operations with profound risk of hypotension, sepsis,
uremia, and respiratory failure are associated with
increased incidence of ulcer complication.
c. Nonsteroidal antiinflammatory drugs (NSAID) and
steroids should be avoided.
2. Active ulcer, requiring elective surgery:
a. Postpone surgery until ulcer has healed.
3. Chronic or recurrent ulcer, requiring surgery:
a. H2 blocker or proton pump inhibitor treatment during
and after surgery until return to baseline status.
b. Discontinue any NSAID 7 to 10 days before.
4. History of peptic ulcer disease, asymptomatic at the time
of surgery:
a. The procedure at hand dictates preoperative actions.34
b. Use above therapeutic measures if frequent recurrence
secondary to previous surgical stress.
CHAPTER 1 • Preoperative Evaluation 9
Management
No treatment
Further evaluation and possible transfusion
Dialysis 24 hr before and possibly 24 hr postoperatively
Desmopressin or cryoprecipitate can be considered
Dialysis
GI reduction (Kayexalate)
Intracellular shift (insulin/glucose)
Cardiac membrane stability (bicarbonate)
Antibiotic prophylaxis
Aseptic technique
Replace calcium
Phosphate binding antacids
Adjust doses based on renal creatinine clearance
Dialysis, consider invasive monitoring if CHF
Nonsteroidal antiinflammatory, aminoglycosides, contrast dye, chemotherapeutic agents
INFLAMMATORY BOWEL DISEASE (IBD)
Crohn’s disease and ulcerative colitis (UC) are two nonspe-
cific inflammatory disorders of the GI tract that are often
jointly included under the umbrella of IBD.35 Both disorders
unfortunately require multiple diagnostic explorations and
surgical therapies. Of absolute importance in patients afflicted
with these disorders is to first identify Crohn’s versus UC,
next discover the extent of distribution of the disease, and
lastly the amount of the corticosteroid use should be
determined. This then allows the practitioner to plan for
optimal nutritional supplementation and support, stress dose
steroid treatment perioperatively, and meticulous wound
management.36
HEPATIC DISORDERS
This subgroup may include various disease processes (viral,
drug, toxic) with a common pathway. As with other diseases,
the extent of the functional impairment must first be clearly
explored. Through a detailed history and physical examina-
tion, evidence to substantiate hepatic dysfunction can be
amassed. This is then supplemented and substantiated by
further evidence extracted from the hepatic-specific labora-
tory tests and expert consultation and evaluation. Risk strati-
fication is pursued next, based on the Child-Pugh scoring
system37 (Table 1-13). Proper preoperative planning is then
implemented based on the above information to prevent spe-
cific risks37 (Figure 1-2).
To further comprehend hepatic dysfunction, it is important
to discuss some of the main pathophysiologic changes that can
directly affect the course of a procedure.
10 SECTION I ■ Anesthesia and Pain Control

TABLE 1-13 Child-Pugh Scoring System

Points
1 2 3
Encephalopathy None Stage I or II Stage III or IV
Ascites Absent Slight (controlled with diuretics) Moderate despite diuretic treatment
Bilirubin (mg/dL) <2 2-3 >3
Albumin (g/L) >3.5 2.8-3.5 <2.8
PT (prolonged seconds) <4 4-6 >6
INR <1.7 1.7-2.3 >2.3
PT, prothrombin time; INR, international normalized ratio.
Class A = 5-6 points; Class B = 7-9 points; Class C = 10-15 points.

History, examination, and

laboratory studies
indicating liver
dysfunction

Asymptomatic lab Acute liver Chronic liver

abnormalities disease disease

Elective Emergency Acute Fulminant Cirrhosis Noncirrhotic

procedure life-threatening hepatitis hepatic failure
indication

Class C Class B Class A

Investigate Proceed with Elective
prior to extreme caution procedure
surgery Close perioperative
monitoring advised

Proceed with Proceed

caution if with
necessary surgery
Defer if
possible

Consider Consider
candidacy for alternatives
transplantation to surgery

FIGURE 1-2. Approach to the patient with liver disease. (Adapted from Patel T: Surgery in the patient with liver
disease, Mayo Clin Proc 74:593-599, 1999. In Townsend: Sabiston textbook of surgery, ed 17, 2004, Saunders. An
imprint of Elsevier.)

ALTERED CARDIOPULMONARY FUNCTION Maintaining effective arterial oxygenation is an enormous

Patients with severe liver disease have increased cardiac
output and reduced systemic vascular resistance. Ironically the
intravascular volume and perfusion of such organs as the liver
and the kidneys is inadequate.38 This pathophysiologic phe-
nomena makes these patients extremely intolerant to hypo-
volemia and cardiac depressant medications.39
obstacle in a severe liver disease patient during an operation.
The intrapulmonary arteriovenous shunting, increased inter-
stitial lung fluid, restrictive lung disease (as a result of ascites
and pleural effusion), and prevalence of tobacco use in this
population all play grand roles in chronic hypoxemia of the
liver disease patient.40

TABLE 1-14 Drug Metabolism Altered by Cirrhosis
Diazepam
Midazolam
Demerol
Morphine
Beta-Blockers
Lidocaine
Cimetidine
ALTERED DRUG METABOLISM AND
PHARMACOKINETICS
Prolonged drug action secondary to slow metabolism of many
hepatically metabolized medications requires careful and
attentive dosing. Liver disease affects metabolism of medica-
tions through diminished phase I and II biotransformation.
Moreover, reduced first-pass metabolism secondary to porto-
systemic shunts allows orally administered drugs to be further
available for absorption. Hypoalbuminemia allows for increased
availability of albumin-bound medications. Such conditions
as ascites and edema, lead to an increase in the extracellular
fluid volume thus diminishing the effects of certain water-
soluble medications. As with albumin-bound medications,
drugs bound to gamma globulin also are more available sec-
ondary to hypogammaglobulinemia.38 It is critical to be aware
of or have easy reference to the medications that fall into
this category, especially those commonly used in anesthesia
(Table 1-14).
ALTERED CLOTTING FUNCTION
Because the liver is the primary manufacturer of clotting
factors II, VII, IX, and X, any alteration in the factors produc-
tion can lead to significant coagulation abnormality. Defi-
ciency of the above vitamin K–dependant factors is associated
with dysfunction of bile secretion.38 Platelet quantity and
quality is also affected in liver disease because the hypersplen-
ism following portal hypertension sequesters up to 90% of
platelets (usually 30% are in spleen). Anemia secondary to
poor transport of iron, serum proteins, and vitamin B12 is
another manifestation of liver disease.38 The extent of these
dysfunctions needs to be identified through laboratory studies
and proper perioperative treatment with blood component
therapy, such as platelets, fresh frozen plasma, cryoprecipitate,
or vitamin K. This will aid to maximize outcome in these
patients.
ALTERED RENAL AND GI FUNCTION
Malnutrition is extremely common in a cirrhotic patient sec-
ondary to malabsorption and inanition. This has multiple
manifestations with poor wound healing being pertinent to
this chapter. As a result of poor renal blood flow, there is a
significant impairment in excretion of salt and water, leading
to various degrees of ascites and edema. It is therefore unam-
biguous as to why careful fluid, electrolyte, and nutritional
management are absolutely critical in patients with such
CHAPTER 1 • Preoperative Evaluation 11
affliction. This can be accomplished together with renal and
GI specialists.
ALTERED NERVOUS SYSTEM
Perioperative attention to mental status is important, espe-
cially in the face of severe hepatic dysfunction. The accumula-
tion of circulatory toxins, impairment in blood-brain barrier,
and intracranial hypertension can lead to such symptoms
as asterixis, somnolence, obtundation, and coma (hepatic
encephalopathy).38 Cirrhotic patients are most susceptible to
serum ammonia level increases as a result of poor urea
synthesis.
Delirium tremens can be devastating in an operative
patient. Therefore proper prophylaxis with oxazepam or loraz-
epam is necessary in liver disease patients with a significant
alcohol abuse history. Furthermore the chronic alcoholic
population also requires nutritional and vitamin (thiamine
and folate) supplementation.32
■ ENDOCRINE
Endocrine diseases can include common and familiar pro-
cesses, such as diabetes mellitus, to more unusual and rare
disorders, such as carcinoid syndrome. Regardless, this cate-
gory includes some very complex conditions that could have
grave effects on the outcome of a procedure if not planned for
properly. The preoperative evaluation should focus on identi-
fying the extent and type of the endocrine dysfunction and
then place in safeguards to optimize outcome. Careful aware-
ness to and monitoring of metabolic stress related to inade-
quate endocrine control should be the prime goal during the
perioperative course.
■ DIABETES MELLITUS
Diabetes is commonly characterized as either insulin-depen-
dant (type I or juvenile-onset) or non–insulin-dependant
(type II). A surgical procedure can drastically affect carbohy-
drate metabolism; as such it presents a unique risk for the
diabetic patient. More than 10 million people in the United
States suffer from diabetes, and more than half will require
surgery at some point in their lives.32 Approximately 20% of
all diabetics are diagnosed during the preoperative evalua-
tion.32 This diagnosis is confirmed through fasting blood
glucose of greater than 120 mg/dL and a 2-hour glucose toler-
ance test level of 140 mg/dL. The most important aspect of
the preoperative evaluation of the diabetic patient is to iden-
tify the extent of their disease, how well is their blood glucose
being monitored and controlled, and any end-organ disease
process that may be present. Preoperative measurement of
hemoglobin A1C concentration allows caregivers to assess the
level of glycemic control over the past several months. Hemo-
globin A1C values of 7% to 9% indicate good control, whereas
values greater than 12% suggest poor control of glucose
levels.41 It is essential to identify these end-organ diseases,
considering they pose further risk for the patient undergoing
a surgical procedure (Table 1-15). A study by Haffner et al42
found that for patients who have diabetes and a history of
12 SECTION I ■ Anesthesia and Pain Control
End-Organ Diseases Associated
TABLE 1-15
with Diabetes
Occlusive vascular disease Neuropathy
Cholelithiasis Gastroparesis
Ophthalmic disease Infection
Renal disease
coronary artery disease, the risk of developing a myocardial
infarction was equivalent to that of nondiabetic patients who
had a prior myocardial infarction.
Among these end-organ dysfunctions, cardiovascular
disease is especially noteworthy. Cardiovascular events are the
major cause of perioperative mortality in the diabetic
patient.43
A major effect of poorly controlled diabetes on surgery is
infection (most common postoperative complication), sec-
ondary to deleterious effects of hyperglycemia on leukocyte
function, impaired chemotaxis and decreased phagocytosis by
polymorphonuclear leukocytes.32 Autonomic neuropathy
places the patient at increased risk of cardiac arrest. Presence
of gastroparesis increases the risk of aspiration. Renal disease
can complicate fluid and electrolyte management.
Effects of surgery on diabetes are due to the stress response
to the surgical event. This translates itself into a surge of
coregulatory hormones (glucagon, cortisol, catecholamines,
and growth hormone), which is magnified in a diabetic patient
secondary to limited insulin availability or effect. This hor-
monal mismatch leads to severe hyperglycemia and at times
ketoacidosis.32
Care of the surgical patient with diabetes differs based on
the type of diabetes. However, few precautions relate to both
groups, such as surgery being scheduled early in the morning
and coordinated effort by surgeon, anesthesiologist, and inter-
nist or endocrinologist to control the blood glucose levels and
prevent above mentioned risks.
TYPE I DIABETES
The following preoperative recommendations are commonly
instituted:
1. Have the patient discontinue long-acting insulin
(Ultralente) the day before surgery.
2. Have the patient take half of the dose of intermediate-
acting insulin (NPH or Lente) the morning of the
procedure.
3. During the operation use a standard 5% to 10% dextrose
infusion.
4. Use a short-acting insulin or an insulin drip during the
surgery to control the blood glucose levels.
The perioperative goal is to maintain the patient’s blood
glucose levels between 100 to 200 mg/dL with a short-acting
insulin preparation during the procedure and with sliding-
scale insulin postoperatively with frequent blood glucose level
checks.
TYPE II DIABETES
Patients with type II diabetes who are on a shorter acting
sulfonylureas (tolbutamide, tolazamide, acetohexamide, and
glipizide) should have the dose held the day of surgery. Those
on longer acting agents (chlorpropamide and glyburide)
should have the dose held the day before surgery. If periopera-
tive insulin is required, it should be given using a sliding scale
with 5% to 10% dextrose infusion running.44
In summary, the essential goals in diabetes mellitus patients
are to prevent hyperglycemia or hypoglycemia. Furthermore
close attention should be focused on fluid and electrolyte
management, wound care, and cardiovascular monitoring in
high-risk individuals.
■ THYROID
The regulatory effects of thyroid hormones on multiple organ
systems distinguishes thyroid dysfunctions as an extremely
important condition to evaluate and plan for preoperatively.
Furthermore, the significance of thyroid hormones on drug
metabolism should be factored into dose adjustment of anes-
thesia and perioperative medications given.
Thyroid dysfunctions, regardless of cause, manifest into two
clinical scenarios: hypothyroidism or hyperthyroidism. It is
important to be aware of the distinctions that make each
condition unique45 (Table 1-16).
HYPERTHYROIDISM
The objective with patients afflicted with this dysfunction is
to avoid and prevent tachyarrhythmias and life-threatening
thyroid storm.32 In case of elective surgery, patient should be
made euthyroid. This is usually achieved with propylthioura-
cil, methimazole, or iodide treatment.45 Clinical response may
take up to 8 weeks. In case of an emergent procedure, beta-
blockers, such as propranolol, are the mainstay of treatment
(avoid in congestive heart failure [CHF] or patients with bron-
chospasm).45 The diagnosis of thyroid storm is a clinical one,
which relies on such characteristics as hyperthermia, vomit-
ing, hypertension, tachycardia, altered mental status, and
impending vascular collapse.46 This fatal condition is mainly
observed in undiagnosed or poorly managed or those with
initiation of stress response by a concomitant illness. Once
diagnosed immediate attention with beta-blockers, iodide,
antithyroid drugs, and glucocorticoids is essential.47 Further-
more the use of salicylates should be avoided as they will dis-
place T4 from binding proteins.46
HYPOTHYROIDISM
Studies clearly do not provide any evidence that patients with
mild to moderate hypothyroidism are at a higher risk of anes-
thetic complication during an operative procedure.45 However,
with that in mind, it is advisable to postpone elective surgery
until rendered euthyroid.
Myxedema coma is a true surgical and medical emergency
that requires immediate and aggressive treatment, second-
ary to a high degree of mortality. Patients afflicted with
 CHAPTER 1 • Preoperative Evaluation 13

TABLE 1-16 Distinguishing Factors of Hyperthyroidism and Hypothyroidism

System Hypothyroidism Hyperthyroidism
General Fatigue, cold intolerance, coarse/dry skin Weight loss, heat intolerance, warm/moist skin, increased
appetite, proptosis
Neurologic Myxedema coma, cognitive impairment Tremor, nervousness, hyperactive reflexes
Cardiovascular Bradycardia, decreased cardiac output, decreased stroke Tachycardia, atrial fibrillation, CHF, increased stroke volume,
volume, atrioventricular conduction defects, pericardial widened pulse pressure, mitral valve prolapse/insufficiency
effusion, orthostatic hypotension, prolonged QRS,
arrhythmias
Pulmonary Decreased alveolar ventilation (blunt response to anoxia Dyspnea, increased carbon dioxide production, decreased
and hypercarbia), pleural effusion vital capacity, increased oxygen consumption
Renal Decreased glomerular filtration rate, decreased plasma Polyuria, hypomagnesemia, hypercalcemia and hypercalciuria
volume, decreased creatine clearance, peripheral edema,
hyponatremia
Gi Delayed gastric emptying, GI bleeding, constipation Hypermotility, diarrhea
Hematology Anemia, platelet hyperaggregability, factor VIII and IX
deficiency
Musculoskeletal Myopathies, increase of creatinine kinase can produce Myopathies, protein wasting, bone resorption
renal failure
Etiology Idiopathic atrophy, Hashmoto’s thyroiditis, subtotal Grave’s disease, toxic multinodular goiter
thyroidectomy
Confirmatory laboratory tests Decreased T3 (triiodothyronine) Increased T4 (levothyroxine)
Decreased T3 resin uptake Increased T3 resin uptake (RU)
Increased thyroid stimulating hormone (TSH) (unless cause Increased T3 RU/T4
from hypothalamic or pituitary dysfunction) Decreased TSH
Increased thyroxine-binding globulin (TBG) Decreased TBG

myxedema coma will demonstrate stupor, hypothermia,
hypoventilation, hypoglycemia, hyponatremia, and hypoten-
sion.48 Treatment with l-thyroxine given intravenously, glu-
cocorticoids, necessary ventilatory support, and temperature
control are appropriate based on the extent of the
condition.48
■ ADRENOCORTICAL
INSUFFICIENCY
Patients undergoing a surgical procedure rely on an adequate
adrenal reserve to sufficiently deal with the stress associated
with the surgery. There are three groups of adrenal cortical
steroids produced: glucocorticoids (cortisol), mineralocorti-
coids (aldosterone), and androgenic or estrogenic hormones.
GLUCOCORTICOID DEFICIENCY
Cortisol, as the primary glucocorticoid in humans, plays the
role of potentiating the effects of other hormones especially
catecholamines. The hypothalamic-pituitary-adrenal axis,
which is influenced by an intricate loop of negative feedback
signals, controls the amount of cortisol secreted. Idiopathic
(autoimmune) and the withdrawal of chronic steroid use are
the most common reasons for glucocorticoid deficiency32
(Table 1-17).
The importance of understanding the effects of glucocorti-
coid deficiency lies in the cardiovascular changes that can
take place perioperatively. Such changes as hypotension and
decreased cardiac output despite fluid therapy are significant
alterations in physiology that have to be treated. Proper steroid
TABLE 1-17 Causes of Glucocorticoid Deficiency
Withdrawal of glucocorticoid medications Inborn errors of metabolism
Idiopathic (presumably autoimmune) Fungal infections
Tuberculosis Metastatic cancer
AIDS Pituitary disease
Lymphoma Cytotoxic agents
Enzyme inhibitors
replacement therapy and adequate perioperative stress dose
steroid treatment are essential in the perioperative course.
Furthermore the possible use of vasoconstrictors and inotropic
agents are permissible.45
Although the use of stress dose steroids in patients under-
going surgery who have consumed greater than 5 mg of pred-
nisone (or equivalent) per day for more than 2 weeks in the
past year is controversial, this author believes that the ill
effects of not taking this precaution significantly outweigh its
use. Refinements in steroid replacement in the perioperative
period have been introduced by Salem et al in patients with
primary glucocorticoid deficiency.49 Such recommendations
have been illustrated in Table 1-18.49
CUSHING’S SYNDROME
Cushing’s syndrome exemplifies any state characterized by
increased glucocorticoid effect. The most common cause of
this syndrome is exogenous glucocorticoid administration.
14 SECTION I ■ Anesthesia and Pain Control
Recommendations for Perioperative
TABLE 1-18 Glucocorticoid Supplements in Patients
Believed to Have Adrenocorticoid Deficiency
Level of Stress Recommendation
(Hydrocortisone Equivalent/Day)
Minor surgical stress (third molar 25 mg × 1 day
extraction, genioplasty, etc.)
Moderate surgical stress (double 50-75 mg × 2 days
jaw surgery, panfacial fractures, etc.)
Major surgical stress (large head 100-150 mg × 2-3 days
and neck resection and
reconstruction, etc.)
TABLE 1-19 Signs and Symptoms of Pheochromocytoma
Hypertension Orthostasis
Tachycardia Diaphoresis
Headaches Anxiety
Pallor Sense of doom
Palpitations Trembling
Constipation Mild abdominal pain
Common signs and symptoms include obesity, facial plethora,
hirsutism, menstrual irregularities, hypertension, proximal
muscle weakness, back pain, skin striae, euphoria, and psycho-
sis.32 The two screening tests for Cushing’s syndrome are the
1 mg overnight dexamethasone suppression of serum cortisol
and/or measurement of a 24-hour urinary free cortisol level.32
Patients with this disease have higher incidences of hyperten-
sion, cardiovascular disease, diabetes, thromboembolism,
delayed wound healing, and increased susceptibility to infec-
tion.45 These factors should be very present in one’s mind as
the Cushing’s patient is taken through the surgical process.
PHEOCHROMOCYTOMA
Although pheochromocytomas are not a common medical
or surgical problem, they present a unique and potentially
devastating risk to the afflicted patient undergoing a surgical
procedure. Pheochromocytomas arise from chromaffin cells of
the neural crest that migrate to form the adult adrenal medulla
and sympathetic ganglion.32 Incidence of pheochromocyto-
mas are increased in neuroectodermal dysphasias, such as
tuberous sclerosis, Sturge-Weber syndrome, von Recklinghau-
sen’s disease, and in multiple endocrine neoplasia type IIA
and IIB.32 A great degree of variety in signs and symptoms of
pheochromocytomas exists (Table 1-19).
The diagnosis of pheochromocytomas is reached by docu-
menting the excess secretion of catecholamines measured in
blood and/or urine. The usual screening test is 24-hour mea-
surement of urinary metanephrines, vanillylmandelic acid,
and catecholamines.32 In patients diagnosed with this dysfunc-
tion, the preoperative treatment begins with phenoxybenza-
mine (long-acting alpha-blocker) or prazosin at least 10 days
Laboratory Studies to Help Identify
TABLE 1-20
Hematologic Dysfunction
CBC (mean corpuscular volume)
Reticulocytes
Serum iron
Total iron-binding capacity
Ferritin
Vitamin B12
Folate
Platelet function analyzer (PFA-100)
before essential surgery. A beta-blocker is added only after
the establishment of alpha-blockade to prevent unopposed
beta-mediated vasoconstriction.50 Elective surgery should be
avoided in this patient population until the tumor is identified
and properly treated and full recovery has been confirmed by
the endocrinologist.
■ HEMATOLOGY
The hematologic assessment relies heavily on excellent explo-
ration of previous surgical history, anticoagulant medications
being used, family history, and general history of easy bruising
or excessive bleeding. When these indicators of hematologic
dysfunction have been identified, the extent of severity is
made tangible with appropriate laboratory tests that can
include CBC, PT, PTT, bleeding time, or fibrin split products.
With this information as one’s initial arsenal and with the
possible guidance of a hematology specialist, the proper peri-
operative planning can be instituted.
ANEMIA
Anemia is the most common laboratory abnormality encoun-
tered in preoperative patients. It is defined as a hemoglobin
concentration of less than 14 g/dL in males and 12.3 g/dL in
females.32 On the history and physical examinations, such
vague symptoms as malaise, dyspnea, palpitation, pallor, and
cyanosis, can be confronted. Physical examination should
also focus on identifying any lymphadenopathy, hepatomegaly
or splenomegaly, and rectal and pelvic exams should be
performed for presence of blood. To truly understand the
cause of anemia, proper laboratory tests should be conducted
(Table 1-20).
The information from the above laboratory results can help
identify the specific anemia. Algorithms, such as the ones
illustrated in Figure 1-3, can aid one in further narrowing the
diagnosis of the specific anemia.32
Once the anemia is properly diagnosed, the proper treat-
ment can be instituted to correct or reverse the disease process.
This may often require the assistance of a hematologist. The
decision to transfuse a patient preoperatively depends on two
important factors. First the estimated blood loss for the surgi-
cal procedure proposed and then the consideration of the
underlying risk factors for ischemic heart disease.51 Those with
 CHAPTER 1 • Preoperative Evaluation 15

RETICULOCYTE COUNT
⬍2% ⬎2%

Exclude blood
Decreased loss Increased indirect
production Bilirubin
Increased LDH
Decreased
Haptoglobins
Hemoglobinemia
Hemoglobinuria

HEMOLYSIS

Diagnosis

Iron deficiency
⬍80 Anemia of chronic disease
Mircrocytic Thalassemia
Sideroblastic anemia

Acute blood loss

Anemia of chronic disease
80-94 Renal failure
MCV
Normocytic Myelophthistic
Leukemia/aplasptic
Hypothyroidism

Vitamin B12 deficiency

Folic acid deficiency
⬎94
Liver disease
Macrocytic
Erythroleukemia
Hypothyroidism

FIGURE 1-3. Evaluation of anemia begins with a reticulocyte count to determine whether the primary cause is one
of decreased production or increased loss. Blood loss must always be excluded as a source first. LDH, lactic
dehydrogenase.

normovolemic anemia and low cardiac risk undergoing a pro-

cedure with small anticipated blood loss can be managed Approximate Complication Rates for
TABLE 1-21
Homologous Red Blood Cell Transfusion
safely without transfusion with many healthy patients tolerat-
ing hemoglobin levels of 6 or 7 g/dL.51 Levels between 6 to IMMUNE REACTION
10 g/dL will be based more on the surgical specifics and clini- Alloimmunization 1 in 100 to 1 in 5
cal picture. Those with levels greater than 10 g/dL rarely Hemolytic transfusion reaction 1 in 6000
require a transfusion.51 Before transfusion of a patient, con- Fatal transfusion reaction 1 in 100,000
sider these factors: informed consent documenting the risk of Febrile reaction 1 in 100 to 1 in 50
infection, alloimmunization, volume overload, and immediate INFECTION
and delayed transfusion reactions32 (see Table 1-21). Human immunodeficiency virus 1 in 106 to 1 in 40,000
Hepatitis B 1 in 300 to 1in 200
SICKLE CELL SYNDROMES Hepatitis C (non-A, non-B) <1 in 100
Sickle cell anemia is far more common than all other hemo-
globinopathies. Approximately 10% of all African-Americans
living in the United States carry the gene for sickle cell
anemia.1
16 SECTION I ■ Anesthesia and Pain Control
The heterozygous state (sickle cell trait) creates very few
surgical or anesthesia risks. The homozygous state (sickle cell
disease), on the other hand, is of significant importance when
planning a surgical procedure.32 This variation occurs as a
result of a genetic mutation substituting a valine for glutamic
acid in the sixth position of the beta chain of the hemoglobin
molecule.32 The resulting alteration in the shape of the eryth-
rocyte when the hemoglobin is deoxygenated can lead to
anemia, chronic hemolysis, and vascular occlusion.32 The pro-
pensity for sickling directly relates to the quantity of hemo-
globin S (measured by standard hemoglobin electrophoresis
and protein densitometry scanner) available.32 Multiple end-
organ damage can result from these vaso-occlusive events.
Perioperative management is focused on excellent oxygen-
ation, hydration, and keeping hemoglobin S levels below 30%
to 50% while keeping normal hemoglobin A levels greater
than 8 to 10 g/dL.52
ABNORMAL BLEEDING
On every surgeon’s mind before performing an invasive pro-
cedure is the risk for abnormal bleeding because this can have
devastating effects on outcome. The comprehension of the
normal hemostatic mechanism allows one to predict and
prevent abnormal bleeding. The exploration of this mecha-
nism in any detail is beyond the current scope. Such signs and
symptoms as easy bruising, excessive bleeding with previous
surgery or trauma, history of hematuria, hematochezia, melena,
hemarthroses, or muscle hematoma should initialize further
evaluation. Physical exam signs of petechiae, purpura, ecchy-
moses, and mucosal bleeding are also clues that require
exploration. With appropriate laboratory testing, such as
CBC, bleeding time, and liver function tests, one can begin
to identify the bleeding dysfunction as a platelet disorder
(quantitative or qualitative) or a coagulation disorder (inher-
ited or acquired).
THROMBOCYTOPENIA
Thrombocytopenia is a quantitative platelet disorder, where
there is increased platelet destruction, decreased platelet
production, or abnormal distribution and/or increased
sequestration. By far the most common cause of thrombocy-
topenia is immunologic, where autoantibodies destroy exist-
ing platelets. This disorder could be present in concert with
other autoimmune disorders (lupus, autoimmune hemolytic
anemia), human immune deficiency virus, and chronic
lymphocytic leukemia.32 These patients are best treated
preoperatively with either splenectomy, corticosteroids, or
immunoglobulin.32
Another cause of decreased platelet levels is decreased pro-
duction as a result of a lack of sufficient megakaryocytes32
(Table 1-22).
The last major cause of decreased platelet count is increased
splenic sequestration. Normally, only one third of all the cir-
culatory platelets are sequestered by the spleen. In those with
splenomegaly, up to 80% to 90% of the circulatory platelets
are sequestered by the spleen.53
Reasons for Suppression of Megakaryocyte
TABLE 1-22
Proliferation
Medications Chloramphenicol, phenylbutazone,
parenteral gold, alcohol, thiazide diuretics,
sulfa drugs
Cytotoxic chemotherapy and
radiation
Infections Hepatitis
Bone marrow infiltration Leukemic or lymphomatous infiltrates,
fibrosis, granulomas, metastatic cancer
Nutritional Vitamin B12 or folate deficiency
In the last two disease processes, which are nonimmune
dysfunctions, platelet transfusion should be considered in
counts less than 50,000 /uL or if significant blood loss is
expected. A single platelet concentrate usually yields an incre-
mental rise in platelet levels of 10,000 /uL/m2.32 A platelet
count should be obtained approximately 1 hour after the
appropriate transfusion amount is administered to confirm
the desired estimate preoperatively.32 In general a patient
with a platelet count of 60,000 to 100,000 /uL or greater can
tolerate most routine surgeries. Considering that platelet sur-
vival postoperatively is affected by fever, infection, or bleed-
ing, close monitoring of platelet levels followed by proper
supplementation is essential.
COAGULATION DISORDER
Hemophilia
The most commonly inherited clotting factor defect is hemo-
philia A (factor VIII deficiency). Hemophilia B (factor IX
deficiency) is much less frequent; however, it shares in the
X-linked pattern of inheritance with hemophilia A.53 As such
these inherited dysfunctions are restricted primarily to males.
Those with mild hemophilia A can at times be successfully
treated with deamino d-arginine vasopressin (DDAVP),
which increases the level of factor VIII. Those with more
severe disease are best benefited with supplementation with
highly purified factor VIII or factor IX. Factor VIII is given
with an initial loading dose of 50 units/kg, followed by 25
units/kg every 12 hours to reach the minimum factor VIII
level of 30%.53 Factor IX is dosed at 100 units/kg loading dose
followed by 25 units/kg every 12 hours to maintain a minimum
level of 25% to 30%.53 For minor surgery, a greater than 50%
level of factor VIII or factor IX would be sufficient. Whereas
in major procedures, an 80% to 100% level of factor VIII or
factor IX is required.53
Von Willebrand’s Disease
This disease is an autosomal dominant inherited hemorrhagic
disorder with highly variable clinical presentation from severe
bleeding disorder to a mere laboratory abnormality. The von
Willebrand’s factor is designed to bind to platelet glycoprotein
Ib to allow for adherence of the platelet to subendothelial
 CHAPTER 1 • Preoperative Evaluation 17

TABLE 1-23 Perioperative Management of Patients on Chronic Oral Anticoagulation Therapy

Clinical Situation Suggested Anticoagulation Management
Low bleeding risk in surgery (dental, cataract, skin) Reduce dose of OAT to achieve INR ≈2
Low thrombotic risk: aortic valve prosthesis without other Stop OAT 4 nights before surgery
thrombotic risk factors* or AF with low stroke risk or VTE
>3 mo previously
Safe to operate when INR ≤1.4
Restart OAT on evening of surgery
Use prophylactic perioperative UFH/LMWH if indicated (depends on type of surgery)
Moderate thrombotic risk: mitral or multiple prostheses or Stop OAT 4 days before surgery
aortic prosthesis with risk factors for thrombosis or AF at high
stroke risk or VTE within past 3 mo
Begin IV UFH† when INR <2.0 (target aPTT = 2 to 3 × control)
Stop heparin 5 hr before surgery
Begin UFH prophylaxis and OAT as soon as possible postoperatively; continue heparin until
INR has been therapeutic for >48 hr
AF, atrial fibrillation; aPTT, activated partial thromboplastin time; LMWH, low-molecular-weight heparin; OAT, oral anticoagulant therapy; UFH, unfractionated heparin; VTE, venous
thromboembolism.
Adapted from Kaboli P, Henderson MC, White RH: DVT prophylaxis and anticoagulation in the surgical patient, Med Clin North Am 87:77-110, 2003. In Hoffman: Hematology:
basic principles and practice, ed 4, 2005, Churchill Livingstone, An imprint of Elsevier.
*Risk factors include caged-ball or single tilting disk valve; atrial fibrillation; history of stroke, TIA, or other embolic event; left ventricular failure; and underlying hypercoagulable
state, including cancer.
†
LMWH at full treatment doses may also be used for “bridging,” although an FDA warning about their use in patients with mechanical valve prostheses was issued in 2002.

surface proteins.32 An abnormal bleeding time is most common

and time tested laboratory examination to identify a defect in
platelet adhesion. A ristocetin cofactor assay directly relays
the activity of von Willebrand’s factor because it will only
agglutinate with platelets with properly functioning von Wil-
lebrand’s factor.53 Because factor VIII and von Willebrand’s
factor share an intimate association in circulating blood, factor
VIII levels are often found to be deficient in these patients.
The clinical identifiers of this disease are typically related to
recurrent mucosal bleeding (e.g., epistaxis, bruising, and GI
bleeding). The efficient and appropriate treatment of these
patients is reliant on the level of the disease that they suffer
from. Those with the most common form of the disease are
sufficiently treated with DDAVP at a dosage of 0.3 μg/kg
infused over 30 minutes.53 Careful postoperative clinical
assessment is required to determine further treatment. Humate-
P is an excellent source of von Willebrand’s factor in those
with a more severe dysfunction or those undergoing a more
invasive procedure with a high risk of bleeding.53 Platelet
transfusion should also be kept in mind during the periopera-
tive course as a source of possible treatment.
Chronic Oral Anticoagulant Therapy
More and more, patients on anticoagulation therapy are con-
fronted in a clinical and surgical setting. It is extremely critical
that these medications (warfarin, Plavix, etc.) are managed
properly preoperatively (Table 1-23). Failure to do so can
have a catastrophic outcome.54
■ NEUROLOGY
As with other systems, exploration during the preoperative
evaluation of the neurologic dysfunctions require detailed
history and physical, followed by proper laboratory and radio-
graphic studies and specialist advice to correctly stratify the
risks for surgery and plan to minimize such risks and maximize
outcome. However, there is a major lack of literature support
in this area owing to little change in preoperative manage-
ment of those with common neurologic dysfunction and those
without. The distinction is revealed in such disease processes
as neuromuscular conditions (e.g., myasthenia gravis), seizure
disorders, large vessel occlusive disease, and rare neurologic
inflictions.
MYASTHENIA GRAVIS
The cause of myasthenia gravis is an autoimmune attack on
the acetylcholine receptors of the postsynaptic (muscle) mem-
brane of the neuromuscular junction. As such, clinical fea-
tures, such as fluctuating weakness and fatigue in extraocular
muscles and eyelids (leading to diplopia and ptosis), weakness
of the limbs, and most critical respiratory muscle weakness.55
In the face of these devastating muscle weaknesses, the deep
tendon reflexes and sensation remain normal. Even though
these signs and symptoms are rather distinct for myasthenia
gravis, the confirmatory test, such as the edrophonium test,
electrodiagnostic studies, or acetylcholine receptor-antibody
level, is often performed.55 Many effective treatments are
18 SECTION I ■ Anesthesia and Pain Control
TABLE 1-24 Causes of Myasthenic Crisis
Infection
Medications Aminoglycosides, zuinine, magnesium,
neuromuscular blockers, antiarrhythmic agents
Thyroid malfunction
Hypokalemia
available for myasthenia gravis: acetylcholine esterase inhibi-
tors (pyridostigmine), immunosuppression with prednisone,
azathioprine, and/or thymectomy.55 The major preventive
focus during the perioperative period is to prevent a myas-
thenic crisis56 (Table 1-24). Such crisis is characterized by a
progressive respiratory or bulbar weakness, which will then
necessitate intubation and ventilatory support.56
Besides correcting and avoiding these causes, the most
effective treatment options for a myasthenic crisis is plasma
exchange or intravenous γ-globulin (400 mg/kg daily for 5
days).56 Only a well-controlled myasthenia gravis patient
should be subjected to elective surgery. Even then careful
respiratory evaluation and anesthesia planning followed post-
operatively with meticulous pulmonary toilet, pain control,
electrolyte level monitoring, avoidance of infection, and med-
ications that can instigate an exacerbation is critical.
SEIZURES
More than usual, a detailed history in these individuals plays
an important role. Having a tangible knowledge of the nature,
frequency, cause, and current medications and recent blood
concentration of those medications is of great value. If sub-
therapeutic levels of antiepileptic medications are discovered,
these levels can be adjusted to therapeutic range in 24 to 48
hours with proper loading dose. Although unexpected recur-
rence of seizures does not usually occur, the patient should be
continued on their medication throughout the perioperative
course. Furthermore as oral and maxillofacial surgeons per-
forming anesthesia, we should be extremely familiar with
anesthetics promoting convulsion and those preventing it57
(Table 1-25).
LARGE VESSEL OCCLUSIVE DISEASE
The risk of stroke should be assessed carefully in all patients
especially the elderly before the commencement of a surgical
procedure. Such factors as previous history of stroke or myo-
cardial infarction, hypertension, peripheral vascular disease,
coronary artery disease, and detection of a carotid bruit should
trigger alarms in one’s head to pursue further preoperative
evaluation. Obviously elective procedures should be post-
poned if the risk of stroke is significant and the proper
treatment has not been instituted to decrease such risk
(anticoagulation, carotid endarterectomy, etc.). However, in
those who have had a stroke greater than 3 months prior and
have had proper management to decrease the risk of a repeat
event, elective surgery with caution and involvement of the
primary physician or neurologist is advisable.
Proconvulsant and Anticonvulsant Effects of
TABLE 1-25
Anesthetic Drugs
Proconvulsants Methohexital (complex partial seizure only)
Etomidate
Enflurane (in greater concentrations with
hypocapnia)
Meperidine
Ketamine
Local anesthetic (rapidly increasing blood levels)
Laudanosine
Questionable Fentanyl (myoclonic activity; minimal evidence
for convulsive activity in humans)
Anticonvulsants Barbiturates
Benzodiazepines
Propofol
Halothane
Isoflurane
Local anesthetics (intravenous infusion)
OTHER NEUROLOGIC DISORDERS
Mention of such dysfunctions as Parkinson’s disease and mul-
tiple sclerosis (MS) is important in this setting. These patients
have unique challenges that warrant careful preoperative
attention.
In Parkinson’s patients, such obstacles as excessive saliva-
tion and bronchial secretions, gastroesophageal reflux, obstruc-
tive and central sleep apnea, and autonomic insufficiency
create difficulties in airway and blood pressure management
in the perioperative period.56 Special care should be focused
on thorough suctioning of the posterior oropharynx to prevent
accumulation of saliva. Patient’s dopaminergic drugs should
be continued up to the surgery to prevent the potentially fatal
dopamine withdrawal syndrome (neuroleptic malignant syn-
drome).32 Dopamine antagonists, certain narcotics (fentanyl,
meperidine), and certain antihypertensives should be strictly
avoided in these patients. The spotlight of the preoperative
testing centers on pulmonary function and autonomic stabil-
ity, as such the involvement of specialists can be of great
value.
Patients suffering with MS depending on the extent of
their dysfunction can have significant respiratory and bulbar
function compromise. Furthermore in certain patients with
severe contracture, positioning on and transfer to and from
the operating table could create a unique challenge. Preopera-
tive evaluation should also confirm the MS patient is infec-
tion free because pyrexia can exacerbate the conduction block
in demyelinated neurons.1
■ IMMUNOLOGIC
The goal of the preoperative evaluation and treatment in
these patients is the same regardless of the cause of the com-
promise in the immune system. Whether the immune suppres-
sion is caused by antineoplastic drugs in cancer patients or
immunosuppressive therapy in transplant or autoimmune
patients or the result of advanced disease in patients with
acquired immunodeficiency syndrome, the immunologic
 CHAPTER 1 • Preoperative Evaluation 19

TABLE 1-26 Consensus Recommendations for Preoperative Screening Tests

Test Age Procedure Type Disease or Condition
Electrocardiogram Male >40-49 yr Cardiovascular Cardiovascular disease
Female >50-55 yr Hypertension
Diabetes
Pulmonary disease
CNS disease
Radiation therapy
Chest radiograph >60 yr Thoracic Pulmonary disease
Upper abdominal Cardiac disease
Malignancy
Smoking ≥20 pack-year
Radiation therapy
High risk for tuberculosis (immigrants)
Hemoglobin Neonates Procedure with >500 mL blood loss suspected Malignancy
Female all age Renal disease
Male ≥65 Smoking ≥20 pack-year
Anticoagulant use
Known anemia
White blood cell count Fever
Suspected infection
Leukemia
Radiation therapy
CNS disease
Platelet count Suspected bleeding disorder
PT/PTT Suspected bleeding disorder
Anticoagulant treatment
Liver disease
Malignancy (leukemia)
Electrolytes >50 yr Major surgery Major organ system disease
Renal disease
Diabetes
Diuretic use
Digoxin use
Steroid use
CNS disease
Cr/BUN >50 yr Major surgery Cardiovascular disease
Renal disease
Diabetes
Diuretics
Digoxin
CNS disease
Glucose Diabetes
Corticosteroid therapy
CNS disease
Urinalysis Genitourinary Renal disease (relative)
Use of bladder catheter or other infection risks Infection
Pregnancy (qualitative HCG) Women of child-bearing age for whom pregnancy
status is uncertain

function must be optimized and precautions against life-
threatening infections taken before surgery.15
Evaluation should center on the extent of the immune
suppression and nutritional deficiency through a complete
history and physical examination, evaluation of medications
being used, focused laboratory studies, and consultation with
specialists. Based on this information, proper perioperative
nutritional supplementation, immune enhancement, and
antibiotic prophylaxis plans must be instituted. Monitoring
wound healing postoperatively is also critical because those
who have consumed steroids within 3 days of surgery have a
reduced degree of wound inflammation, epithelialization, and
collagen synthesis.58
■ PREOPERATIVE TESTING
In the past 2 decades, there have been numerous studies scru-
tinizing the value of routine preoperative testing and cost
efficacy. Although a certain consensus has been reached, there
is still much room for subjective decision. The purpose of such
testing is twofold: one to quantify existing disease and second
20 SECTION I ■ Anesthesia and Pain Control
to identify new conditions suspected through a thorough
history and physical examination. To use such tests as adjunct
to health maintenance or in the hope of precluding malprac-
tice is both cost prohibitive and inefficient.
The following tests are commonly considered to be the
more usual preoperative tests in patients:
1. Complete blood count
2. Platelet count
3. Electrolyte levels
4. Creatinine and blood urea nitrogen levels (Cr/BUN)
5. Measurement of the prothrombin and partial thromboplas-
tin time (PT/PTT)
6. Urinalysis
7. Electrocardiography
8. Chest radiograph
9. Pulmonary function testing
One conclusion has been made repeatedly by all research-
ers: a healthy patient under the age of 40 does not require any
laboratory testing preoperatively unless the procedure dictates
otherwise (e.g., if severe blood loss is expected a type and
screen, CBC, and possible coagulation studies are warranted).
A general guideline has been provided (Table 1-26) to show-
case when a particular preoperative test is advisable. Please
refer to this table with prudence because it is only indicative
of the most common scenarios.
■ CONSENT AND PREOPERATIVE
PREPARATION
At this point, the preoperative evaluation has been com-
pleted, risk stratification finalized, and the patient is ready to
make his or her final commitment to surgery. This matter
should not be taken lightly, not only because of the possibility
of litigation, more importantly to create a realistic and healthy
expectation of the surgical procedure and outcome. As it is
commonly known, happiness is dependant on one’s expecta-
tions matching reality. It is the clinician’s responsibility to not
only review a cohesive and complete consent form (risks and
benefits of the procedure) with the patient but to make the
information included tangible and understandable. Unique
risks and altered outcomes should be discussed. It is always
advisable to include loved ones in this process with the consent
of the patient. This is a unique chance to engage those
involved in caring for the patient and establish a genuine
caring relationship that sets all parties to attain at the least,
peace of mind.
REFERENCES
1. Cummings: Otolaryngology: head and neck surgery, ed 4, St Louis,
2005, Mosby.
2. Longnecker DE, Murphy FL: Introduction to anesthesia, vol 1, ed
9, Philadelphia, WB Saunders, 1997.
3. Longnecker DE, Murphy FL: Introduction to anesthesia, vol 1, ed
9, Philadelphia WB Saunders 1997.
4. Saklad M: Grading of patients for surgical procedures, Anesthe-
siology 2(3):281-84, 1941.
5. Holt NF, Silverman DG: Modeling perioperative risk: can
numbers speak louder than words? Anesthesiol Clin 24(3):427-59,
2006.
6. Mangano DT, Goldman L: Preoperative assessment of patients
with known or suspected coronary disease, N Engl J Med
333:1750-56, 1995.
7. Dripps RD, Lamont A, Eckenhoff JE: The role of anesthesia in
surgical mortality, JAMA 178:261-67, 1961.
8. Goldman L et al: Multifactorial index of cardiac risk in
noncardiac surgical procedures, N Engl J Med 297:845-50,
1977.
9. Lee TH et al: Derivation and prospective validation of a simple
index for prediction of cardiac risk of major noncardiac surgery,
Circulation 100:1043-49, 1999.
10. Fleischer LA et al: American College of Cardiology/American
Heart Association (ACC/AHA) guideline update on periopera-
tive cardiovascular evaluation for noncardiac surgery: a report,
Circulation 105:1257-67, 2002.
11. Eagle KA et al: Guidelines for perioperative cardiovascular eval-
uation of the noncardiac surgery. A report of the American
Heart Association /American College of Cardiology Task Force
on Assessment of Diagnostic and Therapeutic Cardiovascular
Procedures, Circulation 93:1278-317, 1996.
12. Eagle KA et al: ACC/AHA guideline update for perioperative
cardiovascular evaluation for noncardiac surgery: a report of the
American College of Cardiology/American Heart Association
Task force on Practice Guidelines (Committee to Update the
1996 Guidelines on Perioperative Cardiovascular Evaluation for
Noncardiac Surgery), Circulation 105:1257-67, 2002.
13. Tarhan S et al: Myocardial infarction after general anesthesia,
JAMA 220:1451, 1972.
14. Steen PA, Tinker JH, Tarhan S: Myocardial reinfarction after
anesthesia and surgery, JAMA 239:2566, 1978.
15. Townsend CM: Sabiston textbook of surgery, ed 17, Philadelphia,
Saunders, 2004. An imprint of Elsevier.
16. Fleisher LA et al: ACC/AHA 2006 guideline update on peri-
operative cardiovascular evaluation for noncardiac surgery:
focused update on perioperative beta-blocker therapy, J Am Coll
Cardiol 47(11):2343-56, 2006.
17. Dajani AS et al: Prevention of bacterial endocarditis. Recom-
mendations by the American Heart Association, JAMA
277:1794-801, 1997.
18. Lawrence VA et al: Risk of pulmonary complications after
elective abdominal surgery, Chest 110:744-50, 1996. In Joehl RJ:
Preoperative evaluation: pulmonary, cardiac, renal dysfunction
and comorbidities, Surg Clin North Am 85:1061-73, 2005.
19. Lawrence VA et al: Incidence and hospital stay for cardiac and
pulmonary complications after abdominal surgery, J Gen Intern
Med 10:671-8, 1995. In Smetana GW: Preoperative pulmonary
evaluation, N Engl J Med 340(12):937-44, 1999.
20. Morton JHV: Tobacco smoking and pulmonary complications
after surgery, Lancet 1:368-70, 1994.
21. Smetana GW: Preoperative pulmonary evaluation, N Engl J Med
340(12):937-44, 1999.
22. Warner MA et al: Role of preoperative cessation of smoking and
other factors in postoperative pulmonary complications: a
blinded prospective study of coronary artery bypass patients,
Mayo Clin Proc 64:609-16, 1989.
23. Longnecker DE, Murphy FL: Introduction to anesthesia, vol 1, ed
9, Philadelphia, WB Saunders, 1997.
24. Guidelines for the diagnosis and management of asthma.
National Hear, Lung, and Blood Institute, National Asthma
Education Program, expert panel report. X. special consider-
ations, J Allergy Clin Immunol 88(suppl):523-34, 1991.
25. Wait J: Southwestern Internal Medicine Conference: preopera-
tive pulmonary evaluation, Am J Med Sci 310:118-25,
1995.
26. Cartagena R: Preoperative evaluation of patients with obesity
and obstructive sleep apnea, Anesthesiol Clin North Am 23:463-
78, 2005.

27. Wong D et al: Factors associated with postoperative pulmonary
complications in patients with severe chronic obstructive pul-
monary disease, Anesth Analg 80:276-84, 1995.
28. Berg H et al: Residual neuromuscular block is a risk factor for
postoperative pulmonary complications: a prospective, random-
ized, and blinded study of postoperative pulmonary complica-
tions after atracurium, vecuronium, and pancuronium, Acta
Anaesthesiol Scand 41:1095-104, 1997. In Smetana GW: Preop-
erative pulmonary evaluation, N Engl J Med 340(12):937-44,
1999.
29. Davidson JK, Eckhardt III WF, Perese DA, editors: Clinical anes-
thesia procedures of the Massachusetts General Hospital, ed 4,
Boston, Little, Brown, 1993.
30. Joseph AJ, Cohn SL: Perioperative care of the patient with renal
failure, Med Clin North Am 87:193-210, 2003.
31. Longnecker DE, Murphy FL: Introduction to anesthesia, vol 1, ed
9, Philadelphia WB Saunders, 1997.
32. Lubin MF, Walker HK, Smith III RB: Medical management of the
surgical patient, vol 1, ed 3, Philadelphia, JB Lippincott, 1992.
33. Soll AH, Kurata J, McGuigan JE: Ulcers, nonsteroidal anti-
inflammatory drugs and related matters, Gastroenterology 96:561,
1989.
34. Matthews JB, Tostella BJ, Silen W: Gastroduodenal hemorrhage
and perforation in the postoperative period, Surg Gynecol Obstet
167(5) 389-92, 1988. In Lubin MF, Walker HK, Smith III RB:
Medical management of the surgical patient, vol 1, ed 3, JB Lippin-
cott, 1992.
35. Friedman S: General principles of medical therapy of inflamma-
tory bowel disease, Gastroenterol Clin North Am 33(2):191-208,
2004.
36. Zenilman ME, Becker JM: Emergencies in inflammatory bowel
disease, Gastroenterol Clin North Am 80:682-9, 1985.
37. Patel T: Surgery in the patient with liver disease, Mayo Clin Proc
74:593-9, 1999. In Townsend: Sabiston textbook of surgery, ed 17,
Philadelphia, 2004, Saunders. An Imprint of Elsevier.
38. Brown BR Jr: Anesthesia in hepatic and biliary tract disease, Phila-
delphia, 1988, FA Davis. In Longnecker DE, Murphy FL: Intro-
duction to anesthesia, vol 1, ed 9, Philadelphia, WB Saunders
1997.
39. Schneider PD: Preoperative assessment of liver function, Sur
Clin North Am 84(2):355-73, 2004.
40. Longnecker DE, Murphy FL: Introduction to anesthesia, vol 1, ed
9, Philadelphia, WB Saunders 1997.
41. Jaspan JB: Monitoring and controlling the patient with non-
insulin-dependent diabetes mellitus, Metabolism 36:22-7, 1987.
42. Haffner SM: Mortality from coronary heart disease in subjects
with type 2 diabetes and in nondiabetic subjects with and
without prior myocardial infarction, N Engl J Med 339:229-34,
1998.
CHAPTER 1 • Preoperative Evaluation 21
43. Fonseca RJ: Oral and maxillofacial surgery, vol 1, ed 1, Philadel-
phia, WB Saunders 2000.
44. Gavin LA: Preoperative management of the diabetic patient,
Endocrinol Metab Clin North Am 21:457-75, 1992.
45. Connery LE: Assessment and therapy of selected endocrine dis-
orders, Anesthesiol Clin North Am 22(1):93-123, 2004.
46. Baeza A et al: Rapid preoperative preparation in hyperthyroid-
ism, Clin Endocrinol (oxf) 35:439-42, 1991.
47. Geffner DL, Hershman JM: Beta-adrenergic blockade for the
treatment of hyperthyroidism, Am J Med 93:61-8, 1992. In Lubin
MF, Walker HK, Smith III RB: Medical management of the surgical
patient, vol 1, ed 3, Philadelphia, JB Lippincott 1992.
48. Ladenson PW et al: Complications of surgery in hypothyroid
patients, Am J Med 77:261-6, 1984. In Lubin MF, Walker HK,
Smith III RB: Medical management of the surgical patient, vol 1,
ed 3, Philadelphia, JB, Lippincott 1992.
49. Salem M et al: Perioperative glucocorticoid coverage: a reassess-
ment 42 years after emergence of a problem, Ann Surg 219:416,
1994. In Longnecker DE, Murphy FL: Introduction to anesthesia,
vol 1, ed 9, Philadelphia, WB Saunders 1997.
50. Schif RL, Welsh GA: Perioperative evaluation and management
of the patient with endocrine dysfunction, Med Clin North Am
87:175-92, 2003.
51. Simon TL et al: Practice parameter for the use of red blood cell
transfusions: developed by the red blood cell administration
practice guideline development task force of the College of
American Pathologists, Arch Pathologic Lab Med 122:130-8,
1998.
52. Koshy M et al: Surgery and anesthesia in sickle cell disease:
cooperative study of sickle cell diseases, Blood 86:3676-84,
1995.
53. Hoffman R et al: Hematology: basic principles of practice, ed 4,
Philadelphia, 2005, Churchill Livingstone. An imprint of
Elsevier.
54. Kaboli P, Henderson MC, White RH: DVT prophylaxis and
anticoagulation in the surgical patient, Med Clin North Am
87:77-110, 2003. In Hoffman: Hematology: basic principles and
practice, ed 4, Philadelphia, Churchill Livingstone 2005. An
imprint of Elsevier.
55. Johns TR, Howard JF, editors: Myasthenia gravis, Semin Neurol
2:193-280, 1982.
56. Goetz CG: Textbook of clinical neurology, ed 2, Philadelphia, WB
Saunders 2003.
57. Longnecker DE, Murphy FL: Introduction to anesthesia, vol 1, ed
9, Philadelphia, WB Saunders 1997.
58. Gohh RY, Warren G: The preoperative evaluation of the trans-
planted patient for nontransplant surgery, Surg Clin North Am
86(5):1147-66, 2006.
CHAPTER 2
MONITORING FOR THE ORAL AND
MAXILLOFACIAL SURGERY PATIENT
The medical literature shows that inadequate monitoring con-
tributes significantly to anesthesia-related morbidity and mor-
tality; analyses demonstrate that most complications could
have been prevented with better monitoring.1-3 Although
errors in patient management are inevitable, the timely detec-
tion of adverse physiologic changes through monitoring can
enable practitioners to take action to prevent these errors
from harming the patient.
Monitoring during anesthesia encompasses continuous
observation and integration of all incoming information. Early
recognition of changing signs and symptoms and evaluation
of responses to therapeutic interventions enable us to provide
safe and effective patient care. Advances in technology have
made it possible to combine the information provided by
instrumental monitors with that provided by our senses so that
we can increase the safety of anesthesia delivery to our patients.
Equal in importance to the actual parameters measured is the
understanding of how monitors work, the information they
provide, and the interpretation of that information to properly
assess the patient.
Ideal monitors should be accurate, convenient, inexpen-
sive, reliable, continuous, and noninvasive. During anesthe-
sia, monitors primarily evaluate the circulatory, respiratory,
central nervous, neuromuscular, and renal systems. Monitor-
ing may be classified as either routine or specialized. This
chapter will focus on the basic routine monitoring of patients
undergoing anesthesia. The following definitions, approved by
the House of Delegates at the 2007 Annual Meeting of the
American Dental Association, explain concepts that are
important for an understanding of the basis of anesthesia
delivery to patients undergoing oral and maxillofacial surgery
in the office, outpatient, and inpatient settings.
■ DEFINITIONS
Minimal sedation: a minimally depressed level of conscious-
ness, produced by a pharmacologic method, that retains the
patient’s ability to independently and continuously maintain
an airway and respond normally to tactile stimulation and
verbal command. Although cognitive function and coordina-
tion may be modestly impaired, ventilatory and cardiovascular
functions are unaffected.
Conscious sedation: a drug-induced depression of con-
sciousness during which patients respond purposefully to verbal
22
Bethany L. Serafin • Jeffrey Dembo
commands, either alone or accompanied by light tactile stimu-
lation. No interventions are required to maintain a patent
airway, and spontaneous ventilation is adequate. Cardiovas-
cular function is usually maintained.
Deep sedation: a drug-induced depression of conscious-
ness during which patients cannot be easily aroused but
respond purposefully following repeated or painful stimula-
tion. The ability to independently maintain ventilatory
function may be impaired. Patients may require assistance in
maintaining a patent airway, and spontaneous ventilation
may be inadequate. Cardiovascular function is usually
maintained.
General anesthesia: a drug-induced loss of consciousness
during which patients are not arousable, even by painful stim-
ulation. The ability to independently maintain ventilatory
function is often impaired. Patients often require assistance
in maintaining a patent airway, and positive pressure ventila-
tion may be required because of depressed spontaneous
ventilation or drug-induced depression of neuromuscular
function. Cardiovascular function may be impaired.
Continual: repeated regularly and frequently in steady
succession.
Continuous: prolonged without any interruption at any
time.
Time-oriented anesthesia record: documentation at
appropriate time intervals of drugs, doses, and physiologic data
obtained during patient monitoring.
■ HISTORY AND EVOLUTION OF
MONITORING GUIDELINES
“Practice guidelines” are devised by a team of experts and
provide recommendations that are based on analysis of the
current literature with the goal of aiding the practitioner in
performing patient care. Such guidelines are not considered
requirements or standards of care. “Standards of care” specify
appropriate treatment protocols for a typical patient or proce-
dure but are still not hard-and-fast rules, and there may be
deviation under exceptional circumstances. “Requirements”
are obligatory codes of conduct or procedures that are deemed
mandatory by the relevant governing body. In the practice of
oral and maxillofacial surgery, most monitoring protocols are
defined either by guidelines from the specialty or from state
boards of dentistry.
 CHAPTER 2 • Monitoring for the Oral and Maxillofacial Surgery Patient
American Dental Society of Anesthesiology (ADSA) Guidelines for Intraoperative Monitoring of Patients
BOX 2-1 Undergoing Conscious Sedation, Deep Sedation, or General Anesthesia
Standard I: Qualified Personnel
Qualified personnel shall be present in the operating room during the anesthesia
period.
Objectives
1. During conscious sedation, a minimum of two qualified persons (e.g., doctor and
assistant trained to monitor appropriate physiologic parameters) should be
present.
2. Because deep sedation and general anesthesia are often indistinguishable entities
with regard to the levels of consciousness or unconsciousness, a minimum of three
qualified persons must be present during deep sedation and general anesthesia.
There should be one person whose sole responsibility is monitoring and recording
vital signs continually. This person may be classified as an anesthesia assistant,
anesthesia technician, nurse, physician, or dentist.
3. In the event of special circumstances (e.g., an emergency in another location,
radiation exposure to personnel), a modification in the number of personnel present
may be made according to the best judgment of the clinician responsible for the
patient under anesthesia. However, at no time should the monitoring of the patient
be interrupted.
Standard II: Oxygenation
During the anesthesia period, the oxygenation of the patient shall be continually evalu-
ated and ensured.
Objective
Adequate oxygen concentration must be delivered through inspired gases to be deliv-
ered to the body tissues.
Methods
Inspired gas. Fail-safe mechanisms (e.g., automatic nitrous oxide turnoff) must be
used on delivery systems before the entry of the gas mixture to the patient’s respiratory
system. If an anesthesia machine that is capable of delivering more than 80% nitrous
oxide (i.e., <20% oxygen) is used, then low-oxygen alarms and oxygen analyzers
should be used.
Blood oxygenation. The color of mucosa, skin, or blood should be evaluated on a
continual basis. In certain circumstances (e.g., deep sedation, general anesthesia),
mechanical monitors should be used to supplement clinical signs. Pulse oximetry is
strongly encouraged during deep sedation and general anesthesia, especially in pedi-
atric patients.
Standard III: Ventilation
During the anesthesia period, the ventilation of the patient shall be continually evalu-
ated. When inhalation agents other than nitrous oxide are used, continuous observation
of the patient is required.
Objective
The exchange of oxygen and carbon dioxide from the lungs must be adequately
maintained.
Data from Rosenberg MB, Campbell RL: Guidelines for intraoperative monitoring of dental patients undergoing conscious sedation, deep sedation, and general anesthesia, Oral
Surg Oral Med Pathol 71(1):2-8, Jan 1991.
The first detailed mandatory standards for monitoring
during anesthesia were the Harvard minimal intraoperative
monitoring standards. Devised in 1985, these guidelines were
created in response to anesthesia-related incidents that
were considered to have been preventable if there had been
better intraoperative monitoring. The guidelines stressed con-
tinuous monitoring of ventilation and circulation. In 1986 the
American Society of Anesthesiologists’ (ASA) committee on
standards of care developed standards for basic intraoperative
monitoring, based primarily on the Harvard standards, that
stressed quantitative versus qualitative measurements. The
ASA monitoring standards became widely accepted by the
anesthesia community. This acceptance prompted the Ameri-
23
Methods
1. During conscious sedation, clinical signs including chest excursion, auscultation of
breath sounds, and movement of the reservoir bag on the gas machine (except
when a nasal cannula is being used) should be continually monitored. Auscultation
of breath sounds can be performed by a precordial or suprasternal stethoscope.
2. During deep sedation and general anesthesia, clinical signs including chest excur-
sion, auscultation of breath sounds, and movement of the reservoir bag on the gas
machine must be continuously monitored.
3. During endotracheal anesthesia, breath sounds and chest excursion must be veri-
fied after intubation and monitored continually. The use of capnography to measure
carbon dioxide levels is encouraged.
Standard IV: Circulation
During the anesthesia period, the circulation and its related organ (e.g., heart) should
be evaluated.
Objectives
Adequate perfusion of blood must be maintained to permit the exchange of oxygen
from the blood to the tissues and carbon dioxide from the tissue to the blood.
Methods
1. When conscious sedation is being used, a blood pressure reading should be made
before its use and after its use before discharge.
2. A blood pressure device must be used to continually monitor systolic and diastolic
pressure during deep sedation, and the pulse and blood pressure should be prop-
erly recorded at regular intervals during deep sedation and general anesthesia.
3. The ECG should be used to continuously display cardiac rhythm during deep
sedation and must be used during general anesthesia throughout the anesthesia
period.
Standard V: Body Temperature
During the anesthesia period, the patient’s body temperature may need to be
evaluated.
Objective
Body temperature should be maintained at or as near to normal as possible. Certain
types of anesthetic agents are more commonly associated with excessive body tem-
perature changes. Low body temperatures, although generally less likely to develop
during dental or office-type anesthesia, may cause a delay in drug metabolism
and patient recovery. High body temperatures may cause a hypermetabolic state and
increase oxygen consumption.
Methods
1. An enteral or transcutaneous device should be readily available to monitor body
temperature during or after general anesthesia.
2. During general anesthesia, when anesthetic agents that are frequently implicated
in malignant hyperthermia (e.g., depolarizing muscle relaxants and volatile gaseous
agents) are used, monitoring body temperature continually is encouraged.
can Dental Society of Anesthesiology (ADSA) to create
detailed guidelines for intraoperative monitoring in the dental
setting. In 1991 the ADSA established its guidelines for intra-
operative monitoring of patients undergoing conscious seda-
tion, deep sedation, and general anesthesia (Box 2-1). These
guidelines applied to all nonregional dental anesthesia
care and considered sedation and delivery of anesthesia in
the dental office setting. The ADSA guidelines combined the
Harvard and ASA standards; they defined which methods of
monitoring should be continually or continuously used and
maintained a focus on oxygenation, ventilation, and circula-
tion. The intent was to unify standards throughout dentistry
and to incorporate the guidelines used within the dental
24 SECTION I ■ Anesthesia and Pain Control
specialties of periodontology, oral and maxillofacial surgery,
and pediatric dentistry. In 1995 the ASA created a task force
to develop recommendations for practioners who are not anes-
thesiologists but who perform therapeutic procedures involv-
ing moderate and deep sedation. The ASA adopted guidelines
for sedation and analgesia by nonanesthesiologists, and in
2002 the ASA task force updated these guidelines. These
practice guidelines, however, do not apply to patients receiv-
ing minimal sedation or general anesthesia.
CIRCULATORY SYSTEM MONITORING
Intraoperative monitoring of the circulatory system is
performed with continuous electrocardiography, pulse oxime-
try, and measurement of arterial blood pressure and heart
rate.
Blood Pressure Monitor
Large intraoperative swings in blood pressure can occur rapidly
and can contribute to perioperative morbidity. Particularly
alarming is rapid onset hypotension following drug adminis-
tration because it is a well-known antecedent to cardiac arrest.
During acute hypotension, myocardial wall tension decreases,
thereby decreasing oxygen demand; however, coronary artery
perfusion diminishes to an even greater extent, putting the
patient at risk of cardiac morbidity. Hypertension decreases
coronary blood flow by increasing myocardial wall tension,
thereby creating increased demand for and consumption of
oxygen. Either extreme increases the risk of cardiac ischemia
with possible adverse outcome. In addition to cardiac perfu-
sion, cerebral and renal perfusion must also be maintained if
patient morbidity is to be prevented, and these can be affected
by wide swings in blood pressure. It would be ideal to routinely
monitor blood pressure continuously to prevent hemodynamic
events; however, the most widely used method of continuous
measurement, an indwelling arterial catheter, is invasive. In
the outpatient clinic, the most common methods of blood
pressure recording are noninvasive and intermittent with
various automated methods of measurement replacing manual
methods.
In traditional sphygmomanometry, the observer detects
Korotkoff’s sounds by stethoscope upon release of a cuff-
occluded brachial artery. The pressure recording at the first
sound is referred to as the systolic blood pressure. The diastolic
pressure is recorded as the point at which the sounds cease
upon further deflation of the cuff. Several factors affect the
accuracy of measurement. The relationship between cuff size
and arm circumference is the most important determinant of
accurate blood pressure readings. In the outpatient clinic, the
most common blood pressure measuring error (84% of errors)
is miscuffing, specifically, using small cuffs on large arms.4 The
proper cuff length should be 80% of arm circumference, and
the proper cuff width, at least 40% of arm circumference.5
Undersized cuffs can cause falsely high readings, whereas over-
sized cuffs cause falsely low readings; however, because the
error caused by an oversized cuff is smaller than that caused
by an undersized cuff, a larger cuff is preferable.
The site of placement is also important. As the site of
monitor placement becomes more distal, the systolic pressure
increases while the diastolic decreases. For patients with
peripheral vascular disease, it is important to measure the
pressure as proximal as possible because peripheral sites may
give erroneously low pressure readings.
The position of the arm is a very important determinant of
blood pressure measurements. The cuff should be at the same
level as the patient’s heart; otherwise hydrostatic pressure will
create an error in the measurement. For every 10 cm above
or below the level of the heart, 7.5 mm Hg must be added or
subtracted from the reading.6 For example, if the upper arm is
below the level of the right atrium (as it is when it is hanging
down while the patient is seated), the reading will be falsely
elevated. Similarly, if the arm is above the level of the heart,
the reading will be falsely low. The reading will also be high
if isometric effects are involved, as when the patient actively
holds the arm up instead of allowing the arm to be passively
supported or if the patient is positioned so that the back is
unsupported or the legs are dangling.
Most of the automated noninvasive blood pressure moni-
tors in use today determine blood pressure measurements by
detecting a sequence of oscillations in cuff pressure using
a pressure transducer. The cuff is inflated by an air pump to a
predetermined pressure that is held while pressure pulsations
are still present in the arterial wall. These oscillations are
transmitted through the cuff to the transducer, and this pres-
sure becomes the point at which the systolic blood pressure
reading is determined. Cuff pressure increases until no pulsa-
tions (oscillations) are detected; then the cuff pressure is
released and blood starts to flow again in the occluded artery.
The pressure oscillations are once again transmitted through
the cuff, and this becomes the point for diastolic pressure deter-
mination. The monitor measures the magnitudes of these oscil-
lations and compares them against algorithms to determine
measurements for systolic, diastolic, and mean pressures.
The advantages of automated blood pressure monitors are
ease of use, safety, and freedom from operator bias; in addition,
accurate placement over an artery is not as crucial as with
traditional sphygmomanometers. The automated monitors
work when peripheral vasoconstriction is present and, unlike
traditional mercury-gravity manometers, do not need to allow
time for venous drainage to obtain accurate measurements.
They also work in very noisy environments and are not sensi-
tive to electrosurgical interference. The complications and
limitations associated with the use of automatic arterial blood
pressure monitors include the risk of compartment syndrome
and nerve palsies because of repeated inflation and device-
related failures, such as the inability of the monitor to
detect blood pressures in patients with dysrhythmias.7,8 Auto-
matic blood pressure monitors may also contribute to loss of
vigilance by the anesthetist.
Although widely used only in research, noninvasive con-
tinuous blood pressure monitors are available. One monitor,
based on a technique described in the early 1970s by Penáz,
incorporates an inflatable finger cuff with an infrared
 CHAPTER 2 • Monitoring for the Oral and Maxillofacial Surgery Patient
photoplethysmograph devised to measure the blood volume of
the finger artery under the cuff.9 With each heartbeat, the
blood volume in the digital artery increases during systole and
decreases during diastole. Because the pressure in the cuff is
kept equal to that inside the artery, the vessel wall is consid-
ered to be unloaded (i.e., its transmural pressure is zero). This
method is also known as the vascular unloading technique.
This mean arterial set-point is then maintained by small
adjustments to the cuff volume; the size of the adjustments is
determined by changes in arterial wall pressure as detected by
a computer. This principle is the basis for the beat-by-beat
measuring of blood pressure.
Another method of noninvasive continuous blood pressure
monitoring is based on arterial applanation tonometry. A
superficial artery is flattened between its supporting bone and
an externally placed transducer. The transducer senses the
pulse, the maximal pulse amplitude, and the widest pulse pres-
sure. These measurements are then calibrated to a previously
recorded oscillometric brachial artery pressure measurement,
and continuous calibration and measurement of blood pres-
sure are obtained. Early research has shown that these nonin-
vasive monitors are accurate; however, further studies are
needed to compare data with standards and to validate the use
of these monitors in the clinical setting.
Electrocardiogram
The contraction of the heart muscle is associated with electri-
cal changes. These changes, or depolarization and repolariza-
tion, can be detected at the surface of the body with skin
surface electrodes that are joined to the electrocardiograph
(ECG) by wires. This machine compares the electrical activity
in each of the electrodes and forms a picture of the heart from
different directions. This picture is displayed in a pattern (the
ECG tracing) that is characteristic from each view. This
tracing can then be used to analyze, in detail, the electrical
activity of the heart.
The ECG is used to monitor heart rate and to detect dys-
rhythmias, conduction defects, or other alterations in the
electrical activity of the myocardium, such as ischemia or
electrolyte imbalance. Standard leads I, II, and III are the most
commonly used during anesthesia and are excellent for detect-
ing dysrhythmias. Lead II allows detection of ischemia of the
inferior wall and also reveals maximal P-wave amplitude for
good detection of dysrhythmias. With the addition of lead V,
ischemia of the anterior and lateral walls of the left ventri-
cle—the common and deleterious sites of ischemia—can
be detected. Therefore a five-lead system is often used to
monitor patients undergoing general anesthesia, with which
the appearance of dysrhythmias might be anticipated. The
ECG allows us to detect myocardial changes and intervene
when normal rhythm is crucial; however, the ECG only pro-
vides information about electrical activity—it does not give
us information about the heart’s mechanical ability to pump
and maintain circulation. Therefore the ECG monitor is best
used in conjunction with the pulse oximeter for circulatory
system monitoring.
25
For detecting myocardial ischemia, the ECG monitor is
essential. Hypoxia and the release of endogenous catechol-
amine because of pain are common causes of dysrhythmias
during sedation. Myocardial ischemia resulting from hypoxia
is indicated by depression or elevation of the ST segment.
On a normal ECG tracing, the ST segment should be iso-
electric, or at the same level as the T wave and the next P
wave. If the ST segment is elevated, acute myocardial injury
or recent infarction may have occurred. The lead through
which elevation is detected indicates the part of the heart
that has been damaged. Pericarditis also causes ST elevation
and is seen in most leads because it affects the entire heart.
Horizontal ST segment depression is usually a sign of isch-
emia rather than infarction. Downsloping ST segment depres-
sion, also indicative of ischemia, may also be associated with
digoxin therapy. Horizontal and downsloping ST segment
depression is a more ominous sign of myocardial problems
than upsloping ST segment depression. T wave changes can
also signify ischemia; however, T wave inversion is also seen
with ventricular hypertrophy, bundle branch block, and
digoxin therapy. T wave inversion is normal in leads III, VR,
and V1. Electrolyte abnormalities may also be reflected in the
ECG tracing. Hypokalemia causes T wave flattening, whereas
hyperkalemia causes peaked T waves and may cause widening
of the QRS complex. Minor changes may also occur regularly
in the ST segment and the T wave; these are considered
nonspecific ST-T changes and are usually of no great signifi-
cance. Although changes in the ST segment and T wave
are not specific for ischemia, when these abnormalities are
detected during anesthesia, they should be immediately
investigated.
RESPIRATORY SYSTEM MONITORING
An inadequate airway during anesthesia contributes signifi-
cantly to morbidity and mortality. Ventilatory changes result-
ing from administered sedative medications tend to precede
cardiovascular system depression. Respiratory system monitor-
ing is an extremely important aspect of patient care during
anesthesia and involves visual methods and the use of moni-
toring devices. Auscultation of breath sounds during con-
scious and deep sedation can be performed with a precordial
or suprasternal stethoscope. Movement of the reservoir bag (if
the patient is undergoing endotracheal, or nitrous oxide/
oxygen anesthesia) and visualization of chest excursion should
be continually monitored, as should the color of the mucous
membranes. However, these observational methods alone are
not sufficient for assessing respiratory adequacy. The use of
pulse oximetry and capnography has greatly increased the
safety of anesthesia care.
Precordial/Pretracheal Stethoscope
The precordial/pretracheal stethoscope is an inexpensive yet
invaluable device for monitoring the circulatory and respira-
tory systems during anesthesia. The precordial/pretracheal
stethoscope consists of a weighted stethoscope head con-
nected via conduction tubing to a custom-molded monaural
26 SECTION I ■ Anesthesia and Pain Control
B oxygen reserves are small, a decrease in SpO2 can occur
FIGURE 2-1. A, B, The precordial/pretracheal stethoscope consists of a
weighted stethoscope head connected via conduction tubing to a custom-
molded monaural earpiece.
earpiece (Figure 2-1). Small circular disposable adhesive
patches are available for attaching the stethoscope’s head to
the skin of the chest or neck. When placed in the precordial
region, the stethoscope monitors heart and breath sounds;
when placed on the neck over the trachea, it monitors respira-
tory sounds over heart sounds (Figure 2-2). It could be argued
that using the stethoscope in the pretracheal position is ideal
for respiratory monitoring during ambulatory anesthesia for
oral surgery because the drugs we use commonly in sedation
are depressors of respiration with a much lower chance of
causing changes in cardiovascular function that would be
diagnosed through auscultation. When used in the precordial
position, the stethoscope’s head should be placed on the chest
wall between the sternal notch and the left nipple for optimal
evaluation of respiratory and heart sounds. Studies show that,
although the design of the stethoscope has been changed so
that it can electrically and selectively amplify and filter heart
and breath sounds, the use of the stethoscope in the past
decade has decreased dramatically.10,11 One limitation of the
stethoscope is that, although breath sounds may be audible,
the stethoscope cannot determine whether tidal volume is
adequate. For this reason, other monitors of oxygenation, such
as the pulse oximeter, are added.
Pulse Oximeter
Desaturation of as much as 10% frequently occurs during
outpatient oral surgical procedures involving intravenous con-
scious sedation.12,13 In as many as 53% of anesthetized patients,
FIGURE 2-2. Using the stethoscope in the pretracheal position monitors
respiratory sounds and heart sounds.
desaturation of more than 10% occurs.6 Because the body’s
quickly. Monitoring oxygenation during delivery of anesthesia
is therefore essential, and hypoxemia must be detected quickly.
Detection allows restoration of oxygenation before irrevers-
ible and potentially life-threatening events can occur. Pulse
oximetry is one of the most important advances in the clinical
monitoring of arterial oxygen saturation. Before its develop-
ment, physical assessment and arterial blood gas analysis were
used to detect hypoxemia in anesthetized patients. It is diffi-
cult to recognize cyanosis by physical examination alone until
the deoxyhemoglobin (Hb) level reaches 5g/dL, which corre-
sponds to an arterial oxygen saturation of about 67%.14 The
pulse oximeter is a sensitive continuous monitor of oxygen-
ation and therefore is an important component of our current
monitoring protocols.
Oximetry is the optical detection of oxygenated (HbO2)
and deoxygenated hemoglobin within blood. The principle
behind pulse oximetry is the tenet that the different compo-
nents of solutions (such as hemoglobins in blood) absorb
different amounts of light. By detecting and measuring the
absorbed and reflected light, we can assess oxygenation status.
Pulse oximeters emit light at two different wavelengths: one
at 660 nm, which is within the red band of the light spectrum,
and one at 940 nm, which is within the infrared light band.
Once the red (R) and infrared (IR) lights have been emitted
from an LED source, they pass through a cutaneous vascular
bed (such as the finger) and are received by a photodetector
that measures the intensity of the transmitted light at both
wavelengths. At 660 nm, HbO2 allows more red light to pass
through, whereas Hb absorbs more red light. At the 940 nm
wavelength, however, this phenomenon is reversed (i.e.,
HbO2 more infrared light than does Hb).15
The pulse oximeter circuitry filters the input from the pho-
todetector to focus only on light of alternating intensity, such
 CHAPTER 2 • Monitoring for the Oral and Maxillofacial Surgery Patient
as that which pulses through an artery. The peak of infrared
absorption/red reflection is determined to be the arterial inflow
into the capillary bed, and the R/IR ratio calculated. This is
then converted to an arterial oxygen saturation level by means
of an empiric algorithm that is based on calibration curves
derived from studies of induced hypoxemia in volunteers.
The pulse oximeter has become the standard for continu-
ous noninvasive assessment of arterial oxygen saturation,
which has even been referred to as the fifth vital sign.16 Pulse
oximetry has the advantage of being accurate. Many studies
show that the difference between saturation measurements
obtained by pulse oximetry and those obtained by arterial
blood gas analysis is insignificant when SpO2 is higher than
70%.17,18 Studies that have determined the accuracy of pulse
oximeter measurements have used a co-oximeter for compari-
son. A co-oximeter transmits four wavelengths of light through
blood and is believed to be the gold standard for detection of
in vitro saturation. Unlike pulse oximeters, however, co-
oximeters cannot provide continuous monitoring.
The pulse oximeter is a noninvasive, continuous, conve-
nient, and inexpensive tool. However, despite its ease of use,
the pulse oximeter provides us with data that can sometimes
be misinterpreted. It indicates the percentage saturation of
arterial blood (SpO2), but is not a direct measure of the partial
pressure of oxygen dissolved in blood (PaO2). The relationship
of these two is described by the oxygen dissociation curve,
but each can be affected by different factors, and therefore
the oxygen saturation will not always accurately predict the
amount of oxygen actually being delivered to tissues.
Pulse oximetry also has other limitations. There must be a
large change in partial pressure of oxygen (a fall below
75 mm Hg) before a change in saturation is sensed by the
pulse oximeter. This may be especially problematic when a
patient is receiving a high flow of supplemental oxygen.
Another limitation is that the pulse oximeter measures periph-
eral arterial blood saturation rather than central arterial blood
saturation. Because the central arterial saturation decreases
before the peripheral saturation does, the desaturation detected
by the pulse oximeter is a late sign. Because the pulse oximeter
measures saturation in peripheral arteries, its accuracy is also
affected by hypoperfusion, as is the case with cold extremities,
peripheral vascular disease, hemodynamic instability, or
extremity elevation.
Potential technical sources of error in pulse oximetry mea-
surements include interference by ambient light, motion arti-
fact, malpositioning, and sources of electromagnetic radiation,
such as cellular phones and electrocautery devices. Inherent
in the design of the machine is an additional delay in the
detection of hypoxia. The measures received by the photode-
tector are signal averaged over several seconds; thus, the pulse
oximeter may not detect hypoxemia until after a considerable
delay has occurred.
Other sources of error in pulse oximetry readings may be
patient related. Some conditions that may affect the accuracy
of pulse oximetry are several forms of dyshemoglobinemias.
In addition to reduced and oxygenated hemoglobin, blood
27
contains carboxyhemoglobin (HbCO) and methemoglobin
(MetHb). Although normally present in very small amounts,
these dyshemoglobins can influence the determination of
oxygen saturation because they do not carry oxygen but have
absorption properties similar to those of HbO2 and Hb. When
HbCO or MetHb are present in higher quantities, they inter-
fere with the absorbance ratio of reduced hemoglobin and
HbO2 and cause an inaccurate sum of Hbs, thus resulting in
inaccurate SpO2 readings. For nonsmokers HbCO levels will
be less than 2%19; for smokers HbCO levels can be 20% higher
than normal; and for patients who have been exposed to
carbon monoxide, these levels can be 40% higher than
normal.20 Because HbCO and HbO2 absorb the same amount
of 660 nm light, arterial desaturation may occur even though
the pulse oximeter maintains a falsely high reading. In one
study, SpO2 remained at 96%, although the HbCO was 44%
because of carbon monoxide poisoning.20
Normal MetHb levels are ordinarily less than 1%.6 Methe-
moglobinemia can be congenital or acquired; acquired cases
are usually due to exposure to prilocaine, benzocaine, sulfa
drugs, and nitrites.21 Because MetHb absorbs light at both
660 nm and 940 nm, the R/IR ratio is once again erroneous,
causing the calibrated saturation to read approximately 80%
to 85% depending on the percentage of MetHb present. In
short methemoglobinemia can cause persistently low satura-
tion recordings even though functional saturation is normal.
Because co-oximetry uses four wavelengths of light, it can
measure both MetHb and HbCO and can confirm that an
inaccuracy in pulse oximetry readings is due to the presence
of these dyshemoglobins. The validity of pulse oximetry mea-
surements in patients with sickle cell disease is questionable.
Some research has shown that pulse oximetry generally over-
estimates oxygen saturation but that these overestimates are
not serious enough to cause misdiagnosis of hypoxemia as
normoxemia.22 Studies have also shown that pulse oximetry
underestimates oxygenation in patients in vaso-occlusive
crisis.23
Anemia in the presence of hypoxia may also adversely
affect the accuracy of pulse oximetry measurements. Research
reveals that at a saturation below 80%, the SaO2 reading may
be falsely low for anemic patients.17,24 Studies have also shown
that Hb concentrations lower than 5 g/dL cause a falsely low
SaO2 in the presence of hypoxemia.25-27
Findings about the effect of nail polish on pulse oximetry
measurements are inconclusive.28-30 Although red nail polish
appears to have no effect on readings, green, black, and blue
polishes and artificial nails may cause lower saturation read-
ings.28,31 Onychomycosis (nail fungus) and dirt under the nail
also appear to affect measurements.32
Capnography
Understanding the analysis and measurement of carbon
dioxide in respired gases requires a definition of the compo-
nents of the process. Capnometry is the measurement of CO2
concentrations during the respiratory cycle. The capnometer
analyzes the gases and displays the readings, and capnography
28 SECTION I ■ Anesthesia and Pain Control
FIGURE 2-3. Respiratory gases are sampled from a nasal cannula. It
consists of modified nasal prongs, an O2 supply tube (large port), and CO2
sample tube (small port).
is the graphic record of the measured CO2 concentrations,
usually displayed on a monitor screen.
Carbon dioxide analyzers placed along the path of ventila-
tion detect the intensity of infrared light passing across a
stream of inhaled or exhaled gas. Respiratory gases are sampled
from a line that runs from either the endotracheal tube or a
tube connected to the oxygen tubing at the nares of a nasal
cannula and are analyzed by mass spectrometry or infrared
light to generate a waveform or capnogram (Figure 2-3). The
capnogram is often one of many other displayed parameters
on a large multipurpose monitor in the operating room;
however, there are portable battery-powered end-tidal (ET)
CO2 monitors that are used for monitoring during transport.
Of clinical significance during sedation or general anesthe-
sia are the changes in respired CO2 that may reveal the onset
of a potential complication. Evaluating end-tidal carbon
dioxide (ETCO2) levels may aid us in determining the status
of the patient’s circulatory, metabolic, and respiratory
systems.
CIRCULATION
Exhaled CO2 concentrations reflect the circulatory status
of the patient. A reduction in cardiac output or a reduction
in blood flow to and through the lungs causes a reduction in
ETCO2. An abrupt drop in ETCO2 can be the result of a
decrease in venous return caused by hypovolemia, shock, pul-
monary embolism, or cardiac arrest. Although ETCO2 is a
good indicator of circulatory function, administering high
doses of epinephrine may cause peripheral vasoconstriction,
which increases cardiac output and in turn causes an errone-
ous increase in ETCO2.
METABOLISM
Because CO2 is a byproduct of cellular metabolism, measure-
ments of CO2 output may reflect changes in respiration and
circulation or altered tissue metabolism. Increases in ETCO2
indicate increases in the metabolic rate of a mechanically
ventilated patient. Conditions, such as hyperthermia, pain,
anxiety, acidosis, intense muscle activity (seizures), and
reversal of muscle relaxants, can cause an increase in expired
CO2. Even before temperature increases, a massive increase
in CO2 production occurs in malignant hyperthermia. For
early detection of this potentially fatal condition, capnometry
is crucial. ETCO2 will decrease with hypometabolic condi-
tions, such as hypothermia, increased depth of anesthesia, and
increased muscle relaxation.
RESPIRATION
Information about a patient’s respiratory status may also be
obtained through CO2 monitoring. In an intubated patient,
changes in ETCO2 may signal inadvertent esophageal intuba-
tion, bronchial intubation, extubation, change in resistance
of the airway, obstruction, a leak in the endotracheal tube
cuff, disconnection, wearing off of the muscle relaxant, or
ventilator malfunction. The normal range of ETCO2 is 40 to
48 mm Hg, with a predictable waveform. During airway
obstruction, the ETCO2 is higher than 48 mm Hg, and the
waveform flattens. These changes occur before oxygen satura-
tion decreases. If the patient is breathing spontaneously, a
decrease in ETCO2 or the absence of waveform indicates
hypoventilation or apnea. In patients with normal cardiac and
pulmonary functions, the alveolar partial pressure of end-tidal
CO2 (PetCO2) and the arterial partial pressure of CO2 (PaCO2)
are directly proportional, unlike the measurements of partial
pressure of arterial oxygen (PaO2) and oxygen saturation,
which do not correspond linearly.
Before oxygen saturation decreases, a large decrease in arte-
rial oxygenation must ensue. Therefore, ETCO2 monitoring
may allow us to detect anesthesia-related hypoventilation
before the pulse oximeter signals a decline in oxygen satura-
tion. In fact many studies in both adults and children have
shown this to be true.33-35
Although capnography has the advantage of being a fairly
inexpensive, noninvasive adjunct for assessing a patient’s ven-
tilation, it has limitations. Its use during sedation is contro-
versial. Erroneous loss of waveform may occur because of
mechanical obstruction (condensation, secretions, or posi-
tioning) in patients who are breathing spontaneously. From
time to time, the machines go through a purge cycle to clear
the line of moisture and secretions, and the waveform is lost
during this cycle.
The Joint Commission on the Accreditation of Healthcare
Organizations (JCAHO) and the American Academy of Pedi-
atrics advocate capnography as a component of monitoring
for sedated children.36 Other authors, however, do not support
the use of capnography as a standard in monitoring during
sedation, and they argue that its use neither decreases hypoxic
events nor optimizes anesthesia care.37 Sampling via nasal
cannula or nasal hood system is considered to be an open
system that allows delivered oxygen or room air to mix with
and dilute expired air. Those who do not support routine
capnography during sedation claim that the shortcomings of
 CHAPTER 2 • Monitoring for the Oral and Maxillofacial Surgery Patient
an open system, especially in children where mouth breathing,
crying, and breath holding is commonplace, make sampling
less accurate. The use of capnography in outpatient oral and
maxillofacial surgery anesthesia will most likely be standard
of care in the near future.
TEMPERATURE MONITOR
The American Association of Oral and Maxillofacial Sur-
geons’ (AAOMS) committee on anesthesia guidelines state
that temperature should be recorded for all intubated, anes-
thetized patients and may also be recorded for patients who
are not intubated. Whenever patients are anesthetized, a
means of providing continuous temperature monitoring should
be readily available and should be used when changes in
body temperature are anticipated or suspected. While under
general anesthesia, a patient loses the normal mechanisms of
regulating body temperature. Although continuous tempera-
ture measurement in the sedated patient may not be as crucial
as measurement in a patient under general anesthesia, when-
ever a variation from normal is suspected preoperatively it
should be evaluated so that the potential negative outcomes
of hypothermia and hyperthermia, discussed later in this
section, can be prevented.
In pediatric patients, for whom the ratio of surface area to
body mass is increased, in patients who are receiving large
amounts of intravenous fluid, and in patients who are under-
going major surgery involving a body cavity, a decrease in
body temperature is anticipated. Hypothermia may lead to
adverse postoperative outcomes, such as prolonged recovery,
increased risk of wound infection, and increased cardiac mor-
bidity. As core body temperature increases, the patient’s
ability to tolerate stress decreases and the workload of the
respiratory and cardiovascular systems increases. Hyperther-
mia may signal severe physiologic disturbances, such as drug
reaction, transfusion reaction, hyperthyroidism, and malig-
nant hyperthermia. Body temperature should be monitored
continually when agents that may trigger malignant hyper-
thermia, such as volatile anesthetics and depolarizing muscle
relaxants, are used; however, even if these agents are not being
used, a means of monitoring temperature should be at least
readily available.
Temperature monitors depend on a large variation in tech-
nologies to display accurate measurements. A thermistor is a
temperature-sensing element that exhibits a large change in
resistance proportional to a small change in temperature. Its
advantages include disposable probes, sensitivity to small tem-
perature changes, accuracy, and low cost. Like the thermistor,
a thermocouple determines temperature by using an electrical
current. It consists of two wires of dissimilar metals welded
together. Its advantages are similar to those of the thermistor;
however, thermocouples do not reveal small temperature
changes as accurately as the thermistor. Both the thermistor
and the thermocouple contain a platinum wire whose electri-
cal resistance varies linearly with temperature. Like both the
thermistor and the thermocouple, the platinum wire is an
accurate, continuous, inexpensive thermometer. All of these
29
thermometers employ a probe that is sealed within a casing to
insulate it from the wet environment inside the body.
Liquid crystal thermometers use a system of organic com-
pounds that melt and recrystallize at specific temperatures.
They consist of an adhesive-backed strip that is placed on the
skin. They are a practical method of temperature monitoring
because they are inexpensive, convenient, disposable, non-
invasive, and transferable with the patient. They are, however,
less accurate than other thermometers, and their readings can
be influenced by factors in the environment, such as humidity
or the presence of a heating lamp. The infrared thermometer,
although it can be used only for intermittent measurements,
is accurate, noninvasive, and convenient. It measures the
amount of infrared radiation emitted by an object, such as
the ear canal, and converts it to a temperature recording. The
accuracy of this thermometer is somewhat technique sensitive
and depends on the degree of aim and penetration into the
ear canal.
Common sites for measurement during routine general
anesthesia are the nasopharynx, esophagus, tympanic mem-
brane, oral cavity, rectum, bladder, and trachea. Because of
the nature of oral surgical procedures, probes placed into the
nasopharynx or oral cavity can become displaced by instru-
mentation or can relay inaccurate readings because of irriga-
tion or continual disturbance. Because of tolerance issues for
patients under sedation, sites, such as skin and axilla, can be
used for measurement during procedures performed with the
patient under general anesthesia. Skin measurements are fre-
quently taken with a liquid crystal thermometer placed on the
forehead. Most of these thermometers are adjusted to reflect
core body temperature; because the forehead has good blood
flow and little subcutaneous fat, accurate measurements can
be obtained.
As is true of all monitors, temperature monitors have limi-
tations. For thermometry the limitations include incorrect
readings and potential hazards, such as monitoring site damage
from burn or perforation. Faulty probe connections, improper
probe placement, and machine failure are potential sources of
error. To prevent high readings, internal probes must be kept
dry at their connections. Burns from temperature probes acting
as a ground for an electrosurgical unit can occur, as can rectal,
tympanic membrane, and esophageal perforations caused by
temperature probes.
NEUROMUSCULAR TRANSMISSION MONITOR
Some of the primary uses of muscle relaxants during anesthe-
sia are to facilitate endotracheal intubation, eliminate patient
movement, provide relaxation of respiratory muscles, and
create a more favorable surgical environment. Different
degrees of neuromuscular blockade (NMB) may be desirable
for each of the above uses. Because of these various states of
relaxation and because patients exhibit a large variation in
response to muscle relaxants, monitoring the level of NMB is
important. The extent of NMB can be assessed by stimulating
a peripheral motor nerve via electrical current and measuring
the response of the muscles innervated by that nerve.
30 SECTION I ■ Anesthesia and Pain Control
Commonly the ulnar nerve is stimulated at the wrist with a
current of 20 to 60 mA while the presence and degree of
thumb adduction by the adductor pollicis muscle is monitored.6
The response of the facial muscles to electrical stimulation
reflects that of airway musculature and is a good indicator that
NMB is adequate for intubation. Stimulating the facial nerve
may be ideal for determining intubation readiness; however,
the response of the adductor pollicis is usually adequate.
During induction of anesthesia, the nerve stimulator is used
to determine whether the laryngeal muscles are sufficiently
relaxed to allow passage of the endotracheal tube through
open vocal cords. During maintenance of anesthesia, NMB
should be deep enough to prevent patient movement but not
so deep that postoperative respiratory support is needed. At
the end of the procedure, the nerve stimulator allows the
anesthetist to determine whether NMB is reversible and, if so,
the degree of that reversal. At this point, monitoring with a
peripheral muscle, such as the adductor pollicis, is ideal because
this muscle is one of the last to recover. Thus recovery in this
muscle will most likely indicate recovery in the respiratory
muscles.
Patterns of stimulation and response are commonly deliv-
ered as a single twitch, train-of-four (TOF), or tetanus. When
compared with control values, the results achieved by single-
twitch stimulus can be used to identify intubation readiness.
As the block progresses, the twitch response diminishes.
However, the depression of the response is the same with
depolarizing and nondepolarizing muscle relaxants. Thus the
use of single-twitch stimulus will not allow the anesthetist
to distinguish between depolarizing and nondepolarizing
blocks.
The TOF pattern of stimulation consists of four single and
equal twitches delivered over a period of about 2 seconds and
does allow differentiation of depolarizing and nondepolarizing
blocks. A depolarizing muscle relaxant will cause equal depres-
sion of the height of all four twitches. A nondepolarizing
muscle relaxant will cause progressive fading among the
twitches until deep blockade is established and the fourth
twitch is eliminated, followed by the third, and so forth. TOF
stimulation is advantageous because it requires no control
response and is a more sensitive monitor of NMB than the
single twitch.
Tetanic stimulation involves repeated single twitches,
usually on the order of 30 to 100 stimuli per second. With no
NMB, sustained contraction of the muscle is seen. With depo-
larizing drugs, the tetanic contractions are sustained but
depressed uniformly; with nondepolarizing drugs, the tetanus
is both depressed and not sustained. The advantage of tetanic
stimulation is that deeper levels of NMB may be monitored
when a single twitch or TOF fails to produce a response. The
disadvantage is that it is painful and can only be used when
the patient is anesthetized.
DEPTH OF SEDATION
Assessment of depth of sedation is necessary for providing a
good experience for the patient while maintaining patient
BOX 2-2 Ramsay Sedation Scale
1. Patient is anxious and agitated or restless, or both.
2. Patient is cooperative, oriented, and tranquil.
3. Patient responds to commands.
4. Patient is asleep but with brisk response to light glabellar tap or loud auditory
stimulus.
5. Patient is asleep with sluggish response to light glabellar tap or loud auditory
stimulus.
6. Patient is asleep with no response.
Data from Ramsay AE: Controlled sedation with alpaxalone-alphadolone, Brit Med
Assoc 2:656-659, 1974.
safety. Sustaining an adequate level of amnesia, analgesia, and
anxiolysis should be balanced with preventing respiratory
depression, laryngospasm, and cardiac problems, such as hypo-
tension and dysrhythmias.
Subjective measures (scales) include clinical scoring
systems that can evaluate a patient’s level of sedation; however,
the use of such scales requires waking or disturbing patients
repeatedly so that their level of responsiveness can be deter-
mined. These scales are easy to use and are indicated when-
ever sedative medications are given. Although many sedation
scoring systems exist, one commonly used subjective scale is
the Ramsay Sedation Scale.38 This was the first established
scale for determining arousability in sedated patients. It scores
sedation at six levels based on the patient’s ability to respond.
The requirement of response, however, means that the Ramsay
Sedation Scale cannot be used for patients undergoing NMB
(Box 2-2). Other clinical assessment tools are the Observer’s
Assessment of Alertness/Sedation Scale, the Riker Sedation-
Agitation Scale, and the Motor Activity Assessment Scale.
These scales measure the degree of alertness of patients given
sedative medications. Factors limiting the use of such scales
include their reliance on individual interpretation of defini-
tions and measurement criteria.
Bispectral Index (BIS) Monitor
Objective measurements, such as vital signs and physical char-
acteristics (e.g., constricted pupils or lid ptosis), may help
determine the depth of sedation. However, certain anesthetic
agents and muscle relaxants and patient variability may render
these objective measurements unreliable. Another objective
measurement tool, the Bispectral Index (BIS) monitor, may
aid us in accomplishing the appropriate level and effectiveness
of sedation. A 2004 study at multiple centers in the United
States found that the incidence of awareness with recall during
anesthesia ranges from one to two per 1000 patients receiving
general anesthesia.39 Four percent of the total anesthesia-
related claims reported by OMSNIC from 1988 to 2001
involved inadequate anesthesia.40 Can a BIS monitor be used
to reduce this incidence?
The BIS monitor is a relatively new, noninvasive instru-
ment used clinically to assess the depth of anesthesia. It
consists of a self-adhesive sensor placed on the patient’s fore-
head, which detects electroencephalogram (EEG) waveforms
 CHAPTER 2 • Monitoring for the Oral and Maxillofacial Surgery Patient
A level of sedation associated with some of our commonly used
B
FIGURE 2-4. A, B, The BIS monitor consists of a self-adhesive sensor
placed on the patient’s forehead, which detects EEG waveforms generated
within the patient’s cerebral cortex. These signals are transferred to a digital
signal converter and then to a monitor.
generated within the patient’s cerebral cortex. These signals
are transferred to a digital signal converter and then to a
monitor (Figure 2-4). The underlying principle is that these
waveforms change with different levels of alertness. The EEG
waveform of an awake patient typically exhibits high fre-
quency and low amplitude; however, once the patient has
been sedated, the frequency decreases and the amplitude
increases. Approximately 5000 hours of EEG recordings from
volunteers were collected to form a database.41 Various EEG
findings taken from the database of patients ranging from the
fully awake state to the fully anesthetized state were analyzed
and converted to a linear scale ranging from 0 to 100. This
scale became the BIS index. Guidelines for levels of sedation
were then established. Alert, awake patients will have a BIS
score of 90 to 100. A score of 70 to 90 represents light to
moderate sedation; a score of 60 to 70 represents deep seda-
tion; a score of 40 to 60 represents general anesthesia; a score
of 1 to 40 represents a deep hypnotic state; and a score of 0
represents the absence of cortical activity.
Use of the BIS monitor for outpatient anesthesia in the
oral and maxillofacial surgeon’s office is controversial. One
school of thought holds that the monitor is a good gauge of
31
level of sedation and may be beneficial for intravenous con-
scious sedation and deep sedation techniques. Several studies
have shown that BIS analysis allows better titration of medi-
cations and therefore decreases the time needed for recovery
and discharge after oral and maxillofacial surgical proce-
dures.42-44 However, others believe that the use of this monitor
may benefit only new, inexperienced practitioners who have
little experience in judging levels of sedation. Still others
believe that the BIS does not warn clinicians of untoward
anesthesia events and cannot predict complications, such as
hypoxemia.
The BIS monitor may not be accurate in reflecting the
drugs and combinations of drugs. Opioids have a synergistic
effect when combined with other sedative-hypnotic medica-
tions; because they reduce movements at levels that are not
associated with EEG changes, BIS analysis may not reflect the
actual level of sedation. EEG-based monitors cannot reliably
differentiate light sedation from deep sedation.38 Also, the BIS
monitor is not as accurate when ketamine is used.45 When
ketamine is added to other sedative drugs, BIS values
are higher than when ketamine is not used. When nitrous
oxide is used alone or in combination, it does not produce
much change in BIS levels even though it can induce
unconsciousness.46
Despite its promising results as a useful adjunct in monitor-
ing sedated patients, the BIS monitor may be unreliable in
determining the depth of sedation achieved by commonly
used sedative medications. Another area of controversy is the
cost-effectiveness of BIS monitors. The idea that the addi-
tional expense of the monitor is offset by a reduction in the
amounts of drugs given to achieve sedation is not supported
in the oral and maxillofacial surgery literature.47
THE ANESTHESIA RECORD
The importance of establishing a legible, comprehensive, and
concise anesthesia record is well established. Documentation
is a crucial component of anesthesia care and is the responsi-
bility of the anesthetist. Well-documented anesthesia care
should indicate the continuum of care provided to the patient
in a contemporaneous, time-oriented record. The American
Dental Association’s guidelines state that a time-oriented
record must be maintained and must include the names and
doses of all drugs given and measurements of physiologic
parameters, such as ETCO2, pulse oximetry levels, heart rate,
respiratory rate, and blood pressure.48 Anesthesia records vary
widely in the type of information they contain and the way
in which this information is entered. In some cases there is
one anesthesia record that includes the entire perioperative
period, but more commonly there are separate records for
patient monitoring during the preoperative, intraoperative,
and postoperative phases. Advances in monitoring technology
allow us greater access to data generated during the anesthetic
case; however, a basic core of information should be docu-
mented. The amount of additional information added to the
record should be guided by the type of anesthesia care
32 SECTION I ■ Anesthesia and Pain Control
TABLE 2-1 ASA Recommended Documentation to Be Included within the
Preanesthesia Evaluation Intraoperative Anesthesia
• Medical history • Patient reevaluation
• Anesthesia history • Equipment and medication check
• Medication history • Recorded vital signs
• Physical exam • Agent, dose, route and time administered
• Review of diagnostic data • Type and amounts of IV fluids
• ASA physical status • Technique(s) used
• Anesthetic plan • Unusual events during anesthesia
• Discussion of risks and benefits of plan • Status of patient at conclusion
with patient
Data from American Society of Anesthesiologists Standards, Guidelines and Statements.
delivered, the procedure performed, and patient variables.
The ASA’s standards, guidelines, and statements for docu-
mentation of anesthesia care state that the anesthesia record
should be a thorough log of the entire perioperative period
and should consist of three components: the preoperative
period, the intraoperative period, and the postoperative
period49 (Table 2-1). For conscious and deep sedation, moni-
tored variables should be recorded before the procedure, after
drug administration begins, at regular intraoperative intervals,
during initial recovery, and immediately before discharge.
The anesthesia record serves several purposes: It is a data
log, a patient management tool, and a medicolegal document.
Presently, most of the anesthesia records generated in the oral
and maxillofacial surgeon’s office are created manually. Their
utility as medicolegal documents is critically important; yet in
view of the manual record’s limitations, their accuracy can be
brought into question because manual records can be illegible,
incomplete, biased, and inaccurate. New advances in moni-
toring and record keeping allow integration of data from
various sources to form an anesthesia information system
(AIS). The AIS can provide accurate records of patient care
throughout the perioperative period.
Some monitoring systems can convert data into formats
that are compatible with a patient’s electronic medical record.
Eastman Kodak Company’s Dental Systems group and Criti-
care Systems, Inc., have developed an integrated system that
can record and store monitored parameters and then incorpo-
rate this electronic anesthesia record into the patient’s file.
Supporters of the electronic anesthesia record argue that the
record is more legible, complete, and accurate than manual
records; opponents worry that the AIS will increase exposure
to malpractice because plaintiff’s attorneys may misinterpret
recorded data or incorporate artifactual data.50
The anesthesia literature also shows that the use of an AIS
increases departmental revenue by decreasing the number
of nonbillable accounts because the percentage of illegible
or incomplete records is lower than with manual record
keeping.51,52 Published reports also suggest that anesthesia
departments that have transitioned to the electronic anesthe-
sia record find it valuable, if not essential, for risk manage-
ment.50 Whether this trend can be extrapolated into
the practice of oral and maxillofacial surgery and offset the
Anesthesia Care Record
Postanesthesia
• Patient condition on admission and discharge from recovery
area
• Vital signs and level of consciousness
• Agent, dose, route and time of medications administered
• Fluids administered
• Unusual events
• Postanesthesia visits
increased cost of integrated monitoring systems is less clear.
Although this new technology is exciting and promising, it is
beneficial only if it improves patient outcome.
MONITORING DURING RECOVERY
Hospitals and outpatient surgery centers have specific proto-
cols and guidelines for transitioning ambulatory surgery
patients from the operating room to discharge. These guide-
lines usually involve a period of recovery in the postanesthesia
care unit (PACU), the step-down unit, or both. Although
these units have a clearly defined process for safe recovery and
discharge of patients, the recovery protocol is often not so
clearly defined in the oral and maxillofacial surgeon’s office.
Necessary to the success of office-based anesthesia is the timely
recovery and release of patients who have been anesthetized.
Appropriate documentation of recovery is essential, and dis-
charge scoring systems can help facilitate discharge. Various
scoring systems have been devised; these systems are easy to
use and practical for use in the outpatient setting. The modi-
fied Aldrete scoring system assigns a numeric score of 0, 1, or
2 to the patient’s motor activity, respiration, circulation, con-
sciousness, and oxygen saturation; the maximum total score is
10. A score of 9 or higher indicates that the patient is ready
for discharge53 (Table 2-2). Another simple and commonly
used scoring system that can help determine readiness for
discharge is the Postanesthesia Discharge Scoring System
(PADSS), developed by Chung and colleagues.54 The PADSS
measures five criteria to determine a patient’s readiness for
discharge. Patients are given a score of 0, 1, or 2 for vital signs,
ambulation, pain, postoperative nausea and vomiting, and
postoperative bleeding. A patient with a score of 9 or higher
is considered ready for discharge (Table 2-3).
Discharge scoring systems offer the anesthetist an objective
measurement tool that can help determine when it is safe to
discharge the recovering patient. Outcome-based criteria
include vital signs, level of pain, alertness, motor function,
hemostasis, lack of nausea or vomiting, presence of an escort,
and the patient’s receptiveness to discharge. Whether we use
a discharge scoring system or outcome-based criteria to measure
a patient’s level of recovery, it is crucial that both the method
of measurement and the criteria met by the patient are docu-
mented in the patient’s record.
 CHAPTER 2 •
TABLE 2-2 Modified Aldrete Scoring System
Parameter
Activity level
Respirations
Circulation
Consciousness
Oxygen saturation (by pulse oximetry)
Maximum total score = 10
Data from Aldrete JA: The postanesthesia recovery score revisited, Butterworth-Heinemann, J Clin Anesth 1:88-91, Feb 7, 1995.
Postanesthesia Discharge Scoring System
TABLE 2-3
(PADSS)
VITAL SIGNS
2 Within 20% of preoperative value
1 20%-40% of preoperative value
0 40% of preoperative value
ACTIVITY, MENTAL STATUS
2 Oriented and steady gait
1 Oriented or steady gait
0 Neither
PAIN, NAUSEA, VOMITING
2 Minimal
1 Moderate
0 Severe
SURGICAL BLEEDING
2 Minimal
1 Moderate
0 Severe
INTAKE AND OUTPUT
2 PO fluids and voided
1 PO fluids or voided
0 Neither
Total score = 10
Data from Chung F, Chan VW, Ong D: A post-anesthetic discharge scoring system for
home readiness after ambulatory surgery, Butterworth-Heinemann, Ambulatory
Anesthesia 7(6):500-506, Sep 1995.
Emerging technology and increased availability of monitor-
ing devices have had an impact on our clinical practice as oral
and maxillofacial surgeons and will continue to do so. Future
monitoring devices will most likely collect and integrate data
and provide automated feedback to correct a patient’s physi-
ologic abnormalities. Research and development of new tech-
Monitoring for the Oral and Maxillofacial Surgery Patient 33
Description of Patient Score
Moves all extremities voluntarily/on command 2
Moves two extremities 1
Cannot move extremities 0
Breathes deeply and coughs freely 2
Is dyspneic, with shallow, limited breathing 1
Is apneic 0
Is 20 mm Hg ≤preanesthetic level 2
Is 20 to 50 mm Hg >preanesthetic level 1
Is 50 mm Hg >preanesthetic level 0
Is fully awake 2
Is arousable on calling 1
Is not responding 0
Has level >90% when breathing room air 2
Requires supplemental oxygen to maintain level >90% 1
Has level <90% with oxygen supplementation 0
nologies will continue, with the goal of producing clear clinical
benefits for our patients. These “smart” monitors may decrease
the likelihood of some types of human error; however, as
clinicians we must continue our vigilance, maintain and
understand our equipment, know what types of data it can
generate, and be able to interpret these data and respond
appropriately.
REFERENCES
1. Caplan RA: Adverse respiratory events in anesthesia: a closed
claims analysis, Anesthesiology 72(5):828-33, 1990.
2. Cooper JB, Newbower RS, Kitz RJ: An analysis of major errors
and equipment failures in anesthesia management: consider-
ations for prevention and detection, Anesthesiology 60(1):34-42,
1984.
3. Jastak JT, Peskin RM: Major morbidity or mortality from office
anesthetic procedures: a closed-claim analysis of 13 cases, Anesth
Prog 38(2):39-44, 1991.
4. Manning DM, Kuchirka C, Kaminski J: Miscuffing: inappropri-
ate blood pressure cuff application, Circulation 68(4):763-6,
1983.
5. Pickering TG et al: Recommendations for blood pressure mea-
surement in humans and experimental animals: part 1: blood
pressure measurement in humans: a statement for professionals
from the Subcommittee of Professional and Public Education of
the American Heart Association Council on High Blood
Pressure Research, Circulation 111(5):697-716, 2005.
6. Dorsch J: Understanding anesthesia equipment, ed 4, Baltimore,
Williams & Wilkins, 1991.
7. Vidal P et al: Compartment syndrome after use of an automatic
arterial pressure monitoring device, Br J Anaesth 71(6):902-4,
1993.
8. Bickler PE, Schapera A, Bainton CR: Acute radial nerve injury
from use of an automatic blood pressure monitor, Anesthesiology
73(1):186-8, 1990.
9. Gravenstein JS et al: Arterial pressure. In Scott M, editor: Clini-
cal monitoring practice, ed 2, Philadelphia, JB Lippincott, 1987.
10. Prielipp RC, Kelly JS, Roy RC: Use of esophageal or precordial
stethoscopes by anesthesia providers: are we listening to our
patients? J Clin Anesth 7(5):367-72, 1995.
34 SECTION I ■ Anesthesia and Pain Control
11. Watson A, Visram A: Survey of the use of oesophageal and
precordial stethoscopes in current paediatric anaesthetic prac-
tice, Paediatr Anaesth 11(4):437-42, 2001.
12. Hempenstall PD, de Plater RM: Oxygen saturation during
general anaesthesia and recovery for outpatient oral surgical
procedures, Anaesth Intensive Care 18(4):517-21, 1990.
13. Rodrigo MR, Rosenquist JB: Effect of conscious sedation with
midazolam on oxygen saturation, J Oral Maxillofac Surg 46(9):
746-50, 1988.
14. Grace RF: Pulse oximetry. Gold standard or false sense of secu-
rity? Med J Aust 160(10):638-44, 1994.
15. Marino PL: Oximetry and capnography. In Zinner SR, editor:
The ICU book, ed 2, Baltimore, Lippincott Williams & Wilkins,
1998.
16. Neff TA: Routine oximetry. A fifth vital sign? Chest 94(2):227,
1988.
17. Severinghaus JW, Kelleher JF: Recent developments in pulse
oximetry, Anesthesiology 76(6):1018-38, 1992.
18. Tremper KK, Barker SJ: Pulse oximetry, Anesthesiology 70(1):98-
108, 1989.
19. Sinex JE: Pulse oximetry: principles and limitations, Am J Emerg
Med 17(1):59-67, 1999.
20. Buckley RG: The pulse oximetry gap in carbon monoxide intoxi-
cation, Ann Emerg Med 24(2):252-5, 1994.
21. Anderson ST, Hajduczek J, Barker SJ: Benzocaine-induced met-
hemoglobinemia in an adult: accuracy of pulse oximetry with
methemoglobinemia, Anesth Analg 67(11):1099-101, 1988.
22. Ortiz FO et al: Accuracy of pulse oximetry in sickle cell disease,
Am J Respir Crit Care Med 159(2):447-51, 1999.
23. Comber JT, Lopez BL: Evaluation of pulse oximetry in sickle cell
anemia patients presenting to the emergency department in
acute vasoocclusive crisis, Am J Emerg Med 14(1):16-8, 1996.
24. Severinghaus JW, Koh SO: Effect of anemia on pulse oximeter
accuracy at low saturation, J Clin Monitoring 6(2):85-8, 1990.
25. Jay GD, Hughes L, Renzi FP: Pulse oximetry is accurate in acute
anemia from hemorrhage, Ann Emerg Med 24(1):32-5, 1994.
26. Schnapp LM, Cohen NH: Pulse oximetry. Uses and abuses,
Chest 98(5):1244-50, 1990.
27. Lee S, Tremper KK, Barker SJ: Effects of anemia on pulse oxim-
etry and continuous mixed venous hemoglobin saturation moni-
toring in dogs, Anesthesiology 75(1):118-22, 1991.
28. Kataria BK, Lampkins R: Nail polish does not affect pulse oxim-
eter saturation, Anesth Analg 65(7):824, 1986.
29. Rubin AS: Nail polish color can affect pulse oximeter saturation,
Anesthesiology 68(5):825, 1988.
30. Brand TM, Brand ME, Jay GD: Enamel nail polish does not
interfere with pulse oximetry among normoxic volunteers, J Clin
Monitoring Computing 17(2):93-6, 2002.
31. Cote CJ et al: The effect of nail polish on pulse oximetry, Anesth
Analg 67(7):683-6, 1988.
32. Ezri T et al: Pulse oximeters and onychomycosis, Anesthesiology
76(1):153-4, 1992.
33. Miner JR, Heegaard W, Plummer D: End-tidal carbon dioxide
monitoring during procedural sedation, Acad Emerg Med
9(4):275-80, 2002.
34. Hart LS et al: The value of end-tidal CO2 monitoring when
comparing three methods of conscious sedation for children
undergoing painful procedures in the emergency department,
Pediatr Emerg Care 13(3):189-93, 1997.
35. McQuillen KK, Steele DW: Capnography during sedation/
analgesia in the pediatric emergency department, Pediatr Emerg
Care 16(6):401-4, 2000.
36. Cote CJ, Wilson S: Guidelines for monitoring and management
of pediatric patients during and after sedation for diagnostic and
therapeutic procedures: an update, Pediatrics 118(6):2587-602,
2006.
37. Bennett J: A case against capnographic monitoring as a standard
of care, J Oral Maxillofac Surg 57(11):1348-52, 1999.
38. Chisholm CJ et al: Comparison of electrophysiologic monitors
with clinical assessment of level of sedation, Mayo Clin Proc
81(1):46-52, 2006.
39. Sebel PS et al: The incidence of awareness during anesthesia: a
multicenter United States study, Anesth Analg 99(3):833-9,
2004.
40. Crowley KE: Anesthesia complications: avoidance, recognition,
and management. In August M, editor: Complications in oral and
maxillofacial surgery, Philadelphia, Elsevier, 2003.
41. Kearse LA Jr: Bispectral analysis of the electroencephalogram
correlates with patient movement to skin incision during
propofol/nitrous oxide anesthesia, Anesthesiology 81(6):1365-70,
1994.
42. Overly FL et al: Bispectral analysis during deep sedation of pedi-
atric oral surgery patients, J Oral Maxillofac Surg 63(2):215-9,
2005.
43. Bannister CF et al: The effect of bispectral index monitoring on
anesthetic use and recovery in children anesthetized with sevo-
flurane in nitrous oxide, Anesth Analg 92(4):877-81, 2001.
44. Sandler NA, Sparks BS: The use of bispectral analysis in patients
undergoing intravenous sedation for third molar extractions,
J Oral Maxillofac Surg 58(4):364-8, 2000.
45. Overly FL et al: Bispectral analysis during pediatric procedural
sedation, Pediatr Emerg Care 21(1):6-11, 2005.
46. Coste C et al: Nitrous oxide prevents movement during orotra-
cheal intubation without affecting BIS value, Anesth Analg
91(1):130-5, 2000.
47. Sandler NA, Hodges J, Sabino M: Assessment of recovery in
patients undergoing intravenous conscious sedation using bispec-
tral analysis, J Oral Maxillofac Surg 59(6):603-11, 2001.
48. ADA Sedation and General Anesthesia Guidelines and Policy
2007. (Accessed July 1, 2007 at www.ada.org/prof/resources/posi-
tions/statements/proposed_anesthesia_guidelines.pdf . . .)
49. Smith DF: Conscious sedation, anesthesia, and the JCAHO,
Marblehead, Massachusetts, Opus Communications, 1999.
50. Feldman JM: Do anesthesia information systems increase mal-
practice exposure? Results of a survey, Anesth Analg 99(3):840-3,
2004.
51. Spring SF: Automated documentation error detection and noti-
fication improves anesthesia billing performance, Anesthesiology
106(1):157-63, 2007.
52. Reich DL: Development of a module for point-of-care charge
capture and submission using an anesthesia information manage-
ment system, Anesthesiology 105(1):179-86, 2006.
53. Aldrete JA: The post-anesthesia recovery score revisited, J Clin
Anesth 7(1):89-91, 1995.
54. Chung F: Recovery pattern and home-readiness after ambulatory
surgery, Anesth Analg 80(5):896-902, 1995.

LOCAL ANESTHETICS
Nima S. Massoomi
■ HISTORICAL PERSPECTIVE ON
LOCAL ANESTHESIA
The efforts of human kind to find the means to control pain
presents as one of the greatest challenges in medicine. Pain is
a phenomenon wisely instituted by nature as a warning sign
of a condition that may be detrimental to our bodies. From
the earliest antiquities down through the long centuries,
humans have resorted to many measures including supersti-
tion in an effort to blunt this noxious stimulus. Yet thankfully
as our knowledge of the human body grew, so did our under-
standing of pain. As Hippocrates once stated, “Divinium est
opus sedare dolorem”—divine is the work to subdue pain.1
Some of the earliest references to the use of pain-reducing
compounds were found in Homer’s “Odyssey,” when Helen
gave Ulysses and his comrades the “sorrow easing drug,” which
consisted of a mixture of poppy and Indian hemp. During the
siege of Troy, the Greeks used anodyne and astringents to ease
the pain of their wounds, completely unaware of its antiseptic
property.2 It was through trial and error that primitive man
used cold to lessen the pain and in time learned that pressure
on the affected area had a more pronounced effect. In the early
times, the Assyrians applied pressure over the carotid to cut
off the blood supply to the brain, thus producing a transient
syncopal-like episode, to obtain a certain degree of anesthesia
during circumcisions.3 This may explain why the literal Greek
and Russian translation of carotid artery is “the artery of
sleep.”4 In the year 50 ad, Pedanius Dioscorides is said to have
made the first attempt to produce an anesthetic paste, allow-
ing it to act as topical anesthetic. By pulverizing Memphis
stone and mixing it with vinegar, the resultant carbonic acid
produced a cold stimulus, causing anesthesia over the affected
area.5
For reasons unknown, the middle ages of humankind did
not present with any new discoveries or advances in local
anesthesia.6 It was not until the nineteenth century that the
literature began to first describe a chemical with some anes-
thetic properties. Supposedly, dating back to 1532, the Indians
in the highlands of Peru chewed the leaves of coca shrub to
relieve fatigue and hunger and to produce a feeling of exhilara-
tion.6-8 Carl Scherzir in 1856 reported the anesthetic proper-
ties of the coca leaf. In 1859 a German chemist, Albert
Neimann, was given credit for being the first to extract cocaine
in its pure form. This was despite the fact that a year earlier
CHAPTER 3
another German chemist by the name of Friedrich Godeke
had also isolated the active ingredient, but had called it
“erythroxylin.” It was not until 1865 that one of Niemann’s
disciples, Wilhelm Lossen, finally determined the correct for-
mulation of cocaine as C17H21NO4.9
In the mid-1860s, as anesthesia began to receive more
attention, Sir Benjamin Ward Richardson demonstrated the
use of ether spray to anesthetize skin.10 Around the same
time a young Viennese physician, Sigmund Freud, became
interested in cocaine’s effect on mood and the psyche. He
subsequently administered it to a colleague, Ernst Fleischl
Von-Marxow, in an effort to free him of his morphine depen-
dence after a thumb amputation.6,7 Ironically, Freud’s col-
league was able to overcome his addiction, but he himself
began to experiment with cocaine and noticed that it removed
his depression. Subsequently, Freud became addicted to
cocaine, which took him 10 years to overcome. It was during
the same time that Carl Koller, then an ophthalmology resi-
dent at the University of Vienna, began working with Freud
in his physiology lab to perform experiments using cocaine.
Koller, who had read that cocaine made the tongue go numb,
decided to try it on the conjunctiva. The rest is history, as he
became aware of cocaine’s anesthetic and mydriatic effect. He
was successfully able to demonstrate cocaine’s activity on
various animal species and even himself.7 Then in 1884, at
the Congress of Ophthalmologists held in Heidelberg,
Germany, Koller’s findings were read at the conference, propa-
gating the properties of cocaine.7,11
Within a 12-month period, the newly discovered proper-
ties of this drug were used in every important clinic in the
world. Many were thrust into using cocaine, without any
regard for its potent side effects, leading to many fatalities. By
one account between 1884 and 1891, 200 cases of systemic
intoxication and 13 deaths were reported.12 It was not until
Reclus and Schleich’s introduction of “infiltrative anesthesia”
that a drop in fatalities was noted.13 As news of cocaine spread
around the world, some in the United States began to experi-
ment with its use. In 1884 at Roosevelt Hospital in New York,
Richard John Hall and William Stewart Halsted were the first
to describe regional block or “perineuronal” anesthesia.6-8,11
Using cocaine they performed what today is referred to as
infraorbital and inferior alveolar nerve blocks for dental
operations and later perfected many other regional anesthetic
techniques.7 Halsted, Hall, and co-workers held weekly
35
36 SECTION I ■ Anesthesia and Pain Control
demonstrations and in “the best tradition of times, experimented
on themselves and innocently paid the price of becoming habitual
users.”14 It took him 2 years to overcome his addiction.
By the1890s, the adverse effects of cocaine had been real-
ized, leading to a more cautious approach in its use. As known
today, these side effects include: cardiac stimulation, periph-
eral vasoconstriction, and the excitation of the central nervous
system (CNS) along with physical and psychological depen-
dence. The hyperexcitation of the cardiovascular system was
later found to be due to the blockage of norepinephrine (NE)
uptake at the neural terminal end.15 This stimulatory effect on
the cardiovascular system, combined with the vasoconstric-
tive effects on the coronary vasculature is now known to cause
myocardial infarctions in susceptible individuals.16,17 The
euphoric effects and the abuse potential of the drug is related
to its ability to block both dopamine (DA) and NE reuptake
at key sites within the brain.7,17 Some postulate that increased
levels of DA lead to dependence. This is due to DA’s role as
a part of the “reward system” in the complex neurotransmitter
system of the brain.
With advances in compounding and better understanding
of organic chemistry, synthetic derivatives of cocaine were
developed to prevent its unfavorable side effects. The first
major breakthrough was the synthesis of an ester called pro-
caine (Novocain) by Alfred Einhorn in 1904.18 It was not until
nearly 40 years later that this development was followed by the
synthesis of lidocaine (Xylocaine), the first amide local anes-
thetic, by Nils Lofgren.19 In comparison lidocaine possessed a
greater potency, with a more rapid onset and most importantly
less allergenicity.6,7,20,21 As a result, lidocaine displaced pro-
caine as the drug of choice in most clinical settings.
Currently, there are more than a dozen local anesthetics,
each with a distinct set of properties and side effects. With
the outside pressures of the insurance companies, third-party
payers, and the need to reduce hospital stays, “day surgery” is
becoming a crucial element of a surgical practice. As a result,
the use of local anesthetics has become essential in providing
expedient service and care to the patient. This trend has been
seen in most surgical subspecialties, including oral and maxil-
lofacial surgery. A recent survey of 865 board-certified German
plastic surgeons demonstrated an increased use of local anes-
thetics for cosmetic surgery of the head and neck, with 1%
prilocaine as the most popular local anesthetic, followed by
1% lidocaine. Unfortunately, in the same time period, adverse
cardiovascular reactions are also up by 8.1%.22 This increased
use of local anesthetics, along with the aging population and
their associated comorbidities, makes it prudent for clinicians
to be well versed in each type of local anesthetic and their
distinct properties.23
■ CHEMISTRY OF LOCAL
ANESTHETICS
It is now known that local anesthetics exert the majority of
their clinical actions through the blockage of nerve impulses
by inhibiting the normal function of voltage-sensitive Na+
TABLE 3-1 Chemical Classification of Local Anesthetics
Esters Amides
Benzocaine Articaine
Cocaine Bupivacaine
Procaine Lidocaine
Propoxycaine Mepivacaine
Tetracaine Prilocaine
Ropivacaine
channels. This in turn will prevent the noxious stimuli from
reaching the brain and producing the sensation of pain. All
injectable local anesthetics are composed of three structural
domains: aromatic residue, intermediate chain, and amino
terminus (Figure 3-1). The aromatic or lipophilic portion of
the molecule allows the drug to penetrate lipid-rich nerve
sheaths and nerve membranes. The intermediate portion of
the molecule affords the necessary spatial separation between
the lipophilic and hydrophilic portions and divides local anes-
thetics into two distinct chemical classes: the esters (-COO-)
and the amides (-NHCO-). Lastly the tertiary or second amino
end provides the hydrophilic properties to the molecule. This
ensures solubility of local anesthetic in the dental cartridge
and the interstitial fluid after injection. By design benzocaine,
which is the most commonly used topical local anesthetic,
lacks this amino terminus and therefore can only be used topi-
cally (see Figure 3-1).
An easy way to determine whether a local anesthetic is an
ester or an amide is to look at the prefix of the generic name
before “-caine.” If the “I” appears in the prefix, then it is an
“I”de, such as lidocaine or bupivacaine. Ester local anesthetics
do not contain the letter “I,” such as benzocaine or procaine
(Table 3-1).
The esters, represented by drugs, such as benzocaine,
cocaine, procaine, propoxycaine, and tetracaine, are metabo-
lized primarily by plasma pseudocholinesterases. A byproduct
of this metabolism is the formation of para-aminobenzoic acid
(PABA), which has been implicated in the development of
allergic responses in a small but significant portion of the
general population.6,7,21,25,26 A structurally related chemical,
methylparaben, was used as a preservative in amide local anes-
thetic solutions until it was discovered that it also produced
allergic reactions in susceptible patients.7,27 Subsequently,
methylparaben was removed from all dental cartridges, except
in multidose vials.
Amide local anesthetics are represented by articaine, bupi-
vacaine, lidocaine, mepivacaine, prilocaine, and etidocaine.
As a result of their lower risk of allergic reactions, this class
of local anesthetics has replaced the esters as the local anes-
thetic of choice. However, amides, which are metabolized
primarily in the liver,6,7,21,25,26 can become problematic if they
are used in patients with compromised liver function. Esti-
mates show that by the age of 65, liver function is only 65%
of normal. Therefore in healthy patients over 65, it is wise to
 CHAPTER 3 • Local Anesthetics 37

Aromatic Intermediate Amino Aromatic Intermediate Amino

residue chain terminus residue chain terminus
ESTERS AMIDES
CH3
C2H5 C2H5
H2N COOCH2CH2 N NHCOCH2 N
C2H5 C2H5
CH3
Procaine Lidocaine
H7C3O CH3
C2H5 C3H7
H2N COOCH2CH2 N NHCOCH N
C2H5 C2H5 C2H5
CH3
Propoxycaine Etidocaine
CH3
H9C4 CH3 CH3
N COOCH2CH2 N NHCOCH N
H CH3
CH3
Tetracaine Mepivacaine
CH3
CH3 C4H9
COOCHCH2CH N NHCOCH N

COOCH3 CH3
Cocaine Bupivacaine
CH3
CH3 H
H2N COOCH2CH3 NHCOCH N
C3H7
Benzocaine Prilocaine
CH3 CH3 H
H9C4O COCH2CH2 N NHCOCH N
S
C3H7
H3COOC
Dyclonine* Articaine
*Dyclonine is a ketone.

FIGURE 3-1. Local anesthetic structures.24

reduce the maximum amount of local anesthetic to about half

of what would be used in healthy young adults.28
Relationship Between pKa, Ionization, and
TABLE 3-2
Local Anesthetic Onset at a pH of 7.47,30
■ pH EFFECTS ON LOCAL
ANESTHETICS Drug pKa % Cationic % Free Base Onset Time (Min)
Mepivacaine 7.7 67 33 2-4
The pharmacodynamics of local anesthetics is affected by
Lidocaine 7.8 71 29 2-4
several variables, including the pH of the solution and the
Prilocaine 7.8 71 29 2-4
surrounding soft tissue. Injectable local anesthetics are weak
Articaine 7.8 71 29 2-4
bases with a pKa range of 7.7 to 8.9 (Table 3-2). This will
Etidocaine 7.9 76 24 2-4
cause them to exist in two forms: a free base or neutral form
Bupivacaine 8.1 83 17 5-8
and cationic or positively charged form. Because a lipophilic
Propoxycaine 8.9 97 3 9-14
form of local anesthetic is required for better penetration
Procaine 8.9 97 3 14-18
of neuronal tissue, the uncharged free base form readily
38 SECTION I ■ Anesthesia and Pain Control
CH3 O R ⫹H⫹ CH3 O R
⫹
NHCR ⫺ N NHCR ⫺ N
⫺H⫹ H blocked.35,36 Additionally, based on experiments on isolated
CH3 R CH3 R
Free base form Cationic form
FIGURE 3-2. Free base and cationic forms of local anesthetic.24
penetrates neural tissue. Conversely the cationic form has a
more difficult time diffusing through the membrane (Figure
3-2).
The Henderson-Hasselbalch equation for weak bases can
predict what proportion of local anesthetic will exist in the
two ionic states.6,7,20,25,29
When the pH of the surrounding tissue and the pKa are
equal, 50% of each ionic form will exist. As the pKa of the
local anesthetic increases or as the pH of the surrounding
environment is reduced, a greater proportion of the charged,
relatively impermeable cationic species will exist (see Table
3-2).
When the local anesthesia is injected into an inflamed or
acidic environment, the more hydrophilic portion of the drug
will be preponderant, resulting in decreased neuronal penetra-
tion and potency. At physiologic pH of 7.4 or higher, local
anesthetics with a lower pKa, such as mepivacaine, lidocaine,
and prilocaine, will have a higher percentage of their free base
available for neuronal diffusion. For instance if lidocaine with
a pKa of 7.8 is injected into a site with a pH of 6.0, the pro-
portion of the cationic form will increase from 74% to 98%.
This leaves only 2% of the local anesthetic capable of pene-
trating the nerve sheaths, making complete anesthesia improb-
able. Other studies show that in addition to pH there are other
local mediators of inflammation, such as prostaglandins and
bradykinin, that can antagonize the effects of local anesthet-
ics.7,31,32 Local anesthetics are typically manufactured as an
acidic hydrochloride salt, with a pH ranging from 3.5 to 6.0.
This improves the water solubility of the local anesthetic and
stabilizes the vasoconstrictor. Because of the low pH, approxi-
mately 99% of local anesthetic will carry a positive charge. As
a result of the buffering capacity of the soft tissue, it is only
after injection that local anesthetic is converted into the free
base form, capable of penetrating the nerve sheaths.
■ MECHANISM OF ACTION OF
LOCAL ANESTHETICS
Local anesthetics can be used in three modes: topical applica-
tion, local infiltration, and nerve blockade. All will lead to
the blockage of the sensation of pain, touch, temperature, and
proprioception by interfering with the propagation of impulses
along peripheral nerve fibers.33 This is accomplished by reduc-
tion in the rate rise in the depolarization phase, leading to a
slowing of the action potential. At the molecular level, this
deterioration in the action potential is accomplished by block-
ing the influx of sodium through the excitable nerve mem-
branes.34 By completely abolishing the inward movement of
depolarizing sodium while having little effect on outward
movement of repolarizing potassium, the action potential is
nerve preparations, there is a direct relationship between the
concentration of sodium in surrounding tissue and concentra-
tion of local anesthetic needed to completely block the action
potential.37 As the gradient for influx of sodium becomes more
favorable, more local anesthetic is needed to block the action
potential.
At sodium channels, both the basic and cationic species
appear to be active, with the cationic species entering the
sodium channels when they are in the open state and the free
base form entering the sodium channels when they are open
or closed. In a classic study carried out by Ritchie et al, nerves
still possessing their outer covering were most susceptible to
local anesthetics at alkaline pH. Yet when the epineurium was
stripped off the nerve fibers, the local anesthetics were most
effective at the more acidic pH.38,39 These experiments con-
firmed the notion that the cationic form of the local anesthet-
ics was also effective in blocking the propagation of action
potentials. Thus the sequence of events induced by local anes-
thetic molecules is as follows: (1) a reduction in the permea-
bility of the nerve cell membrane to sodium ions, (2) a
decreased rate of rise in the depolarization phase of the action
potential, and (3) failure of a propagated action potential.
■ POTENCY OF LOCAL
ANESTHETICS
Potency is a comparative term that estimates the amount of
one drug relative to another, in terms of how much of each
drug is needed to have same effect. Potency and duration of
action can differ between each drug depending on the
chemical structure and the presence of other additives, such
as vasoconstrictors, which will be discussed later. Generally
speaking the more hydrophobic or lipophilic the agent, the
greater the potency and the longer the duration of action. As
shown in Table 3-3, potency is directly related to lipid solubil-
ity and inversely related to the concentration of the local
anesthetic. The lower the lipid solubility, the higher the con-
centration of local anesthetic that is needed to produce the
same effect. For this reason, local anesthetics with higher lipid
solubility are manufactured at lower concentrations.
The lipid solubility of local anesthetics can be manipulated
by the addition or removal of carbon atoms at key sites on the
molecule. For example, as shown in Figure 3-2, the addition
Relationship Between Lipid Solubility and
TABLE 3-3
Local Anesthetic Concentration7
Drug Lipid Solubility Concentration
Articaine 40 4%
Mepivacaine 42 2%-4%
Prilocaine 55 4%
Lidocaine 110 2%
Bupivacaine 560 0.5%
 CHAPTER 3 • Local Anesthetics 39

of a butyl group (-C4H9) to mepivacaine results in the forma-
tion of bupivacaine, which possesses at least four times the
relative potency from a clinical standpoint.6,7,21 Mepivacaine
is marketed at a 2% to 4% solution, whereas bupivacaine
is marketed as a 0.5% solution. However, when comparing
the two from a potency standpoint, there is no evidence that
one local anesthetic is superior to another in the laboratory
or in the clinical setting.
■ EFFICACY AND DURATION OF
ACTION OF LOCAL ANESTHESIA
There are various factors that influence the efficacy and the
duration of local anesthetic action. First, and the most obvious,
is accurate anatomic placement of the local anesthetic in the
vicinity of the desired nerve. This is especially true of the
mandibular nerve, which has been shown to possess many
accessory branches.40,41 The second factor has to do with the
actual chemical makeup of the local anesthetic. Properties,
such as the solubility of the local anesthetic into the nerve
sheath or the presence or absence of a vasoconstrictor, along
with the intrinsic activity of the local anesthetic, can make a
difference in the efficacy and duration of action. As a general
rule, the duration of anesthesia in soft tissues lasts longer than
pulpal anesthesia by a factor of 2 to 3.7,21,26,42,43 This is shown
in Table 3-4 and holds true even in the presence or absence
of vasoconstrictors. For the listed local anesthetics, there is a
range of maximum dosage recommendations, with the number
in parenthesis based on Malamed’s more conservative guide-
lines. The higher numbers are based on the package inserts
and Jastak et el.
Long-acting local anesthetics, such as bupivacaine, are
highly lipid soluble and bind more tightly to protein and lipid
structures within the nerve membrane than other local anes-
thetics.21,25,39,46,47 When administered via mandibular block,
these long-acting anesthetics with 1 : 200,000 epinephrine
possess a longer duration of pulpal anesthesia than other mar-
keted anesthetic solutions.48,49 However, several studies of
infiltrative or PDL injections of bupivacaine with 1 : 200,000
epinephrine show that in the maxilla the pulpal anesthesia
duration is not longer, and in some cases even shorter,
than the duration of 2% lidocaine with 1 : 100,000
epinephrine.50,51
It is important to note that local anesthetics have an
intrinsic vasodilatory property. This is especially true of lido-
caine, which in the absence of a vasoconstrictor, is rapidly
redistributed away from the site of injection.6,7,21 As shown in
Table 3-4, 2% lidocaine plain without epinephrine maintains
pulpal anesthesia duration of about 5 minutes in the maxilla
and 10 minutes in the mandible. Adding 1 : 100,000 epineph-
rine to this solution increases the duration of pulpal anesthesia
approximately tenfold, to 60 minutes in the maxilla and 85
minutes in the mandible. In contrast both mepivacaine and
prilocaine have less vasodilatory activity than lidocaine.21
Solutions of 3% mepivacaine or 4% prilocaine in the absence
of a vasoconstrictor can produce pulpal anesthetic durations
in the 20- to 55-minute range, which is only doubled in the
presence of a vasoconstrictor.7,21,26,27,52
■ USE OF VASOCONSTRICTORS
WITH LOCAL ANESTHETICS
For decades the use of vasoconstrictors with local anesthesia
has been one of the most contentious topics in dentistry.
Considering today’s aging population and their comorbidities,
this issue will surely continue to be contentious. Because of
the potential adverse effects of vasoconstrictors, it has been
unethical to perform controlled, randomized, and double-
blind studies on humans. Much of what has been debated is
based on anecdotal observations on human case reports and
animal studies with unsubstantiated data. Questions still
remain as to the actual interplay of vasoconstrictors and car-
diovascular disease and the dreaded drug-drug interactions.
Today the two most common vasoconstrictors used in
dental anesthetic solutions in the United States are epineph-
rine and levonordefrin. Local anesthetics containing NE are

TABLE 3-4 Injectable Local Anesthetics7,26,30,44,45

Anesthetic Duration in Minutes
Maxillary Infiltration Mandibular Block Maximum Dosage Maximum Total
Pulp Soft Tissue Pulp Soft Tissue mg/kg mg/lb Dosage (mg)
Lidocaine 2% plain 5 60 10 120 4.5 2.0 300
2% + 1 : 50,000 epinephrine 60 180 90 240 7.0 (4.5) 3.18 (2.0) 500 (200)*
2% +1 : 100,000 epinephrine 60 180 85 240 7.0 (4.5) 3.18 (2.0) 500 (300)
Mepivacaine 3% plain 20 120 40 180 6.6 (4.5) 2.2 (2.0) 400 (300)
2% + 1 : 100,000 epinephrine 60 170 85 190 6.6 (4.5) 2.2 (2.0) 400 (300)
2% + 1 : 20,000 levonordefrin 45 120 75 240 6.6 (4.5) 2.2 (2.0) 400 (300)
Articaine 4% + 1 : 100,000 epinephrine 60 180 75 360 7.0 [5.0]† 3.2 [2.72]† 500 [144]†
4% + 1 : 200,000 epinephrine 45 120 60 300 7.0 [5.0]† 3.2 [2.72]† 500 [144]†
Prilocaine 4% plain 20 105 60 240 8.0 (6.0) 3.64 (2.7) 600 (400)
4% + 1 : 200,000 epinephrine 45 120 90 240 8.0 (6.0) 3.64 (2.7) 600 (400)
Bupivacaine 0.5% +1 : 200,000 epinephrine 45 240 240 540 1.3 0.6 90
*Based on the 200 mg of epinephrine limit.
†
Represents maximum recommended dose in children ≤30 kg or ≤13.6 lb.
40 SECTION I ■ Anesthesia and Pain Control
no longer manufactured in the United States, but continue to
be used elsewhere in the world.24 In general vasoconstrictors
are classified as adrenergic or sympathomimetic because they
are, or closely resemble, the natural mediators of the sympa-
thetic nervous system.43 Chemically, they are classified as cat-
echolamines because of their direct action on the adrenergic
receptors.7,43,53 By design vasoconstrictor concentrations
within local anesthetics are titrated to approximate the same
α-adrenergic activity. This explains the varying concentra-
tion of vasoconstrictors that are found in commercial
formulations.
The adrenergic system is composed of both β and α recep-
tors. Each receptor type is further subdivided into β1 or β2 and
α1 or α2. For the most part, the β-adrenergic system is mostly
systemic, whereas the α-adrenergic system is mainly periph-
eral with less systemic action.54 The main action of the β1
receptor is at the heart, where its activation increases heart
rate and automaticity of the heart via the SA node, along with
increasing contractility and conduction of the heart. β2 recep-
tors are located in the vascular beds of skeletal muscles and
pulmonary vasculature. Their activation leads to vasodilation
or relaxation of the trachea and bronchioles. On the other
hand, α1 receptors are found in the peripheral vasculature and
cause severe vasoconstriction of the peripheral arterioles
and veins on stimulation. For this reason, the use of local
anesthetic with vasoconstrictors is contraindicated in distal
appendages with an end vascular supply, such as nose, ears,
fingers, and toes. Lastly the stimulation of α2 receptors, which
are mostly found in the CNS, leads to decreased sympathetic
outflow from the brain and a decrease in the release of NE
from the presynaptic neurons.
The physiologic result of β1 stimulation is an increase in
blood pressure, whereas the stimulation of β2 receptors tends
to decrease blood pressure.7,43,55 The α receptors mainly cause
vasoconstriction at the peripheral circulation, skin, and
mucous membranes, with a nominal increase in the blood
pressure.54,55 For instance the antihypertensive medication
prazosin (Minipress), which is an α1 antagonist, has only
limited effectiveness against minimal to moderate hyperten-
sion with negligible decreases in blood pressure of approxi-
mately 10 to 12 mm Hg.56 Fortunately, because of their
similarity to endogenous catecholamines, their action is ter-
minated within one minute by the enzyme catechol-O-methyl
transferase (COMT), which is readily available in blood, liver,
lungs, and other tissues.57
Examining the actions of catecholamines’ subtle differ-
ences are noted. Table 3-5 shows that epinephrine is the most
potent with respect to α receptor stimulation, as compared
with NE, levonordefrin, and phenylephrine. NE stimulates
the β1 receptor preferentially over β2, therefore causing an
increase in blood pressure when used as a vasoconstrictor in
local anesthetic. On the other hand, epinephrine has an equal
affinity for both α and β receptors, causing no dramatic
increases in blood pressure as a result of β2 vasodilation.54 The
vasodilatory β2 receptors are believed to be more sensitive to
low blood levels of epinephrine than are the vasoconstrictive
TABLE 3-5 Vasoconstrictor Selectivity and Potency59
Vasoconstrictor b1 Selectivity b2 Selectivity Relative a Potency
Epinephrine 50% 50% 100%
Norepinephrine 85% 15% 25%
Levonordefrin 75% 25% 15%
Phenylephrine 95% 5% 5%
α1 receptors. This explains why small doses of epinephrine
often increase heart rate and systolic blood pressure yet actu-
ally reduce diastolic blood pressure, with the mean arterial
pressure (MAP) remaining unchanged.7,43,58
Because of NE’s mostly β1 properties, local anesthetics con-
taining NE have resulted in numerous adverse reactions during
routine dental treatment.60 Some of these reactions were
attributed to “rebound bradycardia,” which is a compensatory
response to the initial hypertension caused by β1 stimulation.
Additionally, NE has shown to impair left ventricular dia-
stolic function, which can be detrimental in patients with
congestive heart failure.61 As a result of systemic side effect,
NE was removed from most local anesthetic formulations in
the United States.
Levonordefrin, which is the least potent of the catechol-
amines, is most similar to NE, possessing less α1 but slightly
more β2 action. It is still available in a 1 : 20,000 solution
(0.05 mg/mL). At low blood levels, it closely resembles NE’s
pressor effects.7,43,53,62 Even though NE and levonordefrin have
less α1 activity, one may think that they would be preferred
over epinephrine in patients with heart disease. On the con-
trary, with the preservation of the patient’s ability to increase
their peripheral vascular resistance more stress can be placed
on the heart when NE or levonordefrin is given.55 Hence
patients with documented hypertension should not receive
NE or levonordefrin because both will exert unrestricted acti-
vation of α1 receptors, which could lead to uncontrolled
increases in blood pressure. This is especially true in patients
with severe, uncontrolled hypertension; refractory arrhyth-
mia, myocardial infarction, or stroke within 6 months;
uncontrolled congestive heart failure; and uncontrolled
hyperthyroidism.63
POTENTIAL BENEFITS OF VASOCONSTRICTORS
The addition of vasoconstrictors to local anesthetics arose
from the desire to reduce or prevent the redistribution of the
local anesthetics away from the site of injection. As an obvious
strategy to reduce the vascular removal of the local anesthetic,
vasoconstrictors, such as epinephrine, were the natural choice.
It is now known that the use of vasoconstrictors decreases the
clearance of the local anesthetic, reduced the total required
amount, increases the duration and depth of anesthesia, and
aids in hemostasis of the surgical wound. Studies show that
with the presence of a vasoconstrictor there is a delay and a
reduction in the peak blood levels of the local anesthetic.*
*References 43,53,55,62,64,65.

This is of importance because excessive blood levels of local
anesthetics are known to cause systemic toxicity, especially in
the pediatric dental population.7,21,66,67
Additionally, local anesthetics, especially lidocaine, inher-
ently cause vasodilation, further strengthening the need for
vasoconstrictors. Experiments show that with the addition
of vasoconstrictors the duration of action of all local anesthet-
ics is prolonged. This is especially true with lidocaine instead
of mepivacaine or prilocaine. As shown in Table 3-4, 2% plain
lidocaine possesses a pulpal anesthesia of about 5 to 10 minutes.
With the addition of 1 : 100,000 epinephrine, the duration is
increased by ten-fold to approximately 60 minutes. This
increase in the duration of action is less dramatic with bupi-
vacaine, possibly as a result of its higher lipophilic proper-
ties.43,55,68 In one study with the absence of a vasoconstrictor,
2% plain lidocaine did not predictably produce pulpal anes-
thesia, and the efficacy of anesthesia was only 38%, obviously
unacceptable in a clinical setting.24,43,69
Some of the inherent properties of vasoconstrictors with
local anesthetics were demonstrated in a recent study by
Sinnott in 2000, where rat sciatic nerves were blocked using
0.5% lidocaine with or without epinephrine. As expected the
use of epinephrine greatly potentiated the duration of action
by four-fold. They were able to show that only after 5 minutes
the total intraneural lidocaine doubled with the presence of
epinephrine, and the rate at which it declined was insig-
nificantly decreased by the vasoconstrictor. This trend was
attributed to epinephrine’s action early in the blockade. By
enhancing the initial neural uptake of the local anesthetic and
sustaining a higher concentration of local anesthetic in the
surrounding tissue, a higher concentration gradient was
created, driving the local anesthetic deeper into the core of
the nerve.70 This results in less local anesthetic needed to
achieve the desired nerve block.
The presence of vasoconstrictor also seems to be beneficial
in patients with cardiovascular disease because it reduces the
release of reactionary endogenous NE.71,72 Dental anxiety,
fear, anesthesia, and surgery are all accompanied by physio-
logic, psychological, and biochemical changes. Physiologi-
cally, this translates into changes in the heart rate and blood
pressure, cardiac arrhythmias, and release of endogenous cat-
echolamines. Multiple studies show that in dental treatment,
even with adequate anesthesia, there are increased levels of
endogenous catecholamines. In turn significant increases in
blood pressure can be seen, leading to adverse reactions.54,73,74
In a randomized, blinded, controlled, and comparative study,
it was noted that perioperative anxiolytics, such as midazolam
(Versed), may attenuate the sympathoadrenal response.75 This
was further supported by a Swedish study, where a randomized
controlled trial of 35 atypical odontalgia patients in Sweden
reported that lidocaine injections provided significant, but not
complete, pain relief as compared with saline (placebo) injec-
tions.76 This suggests the pain experienced in these patients is
not solely dependent on peripheral afferent inputs and must
involve higher order neurons.76 When compared with 0.15 mg/
kg of midazolam (Versed), 1.5 μg/kg of clonidine (Catapres)
CHAPTER 3 • Local Anesthetics 41
and 0.3 mg/kg morphine were found to be the more effective
premedications in reducing pain during application of local
anesthesia. This suggests that clonidine (Catapres) should be
selected over morphine as a premedication to reduce anxiety
and pain.77
Today it is generally agreed that the concentration of vaso-
constrictors needs to be somewhere between 1 : 200,000 and
1 : 100,000 to improve the duration of action.53,62 Increasing
the concentration of any vasoconstrictor to 1 : 50,000 does not
only cause significant cardiovascular changes but has also not
shown to be of any benefit in duration of action.6,7,21,62 In a
study of 11 normotensive patients undergoing tooth extrac-
tion with 2% lidocaine with epinephrine (1 : 80,000), it was
found that during surgery there was a significant increase in
systolic blood pressure. Furthermore the serum glucose levels
increased after local anesthesia; plasma insulin concentrations
remained steady. Together these data suggest sympathoadre-
nal outflow is activated by administration of local anesthetic
and tooth extraction, which ultimately leads to an increase in
serum glucose levels in patients with normal blood pressure.54
This is in addition to the stress of the procedure.
As mentioned previously, another advantage of using vaso-
constrictors in local anesthetic is the hemostatic effect it pro-
vides at the surgical site. In one third molar study, there was
a 50% reduction in blood loss with the use of 2% lidocaine
plus 1 : 100,000 epinephrine versus 3% plain mepivacaine.78
Hemostasis also lends itself to a more visible surgical field and
decrease in the risk of aspiration of blood, especially during
intraoral procedure. It is important to note that the optimum
concentration of local anesthetic that is needed for adequate
hemostasis is specific to each local anesthetic. Studies clearly
indicated that with lidocaine a concentration of 1 : 50,000
epinephrine is more effective than the less concentrated solu-
tions of 1 : 200,000.55,79 Along the same lines, 1 : 200,000
mixture of epinephrine seems to impart adequate hemostasis
when used with prilocaine and bupivacaine.7,55
POTENTIAL SYSTEMIC SIDE EFFECTS
OF VASOCONSTRICTORS
Even though vasoconstrictors reduce systemic absorption of
the local anesthetic, there is still systemic absorption of the
vasoconstrictor itself, especially if there is an inadvertent
intravascular injection.58,80-85 Fortunately, even with systemic
absorption of vasoconstrictors, the blood pressure and
heart rate remains unchanged, with minimal effect on the
MAP.58,61,80,86 This is despite the fact that investigators repeat-
edly report a two-fold to four-fold increase in the basal epi-
nephrine levels after an injection of local anesthetics with
1 : 100,000 epinephrine.58,80-83 It is important to note that plain
lidocaine had no effect on plasma epinephrine levels or any
cardiovascular parameter.58,81
Because the majority of patients undergoing elective extrac-
tion of teeth are young and healthy adults, their cardiovascu-
lar response is expected to be different than a 50-year-old
patient with significant atherosclerotic and/or cardiovascular
disease. In a typical third molar extraction case, it is not
42 SECTION I ■ Anesthesia and Pain Control

unusual to administer eight cartridges of 2% lidocaine plus
1 : 100,000 epinephrine. That equates to 288 mg of local anes-
thetic plus 144 μg of epinephrine. In one particular study, this
amounted to a twenty-seven-fold increase in systemic epi-
nephrine levels, resulting in an approximate elevation in sys-
tolic blood pressure of about 20 mm Hg, an increase in the
heart rate of about 20 beats per minute, and a 52% increase
in myocardial oxygen consumption. This may explain why
most fatal outcomes have been in older patients with signifi-
cant cardiovascular disease.
So it seems that even with the use of local anesthetics the
likelihood of systemic toxicity cannot be completely elimi-
nated. This is especially true of inadvertent intravascular
administration of epinephrine, which has been shown to redi-
rect a larger than expected percentage of cardiac output toward
the brain, doubling the delivery of lidocaine to an organ that
is most susceptible during local anesthetic overdoses.64,65,87 In
the event that vasoconstrictors cannot be used, 2% to 3%
mepivacaine or 4% prilocaine are the two dental local anes-
thetics that can provide acceptable pulpal anesthesia without
the use of vasoconstrictors.
POTENTIAL DRUG-DRUG INTERACTION
WITH VASOCONSTRICTORS
Drug-drug interaction with vasoconstrictors is one area that
continues to evolve. Over the years, the risk of drug interac-
tions with vasoconstrictors has been overstated in some
patient groups, and it remains underappreciated in others.88-91
There are two articles that are repeatedly cited as cause for
concern when dealing with drug-drug interactions as related
to antidepressant or antihypertensive medications. Yet an
increasing body of evidence is beginning to question some of
what were once thought to be absolute drug-drug interactions.
Before any conclusions can be drawn, more well-designed
studies are needed.92,93
Table 3-6 summarizes the three main categories of antide-
pressant medications: monoamine oxidase inhibitors (MAOIs),
tricyclic antidepressants (TCAs), and selective serotonin
reuptake inhibitors (SSRIs). In the past, it was widely believed
that the use of MAOIs and TCAs, excluding SSRIs, were an
absolute contraindication to the use of vasoconstrictors.
However, in the past 30 years, there has not been a single case
report of an adverse reaction with local anesthetics plus vaso-
constrictors in the millions of patients taking these antide-
pressant medications.94 The interaction of MAOIs with local
anesthetics plus vasoconstrictors was thought to be related to
the accumulation of serum catecholamines. In turn this was
postulated to cause an increased risk of severe hypertension
or cardiac arrhythmia. However, the short half-life of exoge-
nously administered catecholamines and their quick reuptake
in the nerve terminals makes it unlikely that such an accu-
mulation can take place. Furthermore in animal studies,
the concurrent administration of any catecholamines with the
MAOI phenelzine did not produce any cardiovascular find-
ings.95 A potential drug interaction with MAOIs should only
be a concern with certain adrenergic drugs, such as phenyl-
ephrine and ephedrine, which have a noncatecholamine
structure.
With regard to TCAs, there have been three commonly
cited studies speaking of a potentially dangerous increase in
blood pressure in patients taking TCAs.95,97,98 However, none
of these studies were blinded or randomized, and their statisti-
cal power was low. Interestingly, in one of these studies by
Yagiela et al, even though no significant change was noted
in the MAP for the dogs tested with epinephrine, dogs pre-
treated with desipramine had significant increases in MAP
when NE or levonordefrin were used.95 Nevertheless, without
distinguishing between NE and epinephrine, the interaction
between vasoconstrictors and TCAs was deemed serious
enough to deserve special attention. These studies also failed

TABLE 3-6 Antidepressant Medication Classification

Antidepressant Classification Generic Name Trade Name
Monoamine oxidase inhibitors (MAOIs) Isocarboxazid Marplan
Phenelzine Nardil
Selegiline transcutaneous Emsam
Tranylcypromine Parnate
Tricyclic antidepressant (TCAs) Amitriptyline Elavil
Clomipramine Anafranil
Desipramine Norpramin
Doxepin Sinequan
Imipramine Tofranil
Nortriptyline Aventyl HCL, Pamelor
Protriptyline Vivactil
Trimipramine Surmontil
Selective serotonin reuptake inhibitors (SSRIs) Citalopram Celexa
Escitalopram Lexapro
Fluoxetine Prozac, Sarafem
Fluvoxamine Fluvox
Paroxetine Paxil, Pexeva
Sertraline Zoloft

to take into account the receptor dynamics. Antidepressant
medications, like other chemicals, are known to cause down-
regulation of CNS β-adrenergic receptors, only 2 to 3 weeks
after the initiation of drug therapy.99-101 Because the subjects
in the above studies were given TCAs for periods of 5 days
or less, the down-regulation of the β-adrenergic receptors
never took place. This may cause one to think that the so-
called hypertensive reactions took place in TCA-naive sub-
jects rather than in adrenergic receptor down-regulated
subjects.
The contaminant use of antihypertensive medications with
vasoconstrictors has always been a critical question on the
mind of many dentists. For this reason in 1955, the American
Heart Association addressed this topic by issuing a statement
that recommended a maximum of 200 μg of epinephrine be
used on patients with heart disease during one dental appoint-
ment. That equals 11 cartridges of 1 : 100,000 epinephrine,
which is slightly below the 13.9 cartridge limitation for local
anesthetic toxicity.102 Then in 1964 in a joint statement, the
American Heart Association and the American Dental
Association concluded, “Concentrations of vasoconstrictors
normally used in dental local anesthetic solutions are not
contraindicated in patients with cardiovascular disease when
administered carefully and with preliminary aspiration.”103
Subsequently, recommendations were made to use 23- through
30-gauge needles for intraoral injections because of their ease
in aspiration. Any needle higher than a 30-gauge makes aspi-
ration very difficult and unreliable.30
As a second-line agent for the treatment of hypertension,
β-blocking agents have been used for years to treat hyperten-
sion and other medical conditions, such as angina and cardiac
arrhythmias. β-blockers are typically classified as either “non-
selective” with both β1 and β2 activity or “selective” meaning
that they preferentially block β1 receptors in the heart (Table
3-7). Because of epinephrine’s 50 : 50 affinity for β1 and β2 if
a nonselective β-blocker, such as propranolol, is used, the β2
vasodilatory effects of epinephrine will be blocked, allowing
only α1 vasoconstrictive effect. This may lead to a serious
increase in blood pressure, with a concomitant reflex brady-
cardia.7,21,43,88,93 For this reason, some advocate complete
avoidance of vasoconstrictor-containing local anesthetic solu-
tions in these patients on nonselective β-blockers, especially
if hemostasis is not required.88,93 Others recommend checking
for any significant change in blood pressure before the initia-
tion of the procedure. This can be accomplished by initially
TABLE 3-7 b-Blocker Classification
Nonselective b-Blockers Selective b1-Blocker
Nadolol (Corgard) Acebutolol (Sectral)
Propranolol (Inderal, Innopran XL) Atenolol (Tenormin)
Sotalol (Betapace) Bisoprolol (Zebeta)
Timolol (Blocadren) Esmolol (Brevibloc)
Metoprolol (Lopressor, Toprol XL)
CHAPTER 3 • Local Anesthetics 43
injecting a 1-mL test dose of vasoconstrictor-containing solu-
tions and monitoring blood pressure for 5 to 10 minutes to
identify any adverse reaction.7,21,88
In a study by Abraham-Inpijn et al, patients with known
hypertension that were injected with 2% lidocaine with
1 : 80,000 epinephrine were noted to have a greater likelihood
of having an elevated blood pressure than those patients who
were thought to be normotensive.104 In a similar study, Meyer
compared the response of normotensive and hypertensive
patients who were injected with plain lidocaine, lidocaine
with 1 : 100,000 epinephrine, and lidocaine with 1 : 20,000
NE. No significant differences were noted in heart rate or
blood pressure between plain lidocaine and lidocaine with
epinephrine. However, with regard to NE, it produced a sig-
nificant increase in blood pressure and a decreased heart rate
when compared with plain lidocaine.86
Recent studies undertaken by Niwa et al have demon-
strated that providing 3.6 mL of lidocaine with 1 : 80,000 epi-
nephrine can be carried out safely on patients with an exercise
capacity of more than 4 metabolic equivalents, which equates
to walking 4.8 km/hr, doing light yard work, or painting.105 In
another study using 10 healthy human subjects and pulsed
Doppler echocardiography of mitral valve, Niwa et al com-
pared the effects of 3.6 mL of 2% lidocaine with either
1 : 80,000 epinephrine or 1 : 25 NE and concluded that epi-
nephrine activates left ventricular diastolic function, and in
contrast NE impairs it.106 In yet another study, Niwa et al
evaluated 27 patients with cardiovascular disease with imped-
ance cardiology to determine hemodynamic responses to an
injection of 1.8 mL of 2% lidocaine with 1 : 80,000 epineph-
rine.61 Based on this study, there was no or very little hemo-
dynamic consequence in patients with cardiovascular disease
who received lidocaine with epinephrine. From the preceding
studies, it is safe to say that two to three cartridges of 2%
lidocaine with 1 : 100,000 epinephrine appear to be well toler-
ated in most patients with cardiovascular disease. The approx-
imate use of 36 to 54 μg of epinephrine appears to outweigh
potential disadvantages of not using vasoconstriction.94
With the increased need to take medically compromised
patients to the operating room for extractions, the contami-
nant use of local anesthetics plus vasoconstriction with halo-
genated general anesthetics is becoming more common. As a
result, agents, such as halothane, enflurane, and isoflurane,
which are known to sensitize the myocardium to both endog-
enous and exogenous catecholamines, can pose a serious risk
of cardiac arrhythmias. Typically the arrhythmias generated
with halothane seem to be the more arrhythmogenic than
either enflurane or isoflurane.7,43,62 Table 3-8 lists the maximum
recommended doses for both epinephrine and levonordefrin
when used in the presence of these inhalation anesthetics.7,43
For instance no more that 100 μg of epinephrine is recom-
mended within a 10-minute period of when halothane is
administered. Obviously, under the realm of general anesthe-
sia, local anesthetics containing vasoconstrictors are usually
used for their hemostatic effects intraoperatively and not for
pain control.
44 SECTION I ■ Anesthesia and Pain Control
Maximum Recommended Dose of
TABLE 3-8 Vasoconstrictors in Patients Receiving
Halogenated Hydrocarbons7
Halothane Enflurane Isoflurane
EPINEPHRINE (0.1 mg/mL)
10 min 100 μg 100 μg 300 μg
60 min 300 μg 300 μg 900 μg
LEVONORDEFRIN (0.05 mg/mL)
10 min 320 μg 320 μg — Uncontrolled cardiac arrhythmias
60 min 960 μg 960 μg — Decompensated congestive heart Failure (CHF)
Finally, it appears that the administration of lidocaine in
combination with a vasoconstrictor has a cardioprotective
effect, thus justifying its limited use in patients with cardio-
vascular disease. Previous concerns about the safety and effi-
cacy of vasoconstrictors have been reduced based on more
recent prospective, blinded, randomized, human clinical trials.
They speak to the safety of epinephrine as a local anesthetic
vasoconstrictor.*
PATIENT CONSIDERATIONS AND MAXIMUM
DOSAGES FOR VASOCONSTRICTORS
There are certain patient populations that may have difficulty
tolerating additional increases in systemic epinephrine levels.
This is especially true in high-risk, medically compromised
patients who receive therapeutic doses of local anesthetic with
vasoconstrictor.110,111 As mentioned previously, adverse out-
comes associated with vasoconstrictors can occur even under
the recommended dose limitations. Table 3-9 summarizes the
maximum recommended dosages of vasoconstrictors from
the 1955 American Heart Association guidelines. Addition-
ally a simple mnemonic has been devised for calculating the
maximum safe dosages of any local anesthetic. “The rule of
25” states that one may safely use one cartridge of any mar-
keted local anesthetic for every 25 lbs of the patient. For
instance in a 100-lb patient, four cartridges will be a safe
cutoff.112
As expected most patients with cardiovascular disease
would seem to be most prone to adverse effects from catechol-
amine administration. Yet conflicting data fails to consistently
show the deleterious effects of local anesthetics with vasocon-
strictors in patients with hypertension or cardiovascular
disease.† Recommendations from various authorities range
from absolute avoidance of vasoconstrictors to a maximum
dose of 200 μg set by the American Heart Association in
1955.113 The dosages shown in Table 3-9 are recommended
for healthy American Society of Anesthesiologists (ASA)
class I patients, keeping in mind that the 1 : 50,000 should
only be used for local hemostasis and not routine use.21,43
Another commonly used dosage limitation for a group of
patients is 40 μg of epinephrine, which equates to one car-
*References 54,61,71,72,80,83,86,105-109.
†
References 58,61,80,86,102,107.
Conditions in Which the Use of
BOX 3-1 Vasoconstriction Should Be Avoided or
Minimized30,114,115,117
Heart Diseases
Resting blood pressure >200/115
Unstable angina
Myocardial infarct (MI) within 6 mo
Cerebrovascular accident (CVA) within 6 mo
Coronary artery bypass graft (CABG) within 6 mo
Thyroid Disease
Untreated hyperthyroidism
Asthma
Sulfite-sensitive asthma
True allergy to sulfite antioxidant
tridge of a 1 : 50,000 solution, two cartridges of a 1 : 100,000
solution, or four cartridges of a 1 : 200,000 solution; or 200 μg
of levonordefrin, which equates to two cartridges of a 1 : 20,000
solution.21 Yet even with these recommendations, one must
realize the great variability that exists in this patient popula-
tion; for there are no absolutes when it comes to patient
stratification. Last but not least are the ASA class III and IV
patients with unstable angina and poorly controlled ventricu-
lar arrhythmias that require emergency treatment under local
anesthesia.55 In this patient population, elective surgery should
be delayed until the underlying medical condition is brought
under control. Box 3-1 lists a number of conditions in which
it would be prudent to completely avoid the use of vasocon-
strictors.21,114,115 In 1986 in a joint statement by the American
Heart Association and the American Dental Association, it
was concluded that “vasoconstrictor agents should be used in
local anesthesia solutions during dental practice only when it
is clear that the procedure will be shortened or the analgesia
rendered more profound. Extreme care should be taken to
avoid intravascular injection and the minimum possible
amount of vasoconstrictor should be used.”116
Patients with untreated hyperthyroidism are especially
sensitive to both endogenous and exogenous catecholamines
and often have concomitant hypertension and/or cardiac
arrhythmias. The excessive release of thyroid hormone can
potentiate both the pressor and the myocardial effects of
epinephrine.7,21,115
As a result of the addition of sodium bisulphate or metabi-
sulfite as an antioxidant to increase the shelf life of vasocon-
strictors in local anesthetics, patients with documented sulfite
allergy should be treated with plain local anesthetic solu-
tions.* Approximately 9 million sulfite-sensitive asthmatics
are also included in this group of patients because they can
also have hypersensitivity reactions.120 Sulfite antioxidants or
sulfur dioxide are typically found in foods, such as salads, dry
fruit, shellfish, and wine.118
*References 6,7,21,115,118,119.

Maximum Recommended Dosages of Vasoconstrictors Derived from the 1955 American Heart Association
TABLE 3-9
Guidelines113
Drug Concentration
mg/mL
Epinephrine 0.02
0.01
0.005
Levonordefrin 0.05
*Maximum number of cartridges is limited by the local anesthetic.
†
Should only be used for local hemostasis.
TABLE 3-10 Use of Local Anesthetics During Pregnancy123
Drug FDA Category
LOCAL ANESTHETICS (INJECTABLE)
Articaine C
Bupivacaine C FROM LOCAL ANESTHESIA
Lidocaine B
Mepivacaine C PROLONGED SENSORY ALTERATION
Prilocaine B
LOCAL ANESTHETICS (TOPICAL)
Benzocaine C
Lidocaine B the informed consent because the risk was so “infinitesi-
VASOCONSTRICTORS
Epinephrine 1 : 200,000 or 1 : 100,000 C (at higher doses)
Levonordefrin 1 : 20,000 Not ranked
Lastly the pregnant and lactating women, when it comes
to this patient population, local anesthetics and vasoconstric-
tors are always a cause for trepidation in practitioners.
However, repeated studies show local anesthetics and vaso-
constrictors can safely be used in pregnant or nursing patients.
Definitive treatment of an odontogenic infection should not
be put off because definitive treatment is the best way to
prevent the problems of prolonged use of systemic analgesics
and antibiotics. In a study of healthy, nursing mothers under-
going dental treatment, it was found that it is safe for an infant
to breast-feed from a mother who has received an injection of
3.6 to 7.2 mL of lidocaine without adrenaline.121 Because all
local anesthetics cross the placental barrier, it is important to
avoid intravascular injection via aspiration. The highest level
transplacental delivery to the infant is seen with prilocaine,
followed by lidocaine, and the lowest level with bupivacaine.122
Table 3-10 summarizes the Food and Drug Administration
(FDA) drug category for the major local anesthetics and vaso-
constrictors that may be used.44 Lidocaine and prilocaine
obtained the best FDA ranking, with lidocaine more prefera-
ble because of its lower concentration and decreased risk of
systemic toxicity. As far as topical anesthetics, lidocaine also
has the safest rating. Although high-dose vasoconstrictors are
used to manage significant hypotension episodes in pregnant
patients, the doses of epinephrine used in local anesthetic
formulations are so low that they are unlikely to cause any
significant change in uterine blood flow. With careful use the
CHAPTER 3 • Local Anesthetics 45
Maximum Recommended Dose
Parts/1000 mg mL No of Cartridges
1 : 50,000† 0.2 10 5
1 : 100,000 0.2 20 11
1 : 200,000 0.2 40 11*
1 : 20,000 1.0 20 11
benefits of vasoconstrictors in local anesthetics, outweigh the
risks of systemic toxicity in pregnant patients.123
■ LOCALIZED COMPLICATIONS
In 1989 the Ontario (Canada) high court ruled that prolonged
sensory alteration did not need to be an essential part of
mal, minimal, extremely small, or in order of magnitude
1 : 800,000.”124 Based on Dower’s data analysis, the frequency
of paresthesia is most common with articaine at 1 : 219,949
and least frequent with lidocaine at 1 : 4,405,130.125 Even
though the chance of prolonged sensory alteration is quite
small, every clinician should try to prevent this outcome
because each case can become a nuisance, not just for the
patient but also the clinician. Persistent sensory alteration is
reportedly the most common reasons for lawsuits against oral
and maxillofacial surgeons.126
Prolonged sensory alteration is defined as persistent anes-
thesia or altered sensation, such as itching or tingling, that
persists well beyond the expected duration of anesthesia. It
can also mean dysesthesia, painful sensation, or hyperesthesia,
an increased sensitivity to stimuli. The most common com-
plaints as a result of paresthesias are speech changes and loss
of taste and drooling, with the lingual nerve being the most
common cause. Most of these are transient sensory alterations
that resolve within 8 weeks, but may also become irrevers-
ible.127 If the damage to the nerve is more severe, the risk of
permanent paresthesia is increased, most commonly involving
the tongue then the lower lip.124 If the patient’s neurodeficit
persists beyond 2 months, he or she should be referred to an
oral surgeon or a neurologist for consultation. In a study by
Hillerup, third molar extractions accounted for the majority
of injuries to the lingual, inferior alveolar, and buccal nerves.
The injection of local anesthetics was the second most fre-
quent cause. In the same study, the female gender was over-
represented in incidence of injured nerves (Figure 3-3),
although no gender difference was found in the severity of
paresthesias.12
Although it is known that the most frequent cause of pro-
longed sensory alteration is direct surgical trauma,130-132 studies
46 SECTION I ■ Anesthesia and Pain Control

TABLE 3-11 Distribution of Analgesic Solution and Nerve Affected Including 54 Nerve Injuries in 52 Patients129
Local Anesthetic Inferior Alveolar Nerve Lingual Nerve Sum N (%)
Articaine 4% 5 24 29 (54%)
Prilocaine 3% 4 6 10 (19%)
Lidocaine 2% 3 7 10 (19%)
Mepivacaine 3% 0 4 4 (7%)
Mepivacaine 3% + Articaine 4% 0 1 1 (2%)
Number of nerve injuries 12 42 54 (100%)

Number of cases 3.1 million for lidocaine, 2.4 million for prilocaine, 1.6 million
12 for mepivacaine, and 0.2 million for bupivacaine. So the
actual incidence of paresthesias does not correlate with the
10 usage of each local anesthetic. Interestingly, before the intro-
duction of articaine in the United States in 2000, the occur-
8 rence of paresthesia was studied and found to be mostly related
to lidocaine 51% of the time. Based on all the reported data,
6 nerve damage seems to be concentration dependent, which
would explain the recent increase in paresthesia cases. Yet
4 contradictory results were obtained by Hoffmeister, who
studies direct nerve injury caused by toxicity. He noted no
2 histologic changes with intrafascicular administration of artic-
aine, claiming that “when used in normal concentrations,
0 local anesthesia does not have a toxic effect.”135 The jury is
1997 1998 1999 2000 2001 2002 2003 2004
still out on this issue, requiring further investigation into this
Females
Males
matter before making any definitive conclusions. For this
reason, some recommend that 4% articaine and 4% prilocaine
FIGURE 3-3. Distribution of 52 patients referred with 54 injection injuries should only be used for infiltrative anesthesia and not for
of inferior alveolar and/or lingual nerves from 1997 to June 2004. Female/male inferior alveolar nerve blocks.136 The package insert from
ratio = 2/1, P = 0.012.129
the articaine manufacturers puts the overall rate below 1%,
based on clinical trials in the United States and United
Kingdom.137
show that the local anesthetic itself can be a source of nerve In terms of direct injury to the lingual or inferior alveolar
trauma. Concentration-dependent neurotoxicity has been nerve, the neurovascular bundle can be traumatized by
reported in many studies.53,133,134 In a 21-year retrospective the sharp needle tip, the subsequent repositioning of the
study in Ontario, Canada, Haas and Lennon demonstrated needle.124,130-132 Using the “traditional” inferior alveolar block,
that in nonsurgical extractions cases 4% articaine and 4% otherwise known as the Halstead approach, local anesthetic
prilocaine were significantly more likely to cause prolonged is deposited near the mandibular foramen. Coincidentally the
neurologic deficits than were other local anesthetic solu- lingual nerve is directly in the path of needle insertion. Fur-
tions.124 It should be noted that both articaine and prilocaine thermore with the mouth wide open during the injection, the
are marketed as 4% solutions, the highest concentrations lingual nerve becomes more taut, reducing its chance of being
available in dentistry. All reported cases involved anesthesia deflected by the searing needle. This will lead to a higher
of the mandibular arch, with symptomatic tongue or the lip. likelihood that the needle will penetrate the nerve potentially
Articaine was the offending anesthetic in 49% of cases, prilo- (1) severing nerve fiber; (2) damaging small blood vessels
caine in 42.2%, lidocaine in 4.9%, and mepivacaine in 3.9%. located within the epineurium and leading to intraneural
Table 3-11 indicates that 4% articaine is 20 times more likely hemorrhage; or (3) damaging connective tissues within the
to cause prolonged sensory alteration as compared with 2% nerve via edema. All three events can lead to prolonged
lidocaine.125 This claim has been further strengthened by sensory alteration, which may be transient or permanent.138
another study in Denmark where 54% of nerve injuries were Some report an increased incidence of paresthesia in patients
associated with 4% articaine, a substantial increase in the who report an “electric” sensation along the path of a nerve
number of injuries after its introduction in the Danish during the injection. This may indicate that the lingual
market.129 nerve is in direct contact with the injecting needle, in which
In the same time period, the number of anesthetic car- case the needle should be retracted away from the nerve before
tridges used totaled approximately 4.4 million for articaine, the injection of the local anesthetic.124,138

TRISMUS
Trismus is a relatively uncommon complication after
local anesthetic injection. It may be due to injury, spasm, or
infection within the medial pterygoid muscle, which is
typically violated during an inferior alveolar nerve block.
This can be prevented by following the basics of atraumatic
injection technique.21 With the application of hot, moist
towels to the effected side, in conjunction with range of
motion exercises, improvement should be noted in about 2 to
3 days.
HEMATOMA
This is typically seen right after the injection as a localized
mass of extravasated blood that follows inadvertent injury to
the underlying blood vessels. Vessels most commonly involved
are: pterygoid plexus of veins, the posterior superior vessels,
and the mental vessels.139 Prevention is the best measure, by
reducing the number of times the mucosa is penetrated. If a
visible hematoma develops, apply direct pressure. If subacute,
wait 6 hours before the application of ice. Analgesics may be
indicated.
PAIN ON INJECTION
This is most often due to the speed of local anesthetic delivery.
If the solution is injected too quickly, it distends the tissue
rapidly causing a painful stimulus. Furthermore if the tempera-
ture of the anesthetic is at the extremes of temperature,
more pain will be sensed. According to Malamed each car-
tridge should be injected over a 1-minute period, and the
anesthetics should be stored at room temperature.30
NEEDLE BREAKAGE
Although uncommon a sudden unexpected movement from
the patient or a bent needle can lead to a breakage of the
needle, which most commonly occurs at the hub. As expected
smaller-diameter needles, such as 30-gauge needles, tend to
break more often than larger-bore needles of 25-gauge or
higher. To prevent this complication, the following are rec-
ommended: The needle should not be bent more than once,
never insert the needle up to its hub, do not apply excessive
force or redirect the needle once within the soft tissue. If a
breakage event occurs, inform the patient and document the
event. Refer the patient to an oral and maxillofacial surgeon
with all the pertinent radiographic images and documentation
for prompt retrieval of the foreign object.139
FACIAL NERVE PARALYSIS
Because facial nerve (CN VII) traverses the parotid capsule,
it is not surprising that transient paralysis can occur if the local
anesthetic is deposited within the parotid capsule. Again pre-
vention is the best medicine, paying attention to the direction
and depth of the needle. If facial paralysis occurs, reassure the
patient, create an eye patch to protect the cornea, and have
the patient remove contact lenses if indicated. Eyedrops may
also be indicated. Return of function will occur within a few
hours depending on the type of local anesthetic used.
CHAPTER 3 • Local Anesthetics 47
■ SYSTEMIC COMPLICATIONS FROM
LOCAL ANESTHESIA
As the injected local anesthetic diffuses away from the site of
injection, it is systemically distributed and absorbed by the
internal organs for metabolism and excretion. The typical
doses of local anesthetic used in dentistry are minimal, and
therefore systemic effects tend to be uncommon. However, in
susceptible patients with repeated injections over the recom-
mended limits, systemic overdoses and even death has
occurred. The initial sign of a systemic overdose may be muscle
twitching, tremors, shivering, or even tonic-clonic seizures.140
This excitatory reaction is thought to be due to the disinhibi-
tion of select inhibitory neurons within the limbic system of
the CNS. As the toxic blood concentrations continue to rise,
drowsiness, lethargy, sedation, and respiratory depression will
follow. Eventually, with extremely toxic levels cardiovascular
conductivity will be disrupted leading to cardiac arrhythmia
and bradycardia.
Long-acting local anesthetics bupivacaine and etidocaine
are known to possess a greater risk of producing cardiotoxic
events than do other local anesthetics.7,42,67,141 Bupivacaine’s
cardiotoxic property is related to its ability to produce a dose-
dependent or high-frequency blockade at normal heart rates.
The treatment of these types of toxic events is largely sup-
portive, making prevention the first and foremost strategy
in avoiding systemic toxicities. The local anesthetic dosing
guidelines are typically based on body weight, and because of
this, children tend to be at greater risk for toxic reactions.
True dose-dependent toxicities to local anesthetics are fre-
quently reported in the pediatric population.142 Because local
anesthetics have a relatively narrow therapeutic index, most
overdoses in children are seen with formulations greater than
the 2% concentrations without epinephrine.30,143 Excessive
plasma levels of local anesthetics are the major cause of mor-
bidity and mortality associated with these agents.* This is
commonly seen in children receiving plain 3% mepivacaine
or 2% lidocaine with 1 : 100,000 epinephrine, without any
regard for maximum dosing guidelines.66,143-147
Methemoglobinemia is another unique reaction that can
be seen with the use of local anesthetics. It typically occurs 1
to 3 hours after the administration of the local anesthetic.
Other medications, such as nitrates and sulfonamide antibiot-
ics, can also act as the initiating factor. In terms of local
anesthetics, prilocaine is thought to cause oxidation of the
iron atom in hemoglobin from the reduced Fe2+ state to the
oxidized Fe3+ state, leading to a deficient oxygen transport
phenomenon characterized by a cyanotic-appearing patient.7
The clinical signs of cyanosis are initially noted as the level
of methemoglobin reaches 10% to 20%. With an increase in
the level nearing 35% to 40%, dyspnea and tachycardia will
ensue. Fortunately, in patients without significant cardiovas-
cular or pulmonary disease, this reaction is well tolerated.
However, in pediatric patients and patients with hereditary
*References 6, 7, 20, 21, 24, 26, 66, 67.
48 SECTION I ■ Anesthesia and Pain Control
methemoglobinemia, who already have a portion of their
hemoglobin in the Fe3+ state, small quantities of prilocaine
can cause a serious reaction. Other risk factors for this reaction
include patients with glucose-6-phosphate dehydrogenase and
methemoglobin reductase deficiency. In these patient popula-
tions, an alternative local anesthetic solution should be used.
If a patient becomes cyanotic, treat appropriately with intra-
venous methylene blue (1 to 2 mg/kg).
Table 3-4 lists the maximum recommended dosages of
various local anesthetic solutions. Because these dosages are
based on a patient’s body weight, a 14-kg pediatric patient can
theoretically tolerate only one fifth of the local anesthetic
given to a 70-kg or greater adult patient. Because there is 50%
more local anesthetic per cartridge in 3% mepivacaine solu-
tion (54 mg/cartridge) than in 2% lidocaine solutions (36 mg/
cartridge), the maximum recommended dosages of 3% mepi-
vacaine are more easily exceeded than a 2% lidocaine solu-
tion.45 Additionally recent studies have failed to show that 3%
mepivacaine produces a shorter duration of lip and tongue
anesthesia than an equal volume of 2% lidocaine plus
1 : 100,000 epinephrine. For this reason, the use of 3% mepi-
vacaine and 4% prilocaine should be avoided in young chil-
dren. It should be noted that in very obese children, the
maximum dose should be calculated using the ideal body
weight and not the true body weight.
Malignant hyperthermia (MH) is a rare disorder with an
autosomal dominant pattern of inheritance, which is a major
cause of anesthetic-related morbidity and mortality in other-
wise healthy patients. The role of local anesthetics, stress, and
epinephrine in inducing this syndrome is also controversial.148
MH is characterized by the development of temperature eleva-
tion, muscle rigidity, and increased oxygen consumption in
susceptible patients. Tachycardia, tachypnea, and blood pres-
sure changes are the early clinical signs, with subsequent cya-
nosis, disseminated intravascular coagulation, and renal failure
as a result of myoglobinuria, arrhythmias, cardiac arrest, and
eventual cardiovascular collapse. It was first described by Den-
borough and Lovell in 1960; subsequently, numerous reports
have documented this condition. MH is relatively rare with
incidence estimates of 1 in 15,000 in children with anesthetic
administrations to 1 in 50,000 in adults. Mean age of sus-
pected MH patients is 18 years, with a male preponderance of
roughly 2 : 1. Some early studies expressed concern over amide
local anesthesia as a trigger for MH episodes.149 In particular
lidocaine was thought to be contraindicated in MH patients
because of their in vitro ability to increase calcium release from
sarcoplasmic reticulum isolated from non-MHS animals.
However, these concerns have never been supported by clini-
cal experience. For years lidocaine has also been used in
patients with MH with no reported complications. Currently,
it is widely agreed that local anesthesia is safe in MH patients.
In the recent past, there have been reports of dentists refusing
to treat patients with MH because of concerns that lidocaine
may trigger an MH reaction.150 Hopefully with today’s under-
standing of local anesthetics and MH such circumstances can
be avoided.
Hypersensitivity or allergic reaction to local anesthetics is
rare, especially with amide local anesthetics. In 1975 Verrill
reported only 12 allergic reactions in the United Kingdom
between 1964 and 1971. In that same time period, millions of
local anesthetic injections were given, making the incidence
of allergic reactions less than 1%.151 In general if a patient has
an allergic reaction to a particular agent in one class, they will
most likely be okay with agents from the other class. On the
rare occasion that a patient is allergic to both classes of local
anesthetics, a 0.5% to 1% solution of diphenhydramine
(Benadryl) plus 1 : 100,000 epinephrine can be used as a pos-
sible alternative, with an onset of action of about 5 minutes
and a duration of at least 30 to 50 minutes.152 As compared
with the actual local anesthetics, this mixture tends to cause
more pain on injection and is less efficacious. It also carries a
risk of tissue necrosis or dermal sloughing at more than recom-
mended concentrations of 2% to 5%.153-155 Subsequently,
these patients should be referred to an allergy specialist to
initiate the process of evaluating a patient for allergy to a
local anesthetic because this can be an arduous and time-
consuming process.
■ TOPICAL ANESTHETICS
Painful procedures, such as venipuncture, extractions of teeth,
and repair of simple to complicated lacerations, are common
in the pediatric population. To reduce distress in the child
and sometimes the parent, the use of topical anesthetic has
been recommended to provide a pleasant experience. It has
been reported that painful dental treatment in children is
relatively frequent even in specialized pediatric practice with
42 out of 361 (11.6%) children experiencing ineffective pain
control. Additionally, in another study, 14 out of 17 dentists
(82.4%) had one or more patients in whom pain control was
not effective.156
Topical anesthetics can be applied painlessly to reduce
physical and psychological stress and the need for physical and
chemical restraint.157 Additionally the use of topical anes-
thetic can help with the repair of lacerations, without distor-
tion of the tissue margins that typically occurs with use of
infiltrative anesthesia.158 Because of the reduced blood supply
at the skin level, the concentration of a topical anesthetic are
typically higher to adequately anesthetize the soft tissue. If not
careful, this can lead to rapid and excessive systemic uptake
of the local anesthetic, which can lead to systemic toxicity.
Anesthetic sprays, such as Cetacaine, can be especially haz-
ardous and should only be used as directed.7 Below is a list of
the most common agents used.
LIDOCAINE
A 5% topical lidocaine base is commonly used for the reduc-
tion of needle-stick pain and has demonstrated an efficacy
with needles not larger than 27-gauge.159-161 The onset is typi-
cally within 2 to 3 minutes, with a duration of 15 minutes.
Two percent viscous lidocaine is also available for use in the
management of alveolar osteitis. When placed directly into
the extraction socket, patients report relief in a few minutes.162

A mucoadhesive patch called Denti-patch containing 46.1 mg
of lidocaine base can also be highly efficacious in reducing the
pain produced by 25-gauge labial needle sticks.163,164 Anes-
thetic onset ranges between 2.5 to 5 minutes, with durations
lasting at least 30 minutes after removal of the patch. With
respect to safety, systemic blood levels produced by these
patches are approximately one ninth that of a typical lido-
caine plus epinephrine injection and one half-that of an
equivalent amount of lidocaine ointment.163,164
LMX
LMX, formally known as ELA-max, is a preparation of lido-
caine encapsulated liposomes. It comes in different formula-
tions of LMX4 or LMX5, which refers to 4% or 5% of lidocaine.
The liposomes facilitate the rate and the extent of absorption
in a controlled fashion, while preventing rapid metabolism of
the drug. Unlike EMLA cream, the application of LMX does
not require any occlusive dressing, and a prescription is not
required. The cost of LMX approximately equals EMLA
cream. Its efficacy has been demonstrated in the success rates
and the shortened duration of venipuncture in children when
compared with placebo.165 LMX is an over-the-counter prepa-
ration and should be applied to the indicated area 30 minutes
before the initiation of the procedure. One to 2 g of LMX can
be applied to 10 cm2 of skin, with the total maximum dose in
kids more than 20 kg set at 2000 cm2.
BENZOCAINE
As mentioned in the beginning of the chapter, benzocaine is
poorly water soluble, making it the drug of choice for anes-
thetizing mucosal surfaces because it is not absorbed systemi-
cally. In spite of this, benzocaine is not totally innocuous, as
evidenced by case reports of methemoglobinemia in children
who received large doses.24 Methemoglobinemia is more likely
to occur with benzocaine in patients with predisposing condi-
tions, such as glucose-6-phosphate dehydrogenase deficiency
or concurrent use of medications that cause methemoglobin.
As mentioned earlier, if a patient becomes cyanotic, treat
appropriately with intravenous methylene blue (1 to 2 mg/kg),
if medically indicated. A 20% ointment is typically sufficient
at the mucosal surface and will reduce needle-stick pain. Its
onset and duration characteristics are similar to those of 5%
lidocaine ointment, with the onset typically between 2 to 3
minutes and a duration of 15 minutes.
TETRACAINE
Tetracaine is an ester local anesthetic that is highly lipid
soluble and rapidly absorbed when placed on mucous mem-
branes. It is the most potent topical anesthetic and thus the
most toxic. It is typically sold in a spray form, composed of
14% benzocaine, 2% butyl aminobenzoate, and 2% tetracaine
and sold under the name Cetacaine. It is indicated for the
production of anesthesia and control of pain at all accessible
mucous membranes except the eyes. It has been used to control
gagging during endoscopic procedure and other surgical pro-
cedures of the ear, nose, mouth, pharynx, larynx, trachea,
CHAPTER 3 • Local Anesthetics 49
bronchi, and esophagus.30 Because of its rapid absorption and
toxic potential, the maximum recommended dose for an adult
is only 20 mg. Care should be taken not to exceed the “two
second spray” rule. Average expulsion rate of residue from
spray, at normal temperatures, has been calculated at 200 mg/
sec. Mindful of its content, on rare occasions, methemoglo-
binemia has been reported in connection with Cetacaine as a
result of the presence of benzocaine. Injudicious administra-
tion, especially in the form of unmetered sprays for widespread
surface anesthesia or to reduce the gagging reflex, can lead to
serious toxicity because fatalities have been reported.7 Remem-
ber that the onset of action is rapid, approximately 30 seconds,
and the duration of anesthesia is typically 30 to 60 minutes.
COCAINE
As discussed in the history of local anesthetics, cocaine’s
intrinsic vasoconstrictive properties were widely used in the
nineteenth century. However, with the development of syn-
thetic local anesthetics, its use has fallen out of favor. Today
because of its abuse potential and toxic stimulation of the
sympathetic nervous system, cocaine has no place in routine
oral surgery procedures, unless it is used as part of simple closed
nasal reduction.7,6,17 Because of its excellent topical anesthetic
and vasoconstrictive activity when used in concentrations of
1% to 10%, it makes for an excellent tool for intranasal
surgery.
EMLA
EMLA cream is a topical anesthetic that has been widely used
for superficial procedures, such as lacerations, circumcisions,
venipunctures, and lumbar punctures. It has been shown to
be just as effective as lidocaine with epinephrine, which war-
rants its use as a matter of practicality rather than its effi-
cacy.166 When it was discovered that crystalline bases of
lidocaine and prilocaine could be combined to produce a
liquid at room temperature, finally the goal of achieving local
anesthesia without inflicting pain was realized. The “E and M”
in EMLA cream signifies an “eutectic mixture” because the
mixture of the two substances has a melting point lower than
that of either substance by itself. The eutectic mixture con-
tains 2.5% lidocaine and 2.5% prilocaine in a cream base and
has excellent penetration as a result of its micron-sized drop-
lets. There is very little irritation or toxicity noted, mostly
consisting of local vascular signs, such as pallor, erythema,
pruritus, and numbness.167
The onset of action can vary based on the vascularity of
the affected area. For the face, the onset can be as fast as 15
minutes, although for most sites at least 60 minutes is required.
Generally speaking the depth of anesthesia increases by
1 mm/30 min, with an approximate maximum depth of 5 mm
by 120 minutes. Anything deeper than 5 mm requires addi-
tional infiltrative local anesthesia of choice, keeping in mind
the use of prilocaine and the resultant methemoglobinemia
in susceptible pediatric patients. EMLA cream is supplied in
many forms, but the most popular form includes the EMLA
Anesthetic Disc or just the EMLA cream supplied with an
50 SECTION I ■ Anesthesia and Pain Control
occlusive dressing similar to Tegaderm. Typically 1 to 2 g of
EMLA cream is sufficient for 10 cm2. Both should be in place
for at least 1 hour before the initiation of any procedure.168
EMLA is still not recommended for use on mucous mem-
branes because of its rapid and pronounced systemic absorp-
tion; however, its use is becoming more commonplace,
especially in Europe.169 There have been several published
reports of its application on oral mucosa, and it seemed to
cause significantly more anesthesia than placebo ointments or
5% lidocaine ointment.169,170 EMLA was also more effective
than placebo or 5% lidocaine ointment in reducing the dis-
comfort of gingival probing or gingival scaling after only a few
minutes.171,172 EMLA cream has also been used during the
removal of arch bars, with the simple application of 4 g on a
toothbrush.173 At these dosages of EMLA, lidocaine blood
levels resemble those of a 1.8-mL intraoral injection.173,174
LET
LET is a combination of 4% lidocaine, 0.1% epinephrine, and
0.5% tetracaine, available in methylcellulose gel or aqueous
solution. It is most frequently used for repair of lacerations in
children. It provides adequate anesthesia for the closure of
75% to 90% of scalp lacerations.175,176 If the anesthesia is
inadequate, then supplemental lidocaine can be provided after
the initial onset of the LET ointment. As a precautionary
measure, because of the presence of epinephrine, LET should
not be used in areas that have end arterial supplies, such as
digits, ears, and nose. In the aqueous form, it can be painted
onto the skin, and after 20 minutes anesthesia becomes effec-
tive. The gel formulation is also applied in the same manner
with the same onset of action, although the duration is longer
at 40 minutes.175
IONTOPHORESIS
Iontophoresis is a recent technique for transdermal adminis-
tration of lidocaine. It used an electric current from two exter-
nally placed electrodes to move ionized lidocaine across the
stratum corneum barrier to the dermis to block free nerve
endings.177 As expected the rate of transport is much higher
than passive diffusion. In a randomized crossover study, pedi-
atric patients who required repeated venous cannulation pre-
ferred iontophoresis over EMLA.177 In another study of 100
children, significantly less pain was perceived when using ion-
tophoresis during venipuncture.178 0.6 to 1.0 mL of 2% lido-
caine with epinephrine is first administered. Then a titrated
electric current of 0 to 4 mA is provided over a 10-minutes
period to achieve a depth of 5 to 7 mm of anesthesia.
THERMAL
Ice can be used for short-term topical anesthetic for such
procedures as simple laceration, venipuncture, and injections.
For adequate anesthesia, the ice must be applied to the skin
for more than 10 seconds. Alternatively, “vapo-coolants,”
such as ethyl chloride, can be used by spraying the indicated
area for 1 to 2 seconds, although its effects are short lived
versus regular ice. As with any other allergy, caution needs to
be used in patients with a history of temperature or cold sen-
sitivities because this may lead to blistering.166 A three-step
method that initially uses ice to reduce pain from the needle,
followed by benzyl alcohol–containing saline to painlessly
reduce the sting of lidocaine with epinephrine has been used
during hair transplant surgery.179
■ LATEST DEVELOPMENT AND
THE FUTURE DIRECTION OF
LOCAL ANESTHESIA
With the patients becoming less tolerant of painful proce-
dures, the last few decades has seen increased research activity
into alternative methods to the transitional techniques, such
as the inferior alveolar nerve block. Although some of these
alternative methods have been on the market for some time,
some still require further perfecting before it will be widely
accepted by general practitioners. Below is a brief synopsis of
these techniques and what to expect over the near future; it
is not meant to be comprehensive.
Microparticulate formulations—With the push to provide
better postoperative pain relief, development of a variety of
controlled-release formulations has taken place. Generally
they have longer duration of action with less side effects as
demonstrated in different animal models. Studies show that
nerve blockade can be further prolonged by co-encapsulating
a second drug.180 For example, in a recent study, the addition
of dexamethasone to lipid-protein-sugar particles (LPSP)
containing bupivacaine leads to an almost doubling of the
duration of block, while maintaining good long-term biocom-
patibility.181 Such formulations could be useful in clinical
applications when a nerve blockade is needed for 24 hours or
less. Prolonged anesthesia can be useful in some myofascial
pain patients, via a simple injection at the trigger sites to
reduce the pain stimuli. In others it can facilitate physical
therapy in certain skeletal muscle disorders, such as
torticollis.
Intraosseous anesthesia—Intraosseous anesthesia is useful
for anesthetizing a single tooth by providing local anesthesia
directly into the cancellous bone surrounding the root of the
indicated tooth. There are essentially two systems that
create a hole in the cortical bone, allowing for a smaller-
circumference needle to penetrate the cancellous bone and
provide local anesthetic to the indicated teeth. Each system
offers both advantages and disadvantages. Stabident (Fairfax
Dental, Miami, Fla) was the first such system developed, with
the X t.i.p. (X t.i.p Technologies, Lakewood, N.J.) introduced
in 1999.
Computer-controlled injections—There are currently a
number of computer-controlled injection devices. They also
offer a number of advantages and disadvantages. As compared
with traditional syringes, these devices are larger, require more
space, and are more expensive. Because of a more aesthetically
appearing needle and handle, they are generally better received
by patients with needle phobias. The computer is able to
control the rate and the pressure of the injection, allowing
for titration of the anesthetic for patient comfort. In 1997

Milestone Scientific launched a Computer Controlled Local
Anesthetic Delivery System (CCLADS known as the “wand,”
which has subsequently been renamed “CompuMed-Featuring
the Wand Hand-Piece.” The CCLAD was designed to deliver
a potentially painless injection of local anesthetic. Since the
availability of the CCLAD numerous studies have been con-
ducted to compare pain associated with the CCLAD and a
hypodermic needle and syringe. In a study of 40 patients
undergoing either Mohs’ microscopic surgery for treatment of
skin cancer removal or a skin biopsy procedure to determine
a positive skin cancer for Mohs’ surgery, the CCLAD was
reported in patients with a normal to low tolerance to cause
less pain than what was experienced with prior injections or
the control group using hypodermic syringes.182 In a study of
101 patients undergoing hair transplant, True et al reported
that anesthesia with the CCLAD was less painful than the
conventional syringe technique.127 In contrast Whalen et al
reported in their study that 11 of 15 patients experienced
less pain with the traditional injection than with CCLAD-
administered local anesthetic.183 The contradictory results
reported by these two groups could perhaps be due to the
experience of the person administering the local anesthetic.
Needleless injections—The administration of medication
without the use of a needle has always been highly desirable.
Initial reports of this novel approach was first reported in 1947
by Hingson and Hughes.184 Refinement of this technique took
place over the next few decades, where in the 1970s multiple
reports showed promising reduction of pain in patients with
cancer. These systems can be divided into three types. The
first group is the disposable, single-use tips, such as J-Tip and
Biojector 2000. The second type has multiple-use nozzles,
such as Ped-O-Jet, Med-E-Jet, and Syrijet. With the third
type, the device is designed for single patient use: Medi-Jector,
which is used for self-administration of variable doses of
insulin. Generally speaking they all employ a technology
based on a piston-pressure expulsion system that forces local
anesthetic into the desired area. In 2000 Cooper et al com-
pared the efficacy of needle-free injections versus injections
using 25-gauge needles before venous cannulation and found
that patients reported less pain on injection with the needle-
free system.
Electronic dental anesthesia (EDA) is one of the latest
developments in pain control. Based on the same principles
as transcutaneous electronic nerve stimulation (TENS), it
uses electrical wave forms and voltage/amperage parameters
to facilitate the disruption of the neuronal pathways transport-
ing the pain stimuli to the brain. Although there has been
success with this technology in the field of medicine for back
pain and sports injuries, its impact in the dental field still
remains to be seen.
REFERENCES
1. Ture H et al: The art of alleviating pain in Greek mythology,
Neurosurgery 56(1):178-85, 2005.
2. Zorab J: History of anaesthesia, Anaesthesia 58(9):935, 2003.
CHAPTER 3 • Local Anesthetics 51
3. Wilkinson K: Anaesthetists and care of the critically ill child 3,
Anaesthesia 58(8):804-5, 2003.
4. Reiling J: Miscellany, JAMA 287(16):2042, 2002.
5. Greene R, Institute for Research in History: History of medicine,
New York, Institute for Research in History and the Haworth
Press, 1988.
6. Hersh EV, Condouris GA: Local anesthetics: a review of their
pharmacology and clinical use, Compendium 8(5):374,376,378-
81, 1987.
7. Jastak JT et al: Local anesthesia of the oral cavity, Philadelphia,
Saunders, 1995.
8. Covino BG, Vassallo HG: Local anesthetics: mechanisms of action
and clinical use. The scientific basis of clinical anesthesia, New
York, Grune & Stratton, 1976.
9. Buhler A: Zur erforschung des kookanenusses, Ciba Z 8:3353-9,
1994.
10. Becker HK: Carl Koller and cocaine, Psychoanal Q 32:309-73,
1963.
11. Fink BR: Neural blockade in clinical anesthesia and manage-
ment of pain. In Cousins MJ, Bridenbaugh PO, editors: History
of neural blockade, ed 3, Philadelphia, Lippincott-Raven,
1998.
12. Cocaine, Br Med J 1(6169):971-2, 1979.
13. Allen C: Local and regional anesthesia, WB Saunders, 1918.
14. Fink BR: Leaves and needles: the introduction of surgical local
anesthesia, Anesthesiology 63(1):77-83, 1985.
15. Macmillan WH: A hypothesis concerning the effect of cocaine
on the action of sympathomimetic amines, Br J Pharmacol
Chemother 14:385-91, 1959.
16. Lathers CM et al: Cocaine-induced seizures, arrhythmias and
sudden death, J Clin Pharmacol 28(7):584-93, 1988.
17. Katzung BG: Clinical pharmacology, ‘88/’89. A Lange clinical
manual, Norwalk, Conn, Appleton & Lange, 1988.
18. Hadda SE: Procaine: Alfred Einhorn’s ideal substitute for
cocaine, J Am Dent Assoc 64:841-5, 1962.
19. Dobbs EC: A Chronological history of local anesthesia in den-
tistry, J Oral Ther Pharmacol 21:546-9, 1965.
20. Yagiela JA: Management of pain and anxiety in dental practice.
In Dionne R, Phero JC, editors: Local anesthetics, New York,
Elsevier, 1991.
21. Malamed SF: Handbook of local anesthesia, ed 4, St Louis, Mosby,
1997.
22. Koeppe T et al: Current trends in local anesthesia in cosmetic
plastic surgery of the head and neck: results of a German
national survey and observations on the use of ropivacaine,
Plast Reconstr Surg 115(6):1723-30, 2005.
23. George EN et al: Re-evaluating selection criteria for local
anaesthesia in day surgery, Br J Plast Surg 57(5):446-9,
2004.
24. Yagiela JA, Neidle EA, Dowd FJ: Pharmacology and therapeu-
tics for dentistry. In Yagiela JA, editor: Local anesthetics, ed 4,
St Louis, Mosby, 1997.
25. Covino BG, Giddon DB: Pharmacology of local anesthetic
agents, J Dent Res 60(8):1454-9, 1981.
26. Hersh EV: Local anesthetics in dentistry: clinical consider-
ations, drug interactions, and novel formulations, Compendium
14(8):1020, 1022, 1024 passim, 1993.
27. Luebke NH, Walker JA: Discussion of sensitivity to preserva-
tives in anesthetics, J Am Dent Assoc 97(4):656-7, 1978.
28. Meechan J: How to avoid local anaesthetic toxicity, Br Dent J
184(7):334-5, 1998.
29. Strichartz GR et al: Fundamental properties of local anesthet-
ics. II. Measured octanol : buffer partition coefficients and pKa
values of clinically used drugs, Anesth Analg 71(2):158-70,
1990.
30. Malamed SF: Handbook of local anesthesia, ed 5, St Louis, Mosby,
2004.
52 SECTION I ■ Anesthesia and Pain Control
31. Horrobin DF, Durand LG, Manku MS: Prostaglandin E1 modi-
fies nerve conduction and interferes with local anaesthetic
action, Prostaglandins 14(1):103-8, 1977.
32. Brown RD: The failure of local anaesthesia in acute inflamma-
tion: some recent concepts, Br Dent J 151(2):47-51, 1981.
33. Aceves J, Machne X: The action of calcium and of local anes-
thetics on nerve cells, and their interaction during excitation,
J Pharmacol Exp Ther 140:138-48, 1963.
34. Strichartz G: Molecular mechanisms of nerve block by local
anesthetics, Anesthesiology 45(4):421-41, 1976.
35. Hille B: Common mode of action of three agents that decrease
the transient change in sodium permeability in nerves, Nature
210(5042):1220-2, 1996.
36. Strichartz GR: The inhibition of sodium currents in myelinated
nerve by quaternary derivatives of lidocaine, J Gen Physiol
62(1):37-57, 1973.
37. Condouris GA: A study on the mechanism of action of cocaine
on amphibian peripheral nerve, J Pharmacol Exp Ther 131:243-
9, 1961.
38. Ritchie JM, Ritchie B, Greengard P: The effect of the nerve
sheath on the action of local anesthetics, J Pharmacol Exp Ther
150:160-4, 1965.
39. Ritchie JM, Ritchie B, Greengard P: The active structure
of local anesthetics, J Pharmacol Exp Ther 150(1):152-9,
1965.
40. Wilson S, Johns P, Fuller PM: The inferior alveolar and
mylohyoid nerves: an anatomic study and relationship to local
anesthesia of the anterior mandibular teeth, J Am Dent Assoc
108(3):350-2, 1984.
41. Pyle MA et al: Prevalence and implications of accessory retro-
molar foramina in clinical dentistry, Gen Dent 47(5):500-3,
1999.
42. Yagiela JA: Local anesthetics, Anesth Prog 38(4-5):128-41,
1991.
43. Jastak JT, Yagiela JA: Vasoconstrictors and local anesthesia: a
review and rationale for use, J Am Dent Assoc 107(4):623-30,
1983.
44. Haas DA: An update on local anesthetics in dentistry, J Can
Dent Assoc 68(9):546-51, 2002.
45. Guideline on appropriate use of local anesthesia for pediatric
dental patients. In Reference manual 2005-2006, 2005, Ameri-
can Academy of Pediatric Dentistry.
46. Moore PA: Long-acting local anesthetics: a review of clinical
efficacy in dentistry, Compendium 11(1):22, 24-6, 28-30,
1990.
47. Sisk AL: Long-acting local anesthetics in dentistry, Anesth
Prog 39(3):53-60, 1992.
48. Chapman PJ, Macleod AW: A clinical study of bupivacaine for
mandibular anesthesia in oral surgery, Anesth Prog 32(2):69-72,
1985.
49. Giovannitti JA, Bennett CR: The effectiveness of 1.5% etido-
caine HCl with epinephrine 1:200,000 and 2% lidocaine HCl
with epinephrine 1:100,000 in oral surgery: a clinical compari-
son, J Am Dent Assoc 107(4):616-8, 1983.
50. Danielsson K, Evers H, Nordenram A: Long-acting local anes-
thetics in oral surgery: an experimental evaluation of bupiva-
caine and etidocaine for oral infiltration anesthesia, Anesth
Prog 32(2):65-8, 1985.
51. Johnson GK, Hlava GL, Kalkwarf KL: A comparison of peri-
odontal intraligamental anesthesia using etidocaine HCl and
lidocaine HCl, Anesth Prog 32(5):202-5, 1985.
52. McLean C et al: An evaluation of 4% prilocaine and 3%
mepivacaine compared with 2% lidocaine (1:100,000 epineph-
rine) for inferior alveolar nerve block, J Endod 19(3):146-50,
1993.
53. Sisk AL: Vasoconstrictors in local anesthesia for dentistry,
Anesth Prog 39(6):187-93, 1993.
54. Nakamura Y et al: Cardiovascular and sympathetic responses
to dental surgery with local anesthesia, Hypertens Res 24(3):209-
14, 2001.
55. Yagiela JA: Vasoconstrictor agents for local anesthesia, Anesth
Prog 42(3-4):116-20, 1995.
56. Larochelle P et al: Prazosin plasma concentration and blood
pressure reduction, Hypertension 4(1):93-101, 1982.
57. Pallasch TJ: Vasoconstrictors and the heart, J Calif Dent Assoc
26(9):668-73, 676, 1998.
58. Chernow B et al: Local dental anesthesia with epinephrine.
Minimal effects on the sympathetic nervous system or on
hemodynamic variables, Arch Intern Med 143(11):2141-3,
1983.
59. Henslee TM et al: Vasoconstrictive agents commonly used in
combination with local anesthetics: a literature review, J Foot
Surg 26(6):504-10, 1987.
60. van der Bijl P, Victor AM: Adverse reactions associated with
norepinephrine in dental local anesthesia, Anesth Prog
39(3):87-9, 1992.
61. Niwa H et al: Cardiovascular response to epinephrine-
containing local anesthesia in patients with cardiovascular
disease, Oral Surg Oral Med Oral Pathol Oral Radiol Endod
92(6):610-6, 2001.
62. Cassidy JP, Phero JC, Grau WH: Epinephrine: systemic effects
and varying concentrations in local anesthesia, Anesth Prog
33(6):289-97, 1986.
63. Holm SW et al: Hypertension: classification, pathophysiology,
and management during outpatient sedation and local anesthe-
sia, J Oral Maxillofac Surg 64(1):111-21, 2006.
64. Goebel WM, Allen G, Randall F: The effect of commercial
vasoconstrictor preparations on the circulating venous serum
level of mepivacaine and lidocaine, J Oral Med 35(4):91-6,
1980.
65. Cannell H et al: Circulating levels of lignocaine after peri-oral
injections, Br Dent J 38(3):87-93, 1975.
66. Hersh EV, Helpin ML, Evans OB: Local anesthetic mortality:
report of case, ASDC J Dent Child 58(6):489-91, 1991.
67. Bacsik CJ, Swift JQ, Hargreaves KM: Toxic systemic reactions
of bupivacaine and etidocaine, Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 79(1):18-23, 1995.
68. Chilton NW: Clinical evaluation of prilocaine hydrochloride
4 percent solution with and without epinephrine, J Am Dent
Assoc 83(1):149-54, 1971.
69. Berling C: Carbocaine in local anesthesia in the oral cavity,
Odontol Rev 9:254-67, 1958.
70. Sinnott CJ et al: Addition of sodium bicarbonate to lidocaine
decreases the duration of peripheral nerve block in the rat,
Anesthesiology 93(4):1045-52, 2000.
71. Knoll-Kohler E, Fortsch G: Pulpal anesthesia dependent on
epinephrine dose in 2% lidocaine: a randomized controlled
double-blind crossover study, Oral Surg Oral Med Oral Pathol
73(5):537-40, 1992.
72. Knoll-Kohler E et al: Cardiohemodynamic and serum catechol-
amine response to surgical removal of impacted mandibular
third molars under local anesthesia: a randomized double-blind
parallel group and crossover study, J Oral Maxillofac Surg
49(9):957-62, 1991.
73. Brand HS et al: Cardiovascular and neuroendocrine responses
during acute stress induced by different types of dental treat-
ment, Int Dent J 45(1):45-8, 1995.
74. Brown RS: Local anesthetics, Dent Clin North Am 38(4):619-
32, 1994.
75. Middlehurst RJ, Gibbs A, Walton G: Cardiovascular risk: the
safety of local anesthesia, vasoconstrictors, and sedation in
heart disease, Anesth Prog 46(4):118-23, 1999.
76. List T et al: Effect of local anesthesia on atypical odontalgia—a
randomized controlled trial, Pain 122(3): 306-14, 2006.

77. Beer GM et al: Oral premedication for operations on the face
under local anesthesia: a placebo-controlled double-blind trial,
Plast Reconstr Surg 108(3):637-43, 2001.
78. Sveen K: Effect of the addition of a vasoconstrictor to local
anesthetic solution on operative and postoperative bleeding,
analgesia and wound healing, Int J Oral Surg 8(4):301-6,
1979.
79. Buckley JA, Ciancio SG, McMullen JA: Efficacy of epineph-
rine concentration in local anesthesia during periodontal
surgery, J Periodontol 55(11):653-7, 1984.
80. Cioffi GA et al: The hemodynamic and plasma catecholamine
responses to routine restorative dental care, J Am Dent Assoc
111(1):67-70, 1985.
81. Tolas AG, Pflug AE, Halter JB: Arterial plasma epinephrine
concentrations and hemodynamic responses after dental injec-
tion of local anesthetic with epinephrine, J Am Dent Assoc
104(1):41-3, 1982.
82. Knoll-Kohler E et al: Changes in plasma epinephrine concen-
tration after dental infiltration anesthesia with different doses
of epinephrine, J Dent Res 68(6):1098-101, 1989.
83. Lipp M et al: Examination of central venous epinephrine level
during local dental infiltration and block anesthesia using
tritium-marked epinephrine as vasoconstrictor, Anesthesiology
69:A371, 1988.
84. Dionne RA, Goldstein DS, Wirdzek PR: Effects of diazepam
premedication and epinephrine-containing local anesthetic on
cardiovascular and plasma catecholamine responses to oral
surgery, Anesth Analg 63(7):640-6, 1984.
85. Troullos ES et al: Plasma epinephrine levels and cardiovascular
response to high administered doses of epinephrine contained
in local anesthesia, Anesth Prog 34(1):10-13, 1987.
86. Meyer FU: Haemodynamic changes under emotional stress fol-
lowing a minor surgical procedure under local anaesthesia, Int
J Oral Maxillofac Surg 16(6):688-94, 1987.
87. Yagiela JA: Vasoconstrictors: their role in local anesthesia tox-
icity, J Jpn Dent Soc Anesthesiol 21:261-78, 1993.
88. Becker DE: Drug interactions in dental practice: a summary of
facts and controversies, Compendium 15(10):1228, 1230, 1232
passim, 1994.
89. Fitzgibbon M et al: Reference values for urinary HMMA, HVA,
noradrenaline, adrenaline, and dopamine excretion in children
using random urine samples and HPLC with electrochemical
detection, Ann Clin Biochem 29(Pt 4):400-4, 1992.
90. Kocher T et al: Association between bone loss in periodontal
disease and polymorphism of N-acetyltransferase (NAT2),
J Clin Periodontol 29(1):21-7, 2002.
91. Shishikura K, Hohjoh H, Tokunaga K: Novel allele containing
a 190C>T nonsynonymous substitution in the N-acetyltrans-
ferase (NAT2) gene, Hum Mutat 15(6):581, 2000.
92. Yagiela JA: Adverse drug interactions in dental practice: inter-
actions associated with vasoconstrictors. Part V of a series,
J Am Dent Assoc 130(5):701-9, 1999.
93. Perusse R, Goulet JP, Turcotte JY: Contraindications to vaso-
constrictors in dentistry: part III, Pharmacologic interactions,
Oral Surg Oral Med Oral Pathol 74(5):692-7, 1992.
94. Brown RS, Rhodus NL: Epinephrine and local anesthesia revis-
ited, Oral Surg Oral Med Oral Pathol Oral Radiol Endod
100(4):401-8, 2005.
95. Yagiela JA, Duffin SR, Hunt LM: Drug interactions and vaso-
constrictors used in local anesthetic solutions, Oral Surg Oral
Med Oral Pathol 59(6):565-71, 1985.
96. Newcomb GM: Contraindications to the use of catecholamine
vasoconstrictors in dental local analgesics, N Z Dent J
69(315):25-30, 1973.
97. Boakes AJ et al: Interactions between sympathomimetic amines
and antidepressant agents in man, Br Med J 1(5849):311-5,
1973.
CHAPTER 3 • Local Anesthetics 53
98. Svedmyr N: The influence of a tricyclic antidepressive agent
(protriptyline) on some of the circulatory effects of noradrena-
line and adrenaline in man, Life Sci 7(1):77-84, 1968.
99. Gurguis GN et al: Adrenergic receptor function in panic dis-
order. II. neutrophil beta 2 receptors: Gs protein coupling,
effects of imipramine treatment and relationship to treatment
outcome, J Psychiatr Res 33(4):309-22, 1999.
100. Stahl SM: Serotonin receptor down regulation by antidepres-
sants: platelet and neuroendocrine markers in humans, Clin
Neuropharmacol 15(Suppl 1) Pt A:97A, 1992.
101. Charney DS, Heninger GR, Sternberg DE: Serotonin function
and mechanism of action of antidepressant treatment. Effects
of amitriptyline and desipramine, Arch Gen Psychiatry 41(4):
359-65, 1984.
102. Little JW: Dental management of the medically compromised
patient, ed 6, St Louis, Mosby, 2002.
103. Akutsu A et al: Management of dental problems in patients
with cardiovascular disease, J Am Dent Assoc 68:333-42,
1964.
104. Abraham-Inpijn L, Borgmeijer-Hoelen A, Gortzak RA:
Changes in blood pressure, heart rate, and electrocardiogram
during dental treatment with use of local anesthesia, J Am Dent
Assoc 116(4):531-6, 1988.
105. Niwa H, Satoh Y, Matsuura H: Cardiovascular responses to
epinephrine-containing local anesthetics for dental use: a com-
parison of hemodynamic responses to infiltration anesthesia
and ergometer-stress testing, Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 90(2):171-81, 2000.
106. Niwa H et al: The effects of epinephrine and norepinephrine
administered during local anesthesia on left ventricular dia-
stolic function, Anesth Prog 38(6):221-6, 1981.
107. Niwa H, Sato Y, Matsuura H: Safety of dental treatment in
patients with previously diagnosed acute myocardial infarction
or unstable angina pectoris, Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 89(1):35-41, 2000.
108. Meechan JG: Differences between men and women regarding
attitudes toward dental local anesthesia among junior students
at a United Kingdom dental school, Anesth Prog 52(2):50-5,
2005.
109. Goldstein DS et al: Circulatory, plasma catecholamine, corti-
sol, lipid, and psychological responses to a real-life stress (third
molar extractions): effects of diazepam sedation and of inclu-
sion of epinephrine with the local anesthetic, Psychosom Med
44(3):259-72, 1982.
110. Yagiela JA: Death in a cardiac patient after local anesthesia
with epinephrine, Orofac Pain Manage 1:6, 1991.
111. Umino M et al: Unexpected atrial fibrillation during tooth
extraction in a sedated elderly patient, Anesth Prog 41(3):77-80,
1994.
112. Moore PA, Hersh EV: Dental therapeutics update. Introduc-
tion, Dent Clin North Am 46(4):xv-xviii, 2002.
113. Use of epinephrine in connection with procaine in dental pro-
cedures: report of the special committee of the New York Heart
Association, Inc. on the use of epinephrine in connection
with procaine in dental procedures, J Am Dent Assoc 50:108,
1955.
114. Perusse R, Goulet JP, Turcotte JY: Contraindications to vaso-
constrictors in dentistry: part I. Cardiovascular diseases, Oral
Surg Oral Med Oral Pathol 74(5):679-86, 1992.
115. Perusse R, Goulet JP, Turcotte JY: Contraindications to
vasoconstrictors in dentistry: part II. Hyperthyroidism, diabe-
tes, sulfite sensitivity, cortico-dependent asthma, and pheo-
chromocytoma, Oral Surg Oral Med Oral Pathol 74(5):687-91,
1992.
116. Kaplan EL: Cardiovascular disease in dental practice, American
Dental Association, American Heart Association, Dallas, 1986,
American Heart Association.
54 SECTION I ■ Anesthesia and Pain Control
117. Goulet JP, Perusse R, Turcotte JY: Contraindications to vaso-
constrictors in dentistry: part III. Pharmacologic interactions,
Oral Surg Oral Med Oral Pathol 74(5):692-7, 1992.
118. Simon RA: Sulfite sensitivity, Ann Allergy 56(4):281-8, 1986.
119. Seng GF, Gay BJ: Dangers of sulfites in dental local anesthetic
solutions: warning and recommendations, J Am Dent Assoc
113(5):769-70, 1986.
120. Bush RK et al: Prevalence of sensitivity to sulfiting agents in
asthmatic patients, Am J Med 81(5):816-20, 1986.
121. Giuliani M et al: Could local anesthesia while breast-feeding
be harmful to infants? J Pediatr Gastroenterol Nutr 32(2):142-4,
2001.
122. Watson AK: Local anaesthetics in pregnancy, Br Dent J
165(8):278-9, 1988.
123. Haas DA, Pynn BR, Sands TD: Drug use for the pregnant or
lactating patient, Gen Dent 48(1):54-60, 2000.
124. Haas DA, Lennon D: A 21 year retrospective study of reports
of paresthesia following local anesthetic administration, J Can
Dent Assoc 61(4):319-20, 323-6, 329-30, 1995.
125. Dower JS Jr: A review of paresthesia in association with
administration of local anesthesia, Dent Today 22(2):64-9,
2003.
126. Colin W, Donoff RB: Restoring sensation after trigeminal
nerve injury: a review of current management, J Am Dent Assoc
123(12):80-5, 1992.
127. True RH et al: Microprocessor-controlled local anesthesia
versus the conventional syringe technique in hair transplanta-
tion, Dermatol Surg 28(6):463-8, 2002.
128. Hillerup S: Iatrogenic injury to oral branches of the trigeminal
nerve: records of 449 cases, Clin Oral Investig, 2006.
129. Hillerup S, Jensen R: Nerve injury caused by mandibular block
analgesia, Int J Oral Maxillofac Surg 35(5):437-43, 2006.
130. Pogrel MA, Bryan J, Regezi J: Nerve damage associated with
inferior alveolar nerve blocks, J Am Dent Assoc 126(8):1150-5,
1995.
131. Pogrel MA, Kaban LB: Injuries to the inferior alveolar and
lingual nerves, J Calif Dent Assoc 21(1):50-4, 1993.
132. Pogrel MA, Thamby S: Permanent nerve involvement result-
ing from inferior alveolar nerve blocks, J Am Dent Assoc
131(7):901-7, 2000.
133. Lambert LA, Lambert DH, Strichartz GR: Irreversible conduc-
tion block in isolated nerve by high concentrations of local
anesthetics, Anesthesiology 80(5):1082-93, 1994.
134. Sakura S et al: The addition of 7.5% glucose does not alter the
neurotoxicity of 5% lidocaine administered intrathecally in the
rat, Anesthesiology 82(1):236-40, 1995.
135. Hoffmeister B: Morphological changes of peripheral nerves
following intraneural injection of local anesthetic, Dtsch
Zahnarztl Z 46(12):828-30, 1991.
136. Yagiela JA: Recent developments in local anesthesia and
oral sedation, Compend Contin Educ Dent 25(9):697-706,
2004.
137. Wynn RL, Bergman SA, Meiller TF: Paresthesia associated
with local anesthetics: a perspective on articaine, Gen Dent
51(6):498-501, 2003.
138. Malamed SF: Nerve injury caused by mandibular block analge-
sia, Int J Oral Maxillofac Surg 35(9):876-7, 2006.
139. Haas DA: Localized complications from local anesthesia, J Calif
Dent Assoc 26(9):677-82, 1998.
140. Moore PA: Adverse drug interactions in dental practice: inter-
actions associated with local anesthetics, sedatives and anxio-
lytics. Part IV of a series, J Am Dent Assoc 130(4):541-54,
1999.
141. Clarkson CW, Hondeghem LM: Mechanism for bupivacaine
depression of cardiac conduction: fast block of sodium channels
during the action potential with slow recovery from block
during diastole, Anesthesiology 62(4):396-405, 1985.
142. Moore PA, Goodson JM: Risk appraisal of narcotic sedation for
children, Anesth Prog 32(4):129-39, 1985.
143. Moore PA: Preventing local anesthesia toxicity, J Am Dent
Assoc 123(9):60-4, 1992.
144. California Board of Dental Examiners: Dentist loses license in
child death case, Anesth Prog 26:24-25, 1979.
145. Goodson JM, Moore PA: Life-threatening reactions after pedo-
dontic sedation: an assessment of narcotic, local anesthetic, and
antiemetic drug interaction, J Am Dent Assoc 107(2):239-45,
1983.
146. Moore MA: Current management of hypertension, Am Fam
Physician 32(6):129-36, 1985.
147. Tarsitano JJ: Children, drugs and local anesthesia, J Am Dent
Assoc 70:1153-8, 1965.
148. Murray C, Sasaki SS, Berg D: Local anesthesia and malignant
hyperthermia: review of the literature and recommendations for
the dermatologic surgeon, Dermatol Surg 25(8):626-30, 1999.
149. Winder RL, Simon JF Jr, Wingard DW: Malignant hyperther-
mia and stress: a concern in dental therapy, J Pedod 3(2):142-
54, 1979.
150. Minasian A, Yagiela JA: The use of amide local anesthetics in
patients susceptible to malignant hyperthermia, Oral Surg Oral
Med Oral Pathol 66(4):405-15, 1988.
151. Verrill PJ: Adverse reactions to local anaesthetics and vasocon-
strictor drugs, Practitioner 214(1281):380-7, 1975.
152. Gallo WJ, Ellis E III: Efficacy of diphenhydramine hydrochlo-
ride for local anesthesia before oral surgery, J Am Dent Assoc
115(2):263-6, 1987.
153. Howell JM, Chisholm CD: Wound care, Emerg Med Clin North
Am 15(2):417-25, 1997.
154. Ramsdell WM: Severe reaction to diphenhydramine, J Am
Acad Dermatol 21(6):1318-20, 1989.
155. Ramsdell WM: Skin cancer: a primer for the nondermatologist,
Tex Med 85(2): 52-5, 1989.
156. Nakai Y et al: Effectiveness of local anesthesia in pediatric
dental practice, J Am Dent Assoc 131(12):1699-705, 2000.
157. Hollander JE, Singer AJ: Laceration management, Ann Emerg
Med 34(3):356-67, 1999.
158. Smith GA et al: Comparison of topical anesthetics without
cocaine to tetracaine-adrenaline-cocaine and lidocaine infiltra-
tion during repair of lacerations: bupivacaine-norepinephrine
is an effective new topical anesthetic agent, Pediatrics 97(3):
301-7, 1996.
159. Yaacob HB, Noor GM, Malek SN: The pharmacological effect
of xylocaine topical anaesthetic–a comparison with a placebo,
Singapore Dent J 6(2):55-7, 1981.
160. Holst A, Evers H: Experimental studies of new topical anaes-
thetics on the oral mucosa, Swed Dent J 9(5):185-91, 1985.
161. Rosivack RG, Koenigsberg SR, Maxwell KC: An analysis of the
effectiveness of two topical anesthetics, Anesth Prog 37(6):290-
2, 1990.
162. Betts NJ et al: Evaluation of topical viscous 2% lidocaine jelly
as an adjunct during the management of alveolar osteitis, J Oral
Maxillofac Surg 53(10):1140-4, 1995.
163. Hersh EV et al: Analgesic efficacy and safety of an intraoral
lidocaine patch, J Am Dent Assoc 127(11):1626-34, 1996.
164. Houpt MI et al: An evaluation of intraoral lidocaine patches
in reducing needle-insertion pain, Compend Contin Educ Dent
18(4):309-10, 312-4, 316, 1997.
165. Taddio A et al: Liposomal lidocaine to improve procedural
success rates and reduce procedural pain among children: a
randomized controlled trial, Cmaj 172(13):1691-5, 2005.
166. Zempsky WT, Karasic RB: EMLA versus TAC for topical anes-
thesia of extremity wounds in children, Ann Emerg Med
30(2):163-6, 1997.
167. Berde CB: Toxicity of local anesthetics in infants and children,
J Pediatr 122(5 Pt 2):S14-20, 1993.

168. Gajraj NM, Pennant JH, Watcha MF: Eutectic mixture of
local anesthetics (EMLA) cream, Anesth Analg 78(3):574-83,
1994.
169. Paschos E et al: Efficacy of intraoral topical anesthetics in
children, J Dent 34(6):398-404, 2006.
170. Svensson P, Petersen JK: Anesthetic effect of EMLA occluded
with Orahesive oral bandages on oral mucosa: a placebo-
controlled study, Anesth Prog 39(3):79-82, 1992.
171. Donaldson D, Meechan JG: A comparison of the effects of
EMLA cream and topical 5% lidocaine on discomfort during
gingival probing, Anesth Prog 42(1):7-10, 1995.
172. Svensson P, Petersen JK, Svensson H: Efficacy of a topical
anesthetic on pain and unpleasantness during scaling of gingi-
val pockets, Anesth Prog 41(2):35-9, 1994.
173. Pere P et al: Topical application of 5% eutectic mixture of lig-
nocaine and prilocaine (EMLA) before removal of arch bars,
Br J Oral Maxillofac Surg 30(3):153-6, 1992.
174. Haasio J et al: Topical anaesthesia of gingival mucosa by 5%
eutectic mixture of lignocaine and prilocaine or by 10% ligno-
caine spray, Br J Oral Maxillofac Surg 28(2):99-101, 1990.
175. Kennedy RM, Luhmann JD: The “ouchless emergency depart-
ment.” Getting closer: advances in decreasing distress during
painful procedures in the emergency department, Pediatr Clin
North Am 46(6):1215-47, vii-viii, 1999.
176. Resch K et al: Topical anesthesia for pediatric lacerations: a
randomized trial of lidocaine-epinephrine-tetracaine solution
versus gel, Ann Emerg Med 32(6):693-7, 1998.
CHAPTER 3 • Local Anesthetics 55
177. Galinkin JL et al: Lidocaine iontophoresis versus eutectic
mixture of local anesthetics (EMLA) for IV placement in chil-
dren, Anesth Analg 94(6):1484-8, table of contents, 2002.
178. Squire SJ, Kirchhoff KT, Hissong K: Comparing two methods
of topical anesthesia used before intravenous cannulation in
pediatric patients, J Pediatr Health Care 14(2):68-72, 2000.
179. Swinehart JM: The ice-saline-Xylocaine technique. A simple
method for minimizing pain in obtaining local anesthesia,
J Dermatol Surg Oncol 18(1):28-30, 1992.
180. Castillo J et al: Glucocorticoids prolong rat sciatic nerve block-
ade in vivo from bupivacaine microspheres, Anesthesiology
85(5):1157-66, 1996.
181. Colombo G et al: Prolonged duration local anesthesia with
lipid-protein-sugar particles containing bupivacaine and dexa-
methasone, J Biomed Mater Res A 75(2):458-64, 2005.
182. Anderson ZN, Podnos SM, Shirley-King R: Patient satisfaction
during the administration of local anesthesia using a computer
controlled local anesthetic delivery system, Dermatol Nurs
15(4):329-30, 392, 2003.
183. Whalen K, Rabinovitz HS, Oliviero MC: Microprocessor-
controlled local anesthesia versus the conventional syringe
technique in hair transplantation, Dermatol Surg 29(1):113,
2003.
184. Hingson R, Hughes J: Clinical studies with jet injection: a new
method of drug administration, Curr Res Anesth Analg 26:221-
30, 1947.
CHAPTER 4
PHARMACOLOGY OF DRUGS IN
AMBULATORY ANESTHESIA
■ BENZODIAZEPINES
DISCOVERY AND DEVELOPMENT
During the summer of 1949, neurochemistry researcher Eugene
Roberts was working in a laboratory in Bar Harbor, Maine,
studying the amino acid content of neuroblastomas in mice.
Using paper chromatography, Roberts analyzed brain extracts
of mice with neuroblastoma to compare them with mice that
were tumor free. He discovered a chemical that was present
in the tumor-free mice and was absent when neuroblastoma
was present. This chemical was soon afterwards identified as
γ-amino butyric acid (GABA), but its role was unclear at the
time. It was not until 1957 that GABA was identified as an
important inhibitory neurotransmitter of the central nervous
system (CNS).1
The 1950s also represented an earnest search for sedative-
hypnotics that could work as effectively as the barbiturates
and phenothiazines but with fewer side effects and lower abuse
potential. Dr. Leo Sternbach, a scientist at Hoffman-LaRoche,
was working with a class of compounds that held promise as
barbiturate replacements, but found only one compound in
this group that had any chemical activity. The compound was
shelved and forgotten for several years, and, while cleaning
his laboratory, Sternbach came across the compound and
decided to test it further. This compound was chlordiazepox-
ide, a benzodiazepine (BZD)—it was found to have sedative
and muscle relaxant properties and later to also possess anti-
convulsant and amnestic effects.2 It was approved by the FDA
in 1960 and marketed by Hoffman-LaRoche as Librium, the
prototype of a drug group that would dramatically change the
landscape of anesthesia practice.
The connection between the BZD and GABA was not
fully elucidated until the 1970s when GABA receptors were
identified in the CNSs of mammals.3 This led to the develop-
ment of additional BZD agonists and the search for antago-
nists. The first true antagonist, flumazenil, was synthesized in
1979.
STRUCTURE AND ACTIVITY OF BZD
All BZD are characterized by having one benzene ring fused
to a seven-membered diazepine ring. They act in two loca-
tions: at central receptors on neuronal membrane and periph-
erally on receptors on mitochondria. The pharmacologic
56
Jeffrey Dembo • Bethany L. Serafin
actions of the BZD are closely related to the inhibitory neu-
rotransmitter GABA. GABA exerts its inhibitory effect by
opening the chloride ion channel on neuronal membranes,
thus hyperpolarizing the cell membrane and making it less
likely to depolarize. BZD bind to benzodiazepine receptors
presynaptically and postsynaptically, which facilitates the
binding of GABA and potentiates its activity, causing CNS
inhibition. In the absence of GABA, the BZD have no innate
pharmacologic effects.
The GABA-BZD receptor complex has been studied
extensively and, although the precise three-dimensional con-
figuration has not been mapped, there is general agreement
that it is a macromolecular complex containing at least 16
different types of subunits.4 These subunits include GABAA
receptors, a BZD receptor, a barbiturate receptor, and a chlo-
ride ionophore (channel). A BZD receptor must be linked to
GABAA receptors, but not all GABAA receptors are paired
with BZD receptors.5 It is still unknown why there exists
a BZD receptor because to date there have been no
endogenous BZD-like chemicals identified. All BZD, both
agonists and antagonists, bind to the receptors reversibly and
competitively.
Other drugs have been found to bind to the GABA-BZD
receptor complex, although their relationships to GABA
activity do not appear to be as specific as the BZD. These
include barbiturates, propofol, steroids, etomidate, and inhala-
tion anesthetic agents. Other anesthetics, such as ketamine
and nitrous oxide, appear to have no activity at the GABA-
BZD receptor complex.
CLINICAL EFFECTS
The pharmacodynamic effects of BZD have been well charac-
terized and include anxiolysis, sedation-hypnosis, muscle
relaxation, amnesia, and anticonvulsant activity. Each BZD
has a differing affinity for the receptor, causing differences in
potency and pharmacokinetics between drugs. Nevertheless,
regardless of the BZD administered, the clinical effects are
similar between drugs and are closely related to receptor satu-
ration.6 At present the clinical effects are linked and one
cannot administer a BZD to achieve one therapeutic effect
(e.g., anxiolysis) without risking amnesia or sedation. However,
there are ongoing research efforts to identify and isolate com-
pounds that can selectively create anxiolysis alone without
creating amnesia, sedation, or muscle relaxation. As more is
 CHAPTER 4 • Pharmacology of Drugs in Ambulatory Anesthesia
learned about the BZD receptor subunits, it may provide
future clinicians with classes of drugs that can selectively
provide anxiolysis with no other effects.7
Anxiolysis is the first therapeutic effect achieved when
titrating the BZD. There are few studies that support any
particular BZD as being most effective in creating anxiolysis.
The level of anxiolysis is dose related. Older textbooks
instructed clinicians to titrate a BZD until Verrill’s sign was
noted (i.e., relaxation causing ptosis of the eyelids to the point
that the lower border of eyelid bisected the pupil). However,
Verrill’s sign is a sedative—not an anxiolytic—end point, and
it is possible that some patients will have benefited sufficiently
from anxiolytic doses of the BZD that there would be no need
to administer additional drug toward a sedative end point.
The inherent benefit of titrating to an anxiolytic end
point would be to minimize the total drug dose and therefore
decrease the time for recovery. The liability of this practice,
however, is that amnesia to the surgery would occur less
predictably.
The sedative-hypnotic effects of the BZD are linearly
related to dose and receptor saturation. Anxiolysis is produced
when less than 20% of receptors are occupied: Sedation
occurs when there is 30% to 50% occupancy and unconscious-
ness when greater than 60% of receptors are occupied.8
Anterograde amnesia is a well-documented effect of the
BZD and is dependent on dose and route of administration.
For example, diazepam 10 mg given orally can provide
anxiolysis and sedation, but only 40% of patients will have
some degree of amnesia.
For greater than 70% of patients to be amnestic, oral
doses of 20 mg or more would have to be administered.
Intravenously, doses of 5 mg and 10 mg of diazepam can
produce amnesia in 50% and 90% of patients, respectively.9
The incidence is similar with midazolam, with complete
amnesia in 67% of patients who received 5 mg midazolam
intravenously.
Patients often appreciate being amnestic to an oral surgical
procedure, and the degree of amnesia roughly follows in a
linear fashion the depth of sedation. However, despite an
adequate depth of sedation, it is possible there still may be
recall, and there are no reliable predictors to tell us which
patients may remember portions of the surgery. Therefore
unless absolute general anesthesia is planned throughout the
entire surgery, it would be wise to inform patients that aware-
ness during the anesthetic may occur and the patient may
retain some memory of the surgery.
The muscle relaxant effect of the BZD occurs both cen-
trally and at the spinal cord. Glycine is the major inhibitory
neurotransmitter in the brainstem and spinal cord, and BZD
mimic glycine thus causing decreased muscle tone.10 The
actions of the BZD are not related to the motor end plate or
neuromuscular transmission.
The BZD depress the central respiratory drive and CO2
response curve. When BZD are used alone and in typical doses
to achieve conscious sedation, the respiratory depressant
effects rarely cause clinically significant hypoventilation or
57
apnea. However, when used with other agents (e.g., opioids)
or when used in elderly or medically compromised patients,
the respiratory depressant effects can be significant and long
lasting. It was in elderly patients undergoing endoscopic pro-
cedures that the respiratory depressant effects of midazolam
were first noted to be potentially dangerous, primarily because
of respiratory arrest. For diazepam there may be a 50% to 65%
decrease in minute ventilation, and for midazolam it can be
anywhere from a 25% to 65% decrease that can last for
hours.
When used alone in healthy patients, BZD cause very
slight changes in heart rate, blood pressure, left ventricular
end diastolic pressure, and systemic vascular resistance. This
cardiovascular stability is thought to result from the main-
tenance of normal baroreceptor function. Diazepam has a
beneficial effect on coronary blood flow, increasing it 22% in
healthy patients and 73% in patients with coronary disease.11
Midazolam neither increases nor decreases coronary blood
flow.
Whereas the effects of BZD in younger patients may not
become clinically significant, the elderly are much more sensi-
tive to these effects and may, in fact, show significant cardio-
vascular changes. Even with modest doses and with minor
surgical procedures, a significant number of patients can expe-
rience hypotension after administration of midazolam.12
When the BZD are combined with other drugs (e.g.,
opioids), there may be significant changes in mean arterial
pressure, systemic vascular resistance, cardiac index, and
stroke volume.
PHARMACOKINETICS AND METABOLISM
Plasma concentrations of BZD follow a linear to slightly
sigmoid dose-response curve. All are highly bound to plasma
proteins, with slight differences between drugs (Table 4-1).
Metabolism occurs in the liver through glucuronide conjuga-
tion and hepatic microsomal enzymes. Because liver function
can diminish with age and with disease, metabolism can be
expected to occur more slowly in the elderly and in patients
with cirrhosis or hepatitis. Concomitant administration of
certain drugs can also increase elimination time; this includes
erythromycin, oral contraceptives, and calcium channel
blockers. All BZD are eliminated through the kidneys.
The BZD have among the widest toxic-therapeutic ratios
of any agent used for sedation and anesthesia, making them a
safe drug class. There have been reported cases of ingestion of
2000 mg diazepam orally by an adult and 300 mg by a 2-year-
old, with complete recovery in both cases.13
The only true contraindication to the use of any BZD is
allergy to the drug and acute narrow-angle glaucoma.
Diazepam
In 1965 the introduction of diazepam to dental practice greatly
improved the dentist’s ability to provide conscious sedation.
Compared with the multidrug regimens that were commonly
used, diazepam represented a drug that could be very effective
as the sole sedative and anxiolytic agent.
58 SECTION I ■ Anesthesia and Pain Control

Benzodiazepines Half-Lives and Protein diazepam: It had a much shorter half-life, did not have active
TABLE 4-1 metabolites, and was water soluble. This provided shorter
Binding
Elimination 1/2 Life (hr) % Protein Bound recovery time for patients and avoided the injection of sol-
Midazolam 1-5 95 vents that were irritating to veins. Midazolam’s water solubil-
Diazepam 20-40 97 ity derives from an imidazole ring that can selectively open
Lorazepam 10-20 88-92 and close, depending on ambient pH. At an acidic pH of less
Triazolam 1-5 85-90 than 4.0, the ring is open, conferring hydrophilicity to the
Alprazolam 9-15 70 molecule and thus making it water soluble. Hence midazolam
Flumazenil 0.7-1.3 54-64 is packaged in vials that have an adjusted pH of 2.9 to 3.7.
Once the solution is injected and is exposed to plasma pH
Modified from Smith RB, Corey SE, Kroboth PD: Pharmacokinetics of benzodiazepines.
of 7.4, the ring closes and the molecule becomes lipophilic
In Bowdle TA, Horita A, Kharasch ED, editors: The pharmacologic basis of
anesthesiology, New York, Churchill Livingstone, 1994, p 263. and is able to bond to receptors on the neural membrane.
The ring closure is not instantaneous, and complete closure
may not occur for 5 to 10 minutes after injection.15 Because
the clinical effects cannot occur until the ring has closed,
Diazepam peak drug effects may not be seen immediately after
injection.
Its water solubility has permitted midazolam liquid to be
Temazepam Desmethyldiazepam administered intramuscularly, nasally, rectally, and orally,
(Restoril®)
routes that were not available for use with diazepam. Oral
administration of midazolam was first investigated in 1988,
(bold indicates active) Methoxazepam
and a number of clinical studies confirmed its effectiveness in
children. In 1997 the FDA approved the use of midazolam
Oxazepam in children, and it became available in an oral syrup form in
(Serax®) 1998.
FIG. 4-1. Metabolites of diazepam. Triazolam (Halcion)
This BZD was originally marketed in the Netherlands in 1977
as a hypnotic and suspended from use after allegedly causing
“raving madness” in some patients, but a thorough investiga-
tion failed to provide sufficient evidence to keep the drug off
The pH of diazepam ranges from 6.2 to 6.9 and has an the market. A similar concern was raised in the United States,
elimination half-life of more than 40 hours. but it was never removed from the market, although the
Because it is not water soluble, a number of different sol- manufacturer discontinued manufacturing the highest dose
vents have been used over the years to create a preparation (0.5 mg) tablet.
for parenteral use. The preparation approved by the FDA It has a rapid onset of action (1 hour), a short elimination
included the solvent propylene glycol, whose irritating proper- half-life, and is eight times more effective than diazepam as a
ties cause the risk of phlebitis and venous thrombosis. To hypnotic. Because of its favorable pharmacokinetics, it has
minimize this risk, the manufacturer’s package insert cautions remained popular as an oral premedicant before outpatient
that the drug must be administered slowly—no more than surgical procedures. Most recently there has been increased
1 mL (5 mg) per minute—and it should not be injected into attention focused on sublingual administration of triazolam.
small veins, such as the dorsum of the hand or the wrist.14 The Because the first-pass effect through the liver is eliminated
injectable solution also contains 10% ethanol, 5% sodium compared with traditional oral administration, there is a
benzoate (a buffer), and 1.5% benzyl alcohol (a preservative). 28% increase in bioavailability of the drug when given sub-
For several years, a preparation of diazepam became available lingually compared with orally, causing greater anxiolysis and
that used a solvent containing the same lipid emulsion as amnesia.16
propofol (Dizac), but this product was discontinued in 2000.
Diazepam is metabolized into several other BZD, some of Lorazepam (Ativan)
which have sedative properties (Fig. 4-1). The long half-life This drug, frequently used in intensive care units for pro-
of the drug and the presence of active metabolites make this longed sedation, does not have a favorable profile for ambula-
drug less than ideal for use in elderly patients or those who tory anesthesia. It has a short distribution half-life and a long
are medically compromised. elimination half-life. As a result of its lower lipid solubility,
its effects do not reach a peak until 30 to 60 minutes after the
Midazolam initial IV dose. It is more effective at producing amnesia than
Midazolam was synthesized in 1975 and introduced for clini- diazepam, and the amnestic effects may last many hours after
cal use in 1986, offering several notable advantages over administration.
 CHAPTER 4 • Pharmacology of Drugs in Ambulatory Anesthesia
Flumazenil
At the time the most popular BZD, diazepam and midazolam,
were introduced for clinical use, there were no specific antago-
nists available. Nonspecific antagonists, physostigmine or
aminophylline, were used to reverse the effects of BZD. The
“reversal” effects were actually generalized CNS excitation
that frequently would overshadow some of the sedative effects
of the BZD. However, this was not true reversal because no
specific action occurred at the BZD receptor. Flumazenil, the
first true antagonist, was synthesized in 1981 and introduced
into clinical practice in 1992. Flumazenil is an imidazobenzo-
diazepine that interacts with GABA-BZD complex and com-
petitively displaces the BZD. It is not protein bound, and its
half-life is roughly 1 hour, making resedation a risk when
longer acting BZD or high doses have been administered.
Flumazenil reverses all BZD effects, but does not antagonize
the effects of other drugs that affect the GABA receptors, such
as ethanol, barbiturates, opioids, or ketamine.
Flumazenil is a very safe drug, with extremely high doses
reported to be given with generally no adverse effects. The
few adverse effects that have been reported, including anxiety,
crying, tachycardia, and nausea and vomiting, are likely
related to the sudden reversal of the therapeutic effects of the
BZD.
■ OPIATES AND OPIOIDS
DISCOVERY AND DEVELOPMENT
Archaeologic evidence and written records confirm that the
pharmacologic effects of the juice from the opium poppy,
papaver sominferum, were known to prehistoric man and early
ancient civilizations. Over centuries of time, opium was used
as an analgesic, antidepressant, antidiarrheal, and cough sup-
pressant. The drug was ingested orally as a tea or mixed with
alcoholic beverages, and it was smoked.
In 1805 morphine was isolated from opium in Germany. It
and its methylated derivative codeine are still produced today
directly from commercially grown opium. In the mid-1800s
when the syringe and needle became available, morphine was
the first drug injected using the newly designed syringe. Hence
by the time of the Civil War, it was possible to treat soldiers
injured in combat by injecting morphine.
The first semisynthetic opioids were heroin and hydromor-
phone (Dilaudid), produced by making simple chemical
changes to morphine’s piperidine ring, the portion that confers
its pharmacologic activity. The next breakthrough was the
synthesis of meperidine, discovered during the search for an
atropine-like drug. It was serendipitously learned that meperi-
dine, in addition to antimuscarinic effects, also possessed
opiate-like effects even though its chemical structure was dif-
ferent. Later, the phenylpiperidine structure of meperidine
was used as the basis for creating a whole series of synthetic
opioids beginning with fentanyl, and later alfentanil, sufent-
anil, and remifentanil. The only ones in the fentanyl series
that have not been used for humans are carfentanil and lofen-
tanil, whose potency is so great that they are generally con-
59
sidered to be useful only for veterinary management of large
animals.
A class of agonist-antagonists was also developed, begin-
ning with pentazocine (Talwin) that was introduced in
1967. The major goal of developing this class of drugs was to
provide dose-dependent analgesia while limiting the adverse
effects (e.g., respiratory depression). Later other agonist-
antagonists were developed, including butorphanol (Stadol),
nalbuphine (Nubain), buprenorphine (Buprenex), and dezo-
cine (Dalgan).
STRUCTURE AND ACTIVITY
From the 1950s until the early 1970s, the idea of an opioid
receptor had been postulated but unproven. In 1973 the first
articles appeared demonstrating the presence of opiate recep-
tors, followed by studies that demonstrated the presence of
endogenous opiates.17,18 Later a number of different opiate
receptor subtypes were characterized. There are three
major receptors (mu, delta, kappa) with as many as eight
subtypes.
The agonist-antagonists possess partial agonist activity at
μ and other receptors in addition to competitive antagonist
activity. This has been shown to create a ceiling effect that
limits respiratory depression regardless of dose administered.
It also limits the possibility of physical dependence.
The antagonists competitively bind at opioid receptors,
displacing any agonists present and thus reversing the effects
of the agonist.
CLINICAL EFFECTS
The primary desirable effect of opioids is analgesia. Analgesia
can be created at the spinal level through activation of pre-
synaptic opioid receptors. This leads to decreased levels of
neurotransmitters and thus decreased transmission of pain-
induced action potentials. Supraspinal analgesia occurs by
activation of postsynaptic opioid receptors in the brainstem
and midbrain, leading to hyperpolarization and thus neuronal
inhibition. There may also be analgesia created through
peripheral mechanisms, as evidenced by reduction of
pain when morphine is injected directly into joints
postoperatively.19
When used as an adjuvant drug for ambulatory anesthesia,
the desired effects of opioids and opiates are not necessarily
analgesia but rather sedation and euphoria, both of which
supplement and augment the actions of other sedative
agents.
The respiratory depressant effects of the opioids are caused
by a dose-dependent depression of the brainstem response to
increased CO2 and decreased O2. The respiratory pattern
changes as well, characterized by a low respiratory rate with a
large tidal volume. Respiratory depression is accentuated by
a variety of factors, including increasing age, concomitant
administration of other CNS depressants, circadian rhythms,
and sleep deprivation.
Opioids are known to cause histamine release. There is also
a central decrease in sympathetic tone, leading to a tendency
60 SECTION I ■ Anesthesia and Pain Control
toward vagal-dominated bradycardia. As a result of these two
effects, direct and indirect vasodilation occurs.
Opioids can rapidly cross the placental barrier and are
found at significant concentrations in the breast milk of
nursing mothers. After opioid administration has ceased, it
can take up to 96 hours for these concentrations to clear,
making it necessary for nursing mothers to feed their infants
using stored milk and to express and discard breast milk pro-
duced during this period of time.20
Opioids have been associated with chest wall rigidity that
usually occurs only after loss of consciousness and is associated
with high doses and rapid administration. That said, there are
cases reported where it occurred in an awake patient who
received a small dose. The mechanism is still not completely
understood. Some have concluded that it results solely
from glottic closure.21 Others have opined that it relates
to the effects of opioids on specific sites in the CNS, such
as the nucleus raphe pontis in the reticular formation
of the brainstem.22 It is not caused by direct stimulation of
skeletal muscle because it can be prevented by pretreatment
with muscle relaxants. Of all the opioids, fentanyl is the one
most prominently implicated in causing chest wall rigidity.
Meperidine
Meperidine, the first totally synthetic opioid, is also known by
its non-U.S. name “pethidine.” Its duration of action is any-
where from 3 to 5 hours.
The atropine-like effects of meperidine differ from those of
other opioids: tachycardia, decreased myocardial contractility,
and mydriasis. One of the metabolites, normeperidine, is long
acting and pharmacologically active and can cause toxic
effects in the CNS that can result in increased EEG activity,
myoclonus, and seizures. These effects are not reversible by
naloxone.
Of all the opioids, meperidine is the one most likely to
cause histamine release. In one study patients showed as high
as a 200-fold increase in serum histamine levels several minutes
after its administration, a far greater amount than either mor-
phine, fentanyl, or sufentanil.23 In addition to the potential
to create symptoms similar to anaphylaxis, this histamine
release may also be responsible for vasodilation that can lead
to clinically significant hypotension.
Fentanyl
Fentanyl is 60 to 80 times more potent than morphine, and
there is a 2 to 3 times greater affinity for fentanyl at the opiate
receptor compared with morphine.24 After injection fentanyl
is characterized by a rapid onset of action owing to its ease
of crossing the blood-brain barrier. It is rapidly eliminated,
with 99% of a single dose cleared from the plasma within
60 minutes.25
Remifentanil
Remifentanil, the most recently introduced opioid, possesses
unique properties by being μ-selective. It also has an ester
linkage and is thus metabolized by tissue and plasma esterases.
This imparts an extremely short half-life and limits the accu-
mulation of the drug in the tissues. This pharmacokinetic
profile makes it ideal for continuous infusion because a steady-
state level can be reached very rapidly, and after discontinuing
the infusion, the level of detectable drug in the serum drops
very quickly.
Naloxone
This short-acting antagonist can be used to quickly reverse
the effects of opioids. Its short duration of action, however,
implies there could be recurrence of the agonist effects when
a long-acting opioid was used. Naloxone is associated with
nausea and vomiting, the incidence of which increases
with dose and rapidity of administration. Sudden reversal of
an opioid with naloxone has also been associated with
rebound sympathetic stimulation that can cause dysrhythmias,
hypertension, myocardial infarction, stroke, and pulmonary
edema.
■ INTRAVENOUS
SEDATIVE-HYPNOTICS
DISCOVERY AND DEVELOPMENT
The barbiturates were the mainstay of intravenous anesthetic
agents for more than 80 years. Their use began with the dis-
covery of barbituric acid by von Baeyer in 1864 who mixed
malonic acid with urea. Although it had no discernable
pharmacologic properties, chemists substituted and added side
chains to the molecule until, in 1903, the first pharmacologi-
cally active barbiturate, diethylbarbituric acid (Veronal), was
identified. Shortly afterwards in 1912, phenobarbital (Luminal)
was synthesized, a drug that became popular as an anticonvul-
sant, sedative, and anxiolytic. Thiopental (Penthothal), a
thiobarbiturate, was synthesized during this same time period
and introduced into clinical practice in 1929. It became the
prototype as an anesthesia induction agent owing to its rapid
onset of action and short duration of action.
Methohexital, an oxybarbiturate, was adopted into clinical
practice in the 1960s and was found to offer some advantages
over thiopental, in particular a shorter duration of action. For
this reason, it became among the most widely used parenteral
anesthetics in dentistry. It is uncertain whether methohexital
will remain a part of our anesthetic armamentarium because
there have been intermittent shortages of methohexital in the
United States over the past decade, and its use in the United
Kingdom has been discontinued since 1999.
In an effort to identify new intravenous nonbarbiturate
anesthetics, propofol (2,6 di-isopropyl phenol) was developed
during the early 1970s. Clinical trials began in 1977, resulting
in availability for clinical use in the United Kingdom in 1986.
Stuart Pharmaceuticals received FDA approval in 1989 for
sale of propofol in the United States under the brand name
Diprivan. Because propofol is not water soluble, it is formu-
lated in a lipid emulsion containing soybean oil, egg phospha-
tide (lecithin), and glycerol. After its introduction, case
reports of septicemia began to surface, with the subsequent
 CHAPTER 4 • Pharmacology of Drugs in Ambulatory Anesthesia
discovery that the lipid emulsion was an excellent culture
medium for bacteria. The manufacturer responded by adding
a preservative, EDTA, to the preparation and by including a
warning in the package insert stating that “strict aseptic tech-
nique must always be maintained during handling.”26 Over the
past several years, two generic products have since been for-
mulated with the only difference being the use of either
sodium bisulfite or benzyl alcohol as preservatives instead of
EDTA that was used in the original patented product.
There is ongoing research using fospropofol, a prodrug that
is converted by alkaline phosphatase to propofol once
injected.27 The putative advantage is that fospropofol is water
soluble, avoiding the need for a lipid solvent. This eliminates
the risk of bacterial growth in the solvent and diminishes
the pain on injection. However, owing to the fact that it
takes time for the prodrug to be converted to active drug,
there would be a potential delay in onset of action once
injected.
STRUCTURE AND ACTIVITY
Methohexital and propofol are thought to exert their action
by interacting with GABA receptors. Although it is unclear
whether they both have common sites of action, it is certain
those sites are different from the sites associated with the
BZD.
CLINICAL EFFECTS
Methohexital
Excitatory effects, such as hiccups and myoclonic movement,
have classically been associated with methohexital, occurring
as frequently as 90% of the time in patients who receive
methohexital.28 Methohexital causes tachycardia and hyper-
tension because there is cardiac compensation for peripheral
vasodilation. It also tends to cause increased EEG activity and
has potential as an epileptogenic.29 Methohexital and other
barbiturates appear to lower the pain threshold and have been
credited with antianalgesic properties, but there is still debate
whether this is a real phenomenon.30
Propofol
Propofol tends to provide cardiovascular stability by exerting
a central sympatholytic effect that maintains a stable heart
rate. There is also an accompanying decrease in systemic vas-
cular resistance, but in the healthy patient and in the doses
typically used in oral and maxillofacial surgery, there might
be a slight—but clinically insignificant—decrease in blood
pressure.31 However, in the patient with significant cardiac
disease, in the hypovolemic patient, or when very large boluses
are given, there may be hypotension on induction. Propofol
appears to cause few changes in electrical activity of the heart
and is not typically associated with dysrhythmias. Both pro-
pofol and methohexital can cause apnea following large induc-
tion doses.
Because sensitivity to propofol increases with age and
clearance of the drug decreases, a 30% to 50% reduction in
drug dose may be required to prevent oversedation.32
61
Propofol has relatively few side effects. It does not cause
nausea and vomiting; to the contrary, it possesses antiemetic
properties and has been administered in subhypnotic doses for
the treatment of nausea and vomiting.33 The mechanism
for its antiemetic effect has not yet been elucidated.
Propofol causes little or no histamine release and has not
been associated with allergic reactions.34 Propofol has bron-
chodilating properties that may be due to direct effects on
smooth muscle.35 The literature also suggests that propofol
may have analgesic effects, as evidenced by decreased need for
postoperative analgesics by patients who received propofol
compared with another anesthetic agent.36
Propofol does not cause tissue damage when given intraar-
terially or when accidentally infiltrated into tissues.37 However,
it is associated with pain on injection, particularly when small
veins are used. Some clinicians have recommended injecting
1% lidocaine into the intravenous catheter before beginning
injection of propofol, and others have admixed lidocaine into
the vial or syringe containing propofol.38
A recently identified adverse effect associated with the
drug has been labeled “propofol infusion syndrome.” It tends
to occur with propofol infusions of greater than 48 hours, but
has also been reported after short-term infusions using large
doses. The syndrome is characterized by the combination of
metabolic acidosis, acute bradycardia and/or asystole, and
rhabdomyolysis, and it can be fatal. Although the mechanism
is not entirely understood, it is thought to result from direct
effects on mitochondria.39
PHARMACOKINETICS AND METABOLISM
Methohexital
The short clinical effects of methohexital are due largely
to redistribution of drug, first to vessel-rich tissues, then to
muscle, and finally to fat. The elimination phase, however, is
long, with slow metabolism of the active drug given up by
extravascular tissues (Table 4-2). Although it would be possi-
ble to keep a surgical patient asleep for many hours using
incremental boluses or a continuous infusion of methohexital,
the patient would remain obtunded for a lengthy period of
time postoperatively owing to significant pooling of non-
metabolized drug in muscle and fat.
Barbiturates, including methohexital, remain contraindi-
cated in patients with inducible porphyria. Because metho-
hexital induces the enzyme δ-aminolevulinic acid, porphyrin
synthesis is increased leading to increased production of heme
and its precursors. In those with porphyria, this could lead to
excessive accumulation of porphyrins and thus would exacer-
bate the disease.
Propofol
Propofol has a favorable pharmacokinetic profile because
recovery from the drug is based on drug clearance and redis-
tribution, not redistribution alone (see Table 4-2). There is
a large volume of distribution and very rapid clearance as a
result of rapid and efficient hepatic metabolism. At 30 minutes
following a bolus does of propofol, less than 20% of unchanged
62 SECTION I ■ Anesthesia and Pain Control
TABLE 4-2 Pharmacokinetics of Intravenous Agents
Distribution 1/2 Life (min)
Midazolam 7-15
Diazepam 3-10
Methohexital 5-6
Propofol 2-4
Ketamine 11-17
drug can be recovered from the serum.40 Because propofol is
metabolized so rapidly, there continues to be speculation that
there are sites outside the liver where metabolism also occurs.41
This rapid metabolism makes propofol an ideal drug for con-
tinuous infusion anesthesia. When a propofol infusion is dis-
continued at the end of a 2-hour case, eye opening will occur
within 5 minutes.42
The quality of recovery also appears to benefit from this
rapid metabolism. Patients who received propofol typically
appear to be alert and clearheaded, often within 20 minutes
of discontinuing the agent.43 This subjectively favorable
recovery may also be due to the euphorigenic properties of
propofol, promoting positive mood changes and thus a better
quality of recovery.44
There is still concern regarding whether or not propofol
can be used for patients with allergies to eggs or soy. Allergic
reactions to food stems from an immune response to proteins
or glycoproteins contained within that food. Until recently
the propofol package insert only stated that a contraindication
to the use of propofol was a “known hypersensitivity to pro-
pofol or its components . . .” However, the FDA issued a label-
ing revision in February of 2007 by adding a new caution
regarding propofol infusion syndrome and, along with that
warning, it became more explicit by stating that propofol is
“contraindicated in patients with allergies to eggs, egg prod-
ucts, soybeans or soy products.”45 However, because the organic
components (egg lecithin and soybean oil) are highly purified
and protein free, it would appear unlikely that propofol would
trigger an allergic response even in a patient with an undiag-
nosed allergy to soy or eggs. The very low incidence of allergic
reactions to all propofol preparations would seem to bear this
out, and the few reported cases of acute immune responses
were usually characterized by co-administration of or sensitiv-
ity to other agents (e.g., muscle relaxants) that are more
strongly associated with allergic reactions.46
■ KETAMINE
DISCOVERY AND DEVELOPMENT
Phencyclidine (PCP) was originally developed in the late
1950s for an analgesic screening program and was found to
produce anesthetic effects in monkeys. It was introduced as
the intravenous anesthetic Sernyl for human clinical trials in
1957. Its effectiveness was hampered by a high incidence of
Elimination 1/2 Life (hr) Clearance (mL/min)
2-4 300-550
20-40 15-35
2-5 700-900
1-3 1400-2800
2-3 1250-1400
postanesthetic emergence reactions. Agitation, excitement,
delirium, and hallucinations were seen in a significant number
of patients, and these unpleasant side effects led the investiga-
tors to abandon further clinical investigation. PCP (also
known as “angel dust”) is now solely a drug of abuse and is
used specifically for its hallucinogenic effects.
Following the negative experiences with PCP, a search
began for a PCP analog that would retain the anesthetic
effects but with a reduced incidence of emergence phenom-
ena. This led to the discovery of ketamine in 1963. Clinical
trials of ketamine began in 1966, and the drug was introduced
for clinical use as Ketalar in 1970. Although it has remained
a cornerstone of veterinary anesthesia, there have been cycles
of enthusiasm for its use in human anesthesia, Over the past
decade, it has enjoyed a resurgence of popularity, particularly
when used in lower doses and in combination with other
intravenous anesthetics.
STRUCTURE AND ACTIVITY
Glutamate is an excitatory neurotransmitter in the brain and
is important for many higher CNS functions, including learn-
ing and memory. Glutamate receptors have multiple subtypes,
of which the N-methyl-D-aspartate (NMDA) receptor is a
cationic subtype. These receptors are found ubiquitously
throughout the brain and spinal cord, but are concentrated
more heavily at higher levels of the cerebral cortex. Gluta-
mate, particularly in the presence of glycine, binds to the
NMDA receptor and causes increased flow of sodium, potas-
sium, and calcium, resulting in neural excitation.
Ketamine is a noncompetitive antagonist of NMDA, thus
inhibiting glutamate activity and causing CNS depression.
There are other drugs that cause NMDA antagonism as well,
including certain opioids (e.g., methadone) and the over-the-
counter antitussive dextromethorphan. Ketamine is also
thought to selectively bind to opioid receptors, possibly pro-
viding an explanation for the analgesic effects of the drug.47
Ketamine is a water-soluble racemic mixture of S(+) and
R(−) isomers. Its antagonism of the NMDA receptor is ste-
reospecific, with the S(+) enantiomer possessing a threefold
to fourfold greater affinity for the NMDA receptor and has
greater dissociative potency than the R(−) form, thus making
it more potent than the racemic mixture.48 The R(−) form,
in addition to being less effective, is also associated with a
greater incidence of emergence phenomena. Hence there is
 CHAPTER 4 • Pharmacology of Drugs in Ambulatory Anesthesia
increasing interest in the clinical use of S(+) ketamine for
anesthesia, postoperative analgesia, and sedation. In 2004 a
U.S. patent was granted for a process to isolate S(+) ketamine
and, although it is not yet commercially available, S(+) ket-
amine offers promise for use in ambulatory anesthesia in oral
and maxillofacial surgery.
Ketamine has partial affinity for opioid receptors and thus
can cause analgesia by inhibition of excitatory transmission at
spinal and supraspinal sites. Despite the implication of involve-
ment of opioid receptors, it does not appear that ketamine
analgesia can be predictably reversed by naloxone.
CLINICAL EFFECTS
Ketamine is described as causing a functional dissociation of
EEG activity between hippocampus and the thalamoneocorti-
cal system. Other sedative-hypnotics act more specifically on
discrete locations within the midbrain and brainstem.
Ketamine causes a profound dose-dependent analgesia.
Because the analgesia occurs at subanesthetic doses and out-
lasts the anesthetic effects, ketamine becomes a very useful
adjunct for patients where it is not possible to achieve absolute
local anesthesia (e.g., when maxillofacial infections require
incision and drainage). The analgesic effect of ketamine is
equal to that of opioids along with the benefit of less respira-
tory depression.
Ketamine is sympathomimetic through direct CNS stimu-
lation, thus causing an increase in heart rate, cardiac contrac-
tility, and rate pressure product. This can result in increased
coronary and cerebral blood flow and increased intracranial
pressure. Regarding electrical activity in the heart, ketamine
has been variably described as causing arrhythmias and pre-
venting them.
Ketamine causes a mild respiratory depression that is not
usually of clinical significance except when very large doses
are given rapidly. The brainstem response to hypercarbia is
maintained, as is the functional residual capacity. Ketamine
is a bronchodilator by relaxing smooth muscle as a result of
its sympathomimetic effects. There is increased secretion from
respiratory mucous glands and salivary glands.
PHARMACOKINETICS AND METABOLISM
Ketamine is metabolized in the liver by the cytochrome P-450
system, and the metabolites are excreted in the kidney. The
principle metabolite is norketamine, an active drug that has
been described as being anywhere from one third to one tenth
the potency of ketamine. There are three other minor metabo-
lites, all of which are inactive.
CONTRAINDICATIONS AND ADVERSE EFFECTS
Over the decades that ketamine has been available, the
adverse effects receiving the greatest amount of attention are
the psychoactive effects. These can range from mild confusion
and distorted perceptions to paranoia, delusions, and halluci-
nations. These psychoactive effects occur more frequently in
adults than children and more often in females compared with
males. They are also more common with large doses (greater
63
than 2 mg/kg IV) and rapid administration (greater than
40 mg/min). Patients with preexisting personality disorders or
psychiatric disease are at greater risk for these psychoactive
effects.
A number of studies have addressed the incidence and
prevention of these psychoactive effects. Some benefit has
been found in informing the patient about possible vivid
imagery and playing music during the anesthetic, and
nitrous oxide may also diminish the severity. However, co-
administration of BZD is the single most effective method of
suppressing or eliminating psychoactive effects.
Contraindications to ketamine include patient situations
where the sympathomimetic effects could be dangerous:
uncontrolled hypertension, unstable angina, recent myocar-
dial infarction, open globe injury, poorly controlled conges-
tive heart failure, and uncontrolled hyperthyroidism. Ketamine
would also be contraindicated in the presence of intracranial
trauma or an open globe injury. Ketamine should be avoided
for patients with psychiatric disorders with a history of recre-
ational drug use.
■ INHALATION ANESTHETICS
DISCOVERY AND DEVELOPMENT
The story of the discovery of nitrous oxide has been published
extensively in many texts and articles. In the late 1700s,
Joseph Priestly had discovered a number of gases, among them,
oxygen and nitrous oxide. At the end of the eighteenth
century, Sir Humphrey Davy reported on the pharmacologic
effects of nitrous oxide, describing its analgesic and mood-
altering properties, yet over the 40 years that followed, nitrous
oxide was not used therapeutically, but was mainly a
source of amusement at demonstrations. It was not until
Horace Wells, a dentist in Hartford, Connecticut, attended
a nitrous oxide demonstration that the therapeutic effects
of nitrous oxide were explored. Wells had witnessed a young
man who, under the influence of nitrous oxide at a town
demonstration, injured his leg and appeared unaware of the
injury. This caused Wells to wonder if exodontia could be
performed painlessly using nitrous oxide. The following day
Wells self-medicated with nitrous oxide and had a fellow
dentist remove one of his wisdom teeth. Afterwards Wells
reported there was no pain with the extraction. Wells was
permitted to demonstrate a tooth extraction on a patient
under the effects at Harvard in front of a group of students
and faculty; however, because the patient cried out during the
extraction, Wells was booed off the stage.
Around the same period of time there was development of
and experimentation with other gaseous agents, including
diethyl ether and chloroform. Over the next 80 years, these
agents, along with nitrous oxide, were the only inhaled anes-
thetics available to support the growing practice of surgery
under anesthesia.
In the 1920s, there began a new effort to design drugs based
on structure-activity relationships. It was during this time
that divinyl ether (Vinethene), a flammable agent, was
64 SECTION I ■ Anesthesia and Pain Control
synthesized. A decade later cyclopropane, another flammable
agent, was introduced for use in anesthesia. However, the
dangerous risks of fire and explosion made these agents less
than ideal, and research continued. In 1951 a new, nonflam-
mable compound called halothane was synthesized and intro-
duced as Fluothane for clinical use in 1956. Shortly after
methoxyflurane (Penthrane) was introduced followed by
enflurane (Ethrane) in 1966 and its isomer isoflurane (Forane)
in 1971. These agents became the mainstay of inhalation
general anesthesia for the next 2 decades. Two newer agents
have all but replaced these because of their superior pharma-
cologic properties: desflurane (Suprane) and sevoflurane
(Ultane), introduced in 1993 and 1995 respectively.
STRUCTURE AND ACTIVITY
The activity of all inhalation agents is based on diffusion of
the gas from the alveoli into the bloodstream. The amount
and speed of diffusion is determined by the partial pressure of
the gas in the alveoli compared with that in the bloodstream.
Once in the bloodstream, the amount of gas available to exert
its pharmacologic effect is determined by the blood-gas solu-
bility coefficient (i.e., the amount of gas that can be dissolved
in blood). The more soluble the gas, the less an amount of
active gas is present to exert its effect. This property also influ-
ences the rapidity of onset of an agent and the recovery from
its effects. Of all the gases, nitrous oxide is the least soluble,
providing a very rapid onset of action and recovery (Table
4-3).
The location at which inhalation agents exert their anal-
gesic effect has been identified in at least two locations: supra-
spinal opiate receptors in the brainstem and adrenergic
receptors in the spinal cord.49 The precise location at which
inhalation agents produce unconsciousness and amnesia has
not been identified, although proposed sites of action include
the hippocampus and the thalamus.50 There is sufficient evi-
dence, however, to indicate that the potent inhalation agents
(not including nitrous oxide) increase inhibitory transmis-
sions via the GABA pathway by interaction with the GABA
receptor. Nitrous oxide, it appears, interacts with and blocks
NMDA receptors and does not have any activity at the GABA
receptor.51
TABLE 4-3 Physical and Chemical Characteristics of Inhaled Anesthetics
Nitrous Oxide Halothane
Boiling pt (°C) 50.2
Vapor pressure (mm Hg) Gas 244
Odor Sweet Organic
Stability in soda lime Yes No
Blood : gas partition coefficient 0.46 2.54
MAC (37 °C) 104 0.75
% Metabolized 0.004 15-20
Modified from Stoelting RK: Pharmacology and physiology in anesthetic practice, ed 3, Philadelphia, Lippincott-Raven, 1999, pp 36, 67.
The potency of anesthetic agents is described by the
minimum alveolar concentration (MAC), the alveolar con-
centration of anesthetic at which 50% of the patients are
unresponsive to a standard surgical stimulus (see Table 4-3).
However, there is a lower concentration at which most
patients will be asleep—this has been termed the MACawake,
or the alveolar concentration at which 50% of patients are
asleep. MAC can be affected by many factors, most notably
co-administration of other anesthetics or sedative drugs.
CLINICAL EFFECTS
Nitrous Oxide
Nitrous oxide is a weak general anesthetic but a powerful
analgesic. It has been estimated that a 20% concentration of
nitrous oxide affords the same degree of analgesia as a dose of
15 mg of morphine.52 Nitrous oxide is also a euphorigenic
agent and a sedative.
Nitrous oxide is poorly soluble in blood and tissues, thus
making induction and recovery rapid. Within 5 minutes after
induction, tissue saturation is 90% of inspired concentration.
Upon discontinuation of the agent, 95% will be eliminated
after 10 minutes.
This rapid diffusion of N2O from blood to lungs can result
in a decreased CO2 arterial tension, thus causing decreased
stimulus for respiration. This rapid diffusion dilutes alveolar
O2 as well with a resultant hypoxic gas mixture in the alveoli.
This leads to a potential effect called diffusion hypoxia, a
phenomenon that is more theoretical than clinically signifi-
cant. However, it is recommended in many texts that patients
should receive 100% oxygen (and not room air) for 5 minutes
after nitrous oxide is discontinued.
Nitrous oxide causes a decrease in myocardial contractility,
peripheral vascular resistance, cardiac output, and blood pres-
sure. It causes a decrease in respiratory rate but an increase in
minute ventilation because of increased tidal volume. There
is no change in the CO2 response curve.
At higher doses, nitrous oxide can cause nausea and vomit-
ing through a central effect.
The toxic effects of nitrous oxide continue to receive atten-
tion, particularly because of the prevalent use of nitrous oxide
in dental operatories. Chronic exposure can lead to peripheral
Isoflurane Desflurane Sevoflurane
48.5 22.8 58.5
240 669 170
Ethereal Ethereal Ethereal
Yes Yes No
1.46 0.42 0.69
1.17 6.6 1.80
0.2 0.02 5
 CHAPTER 4 • Pharmacology of Drugs in Ambulatory Anesthesia
neuropathies and bone marrow suppression through inactiva-
tion of the methionine synthetase pathway. Surveys have
suggested an increased incidence of spontaneous abortion and
decreased fertility in health care providers exposed to nitrous
oxide on a regular basis.
Nitrous oxide diffuses into empty body cavities because it
displaces nitrogen. This can create morbidity in the presence
of emphysema, pneumothorax, an open globe, or following
middle ear surgery.
Isoflurane
Isoflurane is an ether that is nonexplosive. Its blood-gas parti-
tion coefficient is 1.4, making it the most soluble of the current
gases in widespread use. Its MAC with oxygen is 1.15%, and
when used with 70% nitrous oxide, it is 0.5%. Compared with
the older gases, such as halothane, it has greater respiratory
depression but less myocardial depression and does not sensi-
tize the myocardium to catecholamines. There is no kidney or
liver toxicity, and only 0.4% is metabolized. Its pungency does
not make it a good choice for an inhalation induction.
Desflurane
Because of its low boiling point, it requires a special heated
vaporizer. Its blood-gas coefficient is 0.42, providing a rapid
onset and recovery from the anesthetic. It is also less soluble
in tissues compared with the other inhalation agents. The
MAC of desflurane is 6% when used with oxygen and 3%
when used with 70% nitrous oxide. The usual maintenance
concentration is 6% to 8%. The pungent odor of desflurane
precludes its use for inhalation induction. Desflurane causes
little change in heart rate and a mild decrease in systemic
arterial pressure. It is metabolized significantly less than other
inhalation agents and does not cause any organ-specific
toxicity.
Sevoflurane
This agent is nonflammable and has an MAC of about 2%
alone and 0.66% when used with nitrous oxide. The usual
maintenance concentration is 2% to 3%. Sevoflurane is a
good agent to use for inhalation induction and does not cause
the coughing and breath holding associated with isoflurane or
desflurane.
Sevoflurane depresses respiration at high concentrations
and relaxes bronchial smooth muscle. It decreases systemic
arterial pressure and cardiac output while causing little change
in heart rate. Sevoflurane has been associated with increased
EEG activity and seizurelike activity. Some metabolism (2%)
occurs in the liver, and two of its metabolites include formal-
dehyde and fluoride, the latter of which has the potential to
cause renal toxicity.
Sevoflurane is known to react with certain carbon dioxide
absorbents used in breathing circuits (soda lime and Baralyme)
causing formation of several breakdown products, the one
most studied identified as Compound A. During a lengthy
anesthetic with sevoflurane, there may be enough accumula-
tion of Compound A to cause nephrotoxicity. Ongoing
65
research is aimed at identifying absorbents that do not interact
with sevoflurane.
REFERENCES
1. Roberts E: The establishment of GABA as a neurotransmitter.
In Squires RF, editor: GABA and benzodiazepine receptors, Vol I,
Boca Raton, Fla, CRC Press, 1988.
2. Randall LO et al: The psychosedative properties of methamino-
diazepoxide, J Pharmacol Exp Ther 129:163, 1960.
3. Squires RF, Braestrup C: Benzodiazepine receptors in rat brain,
Nature 266:732, 1977.
4. Martin IL, Dunn SMJ: GABA receptors, Tocris Rev No 20,
Mar 2002. (Accessed 11-13-07 at http://www.biotrend.com/
download/gabarev.pdf.)
5. Briley MS, Langer SZ: Influence of GABA receptor agonists and
antagonists on the binding of 3H-diazepam to the benzodiaze-
pine receptor, Eur J Pharmacol 52:129, 1978.
6. Amrein R et al: Clinical pharmacology of flumazenil, Eur J
Anaesthiol Suppl 2:65-80, 1988.
7. Basile AS, Lippa AS, Skolnick P: Anxioselective anxiolytics:
can less be more? Eur J Pharmacol 500:441-51, 2004.
8. Stoelting RK: Pharmacology and physiology in anesthetic practice,
ed 3, Philadelphia, Lippincott-Raven, 1999.
9. Dundee JW, Pandit SK: Anterograde amnestic effects of pethi-
dine, hyoscine, and diazepam in adults, Br J Pharmacol 44:140,
1972.
10. Young AB, Zukin SR, Snyder SH: Interaction of benzodiazepines
with central nervous system glycine receptors: possible mecha-
nism of action, Proc Natl Acad Sci 71:2246, 1974.
11. Ikram H, Rubin AP, Jewkes RF: Effect of diazepam on myocar-
dial blood flow of patients with and without coronary artery
disease, Br Heart J 35:626, 1973.
12. Lind LJ, Mushlin PS, Schitman PA: Monitored anesthesia care
for dental implant surgery: analysis of effectiveness and compli-
cations, J Oral Implantol 16:106, 1990.
13. Greenblatt DJ et al: Rapid recovery from massive diazepam over-
dose, JAMA 240(17):1872-4, 1978.
14. Valium injectable package insert, Nutley, NJ, Roche Pharma-
ceuticals, 1999.
15. Stanski DR, Watkins WD: Drug disposition in anesthesia, New
York, Grune and Stratton, 1982.
16. Berthold CW, Dionne RA, Corey SE: Comparison of sublin-
gually and orally administered triazolam for premedication before
oral surgery, Oral Surg Oral Med Oral Pathol Oral Radiol Endod
84:119, 1997.
17. Pert CB, Snyder SH: Opiate receptor: demonstration in nervous
tissue, Science 179:1011, 1973.
18. Lord JAH et al: Endogenous opioids peptides: multiple agonists
and receptors, Nature 267:495, 1977.
19. Stein C et al: Analgesic effect of intraarticular morphine after
arthroscopic knee surgery, N Engl J Med 325:1123, 1991.
20. Wittels B, Scott DT, Sinatra RS: Exogenous opioids in human
breast milk and acute neonatal neurobehavior: a preliminary
study, Anesthesiology 73:864, 1990.
21. Bennett JA et al: Difficult or impossible ventilation after sufen-
tanil-induced anesthesia is caused primarily by vocal cord closure,
Anesthesiology 87:1070, 1997.
22. Blasco TA et al: The role of the nucleus raphe pontis and the
caudate nucleus in alfentanil rigidity in the rat, Brain Res
386:280, 1986.
23. Flacke JW et al: Histamine release by four narcotics: a double-
blind study in humans, Anesth Analg 66:723, 1987.
24. Bovill JG: Pharmacokinetics of opioids. In Bowdle TA, Horita
A, Kharasch, editors: The Pharmacologic basis of anesthesiology,
New York, Churchill Livingstone, 1994.
66 SECTION I ■ Anesthesia and Pain Control
25. McClain DA, Hug CC Jr: Intravenous fentanyl kinetics, Clin
Pharmacol Ther 28:106, 1980.
26. Diprivan package insert, Wilmington, Del, AstraZeneca
Pharmaceuticals LP, 2001.
27. Fechner J et al: Sedation with GPI 15715, a water-soluble
prodrug of propofol, using target-controlled infusion in volun-
teers, Anesth Analg 100:701, 2005.
28. Mackenzie N, Grant IS: Propofol (Diprivan) for continuous
intravenous anaesthesia. A comparison with methohexitone,
Postgrad Med J 61(Suppl 3):70, 1985.
29. Reddy RV et al: Excitatory effects and electroencephalographic
correlation of etomidate, thiopental, methohexital, and propo-
fol, Anesth Analg 77:1008, 1993.
30. Kitahata L, Saberski L: Are barbiturates hyperalgesic? Anesthesi-
ology 77:1059, 1992.
31. Werner ME, Bach DE, Newhouse RF: A comparison of propofol
with methohexital and isoflurane in two general anesthetic tech-
niques, J Oral Maxillofac Surg 51:1076, 1993.
32. Schnider TW et al: The influence of age on propofol pharma-
codynamics, Anesthesiology 90:1502, 1999.
33. Borgeat A et al: Subhypnotic doses of propofol possess direct
antiemetic properties, Anesth Analg 74:539, 1992.
34. Doenicke A et al: Effects of propofol (Diprivan) on histamine
release, immunoglobulin levels and activation of complement in
healthy volunteers, Postgrad Med J 61(suppl): 15, 1985.
35. Smith I et al: Propofol-an update on its clinical use, Anesthesiol-
ogy 81:1005, 1994.
36. Miranda AF, Kyi W, Sivalingam N: Propofol and methohexi-
tone for elective caesarean—a comparative study, Med J Malaysia
47:280, 1992.
37. Chong M, Davis TP: Accidental intra-arterial injection of pro-
pofol, Anaesthesia 42:781, 1987.
38. Picard P, Tramer MR: Prevention of pain on injection with
propofol: a quantitative systematic review, Anesth Analg 90:963,
2000.
39. Kam PC, Cardone D: Propofol infusion syndrome, Anaesthesia
62:690, 2007.
40. White PF: Propofol: pharmacokinetics and pharmacodynamics,
Sem Anesth 7(suppl 1):4, 1988.
41. Shafer SL: Advances in propofol pharmacokinetics and pharma-
codynamics, J Clin Anesth 5(Suppl 1):14S, 1993.
42. Edelist G: Propofol for laser endoscopic procedures, Sem Anesth
11(suppl 1):16, 1992.
43. Steegers PA, Foster PA: Propofol in total intravenous anaesthe-
sia without nitrous oxide, Anaesthesia 43(suppl):94,1988.
44. Zacny JP et al: Subjective and psychomotor effects of subanes-
thetic doses of propofol in healthy volunteers, Anesthesiology
76:696, 1992.
45. www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm?
fuseaction=Search.Label_ApprovalHistory. (Accessed 10/22/
2007).
46. Laxenaire MC et al: Life-threatening anaphylactoid reactions to
propofol (‘Diprivan’), Anesthesiology 77:275, 1992.
47. Fink AD, Ngai SH: Opiate receptor mediation of ketamine anal-
gesia, Anesthesiology 56:291-7, 1982.
48. Oye I, Paulsen O, Maurset A: Effects of ketamine on sensory
perception: evidence for a role of N-methyl-d-aspartate recep-
tors, J Pharmacol Exp Ther 260:1209, 1992.
49. Guo TZ et al: Antinociceptive response to nitrous oxide is medi-
ated by supraspinal opiate and spinal alpha2 adrenergic receptors
in the rat, Anesthesiology 85:846, 1996.
50. Evers AS, Koblin DD: Inhalational anesthetics. In Evers AS,
Maze M, editors: Anesthetic pharmacology—physiologic principles
and clinical practice, Philadelphia, Elsevier, 2004.
51. Jevtovic-Todorovic V et al: Nitrous oxide (laughing gas) is an
NMDA antagonist, neuroprotectant, and neurotoxin, Nat Med
4:460, 1998.
52. Chapman WP, Arrowood JG, Beecher HK: The analgesia effects
of low concentrations of nitrous oxide compared in man with
morphine sulfate, J Clin Invest 22:871, 1943.

ANESTHETIC CONCEPTS AND
Jeffrey D. Bennett
Providing office-based sedation, anxiolysis, and analgesia to
the oral and maxillofacial surgery patient has been standard
practice for decades. The goal has always been to establish an
environment in which the patient is comfortable and coopera-
tive and hemodynamically stable. The focus has also been on
rapid patient recovery with efficient use of time. Numerous
advancements in pharmacology, equipment, and techniques
over the years provide the surgeon with various alternatives.
There may be several different adequate choices in regard to
anesthetic agent or technique for a particular situation. Many
surgeons have a standard technique, which works well for
them for most situations. However, the standard anesthetic
regimen may be inappropriate for a particular patient or situ-
ation, and the surgeon must avoid a reflexive thought process
of using the same drug or technique for all patients or all surgi-
cal procedures.
■ LEVELS OF SEDATION
Anesthesia is a continuum from consciousness to general
anesthesia. The recognized levels of sedation are: minimal
sedation (formerly referred to as anxiolysis), moderate seda-
tion/analgesia (formerly referred to as conscious sedation),
deep sedation/analgesia, and general anesthesia. The patient’s
responsiveness, airway maintenance, spontaneous ventila-
tions, and cardiovascular function categorize these different
levels or depths of sedation.
Minimal sedation is defined as a “drug induced state during
which patients respond normally to verbal commands.
Although cognitive function and coordination may be
impaired, ventilatory and cardiovascular functions are
unaffected.”1,2
Moderate sedation/analgesia (which we will refer to as
moderate sedation) is defined as a “drug induced depression of
consciousness during which patients respond purposefully to
verbal commands, either alone or accompanied by light tactile
stimulation. No interventions are required to maintain a
patent airway, and spontaneous ventilation is adequate.
Cardiovascular function is usually maintained.”1,2
Deep sedation/analgesia (which we will refer to as deep
sedation) is defined as a “drug induced depression of con-
sciousness during which patients cannot be easily aroused but
respond purposefully following repeated or painful stimula-
tion. The ability to independently maintain ventilatory func-
CHAPTER 5
TECHNIQUES
tion may be impaired. Patients may require assistance in
maintaining a patent airway, and spontaneous ventilation
may be inadequate. Cardiovascular function is usually
maintained.”1,2
General anesthesia is defined as a “drug induced loss of
consciousness during which patients are not arousable, even
by painful stimulation. The ability to independently maintain
ventilatory function is often impaired. Patients often require
assistance in maintaining a patent airway, and positive pres-
sure ventilation may be required because of depressed sponta-
neous ventilation or drug induced depression of neuromuscular
function. Cardiovascular function may be impaired.”1,2
These levels of sedation are not dependent on the route of
drug administration nor the specific anesthetic agent or com-
bination of agents administered. For example, given a large
enough dose or a more typical dose in a medically compro-
mised patient, an oral benzodiazepine could induce a level
of moderate sedation/analgesia to deep sedation/analgesia.
Various oral agents (e.g., benzodiazepines or chloral hydrate)
when co-administered with nitrous oxide have produced more
profound levels of sedation inducing deep sedation/analgesia
or general anesthesia.3,4 Alternatively, propofol and metho-
hexital, which are commonly associated with deep sedation/
analgesia and general anesthesia, can be administered such as
to produce levels of sedation that range from minimal sedation
to moderate sedation/analgesia.
■ GOALS OF SEDATION
The goal of sedation is to: (1) provide an optimal environ-
ment for completion of the surgical procedure, (2) minimize
patient anxiety and optimize patient comfort, (3) control the
patient’s behavior and movement and optimize patient coop-
eration, (4) optimize analgesia and minimize patient discom-
fort and pain, (5) maximize the potential for amnesia, and (6)
optimize patient safety and maintain hemodynamic stability.
Each situation (involving the patient and the specific surgical
procedure) is independently evaluated to determine the depth
or level of sedation required to achieve these goals.
The sedation of a child is different then that of an adult.
For the young child, who lacks the coping capability and the
social adaptability, the primary goal is to control the child’s
behavior and movement and to optimize patient cooperation.
This differs from that of an adult patient in which the primary
67
68 SECTION I ■ Anesthesia and Pain Control
goal is to minimize patient anxiety and optimize patient
comfort. Because of the different goals, the child frequently
will require a greater depth of anesthesia. Alternatively, if a
moderate sedation or a deep sedation is used instead of a
general anesthetic for the management of the pediatric patient,
the practitioner will need to have a different level of tolerabil-
ity. For example, the practitioner must be willing to accept
some crying and possible movement that may require minimal
restraint if a level of moderate sedation (or possibly deep seda-
tion) is planned for a pediatric patient.
The practitioner must also select which medications that
will be used to achieve the anesthetic plan. Although there
may be specific medications, such as propofol or methohexital,
which may more commonly be used to achieve an anesthetic
depth of deep sedation or general anesthesia, all of the anes-
thetic drugs that are used for “lighter” levels of anesthesia,
such as minimal sedation, can result in effects associated with
deep sedation or general anesthesia. Alternatively, in appro-
priate doses propofol or methohexital can be titrated to
achieve a level of moderate sedation. Ketamine has seen a
resurgence in interest in the past decade. The dissociative
state resulting from ketamine provides a favorable surgical
environment in which the patient becomes relatively immo-
bile while maintaining an intact and stable airway. The desire
to incorporate the drug into every technique needs to be
weighed against an understanding of the drug’s sympathetic
effect. For example, nonjudicious use of the drug in a cardio-
vascularly compromised patient or a patient on a tricyclic
antidepressant can have unfavorable consequences. In the
former, the increased sympathetic stimulation can negatively
impact the myocardial imbalance of oxygen supply and
demand, and in the latter the patient may have prolonged
sympathetic effects because of the interaction of the two
drugs.
■ CONCEPT OF RESCUE
There is a prevailing thought in medicine that human errors
are inevitable and that these errors are not necessarily second-
ary to incompetence. An American Society of Anesthesiolo-
gists (ASA) closed claims analysis reported that up to 80% of
anesthetic mishaps could have been prevented and were
attributable to human error.5 The concept of rescue therefore
is essential to safe sedation. The office-based environment
cannot be dependent on emergency medical services (EMS)
as the primary intervention for adverse events. The office must
be equipped and the staff able to manage the most serious of
adverse events. The first line in preventing an adverse event
is prevention. This has two components: (1) preoperative
assessment and (2) ensuring that the practitioner who is
administering the anesthetic is trained and capable of rescuing
the patient from a deeper level of sedation than was initially
planned.
Preanesthetic assessment is the focus of a separate chapter.
However, there are a few points that I would like to emphasize
here. The preanesthetic or preoperative assessment is the
process in which the practitioner ensures that the patient is
fit for anesthesia and surgery. The aim of the assessment is to
obtain a good medical history and complete a focused physical
examination. The medical history alone reveals up to 90% of
the needed information. Two distinct types of office-based
surgery practices exist among our oral and maxillofacial surgery
colleagues. Those who perform this preanesthetic assessment
solely on the day of surgery and those who perform this on a
separate appointment before the scheduled surgery date. There
are a few advantages to the latter methodology: (1) the ability
to assess the patient’s level of anxiety and provide psychologi-
cal intervention either behaviorally or pharmacologically and
(2) the ability to modify and direct treatment based on the
patient’s medical history (e.g., management of long-term
medication, such as what medications should be taken and
what drugs not taken on the day of surgery).
Rescue therapies require continuous and repeated training
to ensure a level of skill and knowledge. This is particularly
important in an environment, such as the oral and maxillofa-
cial surgery office, in which there is a rarity of a significant
adverse event occurring. There are several measures that can
be taken by the practitioner to prevent the occurrence of an
adverse event or minimize the undesirable consequences of
such an adverse event. The practice of ambulatory office-based
anesthesia in the oral and maxillofacial surgeon’s office empha-
sizes team management. The concept of team management
has been shown to optimize performance and minimize errors
in medicine.6,7 Additionally the practitioner and the anes-
thetic team should prepare for anesthetic care similar to a
flight crew. Using this comparison, the anesthetic team must
be comfortable and familiar with the anesthetic equipment. If
the equipment is new to their office, this may entail a more
detailed review to ensure familiarization. If the equipment is
older, although the office may be familiar and fairly comfort-
able with it, its inspection must focus on potential effects
resulting from age and ensure that it remains optimally func-
tional. This requires a protocol in which the equipment (both
that used for routine care and emergency intervention) is
regularly inspected and the anesthetic team has the opportu-
nity to practice with it. The latter point emphasizes the other
concept in training and performance testing among pilots.
Pilots use simulators to artificially create a scenario that is
analogous to real life. Simulators can provide scenarios that
represent normal anesthetic management and emergency situ-
ations. The ability to represent emergency situations is of
particular interest because many individuals may never
encounter a particular emergency during training until
they encounter such a situation during actual clinical patient
care.
There are four different types of simulators: screen-based
text simulators, screen-based graphical simulators, mannequin-
based simulators, and virtual reality simulators. The manne-
quin-based simulator includes an anatomically correct physical
model of a patient. The mannequins vary in complexity. The
level of mannequin sophistication may allow the trainee to
ventilate and/or intubate the mannequin, auscultate heart
and lung sounds using anatomically placed speakers, assess
 CHAPTER 5 •
respiratory efficacy by measuring end-tidal CO2 and pulse
oximetry, palpate carotid and radial pulses, and establish
intravenous (IV) access. These simulators have been shown
to enhance skills without endangering the health of patients.8
They facilitate acquisition of knowledge and skills that are
transferable back to clinical care. However, the mannequin
simulators are expensive and lack easy portability. The screen-
based graphical simulators attempt to visually recreate the
clinical environment. The simulation programs provide physi-
ologic data (such as HR, BP, ECG, O2Sat, end-tidal CO2),
provide patient interaction (such as patient responses to preset
questions), allow responses to physical examination (such as
breath or heart sounds or level of responsiveness), and provide
realistic responses to drug administration based on the phar-
macokinetic and pharmacodynamic properties of the medica-
tions. Two studies completed at the University of Washington
demonstrated that the use of the screen-based graphical simu-
lator demonstrated better retention and better application of
skills and knowledge than those who used a text solely.9,10
■ AIRWAY ASSESSMENT
Assessment of the airway is one of the most critical compo-
nents of the preoperative assessment. This is exemplified by
two separate ASA closed claims analysis publications that
reported respiratory adverse events as the most common
mechanism of injury to the patient. Forty-one percent of these
claims were for death or permanent brain damage. The inci-
dence of respiratory adverse events, most of which were inad-
equate oxygenation/ventilation, was comparable between
monitored anesthesia care (MAC) and general anesthesia.11,12
The first step in preventing these adverse respiratory events is
to identify a potential difficult airway.
Airway assessment consists of both history and examina-
tion. The history obtained from the patient should inquire
about prior surgeries on the airway or difficulties with airway
management during prior surgeries. The examination com-
ponent of the assessment focuses on several anatomic
components to the airway that can predict difficult airway
management: (1) modified Mallampati test, (2) thyromental
distance, (3) mandibular retrognathia, (4) interincisal opening
less than 3 cm, (5) short neck, (6) thick neck (increased neck
circumference of 17 inches for males and 16 inches for
females), and (7) diminished range of motion of head and
neck with the inability to extend or flex the neck (such that
the tip of the chin can touch the chest). The modified Mal-
lampati test assesses the airway based on the ability to visualize
the uvula and faucial pillars when the mouth is wide open,
the tongue is maximally protruded, the neck is extended
forward into the sniffing position, and the patient phonates.
The modified Mallampati classification has five categories that
are defined in Table 5-1, with the higher class supposed to
predict greater difficulty in intubation.
The thyromental distance is a measurement from the man-
dibular menton to the prominence of the thyroid cartilage
with the neck in full extension. The distance should be at
least 6 cm or approximately three ordinary fingerbreadths.
Anesthetic Concepts and Techniques 69
TABLE 5-1 Mallampati Classification
Class 0 Ability to see any part of the epiglottis on mouth opening
and tongue protrusion
Class 1 Soft palate, fauces, uvula, anterior and posterior pillars
seen
Class 2 Soft palate, fauces, and uvula seen
Class 3 Soft palate and base of uvula seen
Class 4 Soft palate only seen
These tests were initially proposed, and most studies to date
have investigated their ability to predict difficult intubations.
Used independently, none of these tests was sufficient to con-
sistently predict the difficulty of airway intubation.13 Combin-
ing several different tests (such as the Mallampati test and the
thyromental distance) to assess a patient’s intubatability did
result in a higher sensitivity, higher positive predictive value,
and fewer false-negative results.14 Because most office-based
anesthesia for oral and maxillofacial surgery is done on the
nonintubated patient, we are actually more interested in
the ability to ventilate and to maintain airway patency than
we are in the ability to intubate a patient. There are fewer
studies assessing the ability to ventilate a patient or mainte-
nance of airway patency. The incidence of being unable to
ventilate a patient is approximately 5% of the general adult
population. The Mallampati test was found to be no better in
predicting difficult mask ventilation than difficult airway intu-
bation. One publication did show a correlation in difficulty in
mask ventilation among patients who were difficult to
intubate.15
Maintaining airway patency in the nonintubated patient is
always potentially a risk because operating in the oral cavity
can result in airway obstruction secondary to such factors as
the positioning of the mandible, head-neck flexion-extension,
or posterior displacement of the tongue. The above criteria
provide some guidance as to the level of sedation, which
would be appropriate or inappropriate for a particular patient
in regard to the potential for airway difficulty. The surgeon
may decide to manage the patient with significant findings
either with a minimal sedation in the office or plan on using
advanced airway techniques (either a laryngeal mask airway
(LMA) or intubation) either in the office or hospital or surgery
center. If the potential for a difficult airway is recognized, then
the appropriate preparations can be made to increase the
likelihood of a good outcome. The complexity with the ability
to predict a difficult airway remains not with the extremes
of the assessment criteria but with those patients who fall
within the middle. Other factors, such as obesity, history of
snoring, abnormal oropharyngeal or neck masses, prior airway
surgeries, or congenital, developmental or acquired facial
deformities (e.g., craniofacial syndromes, burns to the head
and neck), may provide further guidance.
Obesity warrants further comment because its incidence is
rapidly increasing in the United States with an incidence in
children and adolescents that exceeds 15% and in adults that
70 SECTION I ■ Anesthesia and Pain Control
exceeds 30% and is predicted to approach 40% in 2008.
Physical findings previously discussed that are found in the
obese patient include: a decrease in cervical and mandibular
range of motion, a decrease in thyromental distance, and a
less favorable Mallampati class. The patient’s airway is more
likely to collapse during anesthesia, and the distribution of
tissue in the patient’s neck and chest will complicate airway
management. This is compounded by the fact that the patient
is more susceptible to developing hypoxemia or hypercapnia
because of restrictive lung disease (an increased chest wall
mass decreases chest wall compliance and diaphragmatic
excursion), increased closing volume, and ventilation-
perfusion mismatch. There is also a higher incidence of
obstructive sleep apnea (OSA) in the obese patient. It is
estimated that OSA is undiagnosed in 80% of patients who
have the condition. This extends the concern with airway and
respiratory management beyond the intraoperative period
into the postoperative period. The literature is insufficient to
evaluate the effects of various analgesic medications on OSA.
These patients will benefit from multimodal analgesic tech-
niques (e.g., preemptive NSAIDs) and minimization of
opioids, and their respiratory depressant effects will most likely
reduce the potential for adverse events.16 The ASA guidelines
suggest that the “OSA patient be monitored for a median of
three hours longer than their non-OSA counterparts before
discharge from the facility.”17
■ LARYNGEAL MASK AIRWAY
Traditional anesthetic management for intraoral surgery is
unique in that the surgical site is contiguous with the unpro-
tected nonintubated airway. The patient is susceptible to
airway obstruction, airway irritation, and hypoventilation or
apnea. This can necessitate surgical interruption to manipu-
late the airway to eliminate the obstruction and establish
airway patency. This may be as easy as readjusting the pha-
ryngeal curtain or performing a head-tilt maneuver. Various
interventions may also be required to remove airway irritation.
These could likewise include repositioning the pharyngeal
curtain, which could be an irritant to the pharynx, or suction-
ing the pharynx of some irrigating solution that may have
passed beyond the pharyngeal curtain. Rarely the patient may
require positive pressure ventilation.
The LMA forms an intermediate form of airway manage-
ment between the face mask and the endotracheal tube. For
intraoral surgery, it provides the ability to obtain, maintain,
and secure a patent airway. The advantage of the LMA is that
it is passed beyond the tongue, forming a seal with the laryn-
geal inlet and eliminating the most common cause of upper
airway obstruction in the nonintubated patient. Because there
is not a direct conduit into the trachea as achieved with
endotracheal intubation, there is a potential for airway
obstruction, which has been reported as high as 30%. This
obstruction generally responds to head repositioning with the
need to neither reposition the LMA nor interrupt surgery.
Breathing may be spontaneous, assisted, or controlled with the
LMA, avoiding the need to interrupt surgery to provide posi-
tive pressure ventilations. The LMA is also an excellent
barrier against aspiration of irrigating solution, surgical debris,
and blood. A pharyngeal curtain, however, is recommended
to keep any surgical debris contained within the oral cavity
and minimize the potential for aspiration of any surgical debris
when the LMA is removed.
General anesthesia is indicated when using the LMA.
Using the standard technique, the LMA is inserted blindly
after induction of general anesthesia. The blind insertion
technique, which requires less airway manipulation compared
with intubation, is associated with less sympathetic stimula-
tion and potential hemodynamic fluctuations. Campbell et al
recommends laryngoscopy and direct visualization of LMA
insertion as an alternative to optimize anatomic placement
and minimize the epiglottis from impinging on the glottic
opening.18 Theoretically, this should improve airflow dynam-
ics. These authors reported that the brief laryngoscopy for
LMA placement did not adversely result in sympathetic stim-
ulation and hemodynamic changes. Neither the blind nor
laryngoscopic insertion technique require neuromuscular
blockade. The LMA is also advantageous compared with
endotracheal intubation in that its anesthetic requirements
both during maintenance and emergence are less.
■ SMOKING
Approximately one-quarter of the American adult population
smoke cigarettes.19 Cigarette smoking is a cause of increased
perioperative morbidity. This may be secondary to the chronic
diseases associated with smoking, such as ischemic heart
disease and chronic obstructive pulmonary disease. The con-
stituents of cigarette smoke, such as nicotine and carbon mon-
oxide, also have acute effects on both the cardiovascular and
respiratory systems.
From a cardiovascular perspective, nicotine activates the
sympathoadrenergic system. This increases heart rate, blood
pressure, and peripheral resistance and increases oxygen
demand. Expired carbon monoxide levels have also been
shown to correlate with ST depression under general anesthe-
sia.20 Cigarette smoking also promotes a hypercoagulable state
contributing to arterial thromboembolism and coronary
vasospasm.
Effects on the respiratory system include impaired muco-
ciliary clearance and mucous hypersecretion, which results in
increased airway irritability. This may be manifested clinically
by a higher incidence of laryngospasm and airway obstruction.
Small airway narrowing contributes to increased closing
capacity, which results in ventilation-perfusion mismatch.
Cigarette smoking also increases the blood carbon monoxide
level and a leftward shift in the oxygen-hemoglobin dissocia-
tion curve. The increase in the carboxyhemoglobin level (8%
to 10%) results in less oxygen being carried by hemoglobin.
The leftward shift in the oxygen-hemoglobin dissociation
curve results in less oxygen being released to the peripheral
tissues. The net effect is a decrease in tissue oxygenation.
Passive smoke exposure has also been shown to be a risk
factor in children contributing to airway complications
 CHAPTER 5 •
(laryngospasm ∼5 times greater and airway obstruction ∼3
times greater) during the intraoperative and postoperative
period.21
Smoking can also have a detrimental effect on wound
healing including wound dehiscence, infection, and impaired
bone healing.22 This may be secondary to effects on the
immune system or changes in tissue oxygenation.
Patients are usually counseled to stop smoking during the
perioperative period. To achieve the greatest benefit from this
counseling, the period of smoking cessation should be at least
6 to 8 weeks. The benefit from abrupt cessation before surgery
is related to the half-life of nicotine and carboxyhemoglobin,
which are 2 hours and 4 hours, respectively. The elimination
of nicotine and carboxyhemoglobin decreases adrenergic stim-
ulation minimizing adverse cardiovascular effects and increases
both the oxygen carrying ability of the blood and the amount
of oxygen released to the peripheral tissues resulting in
increased tissue oxygenation, respectively. Overnight absti-
nence of smoking is beneficial, however, as the half-life of
both nicotine and carboxyhemoglobin can be prolonged
during sleep; a 24-hour “cigarette smoke-free” period is
preferable.23
There has been controversy over smoking cessation beyond
the initial 24 hours and a 6- to 8-week period. This contro-
versy focuses on a paradoxic effect in which there is a transient
increase in airway secretions and airway irritability associated
with smoking cessation. This concept is best understood by
recognizing that many smokers complain of increased airway
secretions and airway irritability during the first several weeks
after smoking cessation. Anesthetically, it is best to appreciate
that it takes several weeks for the reduction in pulmonary
complications to be apparent. During this time there may be
a slight but not significant increase in pulmonary complica-
tions seen in anesthetized patients.24,25
The polycyclic hydrocarbons present in cigarette smoke are
potent inducers of liver enzymes. Smoking cessation decreases
these metabolic enzymes potentially increasing blood levels of
drugs that interact with the cytochrome P-450 pathway. Cou-
madin is one drug that is metabolized by the affected enzymes,
which may result in increased postoperative bleeding. Inter-
estingly, postoperative nausea and vomiting is less in smokers.
This may be attributed to the induction of liver enzymes.
These enzymes may be responsible for the metabolization and
excretion of various chemicals that may affect postoperative
nausea and vomiting.26
■ PREOPERATIVE FASTING
The concept for preoperative fasting exists to minimize the
risk of pulmonary aspiration, which may result in laryngo-
spasm, chemical pneumonitis, or partial or complete airway
obstruction as a result of particulate matter. The concept dates
back to the mid-1940s when Mendelson (who was an obstetri-
cian) described a series of patients undergoing general anes-
thesia for vaginal delivery in which he documented respiratory
complications secondary to aspiration. He noted two distinct
situations: (1) aspiration of particulate matter resulting in
Anesthetic Concepts and Techniques 71
obstruction and (2) aspiration of liquid gastric contents result-
ing in dyspnea and cyanosis consistent with what is now
referred to as aspiration pneumonitis.27 Since this report sub-
sequent studies have sought to determine the minimum pH
and volume of the aspirate. A pH less than 2.5 is associated
with pathologic changes. The actual residual gastric volume
associated with aspiration is more difficult to determine
because not all regurgitated fluid is aspirated. A classic study
suggested that a volume of 0.8 mL/kg with a pH of less than
2.5 when directly instilled into the trachea produces an aspira-
tion pneumonitis.28 Other authors have suggested that this
equates to a residual gastric volume of greater than 200 mL
for passive regurgitation and pulmonary aspiration to occur
during anesthesia. Gastric volumes of this magnitude may be
found, but they are not normal. The typical residual gastric fluid
volume in a fasted patient of greater than 8 hours for solids and
2 hours for clear liquids should be less than 30 mL.29
The basic premise of preoperative fasting is to minimize the
volume and the acidity of the residual gastric volume. The
ASA adopted new fasting guidelines in 1999. A basic knowl-
edge of gastric emptying times facilitates an understanding of
these modifications. Gastric emptying for solid food is vari-
able. A surgeon should be aware that approximately 50% of
the contents of an ingested solid meal will have remained
in the stomach after 2 hours. Alternatively, gastric emptying
for liquids is rapid with a mean half-time of 10 minutes.
Approximately 80% of ingested clear liquid will have passed
into the duodenum after the first hour.
The current ASA recommendation allows the consump-
tion of clear liquids up to 2 hours before the anesthetic. It is
recommended that an individual should fast for a minimum
of 6 hours after the consumption of a “light meal” (e.g., toast
and avoidance of fat-containing solids and liquids) and up to
8 hours after the consumption of “fatty” solids.30 The advan-
tage of allowing clear liquid consumption up to 2 hours before
the anesthetic is that it minimizes the risk of dehydration and
hypoglycemia. It also decreases the potential for noncompli-
ance and patient irritability (especially among children).
A preoperative evaluation assessing for comorbidities may
result in a modification of the general guidelines of 2 hours
NPO for clear liquids and 6 hours NPO for a “light meal.”
There are numerous situations that may delay gastric empty-
ing: high sympathetic tone as a result of pain and anxiety,
opioid use, cigarette smoking, cannabinoids, and functional
dyspepsia. Several clinical conditions are associated with gas-
troparesis: diabetes mellitus, systemic lupus erythematosus,
lack of coordination of swallowing or respiration, functional or
mechanical obstruction to digestion, gastroesophageal dys-
function, Parkinson’s disease, and anorexia or bulimia. Of
these diabetes is the most commonly associated with gastropa-
resis. And in the diabetic patient, the delay in gastric emptying
is more significant for solids than for liquids. Obese patients are
not an increased risk for aspiration as a result of acidity and
gastric volume, but have a higher incidence of difficulty in
airway management with the potential for resultant gastric
distention that may translate into an aspiration risk.
72 SECTION I ■ Anesthesia and Pain Control
The use of gastrointestinal stimulants (e.g., metoclo-
pramide), histamine-2 receptor antagonists (e.g., cimetidine),
nonparticulate antacids (e.g., sodium citrate), and antiemetics
are not routinely recommended to reduce the risk of aspiration
in patients who have no increased risk of aspiration.
■ FLUID ADMINISTRATION
Total body water is approximately 60% of total body weight.
It exists in two major compartments: intracellular and extra-
cellular. Two-thirds of the total body water is compartmental-
ized into the intracellular space, and the remaining one third
is compartmentalized into the extracellular space. The extra-
cellular compartment is further subdivided into intravascular
and extravascular compartments. The intravascular compart-
ment consists of one-fourth of the extracellular body water or
one-twelfth of the total body water.
Sodium and chloride are primary extracellular electrolytes.
These electrolytes are not diffusible between compartments.
The distribution of free water is dependent on ionic and
osmotic pressures.
Understanding fluid compartmentalization is critical to
understanding intraoperative fluid administration. The admin-
istration of a hypotonic solution, such as D5W, will result in
a rapid redistribution of free water with only one-twelfth of
the water remaining in the intravascular space. Alternatively
the administration of an isotonic solution, such as 0.9%
normal saline, will result in a preferential distribution of the
fluid within the extracellular space. The fluid will remain
within the intravascular compartment for the first 15 to 30
minutes before equilibration within the extracellular compart-
ment. This provides the advantage of countering the vasodi-
latation secondary to the anesthetic agents.
The use of D5W or the inclusion of dextrose in the intra-
operative IV fluid is controversial for other reasons as well.
The perioperative period is usually associated with a transitory
hyperglycemia secondary to the release of the hormones: epi-
nephrine, cortisol, and glucagon. The infusion of a dextrose
solution may intensify the hyperglycemia. In the event of
hypoxemia and anaerobic metabolism, the hyperglycemia will
result in increased carbon dioxide production and intracellular
lactic acidosis potentially worsening neurologic injury associ-
ated with the hypoxemia.31,32 The above is relevant in regard
to resuscitation of the trauma patient and fluid management
for major surgery. It also has relevance in the event of resus-
citation of a patient in the office. However, for dentoalveolar
surgery, a minor risk surgical procedure, as defined by the
AHA/ACC, the stress induced hyperglycemia is transitory
and can be followed by a period of hypoglycemia.33 The post-
operative hypoglycemia may be compounded by limited
caloric intake during this period because of local wound dis-
comfort and soft tissue swelling that compromise the patient’s
ability and desire to take postoperative fluids.
Perioperative fluid administration for office-based surgery
consists of the administration of crystalloid solutions (e.g.,
0.45% saline, 0.9% saline, D5/0.45% normal saline, D5/0.9%
saline). In minor surgery, there is no concern about fluid loss
or fluid shift; however, fluid administration provides the
ability to correct the preexisting fluid deficit secondary to
preoperative fasting guidelines. Rehydration of the patient’s
fluid deficit during the perioperative period has been shown
to improve the “quality” of recovery.34 The fluid deficit can
be calculated using the formula for maintenance require-
ments, which is 4 mL/kg/hr for the first 10 kg, 2 mL/kg/hr for
the second 10 kg, and 1 mL/kg/hr for each additional kilo-
gram. For a 70-kg lean individual who has fasted 8 hours
(between midnight and 8 am), the fluid deficit approximates
1 L. Whereas the current fasting guidelines allow unrestricted
clear fluid consumption up to 2 to 3 hours before surgery,
there are many patients for various reasons who have a 1- to
2-L fluid deficit. For office-based anesthesia in the healthy
patient, it would be reasonable to administer 500 to 1000 cc
of a crystalloid solution instead of simply using the IV access
solely as a route of drug administration. Considering the
patient’s potential limited ability to take sustenance postop-
eratively, the administration of a 1-L dextrose supplemented
0.45% or 0.9% saline solution could provide approximately
250 kcal of carbohydrate energy.
Whereas the above paragraph focuses on the recommenda-
tion to adequately rehydrate a patient, the practitioner must
also be cognizant of excessive fluid administration. Most prac-
titioners will be attentive to the patient who has a history of
a systemic disease that requires fluid restriction, such as con-
gestive heart disease. Special consideration must be given to
the young pediatric patient. Overhydration can occur with
any solution; however, with a hypotonic solution (such as
D5W) overhydration can rapidly result in cerebral edema and
significant morbidity or patient mortality. This is merely
another reason to consider administering either maintenance
or replacement fluids (e.g., 0.45% or 0.9% normal saline).
Prevention of overhydration can also be minimized by using
a microdrip infusion set in the pediatric patient.
■ ANESTHETIC TECHNIQUES IN
OFFICE-BASED ANESTHESIA
The guiding principle of ambulatory anesthesia for office-
based oral and maxillofacial surgery is to achieve adequate
anxiolysis, sedation, amnesia, analgesia, and hemodynamic
stability, such as to provide for a safe surgical environment
resulting in rapid recovery and discharge of the patient home.
There are several aspects to anesthetic technique manage-
ment that are controversial. In this section, we are going to
focus on depth of anesthesia monitoring, anesthetic delivery
techniques (bolus versus continuous infusion), and choice of
anesthetic agents or combinations.
Depth of anesthetic monitoring: When anesthetizing a patient
in the office, the desired depth of anesthesia is most commonly
assessed by subjectively assessing the patient’s movements and
facial expressions or lack thereof and objectively assessing the
patient’s respiratory (respiratory rate and oxygen saturation)
and cardiovascular (blood pressure, pulse, and rhythm) func-
tion and stability. The anesthetic plan may be driven simply
to achieve patient comfort and cooperation. Alternatively the
 CHAPTER 5 •
anesthetic plan may be dictated by the intent to maintain a
specific anesthetic depth. There may be several factors that
influence the selection of the anesthetic plan of which are the
patient’s desired depth of anesthesia or lack of awareness, the
surgeon’s desired depth of anesthesia or amnesia, the surgical
procedure, and/or the patient’s systemic health.
Awareness with intraoperative recall is a major concern for
all surgeons and anesthesiologists. Without minimizing the
problem of intraoperative awareness, the situation is different
in the intubated patient compared with the nonintubated
patient. Awareness is frightening in the intubated patient
because of a lack of ability to communicate both their aware-
ness and inadequate anesthetic depth. For the nonintubated
patient who always maintains their ability to communicate,
there are different potential problems. For a planned general
anesthetic, how does the surgeon optimally assess the anes-
thetic depth of a patient who appears relaxed, comfortable,
eyes closed, and hemodynamically stable without unnecessar-
ily administering an excess of anesthetic agent, which can be
associated with adverse effects and delay recovery, or admin-
ister inadequate anesthetic agent such that the patient makes
comment that they were awake despite appearing very com-
fortable and asleep?
The bispectral index (BIS) is a monitor that focuses on
changes in the EEG and uses an algorithm to assign a linear
dimensionless number that correlates with anesthetic depth
(Table 5-2). For the agents frequently used in oral and maxil-
lofacial surgery (propofol, methohexital, midazolam), BIS is
relatively agent independent. However, BIS is not entirely
agent independent and does not reflect the clinical effects
of ketamine or nitrous oxide in addition to the low dose of
opioids generally used for office-based oral and maxillofacial
surgery.35 As many surgeons use nitrous oxide in combination
with IV agents, and ketamine is making a resurgence as a
component of the anesthetic cocktail in oral and maxillofacial
surgery practices, BIS monitoring has clear limitations. Addi-
tionally, there is individual variation in BIS’s correlation with
clinical indices of sedation, which may make it less accurate
for any particular patient.36 Sandler et al has demonstrated the
use of BIS in oral and maxillofacial surgery.37 Whereas these
studies demonstrated a strong positive relationship between
BIS and the Observer’s Assessment of Alertness and Sedation
Scale (OAA/S) and a trend toward earlier return of motor
function, they also showed a lack of correlation between BIS
and the OAA/S at deeper levels of sedation consistent with
deep sedation and only a trend toward earlier recovery. Periods
TABLE 5-2 Correlation of BIS Value with Sedation Level
BIS Value Sedation Level
100 Awake
70 Light hypnotic effect
Low probability of recall
60 Moderate hypnotic effect
Unconscious
40 Deep hypnotic effect
Anesthetic Concepts and Techniques 73
of more intense stimulation balanced by less stimulating
periods and relatively brief surgical procedures, which are not
atypical for dentoalveolar surgery, may further limit BIS effec-
tiveness in this environment.
Even if BIS is demonstrated to reliably define depth of
sedation, what impact would this have on anesthetic manage-
ment in the oral and maxillofacial surgery office? To use less
drug and to expedite recovery, would the goal be to maintain
a level of general anesthesia as close to the transition between
general anesthesia and deep sedation? Would titration of anes-
thesia to this specific zone increase the risk of the patient
transitioning to a level of anesthetic excitability with its
inherent risks? Alternatively, for the nonintubated patient
who appears to be at an appropriate anesthetic depth and is
dependent on spontaneous ventilation, would it be more
appropriate to monitor ventilations and oxygen saturation in
conjunction with clinical assessment of anesthetic depth or
titrate the anesthetic agents based on BIS monitoring? Could
administering anesthetic medications based on BIS readings
potentially result in a patient who no longer maintains
adequate ventilations or a patent airway? The literature is
inadequate in regard to BIS analysis demonstrating that it
optimizes anesthetic management and that it decreases anes-
thetic morbidity and mortality when incorporated into
anesthetic care for the typical office dentoalveolar surgical
procedure.
The above discussion focuses on the use of BIS in monitor-
ing a deep sedation/general anesthetic. BIS may have more
benefit in monitoring a patient with moderate to deep seda-
tion for a prolonged procedure. The goal would be to maintain
a BIS value between 70 and 80, which would correlate with
eyelid ptosis and patient response only to loud or repeated
calling of their name or mild prodding or shaking. A deviation
outside these values would suggest a level of anesthesia either
too light or too deep warranting either additional administra-
tion of the bolus agent, an increase or decrease in the continu-
ous infusion, and/or more attentive monitoring to ensure
airway patency and spontaneous ventilations.
Additional controversy focuses on BIS cost-effectiveness.
There is a cost for each unit and the disposable electrodes that
may not be countered by the reduced anesthetic agent and
ability to discharge the patient more rapidly. Obviously the
questions raised cannot be taken individually, and a multitude
of factors need be used in optimizing anesthetic management.
Anesthetic delivery technique and choice of anesthetic agents or
combinations: Rapid recovery and early return to preoperative
function are fundamental principles in ambulatory anesthesia.
Pharmacokinetic and pharmacodynamic properties of many of
the current IV and inhalational anesthetic agents facilitate
these objectives. This section will focus on techniques of
administration and choice of agent(s). A separate chapter will
discuss the pharmacology of the drugs.
IV anesthesia is the principal anesthetic technique used by
oral and maxillofacial surgeons. It can be achieved with single
or multiple IV drug combinations, with or without nitrous
oxide. The administration of the anesthetic drug(s) can be
74 SECTION I ■ Anesthesia and Pain Control
solely at the beginning of the surgery or titrated throughout
the surgery. The anesthetic drugs can be administered by
intermittent bolus, by continuous infusion, or a combination
of both. The goal for all forms of administration is to achieve
and maintain an appropriate concentration of anesthetic drug
at the effector site within the central nervous system to
achieve a desired anesthetic depth.
The choice to administer anesthetic drugs solely at the
beginning of the surgery is commonly due to the following
objectives: (1) to achieve a sedative depth to facilitate the
local anesthetic administration; (2) the pharmacologic profile
of the selected agents is such that they will provide a satisfac-
tory depth of sedation of appropriate duration for the planned
surgery; and/or (3) the surgical time is of such short duration
that additional drug administration is not required.
The benzodiazepine-opioid combination of midazolam and
fentanyl is commonly titrated to a selected anesthetic depth
before the administration of the local anesthetic agent. The
pharmacologic profile of these agents is such that they provide
a satisfactory depth of sedation of appropriate duration for
many surgeons to perform dentoalveolar surgery without
additional drug administration. There is a benefit to this drug
combination in that it provides anxiolysis, amnesia, sedation,
and analgesia. Of additional benefit is the availability of a
reversal agent for each class of drug. There is a limitation to
the anesthetic combination in that the onset and recovery of
each agent is relatively slow. An induction agent, such as
propofol or methohexital, may be bolused before the admin-
istration of the local anesthetic agent to provide a more pro-
found anesthetic depth of brief duration.
The pharmacokinetics and pharmacodynamics of propofol
and methohexital are ideal for office-based anesthesia because
they provide rapid onset and rapid recovery and return to
“street readiness.” An intermittent bolus technique remains
the most commonly used technique for administration of
these agents in oral and maxillofacial surgery. The disadvan-
tage to this technique is the potential for high peak plasma
concentrations of anesthetic drug with resultant unwanted
effects (primarily hypoventilation or apnea or airway obstruc-
tion). An alternative to the intermittent bolus technique is a
continuous infusion technique with or without intermittent
boluses.38 The use of the infusion pump endeavors to parallel
the simplicity of administering an inhalational agent with a
vaporizer. The infusion can be titrated up or down in response
to clinical signs and/or BIS monitoring. The intermittent
bolus can be administered to adjust the sedative depth before
an anticipated increased surgical insult. The sustained base-
line plasma level achieved from the continuous infusion
should result in a more rapid response to the intermittent
bolus administration. Ideal application of this technique
requires the use of an infusion pump in which the practitioner
can set a dose per weight per time infusion. Newer target-
controlled infusion delivery systems use pharmacokinetic
models to achieve effect-site concentrations. Mathematical
calculations alter the infusion based on interindividual vari-
ability and surgery. Advocates of a continuous infusion anes-
thetic technique claim that the technique will result in a more
stable plasma level of anesthetic drug, which will provide a
safer and more optimal anesthetic.39
An alternative and nontraditional method of sedation is
patient-controlled sedation. The concept of patient-controlled
sedation is that it enables the patient to vary the degree of
sedation. A patient has the ability to administer a predefined
bolus of IV anesthetic agent. Various parameters can be set
into the devices that limit the total amount of drug, the inter-
vals in which a patient can self administer the anesthetic
agent and the rate at which a drug is administered. Although
various agents have been used, the pharmacokinetic proper-
ties of propofol make it the most appropriate agent for patient-
controlled sedation.40,41,42
Choose of anesthetic agent: Nitrous oxide is the most com-
monly used inhalational agent among oral and maxillofacial
surgeons. Use of nitrous oxide in conjunction with either
IV agents (e.g., propofol) or potent inhalational agents
(e.g., sevoflurane) potentiates the effect of the other anes-
thetic agent. This can reduce the amount of required
anesthetic agent and result in a shorter wake-up time. However,
many surgeons feel that the excellent pharmacokinetic proper-
ties of the current IV agents minimize these benefits potentially
achieved with nitrous oxide. It has also been suggested that
nitrous oxide contributes to a higher incidence of nausea and
vomiting, although this has been challenged.43
IV sedation is most commonly achieved with a combina-
tion of midazolam, fentanyl, and propofol or methohexital.
Ketamine has gained in popularity and can be incorporated
into a standard anesthetic regimen or used as a drug to scav-
enge an anesthetic. Ketamine provides two effects that are
advantageous in optimizing the anesthetic. First the cataleptic
state establishes a degree of immobility, and as the patient
recovers from the effect of ketamine, there is a slow “robotic”
type of return to purposeful patient movement compared with
the rapid and “violent” type of movement that may be seen
with either propofol or methohexital. Second when ketamine
is administered as a slow bolus in doses of 0.25 to 1 mg/kg
(that are customary for office-based ambulatory oral and max-
illofacial surgery), airway patency, spontaneous ventilations,
and functional residual capacity (FRC) are maintained.
Remifentanil is an ultrashort-acting opioid. It has advan-
tages over other opioids because of its rapid onset (∼90 seconds,
compared with fentanyl ∼5 minutes) and rapid offset (context
sensitive half-life of 3 to 6 minutes). Because of its pharma-
cokinetic profile, it is frequently administered as an infusion.
Remifentanil can be combined with midazolam (for amnesia
and anxiolysis) instead of propofol or methohexital.44,45 The
use of remifentanil provides a degree of intense analgesia in
which the patient has excellent pain control. When com-
bined with midazolam, the patient is frequently awake and less
amnestic of the procedure than if propofol or methohexital
were administered. However, the use of remifentanil estab-
lishes a surgical environment in which the patient, although
less sedated and clinically more awake, does not move and
does not transition from lighter to deeper anesthetic depths
 CHAPTER 5 •
with the associated patient movement and potential airway
irritability. Attentive respiratory monitoring is required with
remifentanil with different authors reporting varying degrees
of hypoxia and ventilator depression.
■ PATIENT POSITIONING
Patient positioning for office-based oral and maxillofacial
surgery is usually dependent on the surgeon’s preference and
the specific surgical procedure. The typical positioning varies
between supine to a head-up position of approximately 60°
with most surgeons’ using some variation of head-up position-
ing. Head-up positioning has some physiologic advantages.
In the erect individual, the rib cage, the diaphragm, and
the abdomen expand with inspiration. In the supine individ-
ual, thoracic expansion is more dependent on rib cage expan-
sion, abdominal expansion is lessened, and the contents of the
abdomen displace the diaphragm cephalad. The cephalad dis-
placement of the diaphragm in the supine patient can cause
a decrease in the FRC of approximately 0.5 L.46
FRC is the lung volume at the end of normal expiration.
In the normal adult patient, the FRC is approximately 2 L
with the total lung capacity being approximately 5 L. In the
anesthetized patient, the FRC can further decrease by another
0.5 L in the supine patient. The importance of the FRC is that
it provides an oxygen reserve in the event of impaired ventila-
tions. Several studies have demonstrated the benefit of head-
up positioning of varying degrees on minimizing oxygen
desaturation after preoxygenation and induction of
anesthesia.47,48
In addition to nonerect patient positioning, several other
factors decrease FRC including obesity, pregnancy, restrictive
pulmonary disease, and short stature.
Patient positioning is also important in regard to preven-
tion of neurologic injuries. In an ASA closed claims analysis,
nerve injuries were the second most common type of com-
plaint. Ulnar neuropathies were preponderant in these case
reports.49 These injuries may occur secondary to stretching or
compression. Diabetes, alcohol, or smoking may contribute to
an increased incidence of postoperative neuropathies.50 The
patient seated in a dental surgical chair is most susceptible to
ulnar or radial nerve injuries, as opposed to lower extremity
nerve injuries. Whereas patient positioning may contribute to
neural deficit, the present observation of the ulnar or radial
nerve injuries suggests that these neuropathies are not second-
ary to patient positioning.51,52
■ POSTOPERATIVE RECOVERY
AND DISCHARGE
Office-based surgery typically is of short duration with a focus
on rapid recovery. Anesthetic recovery is a continuum from
the end of surgery when the last sedative/anesthetic agent has
been administered and the patient emerges from sedation/
anesthesia (early recovery) to a time in which the patient has
satisfactorily achieved “selected” criteria that indicate that the
patient is stable to be discharged (intermediate recovery) to a
time in which the patient returns to their preoperative physi-
Anesthetic Concepts and Techniques 75
ologic state (late recovery). Clinically, early recovery is cate-
gorized by the patient awakening, having intact airway reflexes,
maintaining a patent airway, ventilating, oxygenating, and
being hemodynamically stable. Most patients who have been
sedated without advanced airway devices for office-based oral
surgery progress almost immediately through early recovery to
the intermediary recovery phase. Until the patient progresses
into the intermediary recovery phase, they need to be inten-
sively observed, generally by the oral and maxillofacial surgeon
or recovery nurse. Pediatric patients have less reserve and
warrant diligent care.
During intermediary recovery, continued observation by a
trained individual to recognize complications should persist
until the patient is discharged. During intermediary recovery,
the observation need not be as intensive requiring one-on-one
observation. Monitoring as described later with set audible
alarms and diligent periodic observation is acceptable. To
avoid having the patient unattended, the patient’s escort can
be allowed to remain with the patient at this time.
Respiratory and cardiovascular monitoring should be con-
tinued throughout the early and intermediary phases of recov-
ery. Respiratory monitoring should assess oxygenation (pulse
oximetry) and ventilation (respiratory rate and airway
patency). Oxygen administration is generally discontinued
during the intermediary recovery period. This assesses the
patient’s ability to maintain oxygenation on room air. Cardio-
vascular monitoring should minimally assess blood pressure
and pulse. Electrocardiographic monitoring is not absolutely
mandated, but should be immediately available. For selected
patients with significant cardiovascular disease, continual
ECG monitoring should be considered. Vital signs consisting
of blood pressure, pulse, respiratory rate, and oxygen satura-
tion should be recorded at regular intervals. IV fluid hydration
is not routinely indicated at this time, and continued admin-
istration may mask hemodynamic stability or lack thereof.
Maintaining IV access, however, provides the ability to
manage adverse events if necessary and is recommended to be
removed just before discharge.
Intermediary discharge criteria determining home readi-
ness are a continuum from the several parameters mentioned
above. Vital signs (blood pressure, pulse, respiratory rate, and
oxygen saturation) must be stable and consistent with preop-
erative values within acceptable parameters. In general blood
pressure and pulse should be within 20% of preoperative
values, and a deviation from 40% warrants investigation.
Oxygen saturation should be maintained above 90% on room
air or consistent with preoperative value. The patient should
be alert and oriented unless their mental status was initially
abnormal at which the patient’s mental status should have
returned to their baseline. The patient must be able to ambu-
late at preoperative levels. Nausea and vomiting should be
minimal and responsive to treatment. Routine antiemetic pro-
phylaxis is only indicated in selected patients with a high
incidence of postoperative nausea and vomiting. There should
be minimal to no pain. Good local anesthesia is beneficial in
reducing the anesthetic requirements and providing prolonged
76 SECTION I ■ Anesthesia and Pain Control
patient comfort minimizing sympathetic stimulation, which
can adversely affect hemodynamic stability and nausea
and vomiting (because sympathetic stimulation increases
incidence of nausea and vomiting). Lastly, surgical bleeding
should be minimal and consistent with that expected for
the surgical procedure.53 Gauze pressure dressing applied to the
intraoral wound for hemostasis should consist minimally of
4 × 4 gauze sheets that partially protrude from the mouth
until the patient has fulfilled discharge criteria. Smaller gauze
sheets or gauze packed solely intraorally increase the potential
risk for aspiration and airway obstruction.
For select patients, fluid intake (diabetic patient) and
urinary voiding may be indicated. Routinely mandating fluid
intake, however, is unnecessary and can contribute to nausea
and vomiting prolonging discharge.54 There is a higher inci-
dence of nausea and vomiting in ambulatory patients who
have received opioids. This is secondary to the interaction
between the labyrinthine vestibular system, opioids, and the
chemoreceptor trigger zone. Because the potential for hypo-
glycemia and the associated morbidity as a result of a lack of
glucose intake is high in the diabetic patient, mandating fluid
intake both in the office before discharge and providing home
instructions to ensure fluid intake and glucose monitoring
upon discharge is critical. Urinary voiding is also not routinely
recommended. Perioperative medications that could contrib-
ute to urine retention include the opioids and anticholinergic
agents. For patients at low risk for urine retention, most have
voided within 3 hours of surgery.55 There are also several
reasons as to why there may be a lack of urinary urgency in
the ambulatory oral surgical patient. Many patients are asked
to void before surgery. This has the benefit of minimizing
perioperative bladder distention, which could contribute to
patient discomfort, sympathetic stimulation (associated with
hypertension and tachycardia), subsequent urine retention,
and/or inadvertent urinary incontinence. Additionally, unless
the patient’s fluid deficit is replaced during surgery, the patient
may not have a volume of urine to void. Patients should be
instructed to seek medical assistance if they are unable to void
within 6 to 8 hours of discharge.
The final determination and responsibility to discharge the
patient is the responsibility of the anesthetist-surgeon. This
task should not be delegated to office staff. Patients should be
discharged to a responsible adult who will accompany them
home and provide postoperative care.
■ KNOW WHEN TO STOP
Sedation is a wonderful modality that optimizes the quality of
care within our offices. Office-based anesthesia in oral and
maxillofacial surgery is mostly accomplished in the nonintu-
bated patient. The technique of providing such anesthesia is
both art and science. The “art” in anesthesia as administered
by the oral and maxillofacial surgeon involves the ability to
establish a good surgical environment in a patient who main-
tains spontaneous ventilations. However, there are times in
which the balance of having a good surgical environment
in which the patient is “asleep, immobile, cooperative, and
comfortable” and maintains a patent airway with spontaneous
ventilations is not accomplished.
When such a situation arises, the anesthetic team is con-
fronted with a decision. The question that most frequently is
on individuals’ minds is how to achieve the anesthetic and
complete the planned surgery. It may not be appropriate to
consider alternative pharmacologic agents or techniques.
Ketamine is one such alternative agent that many practitio-
ners may consider. It can establish a dissociative state and
“scavenge” many such anesthetics. Some practitioners may
convert a failed anesthetic in the nonintubated patient to a
technique in which the airway is secured with either an endo-
tracheal tube or an LMA. However, ketamine may not “smooth”
out the anesthetic, and the patient may have a difficult airway
that cannot be secured with various airway devices.
When deviating from the planned anesthetic treatment,
there must be limits as to what is acceptable. Not all patients
can be anesthetized “as planned” in the office. For example, a
patient who was planned for general anesthetic may only be
able to be minimally or moderately sedated. If a patient
requires a general anesthetic, it may be more appropriate to
seek the assistance of an anesthesiologist. Although there is a
natural desire not to want to admit defeat, optimal patient
care is the goal, and the practitioner needs to “know when to
stop.”
REFERENCES
1. Joint Commission on Accreditation of Healthcare Organiza-
tions: 2001 Sedation and anesthesia care standards, Oakbrook
Terrace Ill, JCAHO (Accessed at www.jcaho.org/standard/
aneshap).
2. American Society of Anesthesiologists: Standards: continuum of
depth of sedation/definition of general anesthesia and levels of
sedation/analgesia. (Accessed at http://www.asahq.org/publica-
tionsAndServices/standards/20.pdf). Jan 2007.
3. Litman RS et al: Upper airway obstruction during midazolam/
nitrous oxide sedation in children with enlarged tonsils,
Pediatric Dent 20:318, 1998.
4. Litman RS, Berkowitz RJ, Ward DS: Levels of consciousness and
ventilator parameters in young children during sedation with
oral midazolam and nitrous oxide, Arch Pediatr Adolesc Med
150:671, 1996.
5. Cooper JB, Newbower RS, Kitz RJ: An analysis of major errors
and equipment failure in anesthesia: considerations for preven-
tion and detection, Anesthesiology 60:34, 1984.
6. Sexton J, Thomas E, Helmreich R: Error, stress and teamwork
in medicine and aviation: cross sectional surveys, BMJ 320:745,
2000.
7. Bellomo R et al: Prospective controlled trial of effect of medical
emergency team on postoperative morbidity and mortality rates,
Crit Care Med 32:916, 2004.
8. Abrahamson S, Denson JS, Wolf RM: Effectiveness of a simula-
tor in training anesthesiology residents, J Quality Safety Health
Care 13:395, 2004.
9. Schwid HA et al: Use of a computerized advanced cardiac life
support simulator improves retention of advanced cardiac life
support guidelines better than a textbook review, Crit Care Med
27:821, 1999.
10. Schwid HA et al: Screen based anesthesia simulation with
debriefing improves performance in a mannequin-based anesthe-
sia simulator, Teach Learn Med 13:92, 2001.
 CHAPTER 5 •
11. Bhananker SM et al: Injury and liability associated with moni-
tored anesthesia care: a closed claims analysis, Anesthesiology
104:208, 2006.
12. Caplan RA et al: Adverse respiratory events in anesthesia: a
closed claims analysis, Anesthesiology 72:828, 1990.
13. Lee A et al: A systematic review (meta-analysis) of the accuracy
of the Mallampati tests to predict the difficult airway, Anesth
Analg 102:1867, 2006.
14. Krobbuaban B et al: The predictive value of the height ratio and
thyromental distance: four predictive tests for difficult laryngos-
copy, Anesth Analg 101:1542, 2005.
15. Langeron O et al: Prediction of difficult mask ventilation,
Anesthesiology 92:1229, 2000.
16. ASA Task Force on Obstructive Sleep Apnea: Practice guide-
lines for the perioperative management of patients with obstruc-
tive sleep apnea, Anesthesiology 104:1081, 2006.
17. Joshi GP: Are patients with obstructive sleep apnea syndrome
suitable for ambulatory surgery? ASA Newsletter 70(1), Jan
2006.
18. Campbell RL et al: Fiberoptic assessment of laryngeal mask
airway placement: blind insertion versus direct visual epiglot-
toscopy, JOMS 62:1108, 2004.
19. Cigarette smoking among adults-United States, 2000, Morb
Mortal Wkly Rep 51:642, 2002.
20. Woehlck HJ et al: Acute smoking increases ST depression in
humans during general anesthesia, Anesth Analg 89:856, 1999.
21. Jones DT, Bhattacharyya N: Passive smoke exposure as a risk
factor for airway complications during outpatient pediatric pro-
cedures, Otolaryngol Head Neck Surg 135:12, 2006.
22. Kwiathkowski TC, Hanley EN Jr, Ramp WK: Cigarette smoking
and its orthopedic consequences, Am J Orthop 25:590, 1996.
23. Munday IT et al: The effectiveness of pre-operative advice to
stop smoking: a prospective controlled trial, Anaesthesia 48:816,
1993.
24. Bluman LG et al: Preoperative smoking habits and postoperative
pulmonary complications, Chest 113:883, 1998.
25. Moores LK: Smoking and postoperative pulmonary complica-
tions: an evidence-based review of the recent literature, Clin
Chest Med 21:139, 2000.
26. Whalen F et al: Recent smoking behavior and postoperative
nausea and vomiting, Anesth Analg 103:70, 2006.
27. Mendelson CL: The aspiration of stomach contents into the
lungs during obstetric anesthesia, Am J Obstet Gynecol 52:191,
1946.
28. Raidoo DM et al: Critical volume for pulmonary acid aspiration:
reappraisal in a primate model, Br J Anaesth 65:248, 1990.
29. Maltby JR et al: Drinking 300 mL of clear fluid two hours before
surgery has no effect on gastric fluid volume and pH in fasting
and non-fasting obese patients, Can J Anesth 51:111, 2004.
30. Practice guidelines for preoperative fasting and the use of phar-
macologic agents to reduce the risk of pulmonary aspiration:
application to healthy patients undergoing elective procedures.
A report by the American Society of Anesthesiologists task force
on preoperative fasting, Anesthesiology 90:896, 1999.
31. Hagerdal M, Caldwell CB, Gross JB: Intraoperative fluid man-
agement influences carbon dioxide production and respiratory
quotient, Anesthesiology 49:48, 1983.
32. Nicolson SC: Glucose: enough versus too much, J Cardiothorac
Vasc Anesth 11:409, 1997.
33. Gowan C: Fluid management for major surgical cases in the
operating room, Certified Registered Nurse Anesthetist 7:81,
1996.
Anesthetic Concepts and Techniques 77
34. Bennett J et al: Perioperative rehydration in ambulatory anes-
thesia for dentoalveolar surgery, Oral Surg Oral Med Oral Path
Oral Radiol Endod 88:279, 1999.
35. Barr G et al: Nitrous oxide does not alter bispectral index: study
with nitrous oxide as sole agent and as adjunct to i.v. anaesthe-
sia, Br J Anaesth 82:827, 1999.
36. Liu J, Singh H, White PF: Electroencephalographic bispectral
index correlates with intraoperative recall and depth of propofol-
induced sedation, Anesth Analg 84:185, 1997.
37. Sandler NA, Hodges J, Sabino M: Assessment of recovery of
patients undergoing intravenous conscious sedation using bispec-
tral analysis, JOMS 59:603, 2001.
38. Bennett J et al: Incremental bolus versus continuous infusion for
deep sedation/general anesthesia during dentoalveolar surgery,
JOMS 56:1049, 1998.
39. Cillo JE, Finn R: Moderate intravenous sedation for office based
full face laser resurfacing using a continuous propofol pump,
JOMS 63:903, 2005.
40. Rodrigo C et al: Patient-controlled sedation with propofol in
minor oral surgery, JOMS 62:52, 2004.
41. Kucukyavuc Z, Cambazoglu M: Effects of low-dose midazolam
with propofol in patient-controlled sedation (PCS) for apicec-
tomy, BJOMS 42:215, 2004.
42. Oei-Lim VLB et al: Patient-controlled versus anesthesiologist-
controlled conscious sedation with propofol for dental treatment
in anxious patients, Anesth Analg 86:967, 1998.
43. Arellano RJ et al: Omission of nitrous oxide from a propofol-
based anesthetic does not affect the recovery of women undergo-
ing outpatient gynecological surgery, Anesth 93:332, 2000.
44. Akcaboy ZN et al: Can remifentanil be a better choice than
propofol for colonoscopy during monitored anesthesia care? Acta
Anaesthesiol Scand 50:736, 2006.
45. Mingus ML et al: The remifentanil 3010 study group: remifent-
anil versus propofol as adjuncts to regional anesthesia, J Clin
Anesth 10:46, 1998.
46. Faust RJ, Cucchiara RF, Bechtle PS: Patient positioning. In
Miller RD, editor: Miller’s anesthesia, ed 6, Philadelphia, Elsevier
Churchill Livingstone, 2005.
47. Altermatt FR et al: Pre-oxygenation in the obese patient:
effects of position on tolerance of apnea, Br J Anaesth 95:706,
2005.
48. Lane S et al: A prospective, randomized controlled trial compar-
ing the efficacy of pre-oxygenation in the 20 head up vs supine
position, Anaesth 60:1064, 2005.
49. Cheney FW et al: Nerve injury associated with anesthesia,
Anesthesiology 90:1062, 1999.
50. Warner MA et al: Lower extremity motor neuropathy associated
with surgery performed on patients in a lithotomy position,
Anesthesiology 81:6, 1994.
51. Warner MA et al: Ulnar neuropathy in medical patients, Anes-
thesiology 92:613, 2000.
52. Warner MA et al: Ulnar neuropathy in surgical patients, Anes-
thesiology 90:54, 1999.
53. Marshall S, Chung F: Assessment of “home readiness”: discharge
criteria and postdischarge complications, Curr Opin Anaesthesiol
10:445, 1997.
54. Kearney R, Mack C, Entwistle L: Withholding oral fluids from
children undergoing day surgery reduces vomiting, Paediatr
Anaesth 8:331, 1998.
55. Pavlin DJ et al: Voiding in patients managed with or without
ultrasound monitoring of bladder volume after outpatient surgery,
Anesth Analg 89:90, 1999.
CHAPTER 6
MANAGEMENT OF
John D. Matheson • David Lee Hill Jr. • Michael A. Gentile
“The art of life is the art of avoiding pain; and he is the best pilot, who steers clearest of the rocks and shoals with
which it is beset.” — Thomas Jefferson
This quote summarizes many patients’ attitudes when visiting
the oral and maxillofacial surgeon. Unfortunately, many of
the procedures commonly performed by oral surgeons result in
moderate to severe pain. In fact, the third molar extraction
pain model has become an accepted method of evaluating the
management of acute postoperative pain.1 As clinicians we
must be cognizant of our patients’ comfort during and after
surgery. The importance of pain control following oral and
maxillofacial surgery is evidenced by the growing body of lit-
erature aimed at evaluating postoperative quality of life out-
comes.2-7 One study shows that the adverse impact on quality
of life following third molar surgery is three times greater when
patients are experiencing postoperative pain.4 Although this
may seem obvious, its importance cannot be underestimated.
Undergoing painless surgery and having limited postoperative
pain is a major concern for our patients.
Pain is an unpleasant sensory experience perceived as
arising from a specific location of the body and frequently
associated with actual or potential tissue damage.8 In his
review of acute and chronic craniofacial pain, Sessle describes
pain as “a complex, multidimensional experience encompass-
ing sensory-discriminatory, cognitive, affective, and motiva-
tional aspects.”9 In other words, an individual’s response to
pain is dependent not only on the extent and site of tissue
damage but also by its processing in the central nervous system.
Pain should not be seen only as a burden. It has a useful func-
tion. It is a diagnostic tool for clinicians and acts as a protec-
tive mechanism for patients.
Pain management also plays an important role in develop-
ing the patient-physician relationship. Patient perception
regarding pain, particularly in relation to oral and maxillofa-
cial surgery, can be difficult for the surgeon to overcome. In
fact, undue worry and an overestimation of the pain they will
encounter can lead to the avoidance of treatment. Patient
education is an essential part of any pain control strategy. By
educating patients on pain expectations and the pain control
regimen to be employed after surgery, we can better prepare
them for their postoperative recovery and alleviate unneces-
sary anxiety.
78
ACUTE POSTOPERATIVE PAIN

The goal of this chapter is to give a comprehensive review
of the management of acute postoperative pain in the oral
and maxillofacial surgery patient. Although considerable
attention has been given to nonpharmacologic methods of
pain management10 (behavioral modification, music therapy,
massage, acupuncture, transcutaneous nerve stimulation), this
chapter will describe the most common pharmacotherapies
used by oral and maxillofacial surgeons. In addition, the dis-
cussion will be geared toward acute pain management—pain
that is of recent onset and limited duration (i.e., surgical
pain).11 We start by examining the neurobiology and patho-
physiology of pain. The major classes of analgesics are then
described. Finally, specific strategies in the ambulatory and
nonambulatory oral and maxillofacial surgery patient are
given. Keeping in mind that evidence-based practice will con-
tinue to change the management of pain in our specialty, the
basic principles will remain the same. It is the responsibility
of the surgeon to: (1) develop an effective pain management
strategy that is patient specific and takes into account both
physiologic and psychosocial factors, (2) communicate that
plan with the patient before surgery, and (3) adjust that strat-
egy as necessary depending on patient feedback and clinical
information. This ultimately leads to greater patient satisfac-
tion and the building of a successful practice.
■ NEUROANATOMY AND
PATHOPHYSIOLOGY OF PAIN
Tissue is inherently damaged during oral and maxillofacial
surgery. Nociception is the electrical transmission of a noxious
stimulus from a site of injury to higher brain centers.12 Follow-
ing tissue damage outside of the craniofacial region, free nerve
endings present in peripheral tissue are stimulated by mechan-
ical, thermal, and chemical means. These free nerve endings
act as afferent pain receptors, or nociceptors. After being
stimulated, an electrical event is initiated and is propagated
via primary afferent nerve fibers to the dorsal horn of the
spinal cord via the dorsal root ganglia. The main two types of
afferent nerve fibers associated with nociception are A-delta
and C-polymodal fibers. A-delta fibers are lightly myelinated,
 CHAPTER 6 • Management of Acute Postoperative Pain 79

Somatosensory Cerebral cortex

cortex
E

Limbic Thalamus
system D
E

Midbrain and
brainstem

F
Ascending Descending, pain
projection modifying pathways
neuron
C
Spinal or medullary Dorsal root
dorsal horn ganglion

B Nociceptive
afferent neuron

Skin, mucosa,
dental pulp
A

Spinal
cord

FIGURE 6-1. Overview of peripheral and CNS pathways involved in nociceptive signaling. The peripheral endings
of nociceptive afferent neurons (A) are activated by various stimuli (e.g., thermal, mechanical, biomechanical). Once
activated, these specialized afferent neurons transmit an action potential to the spinal (or medullary) dorsal horn of the
CNS (B). Within the dorsal horn, the signal from the periphery may be relayed to ascending projection neurons (C) that
send the message to specific regions of the thalamus (D). Various regions within the CNS (E) that determine the sensory,
motivational, and affective responses to painful stimuli receive input from the thalamus. Descending inhibitory pathways
within the CNS (F) suppress excitatory activity at the level of the dorsal horn.

have a larger diameter, and are fast conducting. They are pri-
marily activated by mechanical stimuli and are characterized
by sharp, stabbing, and shooting sensations. C fibers are termed
polymodal because they are activated by mechanical, chemi-
cal, and thermal stimuli. They have a smaller diameter, are
unmyelinated, transmit impulses at a slower rate, and are
associated with dull, achy pains. After synapsing with second
order neurons in the dorsal horn, the impulse then crosses to
the contralateral ascending spinothalamic tract where it
travels to the thalamus. From the thalamus, the impulse travels
to higher brain centers, including the somatosensory cortex
and limbic system. The transmission of this impulse may also
be affected by descending pain-modifying pathways from the
cerebral cortex, midbrain, and brainstem.13 These descending
pathways generally synapse in the dorsal horn in the vicinity
of second order ascending fibers and suppress excitatory trans-
mission, thus inhibiting the transmission of pain sensation
(Figure 6-1).
Pain sensation of oral and craniofacial origin follows a
similar pathway to that outlined earlier. The main differences
are in the specific nerves involved in transmission and the
level of the central nervous system (CNS) at which they are
transmitted to higher brain centers. The main sensory nerve
of the orofacial region is the trigeminal nerve (cranial nerve
V). There are also some tissues in the craniofacial region
receiving afferent sensory innervation from other cranial
nerves (cranial nerves VII, IX, X, and XII) and branches of
the upper cervical spinal nerves (C1, C2, C3). After stimulat-
ing nociceptors in tissues innervated by the trigeminal nerve,
an afferent impulse is directed toward the CNS via the tri-
geminal (Gasserian) ganglion. Whereas in the rest of the body
the impulse travels to the dorsal root of the spinal cord, in the
craniofacial region, sensory information is passed through a
special area of the brainstem known as the trigeminal brain-
stem sensory nuclear complex (VBSNC). This is a bilateral,
multinucleated structure in the dorsolateral brainstem extend-
ing from the pons to the upper cervical spinal cord.14 The
VBSNC is divided into two major nuclei: the main sensory
nucleus and the spinal tract nucleus. The spinal tract nucleus
is further divided into the subnucleus oralis, the subnucleus
interpolaris, and the subnucleus caudalis. After synapsing in
the VBSNC, the impulse travels to the thalamus where it can
be relayed to higher brain centers, including the somatosen-
sory cortex and the limbic system. The impulse can also be
80 SECTION I ■ Anesthesia and Pain Control
Cerebral
cortex
Thalamus
Main sensory
Oralis
Motor
nuclei
RF
Interpolaris Brainstem
Trigeminal
ganglion
Caudalis
Spinal
cord
FIGURE 6-2. Transmission of sensory information from the mouth and
face to the somatosensory areas of the cerebral cortex. The major pathway
involves the trigeminal nerve, the primary afferent cell bodies of which are in
the trigeminal (semilunar) ganglion. The peripheral processes of these cells
innervate oral-facial tissues, whereas the central processes enter the brain-
stem and synapse on second-order neurons at various levels of the trigeminal
brainstem sensory nuclear complex. This complex may be subdivided, from
rostral to caudal, into the main (or principal) sensory nucleus and the spinal
tract nucleus, which consists of three subnuclei: oralis, interpolaris, and cau-
dalis. From the brainstem complex, sensory information may then be relayed
to the third-order neurons in the thalamus and from there to the cerebral cortex
or less directly by multisynaptic pathways involving, for example, the reticular
formation (RF). The sensory information relayed from a particular region of the
complex may also pass to other brainstem structures (e.g., cranial nerve motor
nuclei involved in reflex responses to oral-facial stimuli) or to the spinal cord
or other regions of the complex (not shown). (From Sessle BJ: Acute and
chronic craniofacial pain: brainstem mechanisms of nociceptive transmission
and neuroplasticity, and their clinical correlates, Crit Rev Oral Biol Med
11(1):57, 2000.)
directed to a variety of other locations in the brainstem and
the spinal cord. Some of these connections are used in reflex
pathways. Finally, descending modifying pathways are also
present that can affect the transmission and sensation of pain
(Figure 6-2).
Inflammation plays an important role in the development
of postoperative pain. Surgical manipulation of oral and facial
tissues causes damage resulting in acute inflammation. As cells
are disrupted, inflammatory mediators and metabolites are
released into surrounding tissue beds. These factors include
cytokines, substance P, prostaglandins, leukotrienes, kinins,
histamine, and serotonin.13 Some of these factors can directly
stimulate a nerve impulse in afferent pain fibers. Others, such
as prostaglandins, serve to sensitize nociceptors by lowering
their activation thresholds. This leads to the hyperalgesia
found in surgically altered tissue.
As outlined previously, the sensation of pain is propagated
by peripherally located receptors after tissue injury. Local
mediators released into tissue beds contribute to the initiation
of an electrical impulse directed toward the spinal cord and
brainstem. From here, the impulse travels to higher brain
centers where cognitive and emotional input is integrated and
the quality of pain is perceived. The management of pain is
directed at altering the peripheral and central mechanisms
responsible for the propagation of pain impulses. These mech-
anisms should be kept in mind when designing a postoperative
pain control regimen.
■ OPIOID ANALGESICS
The term opioid refers to those compounds that have been
synthetically manufactured to resemble the chemical structure
of the naturally occurring alkaloids of the opium poppy. The
natural by-products of opium, including morphine, codeine,
and their semisynthetic derivatives, are known as opiates. The
opiates can also be grouped under the single term opioid. The
activity of all opioids is related to their binding to a special
set of membrane-bound receptors. These receptors have been
categorized into three groups based on their pharmacologic
selectivity: mu, kappa, and delta. One method of classifying
opioids is by their ability to bind opioid receptors. This clas-
sification groups opioids into agonists, antagonists, and
agonist-antagonists. Agonists, such as morphine and codeine,
elicit their analgesic effects by binding mu and kappa
receptors. In contrast, antagonists bind opioid receptors, but
do not stimulate them. Naloxone, a common narcotic reversal
agent, is an opioid antagonist. Its ability to reverse the effects
of opioid agonists is based on its higher binding affinity for
opioid receptors. Finally, agonist-antagonist drugs act as ago-
nists at one type of receptor and antagonists at others. For
example, pentazocine acts as an agonist at kappa receptors and
an antagonist at mu receptors.
The physiologic effect of opioids is dependent on the type
and location of the receptors that they bind. Their analgesic
effect is generated mainly by the inhibition of nociceptive
impulses in the CNS. They have been found at various levels
of the ascending pain pathway, including the dorsal horn of
the spinal cord, the brainstem, the thalamus, and the somato-
sensory cortex.15 They have also been found in the midbrain
and medulla, where they activate descending inhibitory path-
ways. Recent literature also points to a peripheral effect of
opioid analgesia.16-19 At the cellular level, binding at opioid
receptors may lead to one of several biochemical results:
(1) decrease in calcium influx at afferent nerve terminals
leading to decreased presynaptic neurotransmitter release,
(2) increased potassium efflux leading to hyperpolarization of
postsynaptic neurons and inhibition of impulse propagation,
and (3) inhibition of GABAergic transmission in the brain-
 CHAPTER 6 • Management of Acute Postoperative Pain 81

stem leading to the excitation of descending modulating
circuits.15
In addition to analgesia, activation of opioid receptors can
lead to several undesirable effects (Box 6-1). The activation
of mu receptors in respiratory centers of the brainstem leads
to respiratory depression. This response is dose dependent and
causes reductions in respiratory rate and minute volume.20
This is the most serious side effect of opioid administration,
and overdose can lead to respiratory arrest and death. One of
the more common unwanted effects of opioid use is nausea
and vomiting. This response is produced by the activation of
neurons in the chemoreceptor trigger zone of the medulla and
is worse in ambulatory patients.21 Other CNS effects include
mental clouding, sedation, and euphoria. All patients taking
these medications should be cautioned against operating
motor vehicles and making important decisions. Outside of
the CNS, opioids can also have unwanted effects. In the gas-
trointestinal (GI) system, opioids decrease gastric and intesti-
nal motility leading to constipation. The effects in the
cardiovascular system can be both detrimental and advanta-
geous. Opioids cause arteriolar vasodilation and can result in
orthostatic hypotension. However, the decrease in cardiac
demand caused by opioids can also be a benefit in patients
experiencing angina or myocardial infarction. Opioids also
cause an increase in smooth muscle tone of the bladder and
BOX 6-1 Opioid Adverse Side Effects
Respiratory depression
Nausea and vomiting
Mental clouding
Sedation
Euphoria
Constipation
Hypotension
Urinary retention
Pruritus
urinary sphincter leading to urinary retention. Finally, itching
may occur during opioid use as a result of the release of hista-
mine from mast cells and possibly by the disinhibition of
itch-specific neurons.22
The concepts of tolerance, dependence, and addiction
deserve mention in any discussion of opioid analgesics. Toler-
ance is a state of adaptation in which exposure to a drug
induces changes that result in a decrease of the drug’s effect
over time.23 The continual use of an opioid can lead to physi-
ologic and psychological alterations that can cause withdrawal
symptoms if the drug is discontinued. This is known as depen-
dence. Addiction is a form of psychological dependence asso-
ciated with the behavior patterns of obtaining and consuming
the drug.24 Even though the postoperative use of opioid anal-
gesics is usually for a limited duration, it is important for the
oral and maxillofacial surgeon to keep these concepts in mind
when managing pain. It is not uncommon to encounter
patients with chronic pain conditions who may be tolerant to
and dependent on opioids. In these situations, the choice of
a nonopioid analgesic or an increase in the dose of an opioid
may be warranted in treating acute postoperative pain. The
key to the use of opioids is maximizing the benefit of analgesia
while limiting any undesirable effects.
REVIEW OF OPIOIDS
Table 6-1 lists the most common opioids used by oral and
maxillofacial surgeons. Oral administration is the most
common route of administration in our population of patients.
It is important to keep in mind that opioids absorbed in the
GI tract are subject to first-pass hepatic metabolism. This
limits their efficacy and increases interpatient variability when
administered orally. Opioids may also be administered paren-
terally, intramuscularly, transdermally, transmucosally, sub-
cutaneously, and rectally.
Morphine is considered the prototype for all opioids.
Accordingly, it is the standard by which all opioids are mea-

TABLE 6-1 Commonly Used Opioid Analgesics

Analgesic Dose (mg) Dosing Interval (hr) Comments
AGONIST
Morphine 10-30 4 Standard analgesic dose used for potency comparisons
Codeine 60 3-4 Can be administered as a single agent or in combination with acetaminophen
or aspirin
Hydrocodone 5-10 4-5 Only available in a combination formulation with either acetaminophen, aspirin,
or ibuprofen
Dihydrocodeine 16-32 4-5 Only available in a combination formulation with either acetaminophen or
aspirin
Oxycodone 5-10 4-5 Only available in a combination formulation with either acetaminophen or
aspirin
Propoxyphene 65-130 4-6 Weak analgesic properties
MIXED AGONIST-ANTAGONIST
Pentazocine 50-100 4-6 Will precipitate an abstinence syndrome in patients dependent on opioids
OTHER
Tramadol 50-100 4-6 Not available in a combination formulation; although currently unscheduled by
the Drug Enforcement Administration, abuse potential exists
82 SECTION I ■ Anesthesia and Pain Control
TABLE 6-2 Equianalgesic Dose of Opioid Agents
Drug IM/IV (mg)
Morphine 10
Meperidine 75
Fentanyl 0.1-0.2
Codeine 120
Pentazocine 30
Oxycodone N/A
Hydrocodone N/A
Propoxyphene napsylate N/A
Tramadol N/A
Abbreviations: IM/IV, intramuscular/intravenous; PO, oral.
From Schwartz SR: Perioperative pain management, Oral Maxillofac Surg Clin North
Am 18:139, 2006.
sured. Table 6-2 compares the potencies of the common
opioids. All doses are based on the pain relief elicited from
10 mg of IV morphine. Administration of morphine is indi-
cated for severe pain, and thus its use in oral and maxillofacial
surgery is limited. When administering this drug intravenously
(IV), it is always wise to do so in a monitored setting. Doses
should be started low (i.e., 1 to 2 mg IV) and then titrated to
effect. It is important to remember that opioids have no ceiling
effect for analgesia. Their administration is limited by the
undesirable effects that occur as doses are increased.
Fentanyl and meperidine are two opioids typically admin-
istered via the IV route. Fentanyl is a fast-acting opioid that
is approximately 100 times more potent than morphine. It is
indicated for severe pain and is a common agent used for
conscious sedation in oral and maxillofacial surgical proce-
dures. The respiratory depressive effects limit its use in the
postoperative period. Like morphine, this drug should only be
administered in a monitored setting. In contrast, meperidine
is 10 times less potent than morphine, has a slower onset, and
lasts about twice as long as morphine and fentanyl. Its use has
generally fallen out of favor because of its undesirable effects.
Normeperidine is a neurotoxic metabolite of meperidine. It
has been shown to cause dysphoria, tremors, and generalized
seizures. In addition, use of meperidine with monoamine
oxidase inhibitors (MAOIs) can cause hypertensive crisis,
hyperpyrexia, and cardiovascular collapse.22
Codeine is another naturally occurring alkaloid that is
structurally similar to morphine. It is typically given in the
oral form. Codeine is a weak mu agonist. However a small
percentage of codeine is converted to morphine after admin-
istration. In the oral form, codeine is about four times less
potent than morphine. Doses greater than 60 mg are not rec-
ommended because the side effects above this dose outweigh
the analgesic benefits. Hydrocodone and oxycodone are semi-
synthetic opioids that are similar to morphine and codeine.
These drugs are available only in the oral formulation and
are about 6.5 and 10 times more potent than codeine,
respectively.
Propoxyphene is an opioid from the diphenylheptane
PO (mg) chemical class of opioids. It is structurally similar to metha-
30-60
done, a compound typically prescribed to treat heroin depen-
dence and addiction. Propoxyphene has about two-thirds of
300
the potency of codeine. In addition to the common side effects
N/A
of opioids, it also causes cardiotoxicity, pulmonary edema, and
200
arrythmias.22 It is therefore not generally considered a first-line
150
choice for opioid analgesia. Because propoxyphene is from a
20-30
different chemical class than the more commonly prescribed
30
opioids, it may be of some use in patients that exhibit sensi-
200
tivities to those medications.
100-150
Pentazocine is an opioid agonist-antagonist. It exhibits mu
antagonist activity and kappa agonist activity. It has less respi-
ratory depressive effects than the pure opioid agonists.
However, because it antagonizes mu receptors, it can precipi-
tate opioid withdrawal symptoms in patients concurrently
taking mu agonists. When crushed and given IV, pentazocine
can cause marked euphoria. To prevent illicit use of this drug,
it is commonly formulated to include the opioid antagonist
naloxone. When given orally, naloxone has minimal activity.
However, when taken IV, the naloxone will antagonize the
euphoric effects caused by pentazocine.
Tramadol is an analgesic drug marketed for treatment of
moderate to severe pain. It is a synthetic compound chemi-
cally unrelated to the other opioid classes. It appears to have
several mechanisms of action: (1) it is a weak mu agonist;
(2) it inhibits the serotonin and norepinephrine reuptake
systems. Unlike pure opioids, respiratory effects and abuse poten-
tial are minimal. The efficacy of tramadol for pain relief follow-
ing dental extractions appears to be comparable with codeine
and its oral combinations.25,26 It is typically administered in doses
of 50 to 100 mg and has been associated with side effects such
as headache, nausea, vomiting, somnolence, and seizures.
Most oral opioids are offered in combination with nonste-
roidal antiinflammatory medications. In the acute post-
operative period, inflammation occurring after the surgical
manipulation of tissue is the major cause of pain. Combining
an opioid with a nonsteroidal antiinflammatory drug (NSAID)
attacks multiple levels of the pain pathway and helps reduce
the dose of opioid necessary to reach the desired amount of
analgesia. It also limits unwanted side effects seen with higher
opioid doses.
■ LOCAL ANESTHETICS
Local anesthesia is a loss of sensation in an area of the body
caused by the depression of nerve ending excitation or the
inhibition of nerve impulse conduction.27 Local anesthetics
are an essential component in the arsenal for surgery and
dentistry. They allow for pain-free manipulation of hard and
soft tissues and have permitted the development of numerous
outpatient oral and maxillofacial surgery procedures. Local
anesthetics are an effective tool that should be considered in
the management of postoperative pain.
The two classes of local anesthetics are esters and amides.
The use of ester local anesthetics has generally fallen out of
favor in the practice of oral and maxillofacial surgery. Ester
 CHAPTER 6 •
local anesthetics need to be hydrolyzed in plasma by
pseudocholinesterase as part of their normal metabolism.
ρ-aminobenzoic acid (PABA) is a product of this breakdown
and can cause allergic reactions in many patients. In addition,
patients can have an atypical form of pseudocholinesterase
that fails to hydrolyze ester local anesthetics and can lead to
ester local anesthetic toxicity. Amide local anesthetics are
primarily metabolized in the liver. Caution should be exer-
cised when administering these drugs to patients with liver
disease. However, amide local anesthetics are considered to
be superior in predictability and safety and are therefore more
commonly used in oral and maxillofacial surgery.
Local anesthetics function by blocking sodium channels in
the membranes of neurons. This blockade depresses the rate
of electrical depolarization at these sites. The threshold poten-
tial for impulse propagation cannot be reached, and conduc-
tion is blocked. When conduction is blocked in pain fibers,
pain sensation cannot be transmitted.
The pain produced following oral and maxillofacial surgical
procedures is mainly inflammatory in nature. It can take days
to weeks for inflammation to resolve from certain surgical
procedures. Lidocaine and mepivacaine, the most commonly
used local anesthetics, are short acting. Used in conjunction
with epinephrine, they block conduction for 3 to 5 hours.
Their use for postoperative pain is therefore limited. The long-
acting amide local anesthetics include bupivacaine and etido-
caine. Their increased duration of action is a result of their
increased degree of protein binding. The dental formulations
of these drugs (0.5% bupivacaine with 1 : 200,000 epineph-
rine, 1.5% etidocaine with 1 : 200,000 epinephrine) can block
conduction for up to 8 to 12 hours.27 In third molar surgery,
use of bupivacaine has been shown to improve postoperative
pain experience compared with lidocaine.28 In addition, it has
been suggested that the blockade of nociceptive input by long-
acting local anesthetics decreases hyperexcitability in the
CNS and results in reduced postoperative pain and decreased
analgesic use.29 Recently the development of continuous infu-
sion devices has added to the efficacy of local anesthetics for
postoperative pain control.30 With these devices, the duration
of sensory blockade can be continued throughout the period
of greatest pain intensity.
Whenever using local anesthetics, the clinician should be
cognizant of the maximum doses for each agent. CNS and
cardiovascular toxicity can result from overdose. CNS depres-
sion from local anesthetic overdose typically manifests with
slurred speech, lightheadedness, headache, blurred vision, and
drowsiness. These signs and symptoms are typically preceded
by a period of excitation. Generalized tonic-clonic seizures can
also occur. In the cardiovascular system, initial signs may
include elevations in heart rate, blood pressure, and respira-
tory rate. As levels of systemic local anesthetic increase, myo-
cardial contractility is decreased. Heart rate, blood pressure,
and respiratory rate become depressed, and circulatory col-
lapse can occur.27 With strict adherence to maximum dosing
recommendations and observation for signs and symptoms of
overdose, local anesthetic toxicity can be prevented.
Management of Acute Postoperative Pain 83
■ NONOPIOID MEDIATED
ANALGESIA
Nonopioid analgesics, such as NSAIDs, acetaminophen, or a
combination thereof, are useful in the treatment of acute pain
in the oral and maxillofacial surgery patient (see Table 6-3).
Numerous clinical trials and studies have demonstrated their
effectiveness in the reduction of acute orofacial pain.31 Essen-
tial to the treatment of acute postoperative pain is an under-
standing of the mechanisms of pain and its pharmacologic
modification.
The inflammatory phase of wound healing consists of a
complex series of reparative responses mediated by release of
prostaglandins, histamine, kinins, leukotrienes, and substance
P. Prostaglandin synthesis at the site of tissue injury enhances
pain by increasing the sensitization and reducing the activa-
tion threshold of nociceptors activated to transmit pain signals
to the CNS. Nociceptive afferent neurons are involved in the
recognition and transmission of painful stimuli. Endogenous
mediators of inflammation cause a hyperalgesic effect by
sensitization and excitation of nociceptors at the site of the
surgical wound. This mechanism of increased levels of
aforementioned inflammatory mediators of pain (histamine,
bradykinin, leukotrienes, substance P) increase the action
potential firing of the nociceptors in tissues subjected to
trauma and inflammation. The subjective interpretation of
these inflammatory-mediated events is an increased percep-
tion of pain.
■ NONSTEROIDAL
ANTIINFLAMMATORY DRUGS
NSAIDs are effective analgesic agents with antiinflammatory
and antipyretic activity. They reduce pain, fever, and inflam-
mation. They are nonnarcotic. The primary mechanism of
action is the inhibition of cyclooxygenase (COX) enzymes
responsible for the conversion of arachidonic acid into pros-
taglandins at the site of injury. Modern laboratory techniques
and biochemical studies have determined that two different
isoforms of COX exist, referred to as COX-1 and COX-2. It
is believed that the expression of COX-1 is constitutive (i.e.,
continuously produced) by many cell types throughout the
body. COX-1–mediated prostaglandins maintain homeostasis
pathways in the GI tract, kidney, heart, brain, and vascula-
ture. Prostaglandins protect the GI mucosal integrity by the
stimulation and production of mucus and bicarbonate, which
form a protective barrier against acid secretion. In the kidney,
prostaglandins regulate blood flow, renin release, and renal
tubular salt and water resorption, resulting in an increased rate
of glomerular filtration. In the circulatory system, prostaglan-
dins regulate vascular homeostasis and platelet function. The
expression of COX-2 is induced during the inflammatory
process at the site of tissue injury. Endogenous prostaglandins
mediated by COX-2 release the aforementioned inflammatory
mediators (including histamine, bradykinin, leukotrienes,
and substance P) during tissue trauma. These inflammatory-
84 SECTION I ■ Anesthesia and Pain Control

TABLE 6-3 Nonopioid Analgesics

Generic Proprietary Pain Level Dose (mg) Interval (hr) Maximum Dose/ Additional Comments
Name 24 hr (mg)
SALICYLIC ACID DERIVATIVES
Aspirin Anacin Mild 650-1000 4-6 4000 Increased risk of bleeding with excessive
Bayer alcohol intake (≥3 drinks/day), avoid use with
Ecotrin viral infections in children or teenagers,
Excedrin syndrome of asthma, rhinitis, and nasal
polyps
Diflunisal Dolobid Mild to 500 12 1500 1000-mg loading dose
moderate
r-AMINOPHENOL DERIVATIVES
Acetaminophen Datril Mild 650-1000 4-6 4000 Increased risk of hepatotoxicity with
excessive alcohol intake (≥3 drinks/day)
Panadol
Tylenol
PROPIONIC ACID DERIVATIVES
Ibuprofen Advil Mild to 400 4-6 3200
moderate
Motrin
Motrin-IB
Ketoprofen Ketoprofen Mild to 25-50 6-8 300
moderate
Naproxen sodium Anaprox Mild to 275 6-8 1375 Start 550 mg then 275 mg every 6-8 hr
moderate
Anaprox DS Mild to 550 12 1375 Alternate 550 mg b.i.d.
moderate
INDOLEACETIC ACIDS
Etodolac Lodine Mild to 200-400 6-8 1000 (1200) Primarily COX-2 inhibitor
moderate
HETEROARYL ACETIC ACIDS
Diclofenac Cataflam Mild to 50 8 150 Loading dose up to 100 mg, total of 200 mg
moderate day 1
Ketorolac Toradol Moderate to 60 IM, 30 IV Single dose 120
severe
30 IM/IV 6 120 Transition from IV/IM to PO 20 mg, then
every 4-6 hr; total duration of use ≤5 days
20 then 10 PO 4-6 40
COXIBS
Celecoxib Celebrex Mild to 200 12 400 400-mg loading dose, then 200 mg if
moderate needed, selective COX-2 inhibitor
Abbreviations: IM/IV, intramuscular/intravenous; PO, oral.
From Schwartz SR: Perioperative pain management, Oral Maxillofac Surg Clin North Am 18:139, 2006.

mediated events result in increased vasodilation and permea-
bility of the peripheral vasculature, edema, erythema,
hyperalgesia, loss of function, and pain.
Acute inflammation occurs during surgical manipulation of
tissue, resulting in postprocedural pain. NSAIDs decrease sur-
gically induced inflammation by inhibition of prostaglandins
synthesized by COX-2, decreasing sensitization of peripheral
terminals of nociceptive afferent neurons. They are very effec-
tive in managing postoperative pain of inflammatory origin
where tissue damage has occurred. They are available over-
the-counter, and a wide variety of formulations (oral, tablet,
and liquid) and dosages exist.
NSAIDs possess many advantages, including analgesic,
antiinflammatory, and antipyretic effects and, unlike opioids,
do not result in sedation or respiratory depression or interfere
with bowel and bladder function.12,32 They are relatively safe
and have a very low addiction rate. Side effects are infrequent
when administered judiciously. NSAIDs used as analgesic for
acute postsurgical pain should be limited to 5 days. To mini-
mize negative GI side effects, NSAIDs should be taken after
meals or with food.8,32 Patients predisposed to GI disease
should take NSAIDs with caution, especially if they have a
history of alcohol abuse or peptic ulcer disease. The results of
previous clinical trials establish that the administration of an
NSAID (e.g., ibuprofen), 400 mg, 30 minutes before surgery
delays the onset and reduces the severity of postoperative pain
with outpatient procedures.8 Evidence demonstrates the ben-
eficial effects of postoperative dosing of an NSAID within 30
minutes after the procedure for NPO patients scheduled for
IV anesthesia.12
 CHAPTER 6 •
Recommended Preoperative NSAID Protocol
BOX 6-2
for Postoperative Pain Control
• Ibuprofen (400 mg) 30 min before the initiation of treatment
• Benefits:
1. Delayed onset of postoperative pain
2. Decreased severity of postoperative pain
• Precautions:
1. DO NOT use in patients for whom NSAIDs are contraindicated (e.g., NSAID
allergy or sensitivity, GI ulcerations, renal disease).
2. Doses of ibuprofen in excess of 400 mg are associated with a greater
incidence of unwanted side effects and have not been demonstrated to
increase analgesic efficacy.
■ PREOPERATIVE ADMINISTRATION
OF NSAIDS5
The synthesis and release of local inflammatory mediators
from injured tissue during the postoperative phase persists
because the local anesthetic blocks afferent impulse conduc-
tion. A state of hyperalgesia exists as a result when the local
anesthetic wears off.8 Patient discomfort subsequently increases
during the lag time between NSAID administration and
when therapeutic plasma concentrations of the analgesic are
attained. Activated and sensitized nociceptive afferent
neurons have an elevated response at the spinal and medullary
dorsal horn levels as the effect of local anesthetic diminishes.
Primary and secondary hyperalgesia may develop as a conse-
quence of these modifications at the CNS level. The admin-
istration of an NSAID preoperatively appears to maximize the
usefulness of this drug class as opposed to the conventional
strategy of NSAID administration at pain onset.
Numerous clinical trials have tested whether the efficacy
of various NSAIDs is increased by administering the com-
pound 30 minutes before the beginning of surgery and deter-
mined that, indeed, it improved postoperative comfort.33,34,35
The various NSAIDs evaluated in this preoperative pain man-
agement strategy demonstrate comparable effectiveness, so
the agent of choice should be that with the fewest side effects.
Both aspirin and diflunisal have demonstrated potentially
dangerous side effects—increased swelling and ecchymosis
with aspirin and dry sockets with diflunisal—leaving ibupro-
fen as the best tolerated of the NSAIDs.36,37 Accordingly,
ibuprofen is suggested as the NSAID of choice for pretreat-
ment (Box 6-2). The recommended preoperative administra-
tion of 400 mg of ibuprofen 30 minutes before surgery has
demonstrated delayed onset and decreased severity of post-
operative pain.38,39 Analgesic potency of this strategy does not
appear to strengthen with doses of ibuprofen in excess of
400 mg in comparison with the increased undesirable side
effects.
DISADVANTAGES AND CONTRAINDICATIONS
(Box 6-3)
The most common adverse side effects of NSAIDs are GI,
including gastritis, ulceration, and bleeding, the potential for
which increases with prolonged usage or high daily doses and
Management of Acute Postoperative Pain 85
BOX 6-3 NSAID Contraindications
• History of allergy or sensitivity to aspirin or NSAIDs
• History of gastric ulcers
• Bleeding disorders (does not apply to acetaminophen)
• Renal disease
• Hepatic disease
• Pregnant or lactating females
• Asthma
prior history of such complications.12,32,40 Attention has been
paid to the potential for NSAIDs to increase the possibility
of postoperative bleeding. With the exception of aspirin, the
inhibition of platelet function is reversible with NSAIDs.
This side effect is rarely seen except in select patient popula-
tions additionally taking anticoagulants.12
Great caution should be exercised when using NSAIDs
during pregnancy or with the elderly because there is a higher
risk of ulcerative disease in the elderly population taking
anticoagulants or corticosteroids.41 The systematic action of
NSAIDs contribute to potential adverse effects, the greatest
risk being spontaneous GI hemorrhage. The production of the
powerful platelet aggregating agent, thromboxane A2, is indi-
rectly decreased by NSAID inhibition of COX, increasing the
likelihood for bleeding. In the genitourinary system, NSAIDs
adversely affect kidney function in patients with chronic renal
disease by decreasing renal blood flow and glomerular filtra-
tion rate.32,42 NSAIDs are therefore contraindicated in patients
with severe renal disease and may cause nephrotoxicity when
taken chronically or in combination with other NSAIDs.
Dyspepsia, peptic ulcer, dysphagia, and abdominal pain are
additional GI side effects.32,43 Non-GI side effects include
severe allergic reactions or anaphylaxis secondary to prosta-
glandin synthesis inhibition, tachycardia, edema, dizziness,
headache, and increased liver enzymes.
Most drug interactions associated with analgesics are not
clinically relevant in acute pain management settings second-
ary to their short duration of use. Potential interactions exist,
however, in patients taking a combination of pain medica-
tions or with extended use.32 NSAIDs may diminish the anti-
hypertensive effect of three classes of agents, including the
ACE inhibitors, β-blockers, and diuretics, by inhibiting pros-
taglandin synthesis. Because NSAID use for this effect is at
least 7 to 8 days, their use should be limited to 4 days in
patients taking antihypertensives.44
■ REVIEW OF NONOPIOID
ANALGESICS (Table 6-4)
ASPIRIN
Aspirin is perhaps the most common NSAID and was discov-
ered in 1897 in Germany. It has proven time and time again
to be an effective analgesic, antiinflammatory, and anti-
pyretic.12 Most segments of the population have little negative
reaction to normal doses, and with a new derivative, diflunisal,
having recently been discovered, new applications may be on
86 SECTION I ■ Anesthesia and Pain Control

TABLE 6-4 Commonly Used Nonopioid Analgesics

Analgesic Suggested Dose (mg) Dosing Interval (hr) Maximum Adult Comments
Daily Dose (mg)
SALICYLIC ACID DERIVATIVES
Aspirin 650-1000 4-6 4000
Diflunisal 500 8-12 1500* Slow onset dictates the need for a 1000-mg loading
dose
ANILINE DERIVATIVES
Acetaminophen 650-1000 4-6 4000
PROPIONIC ACID DERIVATIVES
Ibuprofen 400 4-6 3200
Ketoprofen 50-75 6-8 300
Naproxen 250 6-8 1250* Slow onset dictates the need for a 500-mg loading dose
INDOLEACETIC ACIDS
Indomethacin 25 8-12 75 High incidence of side effects
Etodolac 200-400 6-8 1200 Highly selective inhibitor of COX-2
Diclofenac 50-100 8-12 150* Consider a 100-mg loading dose
Ketorolac 15-30 IV or 30-60 IM, 4-6 120 IV or IM, 40 PO Oral dosing only after parenteral administration; therapy
10-20 PO not to exceed 5 days
*Does not include the loading dose.
Abbreviations: IM/IV, intramuscular/intravenous; PO, oral.

the horizon. Despite these positives, it has a low therapeutic
ceiling; can cause gastric ulcerations, perforations, and bleed-
ing; and inactivates platelets for their lifespan following con-
sumption of the drug. It can lead to the development of Reye’s
syndrome in children with viral infections.45
ACETAMINOPHEN
Acetaminophen is similarly common to aspirin and similarly
safe. It provides effective relief for mild pain, can be combined
with opioids for more serious pain, and has minimal short-
term side effects. Most importantly, unlike aspirin, it does not
impact platelet function. It does not possess the antiinflam-
matory properties of aspirin. Its downsides are that it can cause
severe hepatic damage (making it dangerous for alcohol
abusers) and has a low therapeutic ceiling.8,12,40,46
KETOROLAC (TORADOL)
Ketorolac is an analgesic used commonly in conjunction with
facial trauma, orthognathic surgery, and maxillofacial surgery.47
It is injectable and has short-term side effects, such as renal
ischemia, GI perforation, and bleeding, that can be lessened
by limiting prescriptions to less than 5 days.12 Administering
ketorolac or another potent NSAID toward the end of an
operation can reduce the amount of opioid necessary to
maintain postoperative comfort in the patient. A parenteral
NSAID, it has proven at least as effective as parenteral opioids
in treating moderate to severe pain.45,48
COX-2 INHIBITORS
The newest and most controversial NSAID, COX-2 inhi-
bitors are best used with patients with acute or chronic pain.49
After the withdrawal of several versions of the drug from the
market in 2004 and 2005, celecoxib is currently the only
COX-2 up for commercial sale.12 In theory, the drug only
inhibits COX-2–mediated prostaglandins, which cause inflam-
mation, limiting the negative effects on the gastroprotective
qualities of the COX-1 isoform. Despite this benefit, COX-2
inhibitors can disturb the hemodynamic balance between the
body’s organs and adversely affects the cardiovascular system.
Worse yet, trials have shown little difference in postoperative
pain relief between COX-2s and ibuprofen, despite the fact
that the former can be 200 times more expensive.50
STEROIDS
Corticosteroids have been used in oral and maxillofacial
surgery for many years and avert most of the postoperative
edema seen with major oral and maxillofacial surgeries when
used correctly. Corticosteroids act earlier in the cascade by
suppressing arachidonic acid production, inhibiting pros-
taglandins and leukotrienes. They also have central antinoci-
ceptive properties at the spinal cord level.12 This in turn leads
to decreased pain and earlier ambulation, ability to consume
food orally, and ultimately a shorter hospital stay.51
Multiple methods of use, both alone and in combination,
have existed for methylprednisolone, dexamethasone, and
methylprednisolone acetate. For procedures expected to cause
significant inflammation, including impacted third molars and
orthognathic surgery, methylprednisolone and other oral ste-
roids have been routinely prescribed. In fact, Romunstad et al.
have demonstrated a greater opioid-sparing and antiemetic
effect with corticosteroids than the powerful NSAID ketoro-
lac following orthopedic surgery.52 Of note, a disadvantage of
concurrent use of corticosteroids with NSAIDs is the signifi-
cant increase in the risk of life-threatening GI bleeding.
 CHAPTER 6 •
■ PERIOPERATIVE PAIN CONTROL
CONSIDERATIONS
Each oral and maxillofacial surgeon must anticipate a pain
management strategy for individual patients. Attenuation of
the nociceptive impulses to the surgical insult while minimiz-
ing drug side effects, including nausea, diminished cognitive
and motor function, and reduced patient anxiety, should be
the goal of this strategy. Unrelieved pain causes suffering and
can lead to other health problems and delays in recovery. In
February 1992, an 18-member panel concluded, after review-
ing more than 7000 public studies, that conventional pain
management modalities were neither effective nor in the best
interest of the patient (Box 6-4).53
Postoperative pain management begins preoperatively.
Patient education before a painful and sometimes highly emo-
tional experience may improve the ability of the patient to
cope and thereby enhance the pain treatment outcome. Some
key steps in patient education are listed in Box 6-5.54
BOX 6-4 Conclusions of Published Studies
• Half of all patients given conventional therapy for their pain do not get adequate
relief. These patients continue to feel moderate to severe pain.
• Prescribing pain medication only “as needed” can result in prolonged delays
because patients may delay asking for help.
• Aggressive prevention of pain is better than treatment because once established
pain is more difficult to suppress.
• Patients have a right to treatment that includes prevention of pain and adequate
pain relief. The surgeon needs to develop pain control plans before surgery and
inform the patient what to expect in terms of pain after the surgery.
• Fears of postsurgical addiction to properly prescribed and administered opioids
are generally groundless.
BOX 6-5 Key Patient Education Steps
• Describe the expected type of pain and its probable duration to decrease the
uncertainty and fears of the unknown.
• Individualize the information for the patient.
• Discuss goals of pain management and how these goals help the patient’s
comfort, hasten recovery, and reduce complications.
• Reinforce the concept that pain prevention is important to good pain management.
The patient should try to anticipate their pain medication requirements.
• Many drug and nondrug treatment options can be helpful in preventing and
managing pain.
• Inform the patients of when and how to contact the surgeon about his or her
pain.
• Parents of minor patients and the surgeon will decide as a team which treatments
are best to manage their pain.
• Discuss treatment plan and choices including the schedule of medications that
are appropriate to the patient.
■ ASSESSMENT AND
MANAGEMENT OF ACUTE PAIN
The increasing number of patients who have become medi-
cally sophisticated has resulted in requests for specific treat-
ment modalities. Postoperative pain management is no
exception. Reducing the incidence, duration, and intensity of
Management of Acute Postoperative Pain 87
postoperative pain and complications not only increases their
comfort level but also improves their level of satisfaction with
the service provider. The most reliable indicator for the exis-
tence and intensity of pain is the patient. Osler said, “Listen
to the patient and he will give you his diagnosis.” In oral and
maxillofacial surgery, somatic pain is the most common type
of pain we encounter; however, patients may also simultane-
ously experience more than one type of pain (Figure 6-3).54
In assessing and formulating a pain management plan, the
clinician must consider the multiple factors that influence
analgesic requirements (Box 6-6).55
Following assessment and determination of the mechanism
of pain, the surgeon can prescribe a pain-management regimen
that addresses the chief complaint of the patient and his or
her individual requirements and considerations. Figure 6-4 is
an algorithm directed toward the specific treatment of the
patient’s pain.54
Factors That Influence Analgesics
BOX 6-6
Requirements
• Age of the patient. Very old or very young patients require smaller doses.
• Sex.
• Preoperative analgesic use.
• Past history of poor pain management.
• Coexisting medical conditions, such as substance abuse, anxiety disorder, affec-
tive disorder, hepatic or renal impairments.
• Cultural factors and personality.
• Preoperative patient education. Appropriate preoperative education can improve
expectations, compliance, and ability to effectively interact with pain management
techniques.
• Individual variations in response and pain threshold.
• Attitude of the clinical staff.
■ PREEMPTIVE ANALGESIA
THERAPY
As has previously been stated, by preventing the sensitization
of the CNS, which would normally amplify subsequent noci-
ceptive input, one may reduce the severity of postoperative
pain.8,53,54 To this end, the application of opioids, local anes-
thesia blocks, and other analgesic modalities are instituted
and established before surgery to attempt to decrease the
intensity and duration of the postoperative pain. Giving an
NSAID 30 minutes before a surgical visit improves
the patient’s postoperative comfort with delayed onset and
decreased severity of postoperative pain.33,34,35 It has been
established that following a dosing strategy governed by the
clock while awake (e.g., “every 4 hours”) rather than as
needed (p.r.n.) maximizes an orally administered analgesic’s
effectiveness.8 During the postoperative period, regular inter-
val dosing results in steady plasma concentration of the anal-
gesic. Plasma concentrations are less likely to decline lower
than the therapeutic threshold with this dosing routine,
reducing the potential for breakthrough pain. After this
88 SECTION I ■ Anesthesia and Pain Control

period, consideration should be given to switching to an as-
needed analgesic protocol. Administration of intraoperative
ketorolac (Toradol) before completion of a surgical procedure
has demonstrated a decrease in the amount and incidence of
postoperative pain therapy.45,47,48
Local anesthesia is integral to the delivery of ambulatory
oral and maxillofacial surgery. The long-acting local anesthet-
ics bupivacaine (Marcaine) and etidocaine (Duranest) are
preemptive in that they prevent neurotransmission of noci-
ceptive stimuli for up to 8 to 12 hours and thereby result in
decreased analgesia requirements and increased patient
comfort.27,28,29
Corticosteroids have been demonstrated to reduce opioid
requirements in both orthognathic and third molar surgery.12,52
As a time-proven adjunct to the postoperative management
of the oral and maxillofacial surgery patient, steroids are rec-
ommended as a perioperative adjunct medication.
■ PCA
Patient-controlled analgesia (PCA) is a method of inpatient,
self-administered analgesia according to the surgeon’s orders
to control his or her pain. A programmable infusion pump
that delivers opioids at a continuous infusion rate (milligrams
per hour) along with a patient-controlled demand bolus is
administered via an I.V. A lock-out interval, when the pump
will not allow more boluses to be administered, is programmed
into the pump. The primary advantage of the PCA is patient
convenience and preemptive pain control because the patient
controls when a dose of analgesia is given and the patient is
not at the mercy of a nurse-call system. Inappropriate candi-
dates for PCA therapy include those patients who are physi-
cally or mentally unable to self-administer medications.
■ PHYSICAL METHODS
Commonly used physical agents include applications of cold,
massage, movement, transcutaneous electrical nerve stimula-
tion (TENS), and rest or immobilization. TENS may be effec-
tive in reducing pain and improving physical function. It has
been used with various degrees of success in the management
of postoperative pain. Evidence is accumulating that TENS
acts by increasing CNS levels of β-endorphins together with
activation of the pain gate by counterirritation.55 At present,
its use in ambulatory oral and maxillofacial surgery is not
practical.
Patients may simultaneously experience more than one
type of pain. Patients who have had impacted third molars
will certainly experience somatic and visceral pain. Neuro-
pathic pain may also be present in the unfortunate event
where the inferior alveolar nerve is injured during surgery.
Neuropathic pain may be resistant to standard opioid therapy

Patient has pain or is

likely to have pain

Critical first steps:

Detailed history
Focused physical exam

Pain assessment

Determine mechanism of pain

using history and pain assessment
(patient may experience more
than one type of pain)

Neuropathic pain
Somatic pain Visceral pain
Patient reports radiating or
Patient reports localized pin Patient reports generalized
specific burning, tingling, or
prick, sharp or stabbing pain ache or pressure
lancinating pain
(see Treatment algorithm: (see Treatment algorithm:
(see Treatment algorithm:
Somatic pain) Visceral pain)
Neuropathic pain)

FIGURE 6-3. Assessment of acute pain. (Adapted from The Institute for Clinical Systems Improvement (ICSI):
Assessment and management of acute pain.)
 CHAPTER 6 • Management of Acute Postoperative Pain 89

and other nociceptive pain treatment modalities. Anticonvul-
sants and tricyclic antidepressants are the mainstay of therapy.
A continuous burning may respond to antidepressants, whereas
lancinating pain may best respond to anticonvulsants. Gaba-
pentin (Neurontin), however, can treat both continuous and
episodic neuropathic pain.54
■ REASSESSMENT
Clinicians should initiate a strategy early during the post-
operative stage for monitoring a patient’s response to analgesic
treatment because no two patients respond to any specific
analgesic in the same way.8 Analgesic effectiveness and pres-
ence of unwelcome side effects should be assessed and remedied
during postoperative monitoring, enabling the clinician to
adapt the postoperative pain strategy to the particular needs of
their patient. The amount and interval of drug dosage can be
titrated by the clinician to obtain the desired analgesic effect
or decrease undesirable side effects. If the decision is made to
transition to another analgesic based on a patient’s inadequate
pain relief or intolerable side effects, close follow-up monitor-
ing is essential in determining that these problems have been
either removed or minimized to an acceptable level.
If adequate pain relief has yet to be obtained, reassessment
is indicated. Attention should be directed to any remain-
ing dentition to rule out a concomitant pupal pathology or
odontogenic infection. Foremost in consideration would be a
localized osteitis (dry socket). However, a pulpitis or odonto-
genic infection of the remaining dentition needs to be ruled
out. Certainly, if either is present, appropriate treatment
should be instituted.
The oral and maxillofacial surgeon also should be mindful
of signs and symptoms of temporomandibular joint and
muscles of mastication dysfunction because they may have
preceded or have been exacerbated by the surgical event. The
postoperative sequelae of third molar surgery and other dental
extractions might include muscle splinting and possibly tem-
poromandibular joint dysfunction. A clinical exam directed
toward ruling out splinting and spasm of the muscles of mas-
tication and dysfunction of the temporomandibular joint
should be part of the postoperative assessment of a break-
through pain patient. Consideration should be given to
conservative management of the presenting symptoms. A
continuation or addition of NSAIDs to address the mild to
moderate pain or the continued use of opiates for severe pain

Type of Pain
Somatic Pain Visceral Neuropathic Pain
Location Localized Generalized Radiating or specific
Patient Pin prick, or stabbing, or sharp Ache, or pressure, Burning, or prickling, or
Description or sharp tingling, or electric shock-like,
or lancinating
Mechanism of A-delta fiber activity; located in the C Fiber activity; Dermatomal ‡ (peripheral), or
Pain periphery* involved deeper non-dermatomal (central)
innervation*
Clinical • Superficial laceration • Periosteum, • Trigeminal
Examples • Superficial burns joints, muscles • Avulsion neuralgia
• Intramuscular injections, • Muscle spasm • Post-traumatic neuralgia
venous access pain† • Peripheral neuropathy
• Osseous surgery • Osseous surgery (diabetes, human
• Stomatitis immunodeficiency virus
• Extensive abrasion [HIV])
• Herpetic neuralgia
Most • Acetaminophen • Corticosteroids • Anticonvulsants
Responsive • Cold packs • NSAIDs • Corticosteroids
Treatments • Corticosteroids • Opioid via any • Neural blockade
• Local anesthetic either route • NSAIDs
topically or by infiltration • Antispasmodics • Opioids via any route
• Non-steroidal anti- • Tricyclic antidepressants
inflammatory drugs
(NSAIDs)
• Tactile stimulation
* Most post-operative patients experience A-delta and C Fiber pain and respond best to
narcotic of any route and NSAIDs.

† Muscle spasms may be less responsive to opioids. Respond best to antispasmodics,

NSAIDs, benzodiazepines, baclofen.

‡ Segmental distribution follows a dermatome chart. This traces the pathway of

sensation to its nerve root.

The algorithm acknowledges that in most clinical situations the initial treatment of pain
and the diagnostic work-up occur concurrently.

FIGURE 6-4. Acute pain management algorithm (Adapted from The Institute for Clinical Systems Improvement
(ICSI): Assessment and management of acute pain.)
90 SECTION I ■ Anesthesia and Pain Control
is appropriate.54 The addition of antispasmodics (muscle
relaxers) with a diagnosis of spasm would also be appropriate.
Chlorzoxazone (Parafon Forte), metaxalone (Skelaxin), cyclo-
benzaprine (Flexeril), and carisoprodol (Soma) fall into this
family of drugs. However, these drugs, to a varying degree, may
impair mental and physical abilities. Caution should be used
when they are used with other CNS depressants, such as
tranquilizers, narcotics, and alcohol.56
Diazepam (Valium) has been shown to be a very good
adjunct to postoperative pain management. It is a very good
muscle relaxer in low doses. Its potential for complications is
much lower than traditional muscle relaxers, and it does not
seem to cause profound muscle impairment when compared
with other muscle relaxers.57 Valium has the added benefit of
lowering the patient’s anxiety level while potentiating the
analgesic effect of the opioids.
■ CONCLUSION
Speaking broadly, pain can be defined as an unpleasant sensory
experience perceived as arising from a specific location of the
body and associated with actual or even purely potential tissue
damage.59 In particular, the onset of acute orofacial pain often
motivates individuals to seek immediate care. The well-
documented analgesic potency of nonopioid medications and
their success in reducing the severity of acute orofacial pain
have contributed greatly to their popularity. Though formerly
classified as mild analgesics, they have now become estab-
lished in their postoperative use in circumstances involving
tissue damage. Hence surgeons now bear responsibility for
effectively and safely controlling pain during both intraopera-
tive and postoperative periods.
The goals of effective management of acute orofacial pain
should include: (1) maintaining maximal patient comfort,
(2) minimizing the occurrence and severity of unwanted side
effects, and (3) returning function as rapidly as possible to the
injured tissue.8 Accomplishing these goals requires a multifac-
eted approach.60 Comprehensive patient evaluation, prepara-
tion, and planning are all crucial to perioperative pain
management.
This includes a responsibility by the surgeon to thoroughly
review and modify any existing pain medication currently
taken by the patient. Also included in the preparatory phase
of perioperative pain management is the starting of nonopioid
medications (NSAIDs, acetaminophen) preoperatively.
In the postoperative period, evidence supports the use of
two different-acting analgesic agents for providing greater
analgesic efficacy with fewer unfavorable effects and also sug-
gests that two routes of administration may be most effective
in providing perioperative analgesia (see Figure 6-3). Practice
guidelines for acute pain management also support a multi-
modal technique for patients that includes administration of
NSAIDs, coxib, or acetaminophen on a by-the-clock schedule
unless contraindicated.61
Oral and maxillofacial surgeons employ a combination of
pharmaceutic agents and strategies for pain management.
Effective pain management may include use of analgesics (i.e.,
opioids, nonopioids, general and local anesthetics, nitrous
oxide, and oxygen), anxiolytics (i.e., benzodiazepines), seda-
tive hypnotics (i.e., propofol, methohexital), dissociative
agents (i.e., ketamine), and volatile inhalational agents. The
administration of these various agents for the management of
perioperative and postoperative pain may be provided by the
oral and maxillofacial surgeon depending on the type of
procedure.
Several strategies exist for management and reduction of
postoperative pain. Recent evidence indicates that the local
inflammatory component responsible for much of the acute
postoperative pain response is decreased by NSAIDs not only
peripherally with decreased nociception sensitivity but also
centrally with an antihyperalgesic effect. Opioids also effec-
tively manage and reduce the unpleasant postoperative pain
experience by exerting both a central and peripheral analgesic
effect.
The use of long-acting local and regional anesthetics (i.e.,
bupivacaine, etidocaine) are important in delaying the trans-
mission of painful stimuli up to 8 hours postoperatively. These
agents may be given either as a local infiltration or block and
help to lower a patient’s total analgesic demand. Heightened
postoperative pain relief is easily achieved by providing a dose
of long-acting anesthetic at the end of a procedure, allowing
patients a “pain-free window” in which to obtain and self-
administer their prescription medications.
When developing a pain control strategy, it is important
to recognize that the maximum dose of combined pharmaceu-
tic agents excluding codeine and propoxyphene is determined
by the NSAID or acetaminophen dosage, rather than the
opioid.12 Comprehension of this fact combined with the real-
ization that local inflammatory response contributes substan-
tially to acute postoperative pain and hyperalgesia enables the
choice of suitable doses of combination drugs. The most effec-
tive pain control strategies address both the inflammatory
response and the CNS-mediated mechanisms resulting from
surgical manipulation of orofacial hard and soft tissues.8
Clinicians’ flexible pain management strategies should aim
to maximize relief from postoperative discomfort and mini-
mize the number and severity of unwanted side effects. In
addition, clinicians need to consider the physiologic and psy-
chological attributes of patients, all of which help determine
how these patients might respond to and subsequently deal
with pain. Ultimately, clinicians need to be both flexible and
adept in their approach to treating acute pain in the periop-
erative setting.
REFERENCES
1. Cooper SA, Beaver WT: A Model to evaluate mild analgesics
in oral surgery outpatients, Clin Pharmacol Ther 20:241,
1976.
2. Conrad SM et al.: Patient’s perception of recovery after third
molar surgery, J Oral Maxillofac Surg 54:1402, 1999.
3. White RP et al.: Recovery after third molar surgery: clinical and
health-related quality of life outcomes, J Oral Maxillofac Surg
61(5):535, 2003.
 CHAPTER 6 •
4. Slade GD et al.: The impact of third molar symptoms, pain and
swelling on oral health-related quality of life, J Oral Maxillofac
Surg 62(9):118, 2004.
5. Snyder M et al.: Pain medication as an indicator of interference
with lifestyle and oral function during recovery after third molar
surgery, J Oral Maxillofac Surg 63(8):1130, 2005.
6. Shugars DA et al.: Assessment of oral health-related quality of
life before and after third molar surgery, J Oral Maxillofac Surg
64(12):1721, 2006.
7. Grossi GB et al.: Assessing post-operative discomfort after third
molar surgery: a prospective study, J Oral Maxillofac Surg
65(5):901, 2007.
8. Jackson DL, Roszkowski MT, Moore PA: Management of acute
postoperative pain. In Fonseca R, editor: Oral and maxillofacial
surgery: anesthesia, dentoalveolar surgery and office management, vol
1, 2000, WB Saunders.
9. Sessle BJ: Acute and chronic craniofacial pain: brainstem mech-
anisms of nociceptive transmission and neuroplasticity, and their
clinical correlates, Crit Rev Oral Biol Med 11(1):57, 2000.
10. Pyati S, Gan TJ: Perioperative pain management, CNS Drugs
21(3):185, 2007.
11. Strassels SA, McNicol E, Suleman R: Postoperative pain man-
agement: a practical review, part 1, Am J Health-Syst Pharm
62:1904, 2005.
12. Schwartz SR: Perioperative pain management, Oral Maxillofac
Surg Clin North Am 18:139, 2006.
13. Jackson DL, Roszkowski MT, Moore PA: Management of acute
postoperative pain. In Fonseca R, editor: Oral and maxillofacial
surgery, 2001, WB Saunders.
14. Sessle BJ: Acute and chronic craniofacial pain: brainstem mech-
anisms of nociceptive transmission and neuroplasticity, and their
clinical correlates, Crit Rev Oral Biol Med 11(1):57, 2000.
15. Inturrisi CE: Clinical pharmacology of opioids for pain, Clin J
Pain 18(suppl 4):S3, 2002.
16. Fields HL et al.: Multiple opiate receptor sites in on primary
afferent fibers, Nature 284:351, 1980.
17. Stein C, Schafer M, Hassan HA: Peripheral opioid receptors,
Ann Med 27:219, 1995.
18. Stein C et al.: Analgesic effect of intraarticular morphine after
arthroscopic knee surgery, N Engl J Med 325:1123, 1991.
19. Zuniga JR, Ibanez C, Kozacko M: The analgesic efficacy and
safety of intra-articular morphine and mepivacaine following
temporomandibular joint arthroplasty, J Oral Maxillofac Surg
65:1477, 2007.
20. Pasero CL, McCaffrey M: Avoiding opioid-induced respiratory
depression, Am J Nurs 94(4):24, 1994.
21. Silva AC, O’Ryan F, Poor DB: Post-operative nausea and vomit-
ing (PONV) after orthognathic surgery: a retrospective study
and literature review, J Oral Maxillofac Surg 64(9):1385, 2007.
22. Strassels SA, McNicol E, Suleman R: Postoperative pain man-
agement: a practical review, part 2, Am J Health-Syst Pharm
62:2019, 2005.
23. DuPen A, Shen D, Ersek M: Mechanisms of opioid-induced
tolerance and hyperalgesia, Pain Manage Nurs 8(3):113, 2007.
24. Ballantyne JC, LaForge KS: Opioid dependence and addiction
during opioid treatment of chronic pain, Pain 129(3):235,
2007.
25. Moore MA, McQuay HJ: Single-patient data meta-analysis
of 3453 postoperative patients: oral tramadol versus placebo,
codeine and combination analgesics, Pain 69(3):297, 1997.
26. Jung YS et al.: Onset of analgesia and analgesic efficacy of tra-
madol/acetaminophen and codeine/acetaminophen/ibuprofen in
acute postoperative pain: a single-center, single-dose, random-
ized, active-controlled, parallel-group study in a dental surgery
pain model, Clin Ther 26(7):1037, 2004.
27. Malamed SF: Handbook of local anesthesia, ed 4, St Louis, 1997,
Mosby.
Management of Acute Postoperative Pain 91
28. Bouloux GF, Punnia-Moorthy A: Bupivacaine versus lidocaine
for third molar surgery: a double-blind, randomized, crossover
study, J Oral Maxillofac Surg 57:510, 1999.
29. Gordon SM et al.: Blockade of peripheral neuronal barrage
reduces postoperative pain, Pain 70:209, 1997.
30. Banks A: Innovations in postoperative pain management:
continuous infusion of local anesthetics, AORN J 85(5):904,
2007.
31. Zuniga JR: The use of nonopioid drugs in management of
chronic orofacial pain, J Oral Maxillofac Surg 56:1075-1080,
1998.
32. Swift JQ: Nonsteroidal anti-inflammatory drugs and opioids:
safety and usage concerns in the differential treatment of post-
operative orofacial pain, J Oral Maxillofac Surg 58(suppl 2):8-11,
2000.
33. Roszkowski MT, Swift JQ, Hargreaves KM: Effect of NSAID
administration on tissue levels of immunoreactive prostaglandin
E2, leukotriene B4, and (S)-flurbiprofen following extraction of
impacted third molars, Pain 73:339-345, 1997.
34. Jackson DL, Moore PA, Hargreaves KM: Preoperative non-
steroidal anti-inflammatory drugs for the prevention of post-
operative dental pain, J Am Dent Assoc 119:641-647, 1989.
35. Dionne RA et al.: Suppression of postoperative pain by preopera-
tive administration of ibuprofen in comparison to placebo, acet-
aminophen, and acetaminophen with codeine, J Clin Pharmacol
23:37-43, 1983.
36. Hespo HU et al.: Double-blind crossover study of the effect of
acetylsalicylic acid on bleeding and postoperative course after
bilateral oral surgery, Eur J Clin Pharmacol 10:217-225, 1976.
37. Petersen JK: The analgesic and anti-inflammatory efficacy of
diflunisal and codeine after removal of impacted third molars,
Curr Med Res Opin 5:525-535, 1978.
38. Dionne RA, Cooper SA: Evaluation of preoperative ibuprofen
for postoperative pain after removal of third molars, Oral Surg
Oral Med Oral Pathol 45:851-856, 1978.
39. Hill CM et al.: Ibuprofen given pre- and postoperatively for the
relief of pain, Int J Oral Maxillofac Surg 16:420-424, 1987.
40. Mehlisch DR, Markenson J, Schnitzer TJ: The efficacy of non-
steroidal anti-inflammatory drugs for acute pain, Cancer Control
6(2)(suppl 1):5-9, 1999.
41. Dionne RA et al.: Dexamethasone suppresses peripheral
prostanoid levels without analgesia in a clinical model of
acute inflammation, J Oral Maxillofacial Surg 61:997-1003,
2003.
42. Insel PA: Analgesic-antipyretics and anti-inflammatory agents:
drugs employed in the treatment of rheumatoid arthritis and
gout. In Gilman AG et al., editors: Goodman and Gilman’s the
pharmacological basis of therapeutics, ed 8, Elmsford, NY, 1990,
Pergamon Press.
43. Ganzberg S: Analgesics: opioids and nonopioids. In Ciancio SG,
editor: ADA guide to dental therapeutics, Chicago, 1998,
American Dental Association.
44. Haas DA: Adverse drug interactions associated with analgesics,
J Am Dent Assoc 130:397, 1999.
45. Shapiro RD, Cohen BH: Perioperative pain control, Atlas Oral
Maxillofac Clin North Am 4:663-74, 1992.
46. Mehlisch DR: The efficacy of combination analgesic therapy in
relieving dental pain, J Am Dent Assoc 133:861-871, 2002.
47. Walton GM et al.: Ketorolac and diclofenac for postoperative
pain relief following oral surgery, Br J Oral Maxillofac Surg
31:158-160, 1993.
48. Jeske AH: Selecting new drugs for pain control. Evidence-based
decisions or clinical impressions? J Am Dent Assoc 133:1052-
1056, 2002.
49. Huber M, Terezhalmy GT: The use of COX-2 inhibitors for
acute dental pain. A second look, J Am Dent Assoc 137:480-487,
2006.
92 SECTION I ■ Anesthesia and Pain Control
50. Spink M, Bahn S, Glickman R: Clinical implications of cyclo-
oxygenase-2 inhibitors for acute dental pain management. Ben-
efits and risks, J Am Dent Assoc 136:1439-1448, 2005.
51. Bell WH, Proffit W, White R: Surgical correction of dentofacial
deformities, Philadelphia, 1980, Saunders.
52. Romunstad L et al.: Methylprednisolone intravenously one day
after surgery has sustained analgesic and opioid-sparing effects,
Acta Anaesthesiol Scand 48:1223-31, 2004.
53. Carr DB, Jacox A: Acute pain management: operative or medical
procedures and trauma, MEDTEP Update Archive, 1994.
54. Institute for Clinical Systems Improvement: Assessment and
management of acute pain, Bloomington, Minn, 2006, Institute
for Clinical Improvement (ICIS).
55. Thompson C: Virtual anesthesia textbook; postoperative pain
management. Available at: www.virtual-anesthesia-textbook.com
(Accessed Nov 2004).
56. Physician’s Desk Reference, ed 61, Montvale, NJ, 2007, Thomp-
son PDR.
57. Goodman & Gilman’s the pharmacological basis of therapeutics,
ed 11, 2006, McGraw-Hill.
58. Coulthard P et al.: Behavioural measurement of postoperative
pain after oral surgery, Br J Oral Maxillofac Surg 38:127-131,
2000.
59. Fields HL: Pain, New York, 1987, McGraw-Hill.
60. Shapiro A et al.: A comparison of three techniques for acute
postoperative pain control following major abdominal surgery,
J Clin Anesth 15:345-350, 2003.
61. Task Force on Acute Pain Management: Practice guidelines for
acute pain management in the perioperative setting, Anesthesiol-
ogy 100:1573-1581, 2004.

PEDIATRIC PHARMACOSEDATION
GENERAL ANESTHESIA
Larry P. Parworth • Trent W. Listello • Gregory S. Bell
Since the inception of the specialty of oral and maxillofacial
surgery, the delivery of anesthesia has been the cornerstone
of our practice. The control of pain and anxiety is a valuable
service to the public, especially for the pediatric population.
The majority of pediatric patients exhibit fear and anxiety
when coming in for surgical treatment, and providing care for
the pediatric patient can be a challenging but rewarding expe-
rience. When behavioral management techniques fail or when
they are not practical, pharmacologic intervention will be
necessary. The goals of pediatric anesthesia are to provide
efficient, safe, reversible, and profound anesthesia, sedation,
or analgesia to allow safe and effective completion of the surgi-
cal procedure.1
Children are not simply small adults. Children have unique
anatomic and physiologic differences that provide special
challenges during anesthetic management. Maintaining a
patent airway can be problematic as a result of large tonsils
and a pliable funnel shaped trachea to name a few. Airway
loss with subsequent hypoxia and resultant cardiovascular
compromise account for the majority of poor outcomes during
pediatric anesthesia.1
Preanesthetic assessment for children should have areas of
focus different from that of adults. A complete review of
systems must include screening for endocrine disorders, con-
genital cardiac defects, hematologic disorders, and any familial
history of malignant hyperthermia. Children tend to have
more frequent upper respiratory tract infections and a higher
incidence of asthma, and thorough investigation is critical.
Safety in the practice of state-of-the-art anesthesia is of the
utmost importance to all oral and maxillofacial surgeons.
Conditions contributing to major morbidity from office anes-
thetic procedures include unfamiliarity with pediatric anes-
thesia.2 One study concluded that the judgment and skill of
the provider was one of the prime determinants related to
anesthetic mortality.3 Constant review of the literature,
having a thorough knowledge of current advances in technol-
ogy and techniques, and ensuring maintenance of pediatric
anesthesia skills are essential to providing the highest quality
of care for our young patients.
This chapter discusses pediatric anatomy and physiology,
preanesthetic work-up, and equipment and monitoring for
the safe and effective delivery of anesthesia. Current
anesthetic drugs and techniques are reviewed along with the
more common complications and their prevention and
management.
CHAPTER 7
AND
■ PEDIATRIC ANATOMIC/
PHYSIOLOGIC/PHARMACOLOGIC
DIFFERENCES
The successful management of pediatric patients undergoing
anesthesia requires a thorough understanding of the anatomic
and physiologic differences between pediatric patients and
adults. These differences lead to many modifications in the
delivery of anesthesia from the preanesthetic evaluation to the
actual delivery of pharmacologic agents.
CARDIOVASCULAR SYSTEM
The cardiovascular system undergoes significant changes at
birth and continues to change throughout childhood. Transi-
tional circulation describes the changes that take place as the
fetus adjusts to the circulatory changes after birth. The end
product of these changes includes the closure of the foramen
ovale, closure of the ductus arteriosus, and closure of the
ductus venosus, the combination of which causes the fetal
circulation to become an adult-type circulation. These shunts
do not close definitively immediately after birth; as a result,
certain clinical conditions may contribute to the persistence
of fetal circulation or to the reappearance of fetal shunts under
stress. Factors, such as hypoxia, hypercarbia, acidosis, infec-
tion, hypothermia, and anesthesia-induced changes in periph-
eral vascular tone, act as a stimulus for maintaining high
pulmonary vascular resistance and a return to fetal circulation.
Blood may be shunted past the lungs through the patent
foramen ovale, and a rapid downhill spiral may occur and
result in severe hypoxemia.4,5 Furthermore, after the neonatal
period, it is estimated that 50% of children younger than 5
years of age and 28% of adults will demonstrate probe patency
of the foramen ovale,6 indicating the need for careful elimina-
tion of all air bubbles from an intravenous (IV) line in a
pediatric patient.
Cardiac Output and Blood Pressure
Cardiac output in pediatric patients is higher than in adults
and is necessary to meet the higher demands for metabolic
oxygen consumption.7 Cardiac output is defined as stroke
volume multiplied by heart rate. The myocardial structure of
the pediatric heart is significantly less developed than in
adults. In particular the volume of cellular mass devoted to
contractility is less in the pediatric heart resulting in a non-
compliant and poorly developed left ventricle that has minimal
93
94 SECTION I ■ Anesthesia and Pain Control
TABLE 7-1 Typical Vital Signs by Age
Age in Years 1 3 6 12
Respiration 25-35 20-30 18-25 15-22
rate/min
Heart rate/min 100-140 80-125 80-120 75-110
Blood pressure 90/60 100/60 110/60 110/65
mm Hg
Modified from Dembo JB: Pediatric outpatient anesthesia, Selected Readings Oral
Maxillofac Surg 5(4):1-19, 1997.
ability to alter stroke volume.4,8 Therefore without the ability
to alter stroke volume, cardiac output in a pediatric heart is
dependant on heart rate.
Mean arterial blood pressure is proportionate to cardiac
output multiplied by systemic vascular resistance. The pediat-
ric cardiovascular system has little ability to alter systemic
vascular resistance; it is less able to respond to hypovolemia
with vasoconstriction4 and is very sensitive to volume over-
loading as well with little ability to compensate. Therefore
blood pressure in the pediatric patient is largely dependant on
cardiac output. Bradycardia is the most lethal arrhythmia in
pediatric patients7 leading to large decreases in cardiac output
and a resultant decrease in blood pressure. Perhaps the most
frequent cause of bradycardia in pediatric patients is hypox-
emia. Other frequent causes include anesthetic overdose
or activation of the parasympathetic nervous system
(Table 7-1).
Neural Innervation
In pediatric patients, the sympathetic nervous system is not
fully developed, giving the parasympathetic nervous system
greater control and increased tone. A severe and sudden bra-
dycardia can often be the result of this parasympathetic hyper-
tonia or “increased vagal tone.”10 The clinician should always
be prepared to treat a vagal induced bradycardia because it can
happen in people of all ages; however, it is important to
note that the incidence is inversely proportional to age with
a sharp decline in incidence for children over the age of 311
(Table 7-2).
RESPIRATORY SYSTEM
During the first years of life, the respiratory system undergoes
significant changes. Immaturity of the respiratory system in
young children (under age 2) makes anesthesia particularly
dangerous and should only be attempted by providers adept
in pediatric anesthesia. This section will discuss the changes
that occur in the development of the respiratory system, which
will be divided into the upper airways, the chest wall, and the
lungs.
Upper Airways
Differences in airway anatomy between pediatric and adult
airways make airway management and intubation difficult in
pediatric patients. The upper airway of infants differs in a
number of ways making pediatric patients more prone to
Frequency of Bradycardia During Anesthesia
TABLE 7-2
Adult in Children, by Age
8-15 0-1 Yr 1-2 Yr 2-3 Yr 3-4 Yr
Total anesthetics 4645 1932 774 628
60-80 With bradycardia 59 19 5 1
125/80 % Bradycardia 1.27 .98 .65 .16
Modified from Keenan RL et al.: Bradycardia during anesthesia in infants: an
epidemiologic study, Anesthesiology 80: 976, 1994.
obstruction than adults.4,12,13 First the infant’s tongue is large
in relation to the oral cavity. Second the laryngeal cartilage
is located higher in the neck. Third the epiglottis is large and
can cover the soft palate, which makes the airway more prone
to obstruction and encourages nasal breathing, often referred
to as “obligatory” nasal breathing. Most infants can convert
to oral breathing if the obstruction lasts more than 15 seconds,14
and almost all infants can easily convert to oral breathing by
5 months of age.15 Young children also have proportionately
larger tonsils than adults, with tonsils and adenoids reaching
their largest size between ages 4 to 10.9
Endotracheal intubation is also influenced by the upper
airway anatomy of the pediatric patient. The pediatric larynx
is funnel shaped and is narrowest at the cricoid cartilage,
whereas the narrowest part of the adult airway is the glottic
opening (Figure 7-1).
For this reason, endotracheal tubes that pass through the
vocal cords of an adult will sit passively in the trachea.
However, in pediatric patients, an endotracheal tube that
passes through the vocal cords may be tight just below the
cords in the area of the cricoid cartilage. Any endotracheal
tube, cuffed or uncuffed, that is placed in a pediatric patient
must be checked to ensure air will “leak” around the tube at
no more than 25 cm H2O. At pressures greater than 25 cm of
H2O. The mucosal capillaries may become damaged leading
to subglottic inflammation, a dangerous phenomenon leading
to further narrowing of an already narrow airway. The small
diameter of the airways and further narrowing profoundly
increases resistance to airflow because resistance is inversely
proportional to the radius raised to the fourth power.
Over the first 2 years of life, the epiglottis, larynx, and
hyoid bone move downward. The facial skeleton grows verti-
cally, and the mandible lengthens from front to back. This
growth continues until the age of 10 to 12 when the pediatric
airway fully develops into an adult airway.
Another difference between the pediatric and adult upper
airway is that the pediatric trachea is more compliant. The
negative pressures generated during inspiration tend to col-
lapse the trachea. The most compliant region of the upper
airway is the pharynx, which makes this region most suscep-
tible to collapse. The pharynx is usually protected from col-
lapsing by the tone of the upper airway muscles, which also
contract during inspiration. However, small upper airways
have a higher resistance to flow and may necessitate greater
negative pressures to produce sufficient inspiratory flow. This
 CHAPTER 7 • Pediatric Pharmacosedation and General Anesthesia
results in a greater tendency for the pediatric upper airway to
collapse.16,17
Chest Wall
There are several properties of the chest wall and associated
muscles of respiration that diminish the efficacy of ventilation
in the pediatric population.
Pediatric ribs are very pliable because they are composed
mainly of cartilage. As a result, the chest wall of an infant is
FIGURE 7-1. Sagittal section of the adult (A) and infant (B) airway. Notice
that the adult larynx is cylindrical shaped with the narrowest part occurring at
the glottic opening. The infant larynx is funnel shaped with the narrowest part
occurring at the level of the cricoid cartilage.
FIGURE 7-2. A, Newborn and B, adult rib cage. The shaded areas
represent the anterior projection of the diaphragm.16,18 A B
95
very compliant and cannot easily maintain negative intratho-
racic pressure, resulting in a decreased mechanical efficiency
and less ventilatory reserve. In the infant, the compliance of
the chest wall is almost three times that of the lung. By the
age of 3, the ribs mineralize and become stiffer, making the
chest wall and lung compliance similar.16 The efficacy of ven-
tilation in the pediatric patient is further diminished by the
anatomy and composition of the respiratory muscles, which
bear the load of respiration. In an infant, the diaphragm inserts
in an almost horizontal fashion, compared with the oblique
insertion in an adult18 (Figure 7-2).
As a result, there is decreased contraction efficiency in
infants; the flat diaphragm has a shorter downward course with
less rib cage expansion. In addition to having a decreased
inspiratory capacity, the composition of the intercostal muscles
and the diaphragm allow little room to increase ventilation
in the face of increased work of breathing. The diaphragm
is made up of a mixture of fatigue-resistant and fatigue-
susceptible muscle fibers. The number of fatigue-resistant
fibers in the diaphragm at birth is approximately ½ of the adult
level. By 2 years of age, the diaphragm has matured to have
approximately the same number of fatigue-resistant fibers as
an adult.16,19 This decreased inspiratory capacity coupled with
less fatigue-resistant fibers places the pediatric patient at a
higher risk to develop ventilatory fatigue quickly after small
changes in respiratory load.
Lungs
There are several properties of the lungs that influence anes-
thesia delivery to the pediatric patient. Many anatomic differ-
ences exist between the pediatric and adult lung.
Respiration is not possible until both the pulmonary
airways and vascular system have matured enough to allow
gas exchange. Marginal gas exchange capability is possible by
approximately the 24th week of gestation, which is a critical
step in allowing postnatal survival.16 Alveoli form both before
and after birth, and initial studies suggested that postnatal
alveolar multiplication was slow after the age of 4 and ended
by the age of 8.20,21 However, more recent studies with
larger groups of cases have shown that the great bulk of
alveoli are present by the age of 2, and limited or no alveolar
multiplication occurs thereafter.22-25 Following the end of
alveolar multiplication, lung development is considered
96 SECTION I ■ Anesthesia and Pain Control
complete, and the lung enters a period of normal growth until
adulthood.23,24
In the newborn, the partial pressure of oxygen in arterial
blood (PaO2) is approximately 70 mm Hg, versus 97 mm Hg
in the adult.26-28 In theory the low PaO2 values may be due to
ventilation-perfusion mismatch and a short capillary transit
time that does not allow proper diffusion between the
alveolar-capillary interface. The PaO2 rises rapidly during the
first 3 years of age with children aged 1 to 3 having an average
PaO2 of 83 mm Hg. The PaO2 then slowly increases up to the
age of 8 years.27,28 Thereafter, PaO2 values remain stable and
similar to those seen in adults.29 The fairly low PaO2 values in
infants and young children are close to the steep part of the
oxygen-hemoglobin dissociation curve. Any further decrease
in PaO2 can induce severe oxygen desaturation.
The physiology of the pediatric lung is affected by the
limited number of alveoli and compliant rib cage. Functional
residual capacity (FRC) is the volume of gas remaining in the
lung at the end of a normal tidal expiration. It represents the
balance point between the inward elastic recoil of the lungs
and the outward elastic recoil of the chest wall. In infants the
chest wall is very compliant making the outward elastic recoil
very small.30 Conversely the lung is stiff making inward elastic
recoil high, possibly as a result of the small and limited number
of alveoli. As a result of this balance, the FRC of a pediatric
patient is lower than that of an adult, promoting low residual
lung volumes at expiration. During anesthesia FRC represents
oxygen stores during periods of apnea. The closing capacity is
the volume of air that is needed to keep the airways open. If
FRC falls below the closing capacity, airway closure occurs
leading to a shunt. The closing capacity is greater in the
pediatric patient. A decreased FRC coupled with an increased
closing capacity predisposes the pediatric patient to shunting,
or perfusing areas of the lung that are receiving no ventilation.
This requires more energy on top of an already higher meta-
bolic demand and oxygen consumption rate. Clinically, this
correlates to rapid oxygen desaturation during periods of apnea
(e.g., during intubation or airway obstruction). In one model
describing the rate of oxyhemoglobin desaturation during
apnea, a child took 41 seconds to desaturate to 85%, whereas
an adult took 84 seconds to desaturate to 85%31 (Table 7-3).
KIDNEYS
Pediatric patients have decreased renal function under the age
of 2. Multiple renal differences are seen early in life including
decreased glomerular filtration rate, impaired sodium reten-
tion, and impaired glucose excretion. At birth glomerular fil-
tration rate is approximately 15% to 30% of normal adult
values. As a result, renal clearance of drugs is diminished. In
addition, neonates are “obligate sodium losers” because they
resorb less sodium in response to aldosterone than adult
kidneys.7 Finally, glucose excretion is impaired in neonates.
This is intended to offset the impaired glycogen stores present
in neonates and tendency toward hypoglycemia. Meticulous
drug, fluid, and glucose regulation is important in early life
before renal function maturation. Functional maturation may
TABLE 7-3 Respiratory Variables
Newborn 3 Yr 5 Yr 12 Yr Adult
Tidal volume 21 112 270 480 575
Minimum ventilation 1.05 2.46 5.5 6.2 6.4
Vital capacity 120 870 1160 3100 4000
FRC 80 490 680 1970 3000
Modified from Dembo JB: Pediatric outpatient anesthesia, Selected Readings Oral
Maxillofac Surg 5(4):1-19, 1997.
be delayed in premature infants; however, by the age of 2,
functional maturation should be complete.4,32
LIVER
At birth the liver is functionally immature, with minimal
glycogen stores that may lead to hypoglycemia.7 This is coun-
terbalanced by decreased renal excretion of glucose as previ-
ously discussed. An immature liver is also reflected in immature
liver enzyme systems. The cytochrome P-450 system, respon-
sible for phase 1 drug metabolism of many lipophilic com-
pounds, reaches approximately 50% of adult values at birth
suggesting decreased capacity for drugs metabolized by this
system. Phase II reactions involving drug conjugation, which
facilitates renal excretion, is also impaired. These immature
reactions alter drug metabolism and lead to long drug half-
lives. By age 1, these reactions achieve adult activity.7,33
THERMOREGULATION
Pediatric patients have a greater surface area to body weight
ratio, or a larger surface area per kilogram than adults. They
also have less muscle mass and less fat content than adults; as
a result, pediatric patients quickly lose body heat to the envi-
ronment. This makes pediatric patients more prone to hypo-
thermia, which is associated with cardiac instability, respiratory
depression, increased pulmonary vascular resistance, altered
drug responses, and slower awakening from anesthesia. With
a limited ability to shiver, infants respond to the stresses of a
cold environment by increasing release of norepinephrine that
enhances brown fat metabolism, a process called nonshivering
thermogenesis.8,34 Environmental temperature is closely linked
to the metabolic rates of infants, providing important sensory
input.35 Under resting conditions, ambient temperature is the
most important determinant of metabolic rate.16 An infant’s
metabolic rate is the lowest when environmental temperatures
are within a neutral range. Cold stress will lead to increased
metabolic rate of brown fat via nonshivering thermogenesis,
increased oxygen consumption, hypoxemia, and metabolic
acidosis.4
DEVELOPMENTAL PHARMACOLOGY
Pediatric patients have a dramatically different response than
adults to medications. Their response is altered by body com-
position, distribution of cardiac output, protein binding, and
functional maturity of the liver and kidneys. As a result, drugs
that have a very predictable response in adults may have a
very unpredictable response in children.
 CHAPTER 7 • Pediatric Pharmacosedation and General Anesthesia
The body composition of a person changes with age. The
total body water in a term infant accounts for approximately
73% of body weight versus 60% for an adult. As the child
grows, total body water decreases as fat and muscle content
increase.36 The implications of a drastically different body
composition are twofold. First, drugs that are water soluble
have a larger volume of water in which to distribute, which
leads to initially larger doses to achieve the desired effect.
Second, with less fat and muscle content, drugs that depend
on redistribution into fat or muscle will remain intravascularly
longer, leading to a longer clinical effect.
Distribution of cardiac output is different in pediatric
patients, which results in unpredictable drug behavior. Pedi-
atric patients have a higher cardiac output to vessel-rich
groups (brain), which leads to a rapid onset of drugs. Pediatric
patients also have decreased plasma levels of albumin leading
to less protein binding and subsequently greater levels of
free/active drug in the serum. Lastly, immature hepatic and
renal function lead to long drug half-lives and decreased
excretion.
As children grow, their body composition, distribution of
cardiac output, protein binding, and functional maturity of
the liver and kidneys all change to further affect drug behav-
ior. The body composition of a child over the age of 2 is
similar to that of an adult; they have normal adult values for
protein, and the liver and kidney have functional maturity.
Of particular importance is that a greater proportion of cardiac
output is directed toward the already matured liver and
kidneys, giving many medications a shorter half-life. As the
child approaches adulthood, the half-life of many drugs
lengthens to adult values. Overall most medications will have
a prolonged elimination half-life in infants, a shortened half-
life in children aged 2 to the early teen years, and a lengthen-
ing of half-life in those approaching adulthood.4,37
■ PREANESTHETIC ASSESSMENT
The ultimate goal of any preanesthetic assessment is to estab-
lish a treatment plan for the patient. Many medical problems
discovered on the preanesthetic visit will prompt a change in
patient management. One study found that the preanesthetic
evaluation leads to changes in the treatment plan for more
than 15% of American Society of Anesthesiologists (ASA)
class 1 and 2 patients.38 Although a similar study has not been
conducted in pediatric patients alone, the significance of the
study is understood. A focused history and physical examina-
tion with special attention to those medical conditions that
will prompt a change in treatment is necessary. Whereas some
medical conditions that require a change in patient manage-
ment will be obvious and would not escape the attention of
most parents (i.e., insulin-dependant diabetes mellitus, con-
genital cardiac defects), others are quite obscure and may only
be brought to light with focused questions. Specific questions
to ask should focus around gestational age, recent upper respi-
ratory infection (URI), asthma, gastroesophageal reflux, and
history of bleeding problems or hematologic disorders. Prema-
ture infants can have multiple medical problems usually caused
97
by immaturity of major organ systems or intrauterine asphyxia.8
Pulmonary complications of prematurity, including broncho-
pulmonary dysplasia, are particularly important to ask about
because normal respiratory function may be delayed for many
years, even up until age 6.9,39 It is also important to ask about
history of previous anesthesia and family history of musculo-
skeletal diseases or malignant hyperthermia.
The physical examination should include the child’s
general appearance, alertness, color, and activity level. Motor
and verbal skills are also noted. Vital signs including height
and weight are recorded. The physical exam should also focus
on the cardiovascular, pulmonary, airway, and any other
systems as indicated from the patient history. The presence of
a heart murmur in a healthy, asymptomatic child is unlikely
to indicate any significant cardiac pathologic condition.8
Innocent murmurs are usually soft systolic ejection murmurs
that are best heard along the upper left or lower left sternal
border without significant radiation and may occur in more
than 30% of normal children. Endocarditis prophylaxis is
required for children with congenital heart defects. If any
question exists in regard to the significance of a heart murmur,
consultation with a pediatrician or pediatric cardiologist is
recommended.
According to the American Association of Oral and
Maxillofacial Surgeons clinical practice guidelines for anes-
thesia in outpatient facilities, most poor outcomes in pediatric
anesthesia are related to loss of the airway.1 The airway exam
is extremely important in the physical examination of any
patient undergoing anesthesia and especially in the pediatric
patient with little respiratory reserve.
The airway exam should focus around three main charac-
teristics that will help to detect a difficult airway. The first
characteristic assesses the size of the tongue in relation to the
oral cavity. The patient opens their mouth as widely as possi-
ble and protrudes their tongue as far as possible. The airway
can then be classified according to what pharyngeal structures
can be seen, also known as the “Mallampati” classification
(Figure 7-3).
This classification is important because the ability to see
vocal cords on direct laryngoscopy is almost always good in
class 1 patients and almost always poor in class 4 patients.40
Additional factors that can complicate airway management
include large tonsils and loose teeth. The second characteris-
tic assesses the atlanto-occipital joint extension. If the neck
can be flexed to approximately 25° to 35°, the atlanto-occipital
joint is extended, and the oral, pharyngeal, and laryngeal
structures are nearly aligned, allowing for easier laryngoscopy.
It should be noted that children with Down syndrome may
have atlanto-occipital joint instability, and extension of the
neck during intubation may lead to cervical dislocation and
spinal cord trauma. Appropriate clinical assessment including
extension and flexion lateral neck films may be necessary to
detect instability before anesthesia for these patients.41 The
third characteristic in evaluation of the airway is measuring
the mandibular space, also known as the thyromental
distance. This is the space anterior to the larynx and is an
98 SECTION I ■ Anesthesia and Pain Control
Class I Class II Class III
Summary of Fasting Recommendations to
TABLE 7-4
Reduce the Risk of Pulmonary Aspiration
Ingested Material Minimum Fasting Period (Hr)
Clear liquids 2 fasting time. Finally, ASA notes that a “light meal” typically
Breast milk 4 consists of toast and clear liquids. Meals that include fried,
Infant formula 6 fatty foods, or meat may prolong gastric emptying leading to
Nonhuman milk 6 a fasting recommendation of 8 or more hours before elective
Light meal 6 procedures.47 Whereas some published evidence supports the
Modified from American Society of Anesthesiologists: American Society of
Anesthesiologists task force on preoperative fasting and the use of pharmacologic
agents to reduce the risk of pulmonary aspiration practice guidelines for preoperative
fasting and the use of pharmacologic agents to reduce the risk of pulmonary
aspiration: application to healthy patients undergoing elective procedures,
Anesthesiology 90:896, 1999.
indication for how easily the laryngeal axis will align with the
pharyngeal axis during direct laryngoscopy. This value is
expressed by the number of “fingerbreadths,” with more “fin-
gerbreadths” being indicative of easier laryngoscopy. Neonates
should have at least one “fingerbreadth” and adolescents at
least three to ease in direct laryngoscopy.40,42-44
PREOPERATIVE FASTING
Pediatric patients are more prone to dehydration than adults,
as a result their preoperative fasting guidelines have been less
strict. Additionally, asking a pediatric patient to fast for an
extended period of time will lead to increased irritability of
the patient. Conversely the incidence of aspiration is three
times higher in pediatric patients than adults (9 per 10,000
versus 3 per 10,000), indicating the need for careful attention
to the matter.45 Fortunately, if aspiration does occur, serious
respiratory morbidity is rare in the immediate postoperative
period in pediatric patients.45,46 In 1999 the ASA appointed
a task force to establish practice guidelines for preoperative
fasting and the use of pharmacologic agents to reduce the risk
of pulmonary aspiration in healthy patients undergoing elec-
tive procedures (Table 7-4).
The ASA points out that with clear liquids there is no
difference in the gastric volume of children who fasted 2 to 4
hours versus more than 4 hours. Examples of clear liquids
Class IV
FIGURE 7-3. Classification of the upper airway in terms
of the size of the tongue and pharyngeal structures visible
upon mouth opening. In class 1 patients, the soft palate,
fauces, uvula, and anterior and posterior tonsillar pillars can
be seen; in class 2 patients, all of the above can be seen
except the tonsillar pillars, which are hidden by the tongue; in
class 3 patients, just the base of the uvula can be seen; and
in class 4 patients, not even the uvula can be visualized.40,41
include water, fruit juices without pulp, and carbonated bever-
ages. The ASA also points out that nonhuman milk is similar
to solids in gastric emptying time, and therefore the amount
ingested must be considered when determining an appropriate
routine use of pharmacologic agents to reduce the risk of pul-
monary aspiration, the ASA states that routine use of phar-
macologic agents to reduce the risk of pulmonary aspiration
in patients who have no apparent increased risk for aspiration
is not recommended.47
UPPER RESPIRATORY INFECTION
During the preanesthetic evaluation, it is important to ask if
the child has had any recent colds that may indicate a recent
upper respiratory infection (URI). If the child has in fact had
a recent cold, it is important to differentiate between a URI
and simple rhinitis. Clear rhinorrhea is usually not a concern,
and anesthesia is not contraindicated. A URI is usually associ-
ated with fever, mucopurulent green or yellow discharge, and
a productive cough. Children with URIs have irritable airways
and are at an increased risk for laryngospasm, breath holding,
postintubation croup, atelectasis, pneumonia, and episodes of
desaturation.48-51 Furthermore airway hyperreactivity may last
for up to 6 weeks after a URI, and the incidence of complica-
tions in children recovering from a URI is almost the same as
children who have active URIs.51 The presence of URI in a
child is particularly important because increased airway edema
and inflammation in an already narrow airway will cause pro-
found increases in resistance to airflow. Traditional guidelines
for treatment of patients with URIs suggest that the procedure
be delayed for 4 to 6 weeks after cessation of the URI to
decrease the risk to the patient.
ASTHMA
Asthma is one of the most common chronic conditions in the
United States, with the prevalence being highest for people
under the age of 18.52 Moreover, the prevalence among chil-
dren aged 5 to 14 has increased 74% from 1980 to 1994 and
 CHAPTER 7 • Pediatric Pharmacosedation and General Anesthesia
160% among children under the age of 4 from 1980 to 1994.52
Given the degree of prevalence among the pediatric popul-
ation it is likely that oral and maxillofacial surgeons will
treat pediatric patients with asthma. Treating pediatric
patients with moderate to severe asthma can be particularly
dangerous because the overall mortality rates of asthma are
highest between the ages of 5 to 14.53 Moreover, acute and
fatal bronchospasm can occur during anesthesia and endo-
tracheal intubation in children with asthma. Whenever
possible endotracheal intubation should be avoided in these
patients.54
In patients with asthma, elective cases should not be under-
taken unless their asthma is well controlled. During preopera-
tive assessment of the asthmatic patient, it is important that
the disease is assessed by the cause, frequency and severity of
attacks, hospital and intensive care admissions, and by drug
history. A thorough examination is required, which may
reveal expiratory wheezes, use of accessory muscles, or an
overdistended chest. If a child is actively wheezing, elective
surgery should be canceled. A child should be free of wheezing
for at least 1 week before surgery. Attempts to control wheez-
ing with an increase in β-agonists or the addition of steroids
are indicated preoperatively. Preoperative steroids may be
needed for children with asthma who continue to wheeze
despite an increase in β-agonists or as a stress dose for children
who have received steroids over the last year to control their
asthma.42,54 The addition of prednisone, 1 mg/kg given 24 and
12 hours before surgery will considerably decrease airway reac-
tivity.42 If preoperative wheezing cannot be controlled with
conservative therapy as an outpatient, admission for more
aggressive therapy and consultation with a pediatrician is
indicated.
■ MONITORS
The ASA has set the standards for basic anesthetic monitor-
ing for all anesthesia care.55 The goal of these standards is to
encourage quality patient care while noting that it is but one
component of care and that the monitors alone do not offer
patient safety guarantees. Two basic standards rely on both
provider vigilance and basic monitoring. Although the various
monitors and alarms are a very important component of anes-
thesia care, they do not replace the anesthesia provider.
The first standard states that a qualified anesthesia provider
must be present in the room through all stages of anesthesia
care. The objective of this standard is based upon the need for
a qualified anesthesia provider to monitor and address any of
the possible rapid changes in patient status and to be present
continuously. Although it is not currently necessary, it is
highly recommended that providers administering anesthesia
to children have current certification in Pediatric Advanced
Life Support (PALS). The observation of levels of conscious-
ness during anesthesia will reduce risks and most likely prevent
many complications if adverse drug responses are detected in
a timely manner.56
The second standard states how oxygenation, ventilation,
circulation, and temperature are to be continually monitored.
99
Continually is further defined as “repeated regularly and fre-
quently in steady rapid succession.”
Oxygen concentration is assessed in inspired gas and blood
with pulse oximetry during any form of anesthesia delivery.
Pulse oximetry will be accompanied by pitch pulse tone with
audible, low threshold tone alarms. Adequate lighting will
help with visual assessment of physical appearance to ascer-
tain appropriate oxygenation of tissues. This is especially
important in small children because of the rapid rate of desatu-
ration and avoidance of hypoxic episodes.
Adequate ventilation should be evaluated by continual
observance of qualitative clinical signs, such as chest expan-
sion, reservoir breathing bag movements, and chest ausculta-
tion. Carbon dioxide detection is necessary during use of
general anesthesia including verification of placement of an
endotracheal tube or laryngeal mask airways (LMAs) and will
be monitored continually unless undetectable as a result of
nature of patient, procedure, or equipment. This will be done
from initial placement of the airway device until removal.
This measurement will be done with capnography, capnome-
try, or mass spectroscopy. Mechanical ventilation units must
include an audible, disconnect alarm. All other forms of anes-
thesia care should also be evaluated by continual observation
of clinical signs and/or detection of exhaled carbon dioxide,
although it would be expected to be lower if using a nonclosed
breathing circuit, such as a nasal canula, where the presence
of exhaled carbon dioxide is the means of detection.
Circulation will be monitored by continuous electrocardio-
gram and heart rate display and arterial blood pressure display
at minimum 5-minute intervals. Additional measures, such as
pulse palpation or heart sound auscultation and intraarterial
pressure tracings, could also be used for general anesthesia
patients. Blood pressure cuffs should be appropriately fitted for
each child to ensure correct measurements because a cuff that
is too large will underestimate readings. Each patient should
be sized with a blood pressure cuff that has a width 20% to
50% greater than the diameter of the patient’s extremity.57
Every child receiving anesthesia shall have temperature
monitoring when a clinically significant change in body tem-
perature is intended, anticipated, or suspected.
ALTERNATIVE MONITORS
Adjuncts to standard monitors evaluate other clinical and
physiologic processes. The use of a precordial stethoscope adds
the ability to hear heart sounds and airway status easily.
Bispectral analysis (BIS) is a noninvasive method to evaluate
levels of anesthesia, and it is based on the principle that elec-
troencephalogram (EEG) waveforms change with the level of
alertness. The manufacturer has developed numeric value,
known as the BIS index, based on an algorithm of EEG digital
signals. The numeric value corresponds to level of sedation:
90 to 100 awake, 70 to 90 light to moderate sedation, 60 to
70 deep sedation, 40 to 60 general anesthesia, and less than
40 a deep hypnotic state. The BIS index has been shown to
be closely associated to sedation scales, which would prevent
possible oversedation.58
100 SECTION I ■ Anesthesia and Pain Control
Transcutaneous capnometry is being studied as an alterna-
tive method of detecting ventilatory malfunction and preven-
tion of hypoxemia in patients in addition to pulse oximetry.
Pulse oximetry is always accompanied with a delay, and a
combination of the two provides the advantage of monitoring
both alveolar ventilation (capnometry) and oxygen transport
to the periphery (pulse oximetry) noninvasively. Stein et al.
investigated two transcutaneous capnometers for clinical use,
but do not currently recommend their use in clinical condi-
tions in the current form because they provide only an approx-
imate estimation of PaCO2.59
ALARMS
Monitors and associated alarms may only alert the provider
if they are activated. Block et al. reported that a majority of
anesthesiologists routinely disable or mute audible alarms
because of a number of false alarms.60 False alarms are a
common source of disruption and distraction in the operating
suite because they alert the anesthesia provider of known
information that is already being controlled or monitored by
the anesthesia provider. The Joint Commission on Accredita-
tion of Healthcare Organizations and the Anesthesia Patient
Safety Foundation (APSF) both recommend the use of
audible alarms.61,62 Alarms have proven their importance by
preventing and reducing the severity of anesthetic incidents,
but sole reliance on monitors without clinical support may
also lead to inappropriate interventions.63 Providers should
become familiar with their equipment and determine the
proper alarm settings based upon ASA guidance and clinical
judgment.
■ EQUIPMENT AND ROOM
PREPARATIONS
The treatment of pediatric patients requires some adjustments
to the setup in preparation for the procedure and presence of
additional and often helpful elements in the operating arena.
Some of these address emergency medications, equipment,
fluid delivery access, and delivery. Initial preparations should
be to change monitoring and anesthesia equipment to pediat-
ric settings.
All pediatric operatories should have emergency equip-
ment that is located in a well-known, easily accessible area.
This equipment should be well maintained and inspected on
a periodic basis. Appropriate algorithms and medicines to
treat perioperative emergencies should be included in that
location as well. A defibrillator with pediatric paddles along
with emergency suction, auxiliary oxygen supplies, and alter-
native source of light should be available in case of loss of
power. The oxygen source should be able to deliver under
pressure for a minimum of 1 hour. At our institution, each
pediatric patient has their information included in a work-
sheet that takes patient vital statistics and converts that infor-
mation into appropriate equipment sizes, fluid replacement
amounts, and doses of common perioperative medications.
This form is then placed in the operative setting to be reviewed
as needed (Box 7-1).
Laryngeal Mask Airway Sizes and
TABLE 7-5
Inflation Volume
Mask Size Patient Selection *Maximum Cuff
Guidelines Inflation Volume (Air)
1 Neonates/infants up to 5 kg up to 4 mL
1½ Infants 5-10 kg up to 7 mL
2 Infants/children 10-20 kg up to 10 mL
2½ Children 20-30 kg up to 14 mL
3 Children 30-50 kg up to 20 mL
4 Adults 50-70 kg up to 30 mL
5 Adults 70-100 kg up to 40 mL
6 Large adults over 100 kg up to 50 mL
*These are maximum volumes that should never be exceeded. It is recommended the
cuff be inflated to 60 cm H2O intracuff pressure.
Source: LMA North America, Inc.
Broselow Emergency Pediatric Tape provides a reference at
each color bar on the tape to select equipment sizes to perform
emergency resuscitation based on weight zone. The tape also
shows precalculated medication dosages and infusion rates
based upon each colored weight zone. Other commercial
and institutional items are available to provide similar
information.
An average setup of pediatric patient treatment begins
with setup of room and equipment. Because infants and chil-
dren have a greater surface area to body weight ratio causing
greater body heat losses, temperature of the operating suite
should be adjusted to between 80 °F to 90 °F.64 Most oral
surgery procedures completed as outpatient procedures are
relatively short, so clinical judgment should determine suit-
ability of additional measures, such as warm fluid and heating
blankets.
AIRWAY
Items needed to access and control the airway should be
readily available; these include appropriately sized nasal can-
nulas, nasopharyngeal airways, oropharyngeal airway, endo-
tracheal tubes, and LMAs (Table 7-5).
Pocket masks and bag-mask-valve devices with positive
pressure ventilation ability should be included. Inclusion of a
system of emergent airway access, such as a cricothyrotomy
kit, should be available in case situations arise where other
methods have failed to establish a patent airway. Transtra-
cheal catheter jet ventilation may be considered for support
of oxygenation when a surgical airway is required for pediatric
patients, but only in situations where oxygenation and venti-
lation cannot be provided any other way.65 Ravussin et al. used
transtracheal jet ventilation during pediatric endoscopic laser
treatment of laryngeal and subglottic stenosis.66 Adequate
control of the airway and satisfactory gas exchange were
obtained in all cases; however, they reported a severe life-
threatening complication rate of 10.7% including pneumome-
diastinum and bilateral pneumothoraces.
A simple method to size an oropharyngeal airway is by
placing the anterior portion at the commissure and the pos-
 BOX 7-1 Pediatric Anesthesia Worksheet

Patient Name:
Medications
Data Entry Box
Pre-operative mg Muscle Relaxants mg IV Emergency Medications mg IV
Age - Months (0-24) Atropine IM 0.02 mg/kg Atracurium Aminophylline 5 mg/kg
Age - Years (> 2) Glycopyrrolate IV,IM 0.01 mg/kg Intubation 0.5 mg/kg Atropine mg (PRN X2) 0.02 mg/kg
Weight - Pounds Ketamine Stun IM 5 mg/kg Maintenance 0.1 mg/kg Atropine minimum dose 0.1 mg, maximum single dose 0.5 mg
Height - Inches Metoclopramide IV 0.15 mg/kg Cisatracurium Calcium Chloride 10 mg/kg
Hours NPO Midazolam IV 0.05 mg/kg Intubation range 0.1 mg/kg (max dose 500 mg) 20 mg/kg
Respiratory Rate Midazolam PO 0.5 mg/kg 0.2 mg/kg Dantrolene (to 10 mg/kg) 2 mg/kg
Hematocrit Midazolam IM 0.1-0.15 mg/kg Maintenance 0.02 mg/kg Dexamethasone 0.15 mk/kg
Minimum Allowable Hct Midazolam Nasal 0.2 mg/kg Mivacurium Dextrose 0.5 gms/kg
Nasal 0.3 mg/kg Intubation 0.2 mg/kg Epinephrine mg (1:10,000) 0.01 mg/kg
Morphine IM 0.1 mg/kg Maintenance 0.08 mg/kg Subsequent dose (1:1000) 0.1 mg/kg
Calculations Pancuronium
Induction mg IV Intubation 0.1 mg/kg Succinylcholine IM 4 mg/kg
Weight Kilograms Ketamine Maintenance 0.05 mg/kg Fluid Bolus PRN 10 ml/kg
Height Centimeters range = 1-2 mg/kg 0 Rocuronium 20 ml/kg
BSA Square Meter Propofol Intubation 0.6 mg/kg Defibrillation Joules 2 J/kg
range = 2-3 mg/kg 0 Rapid sequence 1.2 mg/kg
Ventilation Thiopental Maintenance 0.15 mg/kg Antibiotics mg IV
range = 3-6 mg/kg 0 Vecuronium Ampicillin 25-50 mg/kg IV q4-6h Max 2-3 g/d
Dead Space ml Intubation 0.1 mg/kg range =
CHAPTER 7 •

Minute Ventilation ml/min mg IV Maintenance 0.025 mg/kg Cephapirin (Cefadyl) 10 - 20 mg/kg IV q6h Max 4 g/d
Alveolar Ventilation ml/min Succinylcholine 2 mg/kg range =
Tidal Volume ml (resting) Succinylcholine 4 mg/kg(IM) Cefazolin (Kefzol) 8.3-25 mg/kg IV q6-8h max 6g/d
Tidal Volume ml @ 10 ml/kg Rocuronium 1.8 mg/kg(IM) range =
Endotracheal tube size mm Atropine 0.01 mg/kg Reversal mg IV Cefotetan (Cefotan) 20-40 mg/kg IV q12h Max 6 g/d
ET-Tube Length @ nose cm Lidocaine 1 mg/kg Atropine 0.015 mg/kg range =
ET-Tube Length @ teeth cm 0.02 mg/kg Cefoxitin (Mefoxin) 30-40 mg/kg IV q6h x 24 hrs
Minimum Narcotics mcg IV Edrophonium 0.75 mg/kg range =
Maximum Sufentanil balanced induction 1 mg/kg Ceftriaxone (Rocephin) 25-50 mg/kg q12-24 hrs
Newborn/Infant length @ lips range = 0.125-0.5 μg/kg Glycopyrrolate 0.01 mg/kg range =
Sufentanil cardiac induction Naloxone PRN 0.005 mg/kg Clindamycin (Cleocin) 6.25-10 mg/kg IV q6h Max 4.8 g/d
Fluids/Blood range = 2-10 μg/kg Neostigmine 0.06 mg/kg range =
Fentanyl balanced may start with half this dose & repeat X1 Gentamicin 1.5-2.5 mg/kg IV q8h
Maintenance ml/hr range = 1-5 μg/kg range =
NPO Deficit Total ml Peri-operative mg IV Vancomycin 10 mg/kg IV q6h Max 1 g/dose
Deficit Replacement ml Diphenhydramine 1.0 mg/kg
1st Hour - Droperidol 0.05 mg/kg
2nd Hour - Ephedrine PRN 0.2 mg/kg Analgesics mg IV
3rd Hour - Hydrocortisone 1 mg/kg Acetaminophen PO 15 mg/kg
Surgical Requirement ml/h Labetalol 0.25 mg/kg loading dose PR 40 mg/kg
Minor (3 ml/kg/hr) - Initial and Subsequent Dosing of Rectal Acetaminophen in Childre: Meperidine 0.5 mg/kg Ibuprofen PO 10 mg/kg
Moderate (5 ml/kg/hr) - A 24-Hour Pharmacokinetic Study of New Dose Recommendations: Morphine Sulfate 0.05 mg/kg Ketorolac (IV) 0.5-0.75 mg/kg
Major (7 ml/kg/hr) - Patrick K.; Tobin, Michael J.; Fisher, Dennis M 0.1 mg/kg SBE prophylaxis mg IV
Blood Replacement Anesthesiology. 94(3):385-389, March 2001. Ondansetron 0.15 mg/kg Gemtamicin 1.5 mg/kg
Estimated Blood Vol ml Promethazine 0.5 mg/kg Ampicillian 50 mg/kg
Allowable Blood Loss ml
Packed RBC (ml) to - Hb 1 Gm Not FDA approved for prophylaxis is children

The authors have exerted every effort to ensure that the drug dosages set forth are in accordance with current recommendations at the time of publication.
The user is urged to check the drug's package insert for any changes in indications and dosages as well as for warnings and precautions.
The responsibility is ultimately that of the prescribing clinician.
Pediatric Pharmacosedation and General Anesthesia
101
102 SECTION I ■ Anesthesia and Pain Control
terior portion to the angle of the mandible. Endotracheal
tubes should also be available and sized appropriately. A
common method for sizing an endotracheal tube for children
over 2 years old is found in the formula:
4 + (age/4) = tube diameter (in mm)
For example, an 8-year-old patient would likely require a
6-mm tube. An alternate method involves selecting an endo-
tracheal tube size equivalent to the diameter of the child’s fifth
finger. Verification of the correct size is based upon ease of
passage into larynx and the development of air leak at 15 to
20 cm H20 pressure. Absence of air passage at that pressure is
an indication that the selected tube is too large. If the leak is
present at less than 10 cm H20, the tube should be changed
to the next larger size. If the patient is planned for intubation,
two endotracheal tubes of selected size and one each of a size
above and below to allow rapid access if the size is incorrect.
Length of the tube placed at the lips can also be figured with
the following formula:
12 + (age/2) = length of tube (in cm)
These formulas are approximate and sizing should always
be confirmed clinically by auscultating bilateral breath sounds,
epigastric auscultation, chest expansion, and presence of
exhaled carbon dioxide. A standard cutoff for use of a cuffed
endotracheal tube has been 8 years or older, but with advent
of low-pressure cuffs, the use of cuffed tubes is becoming more
common.67,68 If desired nasal intubation can be performed with
an RAE design nasal tube, appropriate-size laryngoscopes
should also be available, and lights and attachments verified
before each case. A narrow handle and straight blade aid
intubation in children less than 5 years old. A pediatric circuit
should be used with appropriate face mask for mask induction
or general anesthesia. Tidal volume (8 to 10 mL/kg) and respi-
ratory rates (increased to 18 to 30) should be adjusted for each
patient. A small dental suction should be nearby and func-
tioning appropriately for evacuation of secretions. Reservoir
bags should be 1 L for small children and 2 L for larger chil-
dren. If the child is 8 years or older, an adult circuit may be
used.
INTRAVENOUS ACCESS
IV access may be accomplished in several manners. At the
preoperative appointment, one can employ the “tell-show-do”
method by showing how the procedure will proceed and also
to see how the child reacts. Parents may also inform the pro-
viders how they think that their child will handle the attempts.
A popular choice for cutaneous anesthesia is the use of EMLA
cream (lidocaine 2.5% and prilocaine 2.5%) under an occlu-
sive dressing and intact skin. By applying a thick layer to the
skin at 2 to 3 sites 90 minutes before the procedure, adequate
skin anesthesia should be achieved for IV access.69 Older chil-
dren may benefit from subcutaneous injection of 2% lidocaine
at the site of venipuncture. Younger children may be unable
to cope with the process, and alternative methods may be
used, such as mask induction before IV placement. Emergent
30°
FIGURE 7-4. Emergent situations may call for placement of IO cannula-
tion 1 to 3 cm below the tuberosity in the middle of the anteromedial surface
of the tibia. Care is taken to avoid the epiphyseal plate while gently twisting
the needle. Loss of resistance, aspiration of marrow, and upright needle when
unsupported indicate proper placement. Resuscitation drugs, fluids, and blood
products may be delivered through this route.
situations may require the use of intraosseous (IO) placement
of a catheter for delivery of resuscitation drugs, fluids, and
blood products. An IO infusion needle kit with stylet is avail-
able from Cook Critical Care Co, Bloomington, Ind. If an IO
needle is not available, a butterfly or standard hypodermic
needle can also be used. The location for IO cannulation is
often the tibia, the site being approximately 1 to 3 cm below
the tuberosity in the middle of the anteromedial surface of the
tibia (Figure 7-4).
In this location, the tibia is close to the skin, and it is easy
to palpate the flat, smooth surface to be cannulated. Other
locations include distal femur, medial malleolus, and anterior
iliac spine. The IO needle is inserted through the skin into
the flat anteromedial surface of the tibia with a gentle twisting
motion; it is directed perpendicular to the surface of the tibia
or slightly toward the toes to avoid entering into the epiphy-
seal plate. If using another location, it is preferred to place
away from the nearest joint space. When a loss of resistance
is felt, stop the needle advancement and attempt marrow
aspiration. If marrow is aspirated, irrigate to prevent obstruc-
tion of the needle. Other indications of proper placement
include an upright needle when unsupported and a fluid deliv-
ery without subcutaneous edema.70 IO placement has been
shown to be performed easily after diverse training with
minimal complications. Complications of IO access include
osteomyelitis, subcutaneous access, compartment syndrome,
extravasation, fracture, growth plate injuries, and fat emboli.71
Fractured bones should not be accessed.
INTRAOPERATIVE FLUIDS
Once IV access has been gained, fluid may be delivered. It has
become common to use an IV delivery device, such as a buret-
rol or volutrol, with a microdrip chamber (60 drops/mL)
 CHAPTER 7 • Pediatric Pharmacosedation and General Anesthesia
attached between the IV fluid bag and the IV catheter; it is
used to deliver IV fluids in a controlled manner with 100 mL
placed at a time in the chamber. Lactated Ringer’s (LR) or
another balanced salt solution is usually adequate because of
the fact that most outpatient oral surgery procedures are short,
and hypoglycemia or electrolyte imbalances are not of concern.
For longer outpatient cases in the operating room where hypo-
glycemia becomes a concern, 5% dextrose in LR may be added
or used as the maintenance fluid itself.72
Fluid management is based upon fluid maintenance,
replacement, and deficit. Fluid maintenance is based upon the
4 : 2 : 1 rule: 4 mL/kg for the first 10 kg, then 2 mL/kg for the
second 10 kg and 1 mL/kg/hr for each remaining kg. In a child
weighing 30 kg, the calculations for maintenance regimen
would be:
10 kg × 4 mL = 40 mL
10 kg × 2 mL = 20 mL
10 kg × 1 mL = 10 mL
30 kg = 70 mL/hr
Fluid replacement takes into consideration the amount of
time in hours the patient was nil per os (NPO) multiplied by
the fluid maintenance amount plus hourly maintenance, surgi-
cal blood loss, urine output, and insensible losses (1 to 3 mL/
kg/hr for most oral surgery procedures). The fluid deficit is
given back incrementally; half is given over the first hour and
then the remaining half given over the next 2 hours. If a
patient was NPO for 8 hours with a maintenance rate of
100 mL/hr, 400 mL would be given the first hour, then 200 mL
given each of the next 2 hours. Surgical blood loss would be
replaced with either crystalloid solution (LR) in a 3 : 1
ratio or 1 : 1 ratio for colloid (5% albumin) or actual blood
replacement.
■ PHARMACOSEDATION AND
GENERAL ANESTHESIA
Oral surgery on pediatric patients can be a very pleasant oper-
ative experience if the patients are reasonably calm and coop-
erative. Cooperation is important to provide for patient,
provider, and staff safety; it also allows for proper monitoring
and physical cooperation during the procedure. The primary
goals of pediatric sedation are to reduce typical fear and
anxiety, increase cooperation, and ensure patient comfort by
providing adequate forms of amnesia and analgesia. Pharma-
cosedation or general anesthesia may be needed to meet these
goals by providing the adequate level of anesthesia.
PREMEDICATION FOR FEAR AND ANXIETY
Premedication is used to reduce presurgical anxiety. Children
may be unable to communicate their fears and may express
them in undesirable ways; scared looks, agitation, trembling,
crying, and, most importantly, noncompliance. Most fear
comes from anticipated pain and separation from parents.
Separation from parents is to be expected from children
between the ages of 6 months and 6 years.73 These fears may
be addressed at the initial preoperative appointment when the
103
routines of the day of surgery may be reviewed with the child
and their parents, to include a visit to the surgery suite and a
trial run of the placement of the IV access. Parents should be
counseled to take part in allaying the fear and anxiety of
patients by remaining calm themselves and providing gentle
encouragement. At our institution, the health and physical
exam is completed 2 days before the day of surgery allowing
for the child to become familiar with the surgical environ-
ment. The parents are given details of the patient’s preopera-
tive fasting, postoperative expectations, postsurgical care
instructions, and use of analgesics at this appointment. This
is also the time to determine the need for premedication and
the extent the parents will play in the perioperative period
and if their presence is needed at the time of induction of
anesthesia. Although parental presence decreases their anxiety
and increases satisfaction, parental presence has no effect on
the child’s anxiety.73 Premedication not only allows for greater
patient cooperation, it may also reduce the amount of anes-
thesia provided at induction and intraoperatively.75
MIDAZOLAM
Midazolam is a benzodiazepine with a rapid onset of action,
short duration of action, has no active metabolites, and pro-
vides retrograde amnestic properties. These qualities make
midazolam ideal for both premedication and sedation. Mid-
azolam is available for delivery in many forms, and its dose is
determined by delivery choice. Oral midazolam is available in
a cherry-flavored syrup; this method of delivery is the most
popular and is delivered at 0.5 to 1.0 mg/kg with a maximum
of 15 to 20 mg.8,76,77 Orally delivered midazolam is effective in
approximately 30 minutes and does not result in significant
changes in heart rate, respirations, or blood pressure with
doses of 0.5 to 0.75 mg/kg.77 However, the disadvantages of
orally administered drugs include inability to titrate, unreli-
able absorption as a result of hepatic first-pass metabolism, and
moderate failure rates. At doses greater than 0.75 mg/kg, mid-
azolam may not provide additional sedation at 30 minutes
after premedication and in some instances may be associated
with a greater incidence of side effects including dysphoria
and blurred vision.77 Midazolam may also be delivered nasally
or rectally, both offering adequate sedation if the child is
unwilling to swallow the syrup. Intranasal administration had
been used often in the past, but is not well accepted by chil-
dren because of irritation to nasal mucosa and taste of medica-
tion when swallowed, which also subjects the medication to
absorption in the digestive tract. Roelofse et al. administered
rectal midazolam (1 mg/kg) to 100 children 30 minutes before
dental treatment.78 The rectal delivery was well accepted by
70% of the patients with reliably good anxiolysis and sedation
without loss of respiratory drive or protective airway reflexes.
If patients have IV access, sedation can be accomplished with
0.1 to 0.15 mg/kg and titrated to effect. Because midazolam
has no analgesic properties, it is necessary to achieve adequate
local anesthesia, with possible addition of other analgesic
medications based on the amount time and expected stimula-
tion of the procedure. Golparvar et al. reported an incidence
104 SECTION I ■ Anesthesia and Pain Control
of 3.4% of pediatric patients with paradoxical reactions with
the use of IV midazolam.79 Signs and symptoms included
restlessness, violent behavior, physical assault, self-injury,
restraint, panic, anger, dysphoria, and disorientation. The
time of onset varied between 3 to 6 minutes and was unlikely
to spontaneously resolve. Patients were treated successfully by
the administration of the rescue tranquilizer ketamine.
FENTANYL
Fentanyl is an opioid agent that is most commonly used after
IV access during surgery; it has a rapid onset of action and
duration of action usually under an hour. It may be used for
sedation often in concert with midazolam. Although it is
available in lollipop form, it must be absorbed through the
oral mucosa; if swallowed, effectiveness decreases as a result
of liver first-pass metabolism.80 Similar to other opioid agents,
the most common side effects with fentanyl use are respiratory
depression, pruritus, and postoperative nausea and vomiting.81
Because of the potential respiratory depression and effects of
synergism with additional medications, such as midazolam,
fentanyl should only be delivered with ASA monitors in
place.
KETAMINE
Ketamine is a dissociative anesthetic agent that produces an
anesthetic state consisting of catalepsy, analgesia, amnesia,
and different degrees of consciousness.82 Ketamine produces a
dissociative state that is created by the generation of dissocia-
tion between the cortical and limbic systems, which disrupts
interpretation of visual, auditory, and painful stimuli from the
brain.83 At subanesthetic doses, ketamine has the advantage
of providing analgesia without respiratory depression associ-
ated with opioids, and it also reduces the amount of additional
opioids necessary in the postoperative period.84 Ketamine
directly stimulates smooth muscle dilatation, which decreases
risk of bronchospasm. Ketamine is also beneficial because it
usually maintains upper airway musculature tone and sponta-
neous respirations.17 Ketamine increases saliva production,
heart rate, blood pressure, and intracranial pressure (ICP). If
a closed head injury is suspected, ketamine should not be used
because of increases in ICP. Additional fluids produced by
excess salivation may cause laryngospasm if secretions contact
the vocal cords, so anticholinergics (atropine or glycopyrro-
late) are often given before use of ketamine.85 Emergence
delirium is often cited as one of the possible side effects from
use and can include hallucinations that are pleasant, bizarre,
or terrifying. Risk factors for emergence delirium are age over
10 years, female gender, underlying psychiatric disorder, IV
route, high doses, and excessive noise or stimulation on emer-
gence.86 The addition of Versed before ketamine use reduces
the incidence of emergence delirium.
Ketamine is usually given parenterally, but it can also be
given through oral, rectal, and intramuscular (IM) routes.78
Oral ketamine has been investigated for use in sedating
anxious pediatric dental patients.87 Ketamine 6 mg/kg was
given orally, with an onset of approximately 20 minutes and
a mean duration of sedation of 36 minutes. Nitrous oxide 30%
to 50% was also administered during treatment. The quality
of sedation was rated as good for 65% of the patients, with a
mean recovery time of 56 minutes. IM is also popular because
patient cooperation is not required, and it has been shown to
be an ideal medication for short procedures in the ER. This
can be accomplished by using ketamine (4 mg/kg) combined
with atropine or glycopyrrolate in a single injection to provide
desired dissociation.88 Alternate combinations described used
ketamine 3 mg/kg, midazolam 0.05 mg/kg, and glycopyrrolate
0.005 mg/kg injected into the lateral thigh to provide sedation
for children with minor facial injuries seen in the emergency
department.89 Satisfactory sedation was achieved in 32 of 37
patients, with 5 others requiring a second ketamine injection
of 1 mg/kg. Onset of sedation was within 6 minutes, and ade-
quate working time of 30 minutes was evident in those
children receiving one injection. Emergence delirium and hal-
lucinations were not observed, and protective airway tone and
respiratory drive were preserved.
PROPOFOL
Propofol is an alkylphenol in an oil at room temperature and
only slightly soluble in water with soybean oil, glycerol, and
purified egg phosphatide. It is the only IV anesthetic that can
be used for total IV anesthesia because the recovery period for
others, such as ketamine and midazolam alone, would be too
long. Propofol is chemically unrelated to benzodiazepines, ste-
roids, opioids, and barbiturates.90 Propofol can be used in
infants and young children because it offers a safe and smooth
induction with a low incidence of side effects.91 Respiratory
depression and apnea are common when used and may require
some form of intervention in settings of sedation, including the
simple but effective chin-lift procedures to open the airway or
more aggressive intervention during deep sedation or general
anesthesia. The length of apnea is slightly longer when com-
pared with barbiturates.92,93 The major advantage of using pro-
pofol is the lower incidence of laryngospasm, postoperative
nausea and vomiting, and a rapid emergence.91,94,95,96
The major disadvantage for propofol use is pain at the
injection site, which can be reduced by placing IV access in
larger veins or the use of lidocaine 0.2 mg/kg either directly
before or mixed in with propofol.97 Other disadvantages of
propofol are increased periods of hypotension and bradycardia
at higher doses, both of which occur more often in
children.17
Induction dosages vary with size of the child and whether
it will be used for induction, sedation, or general anesthesia
at higher levels. Propofol maintenance is ideal because of the
rapid and short-acting mechanism of propofol. Infusion pumps
may be used to titrate the drug to the desired level of sedation.
Controlled boluses of propofol may also be used for short pro-
cedures (Table 7-6).
INHALATION ANESTHESIA
Nitrous oxide was the first anesthetic introduced by Horace
Wells in 1844 and is currently known for having a wide
 CHAPTER 7 • Pediatric Pharmacosedation and General Anesthesia 105

TABLE 7-6 Pediatric Drug Doses ing sensitization of myocardium when local anesthetics with
Drug Comment Dosage epinephrine are used, possible development of ventricular
Midazolam Premedication (PO) 0.5 mg/kg
arrhythmias, cardiac depression, and hepatic necrosis. Sevo-
Maximum dose (PO) 20 mg flurane produces a dose-dependent increase in respiratory rate
Premedication (intranasal)* 0.2-0.6 mg/kg and a decrease in tidal volume, as do most volatile anesthet-
Sedation (IM) 0.1-0.15 mg/kg ics. The advantages of sevoflurane over halothane are
Maximum dose (IM) 7.5 mg decreases in incidence of breath holding and laryngospasm,
Sedation (IV) 0.05 mg/kg
faster onset of action and recovery, and improved patient
Fentanyl Pain relief (IV) 1-2 μg/kg
acceptance.101
Pain relief (intranasal) 2 μg/kg
Premedication (Oralet) 10-15 μg/kg Mask induction with sevoflurane is successful because of
Anesthetic adjunct (IV) 1-5 μg/kg patient acceptance and tolerance of large minimum alveolar
Maintenance infusion 2-4 μg kg/hr concentrations (MAC). Sevoflurane demonstrates the least
Main anesthetic (IV) 50-100 μg/kg airway irritation of all the currently available inhalation
Ketamine Initial dose (IM) 4 mg/kg agents. Morgan et al. describe two methods of mask induc-
Supplemental dose (IM) 1-2 mg/kg
tion.8 Mask induction can be accomplished using a single-
With adjunctive agent (N2O) IM 2 mg
Low dose (PR) 5 mg/kg breath technique with 8% sevoflurane and 50% nitrous oxide
Dissociative dose (PR) 10 mg/kg and oxygen or with 100% oxygen. If the child is cooperative,
Induction (IV) 1-2 mg/kg then 0.5% incremental doses every 3 to 5 breaths of sevoflu-
Sedation (IV) 0.5-1.0 mg/kg rane can be added as the child is breathing 70% nitrous oxide
Maintenance infusion 25-75 μg/kg/min
and oxygen 30%. Once the lid reflex is lost, IV access can be
Premedication (PO) 6-10 mg/kg
accomplished and appropriate methods of anesthesia can be
Propofol Induction (IV) 2-3 mg/kg
Maintenance infusion 60-250 μg/kg/min delivered and maintained. The improved acceptance of mask
induction is possible with the use of scented lip balm or sprays
Taken from Morgan GE, Mikhail MS, and Murray MJ: Pediatric anesthesia. In Clinical
placed inside the mask. The MAC of sevoflurane is 2.5% for
anesthesiology, ed 4, New York, 2006, McGraw-Hill, pp 922-950. Gonty AA:
Ketamine-a new look at an old drug, Oral and Maxillofac Surg Clin North Am 4:815- patients 6 months to 12 years and 3.2% to 3.3% for infants
823, 1992. *Shankar V: Procedural sedation in the pediatric patient, Anesthesiol Clin less than 6 months old if general inhalation anesthesia is
North Am 23:635-654, 2005. used.102
TECHNIQUES OF DEEP SEDATION/
GENERAL ANESTHESIA
margin of safety and few side effects that supports its use in At our institution, the majority of scheduled outpatient pedi-
pediatric patients.98 Advantages of nitrous oxide include rapid atric procedures are dentoalveolar surgeries lasting from 10 to
induction and emergence, insignificant cardiovascular and 30 minutes under deep sedation or nonintubated general anes-
respiratory changes, and ability to produce analgesia. Nitrous thesia for apprehensive children. All patients are treated in
oxide can be combined with other anesthetic agents produc- the clinic operating room suite with an oral and maxillofacial
ing sedation and analgesia during pediatric procedures. Litman surgery resident and attending staff managing the anesthetic
et al. premedicated 34 children with 0.7 mg/kg of oral mid- and an additional surgeon performing the procedure. Because
azolam 15 to 20 minutes before administering 40% nitrous of the previously mentioned anatomic and physiologic char-
oxide during pediatric oral procedures.99 This technique did acteristics evident during early childhood, we limit our pedi-
not result in any clinically significant respiratory depression, atric outpatient deep sedations and general anesthetics to
but in three children resulted in a level of deep sedation and include ASA 1 or 2 patients age 3 and older. Children under
a level approaching general anesthesia in one child. Nitrous the age of 3 are scheduled in the main operating room and
oxide can also be combined with volatile anesthetics, creating managed by an anesthesiologist.
the “second gas effect,” where uptake of the blood by the “first” Obtaining IV access preoperatively cannot always be
gas (nitrous oxide) increases both the alveolar concentration accomplished in pediatric patients, but we have experienced
of the “second” gas (e.g., sevoflurane) and the input of addi- good success with the application of EMLA cream 60 to 90
tional second gas into the alveoli via augmentation of the minutes before the appointment in the 6- to 12-year-old age
inspired volume.100 group. Children in this age group may prefer an IV start to
Inhalational anesthetics have two main uses in pediatric the pungent odor of volatile anesthetics during mask induc-
anesthesia, and both are amenable to same day procedures. tion. Our preferred method of pediatric outpatient anesthesia
Sevoflurane is an inhalation agent with a favorable profile, for children able to cooperate for IV access consists of initial
making it useful for mask induction and maintenance. doses of 0.05 mg/kg of midazolam, and 0.50 mcg/kg of fen-
Sevoflurane is halogenated ether, which has rapid onset tanyl. For procedures lasting less than 10 minutes, intermit-
and recovery attributes. It has gained favor in oral surgery tent boluses of 0.25 to 0.50 mg of propofol are then administered
procedures in children as a result of decreased potential for until the desired plane of anesthesia is achieved. For cases
side effects possible with other inhalation anesthetics includ- anticipated to last longer than 10 to 15 minutes, we have
106 SECTION I ■ Anesthesia and Pain Control
found a modification of the technique described by
Blankenstein103 to be effective for pediatric patients. Boluses
of midazolam and fentanyl are administered as described pre-
viously, followed by ketamine 0.2 to 0.3 mg/kg, injected slowly
to reduce the incidence of apnea. Glycopyrrolate 0.01 mg/kg
has been given as an antisialagogue to control secretions.
After this an infusion of propofol at 75 to 125 mcg/kg/min is
started and adjusted as necessary to maintain a plane of deep
sedation/general anesthesia. If required additional boluses of
0.25 mg/kg of propofol are added to deepen anesthesia and
prevent undesirable patient movement. The use of ketamine
and propofol together complement each other, and we find
less airway obstruction than when using propofol alone. Also
the cardiostimulant effects of ketamine and glycopyrrolate are
reduced by the cardiodepressant effects of propofol. Another
advantage of this technique is that the low dose of ketamine
and the antiemetic properties of propofol together result
in a low incidence of postoperative nausea and vomiting.
Prolonged recovery and nausea have been shown to be
insignificant when the total dose of ketamine is less than
0.4 mg/kg.104
If the child is unable or not willing to cooperate for IV
access, we find mask induction with 8% sevoflurane and 60%
nitrous oxide and 40% oxygen mixture to be most effective.
Baum et al. reported faster induction and decreased incidences
of coughing and breath holding with 8% sevoflurane and
nitrous oxide when compared with incremental increases of
halothane or sevoflurane.105 The flow rates of nitrous oxide
and oxygen are set at 4 L and 2 L respectively. The anesthetic
circuit is charged, the patient is instructed to exhale, and the
mask is placed resulting in a single-breath induction. Stage 3
of general anesthesia is reached in approximately 1 to 2
minutes, and when eyelash reflex is lost, the sevoflurane con-
centration is reduced to 2% to 3%, IV access is established,
and anesthesia is maintained with intermittent boluses of 0.25
to 0.50 mg/kg of propofol. If the surgical procedure is very
short (extraction of a primary tooth), it can usually be accom-
plished without additional medications other than the induc-
tion with sevoflurane and nitrous oxide. For cases lasting
longer than 15 minutes, propofol infusion is started after mask
induction at a rate of 125 to 175 mcg/kg/min and turned off
approximately 5 to 10 minutes before the end of the surgery.
The advantage of converting to IV anesthesia with propofol
is that this technique allows full access to the oral cavity
without intubating the patient and reduces the exposure to
the inhalation agent, reducing the likelihood of postoperative
nausea and vomiting.
Although other techniques of anesthesia are available
for treating pediatric patients, we find that the preceding
techniques provide excellent working time, maintenance of
cardiovascular and respiratory function, smooth emergence,
and quick recovery. However, we are always prepared to assist
with ventilation as necessary, have emergency drugs drawn
into syringes placed on the bracket tray and have all equip-
ment required for intubation immediately available if
required.
■ PERIOPERATIVE COMPLICATIONS
Regardless of the type of anesthesia delivered, there are several
important complications that could occur. These may deal
with surgical environment, medications given, and physical
responses of each patient. Complications of the procedure and
type of anesthesia to be delivered should be discussed during
the preoperative appointments and at the time of consent.
The parent’s and child’s questions should be answered and
their understanding reviewed. Each practitioner providing
anesthesia services should be well versed in the signs and
symptoms of each complication to include rapid and appropri-
ate identification and treatment.
LARYNGOSPASM
A common and frightening anesthetic complication is the
occurrence of laryngospasm, which is a forceful involuntary
spasm of the laryngeal musculature, causing a partial or com-
plete airway obstruction. It is caused by the stimulation of the
superior laryngeal nerve by secretions or foreign bodies, such
as an endotracheal tube passing through the larynx during
extubation.8 Signs of laryngospasm are the absence of sound
in a complete obstruction or squeaks, grunts, or whistles in
incomplete obstructions.17 Methods of preventing laryngo-
spasm would include controlling excess secretions, protecting
against foreign body aspiration, avoiding stimulating the
patient during “light” anesthesia, and deepening the level of
anesthesia or extubating the spontaneously breathing patient
while deeply anesthetized.
Treatment of suspected laryngospasm would include an
initial airway assessment with simple head-lift, jaw-thrust
maneuver, elevation of the tongue, suction of oropharynx,
and if confirmed, application of gentle positive pressure ven-
tilation with anesthesia bag and mask using 100% oxygen. If
this does not break the laryngospasm and hypoxia occurs,
succinylcholine or rocuronium should be given to paralyze
the laryngeal muscles, and atropine 0.02 mg/kg should be
administered first when succinylcholine is used in children
to prevent bradycardia. If laryngospasm occurs in patients
where IV access is not available and in whom more conserva-
tive measures have failed, IM succinylcholine can be admin-
istered at a dose of 4 to 6 mg/kg.8 The application of muscle
relaxants should be followed by controlled ventilation until
the patient regains adequate respiratory mechanics. Succinyl-
choline is used for emergency use only in children because
children with undiagnosed myopathies are more susceptible
than adults to hyperkalemic cardiac arrest, malignant hyper-
thermia, and masseter muscle spasm.8 If it is used in an emer-
gency situation, the provider must be vigilant to the signs
and symptoms of evolving malignant hyperthermia (MH) or
hyperkalemia.
A severe complication that could occur from prolonged
airway obstruction accompanied with respiratory efforts is
negative pulmonary pressure edema, which is caused most
commonly by larygnospasm.106 Other causes include obstruc-
tion of the endotracheal tube or a misplaced LMA resulting
 CHAPTER 7 • Pediatric Pharmacosedation and General Anesthesia
TABLE 7-7 Drugs Involved in Perioperative Anaphylaxis
Substance Incidence of Most Commonly Associated
Perioperative with Perioperative
Anaphylaxis (%) Anaphylaxis
Muscle relaxants 69.2 Succinylcholine, rocuronium,
atracurium
Natural rubber latex 12.1 Latex gloves, tourniquets, Foley
catheters
Antibiotics 8 Penicillin and other β-lactams
Hypnotics 3.7 Propofol, thiopental
Colloids 2.7 Dextran, gelatin
Opioids 1.4 Morphine, meperidine
Other substances 2.9 Propacetamol, aprotinin,
chymopapain, protamine,
bupivacaine
From Hepner DL, Castells, MC: Anaphylaxis during the perioperative period, Anesth
Analg 97:1381-1395, 2003.
in the folding of the epiglottis over the opening of the trachea.
Although exact incidence is unknown, it is most likely caused
by the generation of markedly negative intrathoracic pressure
as a result of forced inspirations caused by the laryngospasm,
resulting in transudation of fluid from pulmonary capillaries
to the interstitium following relief of the upper airway obstruc-
tion. Upon relief of the obstruction, developing dyspnea with
pink frothy sputum caused by pulmonary hemorrhage and
frank hemoptysis could be seen. A chest radiograph would
demonstrate bilateral pulmonary infiltrates. Supportive treat-
ment would include observation for several hours in the hos-
pital setting with maintenance of adequate oxygenation and
airway patency. Most cases resolve without lasting conse-
quences, but some patients may require diuretics (furosemide),
intubation, and mechanical ventilation.107
ANAPHYLAXIS
Anaphylaxis is generally an unanticipated severe allergic reac-
tion that can occur suddenly. Anaphylaxis is a Gell and
Coombs classification Type I immunoglobulin IgE-mediated
hypersensitivity reaction causing direct activation of mast
cells and basophils.108 In the clinical setting, this can be caused
by agents that are used commonly in the operative setting
(Table 7-7).
During many same day oral surgery procedures, the initial
signs and symptoms could be easily recognized as a result of
exposure of some or most of the skin, such as pruritus, flushing,
urticaria, angioedema, and conjunctivitis. Severe hypoten-
sion, greater than 40% of baseline, after a slow infusion or
small increments of drugs may indicate an allergic reaction.109
Wheezing and dyspnea may be followed by abdominal pain,
nausea, vomiting, diarrhea, and cardiovascular collapse and
death.108 Initial treatment would be immediate removal or
discontinuation of the offending object or medication fol-
lowed by immediate administration of epinephrine to treat
hypotension, cardiovascular collapse, and provide smooth
muscle relaxation. Diphenhydramine should be administered
107
if urticaria and angioedema are present, and the addition of
steroids and bronchodilators may also be considered.110
BRONCHOSPASM
Bronchospasm is a constriction of bronchial smooth muscles
and is common in the postoperative period. It can be caused by
aspiration, histamine release secondary to medications, aller-
gic response, or existing pulmonary conditions especially asthma
in the pediatric population. Bronchospasm may be caused by
secretions, deep pharyngeal suctioning, aspiration, or intuba-
tion. Treatment consists of removing any possible irritants or
drugs and administering inhaled β2-sympathomimetic agents,
such as albuterol. For uncooperative or obtunded patients, a
subcutaneous injection of epinephrine is appropriate for most
intraoperative occurrences. If the patient is intubated, approx-
imately 5 to 10 puffs of albuterol can be administered through
the endotracheal tube followed by positive pressure ventilation
with 100% oxygen. Nebulized atropine or glycopyrrolate can
be used to control excess secretions. IV epinephrine should not
be used unless hypotension is present and concurrent anaphy-
laxis is suspected. Intubation may be necessary if the patient
continues to be hypoxic.111
ASPIRATION
Aspiration has been shown to be a cause of laryngospasm and
bronchospasm and pneumonitis. Aspiration of gastric con-
tents aspirated in greater than 0.3 to 0.5 mL/kg may cause the
most serious consequences of aspiration, but the aspiration of
food, pus, or dental materials are also serious and may need
to be treated with antibiotic coverage, bronchoscopy, and
removal of foreign objects. Of all aspirated contents, blood is
the least worrisome. Pneumonitis had previously been treated
with antibiotics and steroids, but the current standard of care
is application of continuous positive airway pressure (CPAP)
ventilation. Antibiotics are useful only in cases of purulent
discharge aspiration.112 Control of airway and secretions are
necessary to prevent this type of injury, and the pediatric
patient should have received appropriate perioperative medi-
cations and verification of NPO status before anesthesia is
initiated. Proper surgical techniques, such as consistent use of
throat packs, control of secretions, and securing small instru-
ments continue to be the best preventative measures for pre-
venting aspiration and its potential consequences.
MALIGNANT HYPERTHERMIA
Malignant hyperthermia (MH) is a hypermetabolic syndrome
occurring in genetically susceptible patients after exposure to
either a volatile anesthetic or succinylcholine. Muscle con-
traction is sustained as a result of a reduction in the reuptake
of calcium from the sarcoplasmic reticulum, resulting in a
hypermetabolic state, tachycardia, hypercarbia, hypoxemia,
and increased heat production. The first signs of MH usually
occur in the operating room, but may be delayed for more than
1 hour after termination of anesthesia. MH is rare, with a
higher incidence in pediatric patients (1 : 15,000) than in
adult patients (1 : 40,000).8
108 SECTION I ■ Anesthesia and Pain Control
MH follows an autosomal pattern of dominance in about
50% of susceptible families, and an autosomal recessive form
has also been associated with King-Denborough syndrome.
Diagnosis can be established by exposing a fresh skeletal
muscle biopsy to a contracture test with caffeine, halothane,
or a combination of both. The earliest signs of MH are mas-
seter muscle rigidity (MMR), tachycardia, and hypercarbia,
with two or more of these signs greatly increasing the likeli-
hood of MH. MMR occurs in only 15% to 30% of true MH
episodes, but can also be present following administration of
succinylcholine. The safest course is to assume that masseter
spasm is due to MH and postpone elective surgery; however,
some anesthesiologists may proceed if no other signs of MH
are evident and then change over to nontriggering anesthetic
agents.8
Treatment involves first discontinuing all triggering agents,
changing breathing tubes, breathing bags, and soda lime.
Hyperventilation is initiated with 100% oxygen, and dan-
trolene sodium is mixed with sterile water and administered
2.5 mg/kg as soon as possible. If a significant rise in body
temperature is evident, cooling measures including ice packs
applied to the body, cold IV fluids, and cold solution lavage
of the stomach and body cavities should be initiated. Acidosis
is treated with sodium bicarbonate, 1 to 2 mg/kg IV, and
hyperkalemia is treated with IV insulin and glucose. Calcium
channel blockers should not be used with dantrolene because
hyperkalemia can result. Additional doses of dantrolene can
be administered if needed, and the patient should be trans-
ferred to intensive care for at least 24 hours until vital signs
have returned to normal.
■ RECOVERY AND DISCHARGE
All pediatric patients should be closely monitored while
recovering from anesthesia until ready for discharge. Pediatric
patients are vulnerable to postanesthetic laryngospasm that
can occur in the recovery room as the patient wakes up and
chokes on pharyngeal secretions.8 For this reason, all pediatric
patients should be recovered in the lateral position to allow
oral secretions to drain away from the vocal chords.
Discharge criteria for children are different than those for
adults. Each pediatric patient must appear fully awake and
back to his or her baseline behavior with no clinical signs of
complications from anesthesia or surgery. Pediatric discharge
criteria should address each of the following: state of con-
sciousness, vitals signs, respiratory efforts, age-appropriate
ambulation, return of normal airway reflexes, clear liquid tol-
erance, adequate pain control, and absence of postoperative
nausea and vomiting.113 Patel et al. reported that the most
common cause of unplanned admissions after attempted same-
day procedures in children was protracted vomiting.110 Ondan-
setron, a serotonin receptor agonist, has been shown to reduce
postoperative nausea and vomiting in pediatric patients when
given at a dose of 0.05 to 0.15 mg/kg IV.114 Dexamethasone
has also been shown to decrease the incidence of postopera-
tive nausea and vomiting in children following tonsillectomy
at a dose of 1 mg/kg not to exceed a total dose of 25 mg.115
Although postoperative vomiting was also the most common
postoperative complication reported by parents after ambula-
tory surgery, the cost-effectiveness of routine prophylaxis is
controversial.112 Other common reported complications post-
operatively are sore throat, headache, sore muscles, and surgi-
cal pain.116 These issues are usually easily resolved by use of
appropriate analgesia medications.
SUMMARY
The performance of oral surgery in children frequently requires
pharmacosedation or general anesthesia to reduce fear and
anxiety, increase cooperation, and ensures adequate forms of
amnesia and analgesia to safely and effectively complete the
surgical procedure. Selection of anesthetic technique is based
on the patient’s needs, the nature of the procedure, the facil-
ity, and the surgeon’s training, experience, and level of
comfort.
REFERENCES
1. American Association of Oral and Maxillofacial Surgeons:
Special considerations for pediatric anesthesia in outpatient
facilities. In Parameters of care draft 2007, Rosemont, Ill,
2006, American Association of Oral and Maxillofacial
Surgeons.
2. Jastak JT, Peskin RM: Major morbidity or mortality from office
anesthetic procedures: a closed-claim analysis of 13 cases,
Anesth Proc 38:39, 1991.
3. Marx GF, Mates DV, Orkin LR: Computer analysis of post-
anesthetic deaths, Anesthesiology 39:54, 1973.
4. Cote CT: Pediatric anesthesia. In Miller RD, editor: Miller’s
anesthesia, ed 6, Philadelphia, 2005, Elsevier, Churchill
Livingstone.
5. Strafford MA: Cardiovascular physiology and care. In O’Neill
JA et al., editors: Pediatric surgery, ed 5, St Louis, 1998, Mosby-
Year Book.
6. Scammon RE, Norris EH: On the time of obliteration of the
fetal blood passages (foramen ovale, ductus arteriosus, ductus
venosus), Anat Rec 15:165, 1918.
7. Vassallo SA: Anesthesia for pediatric surgery. In Hurford WE,
editors: Clinical anesthesia procedures of the Massachusetts General
Hospital, ed 6, Philadelphia, 2002, Lippincott Williams &
Wilkins.
8. Morgan GE, Mikhail MS, Murray MJ: Pediatric anesthesia. In
Clinical anesthesiology, ed 4, New York, 2002, McGraw-Hill.
9. Dembo JB: Pediatric outpatient anesthesia, Selected Readings
Oral Maxillofac Surg 5(4):1-19, 1997.
10. Wetzel RC: Evaluation of children. In Longnecker DE, Tinker
JH, Morgan GE, editors: Principles and practice of anesthesiology,
St Louis, 1998, Mosby-Year Book.
11. Keenan RL et al.: Bradycardia during anesthesia in infants: an
epidemiologic study, Anesthesiology 80:976, 1994.
12. Negus VE: The anatomy of the human larynx. In The Compara-
tive anatomy and physiology of the larynx, New York, 1949, Grune
& Stratton.
13. Eckenhoff JE: Some anatomic considerations of the infant
larynx influencing endotracheal anesthesia, Anesthesiology
12:401-410, 1951.
14. De Almeida VL et al.: The effect of nasal occlusion on the
initiation of oral breathing in preterm infants, Pediatr Pulmonol
18:374-378, 1994.
15. Miller MJ et al.: Effect of maturation on oral breathing in sleep-
ing premature infants, J Pediatr 109:515-519, 1986.
 CHAPTER 7 • Pediatric Pharmacosedation and General Anesthesia
16. Gaultier C: Developmental anatomy and physiology of the
respiratory system. In Taussi LM, Landau LI, editors: Pediatric
respiratory medicine, ed 1, St Louis, 1999, Mosby.
17. Bennett JD, Dembo JB, Butterfield KJ: Pediatric sedation. In
Peterson’s principles of oral and maxillofacial surgery, ed 2, Ham-
ilton, Ontario, 2004, BC Decker.
18. Devlieger H et al.: The diaphragm of the newborn infant: ana-
tomic and ultrasonographics studies, J Dev Physiol 16:321-329,
1991.
19. Keens TG et al.: Developmental pattern of muscle fiber types
in human ventilatory muscle, J Appl Physiol 44:909-913, 1978.
20. Davies G, Reid L: Growth of alveoli and pulmonary arteries in
childhood, Thorax 25:669-691, 1970.
21. Dunnil MS: Postnatal growth of the lung, Thorax 17:329-333,
1962.
22. Haddad GG, Fontan JJP: Development of the respiratory
system. In Nelson textbook of pediatrics, ed 17, St Louis, 2004,
Saunders.
23. Zeltner TB et al.: The postnatal development and growth of
the human lung. I. Morphometry, Respir Physiol 67:247-267,
1987.
24. Zeltner TB, Burri P: The postnatal development and growth of
the human lung. II. Morphology, Respir Physiol 67:269-282,
1987.
25. Thurlbeck WM: Postnatal human lung growth, Thorax 37:564-
571, 1982.
26. Koch G: Alveolar ventilation, diffusion capacity and the (A-a)
PO2 difference in the newborn infant, Respir Physiol 4:168-192,
1968.
27. Gaultier CL et al.: Determination of capillary oxygen tension
in infants and children, Bull Eur Physiopathol Respir 14:287-297,
1978.
28. Dong SH et al.: Arterialized capillary blood gases and acid-base
studies in normal individuals 29 days to 24 years of age, Am J
Dis Child 139:1019-1022, 1985.
29. Levison HEA, Featherby EA, Weng TR: Arterial blood gases,
alveolar-arterial oxygen difference, and physiologic dead space
in children and young adults, Am Rev Respir Dis 101:972-974,
1970.
30. Papastamelos C et al.: Developmental changes in chest wall
compliance in infancy and early childhood, J Appl Physiol
78:179-184, 1995.
31. Farmery AD, Roe PG: A model to describe the rate of oxyhae-
moglobin desaturation during apnea, Br J Anaesth 76:284-291,
1996.
32. McCrory WW: Quantitative measurement of renal function
during growth in infancy and childhood. In Developmental
nephrology, Cambridge, Mass, 1972, Harvard University Press.
33. Leeder JS, Kearns GL: Pharmacogenetics in pediatrics. In
Implications for practice, Pediatr Clin North Am 44:55-77,
1997.
34. Himms-Hagen J: Cellular thermogenesis, Annu Rev Physiol
38:315-351, 1976.
35. Johnson P, Andrews DC: The role of thermometabolism on
cardiorespiratory function in postnatal life. In Gaultier C,
Escourrou P, Curzi-Dascalova L, editors: Sleep and cardiorespira-
tory control, vol 227, Paris, 1991, Colloque INSERM/John
Libbey.
36. Friis-Hansen B: Body composition during growth. In vivo mea-
surements and biochemical data correlated to differential ana-
tomical growth, Pediatrics 47:264-274, 1971.
37. Ginsberg G et al.: Evaluation of child/adult pharmacokinetic
differences from a database derived from the therapeutic drug
literature, Toxicol Sci 66:185-200, 2002.
38. Gibby GL et al.: How often does the preoperative interview
change anesthetic management? [abstract], Anesthesiology 77:
A1134, 1992.
109
39. Curran MA: Preoperative assessment of the pediatric patient,
In Kaban LB, Troulis MJ, editors: Pediatric oral and maxillofacial
surgery, Philadelphia, 2004, Saunders.
40. Mallampati SR et al.: A clinical sign to predict difficult tracheal
intubation: a prospective study, Can Anaesth Soc J 32:429,
1985.
41. Wetzel RC: Anesthesia and perioperative care. In Behrman RE
et al., editors: Nelson textbook of pediatrics, ed 17, Philadelphia,
2004, Saunders.
42. Benumof JL: Management of the difficult adult airway, with
special emphasis on awake tracheal intubation, Anesthesiology
75:1087, 1991.
43. Cauldwell CB, Fisher DM: Ambulatory anesthetic and sedative
techniques for children, Oral Maxillofac Surg Clin North Am
6(1):1-11, 1994.
44. Cote CJ, Todres ID: The pediatric airway. In Cote CJ et al.,
editors: A Practice of anesthesia for infants and children, ed 2,
Philadelphia, 1993, WB Saunders.
45. Vischoff D, Limoges P: Outpatient anesthesia. In Bissonnette
B, Dalens B, editors: Pediatric anesthesia: principles and practice,
New York, 2002, McGraw-Hill.
46. Warner MA et al.: Perioperative pulmonary aspiration in
infants and children, Anesthesiology 90:66, 1999.
47. American Society of Anesthesiologists: American Society of
Anesthesiologists task force on preoperative fasting and the use
of pharmacologic agents to reduce the risk of pulmonary aspira-
tion practice guidelines for preoperative fasting and the use of
pharmacologic agents to reduce the risk of pulmonary aspira-
tion: Application to healthy patients undergoing elective pro-
cedures, Anesthesiology 1999:90, 896.
48. McGill WA, Coveler LA, Epstein BS: Subacute upper respira-
tory infection in small children, Anesth Analg 58:331-333,
1979.
49. Schreiner MS et al.: Do children who experience laryngospasm
have an increased risk of upper respiratory tract infection?
Anesthesiology 85:475-480, 1996.
50. Cohen MM, Cameron CB: Should you cancel the operation
when a child has an upper respiratory tract infection? Anesth
Analg 72:282-288, 1991.
51. Tait AR et al.: Risk factors for perioperative adverse respiratory
events in children with upper respiratory tract infections, Anes-
thesiology 95:299-306, 2001.
52. National Institutes of Health, National Heart, Lung, and Blood
Institute: Data fact sheet, asthma statistics, 1999. Available at
www.nhlbi.nih.gov/health/prof/lung/asthma/asthstat.pdf (Accessed
Dec 2006)
53. Ruggiero SL: Evaluation, treatment, and management of the
asthmatic patient, Oral and Maxillofac Surg Clin North Am
10(3):337-348, 1998.
54. Maxwell LG et al.: Systemic disorders in pediatric anesthesia.
In Motoyama EK, Davis PJ, editors: Anesthesia for infants and
children, ed 6, St Louis, 1996, Mosby.
55. Standards for basic anesthetic monitoring (Approved by the
House of Delegates on Oct 21, 1986, and last amended on Oct
24, 2005), American Society of Anesthesiologists Standards,
Guidelines and Statements. Available at: www.asahq.org/
publicationsAndServices/standards/02.pdf#2 (Accessed Oct
2006)
56. Gross JB et al.: Practice guidelines for sedation and analgesia
by non-anesthesiologists. A report by the American Society of
Anesthesiologists task force on sedation and analgesia by non-
anesthesiologists, Anesthesiology 84:459-471, 1996.
57. Morgan GE, Mikhail MS, Murray MJ: Clinical anesthesiology, ed
4, New York, 2006, McGraw-Hill.
58. Overly FL et al.: Bispectral analysis during deep sedation of
pediatric oral surgery patients, J Oral Maxillofac Surg 63:215-
219, 2005.
110 SECTION I ■ Anesthesia and Pain Control
59. Stein N et al.: An evaluation of a transcutaneous and an end-
tidal capnometer for noninvasive monitoring of spontaneously
breathing patients, Respir Care 51(10):1162-1166, 2006.
60. Block FE Jr, L Nuutinen L, Ballast B: Optimization of alarms:
a study on alarm limits, alarm sounds, and false alarms, intended
to reduce annoyance, J Clin Monit Comput 15:75-83, 1999.
61. Bhanaker SM et al.: Injury and liability associated with moni-
tored anesthesia care, Anesthesiology 104(2):228-234, 2006.
62. Stoelting RK: Audible information signals (‘alarms’) and their
role in the operating room, ASA Newsletter 2004. Available
at: www.asahq.org/Newsletters/2004/06_04/subNews06_04.html
(Accessed Nov 2006)
63. James RH: 1000 anaesthetic incidents: experience to date,
Anaesthesia 58:856-863, 2003.
64. Hurford EH: Clinical anesthesia procedures of the Massachusetts
General Hospital, ed 6, Philadelphia, 2002, Lippincott Williams
& Wilkins.
65. Part 12: Advanced pediatric life support. In Circ J Am Heart
Assoc 112:169, 2005. Available at www.circulationaha.org
(Accessed Jan 2007)
66. Ravussin P et al.: Percutaneous transtracheal jet ventilation for
peadiatric endoscopic laser treatment of subglottic lesions, Can
J Anaesth 41:1200-1207, 1994.
67. Cox RG: Should cuffed endotracheal tubes be used routinely
in children? Can J Anaesth 52:669-674, 2005.
68. Newth CJ et al.: The use of cuffed versus uncuffed endotracheal
tubes in pediatric intensive care, J Pediatr 144:333-337, 2004.
69. Kundo S, Achar S: Principles of office anesthesia: part II.
Topical anesthesia, Am Fam Physician 66(1):99-102, 2002.
70. Hazinski MF: Vascular access. In PALS provider manual, Dallas,
2002, American Heart Association.
71. Fiorito BA et al.: Intraosseous access in the setting of pediatric
critical care transport, Pediatr Crit Care Med 6(1):50-53,
2005.
72. Winikoff SI, Rosenblum M: Anesthetic management of the
pediatric patient for ambulatory surgery, Oral and Maxillofac
Surg Clin of North Am 11(4):505-517, 1999.
73. Pang LM, Liu LMP, Coté CJ: Premedication and induction of
anesthesia. In A practice of anesthesia for infants and children, ed
3, Philadelphia, 2001, Saunders.
74. Kain ZN et al.: Parental presence and a sedative premedicant
for children undergoing surgery, Anesthesiology 92:939-946,
2000.
75. Maranets I, Kain ZN: Preoperative anxiety and intraoperative
anesthetic requirements, Anesth Analg 89:1346-1351, 1999.
76. Kain ZN et al.: Premedication in the United States: a status
report, Anesth Analg 84:427, 1997.
77. McMillan CO et al.: Premedication of children with oral mid-
azolam, Can J Anaesth 39:545-550, 1992.
78. Roelofse JA, Joubert JJ, Roelofse GR: Double blind randomized
comparison of midazolam alone with midazolam combined with
ketamine for sedation of pediatric dental patients, J Oral Maxil-
lofac Surg 54:838-844, 1996.
79. Golparvar M et al.: Paradoxical reaction following intravenous
midazolam premedication in pediatric patients—a randomized
placebo controlled trial of ketamine for rapid tranquilization,
Pediatr Anesth 14:924-930, 2004.
80. Vischoff D, Limoges P: Outpatient anesthesia. In Bissonnette
B, Dalens BJ, editors: Pediatric anesthesia, New York, 2002,
McGraw-Hill.
81. Friesen RH, Lockhart CH: Oral transmucosal fentanyl citrate
for preanesthetic medication of pediatric day surgery patients
with and without droperidol as a prophylactic anti-emetic,
Anesthesiology 76:46, 1992.
82. Bennett J: Intravenous anesthesia for oral and maxillofacial
office practice, Oral Maxillofac Surg Clin North Am 11:601-609,
1999.
83. Kitahata LM, Taub A, Kosaka Y: Lamina specific suppression
of dorsal-horn unit activity by ketamine hydrochloride, Anes-
thesiology 38:4-11, 1973.
84. Sadove MS et al.: Analgesic effects of ketamine admini-
stered in subdissociative doses, Anesth Analg 50(3):452-457,
1971.
85. Gonty AA: Ketamine—a new look at an old drug, Oral and
Maxillofac Surg Clin North Am 4:815-823, 1992.
86. White PF, Way WL, Trevor AJ: Ketamine—its pharmacology
and therapeutic uses, Anesthesiology 56:119, 1982.
87. Alfonzo-Echeverri EC et al.: Oral ketamine for pediatric dental
surgery sedation, Pediatr Dent 15:182-185, 1993.
88. Green SM, Johnson NE: Ketamine sedation for pediatric pro-
cedures: part 2, review and implications, Ann Emerg Med
19:1033-1046, 1990.
89. Pruitt JW et al.: Intramuscular ketamine, midazolam, and gly-
copyrrolate for pediatric sedation in the emergency department,
J Oral Maxillofac Surg 53:13-17, 1995.
90. Sebel PS, Lowdon JD: Propofol: a new intravenous anesthetic,
Anesthesiology 71:260-277, 1989.
91. Hannallah RS et al.: Propofol anesthesia in paediatric ambula-
tory patients: a comparison with thiopentene and halothane,
Can J Anaesth 41:12-18, 1994.
92. Kraut RA: Propofol—a rival to methohexital, Oral and Maxil-
lofac Surg Clin North Am 4:825-830, 1992.
93. Reber A et al.: Effect of combined mouth closure and chin lift
on upper airway dimensions during routine magnetic resonance
imaging in pediatric patients sedated with propofol, Anesthesiol-
ogy 90:1617-1623, 1999.
94. Schrum SF et al.: Comparison of propofol and thiopental for
rapid anesthesia induction in infants, Anesth Analg 78:482-485,
1994.
95. Crawford MW et al.: Recovery characteristics of propofol
anaesthesia, with and without nitrous oxide: a comparison with
halothane/nitrous oxide anaesthesia in children, Pediatr
Anaesth 8:49-54, 1998.
96. Bart SM et al.: Ondansetron with propofol reduces emesis and
airway obstruction in pediatric outpatients, Can J Anaesth
46:359-362, 1999.
97. Cameron E et al.: The minimum effective dose of lidocaine to
prevent injection pain due to propofol in children, Anesthesiol-
ogy 47:604, 1992.
98. Duncan GH, Moore PA: Nitrous oxide and the dental patient:
a review of adverse reactions, J Am Dent Assoc 108:213-219,
1983.
99. Litman RS et al.: Breathing patterns and levels of consciousness
in children during administration of nitrous oxide after oral
midazolam premedication, J Oral Maxillofac Surg 55:1372-1377,
1997.
100. Hurford EH: Clinical anesthesia procedures of the Massachusetts
General Hospital, ed 6, Philadelphia, 2002, Lippincott Williams
& Wilkins.
101. Lee M, Bennett HE, Gordon N: Sevoflurane general anesthe-
sia: an alternative technique in the pediatric oral and maxillo-
facial surgery patient, J Oral Maxillofac Surg 61:1249-1252,
2003.
102. Lerman J et al.: The pharmacology of sevoflurane in infants and
children, Anesthesiology 80:114, 1994.
103. Blankenstein KC: Low-dose intravenous ketamine, an effective
alternative to conventional deep conscious sedation, J Oral
Maxillofacial Surg 64:691-692, 2006.
104. Blankenstein KC, Anderson J: A double-blind comparison
of low-dose intravenous ketamine and methohexital in adults,
J Oral Maxillofac Surg 49:468, 1991.
105. Baum VC, Yemen TA, Baum ID: Immediate 8% sevoflurane
induction in children: 8% sevoflurane compared with 5% halo-
thane, Br J Anaesth Analog 85:313, 1997.
 CHAPTER 7 • Pediatric Pharmacosedation and General Anesthesia
106. Padley SPG, Downes MO: Case report. Pulmonary edema sec-
ondary to laryngospasm following general anesthesia, Br J Radiol
67:654, 1994.
107. Kelly JP, Ciavarro C: Postobstructive pulmonary edema in an
obese child after an oral surgery procedure under general anes-
thesia: a case report, J Oral Maxillofac Surg 60:1503-1505,
2002.
108. Hepner DL, Castells MC: Anaphylaxis during the perioperative
period, Anesth Analg 97:1381-1395, 2003.
109. Campbell RL, Campbell JR: Anesthesia complications associ-
ated with ambulatory oral and maxillofacial surgery, Selected
Readings, Oral Maxillofac Surg 9(2), 2001.
110. Castells MC et al.: Anaphylaxis. In Holgate ST, Church MK,
Lichtenstein LM, editors: Allergy, ed 2, London, 2001, Mosby.
111. Complications and emergencies. In American Association of
Oral and Maxillofacial Surgeons: Office anesthesia evaluation
manual, ed 6, 2000.
111
112. Patel RI, Hannallah RS: Anesthetic complications following
pediatric ambulatory surgery: a 3-year study, Anesthesiology
69:1009-1012, 1988.
113. Hannallah RS: Outpatient anesthesia. In Coté CJ, Todres ID,
Ryan JF, editors: A practice of anesthesia for infants and children,
ed 3, Philadelphia, 2001, Saunders.
114. ASHP therapeutic guidelines on the pharmacologic manage-
ment of nausea and vomiting in adult and pediatric patients
receiving chemotherapy or radiation therapy or undergoing
surgery, Am J Health Syst Pharm 56:729, 1999.
115. Pappas ALS et al.: The effect of preoperative dexamethasone
on the immediate and delayed postoperative morbidity in chil-
dren undergoing adenotonsillectomy, Anesth Analog 87:57-61,
1998.
116. Steward DJ: Outpatient pediatric anesthesia, Anesthesiology
43:268-276, 1975.
CHAPTER 8
THE ESSENTIAL ROLE OF THE ORAL AND
MAXILLOFACIAL SURGEON IN THE DIAGNOSIS,
MANAGEMENT, CAUSATION, AND PREVENTION OF
CHRONIC OROFACIAL PAIN: CLINICAL PERSPECTIVES
The previous chapter emphasized pathophysiologic mecha-
nisms leading to chronic orofacial head pain. The important
role of acute trauma and repeated noxious stimuli to the oral
and maxillofacial structures has been well documented as
major etiologic factors that lead to chronic orofacial pain
conditions. It is clear that recurrent noxious stimulation of
the peripheral branches of the trigeminal nerve lead to peri-
pheral and central sensitization of ascending nerve pathways,
ultimately leading to chronic orofacial pain. Stimulation of
these ascending pathways reach the cerebral cortex resulting
in the patient’s awareness of pain at a site localized peripher-
ally in the oral and maxillofacial region. A major challenge
for the oral and maxillofacial surgeon as a clinician is to realize
that the patient’s perception of the site and source of pain is
peripheral, and the patient will frequently request localized
treatment at this peripheral site. If the pain is neuropathic in
origin, with central sensitization, multiple localized treat-
ments not only will fail to alleviate the pain, but will further
stimulate the ascending pathways creating more localized
tissue injury, further exacerbating chronic orofacial pain.
A thorough knowledge of the principles of diagnosis, man-
agement, causation, and prevention of chronic orofacial pain
is essential for every oral and maxillofacial surgeon, regardless
of whether the clinician chooses to actively diagnose and treat
these challenging patients or decides to refer them to other
specialists. The reason for this is that the oral and maxillofa-
cial surgeon is in a key position to prevent the progression
from acute pain to a chronic pain condition. Conversely,
failure to properly diagnose and manage patients who have
pain may lead to multiple surgeries, failed treatments, and
create the physiologic environment for progression to chronic
pain.
The previous chapter reviewed the diagnosis and treatment
of the major types of chronic orofacial pain conditions that
have been classified as being neurologic, musculoskeletal, and
vascular in origin. This chapter will focus on the most practi-
cal clinical aspects of chronic orofacial pain that every oral
and maxillofacial surgeon should know regardless of whether
he or she will be the primary treating clinician for the chronic
112
Howard A. Israel
pain condition or the one who refers the patient for further
specialty care. The major sections of this chapter include:
• Principles of diagnosis and management
• The essential role of the oral and maxillofacial surgeon
in the prevention of progression to chronic orofacial
pain
• Diagnosis and treatment of the most common
inflammatory and degenerative temporomandibular
joint conditions
■ PRINCIPLES OF DIAGNOSIS AND
MANAGEMENT OF PATIENTS
WITH CHRONIC OROFACIAL PAIN
THE INITIAL VISIT
Patients with chronic orofacial pain conditions have complex
histories frequently including misdiagnoses, multiple dental
and surgical procedures, and multiple failed treatments. The
frustration of these patients and their family members is
immense. The chronic pain condition often creates intense
physical and emotional suffering and is frequently associated
with anxiety and depression. The main point here is that the
initial consultation visit requires a significant amount of time
for the patient and the clinician. The patient needs time to
adequately express their chief complaint(s) and recount the
history. The clinician needs time to properly assimilate the
extensive information presented, perform a head and neck
examination, obtain appropriate diagnostic images, review
previous records and diagnostic images, process the informa-
tion, develop differential diagnoses, and provide treatment
recommendations with proper sequencing. Additionally, there
needs to be time set aside for the patient to assimilate the
information provided by the clinician and ask questions. The
time that is required for this initial consultation appointment
will vary with different patients and clinicians. However, it is
rare for the initial appointment to take less than 1 hour, and
in most instances, the time allotment should be 1½ hours.
It is important for the clinician to obtain an appropriate
history without excessive amounts of superfluous information
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon
from the patient. Patients who suffer from chronic orofacial
pain often have extensive histories, and the anxious patient
believes that it is necessary to provide the clinician every
detailed piece of information in the quest for a diagnosis and
successful treatment. Unfortunately, excessive amounts of
superfluous information can often be counterproductive in
assisting the clinician in making the correct diagnosis. There-
fore, a clinician-guided interview is necessary. At the start of
the interview, the clinician should lay down the ground rules
of the interview and ask the patient to respond only to the
question that is asked. However, the clinician must also inform
the patient that after this guided interview is complete, the
patient will be free to provide the clinician with any other
information that he or she believes is helpful. The key com-
ponents of the clinician guided history are as follows:
1. Chief complaint(s) listed in order with the most severe
symptoms being first
2. History of present illness—in chronologic order so that
a timeline of events can be constructed. The patient
should provide a chronologic list of treating clinicians
that includes their specialty, the diagnosis rendered, the
treatment recommended, actual treatment provided, and
the patient’s response to that treatment.
3. Pain history1:
a. Location(s)—one finger with pointing to those spots
that are most painful in descending order to those that
are less severe
b. Duration—continuous or intermittent
c. Quality of the pain
i. Shocklike
ii. Aching
iii. Burning
iv. Numbing
v. Other descriptions
d. Precipitating factors (e.g., light touch, opening jaw,
chewing, drinking hot or cold liquids, stress, exercise,
spontaneous)
e. Temporal predisposition (early AM, progression
throughout course of day, early evening before sleep,
awakens patient from sleep)
f. Factors that reduce pain (effective medications, moist
heat, ice, massage)
Following the completion of a careful clinician-guided
history, the oral and maxillofacial surgeon will be in a better
position to establish a more accurate differential diagnosis.
Additionally the examination that follows this history may
become more focused toward establishing the correct
diagnosis.
The consultation rarely ends at the first visit because the
diagnosis and therapeutic approaches will frequently change
based on the response to treatment and the results of further
diagnostic information as the work-up progresses. The impact
of having a new chronic orofacial pain patient in the middle
of a busy day in an oral and maxillofacial surgeon’s office can
be quite disruptive to the schedule. Therefore, if the clinician
is unable to allocate the appropriate time and energy in the
113
management of these patients, it is often better to be prepared
to refer the patient to a specialist or a group of specialists who
have demonstrated expertise in the diagnosis and manage-
ment of chronic pain.
Assuming the oral and maxillofacial surgeon is willing to
have the responsibility of diagnosis and treatment of the
chronic orofacial pain patient, then the following are some of
the key principles in managing these patients:
FLEXIBLE DIAGNOSES-MANAGEMENT CONCEPT
It is common, even for the experienced clinician, to be uncer-
tain of the diagnosis and treatment of a chronic orofacial pain
patient. This is unlike the more common situation in which
a patient in acute pain has an abscess that is generally easy to
diagnose, treat, and cure. Because this is not the case with
chronic pain patients, it is important for the clinician to have
a different mindset with the development of differential diag-
noses that remain flexible. The concept here is that the clini-
cian develops an initial differential diagnoses and treats the
patient according to the most likely condition(s) causing the
chronic pain. Based on the response to treatment, there is a
continual reevaluation of the diagnoses and treatment.
The following clinical scenario is an example of the flexible
diagnoses-treatment concept in action. A hypothetical patient
is referred to the oral and maxillofacial surgeon who reports
having brief episodes (1 to 5 seconds) of well-localized unilat-
eral facial pain, followed by a dull aching pain that is ipsilat-
eral and poorly localized. The patient has some of the features
of trigeminal neuralgia, but the clinical presentation is not
classic. Patients who have this and similar scenarios will fre-
quently seek a dental evaluation that either fails to reveal any
dental pathologic condition or results in dental treatment that
fails to alleviate the symptoms. When this hypothetical patient
is referred to the oral and maxillofacial surgeon, the clinical
examination is often unremarkable. In this scenario, the head
and neck examination is negative except for tenderness to
palpation of the muscles of mastication, particularly the mas-
seter and temporalis. However, the history of short episodes
of sharp pain suggests trigeminal neuralgia. The initial differ-
ential diagnoses would include trigeminal neuralgia and mas-
ticatory muscle spasm. After the initial evaluation, the patient
may be placed on a course of anticonvulsant medication
therapy (e.g., gabapentin 300 mg t.i.d. or carbamazepine
200 mg b.i.d.). At the follow-up visit, if the patient reports a
significant reduction in symptoms, the primary diagnosis of
trigeminal neuralgia becomes more likely. The response to
treatment and the diagnosis of trigeminal neuralgia warrant
further investigation with a brain MRI to rule out an intra-
cranial tumor or lesion. If the patient had no response to the
anticonvulsant medication, the clinician may proceed to
increase the medication dosage or change the primary diag-
nosis to masticatory muscle spasm and treat the patient with
muscle relaxants and physical therapy. The flexible diagnosis-
treatment concept emphasizes the continual reevaluation of
the diagnoses and therapeutic efficacy, with alterations in the
diagnosis and treatment according to the patient’s response.
114 SECTION I ■ Anesthesia and Pain Control
The clinician must also be aware that patients frequently have
multiple concomitant diagnoses that require diagnosis-specific
treatment for each condition. Therefore, the example pro-
vided previously may require treatment of masticatory myo-
spasm and trigeminal neuralgia once the primary diagnosis is
established.
USE LOCAL ANESTHETIC INJECTIONS TO
ENHANCE DIAGNOSTIC ACCURACY AND
PROVIDE PAIN RELIEF
At the initial visit, the chronic facial pain patient who has
seen multiple clinicians has often lost hope of having pain
relief and is often frustrated about the failure to have an accu-
rate diagnosis to explain the cause of their pain. They will
often believe that the failure of clinicians to provide a specific
diagnosis and cause for their pain means that their health care
providers believe that their pain is psychogenic in origin and
has no physiologic basis. Thus, the patient will often cling to
the belief that the pain is coming from a specific tooth. Their
hope is that removal of that specific tooth, regardless of how
many other teeth have been removed or treated, will relieve
them of their pain, end their suffering, and thus, disprove the
psychogenic cause concept. The clinician will often be unable
to detect any signs of pathologic condition on the clinical and
radiographic examination. However, these patients will often
have pain to percussion or palpation of a specific tooth, and
the clinician may consider the diagnosis of a tooth fracture,
pericementitis, or a nonspecific pulpitis. Diagnostic local
anesthetic injections are extremely valuable at the time of the
initial visit of the chronic orofacial pain patient for the
following reasons:
1. Local anesthetic injections are helpful in differentiating
peripheral pain of dental or musculoskeletal cause versus
central mediated pain.
2. Local anesthetic injections that result in pain relief
provide hope for the patient that there is something that
can “turn off” or reduce the pain. Local anesthetic injec-
tions that provide pain reduction provide a significant
psychological lift and further corroborates for the patient
that the cause of the pain is not psychogenic, but based
on excessive activity of specific neural pain pathways.
3. Local anesthetic injections that successfully reduce pain
provide the patient and clinician an important thera-
peutic adjunct by blocking the pain. This helps to
reduce the repeated stimulation of central ascending
nerve pathways, which contribute to exacerbation of
neuropathic pain.
4. The results of the local anesthetic injections provide
further direction for the clinician concerning
treatment.
The patient who has pain localized to a specific tooth, who
responds favorably with pain reduction from a local anesthetic
block or infiltration may provide the clinician further justifica-
tion for local dental treatment. However, if there is a history
of multiple episodes of localized tooth pain with failed dental
treatments (e.g., extraction, apicoectomy, endodontic
therapy), the clinician should be very cautious about drawing
the conclusion that the pain is solely dental in origin. It is
important for the oral and maxillofacial surgeon to realize that
many central mediated pain conditions, such as trigeminal
neuralgia or atypical facial neuralgia, have a peripherally
located trigger zone, which when stimulated with light touch,
pressure, or other sensory stimuli, can lead to a triggering of
central neuropathic pain. It is not unusual for occlusal pressure
on a specific tooth to be the source of a trigger of central
mediated pain with local anesthetic blocks resulting in pain
reduction. Therefore in the absence of objective signs of local
dental pathologic conditions, the clinician should be very
cautious in providing localized dental treatment in the patient
with chronic facial pain, even if the patient responds favorably
to local anesthetics. As discussed previously, further surgical
trauma can provide additional stimulation of ascending central
neural pathways, leading to a further exacerbation of chronic
pain. The corollary to this is that repeated blocking of the
peripheral stimulus leading to stimulation of ascending central
neural pathways is extremely valuable in treating the
patient with chronic neuropathic pain by reducing central
sensitization.
A regular schedule of local anesthetic blocks can be an
important therapeutic intervention provided by the oral and
maxillofacial surgeon for the chronic facial pain patient. The
initial injections should be as well localized as possible and
use short-acting local anesthetics. Therefore, if the pain is
localized to a maxillary tooth, a small amount of local infiltra-
tion at the apex of the tooth (often without the use of topical
anesthetic, which may obscure the results) would be per-
formed with 3% mepivacaine. In the mandible, the bicuspid
teeth and all teeth anterior to the bicuspids are amenable to
a local anesthetic infiltration. Mandibular molars may require
local infiltration along with a periodontal ligament injection.
Alternatively, an inferior alveolar nerve block can be given
for the mandibular molars, but the diagnostic results of this
injection are less specific because of the broader anatomic area
of anesthesia obtained. If the local anesthetic injection adja-
cent to the suspected tooth fails to provide any pain relief, it
is often helpful to give an injection into the adjacent muscle
of mastication (usually the masseter, temporalis, or lateral
pterygoid) because masticatory muscle spasm is a common
source of referred dental pain (Figure 8-1).
The local anesthetic injection is often delivered following
the clinical and radiographic examination but before the dis-
cussion with the patient concerning the diagnosis and treat-
ment recommendations. This gives the local anesthetic time
to take effect before discharging the patient. Because the
patient has provided the clinician with a preinjection subjec-
tive assessment of their pain intensity using he visual analog
scale (0 = no pain, 10 = the most severe pain), the patient is
then asked to provide a number on the visual analog scale, 5
minutes following the administration of the injection. If the
initial response does not provide at least a 50% reduction in
the pain, then the clinician may consider providing additional
local anesthetic injections in an attempt to identify the
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon
FIGURE 8-1. A 57-year-old female with chronic neuropathic pain and
masticatory muscle spasm. Trigger injections of local anesthetics into muscles
of mastication have provided significant relief of pain lasting 2 to 4 weeks.
peripheral source (or trigger) of the pain. The reason for the
initial use of a short-acting local anesthetic, such as 3% mepi-
vacaine is that certain patients may find that the local anes-
thetic sensation provides a dysesthesia with further exacerbation
of the pain. Although this is rare, it does occur in some
chronic orofacial pain patients. Individuals who have had
trigeminal nerve injuries (from surgery or trauma) seem to be
more susceptible to exacerbation of pain with trials of local
anesthetics.
If the short-acting local anesthetic provides a significant
reduction in pain (greater than 50%), then the oral and max-
illofacial surgeon may consider administration of a long-acting
local anesthetic, such as 0.5% bupivacaine with epinephrine
1 : 200,000 at the same site of the initial injection. This may
be performed at the first visit, or at times it can be saved for
a subsequent visit, to provide a stepwise approach for the
patient to gradually treat and improve their pain condition.
Giving the patient hope, confidence, and pain relief plays an
important role in reversing the deleterious effects of chronic
pain.
The time, site, dose, and response to the injections are
recorded carefully in the chart, and the patient is also given
the task of keeping a log of their pain level following the
initial injection. This log provides very important diagnostic
and potentially therapeutic information (Figure 8-2).
The log includes the following information:
• Preinjection pain level on the VAS
• Time of injection
• Location of injection
• Local anesthetic agent(s) used and dosage
• Patient response after 5 minutes on the VAS
• Patient response after 15 minutes on the VAS
• Patient VAS every hour following the injection (patient
takes the log home)
• Time when the local anesthetic effect has worn off
• Pain VAS every hour following this for 24 hours
115
If the log demonstrates that the pain returns to preinjection
levels following the local anesthetic injection, this provides
additional evidence that the primary pain source is local or
there is a trigger that is local. If the log demonstrates further
effective pain relief following the cessation of the local anes-
thetic effect, this provides evidence that there is a central
neuropathic component of the pain that is being exacerbated
by peripheral impulses. These peripheral impulses may be scar
tissue or neuromas from previous trauma. However, regardless
of the exact mechanism for the pain, the response of contin-
ued pain relief following a wearing off of the local anesthetic
effect is an indication that the central nervous system has had
a chance to temporarily recover from the barrage of ascending
impulses from peripheral nerve pathways. This then provides
the clinician with a therapeutic intervention, which has
potential to reduce the central mediated component of the
pain by blocking peripheral painful sensory impulses.
The results of diagnostic local anesthetic injections in
chronic facial pain patients are often equivocal. There are
some patients who have no benefit and others who have
varying responses at different times. In this scenario, it is not
necessarily recommended to completely abandon the use of
local anesthetics. If the results of the injections are equivocal,
the clinician may then proceed to try to block the pain farther
proximally. Therefore, the patient who had an equivocal
response to a local infiltration in the maxillary anterior region
may need a trial of infraorbital nerve blocks. Those who had
an equivocal response to posterior maxillary molar infiltra-
tions may benefit from a posterior superior alveolar nerve
block or a V2 division block administered through the ptery-
gopalatine fissure or the greater palatine canal. Individuals
who have equivocal responses to injection of mandibular
teeth may benefit from a mental nerve block, lingual nerve
block, buccal nerve block, and/or an inferior alveolar nerve
block. Each trial of local anesthetic injections is assessed using
the aforementioned local anesthetic log. These logs provide
very useful information even when the response to the local
anesthetic does not provide pain relief. A review of the tem-
poral tendencies of the pain will provide useful information
on factors that exacerbate the pain and may also enable the
clinician to more effectively time and dose medications to
reduce or prevent the onset of the pain (see Figure 8-2).
RULE OUT PATHOLOGIC CONDITIONS LOCALIZED
TO THE SURROUNDING ANATOMIC STRUCTURES
The complex regional anatomy of the oral and maxillofacial
region makes diagnosis and treatment of pathologic condi-
tions in this region difficult. Pain is the most common reason
for a patient to seek treatment. The trigeminal nerve is respon-
sible for transmitting sensory impulses from the head and neck
region to the central nervous system. The variable anatomy
of the branches of the trigeminal nerve along with the complex
branching and crossover of nerve fibers makes the head and
neck region very susceptible to referred pain patterns, where
the site and source of pain are different. One of the goals of
the initial visit is to rule out any local pathologic condition
116 SECTION I ■ Anesthesia and Pain Control
3/23/06
11AM 5PM
3/14/2006 0 injection
15-Mar 0 5
16-Mar 0 5
17-Mar 0 0
18-Mar 1 5
19-Mar 0 3
20-Mar 0 0
21-Mar 0 3
22-Mar 0 0
A
FIGURE 8-2. A, B, A 65-year-old female with atypical facial neuralgia being treated with pregabalin 75 mg t.i.d.,
amitriptyline 25 mg OD, and local anesthetic injections. The log helps the clinician determine the efficacy of therapy and
ascertain daily variations in pain patterns. The elevated pain levels toward the evening in this patient require increased
dosages of pain medications later in the day.
that is amenable to routine treatment by the oral and maxil-
lofacial surgeon. Therefore, anatomic regions adjacent to the
oral cavity, maxilla, and mandible may have a localized patho-
logic condition that can cause referred pain. Failure to diag-
nose pathologic conditions from surrounding structures can
contribute to the onset of chronic orofacial pain.
A common example of this is the patient with maxillary
sinusitis. These patients will often come to their dentist com-
plaining of multiple painful posterior maxillary teeth. If the
patient undergoes several dental treatments that fail to reduce
the pain (endodontic therapy, apicoectomy, extraction
therapy), not only is the source of the pain still present, but
the repeated tissue damage from invasive treatment can set
up the environment for the onset of chronic orofacial pain.
If the correct diagnosis of maxillary sinusitis is made too late,
appropriate sinus treatment may alleviate the pain from
the sinusitis, but may have no effect on the chronic central
mediated pain that was created by multiple failed dental
treatments.
Another commonly misdiagnosed condition involving sur-
rounding structures is temporal arteritis. These patients have
severe pain associated with chewing. The pain tends to be
localized to the temporal region, but can also be referred to
the temporomandibular joint, and thus, is frequently misdiag-
nosed. An additional factor that contributes to this misdiag-
nosis is that the patient population with temporal arteritis is
often significantly older than those with typical inflammatory
temporomandibular joint pathologic conditions. Therefore
on clinical examination, chronic osteoarthritis is often dis-
covered with crepitus of the temporomandibular joints on
8PM 11PM
some numbness 4
0 3
0 4
7 9 add’l vicodin
0 3
6 8 add’l vicodin
0 2
0 8
2 3
auscultation and evidence of degenerative changes of the
mandibular condyles seen on panoramic radiographs. Thus,
these patients often undergo treatment for temporomandibu-
lar joint osteoarthritis that fails to alleviate the symptoms.
The use of nonsteroidal antiinflammatory medications
(NSAIDs), a softer diet, physical therapy, and night guard
appliances will not alleviate the symptoms of temporal arteri-
tis. In fact the delay in making a correct diagnosis can lead to
permanent impairment of vision. There are several ways of
preventing misdiagnosis of temporal arteritis. Patients with
temporal arteritis will frequently have pain to palpation of the
temporal artery. An elevation in the serum erythrocyte sedi-
mentation rate (ESR) is a nonspecific laboratory finding in
patients with temporal arteritis. A definitive diagnosis requires
a temporal artery biopsy. Elderly patients who do not fit the
typical profile of the younger patients who are susceptible to
inflammatory temporomandibular joint disease should all be
suspected of having temporal arteritis until it is ruled out.
PERFORM A CRANIAL NERVE EXAMINATION AS A
ROUTINE PART OF THE CLINICAL EXAMINATION
OF THE CHRONIC OROFACIAL PAIN PATIENT
The cranial nerve examination is an essential part of any
thorough head and neck examination. For patients with
chronic orofacial pain conditions, a thorough cranial nerve
examination is essential and should be performed frequently
at follow-up visits. The cranial nerve examination takes very
little time, and if there are no abnormalities, it may seem to
the clinician that the information was not very helpful.
However, this is not the case because an abnormal cranial
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon 117

13-Nov-06

11AM 3PM 8PM 11PM

1-Oct-06 0 0 0 5
10/2/2006 0 0 4 7
10/3/2006 0 0 5 6
10/4/2006 0 0 0 9
10/5/2006 0 0 5 0
10/6/2006 0 0 0 0 8
10/7/2006 0 0 0 0
10/8/2006 0 0 0 0
10/9/2006 0 0 5 0 8 vicodin
10/10/2006 0 0 0 8 vicodin
10/11/2006 0 0 0 8 vicodin
10/12/2006 0 0 5 8 vicodin
10/13/2006 0 0 0 0
10/14/2006 0 0 0 8
10/15/2006 0 0 0 8
10/16/2006 0 7 7 0
10/17/2006 0 5 0 8 vicodin
10/18/2006 0 0 0 0
10/19/2006 0 0 0 7
10/20/2006 0 0 5 8 vicodin
10/22/2006 0 5 0 8 vicodin
10/23/2006 0 6 7 0
10/24/2006 0 0 3 8 vicodin
10/25/2006 0 0 8 0
10/26/2006 0 8 8 0
10/27/2006 0 0 5 0
10/28/2006 0 2 0 4
11/2/2006 0 0 0 0
11/3/2006 0 0 5 8
11/4/2006 2 0 0 6
11/5/2006 2 0 0 0
11/6/2006 0 0 5 0
11/7/2006 0 0 0 7
11/8/2006 2 5 5 8 vicodin
11/9/2006 2 0 7 vicodin 8 vicodin
11/10/2006 0 0 0 0
11/11/2006 2 0 0 0

B
FIGURE 8-2, cont’d

nerve examination usually represents a significant pathologic
condition. The following is a very brief gross cranial nerve
examination that potentially can yield very important
information:
• Cranial Nerve I: Have the patient close his or her eyes,
close one nostril, and ask them to identify a smell (e.g.,
alcohol).
• Cranial Nerves II, III, IV, VI: Check papillary reflexes
to light and accommodation. Check extraocular eye
movements in three planes.
• Cranial Nerve V: Test sensory branches of V1, V2, V3
with a cotton swab and look for differences between left
and right. Check motor division of V by looking for
deviation of the mandible upon opening, representing
unopposed action of the lateral pterygoid muscle. Ask
the patient to clench and check for masseter and
temporalis tone bilaterally.
• Cranial Nerve VII: Ask patient to demonstrate facial
movements by raising the eyebrows, shutting the eyes,
moving the nose, smiling, and pursing lips.
118 SECTION I ■ Anesthesia and Pain Control
• Cranial Nerve VIII: The examiner rubs his or her fingers
together in front of each ear, and differences between
the right and left sides are noted.
• Cranial Nerves IX and X: Test the gag reflex. IX is
sensory, and X is motor.
• Cranial Nerve XI: Have patient elevate shoulders and
look for asymmetry.
• Cranial Nerve XII: Ask patient to protrude their tongue
and look for deviation to one side. Unopposed action of
the right or left genioglossus muscle will cause deviation
to the side that is impaired.
When checking the facial nerve, an abnormal finding may
be complete paralysis of the muscles of one side of the face or
may only involve the lower half of the face. The distinction
between these two types of facial nerve dysfunction is very
important. The temporal branches of the facial nerve on one
side receive input from upper motor neurons bilaterally as a
result of decussation of these nerve fibers in the brain. The
lower peripheral branches of the facial nerve receive upper
motor neuron input from the ipsilateral side only. Thus, a
centrally located lesion that affects the facial nerve will cause
paralysis of only the lower half of the face. A peripherally
located lesion that affects the facial nerve, such as a parotid
tumor, is likely to cause paralysis of all of the branches of the
facial nerve on the side of the tumor (Figure 8-3, A).
Deviation of the mandible upon opening is a sign that is
common in chronic facial pain patients who have a temporo-
mandibular joint disorder. The clinician will often assume
that the facial pain and deviation of mandibular opening is
due to failed translation of a pathologic ipsilateral temporo-
mandibular joint. However, it is extremely important for the
clinician to also check the motor function of the trigeminal
nerve because deviation of the mandible can also be caused
by a pathologic condition impinging on this nerve. Failure to
check for the presence of motor function of the trigeminal
nerve can lead to a significant misdiagnosis, with treatment
of a temporomandibular joint condition when in fact the
patient has a tumor or lesion causing impingement of the
cranial nerve V (Figures. 8-3, B-E).
Patients with chronic orofacial pain often complain of the
symptom of numbness. A careful history will reveal if there is
any evidence of trauma or surgery that may have caused
damage to the sensory nerves that innervate the oral and
maxillofacial region. There are some chronic pain patients,
with no history of acute trauma to the branches of the trigemi-
nal nerve, who complain of facial numbness. Individuals who
complain of sensory disturbances require a careful sensory
examination. The simplest form of this examination is to ask
the patient to close their eyes while the examiner tests for
normal sensation to touch, using a cotton applicator. The
cotton applicator goes from the area where the sensation is
normal toward the area that is abnormal, asking the patient
to identify when the change in sensation has taken place. The
examiner draws a mark at that site (make up pencil) and
repeats the examination from different locations, going from
normal to abnormal. The examiner then draws a map of the
area with altered or reduced sensation and photographs of this
area are taken. If the area of altered sensation follows the dis-
tribution of one of the sensory nerves, then this is highly sug-
gestive of a pathologic condition or trauma that is altering
normal sensory activity (Figure 8-4, A,B). Further investiga-
tion of both peripheral and central causes of altered sensory
activity are required. Local trauma, surgical trauma, and
pathologic conditions can often be diagnosed with radiographs
and diagnostic images (CT or MRI). Pathologic conditions of
the central nervous system that alter sensation require an MRI
and/or CT of the brain. Demyelinating diseases, such as mul-
tiple sclerosis and intracranial tumors, such as acoustic
neuroma, are common central causes of altered sensation of
the oral and maxillofacial region. If the map of the area of
altered sensation does not follow the anatomic distribution of
one of the branches of the trigeminal nerve, it is more likely
that the altered sensation is due to a musculoskeletal disorder.
Patients suffering from masticatory muscle spasm often have
intermittent areas of altered sensation that do not follow an
anatomic distribution. This is most likely due to the effect of
increased muscle activity causing intermittent impingement
of terminal sensory fibers.
CONSIDER SYSTEMIC PATHOLOGIC CONDITIONS
THAT CAN CAUSE FACIAL PAIN
The key to diagnosing systemic pathologic conditions that can
cause pain is taking a careful history. Systemic musculoskeletal
disorders, such as fibromyalgia, rheumatoid arthritis, and
osteoarthritis, commonly affect the temporomandibular joint
and surrounding structures. The pattern of the pain and the
quality of the pain often provide significant clues to a systemic
cause. Unilateral shocklike facial pain is characteristic of tri-
geminal neuralgia. If this type of pain is accompanied with a
history of severe fatigue and patches of sensory alterations in
other areas of the body in a young adult, this would be highly
suggestive of multiple sclerosis, which is associated with a
higher frequency of trigeminal neuralgia. A history of herpes
zoster would be more suggestive of postherpetic neuralgia.
A recent study of patients experiencing significant cardiac
ischemia revealed that craniofacial pain was the only com-
plaint in 6% of individuals.2 In this study of cardiac ischemia
symptoms, an additional 32% of patients had craniofacial pain
along with concomitant pain in other regions. The most
common craniofacial pain locations were the throat, mandi-
ble, temporomandibular joint, and teeth. Overall the study
concluded that in patients with cardiac ischemia who did not
have chest pain, craniofacial pain was the most dominant
symptom. Patients who have risk factors for coronary artery
disease, with atypical orofacial pain should be suspected of
having cardiac ischemia. In particular if the pain history
reveals physical activity to be a precipitating cause of the pain,
the clinician should be highly suspicious of cardiac ischemia.
The implications for the dentist and oral and maxillofacial
surgeon are significant because cardiac ischemia and acute
myocardial infarction require immediate referral and
management.
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon 119

A1 A2

B C1

C2 D
FIGURE 8-3. A, A 43-year-old female who had an 18-month history of right-sided facial pain
and deviation of the mandible to the right with opening. The patient had previously been treated
for a temporomandibular joint disorder without success. Examination revealed a deficit of all of the
branches of the right facial nerve and right V3 paresthesia. B, The mandible deviated to the right
with maximal opening. The clinical examination revealed no evidence of motor function of the right
temporalis or masseter muscles when the patient was asked to clench. C, Temporomandibular
joint MRIs taken 18 months before her presentation were read as normal. Images medial to the
condyle demonstrated a mass in the right pterygomandibular space. D, A new MRI was ordered
that revealed a large tumor medial to the mandible and lateral to the medial pterygoid muscle,
with invasion of the base of the skull. E, The final diagnosis was adenocarcinoma of the parotid
gland. Complete excision of the tumor was not possible because of extensive invasion into the
base of the skull. The patient underwent radiation therapy along with pain management with
E methadone. She passed away within 1 year following the diagnosis of adenocarcinoma of the
parotid gland.
120 SECTION I ■ Anesthesia and Pain Control

A B

FIGURE 8-4. A, A 75-year-old woman with chronic pain of the right mandible. The patient had previously been
treated with two endodontic therapies, two apicoectomies, and two extractions without relief of her symptoms. At the
time of her initial presentation, the clinical examination was normal except for a right V3 paresthesia, which the patient
was not aware of. An initial diagnosis of atypical facial neuralgia was made, and the pain was successfully managed
with gabapentin 300 mg t.i.d. B, Although the pain was successfully controlled, a brain scan was a necessary part of
the work-up. MRI of the brain demonstrated an acoustic neuroma, impinging on the trigeminal nerve. She subsequently
underwent a craniotomy with removal of the tumor, with a continued postoperative course of gabapentin 300 mg t.i.d.
Nine months following the surgery, the patient was free of disease and pain free.

RECOGNIZE AND TREAT BOTH PERIPHERAL AND
CENTRAL MEDIATED PAIN
An important principal in the management of the patient
with chronic orofacial pain is to establish accurate diagnoses.
However, the process of performing an appropriate work-up is
frequently lengthy and may yield negative or equivocal results.
During this process, it is important for the clinician to provide
therapies that reduce the pain. A key principal in the treat-
ment of orofacial pain is to block the peripheral input of
noxious stimuli from reaching the central nervous system to
prevent sensitization of ascending pathways in the central
nervous system. Interventions that successfully reduce the
pain by reducing peripheral noxious stimuli are not only
temporarily beneficial, but have important therapeutic effects
because they reduce stimulation of the central nervous system.
Thus a local anesthetic that blocks peripheral sensory nerves
also reduces the volley of impulses reaching the subnucleus
caudalis of the brainstem. This in turn reduces the stimulation
of the ascending spinothalamic tract of the spinal cord that
eventually reaches the cerebral cortex and is recognized as
pain. Because central neuropathic pain is characterized by
excessive excitability of the ascending nerve pathways, the
local anesthetic block reduces this excitability. This helps to
explain the phenomenon experienced by many chronic oro-
facial pain patients of obtaining significant pain relief beyond
the duration of the local anesthetic.
There are numerous modalities that the clinician can use
to reduce peripherally mediated pain. Medications that
provide antiinflammatory effects (both steroidal and nonste-
roidal) have the capacity to reduce the noxious stimuli
by reducing stimulation of the peripheral nociceptors
caused by tissue injury. Muscle relaxant medications can be
helpful indirectly by reducing painful muscle contraction
that often occurs as a response to injury. This is particularly
true in individuals who have painful musculoskeletal
disorders of the head, such as temporomandibular joint syno-
vitis or masticatory muscle spasm. As described previously, a
series of local anesthetic injections designed to block the
peripheral pain impulses can have important therapeutic
effects.
The reduction of central mediated pain simultaneously
with the reduction of the peripheral mediated pain offers the
chronic orofacial pain patient the best chance of effective
pain relief. Central mediated pain can be reduced with a
variety of medications. Anticonvulsant mediations (gaba-
pentin, pregabalin, carbamazepine) are helpful, but these
medications require careful titration to eventually achieve a
therapeutic dose. Some patients are not able to tolerate the
side effects of these medications as the dosage is increased.
The use of narcotic analgesics in patients with chronic orofa-
cial pain is controversial. The opioid class of medications acts
centrally to reduce pain. However, the potential for tolerance,
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon
abuse, and addiction are possible with narcotic analgesics
when their use is not carefully supervised and documented by
the treating clinician. Short-acting narcotic analgesics are not
indicated in the treatment of chronic orofacial pain. The short
duration of pain relief with medications, such as Tylenol with
codeine, hydrocodone, and oxycodone, result in a brief period
of reduced pain often followed several hours later by a return
of severe pain, resulting in a cycle characterized by an increas-
ing frequency and dose of narcotic medication. In spite of our
knowledge about the negative effects of short-acting narcotics
in the chronic orofacial pain patient, many patients arrive at
the oral and maxillofacial surgeon’s office with a long history
of dependence on short-acting narcotics. In certain select
patients, long-acting narcotic analgesics are indicated3 and are
usually prescribed in a pain management center. If the oral
and maxillofacial surgeon decides to manage patients with
long-acting narcotic analgesics, it is especially important to
have a signed contract with the patient to provide ground
rules for their use. It is extremely important to avoid having
multiple clinicians prescribing medications for pain manage-
ment, and thus communication and coordination with all of
the patient’s physicians is very important. In general it is best
for only one treating clinician to be in charge of prescribing
pain medications.
SUBSEQUENT VISITS OF THE CHRONIC
OROFACIAL PAIN PATIENT
Regularly scheduled follow-up visits are a necessary part of
management of the chronic orofacial pain patient. Each sub-
sequent visit requires that the clinician follow an organized
protocol which should include the following:
1. Review of the diagnoses and treatment recommenda-
tions from the previous appointment
2. Subjective assessment by the patient as to whether the
pain is the same, better, or worse than the previous
appointment
3. Detailed assessment of the pain to determine if it has
changed with respect to:
a. Location
b. Intensity (visual analog scale)
c. Frequency
d. Character
e. Temporal pattern
f. Reevaluation of factors that increase and decrease the
pain
4. Assessment concerning patient compliance with the
treatment recommendations from the previous visit
5. Assessment of any side effects or complications from
the treatment recommendations of the previous visit
6. Review of any changes in the medical history
7. Review of all current medications and compliance with
these medications
8. Patient assessment of the efficacy of each of the treat-
ment recommendations from the previous visit
9. Thorough head and neck examination including cranial
nerve examination
121
10. Review of all new diagnostic images and laboratory test
results ordered
11. Reassessment of the differential diagnoses
12. Treatment plan with the inclusion of the date required
for follow-up
13. Projected plan for the next step in treatment should the
patient not improve or if the symptoms increase
REEVALUATE DIAGNOSES CONTINUALLY
The follow-up appointments for chronic orofacial pain
patients can vary in length, but usually 30 minutes is an
adequate amount of time for this reevaluation process. It is
very important for the clinician not to evaluate the patient
with a preconceived notion of the diagnoses. Rather it is
better for the clinician to view each subsequent visit with
a fresh viewpoint, challenging the accuracy of the working
differential diagnoses based on the patient’s response to
treatment and changes in the history and clinical
examination.
MINIMIZE VARIABLES WHEN INSTITUTING
CHANGES IN TREATMENT
The first consultation visit should ultimately result in a dif-
ferential diagnoses and treatment based on the diagnoses.
Initially, this will involve multiple treatment modalities fre-
quently involving multiple medications. At subsequent visits,
the diagnoses should become clearer as the patient responds
or fails to respond to treatment. Another key principle in the
subsequent evaluation and management of the chronic orofa-
cial pain patient is when providing changes in treatment, it
is preferable to make only one change (or the fewest number
of changes) at a time. This concept of management helps to
reduce multiple variables in treatment changes that may
further confuse evaluation and management of the chronic
orofacial pain patient. For example, if a medication that has
been prescribed at the previous appointment was not effective
or created an untoward side effect, it is generally best to
replace one medication with another single medication. In
this way, the effect of this medication change can be assessed
accurately at the next appointment. If two or more medica-
tions are added to the treatment regimen, then any improve-
ment or untoward effect cannot be attributed with certainty
to either of the medications that were tried. An example of
this would be the patient with chronic orofacial pain in whom
the differential diagnosis includes both atypical facial neural-
gia and a chronic infection. If the clinician decides to treat
the patient with both a course of an anticonvulsant (e.g.,
gabapentin) and an antibiotic, then a favorable response to
this treatment may further confuse the diagnosis and appropri-
ate treatment regimen.
There are many exceptions to the one treatment change
principle that rely on the judgment of the clinician and the
multiplicity of diagnoses being managed. The initial visit basi-
cally maps out a plan and provides treatment for each indi-
vidual diagnosis, so initial management with multiple therapies
and medications are common. However, once the diagnoses
122 SECTION I ■ Anesthesia and Pain Control
become more firmly established, providing one treatment
change is very helpful to the clinician in providing appropri-
ate and successful management of these complex patients. At
the end of each follow-up appointment, it is important for the
clinician to have a plan, should the patient not respond favor-
ably to the treatment recommended at the previous appoint-
ment. For example, if the patient with masticatory muscle
spasm has been unsuccessfully treated with a muscle relaxant,
then the clinician may opt to try a different medication. The
clinician may note in the chart that at the follow-up appoint-
ment if the second muscle relaxant was unsuccessful in reduc-
ing symptoms, a series of muscle trigger injections may be the
next course of action. The key principle here is for the clini-
cian to have a plan in advance based on the patient’s response
to treatment.
AVOID CHANGES IN TREATMENT IF PAIN LEVELS
ARE IMPROVING
Another key principle in treatment of chronic orofacial pain
patients is the following: If the patient is getting better, do
not make any significant changes in the treatment. Because
these patients have been suffering for a long period of time
(often with multiple failed treatments), any reduction in pain
levels must be viewed as a significant event in the course of
their treatment. Patients with chronic orofacial pain are
hoping for a rapid and complete end to their suffering.
Unfortunately, this is rare and often unrealistic, particularly
in cases where there is a central neuropathic component to
the pain. The hyperactivity of excitable central pain path-
ways is particularly difficult to reduce because of the contin-
ued stimulation of these pathways with neuromas, sympathetic
nerve fibers, and fibrous tissue that resulted from multiple
local traumatic episodes (often from multiple surgical proce-
dures). It is important for the clinician to explain to the
patient that if they have had pain for many months or years,
it is unrealistic for the pain to resolve in 1 to 2 weeks. A
general guideline provided to patients is that if the patient
has had the pain for 1 year, it will often take an equal
amount of time for the pain to subside to an acceptable level.
By lowering the patient’s unrealistic expectations, the clini-
cian is better able to provide reassurance and hope for the
patient, which is an important part of pain management.
Therefore, when providing treatment for chronic orofacial
pain, if the patient’s pain level is reduced from the previous
visit, this is considered a significant event, and major altera-
tions in the treatment provided are generally not recom-
mended. It is important to remember that pain reduction is
therapeutic in itself because of decreased stimulation of the
central pain pathways. Patients are informed that as long as
the pain levels are reducing, then the treatment is headed
in the appropriate direction. Some patients have an initial
response to the pain management and then plateau without
any further improvement. When this juncture is reached, it
is advisable to reevaluate the diagnoses and implement
further new treatment modalities designed to further enhance
pain management.
INDIVIDUALIZE PAIN MANAGEMENT FOR EACH
SPECIFIC PATIENT
The pain management regimen must be individualized for
each patient. Therapeutic interventions that are successful for
one patient may be unsuccessful for another patient with the
same diagnosis. It is extremely important for the clinician to
continually evaluate whether the treatment modalities that
are prescribed are in fact helping the patient. Patients with
masticatory myospasm and temporomandibular joint disorders
are often referred for physical therapy and are treated with a
night guard appliance and NSAIDs. If the physical therapy or
the night guard appliance appear to be exacerbating symp-
toms, these modalities must be discontinued. Medications that
are prescribed that are not providing clinical benefit should
not be continued. Some chronic orofacial pain patients are
placed on anticonvulsants (such as gabapentin) or muscle
relaxants (e.g., cyclobenzaprine) for a long time, and it is not
clear if the medication is providing any therapeutic benefit. If
the clinician suspects that one of the medications prescribed
is not providing a therapeutic benefit, then that medication
should be gradually tapered. If the patient starts to develop
increased symptoms during the tapering of the dosage of medi-
cation, this confirms that the medication is in fact helping,
and a return to the previous dosage is indicated. Some patients
who have been on medication for a long time are unhappy
with some of the side effects (e.g., sedation, or weight gain
from gabapentin). Again, it is important for the clinician to
gradually taper the dose of medication for two important
reasons. First an increase in pain symptoms may warrant a
return to the maintenance dosage of the medication (e.g.,
clonazepam cessation can cause seizures). The important
concept here is that the clinician is continually reevaluating
both the diagnoses and response to treatment and adapting
the treatment according the diagnoses and efficacy of the
treatment.
Alternative therapies may play an important role in pain
management. Acupuncture, acupressure, massage therapy,
yoga, exercise, reiki, tai chi, and holistic remedies are exam-
ples of the many modalities that the patient may consider in
an effort to reduce the pain. Regardless of whether the clini-
cian can explain the scientific mechanism behind these
modalities, if the patient believes that the alternative therapy
is effectively reducing the pain, then this treatment should be
continued. However, it is important for the clinician to evalu-
ate if the alternative therapy has the potential to do harm.
Certain holistic remedies can have deleterious side effects.
Manipulative procedures by untrained individuals have the
potential to create tissue damage. Therefore continued reeval-
uation of the effectiveness of these alternative treatment
modalities by the clinician is necessary.
Referrals to appropriate specialists are a necessary com-
ponent in the management of the chronic orofacial pain
patient. A relatively simple algorithm to follow concerning
when to make a referral for a patient with pain who is not
responding to treatment can be seen in Figure 8-5 (Triage of
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon 123

Patient intake

Dentist

Pain: Pain: Pain:

Likely dental origin Possible dental origin Unlikely dental origin

Dental Dental vs. Referral Referral

treatment treatment

Pain Pain Pain Pain

resolution persists resolution persists

Referral Referral

FIGURE 8-5. Triage of the complex/chronic orofacial

pain patient. Pain specialists or pain management center

the Complex/Chronic Orofacial Pain Patient). The most
common reason for patients to seek dental treatment is the
onset of orofacial pain. Following the initial visit with the
clinician, a diagnosis is formulated and treatment instituted.
If it appears likely for the pain to be of dental origin, then the
appropriate dental therapy should be instituted followed by a
reevaluation of the response to treatment. If the pain persists,
regardless of the dental intervention, then an appropriate
referral is indicated. For those patients in whom the diagnosis
of a dental cause is uncertain, the clinician may opt for an
immediate referral and/or may institute dental treatment to
see if the patient responds. However, failure of the patient to
respond to routine dental treatments is a warning sign that
the origin of the orofacial pain may not be of dental origin.
This is a key point in the management of the patient, which
may determine whether a patient with relatively acute pain
evolves into a chronic orofacial pain patient. Multiple dental
interventions that fail to resolve the pain symptoms result in
repeated surgical trauma to the oral and maxillofacial region
and may be the prelude to the development of peripheral and
central sensitization of pain pathways, leading to neuropathic
pain (Figure 8-6). Those patients who initially have a history
of symptoms with clinical signs suggesting a nondental origin
of the pain will often require immediate referral to the appro-
priate specialists(s) who are experienced in the management
of chronic pain.
The oral and maxillofacial surgeon should have a relation-
ship with a group of specialists who are available to provide
assistance in the diagnosis and management of the chronic
orofacial pain patient. The clinician must be confident that
these specialists are individuals who have the time, expertise,
and willingness to take on the challenge of caring for these
complex patients. Listed below are those specialties that are
likely to be included in the management of the chronic
orofacial pain patient.
• Oral and maxillofacial surgery
• Otolaryngology
• Neurology
• Neurosurgery
• Psychiatry
• Psychology
• Anesthesiology
• General dentistry
• Endodontics
• Radiology
• Physical therapy
• Alternative medicine
Psychological evaluation and cognitive behavioral
approaches provided to the patient with chronic pain are
extremely important. How the clinician approaches this with
the patient can be an important factor in the success or failure
of treatment. It is extremely important for the clinician to
understand that while the patient is being worked up for the
appropriate diagnosis and treatment, the patient is suffering
as a result of the significant impact of the chronic pain on the
quality of life. There is both physical and psychological suf-
fering associated with chronic pain, both of which may lead
to a feeling of hopelessness, depression, and anxiety, which
may have further exacerbating effects on pain pathways. A
study of patients with temporomandibular disorders (TMD)
concluded that these patients have a markedly impaired oral
health-related quality of life.4 Therefore, while the clinician
is searching for the cause of the pain and providing treatment
to reduce the pain, psychological evaluation, and manage-
124 SECTION I ■ Anesthesia and Pain Control

FIGURE 8-6. A 48-year-old woman who underwent a lengthy session of multiple crown preparations under general
anesthesia in her dentist’s office. Following this procedure, she developed dental pain that localized to specific teeth,
followed by dental treatment (endodontic therapy, apicoectomy, and/or extraction). Over the course of 9 months, the
patient underwent 12 endodontic procedures, four apicoectomies, four extractions, and placement of five implants. With
each procedure, the pain migrated to a different tooth. After 9 months of chronic pain, this patient was referred for
chronic pain evaluation and management. This is clearly a case of neuropathic pain with central sensitization, and the
patient has been treated successfully with anticonvulsant mediations, long-acting narcotic analgesics, and infraorbital
local anesthetic blocks.

ment are important in reducing the impact of the chronic pain
on the quality of life. Cognitive behavioral therapy5 is not
designed specifically to reduce pain; it provides the patient
with coping strategies to improve quality of life. Cognitive
behavioral therapy focuses on teaching certain strategic skills
and techniques that are incorporated into daily life activities
that help the individual cope with the effects of chronic pain.
Furthermore unlike other interventions provided by health
care professionals, cognitive behavioral therapy requires that
the patient be an active participant in their care, assuming
responsibility for learning these techniques. This is different
from the typical therapies provided by clinicians in which the
patient is a passive recipient of their treatment.
Many patients who are referred for psychological evalua-
tion are extremely resistant to this recommendation. They
will often assume that the physician believes that the pain is
not real and/or is being produced, with the patient having
other reinforcing motivating factors for maintaining the pain.
It is very important for the clinician to emphasize to the
patient that the reason for the psychological evaluation is to
diagnose and treat any concurrent exacerbating psychiatric
disease (such as depression and anxiety) and develop strategies
for improving the quality of life while going through the stress
of living with chronic orofacial pain.
■ PREVENTION OF PROGRESSION
TO CHRONIC OROFACIAL PAIN—
THE KEY ROLE OF THE ORAL
AND MAXILLOFACIAL SURGEON
There are numerous studies that have clearly demonstrated
that repeated damage to peripheral tissues will lead to periph-
eral and central sensitization of pain pathways ultimately
resulting in central neuropathic pain.6-20 Multiple dental
treatments that fail to result in symptom resolution are
common in the population of patients with chronic orofacial
pain. These patients frequently have a history of multiple
failed endodontic procedures, apicoectomies, and extractions
over the course of several months to years, with the repeated
tissue trauma acting as an exacerbating factor in the progres-
sion from acute pain to chronic pain. A study of 120 chronic
orofacial pain patients seen at a multidisciplinary academic
center for orofacial pain concluded that surgical intervention
exacerbated pain in 55% of patients who had undergone
surgery for treatment of their pain.19 Retrospective studies on
the results of endodontic surgery revealed a 2% to 3%
incidence of posttraumatic painful peripheral neuropathy
resulting in phantom tooth pain.10,11 When a patient fails to
improve following an endodontic procedure, it is common
for the patient to be referred to the oral and maxillofacial
surgeon.
Patients who are desperate to get pain relief will often point
to a specific tooth or region, requesting the surgeon to perform
one more procedure to eliminate the source of pain. The
individual who is suffering will frequently beg the oral surgeon
to provide the localized treatment, in spite of the history of
previous multiple failed surgical procedures. The treating cli-
nician who is aware of this scenario as being typical of the
onset of central neuropathic pain will often find it difficult for
the patient to conceptualize the concept of central sensitiza-
tion and neuropathic pain. From the patient’s perspective, the
pain is coming from a local site, and any treatment, other than
local treatment, is often perceived by the patient as being
psychogenic. Therefore, the surgeon is in a key position to
determine whether there is a progression to multiple failed
surgical treatments or more appropriate therapeutic interven-
tions driven by accurate diagnoses. The following are key
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon
principles for the oral and maxillofacial surgeon with regard
to the prevention of progression to chronic orofacial pain:
1. Avoid invasive procedures in the absence of clinical and
radiographic findings.
2. If a patient has failed to experience pain relief after
several dental interventions, reevaluate the diagnosis
and consider alternative diagnoses that have oral pain,
but have a different cause.
3. Perform local anesthetic injections for diagnostic pur-
poses to rule out local sources of pain.
4. Perform local anesthetic injections to provide pain relief
and reduction of the barrage of stimulated neurons
transmitting pain to the central nervous system.
5. When the diagnosis is uncertain in a patient with
chronic orofacial pain, consider a trial course of medica-
tions to reduce the central mediated pain and help to
corroborate the diagnosis.
THIRD MOLAR SURGERY—A POTENTIAL
PRECIPITATING FACTOR FOR CHRONIC
FACIAL PAIN
Evaluation and management of third molars is one of the most
common responsibilities of the oral and maxillofacial surgeon.
Regardless of whether the surgeon is going to be directly
involved in the treatment of the chronic orofacial pain patient,
correct management of patients who are referred for third
molar evaluation is critical in the prevention of chronic oro-
facial pain. A recent retrospective study of third molar extrac-
tions and risk of TMD was performed using data from electronic
dental insurance records.21 The data included 34,491 patients
with a mean of 18.2 years who underwent third molar extrac-
tion. The authors concluded that there was a 60% increased
risk of experiencing TMD in adolescents and young adults
who underwent third molar surgery. It should be noted that
14% of the procedures were performed by general dentists,
whereas 83% were performed by oral and maxillofacial sur-
geons. The authors suggested that in this age population, 23%
of TMD cases might be due to third molar surgery. Although
this retrospective cohort study does not prove that third molar
extraction causes TMD, experienced clinicians are aware that
third molar extraction is a risk factor.
PROTECT THE TEMPOROMANDIBULAR JOINT
DURING SURGICAL PROCEDURES
Oral and maxillofacial surgeons are very aware of the impor-
tance of using atraumatic techniques and supporting the man-
dible while performing surgical procedures. Additionally, it is
extremely important for the oral and maxillofacial surgeon to
perform a complete examination of the temporomandibular
joints and masticatory muscles at the initial consultation for
third molar surgery. The preoperative evaluation should
include questions regarding a history of parafunctional masti-
catory activity (clenching, bruxism), temporomandibular
joint symptoms, disease and/or treatment. The examination
must include palpation of the temporomandibular joints and
masticatory muscles to determine if there is any tenderness.
125
Mandibular range of motion measurements should be
performed, including interincisal opening distance, devia-
tions, lateral excursions, and protrusive movements. Ausculta-
tion of the temporomandibular joints should also be performed
to detect any preexisting joint sounds, such as clicking or
crepitus. The results of this examination must be well docu-
mented in the chart, serving as a baseline should the patient
develop any temporomandibular joint symptoms postopera-
tively. If the patient does have a history of temporomandibular
joint symptoms in the past, it is important for the clinician
and patient to be aware of the likelihood of a potential exac-
erbation, and measures should be taken to minimize the risk
of a TMD flare-up. Therefore, the surgeon may decide to
reduce the time of the surgery by performing the removal of
the third molars in stages, rather than all four extractions at
one time. If the patient is not extremely anxious, the clinician
may opt to avoid general anesthesia or conscious sedation,
thus, allowing the patient to inform the surgeon if there is any
increased joint stress detected by the patient during the pro-
cedure. If the patient has concurrent temporomandibular joint
symptoms, and if the removal of the third molars is elective
(no active infection), the oral and maxillofacial surgeon
should treat the temporomandibular joint symptoms first until
the patient has become asymptomatic before removing the
third molars.
CORROBORATE DIAGNOSIS OF THIRD MOLARS
AS ETIOLOGY OF THE PAIN (IF PATIENT IS
BEING REFERRED WITH A PRESUMPTION OF
DENTAL PAIN CAUSED BY A THIRD MOLAR
PATHOLOGIC CONDITION)
Another extremely important factor in the prevention of
chronic facial pain in the patient referred for third molar
evaluation is the nature of the referral and the patient’s pre-
senting symptoms. A very common scenario is the patient with
oral pain who is referred by the general dentist for removal of
the wisdom teeth. These patients often have a history of being
treated by the dentist with undiagnosed dental pain and nega-
tive clinical findings. In the frustration of pursuing a diagnosis,
the general dentist may note the presence of third molars and
send the patient to the oral and maxillofacial surgeon to either
remove the third molars or rule out the third molars as a cause
of the pain. In this scenario, it is extremely important for the
oral and maxillofacial surgeon to determine if it is likely for
the third molars to in fact be the cause of the dental pain. The
presence of pericoronitis, extensive caries, purulence, and/or
other third molar pathologic condition as the likely cause of
the dental pain is a prerequisite for the removal of the third
molars in this situation. Should the clinician decide to remove
the third molars when these teeth are asymptomatic, in the
presence of dental pain, this situation is likely to significantly
exacerbate the pain since the patient will experience postop-
erative pain from the third molar surgery and additional pain
from the actual source of the pain. It is not uncommon for a
patient to come to the oral and maxillofacial surgeon for a
third molar evaluation and pain, and following a careful history
126 SECTION I ■ Anesthesia and Pain Control
and examination, it is determined that the pain is due to a
TMD. Removal of third molars in this situation will further
exacerbate the symptoms of the TMD and induce further pain
from the surgical procedure. This unfortunate scenario can be
a major factor in setting the patient on a course of chronic
orofacial pain from a severe TMD.
■ TEMPOROMANDIBULAR JOINT
AND MASTICATORY MUSCLE
DISORDERS: CURRENT
CONCEPTS OF DIAGNOSIS
AND MANAGEMENT
TMD represents the major component of chronic orofacial
pain involving the musculoskeletal compartment of the head
and neck region. Although TMD represent a significant
segment of the overall population of patients with chronic
orofacial pain, this patient population requires special atten-
tion by the oral and maxillofacial surgeon. One study has
estimated that approximately 12% of the adult population in
the United States suffers from temporomandibular symptoms
every 6 months.22 The taxonomy of the group of disorders
involving the temporomandibular joint and masticatory
muscles has added further confusion to appropriate diagnosis
and treatment. The term “TMJ” is often inappropriately used
by patients and some health professionals to include the
variety of disorders of the musculoskeletal component of the
head and neck affecting the temporomandibular joint and
surrounding masticatory muscles. Of course the abbreviation
“TMJ” should be avoided and when used, should only refer to
the anatomic structure. The abbreviation “TMD” (temporo-
mandibular disorder) is used to include the vast array of tem-
poromandibular disorders, including those which affect both
the masticatory muscles and the temporomandibular joint.
The abbreviation “MPD” (myofascial pain dysfunction syn-
drome) has been used to describe those disorders that involve
the muscles of mastication and associated fascia, which are
the result of excessive muscle activity causing muscle pain.
For the purposes of this chapter, we will use the term tem-
poromandibular joint disorders to refer to pathologic condi-
tions of the intraarticular structures. The term masticatory
muscle disorders will refer to those conditions in which there
is pain localized to the muscles of mastication. The term
“temporomandibular disorder” will include conditions affect-
ing either the temporomandibular joint, muscles of mastica-
tion, or both.
In the past, many patients suffering from temporomandibu-
lar joint disorders who did not respond to conservative, non-
surgical measures were subject to numerous invasive procedures,
with the belief that the patient had a mechanical problem
inside the joint that could be “fixed.” Over the past 20 years,
research on temporomandibular joint synovial fluids has
provided compelling evidence that patients with the more
common inflammatory/degenerative temporomandibular joint
disorders have alterations in the biochemical composition of
the joint leading to changes in the joint tissues, with resultant
altered joint biomechanics, pain, and dysfunction. Thus, the
oral and maxillofacial surgeon must approach the manage-
ment of these patients with an understanding of the structure
and function of the component tissues, reduce etiologic factors
that alter structure and function, reduce or remove and treat
pathologic tissues, and restore joint and muscle function.
Attempts at solely restoring or reconstructing “normal” joint
and muscle anatomy without addressing the etiologic factors
that lead to altered joint and muscle biomechanics are likely
to fail.
It is extremely important for the oral and maxillofacial
surgeon to be aware of the potential for one or more temporo-
mandibular joint surgeries to be a precursor of centrally medi-
ated neuropathic chronic orofacial pain.20 First, most of these
patients have had pain for a period of more than 6 months,
and for a patient to be a candidate for temporomandibular
joint surgery, most of them have failed multiple nonsurgical
treatments. Thus these individuals have had time for the
localized musculoskeletal pain to cause peripheral and central
sensitization. Additionally, no matter how atraumatic the
surgery is performed, there is tissue damage associated with
any invasive procedure, which can further stimulate periph-
eral and central sensitization of neurons that transmit pain.
This is an additional reason for the surgeon to consider the
least invasive procedure as the surgical procedure of choice.
In general the first surgical procedure has the best chance
of having a successful result. Each invasive procedure follow-
ing this is likely to further exacerbate central mediated pain.
Therefore, multiple temporomandibular joint surgical proce-
dures on the same patient should be avoided in most cases
where there is likely to be an exacerbation of neuropathic
pain. One study from an academic center with a multidisci-
plinary approach to chronic orofacial pain studied 120 con-
secutive patients who were referred to the center for diagnosis
and management.19 Of these patients, 6% (seven patients)
had previously undergone temporomandibular joint surgery.
These seven patients had undergone a total of 26 temporo-
mandibular surgical procedures, an average of 3.7 temporo-
mandibular joint surgeries per patient. Milam20 has concluded
that chronic pain in patients with multiple failed temporo-
mandibular joint operations is primarily due to two factors:
(1) repeated surgical trauma to the region and (2) misdiagno-
sis, with continuation of the previous condition that was
causing the pain and not adequately treated. The pain is often
localized to the preauricular region, and some patients develop
a diffuse regional pain of the head and neck. Many of these
patients develop allodynia, representing peripheral and central
sensitization of neurons, and/or burning, reflecting sympa-
thetic mediated pain.
■ PATHOGENESIS OF COMMON
TEMPOROMANDIBULAR
JOINT DISORDERS
INTERNAL DERANGEMENT THEORY
In the past, internal derangement of the temporomandibular
joint was considered to be central in the pathogenesis of
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon
temporomandibular joint disorders.22 Anterior disk displace-
ment was believed to be an important cause of pain, limita-
tion of motion, and mandibular dysfunction in patients
seeking treatment for their temporomandibular joint condi-
tion. The progression from anterior disk displacement to
osteoarthritis and disk perforation was believed to be inevi-
table, therefore, conservative and surgical treatments were
designed to reposition a displaced disk. Anterior repositioning
splints were used to “recapture” the disk. Temporomandibular
joint arthroplasty was designed to position the posterior band
of the disk over the head of the condyle. Disks that were
deformed or with perforations were often removed and
replaced with a variety of grafts and materials in an attempt
to replace the diseased disk. Acceptance of internal derange-
ment theory led to flawed treatments that were not supported
by valid research. Our current understanding of temporoman-
dibular joint pathogenesis does not support therapeutic
interventions designed to reposition or replace a diseased
disk.23
Today there is overwhelming evidence that internal
derangement is the end result of changes in joint biochemistry
and tissues leading to altered joint biomechanics. Disk dis-
placement by itself without significant symptoms does not
require surgical treatment. The clinician should view disk
displacement as a flaw in joint biomechanics, which has
occurred as a result of joint overloading, which may be ongoing
with associated pain or stable, with the joint being functional
and without pain. Research findings over the past 10 to 15
years, including clinical studies, MRI studies, and synovial
fluid analyses, have provided compelling evidence that inter-
nal derangement theory as a major pathologic entity is
flawed.23-24 This conclusion is based on a variety of clinical
findings, one of which is the high prevalence of disk displace-
ments in individuals without signs or symptoms of a TMD.35,36
Our knowledge of the histology of the temporomandibular
joint disk reveals a structure consisting of fibrocartilage without
a blood supply and lacking any sensory neurons. Studies have
demonstrated that disk repositioning procedures are frequently
associated with a relapse in disk position.26,37 Arthroscopy and
arthrocentesis are treatment modalities that result in signifi-
cant improvement in patient symptoms without changes in
disk position. In the past, it was believed that internal derange-
ment ultimately would lead to degenerative joint disease.
However, a study of degenerative joint disease and disk posi-
tion by Luder38 did not support the conclusion that uncor-
rected disk displacement constitutes a risk for the development
of osteoarthritis. To the contrary, the work of Stegenga et
al.39,40 has supported the concept that abnormal disk position
is the end result of degenerative changes that occur within the
articular tissues. In spite of these research findings, clinicians
often emphasize the importance of disk position without
focusing on the pathologic changes in the tissues that lead to
altered joint biomechanics.
The clinician must ask the following question: Why would
a disk surgically repositioned into the “correct” anatomic loca-
tion relapse into an anterior position? The answer to this
127
question can be found in research findings over the past 15
years. Biochemical changes occur in the tissues in response to
joint overloading and immobilization. These biochemical
changes include elevations in inflammatory mediators26,27,28,41
and proteoglycan degradation products,30,31,42,43 which have
been demonstrated in the synovial fluids of pathologic tem-
poromandibular joints. These biochemical abnormalities
result in morphologic changes in the tissues including synovial
inflammation and cartilage degradation (fibrillation), which
then result in altered biomechanics and impaired joint mobil-
ity. Inflamed synovial tissues result in alterations in the lubri-
cating properties of synovial fluid. Osteoarthritis results in
fibrillation of the articular cartilage, which also impairs the
sliding ability of opposing articular surfaces. Pain from syno-
vial inflammation and impaired biomechanics leads to reduc-
tion in joint mobility. Temporomandibular joint adhesions
have been shown to be directly related to synovial inflamma-
tion.44 Orthopedic studies over the past 30 years by investiga-
tors, such as Salter45 and Akeson46 have shown that joint
immobilization leads to adhesions, impaired cartilage nutri-
tion, and cartilage degradation. Therefore, in patients with
painful limitation of mandibular opening as a result of syno-
vitis and osteoarthritis, there is a cycle of joint overloading
leading to synovitis and osteoarthritis and reduced joint
mobility. This leads to further adhesions, decreases in joint
motion, pain, and more cartilage degradation (Figure 8-7).
With our existing knowledge of how synovial joints work, how
could we expect disk repositioning surgery to reliably alter the
biochemical and biomechanical processes that lead to pain
and dysfunction?
STRUCTURE AND FUNCTION OF SYNOVIAL JOINTS
The temporomandibular joint is a synovial joint that behaves
according to the same biologic principles as other synovial
joints. The articular cartilage lining the condyle, articular
eminence, and disk consists of chondrocytes embedded in a
matrix of fibrocartilage consisting of collagen and proteogly-
cans. The collagen provides structural support, and the pro-
teoglycans are osmotically active, giving the cartilage the
characteristics of elasticity and resiliency. Cartilage that is
loaded deforms at the point of loading as a result of the seepage
of water from the osmotically active proteoglycan molecules.
The loaded cartilage maintains structural integrity because of
the collagen fibers. When the load is removed, water seeps
back into the cartilage as a result of the osmotically active
proteoglycans, and the cartilage resumes its original shape and
contour (Figure 8-8). The loading and sliding functions of the
articular cartilage are dependent on the maintenance of
the collagen and proteoglycan matrix. The chondrocytes are
responsible for producing the collagen and proteoglycan
matrix. Because cartilage has no blood supply, the viability of
the chondrocytes is dependent on nutrition from the synovial
fluid. Therefore joint movement associated with the pumping
action of the synovial fluid is necessary for chondrocyte viabil-
ity and thus the maintenance of an intact articular cartilage
matrix.
128 SECTION I ■ Anesthesia and Pain Control

Joint overloading

Synovial fluid and tissue changes

• ↑ Proteoglycan degradation
• ↑ Inflammatory mediators
• ↓ Lubrication

Osteoarthritis Synovitis

Decreased Joint pain

mobility

Adhesions
FIGURE 8-7. Pathogenesis of temporomandibular
joint synovitis, osteoarthritis, and adhesions.

first is joint overloading, usually through parafunctional mas-

Unloaded cartilage
Collagen
fibrils
Proteoglycans
Subchondral
bone
Loaded cartilage
FIGURE 8-8. Articular cartilage surfaces in unloaded and loaded states.
Proteoglycans are osmotically active, and the collagen fibrils provide structural
support giving the cartilage the characteristics of compressibility and
resiliency.
The synovial membrane lines all surfaces of the joint space
that are not lined by cartilage. The synovial membrane con-
sists of a surface layer of synovial cells and an underlying layer
of loose, vascular connective tissue. The synovium produces
hyaluronate, the main component of synovial fluid, which
functions to lubricate the joint.
MALADAPTIVE CHANGES IN SYNOVIAL JOINTS
There are two major factors that contribute to the loss of
structure and function of the temporomandibular joint. The
ticatory habits, such as clenching or bruxism. Excessive joint
loading can create forces on the cartilage that exceed the
adaptive capacity of this tissue, leading to cartilage degrada-
tion. Furthermore, cartilage degradation products in the syno-
vial fluid will lead to synovitis. The combination of articular
cartilage degradation with irregular cartilaginous surfaces and
altered joint lubrication from synovitis leads to impaired joint
biomechanics and reduced mobility. The altered biomechan-
ics are responsible for joint noises and disk displacement. It is
important for the clinician to understand that the altered disk
position and biomechanics are the end result of biochemical
alterations in the tissues. Therefore, successful management
of temporomandibular joint pathologic conditions must be
based on treatment of the underlying tissue abnormalities.
Gross manipulation of the position of diskal tissues, which is
the aim of disk repositioning surgery, is likely to lead to relapse
of disk position and failure of treatment because it does not
address the tissue abnormalities or etiologic factors that caused
the maladaptive tissue changes.
The second major factor that leads to loss of joint structure
and function is decreased mobility. Because movement is nec-
essary for the diffusion of synovial fluid through cartilage to
provide nutrition of chondrocytes, failure of this movement
leads to chondrocyte dysfunction and death, leading to a
failure of matrix production and a further breakdown of the
articular cartilage. The altered mobility and the pain from
synovial effusion leads to the formation of intraarticular adhe-
sions, which further reduce mobility. These factors ultimately
lead to a self-perpetuating cycle of reduced range of motion,
synovitis, adhesions, and osteoarthritis (Figure 8-9).
Biochemical changes in the tissues lead to osteoarthritis,
synovitis, and adhesions, which are seen by the clinician
arthroscopically and by the pathologist microscopically. These
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon
Mechanical trauma
Biochemical changes in tissues and synovial fluid
Maladaptive tissue responses
Altered joint biomechanics
Reduced motion and pain
FIGURE 8-9. Self-perpetuating cycle of pathologic tissue changes when
the adaptive capacity of the temporomandibular joint tissues is exceeded.
conditions should not necessarily be viewed as totally separate
and independent disease entities. Rather these conditions rep-
resent the end result of changes to the articular tissues (osteo-
arthritis) and synovium (synovitis, adhesions) that have not
been able to adapt to the excessive functional demands placed
on the tissues. Furthermore the altered structure of the tissues
in osteoarthritis, synovitis, and adhesions leads to decreased
functional joint capacity, which leads to a further progression
of the disease process.
It is important to understand that under normal circum-
stances in nonpatient populations, the synovial and cartilagi-
nous tissues have the adaptive capacity to tolerate the
mechanical loads placed on the joint, maintaining tissue
integrity. However, when there is chronic loading of a joint
beyond the adaptive capacity of the tissues, symptoms of joint
pain, limitation of movement, and joint noises will occur.
During the early stages of this process, nonsurgical therapeutic
interventions (designed to reduce joint loading, reduce inflam-
mation, and increase mobility) along with the natural healing
ability of the tissues has the capacity to promote a return to
normal joint structure and function. However, when the etio-
logic factors of excessive joint loading and reduced mobility
continue, over time pathologic conditions develop that are
not reversible with routine conservative therapies, necessitat-
ing surgical intervention. Osteoarthritis, synovitis, and adhe-
sions are dynamic, maladaptive tissue changes that further
contribute to the progression of cartilage degradation, syno-
vial inflammation, and adhesion formation when these condi-
tions are under treated.
■ PRINCIPLES OF NONSURGICAL
MANAGEMENT OF COMMON
TEMPOROMANDIBULAR
JOINT DISORDERS
Patients with symptoms related to pathologic conditions and
dysfunction of the temporomandibular joint are frequently
129
referred to the oral and maxillofacial surgeon for diagnosis and
treatment. The most common symptoms that are associated
with temporomandibular joint disease are intraarticular pain,
limitation of mandibular range of motion, and joint noises
(clicking and/or crepitus). Because these symptoms are non-
specific, they can reflect common temporomandibular joint
pathologic conditions, such as synovitis, adhesions, and osteo-
arthritis, or they may reflect more serious conditions, such as
neoplasia (osteochondroma, chondrosarcoma), fibrous and/or
bony ankylosis, or systemic conditions (rheumatoid arthritis,
psoriatic arthritis). The first and most important principle of
patient management is the establishment of accurate diagno-
ses upon which appropriate treatment is based. Furthermore
the principles of treatment are also based on a thorough
understanding of the pathogenesis of the disease process.
The oral and maxillofacial surgeon must be aware of the
roles of nonsurgical therapies and surgery in the management
of the more common disorders of the temporomandibular
joint. The main focus here is an understanding of the patho-
genesis of the disease process leading to principles of treat-
ment and therapeutic interventions. Nonsurgical therapeutic
interventions are a necessary part of the treatment of common
temporomandibular joint conditions and represent the initial
management intervention by the clinician. A trial period of
nonsurgical therapy is necessary for the surgeon to assess the
severity of the pathologic condition that is present. For
patients who respond to nonsurgical therapies with improved
mandibular function and reduced pain, further progression to
more invasive therapies are often unnecessary. When patients
do not respond adequately to nonsurgical therapies, this is a
reflection of the magnitude of an intraarticular pathologic
condition present, which has entered a phase that is not
reversible with conservative therapy. The preoperative period
of nonsurgical therapy and the patient’s response or lack of
response to this therapy provides important information to the
clinician as to the severity of the pathologic condition that is
present. Furthermore the preoperative period of nonsurgical
therapy that has failed to improve the patient’s symptoms
provides the surgeon with improved patient selection leading
to better surgical outcomes. Evaluation of the patient’s
compliance with preoperative nonsurgical regimens provides
the surgeon with valuable information on how compliant
the patient will be with the postoperative rehabilitation
regimen.
Based on our understanding of the pathogenesis of the
more common temporomandibular joint disorders (synovitis,
osteoarthritis, adhesions), the principles of nonsurgical and
surgical management can be established. The following con-
cepts are essential in the nonsurgical treatment of patients:
REDUCTION OF JOINT LOADING
Because joint overload leads to cartilage degradation, the cli-
nician must be aware of parafunctional masticatory activities
and control their deleterious effects. Furthermore, a synovial
joint that is undergoing osteoarthritic and inflammatory
changes requires a reduction in joint loading to give the tissues
130 SECTION I ■ Anesthesia and Pain Control
a chance to recover and repair. A soft nonchew diet for a
specified period of time is necessary. Unfortunately, many
patients will adhere to this regimen for too short a period of
time, and as soon as the symptoms subside, they immediately
return to a diet that their joint tissues cannot tolerate, con-
tributing to a relapse of symptoms.
Education of patients on the deleterious effects of clench-
ing and making them aware of episodes where their teeth
come together during times of stress are important. It is
common for individuals to spend hours in front of the com-
puter, studying for examinations, or enduring job stress with
an unawareness of their teeth in a clenched position. Simply
making patients aware of times when they are susceptible to
clenching will often help them reduce this deleterious habit.
Occlusal splint appliances that distribute the forces equally
between the maxillary and mandibular teeth can be used at
night to reduce the deleterious effects of clenching and
bruxism. These appliances can also be used during the daytime
hours, usually in nonsocial settings, to help reduce joint load
overloading. The clinician must carefully evaluate the patient’s
response to these appliances since there are some individuals
who tend to clench more when there is an appliance in their
mouth.
MAXIMIZE JOINT MOBILITY
Orthopedic research has clearly demonstrated the deleterious
effects of joint immobilization. All too often, clinicians will
empirically inform patients to reduce their joint movement.
However, joint immobilization will reduce the movement of
synovial fluid and impair nutrition of chondrocytes, leading
to cartilage degradation. Immobilization will also lead to joint
adhesions if accompanied by synovitis, leading to further
decreases in joint range of motion. Passive motion exercises
are an important part of synovial joint rehabilitation. Passive
motion entails joint movement that does not involve the use
of the muscle groups that normally move the joint. Active
motion exercises of the jaw, which involves activation of the
muscles of mastication, has the potential to further aggravate
existing muscle spasm and myalgia.
There are several ways of achieving passive motion of the
temporomandibular joint. Physical therapy has the great
advantage of providing the patient with passive motion
manipulations by a professional who has years of training in
musculoskeletal physiology. Most patients undergo physical
therapy two to three times weekly and undergo passive stretch-
ing and education in passive motion exercises. Unfortunately,
some patients forget about the importance of the home exer-
cises, only to forgo them with the misunderstanding that this
is the function of the physical therapy sessions. Home passive
motion exercises can be achieved with a variety of devices
designed to move the mandible by squeezing the device by
hand. Fingers can be used to passively stretch the jaw open as
well. The thumb of one hand can be placed on the palate, and
the index finger of the other hand can be hooked over the
lower anterior teeth, with gentle stretching of the mandible
to the maximal opening position and holding it in that
position for several seconds. I generally instruct patients to
perform these exercises for 5 minutes 3 to 4 times daily, fol-
lowing massage or moist heat applications. Frequent moist
heat applications, massage, and ice applications are important
adjuncts to passive motion exercises and help to reduce mas-
ticatory muscle spasm and myalgia. A great advantage of home
passive motion exercises by the patient is that their own pro-
prioception can be used to achieve the maximal stretch
without creating significant pain.
REDUCTION OF INFLAMMATION AND PAIN
Inflammation of synovial tissues must be controlled for the
temporomandibular joint to recover normal joint function. If
the patient attempts to function on inflamed synovial tissues,
this will stimulate more inflammation. Furthermore, the pain
associated with synovial inflammation will result in a further
decrease of joint motion and help to exacerbate cartilage
breakdown and joint adhesions. Inflammation and pain can
be managed with NSAIDs, such as ibuprofen and naproxen.
However, it is common for patients to fail to use these medica-
tions properly. Many patients try over-the-counter NSAIDs
as needed for pain. However, once the pain subsides, they stop
using the medication, attempt to function by resuming their
normal diet, followed by a reoccurrence of the symptoms as a
result of persistent joint inflammation. For NSAIDs to be
effective, they must be taken for a course of 7 to 14 days, in
conjunction with joint unloading, to attempt to reduce syno-
vial inflammation. If this course of treatment fails to signifi-
cantly reduce the symptoms, it is an indication that the
synovial inflammation is unlikely to be reversible with stan-
dard nonsurgical treatment. Some patients will benefit from a
short course of steroid medications; however, these should be
used sparingly and with caution because of the potential for
significant side effects.
Pain management is a very important part of the overall
management of patients with temporomandibular joint disor-
ders. Failure to control pain levels, along with chronic tissue
injury, has the potential to lead to central sensitization of
ascending nerve pathways that transmit pain, leading to
chronic neuropathic pain. This leads to symptoms of allo-
dynia, in which nonnoxious stimuli, such as light touch, acti-
vate pain pathways leading to the cerebral cortex. An
important goal in the management of these patients is to
prevent the onset of chronic central neuropathic pain so that
local treatment of the diseased joint reverses the patient’s
symptoms. With the onset of chronic neuropathic pain, local
treatment of the diseased joint and a reduction in the activity
of the central pain pathways is needed. However, successful
management of the patient who has developed chronic neu-
ropathic pain is much more difficult because multiple surgical
procedures and repeated trauma to tissues tend to exacerbate
central sensitization of ascending pain pathways.6-20 Local
anesthetic blocks that reduce pain may be helpful in the
management of chronic neuropathic pain, and medications
(anticonvulsants, such as gabapentin) that reduce activity of
nerve pathways have demonstrated some effectiveness in the
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon
management of chronic neuropathic pain. Acupuncture is
also an extremely valuable adjunct in the management of
pain.
Narcotic analgesics generally are not effective in the man-
agement of temporomandibular joint pain because the pain
relief is often brief, followed by a rebound of more severe joint
pain. Narcotic analgesics do play an important role in man-
agement of pain in the early postoperative period for patients
who undergo surgery.
RECOGNIZE AND TREAT MASTICATORY
MUSCLE DISORDERS
It is important for the clinician to evaluate the relative impact
of masticatory muscle disorders on the degree of orofacial pain.
Masticatory muscle spasm is common in patients with orofa-
cial pain and represents a natural response to immobilize
injured tissues. Patients who have severe pain from intraar-
ticular temporomandibular joint pathologic conditions will
often have significant masticatory muscle spasm and myalgia
(muscle pain). Because joint overload from parafunctional
masticatory activity is a common factor leading to joint patho-
logic conditions, it is often difficult for the clinician to
determine whether the main pathologic condition is intraar-
ticular, with secondary masticatory muscle spasm, or the main
pathologic condition is masticatory muscle spasm and myalgia,
with secondary joint inflammation.
Although there are patients who clearly have primary joint
or muscle pathologic conditions, these individuals are rela-
tively rare. Most patients have both muscle and joint compo-
nents that contribute significantly to their orofacial pain. In
this scenario, when the clinician is unsure of the relative
contributions of joint and muscle pathologic conditions to the
overall pain condition, it is helpful to treat the muscle com-
ponent of the pain with muscle relaxants and muscle trigger
injections to address the masticatory myalgia component of
the pain. If the myalgia component improves with persistent
intraarticular pain, then the clinical picture becomes clearer,
with the focus being shifted to treating an intraarticular
pathologic condition. Unfortunately, there are many patients
in whom the intraarticular pathologic condition and myalgia
components are so severe that it is difficult if not impossible
to determine the relative contributions of each to the overall
orofacial pain condition. These patients are quite challenging
and often require prolonged treatment to manage both the
masticatory myalgia and the intraarticular pathologic
condition.
IMPROVE SLEEP
Getting adequate, uninterrupted sleep is very important in the
management of patients suffering from TMD. Sleep is neces-
sary for joints and muscles to undergo a period of physiologic
rest, recovery, and repair. Individuals who have difficulty
falling asleep or who have interrupted sleep are much less
likely to have the ability to reduce joint loading and permit
the natural process of joint repair. Additionally, the increased
muscle activity without a period of physiologic rest makes
131
individuals more prone to masticatory myospasm and
myalgia.
The clinician should consider prescribing a muscle relaxant
before bedtime to assist in sleep and reduce muscle activity.
Benzodiazepines at a dose that is adequate to promote sleep is
often very beneficial in the management of these patients.
Because most muscle relaxants cause some degree of sedation,
these are usually avoided during the daytime hours.
■ PRINCIPLES OF SURGICAL
MANAGEMENT OF
TEMPOROMANDIBULAR
JOINT DISORDERS
The indications for performing temporomandibular joint
surgery in this patient population are as follows:
1. The patient has severe pain and/or mandibular
dysfunction.
2. The cause of the pain and/or mandibular dysfunction is
due to a diagnosis consistent with significant intrarticu-
lar pathologic condition (usually synovitis, osteoarthri-
tis, adhesions).
3. A full course of appropriate nonsurgical therapy has
failed to improve the patient’s symptoms.
It is important for the clinician to understand that for surgi-
cal management to be successful there must be a significant
temporomandibular joint pathologic condition. Additionally,
surgical management must be considered an adjunct to a com-
prehensive treatment regimen designed to decrease adverse
joint loading, restore range of motion, reduce inflammation,
and decrease pain. Surgical management of temporomandibu-
lar joint pathologic conditions should be designed to maxi-
mize the restoration of structure and function of the joint.
Temporomandibular joint surgery does not necessarily reduce
pain (unless the sensory innervation to the joint is disrupted),
but is designed to restore joint structure and function, and
patients must understand that the postoperative period requires
significant rehabilitation. Thus, a thorough regimen of con-
tinued nonsurgical management techniques must be contin-
ued in the postoperative period. With proper patient selection,
appropriate surgery and postoperative compliance with passive
motion exercises, medications, and reduction of joint loads,
most patients will ultimately have significant reduction in
pain levels and improvement in mandibular functioning.
The principles of surgical management are as follows:
1. Perform the least invasive procedure with the highest
benefit to risk ratio. The more aggressive the surgical
approach, the greater chance there is for tissue injury
and scar tissue formation. Dissection through the layers
of tissue that lead to the joint and invasion of the joint
capsule will cause scar tissue formation, which may
offset some of the benefits of the surgical manipulation
of tissues with open joint surgery.
2. Surgical procedures should be designed to remove and/
or treat the pathologic tissue that is present. Therefore,
intraarticular adhesions and pathologic osteoarthritic
fibrillation tissue should be removed.
132 SECTION I ■ Anesthesia and Pain Control
3. Surgical procedures should assist in the reduction of
synovial inflammation. Open joint procedures, which
involve extensive synovectomy, can be deleterious
because this may increase scar tissue formation and
reduce the lubricating capacity of the joint. Arthroscopic
surgery enables the surgeon to isolate the areas of syno-
vitis and inject a high concentration antiinflammatory
medication under direct vision into the most inflamed
synovial tissues.
4. Surgical procedures should result in maximal preserva-
tion of the synovium, articular cartilage, and disk.
Because there is no compelling evidence to demonstrate
that removal of a disk with a perforation yields a better
outcome than preserving the disk with a perforation, the
clinician may prefer to perform arthroscopic shaving of
the osteoarthritic tissue around a perforation, rather
than removing the disk. This permits the disk to con-
tinue to function as a three-dimensional space filler
between the convex surfaces of the articular eminence
and condyle, similar to the knee meniscus.
5. All operative procedures, whether performed under
general anesthesia, conscious sedation, or local anesthe-
sia, should be accompanied by the administration of
local anesthesia to the surgical site. This will prevent
barrages of noxious stimuli transmitted by peripheral
sensory nerves from reaching the central nervous
system.
The surgical options that are available to treat the more
common temporomandibular joint disorders include arthro-
centesis, arthroscopy, and arthrotomy. For patients who
have a joint space and have a clinical diagnosis of synovitis,
osteoarthritis and/or adhesions, arthrocentesis and arthros-
copy are the least invasive surgical options. Arthrocentesis
has the advantage of being easily performed in the office
setting and is generally more effective when the history of
onset of symptoms are relatively short, usually less than 3
months. Joint lavage has the highest chance of success if
there are no mature joint adhesions. A disadvantage of
arthrocentesis is that the actual pathologic condition cannot
be visualized, and the clinician is not able to obtain a tissue
sample for histopathologic examination. Furthermore, if
mature adhesions are present, the chance for a successful
reduction in symptoms is decreased.
Arthroscopic temporomandibular joint surgery has the
advantage of being minimally invasive and associated with a
rapid recovery compared with open joint surgery. The proce-
dure is performed in an ambulatory setting, permitting the
patient to recover at home on the same day of the surgery.
Arthroscopic temporomandibular joint surgery is a technique
for getting into the joint space, and there is significant varia-
tion in how oral and maxillofacial surgeons treat patients
arthroscopically once they have access to the intraarticular
tissues. Once diagnostic arthroscopy has been completed, the
areas of abnormality can be identified. A second portal of
entry enables the surgeon to perform operative procedures
under direct vision with the arthroscope being present in one
portal and the entry of surgical instruments in the second
portal. Operative arthroscopic surgery is designed to treat the
pathologic condition that is present with maximal preserva-
tion of intraarticular tissues. Adhesions are released with
miniblades and removed with alligator forceps or motorized
shaving instruments. Osteoarthritic fibrillation tissue is
removed with forceps and/or motorized shaving instruments
as well. The removal of tissue specimens enables the surgeon
to obtain histopathologic confirmation of the correct diagno-
sis. Synovitis is treated by directly isolating the most inflamed
tissue and injection of a high concentration of steroid medica-
tion in the subsynovial tissues under direct vision. Anteriorly
displaced disks are mobilized to improve translation in the
superior joint space. Although there are some arthroscopic
surgeons who stabilize the disk in a posterior position through
a variety of techniques, it is this author’s opinion that this is
not necessary or indicated because there are many asymptom-
atic individuals with anterior disk position.
Open joint surgery, which formerly was the mainstay of
surgical treatment of the patient with intraarticular abnor-
malities, still has a place in the armamentarium of the oral
and maxillofacial surgeon for the treatment of intraarticular
temporomandibular joint pathologic conditions. Because less
invasive procedures, such as arthrocentesis and arthroscopy,
have a proven record of success in treating painful intraarticu-
lar abnormalities, these modalities should be considered first.
However, when the joint space is obliterated by fibrous and/or
bony ankylosis, arthrotomy is the surgical treatment of choice.
Conditions, such as neoplasia (osteochondroma), synovial
chondromatosis, and pigmented villonodular synovitis, require
open joint surgical procedures to remove the abnormality and
restore joint function. There are numerous methods of recon-
structing temporomandibular joints including autogenous
reconstruction, distraction osteogenesis, and alloplastic tem-
poromandibular joint reconstruction. Each clinician must
decide on the technique of choice; however, there is currently
no consensus on the best alternative of the ideal temporoman-
dibular joint reconstruction technique. In spite of this, the
principles of nonsurgical and surgical management still apply
to patients with more severe pathologic conditions requiring
more invasive surgical treatments.
Some clinicians still prefer to perform diskoplasty as the
primary treatment for persistent symptomatic internal derange-
ment. These patients often experience improvement in their
pain symptoms for 9 to 12 months during the period of dener-
vation of the joint. However, with eventual recovery of the
sensory branches of the auriculotemporal nerve, the symptoms
of pain may reoccur. Because open joint surgery involves dis-
section through the subcutaneous fascia, parotideomasseteric
fascia and joint capsule, the clinician must be cognizant of the
additional scar tissue formation with these procedures, and
passive mobilization is especially important in the postopera-
tive period. For these cases to be successful, it is extremely
important for the clinician to control those etiologic factors
that led to the intraarticular pathologic condition initially.
Therefore reduction of joint overloading, masticatory muscle
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon
activity, and joint inflammation are particularly important for
those patients who have undergone arthrotomy for internal
derangement.
SURGICAL OUTCOMES
Studies reporting the outcomes of surgical treatment of tem-
poromandibular joint disorders are fairly consistent, with
success rates of 76% to 84%. Randomized controlled studies
in this patient population are relatively impractical because
most patients come to the oral and maxillofacial surgeon with
a long history of failed nonsurgical treatments. Those patients
who have been referred for a surgical evaluation are focused
on treatments designed to relieve their symptoms, and these
individuals are unlikely to submit to randomized treatments.
Therefore the published literature forces us to rely on reported
case series to evaluate the outcomes of surgical treatment of
temporomandibular joint disorders.
One study47 compared clinical outcomes of arthroscopic
lysis and lavage with arthroplasty with disk repositioning. The
investigators reported on the results of arthroscopy on 47
patients (63 temporomandibular joints) and 59 patients (79
temporomandibular joints). Successful reduction in pain and
increased interincisal opening occurred in 79% of arthroscopy
patients and 76% of arthroplasty patients. The complication
rate was 8% for arthroscopy patients and 12% for arthroplasty
patients with all complications resolving, except for one
arthroplasty patient with persistent facial nerve paresis.
Arthrocentesis is the least invasive of the surgical modali-
ties in the treatment of temporomandibular joint disorders.
This modality has emerged as an excellent therapeutic inter-
vention in patients with the recent onset of painful limitation
of opening and associated anterior disk displacement without
reduction. Nitzan et al.48 have reported on the clinical out-
comes in 39 patients who underwent arthrocentesis of 40
temporomandibular joints. The mean follow-up period was
16.6 months, and the mean increase in maximum interincisal
opening distance was 21 mm with significant reduction in
pain levels. Fridrich et al.49 compared the results of arthrocen-
tesis and arthroscopy in a prospective study of 19 patients with
internal derangement. They reported an 82% success rate for
the arthroscopy group and 75% success rate in the arthrocen-
tesis group. Success was based on improvement in maximum
interincisal opening distance and subjective reduction in pain
levels.
More than 20 years of experience with the outcomes of
temporomandibular joint arthroscopy has demonstrated a sig-
nificant reduction in pain, improved interincisal opening dis-
tance, and improved mandibular function without any change
in disk position. Although ideal randomized controlled clini-
cal studies evaluating the outcomes of arthroscopy with other
treatments do not exist, case series reports from different
investigators have yielded remarkably consistent results. A
compilation of 11 studies on the outcomes of arthroscopic
surgery have demonstrated a mean success rate of 84%, with
a mean reduction in pain levels on the visual analog scale of
4.6 after arthroscopy (mean follow-up 17.1 months) and a
133
mean increase in interincisal opening distance of 10.4 mm.49-59
These results are consistent with other published results on
the outcomes of temporomandibular joint arthroscopy.
POSTOPERATIVE REHABILITATION
Once surgery has been performed, the importance of the post-
operative rehabilitation regimen cannot be overemphasized.
Nonsurgical therapies designed to restore mandibular range
of motion, prevent the formation of adhesions, reduce inflam-
mation, and reduce the etiologic factors, such as joint over-
loading, are essential for surgical success. Therefore, a major
point of information to the clinician is that nonsurgical and
surgical therapy of temporomandibular joint disorders are not
mutually exclusive. Nonsurgical therapy is an essential com-
ponent of treatment of these patients and when less serious
temporomandibular joint abnormality is present may be the
sole treatment for the patient. However, nonsurgical thera-
pies are also an integral part of surgical treatment and are
necessary in the preoperative and postoperative periods in
the surgical management of patients with temporomandibular
joint disorders.
Postoperative rehabilitation of the patient undergoing
arthroscopic surgery is essential, using the principles of non-
surgical management that were performed in the preoperative
period. If a patient has been noncompliant with nonsurgical
management in the preoperative period, it is less likely for
there to be successful compliance with the important postop-
erative rehabilitation regimen. Although the regimen for each
patient is different, based on their postoperative clinical
course, the following are the general guidelines that are used.
The patient is placed on a nonchew diet for approximately 3
weeks to prevent loading of intraarticular tissues. This joint
unloading is necessary to permit the tissues to recover because
early function and joint overload will precipitate the same
factors that caused the initial pathologic condition. If the
patient is minimally symptomatic by postoperative week 3, a
gradual progression of the diet is permitted, as long as there is
no exacerbation of pain or dysfunction. If pain occurs during
chewing, the patient is instructed to continue on the nonchew
diet for an additional week, until the loads of mastication on
the temporomandibular joint are tolerated. Passive motion
exercises are essential in the postoperative period. Passive
finger stretching exercises of the mandible to a level of opening
that meets mild resistance without precipitating significant
pain is recommended. These exercises are performed 4 to 6
times daily for 5 to 10 minutes, are preceded by moist heat or
massage, and followed by ice or massage. The passive motion
exercises are necessary to prevent the formation of new adhe-
sions and increase mandibular range of motion. Physical
therapy may be prescribed, particularly if the patient tends to
be noncompliant with the exercises or if the patient’s interin-
cisal opening distance is not increasing as expected. Pain
management rarely requires more than a few days of narcotic
analgesics, which are prescribed. NSAIDs amd muscle relax-
ants (bedtime only) are frequently prescribed. Additional
pain management techniques, such as acupuncture, are also
134 SECTION I ■ Anesthesia and Pain Control
important in the postoperative period. As the patient pro-
gresses into the later postoperative period (4 to 12 weeks),
the exercises are usually gradually reduced to 2 to 3 times
daily, and the medications are used as needed. If there is a
flare-up of symptoms within the first year, the patient is
instructed to immediately go on a 7- to 14-day course of non-
steroidal antiinflammatory and muscle relaxant medications, a
nonchew diet, and regular passive motion exercises 4 to 6 times
daily. The patient’s immediate compliance with this early post-
operative rehabilitation regimen at the onset of the reoccur-
rence of symptoms will frequently abort a flare-up of synovitis
and result in a return to normal mandibular function.
Patients who do not improve following temporomandibular
joint surgery generally fall into two categories. The first group
of surgical failures are those patients in whom there is a mis-
diagnosis and there is minimal intraarticular abnormality. If
the patient underwent arthroscopy, the synovitis tends to be
at a low level, there are few adhesions, and the articular car-
tilage appears normal. These patients have pain that is primar-
ily from the muscles of mastication with secondary and/or
referred joint pain. They tend to have severe masticatory
parafunctional habits that persist in spite of appropriate non-
surgical measures. The second group of patients who are more
likely to fail to improve with temporomandibular joint surgery
are those with a long history of chronic pain associated with
a central neuropathic component. These individuals tend to
have allodynia, with pain associated to a light touch of the
skin in the temporomandibular joint region. They often have
a history of multiple failed temporomandibular joint treat-
ments, and may have had a history of multiple joint surgeries.
It is extremely important for the surgeon to be aware that with
each surgical procedure performed on the temporomandibular
joint there is the potential to increase scar tissue, reduce
mobility, and add more tissue trauma, resulting in central
neuropathic pain.
SUMMARY
The oral and maxillofacial surgeon has a critical position in
the management of patients with chronic orofacial pain.
Regardless of whether the clinician is actively treating the
chronic pain patient or prefers to refer these individuals to
other specialists, it is essential for the oral and maxillofacial
surgeon to have a thorough knowledge of the pathophysiology
of chronic pain. Multiple invasive procedures that are unsuc-
cessful can transform a patient with acute pain to one with
chronic orofacial pain, therefore, the oral and maxillofacial
surgeon is in a key position to prevent this progression. Some
of the key principles described in this chapter include avoid-
ance of multiple invasive procedures, provide treatment based
on the establishment of an accurate diagnosis, and treatment
of both peripheral and central components chronic pain. By
following these principles, the oral and maxillofacial surgeon
will play an important role in reducing the population of
patients who progress to chronic pain and provide successful
management of those individuals who suffer from chronic
complex orofacial pain conditions.
REFERENCES
1. Svensson P et al.: Overview on tools and methods to assess
neuropathic trigeminal pain, J Orofac Pain 18(4):332-338, 2004.
2. Kreiner M et al.: Craniofacial pain as the sole symptom of cardiac
ischemia: a prospective multicenter study, J Am Dent Assoc
138(1):74-79, 2007.
3. Swift JQ, Roszkowski MT: The use of opioid drugs in manage-
ment of chronic orofacial pain, J Oral Maxillofac Surg 56(9):1081-
1085, 1998.
4. John MT, Reissman DR, Schierz O: Oral health-related quality
of life in patients with temporomandibular disorders, J Orofac
Pain 21(1):46-54, 2007.
5. Feinmann C, Newton-John T: Psychiatric and psychological
management considerations associated with nerve damage and
neuropathic trigeminal pain, J Orofac Pain 18(4):360-365,
2004.
6. Robinson PP et al.: Peripheral mechanisms for the initiation of
pain following trigeminal nerve injury, J Orofac Pain 18(4):287-
292, 2004.
7. Dubner R, Ren K: Brainstem mechanisms of persistent pain
following injury, J Orofac Pain 18(4):299-305, 2004.
8. Salter M: Cellular neuroplasticity mechanisms mediating pain
persistence, J Orofac Pain 18(4):318-324, 2004.
9. Bennett GJ: Neuropathic pain in the orofacial region: clinical
and research challenges, J Orofac Pain 18(4):281-286, 2004.
10. Marbach JJ et al.: Incidence of phantom tooth pain: an atypical
facial neuralgia, Oral Surg Oral Med Oral Pathol 53:190-193,
1982.
11. Jacobs R et al.: Appearance of painful or non-painful phantom
tooth after tooth extraction, J Dent Res 77:1008, 1998.
12. Plesh O et al.: The relationship between chronic facial pain and
a history of trauma and surgery, Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 88(1):16-21, 1999.
13. Allerbring M, Haegerstam G: Invasive dental treatment, pain
reports and disease conviction in chronic facial pain patients. A
retrospective study, Acta Odontol Scand 53(1):1995.
14. Vickers ER, Cousins MJ: Neuropathic orofacial pain. Part 2-
diagnostic procedures, treatment guidelines and case reports,
Aust Endod J 26(2):53-63, 2000.
15. Wolf E et al.: Long-lasting orofacial pain-a study of 109 consecu-
tive patients referred to a pain group, Swed Dent J 25(3):129-136,
2001.
16. Hampf G: Dilemma in treatment of patients suffering from oro-
facial dysaesthesia, Int J Oral Maxillofac Surg 16(4):397-401,
1987.
17. Truelove E: Management issues of neuropathic trigeminal pain
from a dental perspective, J Orofac Pain 18(4):374-380, 2004.
18. Benoliel R et al.: Diagnosis and treatment of persistent pain after
trauma to the head and neck, J Oral Maxillofac Surg 52(11):1138-
1147, 1994.
19. Israel H et al.: Oral and maxillofacial surgery in patients with
chronic orofacial pain, J Oral Maxillofac Surg 61:662-667,
2003.
20. Milam SB: Failed implants and multiple operations, Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 83:156, 1997.
21. Huang GJ: Third molar extraction as a risk factor for temporo-
mandibular disorder, J Am Dent Assoc 137(11):1547-1554,
2006.
22. Lipton JA, Ship JA, Larach-Robinson D: Estimated prevalence
and distribution of reported orofacial pain in the United States,
J Am Dent Assoc 124:115-121, 1993. McCarty WL, Farrar WB:
Surgery for internal derangements of the temporomandibular
joint, J Prosthet Dent 42(2):191-196, 1979.
23. Dolwick MF: Intra-articular disc displacement part I: its
questionable role in temporomandibular joint pathology, J
Oral Maxillofac Surg 53:1069-1072, 1995. Katzberg RW et al.:
 CHAPTER 8 • The Essential Role of the Oral and Maxillofacial Surgeon
Anatomic disorders of the temporomandibular joint disc in
asymptomatic subjects, J Oral Maxillofac Surg 54:147-153,
1996.
24. Moore JB: Coronal and sagittal TMJ meniscus position in asymp-
tomatic subjects by MRI, J Oral Maxillofac Surg 47:75, 1989
(abstract).
25. Kircos LT et al.: Magnetic resonance imaging of the TMJ disc
in asymptomatic volunteers, J Oral Maxillofac Surg 45:852,
1987.
26. Trumpy IG, Lyberg T: Surgical treatment of internal derange-
ment of the temporomandibular joint: long-term evaluation of
three techniques, J Oral Maxillofac Surg 53:746-747, 1995.
27. Quinn JH, Bazan NG: Identification of prostaglandin E2 and
leukotriene B4 in the synovial fluid of painful, dysfunctional
temporomandibular joints, J Oral Maxillofac Surg 48:968, 1990.
28. Shafer DM: Tumor necrosis factor alpha as a biochemical marker
of pain and outcome in temporomandibular joints with internal
derangements, J Oral Maxillofac Surg 52:786, 1994.
29. Kopp S: Neuroendocrine, immune and local responses related to
temporomandibular disorders, J Orofac Pain 15:9, 2001.
30. Ratcliffe A, Israel HA: Proteoglycan components of articular
cartilage in synovial fluids as potential markers of osteoarthritis
of the temporomandibular joint. In Sessle BJ, Bryant PS, Dionne
RA, editors: Temporomandibular disorders and related pain condi-
tions, progress in pain research and management, Vol 4, Seattle,
IASP Press.
31. Israel H et al.: Correlation between arthroscopic diagnosis of
osteoarthritis and synovitis of the human temporomandibular
joint and keratan sulfate levels in the synovial fluid, J Oral Maxil-
lofac Surg 55:210, 1997.
32. Kubota E et al.: Interleukin 1 beta and stromelysin (mmp 3)
activity of synovial fluid as possible markers of osteoarthritis in
the temporomandibular joint, J Oral Maxillofac Surg 55:20,
1997.
33. Kubota E et al.: Synovial fluid cytokines and proteinases as
markers of temporomandibular joint disease, J Oral Maxillofac
Surg 56:192, 1998.
34. Israel H et al.: Osteoarthritis and synovitis as major pathoses of
the temporomandibular joint: comparison of clinical diagnosis
and arthroscopic morphology, J Oral Maxillofac Surg 56:1023-
1028, 1998.
35. Orbach S: Meniscal disorders, NY State Dent J 62:24-31, 1996.
36. Romanelli GG et al.: Evaluation of temporomandibular joint
internal derangement, J Orofac Pain 7:254-262, 1993.
37. Stegenga B: Osteoarthritis of the temporomandibular joint organ
and its relationship to disc displacement, J Orofac Pain 15:193-
205, 2001.
38. Luder HU: Articular degeneration and remodeling in human
temporomandibular joints with normal and abnormal disc posi-
tion, J Orofac Pain 7:391-402, 1993.
39. Stegenga B, DeBont LGM, Boering G: Osteoarthrosis as the
cause of craniomandibular pain and dysfunction: A unifying
concept, J Oral Maxillofac Surg 47:249-256, 1989.
40. Stegenga B et al.: Tissue responses to degenerative changes in
the temporomandibular joint: a review, J Oral Maxillofac Surg
49:1079-1088, 1991.
41. Chang H, Israel H: Analysis of inflammatory mediators in TMJ
synovial fluid lavage samples in symptomatic patients and
asymptomatic controls, J Oral Maxillofacial Surg 63:761-765,
2005.
135
42. Shibata T et al.: Glycosaminoglycan components in temporo-
mandibular joint synovial fluid as markers of joint pathology, J
Oral Maxillofac Surg 56:209, 1998.
43. Israel H, Saed-Nejad F, Ratcliffe A: Early diagnosis of osteoar-
throsis of the temporomandibular joint: correlation between
arthroscopic diagnosis and keratan sulfate levels in the synovial
fluid, J Oral Maxillofac Surg 49:708-711, 1991.
44. Israel H, Langevin CJ, Singer M: The relationship between tem-
poromandibular joint synovitis and adhesions: pathogenic mech-
anisms and clinical implications for surgical management, J Oral
Maxillofac Surg 64:1066-1074, 2006.
45. Salter RB: The biologic concept of continuous passive motion
of synovial joints. The first 18 years of basic research and is
clinical application, Clin Orthop 242:12, 1989.
46. Akeson WH et al.: Effects of immobilization on joints, Clin
Orthop 219:28, 1987.
47. Zeitler D, Porter B: A retrospective study comparing arthroscopic
surgery with arthrotomy and disc repositioning. In Clark G,
Sanders B, Bertolame C, editors: Advances in diagnostic and surgi-
cal arthroscopy of the temporomandibular joint, Philadelphia, 1993,
PA Saunders.
48. Nitzan D, Dolwick FM, Heft M: Arthroscopic lavage and lysis
of the temporomandibular joint: a change in perspective, J Oral
Maxillofac Surg 48:798, 1990.
49. Fridrich KL, Wise JM, Zeitler DL: Prospective comparison of
arthroscopy and arthrocentesis for temporomandibular joint dis-
orders, J Oral Maxillofac Surg 54:816, 1996.
50. Sanders, Buoncristiani: Diagnostic and surgical arthroscopy of
the temporomandibular joint: clinical experience with 136 pro-
cedures over a 2-year period, J Craniomand Dis 1:202, 1987.
51. Moses JJ, Poker ID: TMJ arthroscopic surgery: an analysis of 237
patients, J Oral Maxillofac Surg 47:790, 1989.
52. Indresano AT: Arthroscopic surgery of the temporomandibular
joint: report of 64 patients with long-term follow-up, J Oral
Maxillofac Surg 47:439, 1989.
53. Israel H, Roser SM: Patient response to temporomandibular
joint arthroscopy: preliminary findings in 24 patients, J Oral
Maxillofac Surg 47:570, 1989.
54. Montgomery MT et al.: Arthroscopic TMJ surgery: effects on
signs, symptoms and disc position, J Oral Maxillofac Surg 47:1263,
1989.
55. McCain JP et al.: Temporomandibular joint arthroscopy: a 6-
year multicenter retrospective study of 4,831 joints, J Oral Maxil-
lofac Surg 50:926, 1992.
56. Hoffman DC, Cubillos L: The effect of arthroscopic surgery on
mandibular range of motion, J Craniomand Pract 12(1):11,
1994.
57. Murakami K et al.: Short-term outcome study for the manage-
ment of temporomandibular joint closed lock, Oral Surg Oral
Med Oral Pathol 80:253, 1995.
58. Murakami K et al.: Four-year follow-up study of temporoman-
dibular joint arthroscopic surgery for advanced internal derange-
ments, J Oral Maxillofac Surg 54:285, 1996.
59. Chossegros C et al.: Clinical results of therapeutic temporoman-
dibular joint arthroscopy: a prospective study of 34 arthroscopies
with prediscal section and retrodiscal coagulation, Br J Oral
Maxillofac Surg 34:504, 1996.
CHAPTER 9
CHRONIC MAXILLOMANDIBULAR,
HEAD AND NECK PAIN
Note: For further discussion, please see Volume II, Chapter 52 Chronic Facial Pain: Evaluation, Differential Diagnosis and
Management Strategies by James Swift.

The oral and maxillofacial surgeon is often challenged by the
patient with chronic head and neck pain. By its nature, surgery
is oriented toward short-term problem solving for patients
whose needs are primarily surgical. Since the 1970s, however,
it has become clear that there are major differences in the
pathophysiology and psychology of acute versus chronic pain
and that the surgeon can have major impact on the cause,
prevention, or treatment of either form of pain. To be success-
ful in managing chronic pain, the clinician must detect and
measure sources of ongoing trauma or noxious disease, assess
the status of both the peripheral and the central nervous
systems (CNSs) of afflicted patients, and be prepared to use
the full spectrum of surgical, pharmacologic, physical, and
behavioral therapies that are currently available. It is also
apparent that the broad dimensions of the chronic pain condi-
tion often require the perspectives of different medical and
surgical disciplines. Some patients may be effectively managed
by a single clinician; some require simple communication
between two or three clinical colleagues or a small collabora-
tive ad hoc group of clinicians; still others may benefit from a
formal multidisciplinary pain clinic environment. No single
venue is either practical or appropriate for all patients with
chronic pain.
This chapter primarily addresses chronic pain, meaning
sustained or recurrent pain states. It does not attempt an
encyclopedic presentation of all chronic head and neck pain
conditions. Such presentations are available in the two classic
general texts in this field by Bonica1 and by Wall and Melzack2
and the classic work on orofacial pain by Bell,3 the proceed-
ings of the International Association for the Study of Pain
(IASP) and the International Headache Society (IHS), and
in key scientific journals, notably the journal Pain, The Clinical
Journal of Pain, and Journal of Orofacial Pain. This chapter
targets chronic pain syndromes that have origin in three
peripheral anatomic “compartments”: musculoskeletal, tri-
geminovascular, and neurologic (Figure 9-1). It will show how
all chronic pain syndromes originating in these compartments
have a “final common pathway” of a sensitized nervous system,
how the clinician can recognize this sensitization, and how
136
John M. Gregg
central nervous dysfunction has implications for patients with
all forms of sustained pain. This chapter is heavily referenced
to enable readers to pursue topics in greater depth as needed,
particularly with regard to the basic mechanisms and modern
therapies for pain syndromes.
■ INCIDENCE AND DEMOGRAPHICS
Chronic pain is a major health care problem, causing untold
suffering to the individual and major disruption of work pro-
ductivity. It is estimated that 30% of the adult population in
the United States suffers from some form of chronic pain, and
estimates of the cost to society from work loss alone are $80
million per year.2,4 If headache is added to this formula, the
overall incidence of chronic pain in the American population
is more than 60%.5 Chronic orofacial and TM pain occurs
yearly in approximately 22% of the American population.6
Collectively, patients who come to clinicians for treatment of
head and neck pain are more likely to be female, with the
female-to-male ratio being 3 : 1.7 They also tend to be of low
socioeconomic status and younger, with peak pain prevalence
occurring in mid-30s to -40s.2 A further breakdown for par-
ticular syndromes reveals a female-to-male ratio of 8 : 1 for TM
myalgias, 3 : 1 for arthralgias, 2 : 1 for migraine or tension head-
aches, and 2 : 1 for neuropathic pain.8,9
■ PAIN DEFINED
Pain is defined as “an unpleasant sensory and emotional expe-
rience associated with actual or potential tissue damage, or
described in terms of such damage. Each individual learns the
application of the word through experiences related to injury
early in life.”10 Pain can further be divided into acute, chronic,
nociceptive, and neuropathic types. Acute pain is pain of short
duration, from noxious disease or recent injury. Acuity does
not mean severity. Indeed some chronic pain conditions,
such as trigeminal neuralgia (TN), are clearly more intense
than most recent-onset surgical pains. Chronic pain is pain of
longer duration, usually 3 months or longer, although the
neurophysiologic and behavioral changes that accompany
chronic pain are often well established within 2 to 4 weeks
 CHAPTER 9 • Chronic Maxillomandibular, Head and Neck Pain 137

after pain onset. Nociceptive pain refers to pain of nonneural
origin, in which normal peripheral nerve terminals are acti-
vated by inflammation or trauma that acts in tissues, such as
skin, teeth, muscles, glands, and blood vessels. The modern
concept is that no matter where or what the initiating noxious
sources, the final conduit for pain is an activation of a specific
class of neural receptors known as nociceptors. Therefore, as
stated by Devor, “bones don’t hurt, muscles don’t hurt, nerves
hurt.”11 If the underlying causes of nonneural painful disease
or trauma are not controlled, a transition from acute to chronic
pain may occur. This appears to be due to a series of gene-
induced plasticity of transmitting peripheral nerves and
ascending central relay neurons, whereby nociceptive pain
becomes “centralized” as neuropathic pain through a process
known as sensitization.12,13 Neuropathic pain, therefore, is a
chronic state in which the nervous system has been sensitized
by repetitive direct or indirect injury or uncontrolled nocicep-
tive disease. Patients with chronic pain, whether the original
nociceptive event was mucosal, cutaneous, muscular, dental,
vascular, or neurologic, all appear to share certain common
features of neuropathic pain, specifically: (1) lowered pain
thresholds, (2) spontaneous and elicited (triggered) pain
activity, (3) central behavioral changes, and (4) refractoriness
to therapies that would ordinarily relieve acute nociceptive
pain (Table 9-1).

■ PAIN PATHOPHYSIOLOGY
A molecular basis for understanding the common features of
Central modulation chronic pain sensitization in all anatomic compartments has
been emerging since the 1970s.14,15 Sensitization appears to
occur at both the peripheral and CNS (Figure 9-2). In the
peripheral sensitization of trigeminal nerves, small A-delta-
Musculoskeletal fiber and C-fiber nociceptors become chronically hyperreac-
tive to all stimuli because of at least three interacting processes.
Peripheral Central
Neurologic sensitization sensitization

TABLE 9-1 Common Features of Chronic Pain

Vascular
(1) Reduced pain thresholds
Pain compartments (2) Spontaneous and/or elicited pain
(3) Central behavioral dysfunction
FIGURE 9-1. An anatomic and mechanisms-based classification of
(4) Refractory to ordinary acute pain therapies
chronic craniofacial pain syndromes.

Brain stem Cortical-

reticular thalamic
Anatomic pain centers centers
compartments PAG LC

NRM

Musculoskeletal Noxious Enk 5Ht Norepi

inflammatory
mediators Primary nociceptor Descending
Arachidonic acid neuron inhibitory
Prostaglandins Ca2+ pathways Ascending
Neurologic Ca2+
Substance P TN pain pathways
5 HT GABA
Histamine
Aspartate Enk
Vascular ?
Glutamate

Ca2+ NMDA
NMDA
SPG Ca2+
Dorsal Horn Neuron

SCG (Peripheral Sensitization) (Central Sensitization)

FIGURE 9-2. Pathophysiology of chronic head and neck pain.

138 SECTION I ■ Anesthesia and Pain Control

A first mechanism of peripheral sensitization is the sustained

release of inflammatory chemical mediators, such as 5-hydroxy-
tryptamine (5-HT), bradykinin, and prostaglandins at the
nociceptor surface receptor and by the sensitized trigeminal
ganglion.16,17,18 As a result, nociceptor thresholds appear to
decrease such that stimuli that would otherwise not be painful,
such as touch or pressure, are transmitted to the CNS through
the sensitized nociceptors and ultimately perceived as pain.
A second mechanism of peripheral sensitization appears to
be the induction of pathologic ectopic electrophysiologic
activity at specific sites on injured nerve trunks (neuromas)
or the trigeminal ganglion itself.19,20,21 A third mechanism of
nerve sensitization has also been linked to pathologic changes
in autonomic nerves, which become neurochemically linked
to injured peripheral somatosensory nerves through sprouting
or up-regulation of autonomic receptors.22,23 Collectively,
these three mechanisms of peripheral sensitization appear to
alter the neurochemical and electrophysiologic status of the
primary afferent fibers that synapse on second-order neurons
in the dorsal horn regions of the brainstem-trigeminal
complex.
Central sensitization, a feature common to all forms of
chronic pain, appears to be an increase in the tonic excit-
ability of wide dynamic range (WDR) neurons in the dorsal
horn of the spinal nucleus of cranial nerve V (see Figure 9-2).
The WDR neurons appear to become especially permeable to
CA2+ influx as a response to the action of certain key excit-
atory amino acids, particularly glutamate, arriving in excess at
the postsynaptic WDR neurons from the sensitized peripheral
nerve.24,25 The actions of glutamate appear to be mediated by
an important receptor, the N-methyl-D-aspartate (NMDA)
receptor. NMDA-receptor antagonistic drugs have been
shown experimentally to block neuropathologic forms of pain
that are refractory to usual therapeutic levels of opioids, and
they hold promise for future treatments of intractable chronic
pain.
Similar sensitization mechanisms have now been demon-
strated in key central relay pathways and nuclear centers.15,26,27
Plasticity and sensitization have been exposed through PET
scan imaging in the posterolateral thalamus and the somato-
sensory cortical centers that mediate the sensory-discrimina-
tive qualities of pain. Neuroplastic sensitization has also been
demonstrated in the medial thalamus, amygdala, and anterior
cingulate cortex, mediating centers for the affective-
emotional (suffering) aspects of chronic pain.28,29,30 Most
recent brain imaging research has shown that the insular
cortex may be a key integrating center for pain perceptions
and responses.31 The phylogenetically ancient insula is somato-
topically organized and positioned for mediating sensory-dis-
crimination and affective-emotional pain components and
activating visceral-motor pain reactions (Figure 9-3).
Central sensitization may also result paradoxically from loss
of sensory input to the brainstem as occurs with peripheral
nerve damage in addition to resulting from CNS lesions, such
as stroke or demyelinating disease. This condition, known as
deafferentation pain, results in pain and phantom phenomena
A P A
B
FIGURE 9-3. fMRI demonstration of brain localization for primary sites of
tooth pain representation in human brain.
Map A displays tooth pulp stimulus projection (arrow) onto superior and lateral
brain S1 targets for expression of sensory-discriminative pain features.
Map B displays projection (arrow) on anterior cingulated and insular cortex, a
theorized integration system for expression of affective-motivational pain
features. (Jantsch HHF et al: Cortical representation of experimental tooth pain
in humans, Pain 118:390, 2005).
experienced by patents in peripheral nerve distributions that
have been “deafferentated” and that will test deficient on
neurosensory examination.32,33,34
A final basis for chronic central sensitization appears to be
failures in the brain’s descending pain inhibition systems that
originate in forebrain-hypothalamic centers, descend to spinal
cord brainstem levels, and modulate pain through neurochem-
ical mediators, such as 5-HT, norepinephrine, GABA-nergic,
and enkephalinergic interneurons.35 Loss of pain inhibition
may account for the protracted pain often experienced by
patients who have sustained head and neck injuries. They are
also implicated in the generalized neurobehavioral disability
often seen in patients with chronic pain.
In addition to the generalized effects of nervous sensitiza-
tion, certain gross anatomic features of the maxillofacial
region may contribute to the uniqueness of this region’s pain
syndromes. The muscles of mastication and the neck are inter-
dependent and, when involved in pain syndromes, often
present combined symptoms. Arteries and venous plexuses are
encompassed at many levels by muscles, such as those of the
temporal fossa and pterygoid regions, making the vessels
susceptible to extremes of compression from muscle overuse
syndromes. Motor and sensory trigeminal nerves are not ana-
tomically mixed, as in spinal systems, making it more likely
that head and neck disease will cause painful conditions
 CHAPTER 9 •
without accompanying motor signs. The sensory trigeminal
nerves often course through nondistensible bony canals and
foramina, predisposing them to compressive or inflammatory
neuropathies. Finally, the fiber spectrum of the trigeminal
sensory nerves as compared with spinal nerves is heavily
skewed toward larger, rapidly conducting myelinated fibers, a
possible explanation for the occurrence of shocking, more
rapid paroxysmal pains seen in the maxillofacial region in
contrast to the duller, deeper pains experienced in other body
regions.
■ PAIN DIAGNOSIS
The IASP classification of head and neck pain disorders
includes 55 different pain conditions for the head and neck.10
In recent years, pain taxonomists have suggested that pain
syndromes should be grouped according to similar mechanisms
of action.36,37 This is useful for effective treatment planning
and for developing new therapies. However, the clinician is
more likely to be successful in treating patients if pain condi-
tions with common mechanisms are also identified within
anatomic compartments because this parallels the manner in
which patients are logically examined and commonly treated.
The anatomic compartments in which chronic pain syndromes
most commonly manifest are overlapping combinations of the
musculoskeletal-articular, trigeminovascular, and neurologic,
with the central nervous compartment acting as a constant in
all cases (see Figure 9-1). The primary chronic pain syn-
dromes, listed in the contexts of their anatomic compart-
ments, are displayed in Table 9-2.
In any listing of pain entities of the maxillofacial region, it
must be recognized that for many pain syndromes the etiologic
mechanisms and the balance of peripheral and central factors
is not completely known; hence a number of “idiopathic”
disorders are grouped in the text and discussed with vascular
and neurologic disorders. Using this anatomic-compartment
and mechanism-based orientation, the clinician’s diagnostic
tasks are to: (1) characterize and quantify pain, (2) determine
An Anatomic and Mechanism-Based
TABLE 9-2 Classification of Primary Chronic Craniofacial
Pain Syndromes
Anatomic Compartment Pain Syndrome
Musculoskeletal FM
Myofascial pain disorders
TM arthralgias
Trigeminovascular Migraine
Tension-type headache
Cluster and autonomic cephalalgias
Orofacial migraine variants
Neurologic Classic TN
Postherpetic TN
Postconcussion syndrome
Posttraumatic TN
CRPS
Idiopathic Orofacial Pain Syndromes
Chronic Maxillomandibular, Head and Neck Pain 139
the presence or absence of ongoing noxious pathoses or
chronic painful dysfunction in each of the anatomic compart-
ments, and (3) recognize the signs of peripheral and central
sensitization.
■ CHARACTERIZING AND
MEASURING PAIN
A first goal of chronic pain assessment is to determine the
nature and severity of the presenting pain and its related func-
tion impairment. These determinations serve as the basis for
judging the outcomes of treatments used. Although no practi-
cal objective technique exists at this time for measuring pain,
indirect methods using verbal descriptors and visual analog
scaling have proved useful for many types of chronic pain
conditions across many cultures.38,39 The McGill pain inven-
tory is a well-tested instrument that combines a visual analog
with weighted pain descriptors. The pain descriptors of the
McGill pain inventory often assist in diagnosis by exposing
qualitative features that are unique to particular syndromes.
For example, patient selection of descriptors, such as “shock-
ing, flashing, tingling, intermittent” point toward neuralgia;
“throbbing, pulsing, nauseating, pressure” more likely point
toward vascular pain sources; and “pinching, pulling, tight,
tired” direct the clinician toward musculoskeletal compart-
ment syndromes.
Function impairment associated with the pain syndrome
can also be ranked on visual analog scales for global life activi-
ties, such as work, career, family, marriage, and leisure. It can
also measure the perceived impact of pain on dysfunction for
specific personal functions, such as sleep, eating, appetite, sex,
and maintenance of personal and oral hygiene.40
■ CLINICAL AND LABORATORY
EXAMINATION
The clinical examination begins with classic inspection, pal-
pation, and percussion of the patient’s head and neck. The
clinician searches for signs of ongoing noxious pathoses that
might indicate active inflammation, infection, tumor com-
pression, repetitive trauma, neoplasm, or glandular obstruc-
tion. The dentition, oral soft tissues, paranasal sinuses, and
salivary and lymph glands should be examined with classic
techniques to rule out active noxious pathoses that may be
sources of acute or chronic episodic pain.
When acute sources of noxious pathoses have been ruled
out and have been cataloged, clinical indicators associated
with chronic pain are researched. Atrophy, asymmetry, cuta-
neous discoloration, herpetic lesions, mucositis, and hyper-
keratosis are commonly associated with chronic syndromes.
The musculoskeletal compartment is specifically addressed by
palpating all muscle groups, especially the trapezius, sterno-
cleidomastoid, occipital, masseteric, temporal, and medial and
lateral pterygoid groups. They are tested for painful tender
points, trigger points with classic muscle fasciculations, and
restricted or deviant range of motion. The range of motion for
the neck is observed for flexion, extension, and rotation, and
the upper spine is palpated for signs of elicited pain or crepitus.
140 SECTION I ■ Anesthesia and Pain Control
The TM capsule is percussed, and pain responses are noted to
both transmeatal and preauricular percussion. Crepitus,
popping, and clicking joint effects are recorded for both
manual and auscultatory signs.
The vascular compartment is examined with classic inspec-
tion, palpation, and percussion of vascular and related tissues,
beginning with the carotid sheath in the neck and extending
to the pericranial vessels. Pain responses to palpation and
pain radiating distally into the jaws and face suggest associa-
tion with adenitis in the salivary or lymphatic glands through
which the vessels course. Auscultation for bruits may further
define a carotid atherosclerotic contribution to chronic pain
and may signify generalized connective tissue disorder.
Doppler analyses may be useful in further defining the extent
of vascular disease and its possible implication in the pain
syndrome. Inspection of mucocutaneous tissues for erythema
and asymmetric edema may signify either vasculopathy or
autonomic derangement, or both. It is also important to
establish, through vascular analyses and neurosensory testing,
the basis for a patient complaint of regional “numbness.” This
aspect of the examination should differentiate between true
trigeminal nerve branch stimulus-response deficits as com-
pared with normal neurosensory reflexes within an area sensed
as “numb” because of direct neural effects of vasoconstriction
or reduced blood flow. The patient with a vascular basis for
subjective numbness tests normally on trigeminal quantita-
tive sensory testing. Correlation should also be made between
headache patterns and ophthalmologic signs, such as increased
intraocular pressures and, more globally, hypertension.
The neurologic compartment is assessed on a central to
peripheral nervous continuum. The examiner begins with
assessment of global functions: level of consciousness, cogni-
tive functions, speech, status of deep tendon reflexes, and signs
of quadrant paresis or loss of sensation that may point to
central lesions. Cranial motor nerve functions are checked,
especially noting deficits in pupillary accommodation reflexes
and extraocular muscle coordination. The purpose here is to
detect gross signs of generalized neurologic dysfunction as a
possible basis of or contributor to chronic pain, such as space-
occupying intracranial lesions, demyelinating-proliferative
disease, or disseminated metabolic or neuroendocrine disease
(such as pituitary, thyroid, or pancreatic disease).
The examination then proceeds to a study of craniofacial
stimulus responses known as quantitative sensory testing
(QST),40,41,42 noting signs of deficits (anesthesia or hypo-
esthesia) or excessive neurologic “trigger responses” (hyper-
esthesia). This examination is done by presenting a cascade
of stimuli bilaterally, beginning with level A testing, a measure
of patient ability to detect fine-touch stimuli, such as cotton
wisp, two-point touch, or brush direction accuracy. The neu-
rosensory examination then proceeds to a measure of patient
capacity with crude touch, such as pin-touch detection or the
Semmes-Weinstein (von Frey) thresholds (level B testing)
and finally to responses and detection levels to noxious stimuli,
such as heat, pinch, or deep pin (level C testing). Patients
in whom hypoesthetic neuropathies have developed from
peripheral nerve injuries or a metabolic disorder demonstrate
elevation of all thresholds throughout the cascade but espe-
cially for fine-touch (large fiber) discrimination. Despite
having elevated thresholds, even for stimuli that are noxious,
many patients with neuropathic pain syndromes complain of
pain experienced “deeply” within the hypoesthetic tissue
regions. Patients who demonstrate signs of neural sensitization
display lowered thresholds to the stimulus cascade and indi-
cate that their pain is “on the surface” when compared with
contralateral nonpainful distributions. Some patients may
describe instantaneous mucocutaneous pain in response to
light (levels A and B) stimuli that are not painful in their
contralateral nonpainful tissues. This phenomenon of touch-
evoked pain is known as allodynia. Other sensitized patients
report hyperalgesia, or noxious-stimulus pain, experienced at
levels that are elevated when compared with noxious stimula-
tion of contralateral tissues. Hyperpathia is another response
signifying neural sensitization, in this case from repetitive
mechanical stimulation. Finally, QST may demonstrate
spreading of pain sensitivity from the originally lesioned nerve
distributions, known as secondary or surround hyperalgesia.43 At
the completion of the neurologic compartment assessment,
the clinician should have localized sources of nociceptive and
neuropathic pain and determined whether there are signs of
peripheral or central sensitization.41,42,44
■ PHARMACOLOGIC SCREENING
Pharmacologic and block testing have the dual purposes of
helping define the chronic pain mechanism and predicting the
success of specific pain therapies.
LIDOCAINE TESTING
Topical lidocaine. Can be used in diagnoses either through
topical gels applied to tender points and pain triggers or
through overnight testing with transcutaneous 5% patches
(Lidoderm). These agents may also assist in palliative pain
control.45
Paraneural lidocaine. Block injections are done, begin-
ning in the most distal nerve branches with small concentra-
tions and noting reports of pain relief from the patient.
Secondary and tertiary blocks are then repeated at higher
levels of the trigeminal nerve branch being tested, noting the
patient’s report of perceived pain changes after each block.
This technique defines the neuropathic contribution to the
patient’s pain mechanism and may assist in the treatment
planning for surgical decompression in cases of suspected
traumatic neuroma or compression neuropathy or control of
classic TN.
Intravenous lidocaine. It is possible to learn about a given
patient’s locus of pain generation by noting pain responses to
intravenous lidocaine.46 In this test, placebo saline is given
first to check for placebo pain response, followed by intrave-
nous lidocaine infused at 1 mg/kg body weight over a 2-minute
time frame. At 30-second intervals, patients are asked to rank
the severity of their pain, noting changes in its intensity or
its quality. A drop in pain severity of greater than 30% is
 CHAPTER 9 •
considered a positive response, signifying a neuropathic basis
of pain as compared with other sources, such as peripheral
musculoskeletal or vascular inflammation. It may also be pre-
dictive of pain responsiveness to centrally acting drugs, such
as anticonvulsant agents. Although the intravenous lidocaine
test has been proposed as a primary screening technique for
central neuropathic pain, it should be noted that peripheral
neuropathic pain generators, such as active neuromas, are also
responsive to higher levels of systemic lidocaine.47
Myofascial lidocaine blocks. Diagnostic blocks of muscle
myofascial tissues with plain lidocaine may define more pre-
cisely the loci of myofascial tender points. Key targets for
diagnostic blocks are the occipital and masticatory muscle
groups, which may differentiate pain that is exclusively myofas-
cial in origin as compared with spinal or temporomandibular-
articular sources.
Autonomic blocks. Both sympathetic and parasympathetic
components of the autonomic nervous system can be tested
for possible involvement in chronic pain syndromes. Stellate
ganglion blocks are done at the C7 level with 10 mL lidocaine
and induce a hemifacial block of postganglionic sympathetic
fibers to the ipsilateral maxillofacial structures.4,48 Signs of
effective block include skin warming, pupillary dilatation, and
eyelid ptosis. If pain is sympathetically mediated, the patient’s
chronic pain will be transiently relieved, although there will
be little effect on trigeminal nerve or myofascial sources of
pain.
The sphenopalatine ganglion may be blocked either directly
at the posterior junction of the inferior and middle turbinates
through transnasal 4% lidocaine insufflation or through
transpalatal injection into the descending palatine canal. Pain
remission may point toward a vascular pain syndrome because
of the possible parasympathetic role of the sphenopalatine
ganglion in craniofacial migraine and migraine-equivalent
syndromes.49 However, because of the proximity of the maxil-
lary division of trigeminal nerves in the sphenopalatine region,
it may not be possible to differentiate between pain sources
from TN and migraine with the sphenopalatine ganglion
block.
■ SYSTEMIC DISEASE, SLEEP, AND
PSYCHIATRIC DYSFUNCTION
Chronic pain does not exist in a demographic vacuum. The
patient’s general health and psychosocial factors act to some
degree in all cases and can be primary determinants of pain
severity reporting, pain tolerance, and responses to therapy.
Chronic pain is known to be influenced by patient age, gender,
socioeconomic status, educational level, family and marital
status, religious and cultural background, previous life experi-
ences with chronic disease, particularly painful disease, the
presence or absence of litigation, levels of daily exercise, and
avocation satisfaction.1,2
Systemic disease. Assessing past medical history is impor-
tant because chronic oral and maxillofacial pain is known to
cluster with other generalized pain conditions. There are
common associations between arthritis, fibromyalgia (FM),
Chronic Maxillomandibular, Head and Neck Pain 141
irritable bowel syndrome, migraine, hypertension, chronic
paranasal sinus pain, and cervical spinal and low back pain.50,51
Although no common mechanisms have been proven for
these painful conditions, similar psychiatric patient profiles
and known reflex connections between autonomic and tri-
geminal systems have been implicated.52,53,54
Sleep dysfunction. A detailed history of the patient’s sleep
history is important, especially with regard to its relationship
to pain.55 The patient should be asked whether he or she is
awakened by pain or simply notices pain on awakening. Mus-
culoskeletal pain exacerbations tend to awaken individuals, as
does neuropathic pain where a cutaneous trigger is present.
Intracranial-based pain, such as TN, however, is more com-
monly “dormant” during sleep and does not awaken the
patient. Patients lacking in deeper sleep levels III and IV and
rapid eye movement (REM) sleep are prone to myofascial pain
and FM patterns.56 Others with restless leg syndrome may
have more intense oral dyskinesias associated with clenching
or bruxism. Patients with obstructive sleep apnea syndrome
may have many features of FM and oral dyskinesias, and there
is known correlation between nocturnal bruxism dyskinesias
and smoking.57
PSYCHIATRIC DISORDERS
A detailed history for previous and current psychiatric condi-
tions should be discussed openly with patients and family.
Three psychiatric diagnoses are of particular relevance to
chronic pain: drug addition, depression, and somatoform
disorders.
Substance abuse. Abuse and addiction to tobacco, alcohol,
opiates, psychosedatives, or other centrally acting drugs is
more common among patients with chronic pain than in the
pain-free population.58 The paradigm for use of long-acting
opiates for management of all forms of chronic pain has
changed in the last 2 decades and now recognizes the appro-
priateness and safety of this practice.59 Current and past use
of any centrally acting drugs must be discussed openly with
patients, and a substance use contract should be agreed upon
between the patient and treating physician before treatment
begins.
Depression is by far the most common psychiatric illness
found in people with chronic pain, although it is believed that
depression rarely manifests itself as pain.60 Rather, depression
appears to result from the demoralizing and debilitating aspects
of chronic pain and profoundly affects vital functions, such as
sleep efficiency, which in turn has major impact on pain toler-
ance and musculoskeletal and vascular pain cycles.61,62 Patients
with a history of depression should be questioned for details
of whether depression has a familial basis; whether it has been
associated with substance abuse; whether it has been endoge-
nous or situation dependent; has had bipolar features, includ-
ing self-destructiveness; and whether hospitalizations have
occurred.
Somatization is the tendency to experience and communi-
cate somatic distress and symptoms that cannot be explained
on a physical basis.63 Patients with chronic pain are known to
142 SECTION I ■ Anesthesia and Pain Control
catastrophize symptoms, apparently in some cases to convince
others of the truthfulness or severity of their symptoms, and
consequently they seem hypochondriacal.64
The clinician may be assisted in screening for psychiatric
relations to pain by the use of certain instruments. Of proven
value are Beck’s Depression Inventory, Spielberger State-Trait
Anxiety Inventory, SCL90, and Pittsburgh Quality of Life
Inventory. More extensive and long-established psychological
screening instruments, such as the Minnesota Multiphasic
Personality Inventory (MMPI), although helpful in defining
psychological disease trends, require professional psychologi-
cal assistance for full interpretation.
Social dysfunction. Chronic pain commonly disrupts
patients’ relationships with spouse and family, job perfor-
mance, and community engagement. Failure in these spheres
further impairs the patient’s tolerance for ongoing pain, may
lead to further destructive behavior, and jeopardize possible
therapies. It is critical that the clinician gain knowledge of
these dynamic factors before beginning treatment.
■ THE MUSCULOSKELETAL
COMPARTMENT
Pain derived from the musculoskeletal compartment of the
head and neck are the chronic syndromes most frequently
seen in clinical practice comprising 40% of all chronic cases
seen in pain clinics.65 Muscle trauma and overuse, joint inflam-
mation, and mechanical disk derangements are clear periph-
eral sources of pain and often account for the isolated and
episodic pain conditions seen in this compartment. The more
refractory and chronic forms of musculoskeletal pain syn-
dromes, however, are more likely associated with central sen-
sitization patterns similar to those seen in neuropathic and
vascular syndromes.66,67 There is much overlap, continuity,
and common pathophysiology between musculoskeletal pain
that is generalized and syndromes that are confined to the
back, cervical, masticatory, and TM regions. There is also
overlap with vascular and neurologic compartment syndromes,
particularly migraine variants and “atypical” or idiopathic
facial pain syndromes. Three primary syndrome types domi-
nate the musculoskeletal compartment: (1) FM, (2) myofas-
cial pain syndromes of the head and neck, and (3) the TM
arthralgias.
■ FIBROMYALGIA
Fibromyalgia (FM), also known as primary fibromyalgia syn-
drome, is a common condition of muscle aching, stiffness,
generalized fatigue, and nonrestorative sleep pattern with
multiple myofascial “tender points” throughout the trunk and
appendages.68 Pain is described as “aching, radiating, gnawing,
shooting, and burning,” is worse in the mornings on awaken-
ing and later in the evening, and is exacerbated by cold
temperatures and physical activity. Patients complain of both
spontaneous deep muscle aching and localized tender-point
pain responses to 4 kg of digital pressure. Studies have
demonstrated a generalized reduction in muscle pain thresh-
olds for pressure pain.69 Sleep onset and retention are
poor and are associated with daytime sleepiness and work
disability.56
FM is believed to occur in approximately 2% to 4% of the
population, with 80% to 90% being female with a mean age
of 52. There is also considerable overlap between FM and TM
and cervical myofascial pain. Of FM patients, 75% also have
TM-myofascial pain, and approximately 30% of patients diag-
nosed with TM pain are believed to have FM. There appears
to be a hereditary predilection.69 FM is best distinguished from
specific myofascial pain syndromes, such as cervicogenic and
TM syndromes, by the presence of multiple thoracic and
appendage tender points.
PATHOPHYSIOLOGY
A central nervous pathophysiology accounts for the main ele-
ments of FM. Psychological theories have suggested that
patients amplify unpleasant experiences and are hypervigilant
to painful events.70 Studies of serotonin metabolism have also
shown that patients with FM may have deficiencies in CNS
pain modulation owing to serotonin pathway dysfunction.71
Others have postulated that chronic myofascial pain is due to
dorsal horn sensitization induced by increased input from
myofascial nociceptors.72
DIAGNOSIS
FM diagnosis is dependant on the demonstration of at
least 11 trunk and appendage tender points. Rheumatoid
factor analyses are normal. Patients have significantly lowered
pain thresholds for heat and pressure and an incapacity to
inhibit secondary pain stimuli at normal levels.73 The overall
clinical pattern is suggestive of pituitary derangement and
a deficient generalized stress response. FM also has many
features in common with hypothyroidism, but patients
test euthyroid, and adrenocortical functions are depressed
with reduced cortisol levels.56,66 Unfortunately, no definitive
laboratory or imaging studies aid in the differential diagnosis
of FM.
TREATMENT
There are no universally definitive treatments for FM, and
few patients become permanently pain free. Treatment pro-
grams rely on pain-management counseling for patient self-
management and lifestyle modification. Medical treatments
depend on simple nonsteroidal analgesics and the titrated use
of low-dosage tricyclic antidepressant agents to increase pain
tolerance thresholds and normalize sleep.74 Tender-point
injections with local anesthetics and corticosteroids and spray
and stretch physical therapy may bring about sustained remis-
sions. Intravenous lidocaine (administered weekly at 4 mg/kg
infusions) has proven effective in relieving pain symptoms of
chronic FM pain for approximately 1 month and can then be
supplemented by the use of titrated oral mexiletine.75 Although
regular aerobic physical exercise is generally recommended for
chronic pain management, isometric exercise has recently
been shown to have a hyperalgesic (pain exacerbation) effect
on patients with FM.76
 CHAPTER 9 •
■ MYOFASCIAL PAIN
The extremely common myofascial pain syndromes of the
head and neck appear to be interdependent, have overlapping
symptoms and courses, and probably share common patho-
physiologies. The three main recognized head and neck myo-
fascial pain syndromes are the temporomandibular myofascial
syndrome, the cervicogenic (occipital) headache, and the
overlapping neurovascular tension-type headache.
TEMPOROMANDIBULAR DISORDERS
Temporomandibular myofascial pain and dysfunction (TMD)
is a chronic episodic condition in which patients experience
pain in the muscles of mastication and surrounding structures,
often in association with pain in the occipital, cervical, and
upper back muscles. Pain is usually described as preauricular
and temporal and often radiates anteriorly to precipitate ret-
roorbital headaches with photophobia and nausea. TMD
overlaps with primary occipital myalgias; cervicogenic, mixed
tension-type headaches; and so-called “atypical” midfacial
pain patterns.9,51,77,78 The TM and cervical regional syndromes
are distinguished from primary FM by pain being confined to
the head and neck region, by distinct patterns of referred pain,
and by specific “trigger points,” where muscles have taut, pal-
pable band regions that twitch when manually percussed.67
There is also an association with TM joint sounds of clicking,
popping, and crepitus, which are highly variable between
patients and also vary over time for individual patients.
Intraarticular symptoms are often associated with myofascial
pain symptoms, and therefore, may represent parallel or inter-
related clinical problems (see section on temporomandibular
joint disorders). Tinnitus and vertigo are common but incon-
sistent aspects of TMDs.
TMD is common among Americans, with some aspects of
the syndrome present in up to 11 million people, or 6% of the
population.6 Onset is most common in the second decade of
life, with peak incidence in the third and fourth decades and
lowered incidence and severity after age 50. TMD is charac-
terized by episodes of increased pain and dysfunction severity
lasting days to weeks followed by gradual remissions. Like all
of the musculoskeletal pain syndromes, TMD is strongly
female in its frequency, with female-to-male ratios 6 : 1 to
9 : 1.7,79
CERVICOGENIC HEADACHE
Cervicogenic headache appears to be due to myalgia of the
occipital muscles and is possibly related to entrapment-
compression of the greater occipital nerve at the base of the
superior nuchal line.80 Many patients with chronic occipital
myalgia have sustained head or neck trauma as an apparent
precipitating event. Pain is usually unilateral, dull, daily, con-
stant, and radiating from the base of the neck toward the
shoulders to temporal-frontal regions and, in some cases, to
midfacial maxillary arterial or trigeminal distributions. The
latter cases have historically been linked to “atypical” referred
muscular-vascular syndromes that have been attributed to
Chronic Maxillomandibular, Head and Neck Pain 143
psychogenic factors. A more likely neurophysiologic link,
however, is through the cervical and trigeminal primary affer-
ents that converge in the subnucleus caudalis of the spinal
cord.81,82
PATHOPHYSIOLOGY
Two universal mechanisms appear to account for sustained
myofascial pain syndromes: tissue trauma and central nervous
sensitization.8 Trauma to myofascial tissues of the head and
neck is a common pathophysiologic denominator for many of
the myofascial pain syndromes. Direct macrotrauma to the
jaws, particularly the symphysis or lateral mandible, is known
to initiate microstructural focal weakness in muscle tendons
and may precipitate chronic pain.83
Repetitive microtrauma to masticatory structures, from
either iatrogenic trauma, battering, or self-induced overuse
activities, such as bruxism, are possible sources of CNS sensi-
tization and pain chronicity.84 Chronic pain and decreased
pain thresholds following microtrauma may cause central
“windup” sensitization of dorsal horn NMDA receptors result-
ing from stimulation of muscle nociceptors by repetitive and
summating microtraumas.66,85
Cervical musculoskeletal macrotrauma is commonly asso-
ciated with both cervicogenic headache and midfacial and
TM pain. The mechanisms of this association remain unclear.
The theory that indirect trauma, such as rapid extension-
flexion cervical trauma (whiplash), can induce permanent
internal derangement of the TM joints remains controver-
sial.86 It has been proposed that indirect whipping action of
the cervical, facial, and masticatory muscles can induce focal
muscle damage and weakening.87 Alternative mechanisms
involve the central brainstem-trigeminal complex, which may
become sensitized by noxious input from injured cervical spine
and occipital myofascial injury, or more global posttraumatic
brain effects.88
Psychosomatic factors have also been strongly implicated
as precipitating or exacerbating factors, or both, for chronic
myofascial pain, mediated through inadequate stress response
(coping), psychiatric depression, and especially dysfunctional
sleep disorders, acting as perpetuating and sustaining factors
for the muscular pain patterns.35
DIAGNOSIS
Diagnosis of head and neck myofascial pain syndromes is
dependant on the demonstration of specific painful tender
points in muscles, either in response to manual percussion and
palpation or with an algometer. Restricted or irregular jaw or
neck movements are determined to be muscular rather than
articular. Imaging of the mandibular condyles may demon-
strate remodeling from long-term masticatory hyperfunction,
which can be differentiated from true arthrotic inflammatory
imaging changes (see the section on temporomandibular dis-
orders). Cervical spine films may demonstrate osteoarthritic
changes, which can be differentiated from more recently
acquired and purely soft tissue pain sources. Local anesthetic
field blocks in muscles, such as the lateral pterygoid or inferior
144 SECTION I ■ Anesthesia and Pain Control
temporalis attachments, may help define the myologic source
of pain. In the case of cervical syndrome, occipital anesthetic
blocks done between the mastoid process and the external
occipital protuberance will define an occipital myalgia source.
In those cases where there is an occipital to midfacial referred
pain linkage, the occipital block will also relieve midfacial
symptoms. Pain relief from tender-point anesthetic blocks
may be predictive of therapeutic benefit from serial blocks,
physical therapy, or electrotherapy.
The clinician should carry out quantitative sensory testing
for all patients who have musculoskeletal compartment pain
to identify signs of central sensitization.89,90 Diagnostic signs
of central sensitization seen in association with muscle tender
points and limited range of mandibular motion would include
(1) lowered pain thresholds to all forms of stimulation, (2)
spread of pain beyond specific muscle sites, (3) mucocutaneous
touch-evoked pain responses (allodynia) and hyperalgesia,
and (4) failure of peripheral lidocaine nerve blocks to signifi-
cantly decrease pain. Recognition of the central neuropathic
mechanisms of chronic multiple sclerosis (MS) pain will more
correctly direct the therapy toward the primary central mech-
anisms and prevent reliance on ineffective and potentially
destructive treatments.91,92
TREATMENT
Myofascial pain management incorporates behavioral, physi-
cal, pharmacologic, and surgical therapies for overall pain
management. Treatments must be individualized, with avoid-
ance of lock-step, cookbook approaches. Because myofascial
pain is often episodic in nature, some interventions must
address acute pain exacerbation, whereas more supportive
and self-help measures are needed for maintenance and
prevention.
Behavioral management of myofascial pain is based on
patient awareness of his or her own role in disease exacerba-
tion and control. Patients should be counseled to understand
the importance of a healthy lifestyle, sleep hygiene, exercise,
nutrition, and smoking and substance abuse avoidance in pre-
venting and managing their pain condition. Responsibility for
therapy and recovery and prevention should be shifted away
from the therapist and toward the patient for long-term
remission.
Specific behavioral techniques that can be applied in both
intervention and maintenance programs include relaxation
therapies, biofeedback, especially electromyographic (EMG)
and temperature biofeedback, hypnotherapy, and cognitive
behavior therapy. There is a proven crossover of therapeutic
effects of behavioral-relaxation approaches between musculo-
skeletal pain and insomnia.55
Physical therapy programs can also be of value for patients
with myofascial pain syndromes. During phases of acute exac-
erbation of pain, physical tissue stress can be reduced through
use of soft diets, occlusal splinting, and icing of the joint and
muscular tender points. For more chronic pain control, formal
physical therapy can be prescribed, specifically for electro-
therapy using iontophoresis or phonophoresis, and home
therapy with TENS applied to tender points. In chronic phases
and after joint surgery, regular mandibular and cervical mobi-
lization is extremely important, with the primary goal of
improving range of motion through practiced stretching and
toning of antagonistic muscles as directed by the physical
therapist.
Pharmacologic management must also be matched to the
stage of the pain cycles seen with myofascial pain syndromes.
In acute exacerbation stages of myofascial pain, the primary
drugs are antiinflammatory agents, local anesthetics, muscle
relaxants, and in selected cases, opiate analgesics.59 Nonste-
roidal antiinflammatory agents are taken on a schedule of
1200 to 1800 mg/day (acetylsalicylic acid or preferably ibu-
profen equivalents). Muscle relaxants. such as benzodiaze-
pines, are useful with low daily dosing and moderate bedtime
dosing, such as alprazolam (0.25 mg three times daily and
2 mg at bedtime). Cyclobenzaprine is also an effective short-
term agent when used at 5 mg three times daily and 10 to
20 mg at bedtime. This agent facilitates the transition to
more chronic maintenance with tricyclic antidepressants
because they have a similar chemical structure. Narcotic
agents can be effective in reversing more severe and debilitat-
ing pain episodes and can be safely used in short-term situa-
tions in conjunction with muscle relaxants and physical and
behavioral therapies.
For patients with more constant musculoskeletal pain, the
tricyclic antidepressant agents (titrated from 10 to 75 mg ami-
triptyline equivalents) are the most proven medical approach.93
Patients should be counseled about the gradual onset (2 to 3
weeks) of therapeutic effect, the expected side effects of early
sedation and xerostomia, and possible weight gain. Tricyclic
therapy for myofascial pain can often be discontinued or
reduced to low-dose bedtime maintenance after a 3- to 6-
month time frame. The serotonin reuptake inhibitor agents,
such as fluoxetine and sertraline, are also effective for many
patients with myofascial syndrome pain and may be better
tolerated for daytime use. These agents, however, do not have
the proven myofascial syndrome pain-relief efficacy of the
tricyclic agents, and they do not appear to be as uniformly
effective in sleep management, an important factor in pain
management of myofascial pain syndrome.
Recently it has been shown that anticonvulsant drugs
have efficacy in the medical management of chronic sensitized
musculoskeletal pain. Gabapentin (Neurontin), used in
titrated doses between 600 and 2400 mg/day has been shown
to be effective particularly for patients with multifocal
pain triggers, cutaneous hyperalgesia, and touch-evoked pain
triggers.94
The use of narcotics and muscle relaxant agents for chronic
myofascial pain (and other forms of chronic “benign” pain)
remains controversial.58,95 There appear to be many patients
whose pain is well controlled and whose functional status is
clearly improved by a daily program of long-acting narcotic
and sedative agents, without evidence of increasing habituat-
ing drug usage.96 The prudent clinician will establish a con-
tractual agreement with such patients, however, regarding the
 CHAPTER 9 • Chronic Maxillomandibular, Head and Neck Pain
use of narcotics and muscle-relaxant agents. The “contract”
should stipulate a daily dosage schedule set at realistic pain-
controlling limits; avoidance of patient duplication of medica-
tions from other physicians; careful combinations of other
CNS agents, such as alcohol; and maintenance of nonphar-
macologic activities known to aid in the patient’s pain
management.
Musculoskeletal tender-point block therapies, using local
anesthetic in combination with adrenocorticosteroid combi-
nations, such as bupivacaine-dexamethasone, have proven
value.4 Blocks may afford pain reduction and increase range
of motion for 1 to 3 months and may be effectively combined
with physical therapy programs that emphasize range-of-
motion and low-impact muscle-toning activities.
There is little evidence that irreversible surgical or orth-
odontic treatments have a significant direct effect on chronic
centralized myofascial pain.97 They may have indirect value,
however, if traumatic tissue forces are reduced and mandibular
range of motion is increased in the process. Therefore, orthog-
nathic surgery that corrects traumatic malocclusion may help
in overall myofascial pain management.98 Surgical arthrocen-
tesis and arthroplasty may also indirectly influence myofascial
pain if concomitant joint pain is an aggravating factor in the
myofascial pain syndrome.99 The prudent oral and maxillofa-
cial surgeon or orthodontist, or both, will stress the supportive
role of irreversible therapies in the overall management of
patients with myofascial pain syndromes.
■ TEMPOROMANDIBULAR
ARTHRITIS
Intraarticular disease may be a source of radiating preauricular
pain and mechanical joint derangements. The two most
common painful conditions associated with the TM joint are
(1) TM rheumatoid arthritis and (2) TM osteoarthritis.
TEMPOROMANDIBULAR RHEUMATOID ARTHRITIS
Rheumatoid arthritis (RA) is a systemic inflammatory disease
of probable autoimmune origin involving many joints, includ-
ing the TM joint. Approximately 50% of patients with RA
have pain in the TM region, and approximately 10% have
deforming arthroses of the mandibular condyle, often resulting
in progressive malocclusions.100 The incidence of RA in the
general population is 2.5%, with a female predilection of
approximately 3 : 1. Peak onset is in the fourth to sixth decades
of life. A juvenile form of RA is rare, but potentially devastat-
ing in its effects on mandibular growth and joint mobility.
Acute episodes of painful intraarticular inflammation leave
patients with secondary intraarticular soft tissue adhesions,
producing pseudoankylosis, especially for translational and
wide opening movements. When the acute inflammatory
cycle has abated, often through spontaneous remission,
patients may still experience pain from extraarticular myalgia
because of the increased masticatory efforts required to over-
come the effects of the arthrosis. Cervical spine RA is also
often seen in conjunction with TM involvement, and this
combination may summate in craniofacial pain.
145
PATHOPHYSIOLOGY
RA produces pain by initiating a classic intraarticular soft
tissue inflammatory response, involving the synovial tissues
and adjacent capsule, and ultimately producing pain by
peripheral sensitization of C nociceptors.101 The adjacent pre-
auricular tissues may display allodynia and hyperalgesia into
adjacent temporal and facial soft tissues. The actual cause of
RA is unknown, although genetic predilection and autoim-
mune factors have been implicated.102
DIAGNOSIS
RA must be differentiated from psoriatic arthritis, systemic
lupus erythematosus, spondylitis, and gout. There is also con-
siderable overlap with noninflammatory osteoarthrosis with
regard to condylar imaging deformities. However, hypergam-
maglobulinemia with antibodies positive against immuno-
globulin G rheumatoid factor is found with RA in more than
85% of cases and effectively differentiates it from aggressive
arthroses.100,101 Patients typically display soft tissue swelling in
the preauricular regions with surrounding hyperalgesia.
TREATMENT
The treatment of rheumatoid arthralgia is directed toward
reducing the pain of both acute and chronic joint pain, pre-
venting radiation of pain into regional myofascial tissues, and
mobilization of restricted joint movements. With acute pain
exacerbation, antiinflammatory drugs are employed on a
scheduled basis and may be supplemented by direct ionto-
phoresis-phonophoresis of local anesthetic and corticosteroid
ions into the glenoid fossae. Support should also be given
for control of myofascial pain to enable patients to sustain
functional movements around the afflicted joints. Surgical
treatments are directed toward lysis and lavage of dysfunc-
tional joints, less often toward total joint replacements.
For young individuals in whom significant dentofacial
deformity has resulted and the inflammatory phases appear
to be in remission, joint reconstruction with autologous rib
or with total joint replacement may be used to restore lost
function.
TEMPOROMANDIBULAR OSTEOARTHRITIS
TM osteoarthritis, also known as degenerative joint disease,
is a commonly painful disorder of the joints in which there
are combinations of synovitis, destruction and abrasion of
articular cartilage, and reactive formation of compensatory
bone and adhesions.102 It is seen much more often in females,
appears familial, usually begins in the teenage years, peaks
during ages 20 to 40, and decreases in incidence and severity
after age 50.103 Patients appear to go through episodes of spe-
cific preauricular joint pain, sometimes called “arthritic events”
that last days to weeks and then dissipate or “burnout,”
although mechanical problems remain. The condition is also
characterized by progressive mechanical problems of decreas-
ing range of motion, popping, crepitus, occasional tinnitus,
and vertigo.
146 SECTION I ■ Anesthesia and Pain Control
PATHOPHYSIOLOGY
The degenerative responses of osteoarthrosis are believed to
be due to a failed capacity of a given patient’s articular carti-
lage to respond to its mechanical stresses. Both macrotrauma
and microtrauma can be responsible for initiating the disinte-
gration processes. Therefore, the same traumatic factors that
may precipitate myofascial pain caused by masticatory hyper-
function, such as nocturnal parasomnias-bruxism, may also
exacerbate TM arthrotic pain. Painful arthrotic events have
been attributed to the traumatic induction of a low-grade
synovitis of capsular and retrodiskal tissues in which there is
an up-regulation of substance P and sensitization of substance
P and CGRP-containing neurons.104 There is also evidence
that TM arthrotic pain may be further sensitized by trauma-
induced autonomic receptor up-regulation. Patients display
allodynia to fine-touch stimulation over the preauricular skin
and decreased systemic pain tolerance thresholds, suggesting
both peripheral and central sensitization mechanisms possibly
mediated by increased synovial fluid concentrations of sero-
tonin and keratan.102
RELATIONSHIP TO INTERNAL DERANGEMENT
Chronically displaced TM disks produce joint popping, crepi-
tus, and a variety of mechanical joint problems, especially
during opening and translational movements. Patients may
manifest “closed locking,” with difficulty in carrying out full
mandibular rotation or translation, or open locking, in which
mandibular closure to full dental centric occlusion is impaired.
Although patients with internal derangement display osteoar-
throsis more than 50% of the time, there is no convincing evi-
dence that internal disk derangement is the direct cause of
arthrosis.99,103 Early arthrotic changes appear to precede disk
displacement, and arthrosis occurs in patients with normal
disks.102,104 Most patients with acute or chronic disk derange-
ments do not have pain, and recent surgical studies have con-
firmed that many patients treated successfully with intraarticular
open or closed procedures enjoy pain remission without correc-
tion of disk displacement.97,105 Therefore, disk displacements
are probably a sign of osteoarthrosis rather than a cause.
DIAGNOSIS
Pain is specific to the preauricular region and increases with
lateral pressure, movement, and sometimes clenching. Crepi-
tus or popping is usually palpable and auscultatable, although
younger patients may exhibit only pain. Transpharyngeal
imaging displays a range of arthrosis from early anterior lipping
and subchondral hypocalcification through more major con-
dylar deformities, osteophytes, surface erosions, dense sclerotic
zones, subchondral cysts, and, in later stages, marked condylar
thinning.102 Magnetic resonance imaging (MRI) analysis is
helpful for establishing the severity of hard and soft tissue joint
degenerative change, but it is rarely necessary to establish the
basic diagnosis.99 Diagnostic intraarticular local anesthetic
blocks may help differentiate pure arthrotic pain from extraar-
ticular myofascial pain syndromes.
TREATMENT
A single best treatment protocol for painful arthrosis with or
without internal derangement remains elusive. Indeed, most
therapies seem to demonstrate a high rate of success, suggest-
ing the possibility that “natural processes” may also act in
producing remission from painful episodes, if not the degen-
erative arthrotic changes. The specific treatment emphasis
should be individualized, tailored to the stage of the condi-
tion, age of the patient, and level of pain severity.
Acute exacerbations in patients with arthrosis should be
treated with combinations of antiinflammatory physical and
medical therapies. Joint rest with soft splinting, soft diet, and
icing of erythematous or edematous joints twice daily is useful.
A course of nonsteroidal antiinflammatory agents (1200 to
2000 mg daily of ibuprofen equivalents in three divided doses)
should be administered by schedule, using 3 weeks on and 1
week off if gastric tolerance is limited. Narcotic analgesics may
be required for selective individuals to maintain functional
levels. Sleep enhancement with mild psychosedative agents
and muscle pain control with benzodiazepines or cyclobenza-
prine are indicated, similar to the treatment of acute-phase
myofascial pain. If rapid remission from the painful arthrotic
phase does not occur, however, more aggressive physical
therapy is indicated. Electrotherapy with iontophoresis-
phonophoresis two to three times weekly applied to joints and
adjacent myofascial tissues can be effective.
More chronic forms of arthrotic pain usually require a sus-
tained antiinflammatory level of daily medications and some
form of sleep promotion, such as zolpidem (Ambien) 10 mg
for sleep onset and a tricyclic antidepressant (such as 20 to
75 mg amitriptyline) for sustained pain relief. Behavioral
modification with emphasis on a healthy lifestyle, avoidance
of tobacco abuse, and the practice of regular physical exercise
may be important in both pain management and resistance of
the destructive arthroses over the long course of this
condition.
Surgical management of TM joint disorders will be reviewed
in detail in another section of this text (see Israel, HA).
■ THE VASCULAR COMPARTMENT
The primary pain syndromes that occur in the head and neck
vascular compartment are (1) migraine, (2) tension-type
headache, (3) trigeminal autonomic cephalalgias including
cluster headache, and (4) migraine variants. These syndromes
appear to have the common pathophysiologic features of an
episodic vascular inflammatory noxious event transmitted to
and from the CNS by the trigeminal system and regional
parasympathetic fibers. They also have considerable diagnos-
tic, pathophysiologic, and therapeutic overlap with neuro-
pathic and musculoskeletal syndromes.
■ MIGRAINE
Classic migraine headaches are chronic, recurrent painful
conditions that affect 6% of adult males and 17% of females.106
Two general forms are recognized: classic migraine (with aura)
 CHAPTER 9 •
Intracranial,
extracranial
vasculature
Neurogenic Trigeminal
inflammation afferent
(SP, NKA,
CGRP, NO,
5HT, BK) ? ?
SPG
FIGURE 9-4. Pathophysiology of the trigeminovascular system.
and common migraine (without aura), with a variety of inter-
mediate and altered variants. The pathophysiologic relation-
ships between classic and common migraines, cluster
headaches, tension-type headaches, and myofascial pain
remain unclear, although it appears that there are key common
mechanisms and some overlapping treatments.
Classic migraine with aura is characterized by infrequent
abrupt-onset throbbing frontotemporal headaches lasting from
4 to 72 hours with secondary spread to the entire hemicra-
nium. Nausea, vomiting, photophobia, and phonophobia
often accompany the pain. Classic migraine is especially dis-
tinguished by prepain anxiety and mood swings, which are
followed by the classic “aura,” characterized by blurred vision,
flickering changes in the visual fields, “curtain” visual effects,
and flickering “scotomata.” In some cases, facial paresthesias,
mild paresis, and aphasia occur.106
Migraine often begins in childhood and is well established
by the end of puberty, with peak incidence in the 20 to 40
age range.107 A hereditary basis is suspected, and a predilection
for females is well established. Pain attacks may be precipi-
tated by stressful psychic, physical, or traumatic events. A
frequent life pattern is one in which the abrupt classic attacks
occur one to four times per month, then diminish in severity
and frequency to give way to “transformed migraine” in which
pain is milder, more frequent, and with or without aura. In
other cases, a “paroxysmal hemicranial” pattern may emerge
and become chronic.108
Migraine without aura, formerly known as common
migraine, is grossly and anatomically similar to the classic
form, but differs by lacking the distinct aura and overtly auto-
nomic phases. It is seen two or three times as frequently as
classic migraine and tends to be frontal and more often bilat-
eral. Pain is aggravated by mild physical exertion, and pain
attacks tend to be more lengthy, in many cases up to a
week.109
PATHOPHYSIOLOGY
Migraine phenomena appear to be due to the interactive and
reciprocal effects of peripheral and central depression and
Chronic Maxillomandibular, Head and Neck Pain 147
DRN LC
Thalamocortical
5Ht Norepi
Spinal trigeminal
complex
sensitization occurring within the “trigeminovascular
system”110 (Figure 9-4). The peripheral effects occur when
cerebral, dural, and meningeal vessels innervated by trigemi-
nal nociceptors become sensitized, possibly from antidromic
CNS and autonomic spread to the cranial vessels.111 The oph-
thalmic and deep temporal arteries are specifically involved,
although these vessels appear to be histologically normal, with
no correlation between migraine syndromes and congenital or
acquired vasculopathy. In the current model of migraine
pathophysiology, termed the “trigeminovascular system,” a
cascade of events begins within the CNS, triggered by a variety
of events, such as chemical-nutritional, physical trauma, and
psychosocial stress112 (see Figure 9-4). The sensitized trigemi-
nal complex, particularly subnucleus caudalis of V, is believed
to be stimulated by descending neurochemical influences that
arise in forebrain reticular centers, specifically the dorsal raphe
nucleus (serotonin) and locus ceruleus (norepinephrine).113
Through unknown mechanisms, possibly antidromic reflex
activity, the trigeminal and parasympathetic ganglia, such as
the sphenopalatine ganglion, initiate a neurogenic inflamma-
tory response with the release of substance P, neurokinin A,
and CGRP by mast cell degranulation and platelet aggrega-
tion. As the final pathway, perivascular trigeminal nociceptor
C fibers respond to the neurogenic inflammatory response to
mediate the pain response centrally. The final clinical phase
of central sensitization is refractory to the triptan class of
drugs, but do respond to dihydroergotamines and COX inhibi-
tors.112 Nitric oxide has been proposed as a key causative
molecule in migraine, and interestingly, nitric oxide oxygen-
ase has been found in high concentrations in the sphenopala-
tine ganglion.114
DIAGNOSIS
The differential diagnosis of migraine includes tension-type
headaches, cervicogenic headaches, mixed (muscular-vascu-
lar) headaches, TM syndromes, and intracranial vascular
anomalies, such as angioma or aneurysm. The key diagnostic
features of migraine are an initial tenderness to palpation of
pericranial vessels (peripheral sensitization phase) followed by
148 SECTION I ■ Anesthesia and Pain Control
a generalized lowering of pain thresholds with QST and the
presence of cutaneous allodynia (central sensitization
phase).110
TREATMENT
There are no universally effective surgical treatments for
migraine. The management of migraine is divided into symp-
tomatic “rescue” and prophylactic treatments. Prophylactic
treatments rely on both behavioral and pharmacologic thera-
pies.109 Behavioral migraine prophylaxis focuses on stress man-
agement, relaxation therapies, including EMG and temperature
biofeedback, and nutritional counseling for alcohol and caf-
feine consumption control. Stabilizing sleep habits and mini-
mizing disturbances of circadian rhythms seem important in
migraine prophylaxis.
Maintenance drug therapies for migraine are individualized
by patient. The most widespread medical therapy combines
tricyclic antidepressant and β-blocker agents.115 Amitriptyline
(20 to 75 mg at bedtime) and propranolol (40 to 120 mg in
divided daily doses) constitute a standard and usually effective
prophylaxis. Sumatriptan, a selective agonist for 5-HT exter-
nal carotid perivascular receptors, has proven effective in pre-
venting and aborting early phases of migraine attacks.106,116 For
symptomatic rescue treatment of migraine, sumatriptan has
become the primary treatment; its primary action is on
branches of the external carotid arteries. It has also shown
efficacy with tension-type headaches, but not for patients with
myofascial pain involving the temporal muscles.117
The maxillary nerve and adjacent sphenopalatine ganglion
have been targeted for pharmacologic and surgical therapies
for treatment of migraine. Intranasal lidocaine (4% topical
solution) has been shown to be effective in 55% of patients
experiencing classic or common migraine attacks when applied
to nasal mucosa adjacent to sphenopalatine ganglia in the
region posterior to the inferior turbinate.49 There has also
been promising therapeutic effect from helium-neon lasers
focused on the posterior maxillary and sphenopalatine region
in 40 consecutive classic migraine patients, reversing acute
migraine in 85% and autonomic effects in 91% of patients
studied.118
TENSION-TYPE HEADACHE
A highly prevalent condition, episodic tension-type head-
ache, occurs at least occasionally in 38% to 66% of American
adults, with peak incidence in the fourth decade of life and
occurring overwhelmingly in white women of high educa-
tional achievement.5 Tension-type headaches are dull frontal-
parietal and often global headaches that are associated with
scalp muscle contractions and in many cases appear to be an
extension of occipital and TM myalgias. There is also some
question of linkage of tension-type headache with more
chronic forms of common migraine;119 many patients with
tension-type headache respond to migraine medical therapy
algorithms, including sumatriptan therapy in early headache
phases, dihydroergotamine and COX inhibitors for later
phases in chronic, constant types.120
■ CLUSTER HEADACHE AND
TRIGEMINOAUTONOMIC
VARIANTS
Cluster headache is a severe, periodic, middle and upper facial
vascular pain syndrome, occurring preponderantly in males
(90%), with a general population incidence of 0.1% to 0.4%
and appearing mostly in ages 20 to 40.121 Pain is experienced
in a midfacial pattern that follows the maxillary artery distri-
bution. Pain is described as deep, boring, or burning and is
experienced in orbital-frontal, retroorbital, anterior temporal,
and infraorbital regions unilaterally. Cluster headaches are
distinguished from classic migraine by being male dominant
at a 9 : 1 ratio, occurring in attacks of 45 to 60 minutes, some-
times one or more per day, and by being sustained irregularly
over days to weeks before lapsing into remission. Attacks are
also associated with rapidly occurring autonomic features of
rhinorrhea, mucocutaneous edema, erythema, and conjuncti-
vitis. Unlike classic migraine, there is no preattack aura,
nausea, vomiting, photophobia, or phonophobia. Alcohol
consumption and sleep dysfunction, including hypoxic epi-
sodes of obstructive sleep apnea, are known to initiate cluster
pain attacks in some individuals.88,121
PATHOPHYSIOLOGY
Cluster headaches, like other migraines, are mediated through
the trigeminovascular complex and its association with cranial
parasympathetic ganglia, such as the sphenopalatine gan-
glion.111 As in classic migraine, a sterile neurogenic inflamma-
tory response is believed to be initiated by CNS-descending
serotonergic- and norepinephrine-mediated tracts, which,
through unknown mechanisms, stimulate trigeminal and asso-
ciated autonomic centers.122 In the case of cluster headaches,
the sphenopalatine ganglion has been especially implicated as
an intermediary between the central trigeminal complex and
the peripheral periarteriolar vessels, where vasoactive peptides
are detected by perivascular trigeminal nociceptors.113
DIAGNOSIS
Cluster headaches are to be differentiated from classic
migraine, common migraine-mixed headaches, and classic
TN. Referred pain components of occipital myalgia and neu-
ralgia (see the section on myofascial pain syndromes of the
head and neck) may also mimic cluster headache and can be
differentiated by testing with bilateral occipital anesthetic
nerve blocks.123 Sphenopalatine ganglion block with injection
or transnasal lidocaine may produce rapid temporary remission
and help establish the diagnosis while also defining a potential
treatment.49
TREATMENTS
Nonpharmacologic prophylactic techniques used to treat
cluster headaches are similar to those used in classic and
common migraines. Alcohol consumption should be limited
in addition to known vasodilating foods and drugs. Sleep
hygiene and continuous positive air pressure or corrective
 CHAPTER 9 • Chronic Maxillomandibular, Head and Neck Pain
orthognathic surgical treatments are indicated for patients
with obstructive sleep apnea–related headache.
Symptomatic rescue treatments for cluster headache have
relied on the use of verapamil (80 to 160 mg three times daily)
and sumatriptan (25 to 50 mg four times daily or 80 mg SC),
producing remission of acute attacks in approximately 60% of
patients.124,125 Intranasal topical 4% lidocaine and nostril cap-
saicin, positioned adjacent to the sphenopalatine ganglion at
the posterior aspect of the inferior turbinate, have been proven
effective at rescue pain relief for acute cluster pain, although
patient self-treatment is hampered by the technical difficulty
of proper drug localization.49,126 Sphenopalatine blocks with
anesthesia and corticosteroid, done transpalatally through the
greater palatine foramina, may be rapidly effective in aborting
pain attacks and, if done serially, may bring more complete
remission from clustering.
■ OROFACIAL MIGRAINE VARIANTS
A number of idiopathic orofacial pain syndromes display
strong trigeminovascular and central nervous disinhibition
features and may have common mechanisms. They include
chronic paranasal sinus pain, burning mucosa, burning tongue,
and phantom tooth odontalgias.51,112,127,128 Pain in these idio-
pathic syndromes appears to occur mainly in the maxillary and
facial-lingual arterial distributions and may include mucocu-
taneous triggering phenomenon similar to that seen in classic
TN. Other variants of a similar nature have historically been
given labels, such as sphenopalatine ganglion neuralgia, peri-
odic migrainous neuralgia, and atypical neuralgias.129
There is also considerable overlap between the “atypical”
midfacial trigeminovascular conditions and painful occipital
myalgia tender points. This referred pain pattern is likely
mediated through convergence of both trigeminal and cervi-
cal afferents in the upper cervical spinal cord dorsal horn.82
Vascular orofacial pain (VOP) syndromes can best be dif-
ferentiated from classic migraine by older age at onset for VOP
and their location in the midface, jaw, cheek, nasal, lingual,
or dental tissues.128 They are more often female. and 20%
display autonomic signs of erythema, edema, conjunctivitis,
and mucositis. VOP must also be differentiated from chronic
regional pain syndrome (CRPS) where there is a history of
trauma (see the section on CRPS).
TREATMENTS
All of the migraine variants, including VOP, appear to respond
similarly to agents useful for classic and common migraine. Tri-
cyclic antidepressants, β-blockers, and nonsteroidal antiinflam-
matory drug therapies are standard. There have been no definitive
studies of the efficacy of sumatriptan for the migraine variants,
although it would be expected that any 5-HT-1D agonist or
selective serotonin uptake inhibitor could be effective.
■ THE NEUROLOGIC
COMPARTMENT
The primary pain syndromes that arise from direct disorder of
either the peripheral or the central nervous systems are (1)
149
TN (tic douloureux), (2) postherpetic neuralgia (PHN), and
(3) posttraumatic pain disorders.
■ TRIGEMINAL NEURALGIA
Known also by its archaic name, tic douloureux, or idiopathic
TN, classic TN is characterized by intense, shocking, and
stabbing orofacial pain that is triggered by innocuous, gentle,
mechanical surface stimulation. Pain occurs in abrupt episodes
(paroxysms) of seconds duration, with attacks separated by
pain-free intervals. Some individuals also report the presence
of a dull, constant “background” pain in the region. Paroxysms
occur most often in the mandibular division of the trigeminal
nerve, less frequently in the maxillary division, and rarely in
the ophthalmic division. Pain rarely crosses the midline. TN
is a syndrome of aging, with onset unusual before the fifth
decade. Pain-free periods of remission may last months or even
years in the early phases of the disease. Eventually pain
episodes progress and become more refractory to all
treatments.130
PATHOPHYSIOLOGY
A strong association has been established through autopsy
study between ticlike symptoms and the presence of proliferat-
ing and demyelinating plaques found in direct apposition with
compressive loops of the superior cerebellar arteries and
veins.131,132 Although these neurovascular relationships are
not usually demonstrable on routine MRI or computed tomo-
graphic (CT) angiography,133 surgical decompression of these
vessels has been shown to yield TN pain remission in high
percentages of TN patients.134 Recent histologic and ultra-
structural biopsy analyses of trigeminal root entry tissues from
neuralgia patients undergoing microvascular decompression
surgery have confirmed the autopsy relationships seen between
vascular compression and demyelination of afferent neurons.135
These have led to an “ignition theory,” whereby pain paro-
xysms result from synchronized afterdischarges of afferent
root fibers recruited by diseased axon-to-axon “ephaptic”
cross-excitation connections.136
Fifteen percent of patients with MS also suffer from
ticlike TN attributed to multiple brainstem demyelination
plaques.137,138 It is unclear whether the neuropathic pain expe-
rienced by these MS patients is generated by “ignition”
mechanisms.
A few authors have correlated ticlike neuropathic pain
syndromes with the presence of mandibular and maxillary
bone cavities, known as “NICO” lesions, which contain
necrotic and potentially pathogenic anaerobic microorgan-
isms.139 The theory that NICO lesions are a cause of classic
TN has little scientific support.
DIAGNOSIS
The diagnosis of TN is easily established when the full syn-
drome is expressed as shocking and triggered electric pain
bursts that are experienced in precise neuroanatomic distribu-
tions and clustered around the perioral region. At the onset
of TN, however, the clinical pattern may be less classic and
150 SECTION I ■ Anesthesia and Pain Control
may easily mimic toothache, sinusitis, more diffuse stomatitis,
or other inflammatory conditions, unfortunately leading to
numerous unnecessary and ineffective ablative dental proce-
dures until the correct diagnosis is made.92 Patients in active
phases of TN, also known as status tic, display allodynia pain
responses to fine-touch stimulation during neurosensory
examination. Imaging of painful tissues is unremarkable for
consistent lesions. The neuralgiform symptoms in younger
individuals (less than 35 years of age) should alert the diag-
nostician to a possible intracranial space-occupying lesion or
intracranial arteriovenous anomalies. Other differential diag-
noses should include acoustic neurilemoma, MS, postherpetic
neuroma, or posttraumatic neuralgias.
TREATMENT
Because of the protracted and progressive clinical course of
TN, successful treatment seeks to maintain pain remissions
through the use of both medical and surgical therapies that
best fit the patient’s physical status and disease stage. There is
currently no proven permanent cure for TN. However, surgi-
cal decompression of neurovascular elements through poste-
rior fossa decompression appears to afford the most definitive,
long-term remissions, with a 10-year pain-free rate of approxi-
mately 82%.134 For this reason, patients with good health and
long life expectancies should be considered for this most defin-
itive neurosurgical treatment. However, the intracranial pro-
cedure is not without risks, with a 2% mortality rate overall
and potential for side effects of hemifacial hypoesthesia and
cranial motor deficits.140
MEDICAL THERAPY
Lidocaine testing and intravenous infusions are useful in
defining diagnosis and predicting medical efficacy for neural-
gia pain control. Intravenous lidocaine given at 5 mg/kg may
also induce early remissions and may be supplemented with
applications of 5% transdermal lidocaine patches.47
Definitive medical management for TN, however, is pri-
marily achieved with anticonvulsant agents.141 Historically,
titration and maintenance with anticonvulsant drugs (ACDs),
carbamazepine (Tegretol), and phenytoin (Dilantin) have a
high level of efficacy and are the gold standards for neuralgia
pain control. However, toxicities and allergies are common
with these agents when used long term. Many patients enjoy
remissions from more recently developed anticonvulsant
agents with less toxicity and better side effect profiles includ-
ing baclofen (Lioresal), gabapentin (Neurontin), lamotrigine,
felbamate, and pregabalin (Lyrica).142 Early stages of TN pain
may also be co-medicated by more rapidly acting benzodiaze-
pines, such as diazepam (Valium) and clonazepam (Klono-
pin). Anticonvulsant therapy is titrated over a 1- to 4-week
period until either pain remission is achieved or side effects
or toxicity are unacceptable. This class of drugs has primary
side effects of somnolence, dizziness, and ataxia, with rare
cases of hepatic dysfunction, leukopenia, and thrombocytope-
nia. When pain remission has been achieved, the ACD either
is kept at maintenance levels or withdrawn and used again for
subsequent recurrences. ACDs may also be used serially as
needed by progressing to the more potent (and toxic) ACDs
as dictated by progression of the pain syndrome.
ACDs may be used in combination with peripheral tri-
geminal blocks using long-acting anesthetics, such as bupiva-
caine (Marcaine), with or without corticosteroids to achieve
remission more rapidly. Unfortunately, for a subset of TN
patients and for patients whose syndrome has been long stand-
ing, pharmacotherapy often becomes ineffective for pain man-
agement, and surgical alternatives are needed.
SURGICAL TREATMENTS
Four anatomic levels are targeted for surgical management of
TN: (1) peripheral nerve (nerve blocks, neurectomy, radiofre-
quency neurolysis), (2) gasserian ganglion (radiofrequency
thermocoagulation, glycerolysis, balloon compression, stereo-
tactic radiosurgery), (3) trigeminal root and brainstem (micro-
vascular decompression), and (4) the brain (deep brain and
motor cortex stimulation).
PERIPHERAL NERVE PROCEDURES
Peripheral Nerve Anesthetic Blocks
Nerve blocking within trigeminal trigger zones is an effective
means of supplementing medical management of TN to obtain
pain remission and also to help palliate pain until effective
anticonvulsant blood levels can be established. Long-acting
local anesthetic agents, such as bupivacaine HCl may be com-
bined with corticosteroid and given serially as needed at the
most proximal possible nerve site. This technique, although
employed empirically by many practitioners, ironically does
not have definitive support from controlled studies in the
literature.
Blocking the trigeminal nerve with an alcohol application
has a long history of use for TN. Ninety-five percent absolute
alcohol was used in small quantities (0.5 to 2 mL) with rapid
effectiveness. However, alcohol blocks have little advocacy in
recent years because of the high levels of pain recurrence
(84%), the complication of burning alcohol neuritis, and the
availability of better surgical alternatives.143
Cryoneurolysis has also been used for TN control.144 Direct
applications of probe temperatures colder than −60 °C are
known to produce Wallerian degeneration without destroying
the nerve sheath itself. Hence regeneration of axons is
expected, and pain remissions are not usually sustained for
more than 6 weeks with this technique.
Peripheral Neurectomy
Among the oldest and most effective peripheral destructive
techniques used for TN is the simple neurectomy, performed
most commonly on infraorbital, inferior alveolar-mental, and
(rarely) lingual nerves. It is especially indicated for elderly,
debilitated patients with limited life expectancy who have
expressed their preference for neurectomy over injection tech-
niques or radiofrequency lesioning.145 Neurectomy has the
decided advantage of simplicity, reliability, and repeatability.
It has the disadvantage of producing full anesthesia or deep
 CHAPTER 9 •
hypoesthesia-related dysfunction. There is also the expected
eventual return of some pain with proliferation of amputated
nerve stump neuromas, which may be tonically painfully
active or display hyperpathic pain when stimulated
mechanically.143
Peripheral Radiofrequency Neurolysis
Radiofrequency (RF) lesioning of trigeminal nerve branches
has been used sparingly but with success.146 In this technique,
the patient is grounded in an electronic circuit, and the 22-
gauge lesion probe is positioned adjacent to the nerve to be
lesioned (topical anesthesia and mild sedation are used). Par-
esthesias are elicited to ensure proximity to the nerve, and
tissue temperature is measured at the probe tip through the
probe thermocouple. Lesioning is then carried out at 65 °C to
75 °C for 1 to 2 minutes, with repositioning to ensure ade-
quate RF-wave effect on the nerve fiber.
RF neurolysis has been shown to induce pain remission in
approximately 80% of cases, with a 20% per year recurrence
rate. Lesions appear to induce small-fiber deficits with preser-
vation of large-fiber gross-touch functions in the nerve distri-
bution. The primary advantages of this technique are its low
morbidity, even for high-risk and elderly patients. Its disad-
vantages are the need for the electronic armamentarium and
reasonable patient cooperation and the inaccessibility of some
pain-triggering nerve trunks. RF lesioning also has poor effi-
cacy for patients with long-standing chronically active stages
of TN.
GASSERIAN GANGLION PROCEDURES
Radiofrequency Ganglionolysis
The trigeminal ganglion may be approached through the
foramen ovale by percutaneously placing a 22-gauge probe
under fluoroscopic guidance. After probe placement, paresthe-
sias are elicited in the nerve distribution intended for lesion-
ing. Thermal lesions of 30- to 90-second duration are then
made at 65 °C to 75 °C using the RF generator of microwave
energies. The RF ganglion lesions have the advantages of high
pain-control predictability (greater than 97%) and selectivity
for specific nerve distributions with low morbidity risk (less
than 0.001%).147 However, RF lesioning is technically more
difficult, relapse is approximately 10% per year, and a 2% to
4% risk of severe sensory loss with associated anesthesia dolo-
rosa occurs.143 RF lesioning nevertheless has had an excellent
and well-documented record for TN pain management since
the mid-1970s. It is preferred over other percutaneous gan-
glion procedures when MS or tumor are present or when pain
is exclusive to V3 division nerves.
Stereotactic Radiosurgery (Gamma Knife)
Done as an outpatient and minimally invasive procedure, 70
to 90 grays irradiation is directed to the trigeminal ganglion
and root entry zone.148 Outcomes are similar to other neuro-
lytic procedures for TN, although there are often latency
periods of weeks before full pain relief effects are achieved.149,150
Repeat lesions may be made for recurrence as needed, and
Chronic Maxillomandibular, Head and Neck Pain 151
because of the minimal side effects with this procedure, gamma
knife is currently a favored treatment for refractory TN.
Gamma knife’s long-term efficacy is not known.
TRIGEMINAL ROOT AND BRAINSTEM
PROCEDURES
Microvascular Decompression, Posterior Fossa
Decompression (PFD)
In this procedure, an open posterior craniotomy approach is
used to gain access to the trigeminal root entry zone and
adjacent brainstem, where cerebellar arterial loops are identi-
fied, elevated, and separated from the root by an interposed
sponge barrier. This procedure, first described in the 1930s and
popularized more recently by Jannetta, is now the most com-
monly performed open intracranial procedure for managing
TN.134 It results in pain freedom for 75% to 80% of patients
at 5 years and approximately 50% remission retention at 8
years. Many patients can retain good facial sensation without
anesthetic dysfunction after undergoing PFD. It is generally
contraindicated in patients over 65 years of age. It has an
overall mortality rate of 2% and is associated with infrequent
hearing loss, vertigo, and cranial nerve VII weakness.133
BRAIN STIMULATION PROCEDURES
Implantation of deep brain stimulating units in the ventro-
caudal thalamus have demonstrated efficacy for pain manage-
ment of patients with intractable TN and other neuropathic
pain syndromes.151
More recently motor cortex stimulation has proven effec-
tive for relieving medically intractable pain.152 However, the
numbers of patients treated with brain stimulation remain
small, the mode of action is not known, and these “last ditch”
procedures are still under review.
■ POSTHERPETIC NEURALGIA
Acute herpes zoster infections of the trigeminal ganglion and
its peripheral branches are seen as bullous-vesicular eruptions
of the skin and mucosa that are confined to the neural distri-
bution and progress to crusting and finally scarring.153 Zoster
has a predilection for individuals 60 years or older and for
patients with immune suppression or debilitating systemic
disease. The acute lesions are painful, with burning sensed
throughout the affected nerve and allodynia and hyperalgesia
beginning within a few days of the outbreak. Biopsy of vesicles
confirms the presence of viral inclusion bodies within the
basilar cells. In contrast to TN, the lesions appear to involve
all branches of the trigeminal nerve equally and in some cases
may erupt in all branches simultaneously.
PATHOPHYSIOLOGY
PHN is believed to be due to a loss of inhibitory sensory func-
tions with a selective necrosis of larger trigeminal ganglion
cells by the zoster viruses.153 Accordingly, a mild loss of large
fiber fine-tactile senses is often measurable on routine neuro-
sensory examination, especially notable in the loss of vibratory
and two-point tactile sensibilities. The lesions effectively
152 SECTION I ■ Anesthesia and Pain Control
induce a partial deafferentation in the trigeminal-brainstem
complex. There is other evidence that either the deafferenta-
tion itself or the viral lesions may stimulate an up-regulation
or activation of sympathetic nerve fibers in the lesioned tri-
geminal nerve distribution, bringing about a sympathetic-
mediated pain component (see the section on complex
regional pain syndrome).
DIAGNOSIS
Chronic pain may emerge from acute herpetic symptoms and
is manifest in the trigeminal nerve distributions long after the
crusted lesions have disappeared. Patients display allodynia
pain in response to fine-touch stimulation over the face. PHN
pain is more constant than TN paroxysmal pain, and the pain
often interferes with eating, brushing the teeth, or washing
the face. Chronic PHN can be refractory to conventional
medical analgesic therapies. It is important, therefore, that the
clinician recognize the signs of emerging neural sensitization
and take preemptive therapeutic steps before central irritabil-
ity is established. Bonica has taught that two to eight stellate
ganglion blocks, given in the early weeks of zoster infection,
may prevent the emergence of chronic neuralgia.4
TREATMENT
Surgical lesioning of trigeminal nerve branches or ganglion,
effectively applied for classic TN, is ineffective for PHN.
Encouraging results have been seen recently, however, with
the use of implanted subcutaneous infraorbital and supraor-
bital stimulating electrodes for a few patients with posther-
petic TN.154 Serial trigeminal nerve blocks and stellate
ganglion blocks with bupivacaine HCl, given weekly, may
induce remission when combined with medical therapies.
The acute stages of herpetic neuralgia should be managed
aggressively with systemic steroids, such as Dosepak cortisone
(5-day course of 20 mg cortisol equivalent per day) and an
acyclovir medical regimen (200 to 400 mg four times daily for
7 days).155
Medical treatments of chronic PHN consist of both topical
and systemic therapies.156 Topical capsaicin preparations are
now available over the counter in 0.025% to 0.075% prepara-
tions. The salve is applied to painful cutaneous tissues,
frequently daily. Therapeutic effect of capsaicins has been
reported as cumulating over a 30-day time frame and has been
attributed to a depletion of substance P, a neuropeptide medi-
ator of heightened activity in C nociceptors.157
The systemic therapies of choice for constant PHN are
tricyclic antidepressants, anticonvulsant agents, α-adrenergic
blocking agents, and systemic lidocaine. Tricyclic therapy is
initiated at low doses (from 25 to 50 mg amitriptyline equiva-
lents) and titrated until pain remission is achieved.158 The
tricyclic side effects of sedation, fluid retention, and xerosto-
mia are unfortunately not well tolerated by older patients, who
make up the bulk of patients with PHN.
Anticonvulsant agents are indicated, especially for those
cases of PHN in which touch-triggered pain predominates or
shocking paresthesias are present. Gabapentin (Neurontin)
and pregabalin (Lyrica) have shown particular effectiveness
when titrated carefully.159,160
In those cases in which stellate ganglion block testing has
afforded significant but transient pain relief, medical treat-
ment with the α2-agonist clonidine (Catapres) may be effec-
tive.161 This agent, marketed as a transdermal patch system,
delivers 0.1, 0.2, or 0.3 mg clonidine per day, with one patch
applied to the painful region weekly. Patients using the cloni-
dine transdermal systems should be monitored closely for
orthostatic hypotension and excess fatigue.
Topical lidocaine therapy, delivered as a 5% transdermal
patch system, has been shown to be effective for control of
PHN without the side effects of tricyclic or anticonvulsant
therapy.162 This system is available for delivering 5% lidocaine
when applied to the allodynic skin regions for 12-hour periods.
Systemic lidocaine, delivered to patients intravenously with
serial target dosing at 5 mg/kg, has also proven useful for
patients with intractable PHN.47,156
■ POSTTRAUMATIC
NEUROPATHIC PAIN
Trauma to the cranium, neck, face, and jaw is a common ini-
tiator of chronic pain syndromes seen for management by oral
and maxillofacial surgeons. The major posttraumatic chronic
disorders are (1) posttraumatic headache (postconcussion syn-
drome), (2) posttraumatic TN, and (3) complex regional pain
syndrome (CRPS). Acute trauma to the cervical spine and
TM articulation is also a common precipitating event for
chronic head and neck pain. Because these syndromes are
primarily nonneuropathic, however, they are discussed in the
section on the musculoskeletal compartment. A unifying and
paradoxical aspect of all posttraumatic disorders is that there
is a poor relationship, and in many cases an inverse correla-
tion, between the severity of trauma and the level of chronic
neuropathic pain that results.41
POSTTRAUMATIC HEADACHE
Posttraumatic headache, also known as post-closed head
injury syndrome (PCHI) and postconcussion syndrome, is a
chronic central neuropathic pain condition. Primary com-
plaints after head injury are early-onset daily headache, dizzi-
ness, fatigue, and moderate to severe sleep dysfunction.163 The
effects may be delayed for days to weeks following injury.
Cognitive deficits are also seen for short-term memory, the
ability to sustain mental concentration, motivation, voca-
tional performance, and social relationships.164 Sleep dysfunc-
tion and insomnia and flashbacks to the injury are seen along
with deficits in non-REM stage III and IV sleep. Consequently,
there is a common association of head trauma with bruxism
and FM.165
Studies of a large series of patients who had sustained mild
traumatic brain injury (loss of consciousness less than 20
minutes, Glasgow coma scale greater than 13) revealed a 79%
to 89% incidence rate of chronic head and neck pain 3 months
after injury.166 The pain pattern is usually described as con-
stant and poorly localized in frontal, parietal, temporal, and
 CHAPTER 9 • Chronic Maxillomandibular, Head and Neck Pain
occipital regions. Symptoms may persist for months or even
years. Pain persistence for 3 years or more is reported in 15%
to 31% of cases, with pain for more than 4 years likely to imply
permanency. Although increasing age predisposes the patient
to slower and less complete recovery, young persons exposed
to repetitious mild head trauma from sports injuries are also
at risk.167 A high frequency of this syndrome among women
with chronic “idiopathic” headache may be due to battering.
One study reported that 66% of women with idiopathic head-
aches had experienced physical and sexual abuse in the
past.168
The development of posttraumatic headache does not cor-
relate well with severity of unconsciousness, amnesia, or skull
fracture. A number of studies show that there is in fact an
inverse relationship between the severity of trauma and the
incidence and severity of headache.169 A seemingly paradoxi-
cal lack of pain in more severely head-injured patients has
been attributed to an inability of the more severely impaired
patient to integrate or articulate as complex as a symptom
complaint, such as head pain. Persisting symptoms in this
population have often been attributed to a form of “accident
neurosis” associated with malingering, litigation, and insurance
claim seeking.170 Several studies have now refuted this conten-
tion, however, and have shown that legal settlements do not
usually bring a termination of clinical symptoms or the ability
to carry out normal work-related cognitive functions.171
PATHOPHYSIOLOGY
Mechanisms of posttraumatic headache remain controversial.
It has been attributed to three main factors: brain injury,
muscular, and vascular.165 Diffuse axonal necrosis has been
described in human autopsy studies and experimental animal
head injury models.173 Direct blunt trauma of the brain against
the inner skull may produce brain surface microhemorrhage
either from direct injury or from contrecoup (opposite pole)
trauma. Rapid flexion of the cervical spine has been impli-
cated in diffuse injuries to the core reticular system of the
brainstem, causing alteration of central pain processing.174
There is also a known association of chronic posttraumatic
headache with cervical spine injury and associated cervical
muscle strain and possible brain ischemia from vertebral artery
spasm during neck flexion-contraction or rotation.175
Current opinion is that chronic pain after closed head
injury results from a combination of peripheral injury to
muscle, nerve, and vertebra and central disturbances of
pain modulation. The central disturbances are most likely
to involve brainstem neurotransmission, possible NMDA-
receptor sensitization mechanisms, and alterations of both
ascending and descending influences from the anterior
brainstem.35
DIAGNOSIS
A diagnosis of posttraumatic headache remains one of exclu-
sion because there is typically an absence of objective findings
on examination. Electrodiagnostic testing, imaging with
CT scan or MRI, or electroencephalography rarely reveal
153
abnormality. The general neurologic examination is usually
normal, although tender-point pain responses are often noted
in cervico-occipital, trapezial, and temporalis musculature.
Because of the high frequency of roadside bomb blasts and
improvements in cranial and thoracic body protection, sol-
diers are surviving and returning from current Middle Eastern
wars with a high rate of traumatic brain injuries (TBI). Sur-
geons treating these patients for chronic pain disorders should
be aware of the obvious overlap between TBI and “posttrau-
matic stress syndrome,” estimated by lay sources to be as high
as 30% of returning soldiers.
TREATMENT
Because oral and maxillofacial surgeons are often involved in
the management of patients with acute head and neck trauma,
they are often in a favorable position to recognize and to help
manage the chronic effects as well. Treatment of chronic
posttraumatic pain consists of (1) eliminating sources of aggra-
vating extracranial nociceptive pain, such as TM and cervical
myofascial pain; (2) reversing the central neuropathic pain
factors, especially sensitization, depression, and sleep disorder;
and (3) assisting patients in their rehabilitation from neuro-
psychiatric disability.
Medical therapies for posttraumatic headache select from
combinations of antidepressant, anticonvulsant, and narcotic
drugs. The tricyclic antidepressants have a long history of
varying success with central neuropathic pain.176 Amitripty-
line equivalents of 25 to 100 mg (given as single doses at
bedtime) are helpful, especially for patients with insomnia or
frequent sleep arousals. The serotonin reuptake inhibitors,
such as fluoxetine (Prozac) or sertraline (Zoloft; 20 to 40 mg/
day), have not been as extensively tested as the tricyclic
agents for managing neuropathic pain.177 They may be more
useful, however, for patients with excessive daytime anxiety.
The most promising anticonvulsant agent for treatment of
patients with postconcussion pain has been gabapentin and
the recently introduced pregabalin (Lyrica).160,178 Their advan-
tages are lower toxicity and side effects when compared with
more traditional agents, such as carbamazepine, phenytoin, or
valproic acid. Gabapentin can be titrated rapidly to 1800 mg/
day and then increased to 2400 mg/day within 2 weeks if pain
levels are improving. Narcotic use for chronic neuropathic
pain remains controversial. However, it appears that many
patients are helped toward more functional pain management
by maintaining a daily strict regimen of moderate-toxicity
narcotics, such as hydrocodone or slow-release (twice daily)
oxycodone.
Behavioral pain management therapies for brain-injured
patients are important and are directed toward teaching
patients how to reduce negative pain behaviors and disability.
Rehabilitation focuses on cognitive perceptual motor retrain-
ing and is done to assist patients in the reacquisition of fine
motor and reasoning skills. Such programs can often be carried
out through a pain management center, if available, where
psychotherapy and occupational and physical therapeutic
interventions can be coordinated.
154 SECTION I ■ Anesthesia and Pain Control
POSTTRAUMATIC TRIGEMINAL NEURALGIA
Trauma to the peripheral trigeminal nerves is a common
source of chronic neuropathic pain.179 The most common
causes are maxillomandibular contusions and fractures, where
the inferior alveolar and infraorbital nerves are almost always
involved and chronic pain persists in up to 35% of cases.180,181
Iatrogenic injuries to inferior alveolar and lingual nerves also
occur during third molar surgery in approximately 1% to 4%
of cases, and an estimated 13% of those injured experience
chronic pain.182,183 Endosseous implant surgery accounts for an
increasing number of cases of mandibular dysesthesias, espe-
cially in those patients with more severe bony atrophy and in
those who undergo nerve repositioning surgeries.184,185 Chronic
neuropathic pain from local anesthetic injuries, although rare
in comparison with the number of injections carried out, are
nevertheless especially painful and refractory to treatment.186,187
Similarly, nerves injured by root canal instruments or chemi-
cals cause a painful sensory nerve toxicity that is difficult to
treat.188 Orthognathic surgery, especially sagittal mandibular
osteotomies, has a high incidence of direct or indirect nerve
injury and an unknown incidence of chronic neuropathic
pain.189,190
Nerve injuries are historically classified according to the
degree of neuroanatomic disruption, ranging from no gross
surface disruption with electrophysiologic impairment (Type
I, Sunderlund),191 or neurapraxia, Seddon,192 to intermediate
levels of axon damage (Type 2, or axonotmesis), and finally
to total discontinuity or severe mixed nerve injuries (Type 5,
or neurotmesis). This linear classification of nerve injuries is
helpful for defining the degree of severity of tissue disruption
and correlates well with deficits in neurosensory functions.
However, this system breaks down as a predictor of pain sever-
ity. It does not account for injuries such as ischemic, chemical,
burn, or cryologic trauma, where there may be little or no
apparent damage to peripheral neural structures, as in Sunder-
lund Type 2 to 3 injuries, yet pain and dysfunction may be
extreme.
A nearly universal complaint of patients who have sus-
tained peripheral trigeminal nerve injuries from any source is
that they report their surface tissues to be “numb.” The major-
ity do not find their neuropathy to be painful, although they
may complain of a variety of dysfunctions and disabilities.
Among those who complain of pain after nerve injury, two
clinical patterns are preponderant: hypoesthetic (Type I) and
hyperesthetic (Type II).193 Type I (hypoesthetic) patients
complain of deep pain in the injured nerve region that tends
to be constant, dull, deep, and aggravated by mechanical pres-
sures or percussion over the injured region. This phenomenon
is known as hyperpathia, defined as “a painful syndrome char-
acterized by an abnormal painful reaction to a stimulus, espe-
cially a repetitive stimulus, and increased threshold.”10 When
examined with quantitative sensory testing, Type I patients
are deficient in neurosensory responses to all levels of stimula-
tion. When local anesthetic nerve blocks are applied proximal
to the injured nerve region, Type I patients tend to indicate
only partial pain remission, suggesting mechanisms other than
simple peripheral nerve irritability. Patients with type I post-
traumatic syndrome often report minimal pain immediately
after injury and test anesthetic or severely hypoesthetic. With
time, however, often with delays of weeks to months after
injury, the hyperpathic pain emerges and becomes constant.
Type II (hyperesthetic) patients, by contrast, have pain
within hours to days of their nerve injury. This pain is described
as “shocking, tingling, burning, electric, and episodic.”193 A
prime clinical feature of Type II pain is the triggering or
“ticlike” phenomena of allodynia and hyperalgesia. Allodynia
is defined as “pain due to a stimulus which does not normally
provoke pain.”10 In this condition, fine-tactile stimuli, such as
light brushing of mucocutaneous tissues, elicits a shocking,
painful response throughout the nerve distribution. Some
patients find that simple skin movement, windy conditions,
or light activities, such as kissing, elicit pain. Hyperalgesia
means “an increased response to a stimulus which is normally
painful.”10 In this case a moderate tissue pinch with a hemo-
stat or hot instrument applied to the skin is reported as exces-
sive in the neuropathic distribution when compared with their
uninjured normal tissues. Type II patients commonly display
both allodynia and hyperalgesia in their injured nerve distri-
butions. Local anesthetic nerve blocks produce a transient but
complete remission from allodynia and hyperalgesia. Patients
may report, however, that a deeper, aching pain persists after
blocking, in which case the possibility of mixed Type I and
Type II injury pathophysiology may be suspected.
PATHOPHYSIOLOGY
As is the case with cranial trauma and cervical spine injuries,
the severity of chronic pain syndromes that result from periph-
eral nerve injury is often poorly correlated with the degree of
tissue damage. This conclusion is supported by information
from both experimental animal injury pain models and human
case series. The primary experimental model of neuropathic
pain developed by Bennett and Xie demonstrates that a
chromic ligature tied loosely around an exposed rodent sciatic
nerve is more likely to induce response behavior suggestive of
severe pain (squealing to touch) than is full transection of the
nerve.194 Human studies also indicate that partial nerve inju-
ries, such as traction, compression, chemical, and burn trauma,
are more likely to induce the more severe forms of shocking
(Type II) pain patterns than are more complete nerve transec-
tion and mutilating amputation injuries.41
There is evidence that chronic posttraumatic pain is due
to a sensitization of both the injured peripheral nerve and its
associated central nervous centers.18,26 Peripheral mechanisms
known to be significant include a tonic hyperactivity of
peripheral nociceptor, spontaneous pain generation from trau-
matic neuromas, and changes in the peripheral autonomic
nervous system.
Traumatic neuromas occurring in the maxillofacial region
assume the configuration of their locality and the specific
injury type,195 and although a majority of trigeminal neuromas
are likely nonpainful, many are a source of neuropathic pain
 CHAPTER 9 • Chronic Maxillomandibular, Head and Neck Pain
and disturbed sensory function. The mechanisms of neuroma
pain remain controversial. There is evidence that neuromas
contain an excess of hypersensitive, small A delta and C
nociceptive fibers displaying an excess of the excitatory neu-
ropeptides calcitonin gene-related peptide (CGRP), substance
P, and vasoactive intestinal polypeptide.16,17 There is also evi-
dence that human trigeminal neuromas contain cross-fiber
interconnections (ephapses), which could serve as an ana-
tomic basis for the amplification of sensation and tingling that
is characteristic of neuromas.196 A final possible basis for neu-
ropathic pain associated with neuromas is based on a prolifera-
tion or up-regulation of autonomic receptors within the nerve
injury and neuroma region.22,23 This collision phenomenon
between somatosensory nerves (trigeminal) and autonomic
(sympathetic) elements has been postulated as the basis for a
particular type of postinjury neuropathic pain known as
chronic regional pain syndrome (CRSP).197,198
Increased excitability of receptive neurons in the dorsal
horn regions of the spinal nucleus of cranial nerve V is now
considered a primary central basis for chronically sustained
neuropathic pain following nerve injury.29,199,200 In a mecha-
nism of traumatic sensitization known as “windup,” it is pos-
tulated that a barrage of low-level repetitive C fiber noxious
input from the injured nerve and active neuroma activates
excitatory amino acid glutamate, specifically the NMDA
receptor.24 Glutamate is believed to produce a sustained
opening of the calcium channels of the recipient central
neuron, recruiting intracellular enzymes, such as nitric oxide
and cyclooxygenase, to mediate the process.16 This phenome-
non may explain the rapid emergence of triggering with type
II pain, where allodynia and spreading hyperalgesia are promi-
nent clinical features. NMDA-receptor antagonistic drugs
would appear to be important agents for future management
of centralized neuropathic pain.
Nerve injury type I pain, however, with its onset delayed
for days or weeks following injury and its association with
major sensory deficit or anesthesia, is better explained by a
CNS phenomenon known as deafferentation hypersensitiv-
ity.193,201 Such loss of all normal input is more associated with
class IV and V major transection injuries, with resulting
severely disorganized amputation neuroma. In deafferentation
cases, a central irritable focus is postulated that may have an
impact at levels central to the spinal cord, extending to tha-
lamic and possibly cortical levels, where phantom phenomena
and neuropsychologic and neuroendocrine derangements may
accompany the “anesthetic” pain syndrome.202
Although it is tempting to explain Type I versus Type II
posttraumatic pain types on the basis of specific differentiating
neural mechanisms, this attempt often breaks down clinically
because patients have mixed injury types.
DIAGNOSIS
A systematic protocol is recommended for evaluating patients
with chronic pain after nerve injury that incorporates mea-
surement of pain and dysfunction, QST, and neuropharmaco-
logic response testing.
155
The differential diagnostic challenge for posttraumatic TN is
classic TN and PHN. The coexistence of these neuropathic
syndromes is, however, rare and can be easily resolved by
taking a thorough history. More often it will be necessary to
identify sources of pain that are nonneuropathic, such as mus-
culoskeletal and vascular pain sources, often found along with
neuropathic pain following traumatic events. Establishing the
link between injury and posttraumatic neuropathic pain is
usually simple: a history linking the trauma event to pain
onset and a pain distribution that conforms to known periph-
eral neuroanatomic distribution.
A greater diagnostic challenge is in determining the loci
and mechanisms acting in a given posttraumatic pain syn-
drome. CT imaging may reveal paraneural foreign body, hard
tissue lesions, or neurovascular canal distortion. Currently
available MRI, however, does not adequately define the
microanatomy of injured nerve to allow definitive diagnosis
of neuroma.
QST has the dual purpose of detecting triggering phenom-
ena and exposing neurosensory deficits through stimulus-
response testing.41,90,203,204 The neurologic examination begins
with testing of deep tendon reflexes and gross cranial motor
nerve functions. Barring generalized findings, the examination
proceeds directly to QST. A three-level “drop-out” test scheme
is recommended in which increasingly noxious stimuli are
applied to the painful nerve-injured tissues, and responses are
compared when similar stimuli are applied to contralateral or
adjacent uninjured and nonpainful tissues.40,44 The first level
of stimulus-response testing applies fine-touch stimuli, such as
brush directional stroking or two-point touch stimuli. Painful
responses to these stimuli indicate allodynia, a cardinal feature
of Type II neuropathic pain with central sensitization. If
patients are unable to detect the fine-tactile stimuli or are
measurably deficient, they are considered hypoesthetic and
tend to fit the Type I pain pattern. A second level of response
testing uses crude-touch stimuli, such as graded punctate von
Frey (Semmes-Weinstein) filaments. Percussion or digital
pressure over neurovascular bundles may also lead to painful
hyperpathic responses, which suggests the presence of periph-
eral neuroma at or near these sites. The third level of testing
applies tolerable painful stimuli to control and injured tissues,
such as hemostat pinch, deep pin pressure, or hot stimuli in
the range of 40 °C to 48 °C. A patient report that the pain
is significantly greater in the injured nerve distribution indi-
cates hyperalgesia. If the patient is unable to identify the
noxious stimuli accurately (i.e., they are anesthetic or severely
hypoesthetic), the assumption is that their painful nerve
lesion is an amputation neuroma or severely fibrosed
neuroma-in-continuity.
Neuropharmacologic testing is useful for patients with trau-
matic neuralgias because it helps define loci and mechanisms
of pain generation. It is also used to predict the efficacy of and
to direct potential surgical, pharmacologic, and physiologic
therapies. Three clinical neuropharmacologic tests are useful:
paraneural lidocaine block, intravenous lidocaine, and stellate
ganglion block (see the section on pharmacologic screening).
156 SECTION I ■ Anesthesia and Pain Control
TREATMENT
A full description of comprehensive treatments for problems
associated with trigeminal nerve injuries is presented in a
separate chapter in this textbook (“Treatment of Trigeminal
Nerve Injuries”). This current chapter therefore will focus
exclusively on treatments for trigeminal injury pain.
Effective treatment of chronic posttraumatic neuralgia is
dependent on a recognition of the widely divergent syndromes
that are encompassed by this term. No single medical, physi-
ologic, or surgical treatment is effective for all forms of trau-
matic neuropathic pain, and unfortunately, at this time there
are some forms of posttraumatic neuropathic pain for which
there are no fully effective treatments.
Acute Nerve Injury Pain Management
A primary goal of acute nerve injury management is to sup-
press the acute pain effects of injury and prevent the emer-
gence of chronic neuropathic sensitization. Emphasis is placed
on removing sources of repetitive secondary trauma or inflam-
mation impacting on the injured nerve, which, even if occur-
ring at low intensity levels, could lead to the sensitization
“windup” process. Observed injured nerves are freed of com-
pressing foreign body, alloplast, implant, and bone or tooth
fragments. If possible the exposed nerve is lavaged with iso-
tonic solution and barrier protected. Infection and inflamma-
tion control, both locally and systemically, should be
maximized. Classic immobilization and local cryotherapy in
the nerve-injury region is employed. Antiinflammatory, opiate
analgesic agents, and psychosedation for anxiety control and
sleep promotion are used aggressively to minimize CNS exci-
tation. Local anesthetic nerve blocks with long-acting agents
and corticosteroids, such as dexamethasone, are applied in the
nerve-injury regions to minimize perineural inflammation
during the first postinjury week.205 Rapid-acting anticonvul-
sant agents, such as clonazepam, in divided doses, 2 to 10 mg
daily may further protect the CNS.206 Topical lidocaine is
delivered either by p.r.n. lidocaine gels or through sus-
tained 12-hour release 5% transcutaneous lidocaine patch
applications.45
Behavioral Management
At all stages after nerve injury or repair, patients can benefit
from sensory reeducation stimulation techniques.207 The psy-
chological support for the nerve-injured patient, with full
attention to his or her needs and expressed concern by the
clinician, is of utmost importance, especially in the acute
injury stage. Full chart documentation of observations, events,
therapies, and patient and professional consultations should
be made to prevent future confusion during the patient’s sub-
sequent nerve-injury recovery.
Pharmacologic Treatments
For intermediate and more chronic forms of nerve-injury pain,
pharmacotherapy stresses anticonvulsant, antidepressant,
and, on occasion, α-adrenergic agents. Currently the most
promising anticonvulsant agents are gabapentin titrated from
900 to 3000 mg daily as tolerated to pain relief.178 The more
recently introduced agent pregabalin (Lyrica) also has a very
favorable toxicity and side-effect profile, but has not under-
gone control study among trigeminal-injured patients.160
Anticonvulsant drugs may be combined with nightly tricyclic
antidepressants if sleep dysfunction and depression are com-
ponents of the pain syndrome.208 For patients who have dem-
onstrated temporary pain remission with stellate ganglion
block testing, the α2-adrenergic agonist clonidine (0.1 to
0.3 mg/day as tolerated) may be administered through a trans-
dermal patch applied in the painful region.161 Local anesthetic
blocks in proximal regions of the painful injured nerve, with
or without corticosteroid, may also aid in gaining pain remis-
sion and in refractory cases, can be delivered as sustained doses
through indwelling paraneural catheter.4
Because of the central role of NMDA receptors in the
pathophysiology of traumatic neuropathic pain, NMDA
agonist-antagonist agents may eventually have great efficacy
for these patients. And although two NMDA-receptor antag-
onistic drugs, dextromethorphan and ketamine, do exist, no
practical systems are currently available for their clinical
use.209,210
Physiologic Treatments
Approximately half of the patients with chronic posttraumatic
neuralgia report greater than placebo levels of pain relief from
the use of transcutaneous electrotherapy, including transcuta-
neous electrical nerve stimulation (TENS).211 Patients with
triggering neuropathic type II injury pain do not tolerate the
stimulation electrode contacts well, however, and may experi-
ence an exacerbation of allodynia. There appears to be little
uniformity among neuropathic pain patients regarding their
responses to cryologic or thermal physical therapies. Some
patients appear cold sensitive and report increased pain with
any cold stimulus. Others, especially those with complaints of
“burning pain,” find relief with ice applications.
SURGICAL TREATMENTS
Surgical intervention for patients who have sustained periph-
eral nerve injury is done for two reasons: to restore sensory
function and to manage pain. Unfortunately, surgeries that
are effective for improving function are not as successful at
relieving pain. Nevertheless, surgical treatments can be con-
sidered for those patients with chronic posttraumatic neural-
gia whose pain has not improved spontaneously, has been
refractory to nonsurgical therapies, and is associated with sig-
nificant function impairment. The main surgical options for
posttraumatic pain are (1) surgical repairs, (2) ablative surgi-
cal lesioning, (3) stereotactic radiosurgery, and (4) brain
stimulation therapies.
Trigeminal surgical repairs. Microsurgical repair out-
comes of damaged lingual and inferior alveolar nerves
using extraneural decompressions, neuroma resection, and
direct reanastomosis (neurorrhaphy) have produced good
results for restoration of basic neurosensory functions.212,213
 CHAPTER 9 •
Unfortunately, there is a dearth of controlled studies regarding
the efficacy of surgical repairs among patients with traumatic
dysesthesias.214 The available reports indicate that surgical
repairs reduce preoperative pain levels greater than 50% for
those patients who (1) have experienced intractable hyperes-
thetic (Type II) posttraumatic pain; (2) respond favorably to
local anesthetic test blocks in the distribution of nerve injury;
and (3) have sustained recent Level 4 or 5 injury and display
amputation or severe in-continuity neuroma at time of surgi-
cal exposure.214 Unsatisfactory surgical outcomes for patients
have been found among patients with (1) long-standing deaf-
ferentation pain in anesthetic zones, (2) burning pain follow-
ing local anesthetic or endodontic chemical injuries, and (3)
patients who display clinical signs of central or autonomic
sensitization (spreading secondary hyperalgesias, erythema,
and swelling episodes).215
Surgical lesioning. Ablative neurosurgical procedures are
indicated among patients with intractable traumatic dyses-
thetic pain when nonsurgical and reparative surgical proce-
dures are not possible or have been unsuccessful. They are
indicated for patients who experience pain relief after local
anesthetic nerve block of the injured region and especially for
localized triggered pain. They are contraindicated for type I
patients with phantom pain in already anesthetic zones or for
patients whose pain is referred and of broad, hemifacial distri-
bution. A wide spectrum of lesioning techniques have been
used historically with success in selective cases. Lesioning can
be done at peripheral nerve sites or, as described for treatment
of classic TN, at trigeminal ganglion levels.
Neurectomy is the simplest and most proven peripheral
ablative method. Nerve destruction with paraneural injection
of absolute ethanol was widely used in the past, but is no
longer recommended because of high rates of burning pain
recurrences and localized tissue sloughing. Cryosurgical nerve
lesioning has also been advocated as a technique for inducing
Wallerian degeneration with minimal scarring of the nerve
trunk. Regeneration of fibers is expected within weeks to
months, however, and “ice-cold” postlesion pain does occur.
Other ablative techniques have been attempted to lesion
more selectively. RF lesioning of accessible peripheral nerves
is an option that preserves larger-fiber sensitivities while
blocking small-fiber pain functions.146 More recently there
have been promising reports of the use of low-level laser and
peripheral stimulation techniques for diminishing neuropathic
pain and improving dysesthesias.154,216,217,218 These techniques
may be effective in suppressing abnormal neural activity by
producing changes in conduction velocities in the photosensi-
tive peripheral nerves.219
STEREOTACTIC RADIOSURGERY (GAMMA KNIFE)
Available as an outpatient and minimally invasive procedure,
“gamma knife” therapy is stereotactically directed to the tri-
geminal ganglion and root entry zone, radiating with 70 to 90
grays.148 Outcomes are similar to other neurolytic procedures,
although there are often latency periods of weeks to months
before full pain relief effects are achieved.149,150 Repeat radio-
Chronic Maxillomandibular, Head and Neck Pain 157
surgery procedures may be carried out in cases of neuralgia
recurrence. The long-term efficacy of gamma knife is not
known, and studies of its efficacy for posttraumatic neuralgias
are lacking.
BRAIN STIMULATION PROCEDURES
For an unfortunate number of patients with posttraumatic
neuralgia, no reparative or ablative procedure appears to be
effective for relief of pain. Such patients may benefit from the
implantation of CNS microelectric stimulators placed at the
nerve root entry zone or on the surface of the brainstem.220
Implantation of deep brain stimulating units in ventrocau-
dal thalamus have also demonstrated efficacy for pain manage-
ment of patients with intractable forms of TN and other
neuropathic pains syndromes.151 Motor cortex stimulation has
also proven effective for relieving medically intractable pain.152
However, the numbers of patients treated with all forms of
brain stimulation remain small, the mechanism of action is
not known, and these “last ditch” procedures are still under
review.
COMPLEX REGIONAL PAIN SYNDROME
The term complex regional pain syndrome (CRPS) has been
adopted to refer to posttraumatic disorders whose pathophysi-
ologies appear to link dysfunction of both the peripheral affer-
ent and sympathetic nervous systems with secondary spread
into the central pain complex.221 Classic CRPS cases are
sequelae of nerve injuries and are characterized by burning
pain with hyperpathia and allodynia and by pain exacerbated
by fear, anger, or emotional distress.222 CRPS has been further
divided into CRPS I, for complete transection nerve injuries
of the reflex sympathetic dystrophy type, and CRPS II for
partial injuries similar to causalgia. Both forms are best known
for traumas to the upper extremity, occur more often in
women, have a peak occurrence at age 50, and may involve a
genetic predisposition.223 Patients also demonstrate varying
degrees of vasomotor and trophic changes. Pain distributions
often expand with time to extend beyond the confines of the
originally injured nerves, a clear indication of central
sensitization.221
Head and neck CRPS may follow any form of accidental
trauma, including facial fractures or brain injury, but more
often follow incomplete nerve injuries from activities, such as
needle-injection injury, orthognathic surgery, endosseous
implant injury, or dentoalveolar surgery. In other cases, spread-
ing and triggered pain phenomena may follow what would
appear to be minor trauma, such as restorative dental or peri-
odontal procedures.128 Whatever the source, stretch-traction,
ischemia, or partial nerve crush injuries appear to be more
significant than complete transection or avulsion injuries.224
Pain in these cases rapidly follows within hours to a few days
of injury in contrast to postamputation nerve injury, in which
pain slowly emerges weeks to months after the trauma.
Although the incidence of CRPS following extremity inju-
ries is believed to be 5% to 7%, the incidence in the head and
neck is unknown. There are no controlled epidemiologic
158 SECTION I ■ Anesthesia and Pain Control
studies of orofacial CRPS or even large series of patients veri-
fied with consistent criteria. Some authors have speculated
that it is infrequently seen following head and neck trauma
because of the anatomic differences between head and neck
sympathetic anatomy, where postganglionic fibers course sepa-
rated from the primary somatosensory nerves as compared
with the extremities, where the two types of fibers coexist in
singular neurovascular sheaths.225
IDIOPATHIC AND ATYPICAL OROFACIAL
PAIN SYNDROMES
Other authors speculate, however, that CRPS II of the head
and neck and orofacial region following minor or vague injury
history may be quite common. A cluster of idiopathic condi-
tions resemble CRPS II as variants for the orofacial region and
include: idiopathic facial pain IFP,226 atypical facial pain and
odontalgias, “burning tongue or burning mucosa” pat-
terns,227,228,229 and “phantom tooth” syndromes.230,231 These
syndromes have in the past been commonly misdiagnosed and
have been attributed to purely psychogenic mechanisms with
little scientific support.128
PATHOPHYSIOLOGY
Although the full understanding of CRPS pathophysiology is
still not known, it appears that this syndrome results from
impairments in peripheral somatosensory, autonomic, and
central mechanisms.198,221 The exact mechanisms by which
the peripheral sympathetic nerves and the primary afferent
nerves become pathologically coupled following peripheral
injury is also unclear.23 Functional adrenoreceptors somehow
appear in the membranes of afferent neurons, possibly by up-
regulation of existing adrenoreceptors, novel (genetic) syn-
thesis of adrenoreceptor mRNA, or uncovering of “hidden”
adrenoreceptors. Coupling has been theorized as being directly
chemical via α-adrenergic receptors acting on the traumatized
nerve or neuroma or its trigeminal ganglion, or both, or indi-
rectly via the paraneural vascular bed.224 “Ephaptic” fiber cou-
pling has been described for afferent axons in experimental
neuromas.21,197 Connections between sympathetic and afferent
fibers has not been proven, however, in humans. Crush trauma,
however, is known to stimulate nerve growth factor produc-
tion by Schwann cells earlier than following nerve transec-
tion. This in turn may encourage the growth of sympathetic
nerves to invade the injured nerve regions and form abnormal
(ephaptic) contacts.232
Central nervous sensitization is a likely mechanism of
CRPS with ascending thalamocortical pain center activation
and disruption of descending pain inhibition systems.26,27,35,221
DIAGNOSIS
Pain in the orofacial region as a result of sympathetic media-
tion follows the topography of the (sympathetically inner-
vated) vascular system as opposed to the classic trigeminal
nerve branch dermatome. Local anesthetic blocks of the origi-
nally injured trigeminal nerve region often do not afford full
pain relief in CRPS patients. By contrast a cardinal diagnostic
sign for CRPS is pain relief with stellate ganglion blocking.
Imaging with thermography may also demonstrate vasomotor
abnormalities. Patients may have mucocutaneous erythema
and diffuse swelling, although they do not display the dramatic
trophic effects or skeletal dissolution seen for extremity reflex
sympathetic dystrophy (RSD). Neurosensory examination
often reveals little threshold deficits in pain regions; patients
may even respond above thresholds for detection of fine-touch
stimuli. As CRPS progresses in severity, key clinical signs of
CNS derangement are seen: spread of painful territory, decreas-
ing pain thresholds, secondary (surround) allodynia, and
hyperalgesia.221,233
TREATMENT
Patients in whom signs of CRPS appear to be developing
acutely after injury may benefit from oral corticosteroid treat-
ments.234 Although physical therapies with electrotherapy,
regional heat, and range-of-motion exercises are first-line
treatments for CRPS of the extremities,48 there are no reports
of comparable physical therapy being effective for patients
with head and neck CRPS. Classic research points to preven-
tion of autonomic syndrome onset by delivery of repetitious
sympathetic nerve blocks in the early period after injury.4,23
For chronic intractable CRPS, weekly stellate ganglion
blocks may be supplemented by the use of the oral α2-agonist
clonidine.222 With the transdermal patch system applied
directly to the painful region if possible, clonidine is delivered
at doses of 0.1 to 0.3 mg daily over a sustained time frame as
needed.161 Primary side effects of clonidine therapy are hypo-
tension and nausea. It has been shown that topical capsaicin
applications are also effective in some patients with atypical
odontoma and also more generalized oral neuropathic
pain.129
In general patients with CRPS and idiopathic “atypical”
conditions do not respond well to ordinary postsurgical levels
of narcotic analgesics, with an efficacy of less than 40%.58
Tricyclic antidepressants (amitriptyline, imipramine) have
been shown to be more effective than the serotonin receptor
reuptake inhibitors, such as paroxetine or citalopram.176 More
recently anticonvulsant agents with improved side-effect pro-
files, such as gabapentin and pregabalin, have shown improved
efficacy for CRPS and idiopathic pain conditions and may
co-medicate with antidepressant medical therapies.178
There are also no proven effective surgical treatments for
chronic CRPS. Recent repairs of injured peripheral spinal
nerves using collagen entubulation grafting, however, have
shown promise in relieving intractable CRPS pain.235
REFERENCES
1. Bonica JJ: The management of pain, ed 2, Philadelphia, 1990,
Lea & Febiger.
2. McMahon SB, Koltzenburg M, editors: Wall and Melzack’s text-
book of pain, ed 5, Philadelphia, 2006, Elsevier, Churchill
Livingstone.
3. Okeson JP: Bell’s orofacial pains, ed 6, Chicago, 2005, Quintes-
sence Books.
 CHAPTER 9 •
4. Bonica JJ: Local anaesthesia and regional blocks. In Wall PS,
Melzack R, editors: Textbook of pain, ed 2, Edinburgh, 1989,
Churchill Livingstone.
5. Schwartz BS et al.: Epidemiology of tension-type headache,
JAMA 279:381, 1998.
6. Lipton JA, Ship JA, Larach-Robinson A: Estimated prevalence
and distribution of reported orofacial pain in the United States.
J Am Dent Assoc 124:115, 1993.
7. Wijnhoven HAH, de Vet HCW, Picavet HSJ: Explaining sex
differences in chronic musculoskeletal pain in a general popula-
tion, Pain 124:158, 2006.
8. De Leeuw R et al.: Prevalence of traumatic stressors in patients
with temporomandibular disorders, J Oral Maxillofac Surg
63(1):42, 2005.
9. LeResche L et al.: Relationship of pain and symptoms to puber-
tal development in adolescents, Pain 118:201, 2005.
10. Merskey H, Bogduk N, editors: Classification of chronic pain:
descriptions of chronic pain syndromes and definitions of pain terms,
ed 2, Seattle, 1994, IASP Press.
11. Devor M: Pain mechanisms and pain syndromes. In Campbell
JN, editor: Pain 1996: an updated review, Seattle, 1996, IASP
Press.
12. Cervero F, Laird JMA: Mechanisms of touch-evoked pain (allo-
dynia): a new model, Pain 68:13-23, 1996.
13. Jensen TS, Baron R; Translation of symptoms and signs into
mechanisms in neuropathic pain, Pain 102:1-8, 2003.
14. Meyer RA: Peripheral mechanisms of cutaneous nociception.
In McMahon SB, Koltzenburg M, editors: Wall and Melzack’s
textbook of pain, ed 5, 2006, Philadelphia, Elsevier, Churchill
Livingstone.
15. Fields HL, Basbaum AI, Heinricher MM: Central nervous
system mechanisms of pain modulation. In McMahon SB, Kolt-
zenburg M, editors: Wall and Melzack’s textbook of pain, ed 5,
Philadelphia, 2006, Elsevier, Churchill Livingstone.
16. Malmberg AB, Yaksh TL: Hyperalgesia mediated by spinal
glutamate or substance P receptor blocked by spinal cyclooxy-
genase inhibition, Science 257:1276, 1992.
17. Calixto JB et al.: Kinins in pain and inflammation, Pain 87:1,
2000.
18. Robinson PP et al.: Peripheral mechanisms for the initiation of
pain following trigeminal nerve injury, J Orofac Pain 18(4):287,
2004.
19. Long A et al.: Changes in neuropeptide expression in inferior
alveolar nerve neuroma, J Dent Res 74:861, 1995.
20. Bongenheim U, Robinson PP: Spontaneous and mechanically
evoked afferent activity originating from myelinated fibers in
ferret inferior alveolar nerve neuroma, Pain 67:399, 1996.
21. Vora AR et al.: Close apposition and exposure of non-myelin-
ated axons in traumatic neuromas of the human lingual nerve,
J Peripheral Nerv Syst 9(4):200, 2004.
22. Sato J, Perl ER: Adrenergic excitation of cutaneous pain recep-
tors induced by peripheral nerve injury, Science 251:1608,
1991.
23. Jorum E et al.: Catecholamine-induced excitation of nocicep-
tors in sympathetically maintained pain, Pain 127:296, 2007.
24. Kristensen JD, Svensson B, Gordh T Jr: The NMDA-receptor
antagonists CPP abolishes neurogenic “windup pain” after
intrathecal administration in humans, Pain 51:249, 1992.
25. Sabino MAC et al.: Tooth extraction-induced internalization
of the substance P receptor in trigeminal nucleus and spinal
cord neurons: imaging the neurochemistry of dental pain, Pain
95:175, 2002.
26. Dubner R, Ren K: Brainstem mechanisms of persistent pain
following injury, J Orofac Pain 18(4):299-305, 2004.
27. Sessle BJ et al.: Properties and plasticity of the primate somato-
sensory and motor cortex related to orofacial sensorimotor
function, Clin Exp Pharmacol Physiol 32(1-2):109, 2005.
Chronic Maxillomandibular, Head and Neck Pain 159
28. Jantsch HHF: Cortical representation of experimental tooth
pain in humans, Pain 118:390, 2005.
29. Ikeda R et al.: NMDA receptor-independent synaptic plasticity
in the central amygdala in the rat model of neuropathic pain,
Pain 127:161, 2007.
30. Pedersen LH, Scheel-Kruger J, Blackburn-Munro G: Amygdala
GABA-A receptor involvement in mediating sensory-
discriminative and affective-motivational pain responses in
a rat model of peripheral nerve injury, Pain 127:17, 2007.
31. Brooks JCW, Tracey I: The insula: a multidimensional integra-
tion site for pain, Pain 128:1, 2007.
32. Gregg JM: Experimental trigeminal neuropathy, J Oral Surg
29:260, 1971.
33. Friedman AH: Treatment of deafferentation pains following
peripheral nerve injury. In Nashold BS, Ovelmen-Levitt J,
editors: Deafferentation pain syndromes: pathophysiology and
treatment, Adv Pain Res Ther 19:321-330, 1991.
34. Salter M: Cellular neuroplasticity mechanisms mediating pain
persistence, J Orofac Pain 18(4):318-324, 2004.
35. Ren K, Dubner R: Descending modulation in persistent pain:
an update, Pain 100:1-6, 2002.
36. Woolf CJ, Max MB: Mechanism-based diagnosis: issues for
analgesic drug development, Anesthesiology 95:241, 2001.
37. Finnerup NB, Jensen TS: Mechanisms of disease: mechanism-
based classification of neuropathic pain-a critical analysis, Nat
Clin Pract Neurol 2:107, 2006.
38. Melzack R: The McGill pain questionnaire: major properties
and scoring methods, Pain 1:277-299, 1975.
39. Krause SJ, Backonja MM: Development of a neuropathic pain
questionnaire, Clin J Pain 19:306-314, 2003.
40. Zuniga JR, Essick GK: A contemporary approach to the clinical
evaluation of trigeminal nerve injuries, Oral Maxillofac Surg
Clin North Am 4:353, 1992.
41. Jaaskelainen SK, Teerjoke-Oksa T, Forssell H: Neurophysio-
logic and quantitative sensory testing in the diagnosis of
trigeminal neuropathy and neuropathic pain, Pain 117(3):
349, 2005.
42. Svensson P et al.: Overview on tools and methods to assess
neuropathic trigeminal pain, J Orofac Pain 18(4):332-338,
2004.
43. Essick GK, Patel S, Trulsson M: Mechanosensory and thermo-
sensory changes across the border of impaired sensitivity to
pinprick after mandibular nerve injury, J Oral Maxillofac Surg
60(11):1250-1266, 2002.
44. Zuniga JR et al.: The accuracy of clinical neurosensory testing
for nerve injury diagnosis, J Oral Maxillofac Surg 56:2,
1998.
45. Devers A, Galer BS: Topical lidocaine patch relieves a variety
of neuropathic pain conditions: an open-label study, Clin J Pain
16:205, 2000.
46. Marchettini P et al.: Lidocaine test in neuralgia, Pain 48:377,
1992.
47. Mao J, Chen LL: Systemic lidocaine for neuropathic pain relief,
Pain 87:7, 2000.
48. Brody MC, Andary MT: Treatment approaches to reflex sym-
pathetic dystrophy, Phys Med Rehabil Clin North Am 4:165,
1993.
49. Maizels M et al.: Intranasal lidocaine for treatment of migraine.
A randomized, double blind, controlled study, JAMA 276:319,
1996.
50. Cole JA et al.: Migraine, fibromyalgia, and depression among
people with IBS: a prevalence study, Gastroenterology 6:26,
2006.
51. Diatchenko L et al.: Idiopathic pain disorders-pathways of
vulnerability, Pain 123:226, 2006.
52. Bossut DF, Maixner W: Effects of cardiac vagal afferent
electrostimulation on the responses of trigeminal and
160 SECTION I ■ Anesthesia and Pain Control
trigeminothalamic neurons to noxious orofacial stimulation,
Pain 65:101, 1996.
53. Carius A, Schulze-Bonhage A: Trigeminal pain under vagus
nerve stimulation, Pain 118:271, 2005.
54. Kreiner M et al.: Craniofacial pain as the sole symptom of
cardiac ischemia: a prospective multicenter study, J Am Dent
Assoc 138(1):74-79, 2007.
55. Naughten F, Ashworth P, Skevington SM: Does sleep quality
predict pain-related disability in chronic pain patients? The
mediating roles of depression and pain severity, Pain 127:243,
2007.
56. McCain GA, Scudds RA: The concept of primary fibromyalgia
(fibrositis): clinical value, relation and significance to other
chronic musculoskeletal pain syndromes, Pain 33:273, 1988.
57. Lavigne GJ et al.: Cigarette smoking as a risk factor or an
exacerbating factor for restless legs syndrome and sleep bruxism,
Sleep 20:290, 1997.
58. Swift JQ, Roszkowski MT: The use of opioid drugs in manage-
ment of chronic orofacial pain, J Oral Maxillofac Surg
56(9):1081-1085, 1998.
59. Portenoy RK: Chronic opioid therapy in non-malignant pain,
J Pain Symptom Manage 5(suppl):46, 1990.
60. Fishbain DA, Cutler RB, Rosomoff HL: Chronic pain associ-
ated with depression: antecedent or consequence of chronic
pain? Clin J Pain 13:116, 1997.
61. Magni G et al.: Prospective study on the relationship between
depressive symptoms and chronic musculoskeletal pain, Pain
56:289, 1994.
62. Feinmann C, Newton-John T: Psychiatric and psychological
management considerations associated with nerve damage and
neuropathic trigeminal pain, J Orofac Pain 18(4):360-365, 2004.
63. Merskey H: Pain, psychogenesis, and psychiatric diagnosis, Int
Rev Psychiatry 12:99-102, 2000.
64. Buenaver LF et al.: Pain-related catastrophizing and perceived
social responses: inter-relationships in the context of chronic
pain, Pain 127:234, 2007.
65. Donaldson D, Kroening R: Recognition and treatment of
patients with chronic orofacial pain, J Am Dent Assoc 99:961,
1979.
66. Sessle BJ: Masticatory muscle disorders: basic science perspec-
tives. In Sessle BJ, Bryant PS, Dionne RA, editors: Temporo-
mandibular disorders and related pain conditions, Seattle, 1995,
IASP Press.
67. Arendt-Nielsen L, Graven-Nielsen T: Central sensitization in
fibromyalgia and other musculoskeletal disorders, Curr Pain
Headache Rep 7(5):355, 2003.
68. Antonelli MS, Vatuter RL: Nonarticular pain syndromes, Post-
grad Med 91:95, 1992.
69. Kosek E, Ekholm J, Hansson P: Sensory dysfunction in fibro-
myalgia patients with implications for pathogenic mechanisms,
Pain 68:375, 1996.
70. McDermid AJ, Rollman GB, McCain GA: Generalized hyper-
vigilance in fibromyalgia: evidence of perceptual amplification,
Pain 66:133, 1996.
71. Russell IJ et al.: Platelet 3H-imipramine uptake receptor density
and serum serotonin levels in patients with fibromyalgia/
fibrositis syndrome, J Rheumatol 19:104, 1992.
72. Bendtsen L, Jensen R, Olesen J: Qualitatively altered nocicep-
tion in chronic myofascial pain, Pain 65:259, 1996.
73. Lautenbacher S, Rollman GB: Possible deficiencies of pain
modulation in fibromyalgia, Clin J Pain 13:189, 1997.
74. Carette S et al.: Comparison of amitriptyline, cyclobenzaprine,
and placebo in the treatment of fibromyalgia. A randomized,
double-blind clinical trial, Arthritis Rheum 37:32, 1994.
75. Paggioloi JJ, Racz GB: Intravenous and oral anesthetics in pain
management: reflections on lidocaine and mexiletine, Pain
Digest 5:69, 1995.
76. Staud R, Robinson ME, Price DD: Isometric exercise has oppo-
site effects on central pain mechanisms in fibromyalgia patients
compared to normal, Pain 118:176, 2005.
77. Diamond S, Freitag FG: The mixed headache syndrome: a
review, Clin J Pain 4:67, 1988.
78. Pielsticker A et al.: Impairment of pain inhibition in chronic
tension-type headache, Pain 118:215, 2005.
79. De Leeuw R, Klasser GD, Romulo JC: Are female patients with
orofacial pain medically compromised? J Am Dent Assoc
136:459, 2005.
80. Anthony M: Headache and the greater occipital nerve, Clin
Neurol Neurosurg 94:297, 1992.
81. Goadsby PJ, Knight YE, Hoskin KL: Stimulation of the greater
occipital nerve increases metabolic activity in the trigeminal
nucleus caudalis and cervical dorsal horn, Pain 73:23, 1997.
82. Sessle BJ et al.: Convergence of cutaneous, tooth pulp, visceral,
neck and muscle afferents on nociceptive and non-nociceptive
neurons in trigeminal subnucleus caudalis (medullary dorsal
horn) and its implications for referred pain, Pain 27:219,
1986.
83. Pullinger AG, Seligman DA: Trauma history in diagnostic sub-
groups of temporomandibular disorders, Oral Surg Oral Med
Oral Pathol 71:529, 1991.
84. Greco CM et al.: Traumatic onset of temporomandibular dis-
orders: positive effects of a standardized conservative treatment
program, Clin J Pain 13:337, 1997.
85. Fillingim RB et al.: Pain sensitivity in patients with temporo-
mandibular disorders: relationship to clinical and psychosocial
factors, Clin J Pain 12:260, 1996.
86. Howard RP et al.: Assessing neck extension as a basis for tem-
poromandibular joint dysfunction, J Oral Maxillofac Surg
49:1210, 1991.
87. Weinberg S, LaPointe H: Cervical extension-flexion injury
(whiplash) and internal derangement of the temporomandibu-
lar joint, J Oral Maxillofac Surg 45:653, 1987.
88. Goadsby PJ, Lipton RB: A review of paroxysmal hemicranias,
SUNCT syndrome and other short-lasting headaches with
autonomic feature, including new cases, Brain 120:193, 1997.
89. Ursin H, Endresen IM: Sensitization: a neurobiological theory
for muscle pain. In Vaeroy H, Merskey H, editors: Progress in
fibromyalgia and muscle pain, Amsterdam, 1993, Elsevier.
90. Svensson P, List T, Hector G: Analysis of stimulus-evoked pain
in patients with myofascial temporomandibular disorders, Pain
92:399, 2001.
91. Maixner W et al.: Sensitivity of patients with painful temporo-
mandibular disorders to experimentally evoked pain, Pain
76:71-81, 1998.
92. Sharav Y: Orofacial pain, J Am Dent Assoc 136:432, 2005.
93. Sharav Y et al.: The analgesic effect of amitriptyline on facial
pain, Pain 31:199, 1987.
94. Kimos P et al.: Analgesic action of gabapentin on chronic pain
in the masticatory muscles: a randomized controlled trial, Pain
127:151-160, 2007.
95. Portenoy RK: Appropriate use of opioids for persistent non-
cancer pain, Lancet 364:739, 2004.
96. Saper JR, editor: Guidelines for opioid use in non-malignant
pain, Top Pain Manage 11:45, 1996.
97. Israel H et al.: Oral and maxillofacial surgery in patients with
chronic orofacial pain, J Oral Maxillofac Surg 61:662-667,
2003.
98. McNamara JA, Seligman DA, Okeson JP: The relationship of
occlusal factors and orthodontic treatment to temporomandib-
ular disorders. In Sessle BJ, Bryant PS, Dionne RA, editors:
Progress in pain and research management, vol 4, Seattle, 1995,
IASP Press.
99. Dolwick FM: Temporomandibular joint disk displacement:
clinical perspectives. In Sessle BJ, Bryant PS, Dionne RA,
 CHAPTER 9 •
editors: Progress in pain and research management, vol 4, Seattle,
1995, IASP Press.
100. Carlsson GE, LeResche L: Epidemiology of temporomandibular
joint disorders. In Sessle BJ, Bryant PS, Dionne RA, editors:
Progress in pain research and management, vol 4, Seattle, 1995,
IASP Press.
101. Appelgren A et al.: Neuropeptides in the arthritic TMJ and
symptoms and signs from the stomatognathic system with
special consideration to rheumatoid arthritis, J Orofac Pain
9:215, 1995.
102. Kopp S: The influence of neuropeptides serotonin and inter-
leukin 1B on temporomandibular joint pain and inflammation,
J Oral Maxillofac Surg 56:189, 1998.
103. Nickerson JW, Boering G: Natural course of osteoarthrosis as
it relates to internal derangements of the temporomandibular
joint, Oral Maxillofac Surg Clin North Am 1:27, 1989.
104. Milam SB: Articular disk displacements and degenerative tem-
poromandibular joint disease. In Sessle BJ, Bryant PS, Dionne
RA, editors: Progress in pain and research and management, vol
4, Seattle, 1995, IASP Press.
105. Murakami K et al.: Four-year follow-up study of temporoman-
dibular joint arthroscopic surgery for advanced internal derange-
ment, J Oral Maxillofac Surg 54:285, 1996.
106. Silberstein SD: Migraine pathophysiology and its clinical impli-
cations, Cephalalgia 24:2, 2004.
107. Valeriani M, Rinalduzzi S, Vigevano F: Multilevel somatosen-
sory system disinhibition in children with migraine, Pain
118:137-144, 2005.
108. Mitrirattanakul S, Merrill RL: Headache impact in patients
with orofacial pain, J Am Dent Assoc 137(9):1267-1274,
2006.
109. Tepper SJ: A primary care approach to migraine and chronic
headache, Primary Care 2:152, 1996.
110. Burstein R et al.: An association between migraine and cutane-
ous allodynia, Ann Neurol 47:614, 2004.
111. Moskowitz MA: The trigeminovascular system. In Olesen J,
Tfelt-Hansen P, Welch KMA, editors: The Headaches, New
York, 1993, Raven Press.
112. Dodick D, Silberstein S: Central sensitization theory of
migraine: clinical implications, J Head Face Pain 46(4):182,
2006.
113. Goadsby PJ, Zagami AS, Lambert GA: Neural processing of
craniovascular pain, Headache 31:365, 1991.
114. Olesen J et al.: The nitric oxide hypothesis of migraine and
other vascular headaches, Cephalalgia 15:94, 1995.
115. Ziegler DK et al.: Propranolol and amitriptyline in prophylaxis
of Migraine, Arch Neurol 50:825, 1993.
116. Tfelt-Hansen P: Sumatriptan for the treatment of migraine
attacks-a review of controlled clinical trials, Cephalalgia 13:238,
1993.
117. Dao TTT et al.: Is myofascial pain of the temporal muscles
relieved by oral sumatriptan? A cross-over pilot study, Pain
62:241, 1995.
118. Weintraub MI: Migraine-a maxillary nerve disorder? A novel
therapy-preliminary results, Am J Pain Manage 6:77, 1996.
119. Jaeger B: Tension type headache and myofascial pain, J Orofa-
cial Pain 7:106, 1993.
120. Hannerz J, Jogestrand T: Is chronic tension-type headache a
vascular headache? The relation between chronic tension-type
headache and cranial hemodynamics, J Head Face Pain
38(9):668, 1998.
121. Sjaastad O: Cluster headache syndrome, Philadelphia, 1992, WB
Saunders.
122. Weiler C: Brainstem activation in spontaneous human migraine
attacks, Nat Med 1:658, 1995.
123. Anthony M: Arrest of attacks of cluster headache by
local steroid injection of the occipital nerve. In Rose CF,
Chronic Maxillomandibular, Head and Neck Pain 161
editor: Migraine: clinical and research advances, London, 1985,
Karger.
124. Gabai IJ, Spierlings E: Prophylactic treatment of cluster head-
ache with verapamil, Headache 29:168, 1989.
125. Ekbom K et al.: Subcutaneous sumatriptan in the acute treat-
ment of cluster headache. A dose comparison study, Acta
Neurol Scand 88:63, 1993.
126. Fusco BM et al.: Preventive effect of repeated nasal applications
of capsaicin in cluster headache, Pain 59:321, 1994.
127. Benoliel R et al.: Orofacial pain with vascular-type features,
Oral Surg Oral Med Oral Pathol 84:506, 1997.
128. Sarlani E, Balciunas BA, Grace EG: Orofacial pain-Part II:
assessment and management of vascular, neurovascular, idio-
pathic, secondary and psychogenic causes, Am Assoc Crit Care
Nurses 6(3):347, 2005.
129. Vickers RE et al.: Analysis of 50 patients with atypical odon-
talgia. A preliminary report on pharmocological procedures for
diagnosis and treatment, Oral Surg Oral Med Oral Pathol 85:24,
1998.
130. Dubner R et al.: Idiopathic trigeminal neuralgia: sensory fea-
tures and pain mechanisms, Pain 31:23, 1987.
131. Kerr FWL: Pathology of trigeminal neuralgia: light and electron
microscopic observations, J Neurosurg 26:151, 1967.
132. Hardy DG, Rhoton AL: Microsurgical relationships of the supe-
rior cerebellar artery and trigeminal nerve, J Neurosurg 49:669,
1978.
133. Patel NK et al.: How accurate is magnetic resonance angiogra-
phy in predicting neurovascular compression in patients with
trigeminal neuralgia? A prospective, single-blinded compara-
tive study, Br J Neurosurg 17(1):60, 2003.
134. Elias WJ, Burchiel KJ: Microvascular decompression, Clin J Pain
18(1):35, 2002.
135. Devor M, Govrin-Lippman R, Rappaport ZH: Mechanism of
trigeminal neuralgia: an ultrastructural analysis of trigeminal
root specimens obtained during microvascular decompression
surgery, J Neurosurg 96:532, 2002.
136. Devor M, Amir R, Rappaport ZH: Pathophysiology of trigemi-
nal neuralgia: the ignition hypothesis, Clin J Pain 18:4,
2002.
137. Hadjimichael O et al.: Persistent pain and uncomfortable sensa-
tions in persons with multiple sclerosis, Pain 127:35, 2007.
138. Osborne TL et al.: Psychosocial factors associated with pain
intensity, pain-related interference, and psychological func-
tioning in persons with multiple sclerosis and pain, Pain 127:52,
2007.
139. Ratner EJ et al.: Jawbone cavities and trigeminal and atypical
facial neuralgias, Oral Surg Oral Med Oral Pathol 48:3, 1979.
140. Hanakita J, Kondo A: Serious complications of microvascular
decompression operations for trigeminal neuralgia and hemifa-
cial spasm, Neurosurgery 22:348, 1988.
141. McQuay H et al.: Anticonvulsant drugs for management of
pain: a systematic review, Br Med J 311:1047, 1995.
142. Chole R et al.: Drug treatment of trigeminal neuralgia: a sys-
temic review of the literature, J Oral Maxillofac Surg 65:40,
2007.
143. Oturai AB et al.: Neurosurgery for trigeminal neuralgia: com-
parison of alcohol block, neurectomy and radiofrequency coag-
ulation, Clin J Pain 12:311, 1996.
144. Fisher B et al.: Trigeminal neuralgia: a five-year experience
with cryosurgery [abstract], J Oral Maxillofac Surg 55:75, 1997.
145. Murali R, Rovit RL: Are peripheral neurectomies of value in
the treatment of trigeminal neuralgia? An analysis of new cases
and cases involving previous radiofrequency gasserian thermo-
coagulation, J Neurosurg 85:435, 1996.
146. Gregg JM, Small EW: Surgical management of trigeminal pain
with radiofrequency lesions of the peripheral nerves, J Oral
Maxillofac Surg 44:1222, 1986.
162 SECTION I ■ Anesthesia and Pain Control
147. Fraioli B et al.: Treatment of trigeminal neuralgia by thermo-
coagulation, glycerolization, and percutaneous compression of
the gasserian ganglion and/or retrogasserian rootlets: long-term
results and therapeutic protocol, Neurosurgery 24:239, 1994.
148. Brisman R: Gamma knife surgery with a dose of 75 to 76.8 gray
for trigeminal neuralgia, J Neurosurg 100:848, 2004.
149. Kao MC: Gamma knife surgery for trigeminal neuralgia, J Neu-
rosurg 96(1):160, 2002.
150. Lopez BC, Hamlyn PJ, Zakrzewska JM: Stereotactic radiosur-
gery for primary trigeminal neuralgia: state of the evidence and
recommendations for future reports, J Neurol Neurosurg Psychia-
try 75:1019, 2004.
151. Hamani C et al.: Deep-brain stimulation for chronic neuro-
pathic pain: long-term outcome and the incidence of inser-
tional effect, Pain 125:188, 2006.
152. Nuti C et al.: Motor cortex stimulation of refractory neuro-
pathic pain: four year outcome and predictors of efficacy, Pain
118:43, 2005.
153. Nurmikko TJ, Rasanan A, Hakkinen V: Clinical and neuro-
physiological observations on acute herpes zoster, Clin J Pain
6:284, 1990.
154. Johnson MD, Burchiel KJ: Peripheral stimulation for treatment
of trigeminal postherpetic neuralgia and trigeminal posttrau-
matic neuropathic pain: a pilot study, Neurosurgery 55(1):135,
2004.
155. Raj P: Management of herpes zoster pain and postherpetic
neuralgia, Pain Digest 2:201, 1992.
156. Rowbotham M, Reisner-Keller LA, Fields HL: Both intrave-
nous lidocaine and morphine reduce the pain of postherpetic
neuralgia, Neurology 41:1024, 1991.
157. Epstein JB, Marcoe JH: Topical application of capsaicin for
treatment of oral neuropathic pain and trigeminal neuralgia,
Oral Surg Oral Med Oral Pathol 77:135, 1994.
158. Kishore-Kumar R et al.: Desipramine relieves postherpetic neu-
ralgia, Clin Pharmacol Ther 47:305, 1990.
159. Rosenberg JM et al.: The effect of gabapentin on neuropathic
pain, Clin J Pain 13:251, 1997.
160. Dworkin RH, Corbin AE, Young JP: Pregabalin for the
treatment of post-herpetic Neuralgia, Neurology 60:1274,
2003.
161. Davis KD et al.: Topical application of clonidine relieves hyper-
algesia in patients with sympathetically mediated pain, Pain
47:309, 1991.
162. Rowbotham MC et al.: Lidocaine patch: double-blind con-
trolled study of a new treatment method for postherpetic
neuralgia, Pain 65:39, 1996.
163. Andary MT et al.: Traumatic brain injury/chronic pain
syndrome: a case comparison study, Clin J Pain 13:144,
1997.
164. Leininger BE: Neuropsychological deficits in symptomatic
minor head injury patients after concussion and mild concus-
sion, J Neurol Neurosurg Psychiatry 53:293, 1990.
165. Anderson J, Kaplan M: Brain injury obscured by chronic pain:
a preliminary report, Arch Phys Med Rehabil 71:703, 1990.
166. Uomoto J, Essleman P: Traumatic brain injury and chronic
pain: differential types and rates by head injury severity, Arch
Phys Med Rehabil 74:61, 1993.
167. Kelly JP et al.: Concussion in sports: guidelines for the preven-
tion of catastrophic outcome, JAMA 266:2867, 1991.
168. Domino J, Haber J: Prior physical abuse and sexual abuse in
women with chronic Headache, Headache 27:310, 1987.
169. Yamaguchi M: Incidence of headache and severity of head
injury, Headache 32:427, 1992.
170. Pilowski I: Cryptotrauma and “accident neurosis,” Br J Psychia-
try 147:310, 1985.
171. Packard RC: Post-traumatic headache: permanency and rela-
tionship to legal settlement, Headache 32:496, 1992.
172. Dubner R, Basbaum A: Spinal dorsal horn plasticity following
tissue or nerve injury. In Wall PD, Melzack R, editors: Textbook
of pain, ed 3, Edinburgh, 1994, Churchill Livingstone.
173. Jane JA, Stewart O, Gennarelli T: Axonal degeneration
induced by non-invasive minor head injury, J Neurosurg 62:96,
1985.
174. Radanov BP, Dvorak J, Valach L: Cognitive deficits in patients
after soft tissue injury of the cervical spine, Spine 17:127, 1992.
175. Tysvaer AT, Lochen EA: Soccer injuries to the brain: a neu-
ropsychological study of former soccer players, Am J Sports Med
19:56, 1991.
176. Cardenas DD et al.: Efficacy of amitriptyline for relief of pain
in spinal cord injury: results of a randomized controlled study,
Pain 96(3):365, 2002.
177. Sindrup SH, Jensen TS: Efficacy of pharmacological treatment
of neuropathic pain: an update and effect related to mechanism
of drug action, Pain 83:389, 1999.
178. Levendoglu F et al.: Gabapentin is a first line drug for the treat-
ment of spinal cord injury, Spine 29:743, 2004.
179. Hillerup S: Iatrogenic injury to oral branches of the trigeminal
nerve: records of 449 cases, Clin Oral Invest 11:133, 2007.
180. Walter JM, Gregg JM: Analysis of post-surgical neurologic
alteration in the trigeminal nerve, J Oral Surg 37:410, 1979.
181. Halpern LR, Kaban LB, Dodson TB: Perioperative neurosen-
sory changes associated with treatment of mandibular fractures,
J Oral Maxillofac Surg 62(5):576, 2004.
182. Alling CC: Dysesthesia of the lingual and inferior alveolar
nerves following third molar surgery, J Oral Maxillofac Surg
44:454, 1986.
183. Jeries W et al.: Permanent sensory impairment following third
molar surgery: a prospective study, Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 102(4):1, 2006.
184. Ellies LG, Hawker PB: The prevalence of altered sensation
associated with implant surgery, Int J Oral Maxillofac Implants
8:674, 1993.
185. Bartling R, Freeman K, Kraut RA: The incidence of altered
sensation of the mental nerve after mandibular implant place-
ment, J Oral Maxillofac Surg 57:1408, 1999.
186. Pogrel MA, Thamby S: Permanent nerve involvement result-
ing from inferior alveolar blocks, J Am Dent Assoc 131(7):901,
2000.
187. Hillerup S, Jensen R: Nerve injury caused by mandibular block
analgesia, Int J Oral Maxillofac Surg 35(5):437, 2006.
188. Poveda R et al.: Mental nerve paresthesia associated with end-
odontic paste within the mandibular canal: report of a case,
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 102(5):46,
2006.
189. Panula K, Finne K, Oikarinen K: Incidence of complications
and problems related to orthognathic surgery: a review of 655
patients, J Oral Maxillofac Surg 59(10):1128, 2001.
190. Al-Bishri A et al.: Incidence of neurosensory disturbance after
sagittal split osteotomy alone or combined with genioplasty, Br
J Oral Maxillofac Surg 42(2):105, 2004.
191. Sunderlund S: A classification of peripheral nerve injuries pro-
ducing loss of function, Brain 74:491, 1951.
192. Seddon HJ: Three types of nerve injury, Brain 66:237, 1943.
193. Gregg JM: Abnormal responses to trigeminal nerve injury, Oral
Maxillofac Surg Clin North Am 4:339, 1992.
194. Bennett GJ, Xie Y-K: A peripheral mononeuropathy in rat that
produces disorders of pain sensation like those seen in man,
Pain 33:87, 1988.
195. Gregg JM: Studies of traumatic neuralgias in the maxillofacial
region: surgical pathology and neural mechanisms, J Oral Maxil-
lofac Surg 48:228, 1990.
196. Vora AR et al.: A light microscopical study of the structure of
traumatic neuromas of the human lingual nerve, Oral Surg Oral
Med Oral Pathol Oral Radiol Endod 99(4):395, 2005.
 CHAPTER 9 • Chronic Maxillomandibular, Head and Neck Pain
197. McLachlan EM et al.: Peripheral-nerve injury triggers norad-
renergic sprouting within dorsal root ganglia, Nature 363:543,
1993.
198. Turton AJ et al.: Sensorimotor integration in complex regional
pain syndrome: a transcranial magnetic stimulation study, Pain
127:270, 2007.
199. Xie Y: Functional changes in dorsal root ganglion cells after
chronic nerve constriction, J Neurophysiol 73:1811, 1995.
200. Woolf CJ, Salter MW: Neuronal plasticity: increasing the gain
in pain, Science 288:1765, 2000.
201. Rawlings CE, Wilkins RH: Treatment of the deafferentation
pain syndromes of the trigeminal system. In Nashold BS,
Ovelmen-Levitt J, editors: Deafferentation pain syndromes:
pathophysiology and treatment, Adv Pain Res Ther 19:291,
1991.
202. Rasmussen PV et al.: Symptoms and signs in patients with sus-
pected neuropathic pain, Pain 110:461-469, 2004.
203. Jaaskelainen SK et al.: Sensory regeneration following intra-
operatively verified trigeminal nerve injury, Neurology
62(11):1951, 2004.
204. Rolke R et al.: Quantitative sensory testing in the German
Research Network on neuropathic pain (DFNS): standardized
protocol and reference values, Pain 123:231-243, 2006.
205. Seo K et al.: Efficacy of steroid treatment for sensory impair-
ment after orthognathic surgery, J Oral Maxillofac Surg 62:1193,
2004.
206. Bartusch SL et al.: Clonazepam for the treatment of lancinating
phantom pain, Clin J Pain 12:59, 1996.
207. Meyer RA, Rath EM: Sensory rehabilitation after trigeminal
nerve injury or nerve repair, Oral Maxillofac Surg Clin North Am
13(2):365, 2001.
208. Max MB: Antidepressants as analgesics. In Fields HL, Liebe-
skind JC, editors: Progress in pain research and management, vol
1, Seattle, 1994, IASP Press.
209. Price DD et al.: The N-methyl-D-aspartate receptor antagonist
dextromethorphan selectively reduces temporal summation of
second pain in man, Pain 59:165, 1994.
210. Warncke T, Stubhaug A, Jorum E: Ketamine, an NMDA recep-
tor antagonist, suppresses spatial and temporal properties of
burn-induced secondary hyperalgesia in man: a double-blind,
crossover comparison with morphine and placebo, Pain 72:99,
1997.
211. Murphy GJ: Utilization of transcutaneous electrical nerve stim-
ulation in managing craniofacial pain, Clin J Pain 6:64, 1990.
212. Pogrel MA: The results of microneurosurgery of the inferior
alveolar and lingual nerve, J Oral Maxillofac Surg 60:485,
2002.
213. Lam NP et al.: Patient satisfaction after trigeminal nerve
Repair, Oral Surg Oral Med Oral Pathol Radiol Endod 95:538,
2003.
214. Gregg JM, Zuniga JR: An outcome analysis of clinical trials of
the surgical management of traumatic trigeminal sensory
neuropathy, Oral Maxillofac Surg Clin North Amer 13(2):377,
2001.
215. Gregg JM: (Unpublished, 2007). “Clinical signs of CNS and
autonomic dysfunction after trigeminal nerve injury” JG
216. Kuller SM, Emami B, Westmark A, et al.: Effect of low level
laser treatment on neurosensory deficits subsequent to sagittal
split ramus osteotomy, Oral Surg Oral Med Oral Pathol 82:132,
1996.
163
217. Miloro M, Halkias LE, Mallery S, et al.: Low-level laser effect
on neural regeneration in Gore-Tex tubes. Oral Surg Oral Med
OralPathol Oral Radiol Endod 93:27, 2002.
218. Shah RV, Racz GB: Long-term relief of post-traumatic head-
ache by sphenopalatine ganglion pulsed radiofrequency lesion-
ing, Arch Phys Med Rehab 85(6):1013-1016, 2004.
219. Snyder-Mackler L, Bork CE: Effect of heliumn on laser
irradiation on peripheral sensory nerve latency, Phys Ther
68:223, 1988.
220. Kumar K, Toth C, Nath R: Deep brain stimulation for intrac-
table pain. A 15 year experience, Neurosurgery 40:736, 1997.
221. Janig W and Baron R: Complex Regional Pain Syndrome:
mystery explained? Lancet Neurol 2:687, 2003.
222. Schattschneider J, Binder A, Siebrecht D, Wasner G, Baron R.
Complex regional pain syndromes: the influence of cutaneous
and deep sympathetic innervation on pain, Clin J Pain 253:280,
2006.
223. Mailis A, Wade J: Profile of Caucasian women with possible
genetic predisposition to reflex sympathetic dystrophy: A pilot,
Clin J Pain 10:210, 1994.
224. Janig W, Lavine JD, Michaelis M: Interactions of sympathetic
and primary afferent neurons following nerve injury and tissue
trauma, Prog Brain Res 113:161, 1996.
225. Hoffman KD, Matthews MA: Comparison of sympathetic
neurons in orofacial and upper extremity nerves. Implications
for causalgia, J Oral Maxillofac Surg 48:720, 1990.
226. Lang E, Kaltenhauser M, Seidler S, et al.: Persistant idiopathic
pain exists independent of somatosensory input from the painful
region: findings from quantitative sensory functions and
somatotopy of the primary somatosensory cortex, Pain 118:80-
91, 2005.
227. Forssell H, Jaaskelainen S, Tenuvuo O, Hinkka S: Sensory
dysfunction in burning mouth syndrome, Pain 99:41, 2002.
228. Grushka M, Epstein JB, Gorsky M: Burning mouth syndrome
and other oral sensory disorders: a unifying hypothesis, Pain Res
Manag 8:133, 2003.
229. Lauria G, Majorana A, Borgna M, et al.: Trigeminal small-fiber
sensory neuropathy causes burning mouth syndrome, Pain
115:332-337, 2005.
230. Mells M et al.: Atypical odontalgia: a review of the literature,
Headache 43:1060, 2003.
231. List T et al.: Effect of local anesthesia on atypical odontalgia—a
randomized controlled trial, Pain 122:306, 2006.
232. Davis HTO et al.: Consensus and contention in the treatment
of chronic nerve-damaging pain, Pain 47:191, 1993.
233. Thimineur M et al.: Central nervous system abnormalities
in complex regional pain syndrome (CRPS): clinical and
quantitative evidence of medullary dysfunction, Clin J Pain
14:256-267,1998.
234. Christiansen K, Jensen EM, Noer I: The reflex sympathetic
dystrophy response to treatment with systemic corticosteroids,
Acta Clin Scand 148:653, 1982.
235. Inada Y et al.: Surgical relief of causalgia with an artificial nerve
guide tube: successful treatment of causalgia (complex regional
pain syndrome Type II) by in situ tissue engineering with a
polyglycolic acid-collagen tube, Pain 117:251, 2005.
 S E C T I O N II •
PEDIATRIC DENTOALVEOLAR SURGERY
Sean W. Digman • Samuel L. Hayes • Jean-Luc G. Niel
Pediatric dentoalveolar surgery certainly does not make up the
bulk of procedures performed in the majority of oral and max-
illofacial surgery offices, but it does present the clinician with
unique challenges both in patient management and the vast
array of problems not encountered in adults. Whether the
treatment is as simple as the extraction of a deciduous tooth
or as complex as treating a sarcoma, these unique challenges
and the long-term effects that our treatments have on these
children must always be taken into consideration. A clear
understanding of the growth and development of the pediatric
patient is necessary to correctly identify abnormalities of the
dentition.
The tooth bud is a collection of cells that derive from the
ectoderm of the first brachial arch and the ectomesenchyme
of the neural crest cells. The formation of primary teeth is
evident between 6 to 8 weeks in utero, and the permanent
teeth begin to form in the 20th week in utero. The initial
calcification of the primary teeth ranges from 14 weeks for the
incisors to 19 weeks in utero for the second molars. The per-
manent teeth calcify between 3 and 4 months for the incisors
and 7 to 10 years for the third molars. If the dentition does
not develop at these times or there is an event that disrupts
the formation, then the teeth will not develop at all.
An anomaly in dental growth and development may be
indicative of a more ominous problem, and the clinician must
be aware of possible systemic causes including malignancy,
endocrine, nutritional, and genetic abnormalities. These can
be manifested in a combination of oral and extraoral findings,
such as those associated with hereditary ectodermal dysplasia
and Gardner’s syndrome. Thus, a comprehensive evaluation
may be warranted in some cases.
The ensuing eruption pattern of both the primary and per-
manent dentition is also of critical importance when evaluat-
ing patients with impacted teeth. Table 10-1 shows the eruption
patterns for both the deciduous and permanent dentitions.
If a pediatric patient has a tooth or a number of teeth that
have failed to erupt in a timely manner, there can be multiple
causes. These include but are not limited to tooth malposition-
ing, retained primary teeth, arch space/length discrepancies,
Dentoalveolar Surgery
CHAPTER 10
obstruction by a supernumerary tooth or by a cyst (usually seen
in teens, such as keratocysts and dentigerous cysts), or tumors
(usually seen in childhood, such as compound/complex odon-
tomas and fibro-osseous lesions). The most commonly impacted
permanent teeth after third molars are maxillary canines, man-
dibular second premolars, and maxillary incisors.
Congenitally missing teeth are observed on a fairly regular
basis with the most common, of course, being the third molars
followed by the lateral incisors and the mandibular second
premolars.
Finally, in 2003 greater than 12 of 1000 children were
found to be victims of child abuse and neglect. As medical
professionals (and conscientious providers), we are obligated
to document and report cases of suspected child abuse and
neglect in all 50 states to the appropriate law enforcement
agency. It is estimated that more than half of the cases of child
abuse involve the head, face, and neck. With these high
numbers, it is very likely that as oral and maxillofacial sur-
geons we will encounter such cases. We have the training and
expertise to identify potential victims, and we must have the
courage to act in the best interest of the victim who is most
often helpless.
■ IMPACTED TEETH
The management of impacted teeth can pose a significant
challenge to both the oral surgeon and orthodontist. An
understanding of the cause, treatment options, and outcomes
is required when formulating a treatment plan. Open dialogue
between the general practitioner, pediatric dentist, oral
surgeon, and orthodontist is critical for a successful outcome.
This section will review the incidence, causes, diagnosis, and
management of impacted teeth other than third molars.
INCIDENCE
Rates of impacted permanent teeth appear to vary among
populations and range from 1% to 5%. Thilander and Myrberg
performed a study on more than 6000 Swedish school children
and found the prevalence of impacted teeth other than third
molars to be 5.4%.1 Although any tooth can become impacted,
165
166 SECTION II ■ Dentoalveolar Surgery

most studies agree that the maxillary canine has the highest be more than 6 : 1.3
rate of impaction followed by mandibular second premolars, Relative to the permanent dentition, primary teeth rarely
maxillary second premolars, mandibular second molars, and become impacted. When it occurs, it is most often a mandibu-
maxillary incisors. Eruption failure of mandibular incisors is lar molar. It is important to distinguish between an impacted
relatively rare and is often associated with pathologic condi- primary molar and one that appears “submerged” relative to
tions when it does occur. the normal eruption of the adjacent permanent teeth. A con-
Rates of maxillary canine impaction approach 2% of the genitally missing succedaneous tooth will allow for prolonged
general population. Of these, 8% of them show bilateral retention of the primary tooth and often result in ankylosis.
involvement. This is greater than five times the rate of man- As the adjacent permanent teeth erupt, the retained primary
dibular canine impactions (0.35%). Females are twice as likely tooth will take on a “submerged” appearance.
to have an impacted canine as males.2 Jacoby found the rate
of palatally impacted canines to labially impacted canines to ETIOLOGY
Before treatment the cause of an impacted tooth must be
ascertained. In general terms, causes of impacted teeth can be
The Eruption Patterns for Both the Deciduous categorized into localized mechanical obstruction or systemic
TABLE 10-1
and Permanent Dentitions
abnormalities. Mechanical obstruction can be attributed to
Deciduous Dentition Permanent Dentition
arch length deficiency, premature loss of deciduous teeth,
Tooth Eruption Root Completion Tooth Eruption Root
(Mo) (Yr) (Yr) Completion
prolonged deciduous tooth retention, supernumerary teeth,
(Yr) odontogenic tumors and cysts (Figure 10-1), abnormal erup-
Maxillary Maxillary tion path, and cleft lip and palate.
A 7 1½-2 1 7-8 10 Systemic causes include hereditary conditions, such as
B 8 1½-2 2 8-9 11 cleidocranial dysplasia and Down syndrome. Other systemic
C 16-20 2½-3 3 11-12 13-15 causes include endocrine dysfunction, febrile diseases, and
D 12-16 2-2½ 4 10-11 12-13 irradiation. Radiographs of patients with cleidocranial dys-
E 21-30 3 5 10-12 12-14 plasia show many retained deciduous teeth with unerupted
6 6-7 9-10 permanent and supernumerary teeth, frequently with dis-
7 12-13 14-16 torted crown and root shapes. Extraction of the retained
8 17-21 18-25 deciduous teeth does not promote eruption of their perma-
nent successors necessitating surgical exposure and orthodon-
Mandibular Mandibular
tic traction.4
A 6½ 1½-2 1 6-7 9
B 7 1½-2 2 7-8 10 EVALUATION
C 16-20 2½-3 3 9-10 12-14 After determining the cause of an impacted tooth, the clini-
D 12-16 2-2½ 4 10-12 12-13 cian must devise a treatment plan in coordination with the
E 21-30 3 5 11-12 13-14 patient’s general practitioner and/or orthodontist. Impacted
6 6-7 9-10 teeth are evaluated by an initial clinical exam followed by a
7 12-13 14-15 radiographic exam. Clinical signs of abnormal exfoliation and
8 17-21 18-25 eruption sequences can allow the clinician to act early, cir-
This table uses the Zsigmondy system of classification. cumventing future problems.

FIGURE 10-1. Radiograph demonstrating an impacted left

maxillary first premolar. The premolar was removed with an
associated dentigerous cyst.
 CHAPTER 10 •
The initial radiographic exam should include a panoramic
radiograph supplemented with a variety of other modalities
that help determine the position of the impacted tooth in
three dimensions. Aside from determining horizontal and ver-
tical positions of teeth, panoramic radiographs can aid in
determining buccal-lingual positions as well. A tooth that is
positioned outside of the radiographic trough will appear out
of focus and larger or smaller than the adjacent teeth. If posi-
tioned palatal to the adjacent teeth (i.e., further from the
x-ray film), a larger image can be expected (see Figure 10-2).
On the other hand, a smaller image can be expected if the
tooth is positioned labial to the focal trough.
When the location of the impacted tooth is not obvious,
a series of periapical radiographs are used to determine tooth
position. This technique is commonly referred to as the tube-
shift technique or Clark’s rule.
An initial periapical radiograph is taken in the standard
fashion. A second radiograph is then taken after moving the
beam source mesially or distally. If the impacted tooth appears
to move in the same direction as the beam source, it is located
lingual or palatal to the adjacent teeth. If it moves in the
opposite direction, the tooth is buccal or labial to the adjacent
teeth. The common acronym for this is S.L.O.B. (same-
lingual, opposite-buccal) (Figures 10-3, 10-4, and 10-5).
Often impacted teeth can be located in the middle of the
alveolus or angulated so that half of the tooth is on the buccal
side and half on the palatal. In these circumstances, an occlusal
radiograph can be of value in determining tooth angulation.
In 1986 Keur made two improvements on this technique
by suggesting the use of the initial panoramic radiograph and
a single occlusal radiograph taken at 60° in the vertical plane.
Because most panoramic radiographs capture an image at +7°
to the occlusal plane, this produces a vertical angulation
change of about 53°. This offers two distinct advantages: (1)
An occlusal radiograph allows for the capture of the entire
impacted tooth while also allowing for a greater change in
angulation of the beam source. Thus, the relative change
between the impacted tooth and the adjacent teeth is more
obvious. (2) Because the panoramic radiograph is usually the
Pediatric Dentoalveolar Surgery 167
FIGURE 10-2. Radiograph demonstrating palatally
impacted maxillary canines. Note the enlarged image of the
canines relative to the adjacent teeth.
initial film obtained, the need for two additional films is
decreased to one.5
TREATMENT OPTIONS
After determining the location and the cause of the impac-
tion, the clinician should consider the treatment options.
Decisions on extraction are based on associated pathologic
conditions, tooth position, feasibility of orthodontic align-
ment, and cooperation of the patient. Studies by Stivaros and
Mandall evaluated the radiographic appearance of the tooth
and the decision to extract or bring the tooth into the arch.
As the angulation of the tooth to the midline increased, it was
more likely to be extracted. Palatally impacted teeth were
more likely to be retained and brought into the arch than
labially positioned teeth.6 Other treatment options include
serial extractions and spontaneous eruption, exposure and
spontaneous eruption, exposure with orthodontic traction,
autotransplantation, extraction with prosthetic replacement,
and no treatment.
MAXILLARY CANINES
To understand the cause of maxillary canine impaction, it is
important to consider the timing of its development and the
surrounding anatomy. In adolescence the maxillary canine
bud is positioned high in the maxilla between the nasal cavity
and the orbital rim. Posteriorly, this space is limited by the
anterior sinus wall. As root formation progresses, the crown
of the cuspid comes in contact with the roots of the lateral
incisor mesially, the first bicuspid distally, and the resorbing
roots of the deciduous canine. Theoretically, these teeth guide
the developing cuspid into its proper position within the arch.
When anomalies exist in lateral incisor and bicuspid form and
position, the cuspid will waver from its expected eruption
path.
In cases of tooth size and arch length discrepancy, the late
erupting canine is prevented from taking its normal position
in the arch. This will occasionally force the canine labially
unless adequate space is made with extractions or orthodontic
therapy. This situation only accounts for 13% of all canine
168 SECTION II ■ Dentoalveolar Surgery

A B
FIGURE 10-3. A, Tube-shift technique demonstrating a palatally impacted object. B, Depiction of a buccally
impacted object.

FIGURE 10-4. Periapical radiograph demonstrating an inverted FIGURE 10-5. Periapical radiograph after shifting the x-ray beam source
mesiodens. to the patient’s left. Note the impacted mesiodens moves in the same direction
as the shift in beam source demonstrating palatal location.
 CHAPTER 10 •
impactions and probably does not represent a true impaction
because these teeth have been shown to spontaneously erupt
if given adequate space.
More commonly an impacted canine is positioned palatal
to the arch. Jacoby found this to be true 87% of the time, of
which only 15% showed arch length discrepancy.3 To account
for the palatal position of the canine, Jacoby theorized that
an excessive amount of palatal space was available for the
canine to drift into. This is caused by “(1) excessive bone
growth in the canine area, (2) the agenesis or hypodevelop-
ment of the lateral incisor, and (3) stimulated eruption of the
lateral incisor or the first premolar.”3
Some foretelling signs of maxillary canine impaction
include prolonged retention of the deciduous canine beyond
14 years, presence of a palatal bulge, delayed eruption of the
permanent canine with abnormal lateral incisor shape or posi-
tion, and absence of a normal labial canine bulge beyond age
11. Ericson and Kurol found in a study of 505 children between
the ages of 10 and 12 that only 5% had nonpalpable canines
at age 11.7
Treatment
In select cases, prevention of canine impaction can be accom-
plished by extraction of deciduous canines as early as 8 or 9
years of age. These cases are usually limited to dental class 1
patients without crowding. Ericson and Kurol found that the
position of the ectopically erupting canine can be normalized
in 91% of cases by removal of the deciduous canine before the
age of 11 provided that the canine crown is distal to the
midline of the lateral incisor. The success rate decreases to
64% when the canine crown is mesial to the midline of the
lateral incisor.8
After clinically and radiographically determining a labially
positioned cuspid, the clinician has several surgical options to
choose from. These include excisional uncovering, an api-
cally positioned flap, and closed eruption techniques. Tooth
position and the amount of attached gingiva in the area help
determine the correct procedure.
Excisional uncovering is usually done after sufficient space
is created for eruption of the permanent cuspid. The procedure
is most often reserved for the palatally impacted canine;
however, it can be performed on a labially positioned tooth if
there is sufficient attached gingiva in the area to provide 2 to
3 mm of gingival cuff after eruption. Without an adequate
gingival cuff, the erupting cuspid is predisposed to future peri-
odontal complications. This procedure is easily performed
when the majority of the crown is above the mucogingival
line and there is little alveolar bone to remove. When the
impacted tooth is vertically aligned and there is no obstruc-
tion, spontaneous eruption will usually occur. Excisional
uncovering should not be attempted if the tooth is positioned
within the center of the alveolus or apical to the mucogingival
line. In this situation, a closed technique or apically posi-
tioned flap is indicated (Figure 10-6).
Excisional uncovering can be accomplished if the crown of
the tooth is readily palpable. This is ideally performed in the
Pediatric Dentoalveolar Surgery 169
A
B
FIGURE 10-6. A, Impacted canine located above the mucogingival line
(dotted line). B, Excisional uncovering of a maxillary canine.
late mixed dentition period to maximize spontaneous erup-
tion; however, orthodontic traction can be used if accom-
plished later. Local anesthesia is infiltrated over the crown to
aid in hemostasis and hydrodissection. A full-thickness muco-
periosteal window is created directly over the tooth, and the
soft tissue is removed. The remaining bone overlying the
crown is removed with a curette or rotary instrumentation
down to the cementoenamel junction, being careful not to
damage the root surface. The dental follicle is then removed,
and a surgical dressing can be packed in the window for patient
comfort. If spontaneous eruption is not anticipated, an orth-
odontic bracket may be bonded to the crown and secured to
the arch wire with a chain or suture. If adequate bone is
removed and the tooth is uncovered early enough (late mixed
dentition), the tooth will usually spontaneously erupt to the
level of the occlusal plane in 6 to 8 months. Orthodontic
bracketing can then be accomplished and the tooth brought
into correct occlusion.9
Exposure of a labially positioned canine is often accom-
plished using an apically positioned flap. This procedure is
indicated if there is insufficient attached gingiva in the eden-
tulous area to provide a 2- to 3-mm cuff around the erupting
tooth and should only be performed if the impacted tooth is
near the alveolus. In high impaction cases, the use of an api-
cally positioned flap can result in significant reintrusion of the
impacted tooth after orthodontic therapy.9 Before surgery
adequate arch space for eruption is usually obtained by the
orthodontist. After local anesthesia, vertical releasing inci-
sions are made on either side of the edentulous space with the
base wider than the apex. A horizontal incision is made over
170 SECTION II ■ Dentoalveolar Surgery

the edentulous alveolar ridge, connecting the two vertical

incisions and incorporating attached gingiva. A full-thickness
mucoperiosteal flap is then reflected apically past the level of
the impacted tooth. Bone is removed as necessary from around
the crown, and an orthodontic bracket and chain can be
attached if spontaneous eruption is not anticipated. The flap
is then sutured apically to allow for simultaneous descent with
the tooth during orthodontic traction (Figure 10-7).
The closed eruption technique is used for high palatal or
labially impacted teeth in which excisional uncovering or
apically positioned flaps would be difficult or result in peri-
odontal compromise. With the closed eruption technique, the
impacted tooth is exposed in the manner described previously,
and an attachment is fixated to the tooth and connected to a A
chain, which is sutured to the archwire for later activation.
The flap is replaced with the chain exiting near the alveolar
ridge space where the tooth is expected to erupt. The ortho-
dontist then uses the chain to apply traction on the impacted
tooth after 2 weeks of healing and forces eruption into the
arch (Figure 10-8).
In a 30-patient study comparing labially impacted teeth
treated with apically positioned flaps against those treated
with the closed eruption technique, Vermette, Kokich, and
Kennedy found that more periodontal and aesthetic disadvan-
tages can be expected with the apically positioned flap tech-
nique. Those treated with apically positioned flaps were shown
to have clinically increased crown lengths, gingival scarring,
and intrusive relapse when compared with the closed eruption
B
group.10
FIGURE 10-7. A, Impacted maxillary canine positioned apical to the
PREMOLARS mucogingival line (dotted line). B, Apically repositioned flap after exposure of
maxillary canine.
Premolar impactions are more common in the mandible than
maxilla and occur more often in the center of the alveolus and
lingually than buccally. If the impactions are a result of an

A B C
FIGURE 10-8. A, High impaction of maxillary canine. B, Exposure and attachment of orthodontic bracket and chain.
C, Repositioned flap for closed eruption.
 CHAPTER 10 •
arch length discrepancy, extraction should be considered after
consultation with the patient’s orthodontist (Figure 10-9).
When adequate space exists to accommodate moving the
tooth into the arch, the impacted premolar can be treated
with the same techniques as described for the impacted
canine.
IMPACTED INCISORS
Impacted maxillary incisors are commonly the result of pre-
mature loss of the primary incisors or trauma. The impacted
tooth is radiographed, as described previously, to both localize
the tooth and determine root development. If root develop-
ment is not complete, soft and hard tissue removal is often
adequate to promote spontaneous eruption. If root formation
is complete or the inclination of the tooth is expected to
prevent normal eruption, exposure should include bonding of
an orthodontic bracket and chain to allow for traction.
IMPACTED MOLARS
Impactions of permanent first and second molars are rare, but
can have a devastating effect on the dentition. If left untreated,
the resulting periodontal defects, caries, and resorption can
leave a patient without a functioning posterior dentition.
Intervention before complete root formation is paramount to
a successful outcome.
Asymmetric first molar eruption patterns should raise sus-
picion and warrant radiographic exam before age 7. After the
age of 7, spontaneous first molar eruption is considered impos-
sible.11 Treatment options of unerupted molars include
surgical exposure and uprighting, extraction with implant
replacement, or a combined surgical and orthodontic correc-
tion. Orthodontic correction is often complicated from limited
access of the impacted tooth and insufficient anchorage,
although with the current advances in orthodontic anchorage,
this is becoming less of a problem. Patient compliance is also
a concern because of the increased treatment time required to
correct a problem that often presents itself in the later phases
of orthodontic care.
Surgical uprighting of a mesially inclined second molar
provides a quick and predictable answer to these problems if
performed at the right time. This procedure is best accom-
Pediatric Dentoalveolar Surgery 171
FIGURE 10-9. Radiograph demonstrating an impacted
maxillary second premolar with associated resorption of the first
molar roots.
plished when two-thirds of root formation have been com-
pleted. Before that, stabilization of the second molar in its new
position can be compromised. If performed after root develop-
ment is completed, a restricted blood supply from the con-
stricted apical foramen can result in pulpal necrosis.
The surgical procedure for uprighting a mandibular second
molar is described as follows: An incision is made along the
external oblique line of the mandible from the anterior border
of the ramus to the distal of the first molar and carried ante-
riorly as an intrasulcular incision to the mesial extent of the
first molar. A full-thickness mucoperiosteal flap is reflected,
and the developing third molar is removed in a standard
fashion being careful to preserve the mesial bone. The remain-
ing bone overlying the mesially inclined second molar is
cautiously removed, and a straight elevator is used to apply
judicious uprighting force on the second molar, using the
buccal bone as a fulcrum. Special attention is directed at not
violating the integrity of the second molar root and periodon-
tal ligament. Uprighting is continued until the mesial mar-
ginal ridge of the second molar is level with the distal marginal
ridge of the first molar. A wedgelike effect is created between
the lingual and buccal cortices, and this is usually sufficient
to stabilize the second molar in its new position. If stability is
still a concern, an orthodontic bracket and archwire may be
used to secure the tooth in the immediate postoperative phase.
Occlusion is then verified, the incision is irrigated and closed,
and a postoperative panoramic radiograph is taken to evaluate
the position of the second molar.12
Complications from surgically uprighting molars can
include pulpal necrosis, root fracture, dilacerations, internal
and external resorption, and periodontal complications.
However, in Dessner’s retrospective study of 34 patients
treated by surgical uprighting of mandibular second molars, 31
showed complete bony fill of the space previously occupied by
the crown of the uprighted tooth. Only 12 of the 34 teeth
showed pulpal changes, and there was no incidence of a
periapical pathologic condition.12
AUTOTRANSPLANTATION VERSUS EXTRACTION
Autotransplantation of impacted teeth is an acceptable alter-
native for patients who will not tolerate extensive orthodontic
172 SECTION II ■ Dentoalveolar Surgery
treatment. The need to minimize orthodontic treatment for
patients with periodontally compromised teeth or poor dental
hygiene is also a valid reason to perform autotransplantation.
Sagne and Thailander were able to successfully transplant 54
of 56 canines.13 The technique involves ensuring adequate
arch space at the recipient site before surgery. Wide exposure
of the impacted tooth is accomplished followed by careful
luxation from its crypt. Care is directed at not disrupting the
periodontal ligament. The alveolar bone at the recipient site
is conservatively contoured, and the tooth is moved into posi-
tion and stabilized with a segmental orthodontic appliance.
Endodontic treatment is advocated at 6 to 8 weeks beginning
with calcium hydroxide paste. Conventional root canal filling
is performed at 1 year following surgery. Complications associ-
ated with autotransplanted teeth are devitalization, decreased
root length, periodontal compromise, and root resorption.
The decision to surgically remove an impacted tooth is
considered when no other treatment is feasible. Many factors
should be considered including the age of the patient, associ-
ated pathologic conditions, severity of the impaction, and the
morbidity associated with a given procedure. Radiographic
localization should be accomplished before removal. Anterior
teeth are approached from the surface of the maxilla, with
which they are most closely associated. Labially impacted
teeth can usually be removed with judicious force from a
dental elevator. Care is taken to avoid excessive force on
developing tooth buds or adjacent roots. A full-thickness flap
without release is used to expose impacted teeth on the palate.
If wide access is anticipated, a palatal stent can be fabricated
before surgery and placed after closure to prevent hematoma
formation. Conservative bone removal with crown and root
sectioning is accomplished. Longitudinal sectioning of the
root can often be helpful to minimize the amount of bone
removal.
Extraction of impacted premolars can be challenging
because of limited access, adjacent roots, the maxillary sinus,
or the mental nerve in the mandible. Extraction of maxillary
bicuspids is accomplished in a similar fashion to anterior max-
illary teeth. Mandibular bicuspids are usually approached from
the buccal surface. When mandibular premolars are located
on the buccal aspect, a buccal flap is used to gain access, the
mental nerve is identified and protected, and the tooth is
sectioned and delivered. When access is limited as a result of
a lingually impacted premolar, buccal and lingual flaps are
used, and once again the mental nerve is identified and pro-
tected. Bone is conservatively removed from the buccal surface
of the mandible, and the tooth is sectioned and removed from
the lingual aspect. A blunt osteotome or straight elevator can
sometimes be used to “push” the premolar out the lingual
cortex from the buccal. Care must be taken not to damage
adjacent roots or the neurovascular bundle.
ADVANCES IN ORTHODONTIC ANCHORAGE
Orthodontic treatment is a complex process that involves the
transmission of constant force to teeth to move them into
proper alignment within the alveolus. Anchorage control to
counteract these forces is the cornerstone of treatment and is
often the limiting factor when deciding to treat a case with
orthodontics alone or in combination with surgery. In particu-
lar intrusion of posterior teeth to correct an anterior open bite
and distal movement of posterior teeth to correct a class 2 or
3 malocclusion presents significant anchorage challenges.
To supplement orthodontic anchorage, various intraoral
and extraoral appliances have been used with varying degrees
of success. Headgear, lip bumpers, Herbst appliances, magnets,
and multiloop edgewise archwires have been used to maximize
orthodontic anchorage. Unfortunately, these devices are cum-
bersome and become ineffective when patient cooperation
fades. Surgical correction of skeletal malocclusions is often
indicated for these patients, but declined for various social and
economic reasons. Advances in skeletal orthodontic anchor-
age over the past 25 years have revealed other options for
these patients.
Examples of skeletal fixation for orthodontic anchorage
include miniplates fashioned to the posterior mandible or
maxilla, microimplants that can be used in interdental loca-
tions, and palatal implants for distalization of maxillary molars.
Miniplates have been used in the posterior maxilla and man-
dible to intrude molars while closing anterior open bites. In a
study by Sherwood, Burch, and Thompson, anterior open
bites were effectively treated by intrusion of maxillary molars
using miniplates for anchorage.14 The miniplates used for fixa-
tion proved to be stable against orthodontic forces, which
intruded maxillary molars between 1.45 and 3.32 mm. Mini-
plate anchorage has also proven to be effective in the distaliza-
tion of maxillary and mandibular molars. By fixating miniplates
to the anterior ramus, Sugawara et al. showed that mandibular
molars could be distalized (average of 3.5 mm at the crown
level and 1.8 mm at the root level) with minimal relapse
(0.3 mm) at 1 year follow-up.15
Multiple skeletal anchorage systems exist, and their versa-
tility in size and shape allow them to be placed in anterior and
posterior locations of both arches. Common sites for place-
ment include the maxillary buttress and anterior ramus areas.
Ease of placement and removal is a clear advantage; however,
many clinicians recommend a 2- to 3-month healing period
for osteointegration before loading the plates with orthodon-
tic forces.
SUPERNUMERARY TEETH
A supernumerary tooth is any additional one that can be
found beyond that of the normal series of 20 deciduous teeth
or 32 permanent teeth. The cause of these anomalies is con-
troversial as multiple theories exist. One theory states that
there is a dichotomy of the developing tooth bud. Another
theory states that the dental lamina becomes hyperactive and
produces two separate dental follicles. Heredity also seems to
play a role because supernumeraries are more common in
the relatives of affected children than in the general
population.16
Supernumerary teeth are more common in the permanent
dentition (2.1%) than the primary dentition (0.8%).17 The
 CHAPTER 10 •
FIGURE 10-10. Occlusal radiograph of an impacted mesiodens prevent-
ing the eruption of a central incisor.
incidence is greatest with the mesiodens followed by supernu-
merary incisors, fourth molars, and mandibular premolars.18
The mesiodens is located between the central incisors and
more often on the palatal side of the alveolus (Figure
10-10).
Indications for removal include associated pathologic
conditions, interference with the eruption pattern of adjacent
teeth, and prevention of orthodontic tooth movement.
If none of these indications are fulfilled and if access to
the impacted supernumerary is limited, observation is a rea-
sonable decision. However, the patient should be informed of
possible sequelae, and long-term radiographic follow-up is
necessary.
Timing for surgical removal is based upon the development
and the risk of damage to the adjacent roots. Kaban recom-
mends surgical removal when one-half to two-thirds of the
permanent central incisor roots have been formed.18 This
allows for some stabilization of the permanent teeth while
retaining the ability to spontaneously erupt after mesiodens
removal.
The surgical technique is similar to removal of other
impacted teeth. After radiographic localization, a sulcular
incision is made, and a full-thickness mucoperiosteal flap is
reflected. If the mesiodens is palatal, it is necessary to separate
the incisive papilla and cauterize if necessary. After adequate
exposure, overlying bone is conservatively removed with
curettes or rotary instrumentation. Without transmitting
excessive force to the adjacent teeth, the mesiodens is gently
elevated and removed with its associated follicle. The site is
than irrigated and closed.
ODONTOMAS
The odontoma is a benign odontogenic tumor that is consid-
ered to be a hamartoma of aborted tooth formation. It is the
most common odontogenic tumor and is usually found inci-
dentally during radiographic exam in children and young
adults during the ages of tooth development. Others may be
Pediatric Dentoalveolar Surgery 173
discovered after an underlying tooth fails to erupt. It is unlikely
that an odontoma will form after the second decade of life,
and they show no gender predilection.
Odontomas can be classified into two categories based on
morphology. Compound odontomas form multiple toothlike
structures and usually occur in the anterior maxilla or mandi-
ble. Complex odontomas contain an amorphous mass of
enamel, dentin, and cementum and occur most often in the
posterior mandible or maxilla.
Clinically, most odontomas are asymptomatic. Larger
lesions may produce an expansion of bone and can reach up
to 6 cm in diameter.19 Radiographically, compound odonto-
mas will appear as multiple radiodense malformed teeth sur-
rounded by a radiolucent rim. Complex odontomas will appear
as a dense amorphous mass with a radiolucent rim. Both forms
may have varying degrees of density depending on the
maturity of dentin and enamel formation.
Odontomas are treated by enucleation and curettage, and
they do not recur. A bony window is created to access the
lesion, which is easily removed with a curette. An intraopera-
tive radiograph can be used to ensure complete removal, and
the incision is closed.
■ SOFT TISSUE PROCEDURES
LABIAL FRENUM
The maxillary labial frenum is a band of fibroelastic tissue
originating from the upper lip and inserting into the attached
gingiva at the midline. It is usually prominent at birth and can
be associated with a diastema in the primary and early perma-
nent dentition. As the alveolus grows vertically, the frenum
attachment moves apically. Eruption of permanent incisors
and canines will typically close the diastema, but in some cases
a prominent labial frenum can contribute to a persistent dia-
stema. This is usually the result of a frenum attachment that
crosses over the alveolar ridge and inserts into the incisive
papilla. In these cases, a clinical exam may reveal an incisive
papilla that blanches when the lip is pulled up.20
Before considering a patient for maxillary labial frenec-
tomy, it is prudent to allow for eruption of all maxillary ante-
rior teeth. The clinician should rule out the possible causes of
diastema including an impacted supernumerary tooth (i.e.,
mesiodens), social behaviors (i.e., thumb sucking and tongue
thrust), pathologic condition, a midline bony cleft, or notch-
ing of alveolar bone between the incisors.
Technique
It is thought that the fibroelastic tissue of the frenum prevents
the diastema from closing. Therefore, it is necessary to com-
pletely excise the fibroelastic band rather than simply incising
the attachment. The latter results in a high rate of recurrence
of the diastema and frenum.18
After infiltrating with local anesthesia, tension is placed on
the frenum by retracting the upper lip. An incision is placed
at the base of the frenum attachment to the incisive papilla
down to the alveolar bone. A thin margin of attached gingival
174 SECTION II ■ Dentoalveolar Surgery
FIGURE 10-11. A, Prominent labial frenum. B, Proposed
incisions for labial frenectomy. C, Soft tissue defect after exci-
sion of labial frenum and vestibular relaxing incisions. D, Final
closure.
tissue is left on the mesial aspect of each central incisor, and
the incision is carried along the lateral borders of the frenum
to its attachment on the labial mucosa. The resultant elliptical
defect is undermined with scissors in the unattached labial
mucosa and releasing incisions are made at the mucogingival
line. The edges of the labial mucosa are sutured together and
the defect in the attached gingival tissue is left to heal by
secondary intention. Placing the sutures through periosteum
at the depth of the vestibule will preserve length. The patient
is placed on a soft diet for 5 days and asked to refrain from
placing any tension on the upper lip (Figure 10-11).
PROMINENT LINGUAL FRENUM (ANKYLOGLOSSIA)
A prominent lingual frenum is common among infants and is
often tightly bound to the attached gingiva, high on the
alveolus at the midline. Complaints of limited tongue mobil-
ity may initiate consults from concerned parents and pediatri-
cians. Initial fears should be alleviated with the knowledge
that the lingual frenum usually becomes less prominent during
the first 2 to 5 years as the alveolus grows in height and teeth
begin to erupt. Other controversial concerns include sucking
and feeding difficulties, airway concerns, future speech diffi-
culty, periodontal, and aesthetic concerns. A tight frenal
attachment can lead to oral hygiene problems with the accu-
mulation of plaque on the lingual anterior teeth. A frenec-
tomy is indicated to prevent resulting periodontal disease in
these patients. A “knee-jerk” reaction to surgically excise all
prominent lingual frena should be avoided because many of
the concerns will resolve with time. A simple incision to
release the tongue should also be avoided because of the high
rate of relapse and potential for scar formation making future
surgery more difficult.
A B
C
D
Lingual Frenectomy Technique
Considering the average age of patients and the opportunity
for bleeding, lingual frenectomy is best accomplished under
conscious sedation and may require an intubated general anes-
thetic. After infiltration with local anesthesia, the tongue is
retracted using sutures or a double prong skin hook. The band
of fibroelastic tissue is excised from its attachment on the
ventral surface of the tongue to its insertion on the attached
gingiva of the lingual mandibular alveolus. Care is taken to
avoid incising the openings of the submandibular glands on
either side of the frenum. A scissor is then used to undermine
the flap margins on the ventral surface of the tongue. Special
attention is given to obtaining good hemostasis to prevent a
hematoma on the floor of the mouth. At this point, the
surgeon may elect to close the wound by a V-Y closure or Z-
plasty technique as described by Kaban.18 Both closure tech-
niques will result in increased length and mobility of the
bound tongue. The Z-plasty technique may allow for greater
length because back-to-back Z-plasties are possible.
The V-Y closure is begun by creating a releasing incision
at the junction of the floor of the mouth and the ventral
tongue. This converts the previous elliptical defect to a V-
shaped defect. The wound is closed using 5-0 chromic gut in
a Y-pattern with the longest arm represented by the ventral
surface of the tongue (Figure 10-12).
The Z-plasty closure is begun by creating two separate
triangles with approximately 45° angles with respect to the
initial ventral ellipse (Figure 10-13).
After the flaps have been undermined, the triangles are
transposed and sutured to their new locations using 5-0
chromic gut. If required, back-to-back Z-plasties can be used
to gain additional length and mobility.
 CHAPTER 10 • Pediatric Dentoalveolar Surgery 175

A B

C D
FIGURE 10-12. A, Preoperative depiction of a prominent lingual frenum. B, Proposed incisions for a lingual fre-
nectomy with a V-Y closure. C, Soft tissue defect after excision of a lingual frenum and undermining of the wound
margins. D, V-Y closure of a lingual frenectomy.

■ GENERALIZED DISORDERS patients is usually skeletal Class III as a result of a deficient

OF DENTITION
CLEIDOCRANIAL DYSPLASIA
Cleidocranial dysplasia (dysostosis) is an autosomal dominant
condition that affects the growth of the cranial vaults, clavi-
cles, maxilla, nasal, and lacrimal bones. This will typically
result in the absence of at least one clavicle, a hypoplastic
maxilla, delayed closure of cranial sutures and fontanelles
(these can form secondary ossification centers and form
wormian bones), and frontal, parietal, and occipital bossing.21
There are dental characteristics as well. These include: reten-
tion of deciduous teeth, presence of supernumerary teeth, and
noneruption of permanent teeth as a result of serious delay
in root development, usually on the order of 3 years23
(Figure 10-14).
These patients also have a tendency to form cysts around
nonerupted permanent teeth. The jaw relationship in these
maxilla and autorotation of the mandible.22
Different treatment modalities have been described in the
literature and consist of three main groups: (1) replacement
of teeth with dentures; (2) removal of supernumerary teeth,
followed by surgical repositioning and transplantation of the
permanent teeth; and (3) surgical and orthodontic treatment
aimed at extracting unnecessary teeth and aligning permanent
teeth.23 It is important to remember that extraction of retained
primary teeth in these patients does not necessarily stimulate
eruption of the permanent teeth. The current trend increas-
ingly points toward the surgical and orthodontic combination
(Figure 10-15).
Within this group, we find different approaches as well. A
key concept in the following management techniques is that
the staging of extractions and exposure allows teeth to be
guided into their ideal position and serve as vertical stops to
maintain vertical height for the next teeth to be exposed.25 In
 176 SECTION II ■ Dentoalveolar Surgery

A B

C D E
FIGURE 10-13. A, Preoperative depiction of a prominent lingual frenum. B, Proposed incisions for a lingual fre-
nectomy with Z-plasty closure. C, Undermining wound margins. D, Transposition of Z-plasty flaps. E, Final closure.

FIGURE 10-14. Pretreatment panoramic radiograph of a patient with cleidocranial dysplasia showing delayed erup-
tion, impacted teeth, and supernumerary teeth. (From Daskalogiannakis J et al.: Cleidocranial dysplasia: 2 generations
of management, J Can Dent Assoc 72(4):337-42, May 2006, with permission.)
 CHAPTER 10 •
the Belfast-Hamburg approach,23,24 a single surgery is used to
remove all deciduous and supernumerary teeth and expose all
permanent teeth. This usually requires wide exposure of the
alveolus, placement of surgical packing, and healing by
secondary intention. The more conservative Toronto-
Melbourne23,24 approach, a staged treatment protocol, is also
used. The initial stage is aimed at extracting deciduous and
supernumerary teeth; the intermediate stage is focused on using
the erupted permanent first molars as anchors to orthodonti-
cally extrude permanent incisors; and the final stage consists of
surgically exposing and orthodontically extruding permanent
premolars and canines. Finally the Jerusalem approach23,24 is
another staged treatment protocol. Permanent teeth are exposed
in two phases, allowing the maxillary incisors to show at the
appropriate age in addition to the permanent first molar. These
teeth are usually exposed when two-thirds of their roots are
developed. The main aspect of this technique is to force erup-
tion of the incisors early for the patient’s self-image.
It is important to understand that in these patients the
chronologic age is much different than the dental age, so
timing of treatment is of the utmost importance. Finally, treat-
ment of cleidocranial dysplasia occurs over an extended period
Pediatric Dentoalveolar Surgery 177
FIGURE 10-15. Posttreatment panoramic radiograph of
the same patient after surgical and orthodontic treatment.(From
Daskalogiannakis J et al.: Cleidocranial dysplasia: 2 generations
of management, J Can Dent Assoc 72(4):337-42, May 2006,
with permission.)
FIGURE 10-16. Panoramic radiograph demonstrating a patient with
hereditary ectodermal dysplasia. Note the hypodontia and the short clinical
crowns and roots of the existing dentition.
of time and can be unpredictable.25 The patient and parents
should be educated about the length of treatment, the need
for multiple surgical procedures, and continued orthodontic
care.
HEREDITARY ECTODERMAL DYSPLASIA
Hereditary ectodermal dysplasia is an inherited disorder that
involves tissues of ectodermal origin, such as hair, nails, skin,
and teeth, and is characterized by aplasia or dysplasia of these
tissues. This disorder can be further subdivided into two
categories. An X-linked hypohidrotic form (Christ-
Siemens-Touraine syndrome) is characterized by the classic
triad of hypohidrosis, hypodontia, and hypotrichosis in addi-
tion to dysmorphic facial features. The hidrotic form (Clous-
ton’s syndrome) usually spares the sweat glands, but continues
to affect hair, nails, and teeth. This form is autosomal domi-
nant and appears to be found primarily in Canadian families
of French descent, as shown by Lowry et al.27 (Figure
10-16).
The diagnosis of hereditary ectodermal dysplasia is usually
made by the correlation of the patient’s history and physical
examination. Classic features include heat intolerance, inabil-
178 SECTION II ■ Dentoalveolar Surgery
FIGURE 10-17. Panoramic radiograph of a patient with
Gardner’s syndrome. Note the multiple osteomas in the mandi-
ble and maxilla. These types of lesions should raise the suspicion
of Gardner’s syndrome, especially if osteomas are present
around the condyles, as seen here. (From Marx R, Stern D: Oral
and maxillofacial pathology, Chicago, 2003, Quintessence Pub-
lishing, p. 756 with permission.)
ity to perspire, abnormal dentition, and sparse hair. As a
consequence, one of the main aspects of treatment is to
improve the patient’s self-image and to preserve psychological
health. Rezende et al.26 promotes early treatment in these
patients because of psychological and physiologic factors: (1)
missing teeth cause prevention of new appositional bone in
the vertical dimension, and only the sutural growth between
the maxilla and the cranial base affect implant location; (2)
alveolar bone defects caused by anodontia reduces tissue
support for eventual removable prostheses; and (3) the absence
of teeth and impaired aesthetics and phonetics can be socially
damaging.
The management of these patients requires a multidisci-
plinary approach, which will usually consist of a pediatric
dentist, orthodontist, prosthodontist, and oral surgeon. The
principal aims of dental treatment are to restore missing teeth
and bone, establish a closer to normal vertical dimension, and
provide support for the facial soft tissues.
Conventional prosthodontic treatment can be problematic
because of the patient’s anatomic abnormalities of the teeth
(conically shaped) and the alveolar ridge (knife-edged). These
abnormalities will result in poor retention and instability of a
removable prosthesis.
The use of endosseous implants in children with hereditary
ectodermal dysplasia appears to be a viable alternative, even
though their use in the younger population carries a degree of
unpredictability. Further discussion on endosseous implants
will be addressed later in the chapter.
GARDNER’S SYNDROME
The initial association made between generalized intestinal
polyposis, osteomas of the jaws, and multiple sebaceous cysts
and lipomas was first described by Devic and Bussy in 1912.28
It was not until 1953 that Gardner described a family with a
triad of features transmitted in an autosomal dominant fashion
consisting of intestinal polyposis, osteomas, and cutaneous
lesions.29 This disorder showed 80% penetrance. Jaw involve-
ment has usually been described as multiple osteomas and
complex odontomas and dental anomalies including impacted
teeth and hypercementosis. Takeda30 describes a case in which
multiple cemental lesions were found in a patient with Gard-
ner’s syndrome. Histopathologically, these lesions behaved
and appeared more like cementum, which was closely united
to tooth roots, and did not fit any prior descriptions in the lit-
erature. Patel et al31 recently described a previously unreported
case of unicystic ameloblastoma mimicking a dentigerous cyst
in a patient with Gardner’s syndrome (Figure 10-17).
The management of Gardner’s syndrome is similar to that
of cleidocranial dysplasia and requires a multidisciplinary
approach. The goal of treatment is to facilitate the eruption
of impacted teeth. Also surgical management of pathologic
entities as described in the literature may additionally be
required.
GENERALIZED GINGIVAL HYPERPLASIA
Gingival hyperplasia is a condition of gingival overgrowth that
can range from very mild enlargement affecting one or more
interdental papillae to severe enlargement affecting both jaws,
with the potential to cause airway compromise. Other undesir-
able features include interferences in oral hygiene (especially
in delayed patients), speech, mastication, and tooth eruption.
The severe form of gingival hyperplasia has usually been asso-
ciated with patients who are treated with combinations of
anticonvulsants as a result of resistant seizures. Additionally,
these patients are usually developmentally delayed and trache-
ostomy dependent. There can also be a psychological compo-
nent in severe cases where facial aesthetics is affected.
Hyperplasia is mainly attributed to medications, but is also
commonly seen with hormonal changes, such as pregnancy
and puberty. Other causes include leukemia, especially acute
myelocytic leukemia, and can be idiopathic in origin.
In drug-induced gingival hyperplasia, Kimball was among
the first to implicate phenytoin as a causative agent.32 Since
then many other drugs have been shown to cause this condi-
tion, including anticonvulsants, such as barbiturates, valproic
acid, succinimides, and carbamazepine.33 Another drug class,
calcium channel blockers, has also been implicated, of which
nifedipine is the most common. Diltiazem, verapamil, and
amlodipine are other causative agents.33 Lastly, cyclosporine,
an immunosuppressant, and oral contraceptive medications
can also cause gingival hyperplasia.
The mechanism by which drugs cause hyperplasia is still
not very well understood. It is suggested that some drugs cause
the production of an inactive form of collagenase that leads
to an imbalance between the production and breakdown of
collagen.34 Other mechanisms include an altered response of
 CHAPTER 10 •
FIGURE 10-18. Drug-induced gingival hyperplasia. The crowns are
almost completely covered. This particular patient was taking phenytoin. (From
Meraw S, Sheridan P: Medically induced gingival hyperplasia, Mayo Clin Proc
73(12):1196-99, Dec 1998 with permission.)
collagen to plaque and hypersensitivity to these drugs in
certain populations34 (Figure 10-18).
Pregnancy can result in gingival enlargement by causing a
severe inflammatory reaction. It was found that the increase
in sex hormones during pregnancy acted as growth factors for
certain bacteria, such as Prevotella intermedia, which were
present in large amounts during the third and fourth months
of pregnancy. This timeline coincided with the development
of hyperplastic lesions.35 Di Placido also postulated that vas-
cular permeability might be increased, thereby increasing the
edema of gingival tissues. Furthermore Reynolds et al. presents
an animal model that used baboons. In the group that was
estrogen suppressed with aromatase inhibitor CGS 20267, all
females (n = 5) showed gingival enlargement. In the control
group (n = 10), none of the females developed gingival
enlargement. Discontinuation of aromatase inhibitor therapy
resulted in spontaneous regression of the gingival lesions.36
The diagnosis of leukemia can be aided by finding gingival
enlargement in an otherwise healthy patient. This oral finding
should always make the clinician suspicious for leukemia. The
most common form of leukemia associated with gingival
hyperplasia is acute monocytic leukemia, which is a subtype
of the acute myelogenous leukemias (AML). The pathogene-
sis is believed to arise from the infiltration of leukemic cells
in the tissues, which causes progressive enlargement of the
interdental papillae. With appropriate chemotherapy, partial
or complete resolution of gingival enlargement is possible. It
is interesting to note that gingival enlargement in edentulous
leukemia patients has not been shown, suggesting that other
local irritants must be present to trigger enlargement.37
Treatment
In drug-induced gingival hyperplasia, nonsurgical treatment
may include discontinuation of the medication because this
can cause regression of the lesions. In some situations, chang-
ing the drug may be a viable alternative. These alternatives
should be discussed with the patient’s physician because it
Pediatric Dentoalveolar Surgery 179
may be detrimental to the overall patient care. Another
important aspect of nonsurgical treatment is oral hygiene. As
discussed earlier, poor oral hygiene can exacerbate gingival
lesions in susceptible patients. Therefore it is recommended
that patients see their dentist regularly for dental prophylaxis
and practice meticulous home care. For patients who are
developmentally delayed and unable to provide for them-
selves, oral hygiene and the condition may be worse, render-
ing the issue more complicated. Many times these patients’
only viable treatment option may be surgical in an operating
room setting. Surgical treatment includes gingivectomy or
periodontal flap surgery. In either case, some form of scaling
and root planning must be performed to minimize local irri-
tants. These procedures may be done under local anesthesia
or intravenous sedation in the office if tolerated by the patient.
General anesthesia is also a viable option, especially in the
developmentally delayed patient. Gingivectomy in these cases
can be bloody as a result of the amount of inflammation
present. It is recommended that electrocautery or a CO2 laser
be used to minimize bleeding.
LOCALIZED GINGIVAL LESIONS
There are certain localized gingival lesions that are more com-
monly seen in the pediatric population. The following is a
review of the preponderant lesions found in this population.
Congenital epulis of the newborn is a soft tissue hamartoma
consisting of large cells with a granular cytoplasm. They are
usually found in the anterior maxilla and have an affinity for
females (9 : 1). They can vary in size and can become large
enough to interfere with feeding. The histology of this tumor
is similar to that found in the adult granular cell tumor.
The major difference, however, is that it does not contain the
pseudoepitheliomatous hyperplasia that is characteristic of
the adult granular cell tumor. Congenital epulis differs from
its adult counterpart (neural in origin) in that it is derived of
pericytic cells, which undergo myofibroblastic differentiation.
If the epulis becomes large enough and causes feeding prob-
lems, early removal is indicated. Surgical removal is usually
accomplished under general anesthesia in an operating room
setting. These lesions respond very well to conservative
removal, and the surgeon must be aware of the potential
bleeding following removal. They usually do not recur, even
when there is incomplete removal. Some cases of spontaneous
regression have been reported in smaller lesions. After surgical
removal, primary teeth usually erupt uneventfully.
An eruption cyst is essentially another type of dentigerous
cyst. They usually occur in younger children and are seen
within the keratinized gingiva as teeth are actively trying to
erupt. They are rare, accounting for less than 1% of all odon-
togenic cysts. The cavity contains fluid, and if traumatized
(which is common), there is an accumulation of blood that
will lend the lesion a bluish color. Depending on how thick
the overlying soft tissue is, they can grow fairly large predispos-
ing the area to pain, swelling, and in severe cases, infection.
There are two main methods to treating eruption cysts. One
method is to let nature take its course and let the tooth erupt.
180 SECTION II ■ Dentoalveolar Surgery
FIGURE 10-19. Pyogenic granuloma, often ulcerated. These lesions are
highly vascular and tend to bleed easily. The fibrous connective tissue is not
as dense as the peripheral ossifying fibroma. (From Oda D: Soft tissue lesions
in children, Oral Maxillofac Surg Clin North Am 17:383-402, 2005, with
permission.)
As the tooth erupts, it will puncture through the cyst causing
it to naturally marsupialize. The second method is surgical,
where a small incision over the crest of the ridge is made
causing the cyst to marsupialize. This will lead to normal
eruption of the tooth.
The gingival cyst of the newborn can appear as multiple
nodules on the edentulous ridge and are seen in the maxilla
more often than the mandible. Characteristically, these cysts
appear white because of the production of keratin from dental
lamina remnants. They can also occur on the palate along the
midline and are characterized as epithelial inclusion cysts,
which occur as the fusion of the hard palate takes place causing
epithelial entrapment along the fusion line. The other com-
monly used term for these cysts is Epstein’s pearls. Regardless
of their location on the ridge or in the palate, monitoring and
parent reassurance is the preferred treatment. These cysts will
spontaneously rupture into the oral cavity, and biopsy to rule
out other entities is only indicated when there are nodules
that are persistent.
The pyogenic granuloma is of one the most common reac-
tive gingival swellings, accounting for 85% of such cases.38
These lesions are typically red-purple in color as a result of
their rich vascularity and therefore tend to bleed quite easily.
They can also be lobular, sessile, and even ulcerated
(Figure 10-19).
They can occur at any age, but seem to occur more fre-
quently in females with hormonal changes, such as puberty,
pregnancy, or taking oral contraceptives. The precipitating
factors are local irritants, such as plaque, calculus, overhang-
ing restorations, and foreign bodies. Because this is an inflam-
matory process with continuous attempts at healing, the
FIGURE 10-20. Peripheral ossifying fibroma. This mass is firm, has a
broad base, and contains dense connective tissue. (From Oda D: Soft tissue
lesions in children, Oral Maxillofac Surg Clin North Am 17:383-402, 2005,
with permission.)
abundant presence of hyperplastic granulation tissue is a char-
acteristic of the pyogenic granuloma. Treatment consists of
surgical excision, preferably with electrocautery or CO2 laser
to minimize bleeding. Depth of the excision should be to the
underlying periosteum. Removal of the local irritant is impor-
tant in preventing recurrence, which occurs mostly in the
pregnant population. It is important to understand the pyo-
genic granuloma can resemble many other entities, primary
and metastatic malignancy being the most concerning. If
there is clinical suspicion, prompt biopsy and further work-up
may be warranted.
Peripheral ossifying fibroma is a lesion exclusively found on
the anterior gingiva and originates from the periodontal
ligament or the periosteum (Figure 10-20).
Unlike the pyogenic granuloma, this lesion makes up only
10% of gingival swellings found in the pediatric population.
It has a slight female predilection and rarely involves primary
teeth. This mass is more firm and less friable than a pyogenic
granuloma or a peripheral giant cell granuloma and will typi-
cally have a broad base. Histologically, this entity will show
a dense fibrous connective tissue, an abundance of plasma
calls, and calcifications that resemble islands of bone in the
rich cellular areas. The treatment of choice is excision with
surgical margins, paying particular attention to the excision
of the periodontal ligament. If the site of origin is at the level
of the periodontal ligament and the ligament is not excised,
there is a propensity for recurrence.
Peripheral giant cell granuloma is more similar to the pyo-
genic granuloma clinically, presenting as a soft, fleshy mass
that bleeds easily. This swelling constitutes 5% of reactive
gingival swellings. It can arise from the gingiva and unlike
pyogenic granuloma can also arise from the edentulous ridge.
The peripheral giant call granuloma originates from the peri-
osteum or periodontal ligament and consists of vascular granu-
lation tissue containing osteoclasts, which are multinucleated
giant cells. It has a 2 : 1 female predilection and is usually
anterior to the molars. This lesion can act rather aggressively,
 CHAPTER 10 •
FIGURE 10-21. Melanotic neuroectodermal tumor of infancy. Often a
bluish mass seen in the anterior maxilla, which can be locally invasive. (From
Oda D: Soft tissue lesions in children, Oral Maxillofac Surg Clin North Am
17:383-402, 2005, with permission.)
resulting in displacement of teeth and carving out of bone,
showing a saucerlike concave pattern. The treatment is com-
plete excision with adequate curettage. The recurrence rate is
less than 10%.
The adenomatoid odontogenic tumor (AOT) is a fairly
rare tumor that is not seen above the age of 30 and is most
commonly seen in teenagers and females. This tumor has a
propensity to the anterior jaws, specifically the anterior
maxilla, and is usually associated with an impacted tooth.
Originally the tumor was associated with ameloblastoma and
was called adenoameloblastoma because of the histologic
characteristics of pseudoducts and enameloid tissue seen in
AOT. However, the AOT actually behaves more like a ham-
artoma than a neoplasm.39 The presence of ductlike structures
and “rosettes,” as mentioned previously, are characteristic, in
addition to the presence of calcifications in the center of the
capsule. Radiographically an AOT will present as a radiolu-
cency that is well defined and may contain radiopaque foci
from calcifications inside the lesion. Local excision is the
treatment of choice for the AOT. This entity is benign and
typically does not recur.
Melanotic neuroectodermal tumor of infancy is a rare,
benign tumor of neural crest origin that is seen in infants
younger than 6 months of age and occurs in the midline of
the maxillary alveolus. Because it is melanotic in origin, it
usually presents as a pigmented mass that appears bluish-black
(Figure 10-21).
It is an osteolytic lesion that can be invasive and presents
as an ill-defined radiolucency on radiograph. The histology
will mainly show nests of tumor cells that contain melanin.
The treatment of choice is local excision with rare recurrence.
Pediatric Dentoalveolar Surgery 181
Other sites have been described and include the skull, man-
dible, mediastinum, brain, scapula, and genital organs.
■ PEDIATRIC IMPLANTS
The use of endosseous implants in the adult edentulous and
partially edentulous patient is widely accepted and supported
in the literature. On the other hand, implant placement in
the pediatric patient has not been as thoroughly researched
and remains controversial except in certain situations. The
success of an implant is dependant on many factors, which
include the quality and quantity of bone, treatment planning,
sound surgical technique, optimal restorative prostheses, and
good long-term oral hygiene.46 Attention to implant place-
ment in the pediatric population is slowly but consistently
gaining popularity. Successful placement of implants in
children has been demonstrated in patients with hereditary
ectodermal dysplasia, cleidocranial dysostosis, cleft lip and
palate, and tumor resections in which bone grafts are used
(Figure 10-22).
Hereditary ectodermal dysplasia is a disorder of the denti-
tion that has received much attention in the behavior of
implants in growing patients. Kearns et al44 was able to show
that implants placed in the anterior maxilla of these patients
resulted in loss of vertical height at the incisal border with the
adjacent permanent teeth. This was supported by Thilander
et al.43 who showed that this leads to the prosthesis eventually
being out of occlusion and usually requires removal and
replacement with a longer abutment. Kearns was able to dem-
onstrate implants can be successfully placed in these pediatric
patients with a success rate of 97% after the placement of 41
implants. Their group raises the following point: Functional,
aesthetic, and psychological benefits should be weighed against
the need to change abutments and the possibility of removal
at a later date.
Ledermann et al.40 states that another possible consider-
ation for implant placement arises from the fact that the most
commonly lost teeth as a result of trauma in children are the
maxillary incisors (Figure 10-23).
Immediate implant placement after tooth luxation or avul-
sion may be indicated to prevent the rapid resorption of the
alveolus and help preserve bone. Ledermann placed a total of
42 implants in patients aged 9 to 18. Fourteen implants were
placed immediately after traumatic luxation of anterior teeth
and 28 implants after appropriate healing time was given.
Aside from three implants failing as a result of additional
trauma, the remaining implants osseointegrated and were
loaded without complications. Their study did not show a case
of submergence, and implants remained stable despite addi-
tional growth of the patient.
Implants do not behave like natural teeth because of the
absence of a periodontal ligament. One of the periodontal
ligament’s functions is to facilitate eruption of natural teeth
and compensate for the vertical growth of the alveolar process.
Implants instead resemble ankylosed teeth and can impede
dentoalveolar growth in the vertical dimension resulting in
submersion when the adjacent teeth and alveolus continue to
182 SECTION II ■ Dentoalveolar Surgery

A B

FIGURE 10-22. A, 6-year-old boy following resection and reconstruction of the right mandible. He was diagnosed
with aggressive myofibroma. B, Same patient 5 months after anterior hip graft and implant placement. (From Troulis M,
Williams B, Kaban L: Staged protocol for resection, skeletal reconstruction, and oral rehabilitation of children with jaw
tumors, J Oral Maxillofac Surg 62:335-43, 2004, with permission.)

D
B

FIGURE 10-23. A, 14-year-old girl 1 month following placement of crown tooth #9

that was lost as a result of trauma. B, Same patient, 3 years after crown placement. Note
continued growth of the skeleton. C, The porcelain-fused-to-metal crown was removed
and adjusted by adding porcelain to the incisal edge, then reseated. D, Periapical radio-
graph of the Ha-Ti implant 7 years after placement, showing osseointegration and no bone
loss. (From Ledermann P, Hassell T, Hefti A: Osseointegrated implants as alternative
therapy to bridge construction or orthodontics in young patients: seven years of clinical
C
experience, Pediatric Dent 15(5):327-33, Oct 1993, with permission.)
 CHAPTER 10 •
FIGURE 10-24. Illustration showing vectors of growth of the maxilla and
mandible. Note the resorption of bone on the nasal floor and apposition of bone
on the palate and alveolus. In the mandible, there is resorption of bone at the
anterior ramus with bone apposition on the posterior ramus and the free
margins of the condyle, causing the mandible to grow downward and
forward.
erupt and gain height. Odman and Thilander42 showed in
growing pigs that implants placed did not move in any single
vector and remained ankylosed. Additionally the study showed
that in the posterior mandible, bony apposition caused the
implants to move lingually through the alveolar process. In
the maxilla, the implants moved palatally. These implants
also seemed to impede the growth of the alveolar process and
caused tooth buds to change their path of eruption.
Craniofacial growth rate and patterns vary from individual
to individual as a result of genetic and other confounding
factors, such as chronic illness. This can make growth predic-
tions unreliable. To date the best predictors of growth are
serial cephalometric analysis taken at 6-month intervals and
hand-wrist films. The famous Scammon growth curves47 have
shown that the maxilla closely mimics the cranial base,
whereas the mandible more closely resembles the general body
growth curve. From these curves, we can derive that the
maxilla finishes growth before the mandible.
Growth occurs in three vectors: transverse, horizontal, and
vertical. In the maxilla, this occurs transversely at the mid-
palatal sutures (Figure 10-24).
Horizontal growth vectors occur at the palatine sutures and
maxillary tuberosities, and vertical growth occurs by apposi-
tion of bone at the alveolus and resorption on the nasal sur-
faces.45 In the mandible, the transverse growth occurs primarily
in the posterior mandible because the mandibular symphysis
usually closes by 2 years of age. The vertical and horizontal
components tend to occur simultaneously in a continuing
vector because apposition takes place at the free margins of
the condyle, upper edge of the alveolar process, and posterior
margin of the ramus.46 This causes the mandible to “roll”
Pediatric Dentoalveolar Surgery 183
downward and forward, as stated by Björk.41 Lastly, cessation
of growth in these vectors predictably occurs in a specific
order, with the transverse growth ending first, horizontal
second, and vertical last.
At this time, some recommendations can be made regard-
ing the use of implants in the growing patient: (1) Implants
can be placed with fair predictability in patients with ectoder-
mal dysplasia, cleidocranial dysostosis, cleft lip and palate, (2)
Implants will do well in areas of tumor resection in which
bone grafts are used. These patients do not have the potential
for the normal growth patterns of the alveolus, (3) Children
who are completely edentulous can have implants placed with
a good degree of predictability because of the decreased alveo-
lar growth potential, (4) Caution must be exercised in par-
tially dentate pediatric patients with teeth on either side of a
proposed implant because of the risk of submersion and/or
eventual unrestorability especially when placing an implant
in the aesthetic zone, (5) For the most predictable prognosis,
implant placement should be delayed until growth is com-
plete, (6) Close follow-up of pediatric implant patients is
necessary.
Endosseous implants in children is an area of dentoalveolar
surgery that still requires more research to compile more defin-
itive data. There is a definite need for implants in the pediatric
population, and with meticulous treatment planning and
informed consent, the best treatment can be rendered.
REFERENCES
1. Thilander B, Myrberg N: The prevalence of malocclusion in
Swedish schoolchildren, Scand J Dent Res 81:12-20, 1973.
2. Bishara SE: Impacted maxillary canines: a review, Am J Orthod
Dentofacial Orthop 101:2, 2002.
3. Jacoby H: The etiology of maxillary canine impactions, Am J
Orthod 84:2, 1983.
4. Stellzig A, Basdra EK, Komposch G: The etiology of canine
tooth impaction-an overview of classification, diagnosis and
management, J Can Dent Assoc 55:3, 1999.
5. Jacobs SG: Radiographic localization of unerupted maxillary
anterior teeth using the vertical tube shift technique: the history
and application of the method with some case reports, Am J
Orthod Dentofacial Orthop 116:4, 1999.
6. Stivaros N, Mandall NA: Radiographic factors affecting the
management of impacted upper permanent canines, J Orthod
23:169-173, 2000.
7. Ericson S, Kurol J: Radiographic assessment of maxillary canine
eruption in children with clinical signs of eruption disturbances,
Eur J Orthod 8:133-140, 1986.
8. Ericson S, Kurol J: Early treatment of palatally erupting maxillary
canines by extraction of primary canines, Eur J Orthod 10:283-
295, 1988.
9. Kokich VG: Surgical and orthodontic management of impacted
maxillary canines, Am J Orthod Dentofacial Orthop 126:3, 2004.
10. Vermette ME, Kokich VG, Kennedy DB: Uncovering labially
impacted teeth: apically positioned flap and closed-eruption
techniques, Angle Orthod 65:1, 1995.
11. Frank CA: Treatment options for impacted teeth, J Am Dent
Assoc 131:625-632, 2000.
12. Dessner S: Surgical uprighting of second molars: rationale and
technique, Oral and Maxillofac Surg Clin North Am 14:2, 2002.
13. Sagne S, Thilander B: Transalveolar transplantation of maxillary
canines. A follow-up study, Eur J Orthod 12:140-147, 1990.
184 SECTION II ■ Dentoalveolar Surgery
14. Sherwood KH, Burch JG, Thompson WJ: Closing anterior open-
bites by intruding molars with titanium miniplate anchorage,
Am J Orthod Dentofacial Orthop 122:593-600, 2002.
15. Sugawara J: Distal movement of mandibular molars in adult
patients with the skeletal anchorage system, Am J Orthod
Dentofacial Orthop 125:130-138, 2004.
16. Garvey TM, Barry HJ, Blake M: Supernumerary teeth-an over-
view of classification, diagnosis and management, J Can Dent
Assoc 65:612-616, 1999.
17. Brook AH: Dental anomalies of number, form and size: their
prevalence in British schoolchildren, J Int Assoc Dent Child 5:37-
53, 1974.
18. Kaban LB, Troulis MJ: Dentoalveolar surgery. In Pediatric oral
and maxillofacial surgery, Philadelphia, 2004, Saunders.
19. Marx RE, Stern D: Odontogenic tumors: hamartomas and neo-
plasms. In Oral and maxillofacial pathology, a rationale for diagnosis
and treatment, Chicago, 2003, Quintessence Publishing.
20. Edwards JG: The diastema, the frenum, the frenectomy: a clini-
cal study, Am J Orthod 71:489-508, 1977.
21. Angle AD, Rebellato J: Dental team management for a patient
with cleidocranial dysplasia, Am J Orthod Dentofacial Orthop
128(1):110-117, July 2005.
22. Shaikh R, Shusterman S: Delayed dental maturation in cleido-
cranial dysplasia, J Dent Child 65(5):325-329, Sep-Oct, 1998.
23. Becker A, Lustmann J, Shteyer A: Cleidocranial dysplasia: part
1-general principles of the orthodontic and surgical treatment
modality, Am J Orthod Dentofacial Orthop 111(1):28-33, Jan
1997.
24. Becker A: Cleidocranial dysplasia: part 2-treatment protocol for
the orthodontic and surgical modality, Am J Orthod Dentofacial
Orthop 111(1):173-183, Jan 1997.
25. Daskalogiannakis J et al.: Cleidocranial dysplasia: 2 generations
of management, J Can Dent Assoc 72(4):337-342, May 2006.
26. Rubo de Rezende M, Amado F: Osseointegrated implants in the
oral rehabilitation of a patient with cleft lip and palate and
ectodermal dysplasia: a case report, Int J Oral Maxillofac Implants
19(6):896-900, 2004.
27. Lowry RB, Robinson G, Miller J: Hereditary ectodermal dyspla-
sia symptoms, inheritance patterns, differential diagnosis, man-
agement, Clin Pediatr 5:395-402, 1996.
28. Devic A, Bussy MM: Un cas de polypose adenomateuse gener-
alisée aà tout l’intestin, Arch Mal Appar Dig 6:278-289, 1912.
29. Gardner EJ, Richard RC: Multiple cutaneous and subcutaneous
lesions occurring simultaneously with hereditary polyposis and
osteomatosis, Am J Hum Genet 5:139-147, 1953.
30. Takeda Y: Multiple cemental lesions in the jaw bones of a
patient with Gardner’s syndrome Virchows archiv-A, Pathologi-
cal Anat Histopathol 411(3):253-256, 1987.
31. Patel H, Rees RT: Unicystic ameloblastoma presenting in
Gardner’s syndrome: a case report, Br Dent J 198(12):747-748,
Jun 25, 2005.
32. Kimball OP: The treatment of epilepsy with sodium diphenyl
hydantoinate, JAMA 112:1244-1250, 1939.
33. Meraw S, Sheridan P: Medically induced gingival hyperplasia,
Mayo Clin Proc 73(12):1196-1199, Dec 1998.
34. Camargo P et al.: Treatment of drug-induced gingival enlarge-
ment: aesthetic and functional considerations, Periodontol 2000
27(1):131-138, Oct 2001.
35. Di Placido G et al.: Gingival hyperplasia in pregnancy. II. etio-
pathogenic factors and mechanisms, Minerva stomatologica
47(5):223-229, May, 1998.
36. Reynolds M et al.: Estrogen suppression induces papillary gingi-
val overgrowth in pregnant baboons, J Periodontol 75(5):693-
701, May 2004.
37. Dreizen S: Malignant gingival and skin “infiltrates” in adult
leukemia, Oral Surg Oral Med Oral Pathol 55:572-579, 1983.
38. Regezi J et al.: Oral pathology. In Clinical pathologic correlations,
ed 4, Philadelphia, 2003, WB Saunders.
39. Oda D: Soft tissue lesions in children, Oral Maxillofac Surg Clin
North Am 17:383-402, 2005.
40. Ledermann P et al.: Osseointegrated implants as alternative
therapy to bridge construction or orthodontics in young patients:
seven years of clinical experience, Pediatric Dent 15(5):327-333,
Oct 1993.
41. Björk A: Variations in the growth pattern of the human
mandible: a longitudinal radiographic study by the implant
method, J Dent Res 42:400-411, 1963.
42. Odman J et al.: The effect of osseointegrated implants on den-
toalveolar development: A clinical and radiographic study in
growing pigs, Eur J Orthod 13:279, 1991.
43. Thilander B et al.: Osseointegrated implants in adolescents: an
alternative in replacing missing teeth? Eur J Orthod 16:84,
1994.
44. Kearns GJ et al.: Placement of endosseous implants in children
with hereditary ectodermal dysplasia, Oral Surg Oral Med Oral
Path Oral Radiol Endod 88:5-10, 1999.
45. Brahim J: Dental implants in children, Oral Maxillofac Clin
North Am 17(4):375-381, Nov 2005.
46. Cronin R, Oesterle L, Ranly D: Mandibular implants and the
growing patient, Int J Oral Maxillofac Implants 9(1):55-62,
1994.
47. Ulijasjek S, Johnson F, Preece M: The Cambridge encyclopedia of
human growth and development, New York, 1998, Cambridge Uni-
versity Press.

BASIC AND COMPLEX EXODONTIA AND SURGICAL
MANAGEMENT OF IMPACTED TEETH
Manaf Saker • Orrett E. Ogle • Harry Dym
Simple extractions are procedures that are becoming less
common in today’s dental world because preventative den-
tistry and advanced dental techniques have evolved to be able
to more successfully maintain and save teeth from being
removed. Awareness about the importance of maintaining
dentition has also played a significant role in extractions
becoming a last resort as a modality for dental treatment.
The relatively recent onset of high-tech dentistry produced
a greater shift toward achieving not only successful lasting
results, but highly cosmetic and more predictable results. The
basis of exodontia has evolved as well to incorporate a higher
degree of technique improvement, treatment planning, and
diagnosis and timing of replacement treatment to be included
in the work-up of the extraction process. As tooth replace-
ment has become the more commonly accepted treatment,
rather than the abandonment of the extraction site as in the
past, clinicians find themselves involved in the management
of the extraction site as a part of a simple extraction
procedure.
The definition of basic exodontia involves simple luxation
techniques, bone expansion, and forceps delivery. The clini-
cian must pay attention in greater detail to diagnostic tools,
such as x-rays, and employ them to appropriately consider root
form abnormalities, root canal therapies, and other various
factors when planning on simple extraction. If these small
details and basic biologic principals are not paid attention to
and respected, the surgeons might find themselves suddenly
dealing with a complicated or surgical exodontia rather than
a simple extraction.
When a problem is anticipated in the process of diagnosis
and treatment planning, then one should prudently proceed
to planning for surgical extraction to preserve the bony socket
and periodontal apparatus.
■ INDICATIONS
DECAY
Decay is one of the most common reasons leading to tooth
extraction. Decayed teeth will fall into one of two categories:
restorable or nonrestorable decayed teeth. Although the
extraction process itself might be a simple procedure, the deci-
sion is not always as simple.
Thorough examination should first take place and studying
of the radiographs in conjunction with the clinical findings as
CHAPTER 11
well should be an intricate part of the decision process. In
cases of nonrestorable decayed teeth, one must pay extreme
care to treatment planning because some teeth could fracture
during the extraction process and lead to a surgical extraction
rather than simple extraction. If possible, it is always prudent
to plan for a surgical extraction and proceed with sectioning
the roots or laying a surgical flap for better preservation of the
alveolar bone and periodontal apparatus.
Unfortunately, some patients that have decayed but restor-
able teeth would like to have their teeth removed for financial
reasons. Although there is not enough room in this chapter
to discuss the ethical dimension of such a decision, the clini-
cian must always spend time counseling the patient regarding
the various options that are available to try to preserve the
tooth.
■ PERIODONTAL DISEASE
When periodontal disease has progressed so far that it has
caused significant bone and periodontal loss and deemed the
tooth nonrestorable, the obvious answer is simple tooth
extraction and an attempt to regenerate and preserve that site
in preparation for other various prosthetic restoration.
Periodontal disease around fully or partially erupted third
molars has been well studied also and has shown to contribute
to medical systemic illnesses. Should periodontal disease be
uncontrollable with surgical methods, one must always con-
sider the option of extraction as a solution as part of the pre-
ventative medical management.1
■ ORTHODONTICS
The requests for orthodontic extractions of first premolars
have dramatically decreased as a result of a shift in the think-
ing process in orthodontic treatment planning. Except in
cases of severe crowding, extractions of premolars are less
common. Rather orthodontic treatment planning today leans
more toward setting the anterior dentition in a more protru-
sive position, taking into consideration lip support, future
skeletal growth change, and its facial cosmetic impact. Evolu-
tion of various orthodontic technologies leading to better
anchorage, such as the orthodontic minianchor implants, is
changing treatment planning as well. However, cases of
extreme crowdedness do sometimes necessitate the extraction
of premolars, anterior lower centrals, or sometimes molars or
premolars with large restorations.
185
186 SECTION II ■ Dentoalveolar Surgery
The treatment planning must be very clearly communi-
cated between the orthodontic specialist who is managing the
orthodontic care and the surgeon who is removing the teeth.
The treatment plan must be of sound clinical judgment.
■ TOOTH FRACTURE
Tooth fracture is a common, but sometimes difficult, condi-
tion to diagnosis, especially in its early stages because the
radiographic evidence cannot always be helpful and a vertical
fracture cannot always be detected with the naked eye.
The diagnosis comes most of the time from an endodontist
who attempted to treat the tooth endodontically with micro-
scopic magnification; he or she tends to see the fracture in the
base of the pulp chamber and make the appropriate referral.
Other fractured teeth with obvious clinical presentation
that deem the crown nonrestorable as a result of the extension
of the fracture into the furcation or deep into the subosseous
level should be considered for evaluation. Some subosseous
fractures could be considered for salvaging by crown lengthen-
ing procedures and orthodontic eruption, yet some are too
deep to salvage that way and must be extracted.
Careful treatment planning should consider the clinical
condition of the tooth, plan simple extraction versus surgical
extraction, and then proceed accordingly.
■ PREPROSTHETIC PREPARATION
In treatment planning for fabricating a fixed or removal pros-
thesis, it would sometimes be necessary to remove carious
nonrestorable teeth or noncarious teeth because of their severe
malposition or supereruption. In fixed prosthetic cases, some-
times the decision is made to remove severely rotated or mal-
erupted teeth for lack of their value in anchorage or for their
negative impact on the cosmetic outcome.
If maxillary or mandibular teeth were removed and not
replaced for a long time, the opposing and adjacent teeth will
undergo supereruption and shifting. Sometimes salvaging
these teeth or restoring them to a functional status could
involve heroic effort and extensive treatment interventions
that would have a significant impact on the time and cost of
treatment.
The decision to have these teeth removed also needs to
be very carefully discussed with the prosthodontist who will
be making the final decision on the design of the prosthetic
work and the engineering of the occlusal force distribution
on the final prosthesis. Patient education about the various
options, the risk involvement versus the benefits, is extremely
important. In some instances, a few anterior teeth might be
remaining, simply for cosmetic value from the patient’s per-
spective. These teeth could have very little to no value for
full anchorage of a partial denture, and a prosthetic decision
might have to be made to have these removed and alter the
design into a full denture for better stability and cosmetic
outcome.
Combination syndrome is a condition that still is found
commonly in general dentistry practice, and it must be very
prudently prevented. Should the patient have a maxillary full
removable prosthesis and partial remaining anterior teeth
only, analysis of the occlusal forces must be carefully studied
and the patient must be counseled about combination syn-
drome scenario. Fabrication of either a new partial lower pros-
thesis that would provide a stable posterior occlusal support
and/or removal of the anterior teeth and conversion of the
lower mandibular prosthesis into a full arch removable denture
should be suggested.
■ REVERSIBLE PULPITIS
With surgeons mastering the techniques of implantology and
with improvement of implant surfaces, the success of implants
have become very predictable and studies have shown that
implants are as successful or more successful than root canal
therapy. When root canals were done by endodontists, the
success rate was found to be between 70% to 95%. It was even
lower than that when the root canals were performed by
general practitioners.
Root canals that failed secondary to nonsurgical endodon-
tics did so because of periodontal disease, dental decay, verti-
cal root fracture, and a variety of other reasons.2
■ TEETH ASSOCIATED WITH
PATHOLOGIC CONDITIONS
Because some pathologic conditions will develop under the
apices of mandibular or maxillary teeth, treatment for these
pathologic conditions could require a thorough and aggressive
curettage and removal to cure the lesion. Good surgical access
and visibility is essential to prevent damaging some vital struc-
tures, such as the inferior alveolar nerve. The clinician must
make that decision and carefully evaluate, aided by clinical
examination, incisional biopsies, and radiographic studies, to
find out if the teeth adjacent to the pathologic conditions need
to be sacrificed for access and successful removal of the lesion.
■ CHEMOTHERAPY AND RADIATION
The significant focus and research of cancer over the past
decades have led to the development of some very effective
chemotherapeutic agents that have led to a dramatic exten-
sion of the life span of cancer patients. In some cases, these
therapies have even achieved a cure for some treated cancers.
These agents unfortunately come with a significant list of side
effects. Most significant of these effects is the impact on the
immune system and the healing abilities of the body. Because
these are life-preserving medications in most instances, one
must learn how to deal with the negative outcome of side
effects in the most efficient manner to afford a suitable quality
of life for the patient.
■ DIAGNOSIS AND TREATMENT
PLANNING
Appropriate and careful studying of the situation, assessing the
difficulty of the extraction, and collecting relevant infor-
mation would lead to appropriate treatment planning and
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth
preparation for a simple versus surgical extraction. A well-
planned procedure will lead to a more comfortable visit for
both surgeon and patient and a more successful, predictable
outcome reflecting positively on the surgeon’s efficiency, valu-
able chair time, and reputation.
Once the surgeon has collected the various diagnostic data,
one must share the information with the patient and use it for
a good session of preoperative patient education, explaining
to the patient a reasonable surgical course and postoperative
strategies and expectations.
Vallerand et al. demonstrated the positive effect of an
informative preoperative session regarding the postoperative
expectations in significantly increasing pain relief and the
positive outcome of satisfaction with pain control without
increasing medications.4
An important part of diagnosis and treatment planning is
collecting medical data, review of the patient’s medical history,
current medications and their potential impact on the patient’s
healing ability, bleeding, immune system, and potential inter-
actions with postoperative medications prescribed by the
surgeon. The patients must also be counseled regarding
smoking and its negative effect on the healing socket and the
alveolar process, bony dimensions, and the effect of smoking
on the dimensional reduction of the residual alveolar bone
and its potential negative impact on the patient’s ability to
replace the extracted tooth postoperatively either by a bridge
or an implant.5
Thorough clinical examination of the object tooth itself
and the surrounding structures must take place. The patient’s
ability to open wide enough to grant good access and visual
field must be evacuated. The presence of TMJ disease or
trismus limiting the patient to open wide must be appraised
as well. Any swelling in the area of the planned extraction
site must be assessed and determined if it is a peridental abscess
versus neoplasm. If neoplasm is suspected, one must prudently
reassess and delay the extraction if possible until further con-
firmation with a biopsy has been performed. If swelling was
due to a dental abscess, then one must plan accordingly and
realize the potential negative impact of the abscess on the
surgeon’s ability to administer an effective local anesthetic.
Then a thorough clinical examination of the tooth itself
and the extent of decay or large restorations that might lead
to tooth fracture is performed, converting the case into a surgi-
cal extraction versus simple extraction. Examination of radio-
graphic evidence, such as panoramic and periapical x-rays,
must take place to assess the roots of the teeth and the sur-
rounding area. Dilacerated roots, bulbous roots, thin long
roots with thin curved ends, ankylosed roots, and the intimate
proximity of these roots to the anatomic structures, such as
the maxillary sinus and inferior alveolar nerve, must all be
considered in forming a treatment plan.
Once all of the data has been thoroughly collected and
analyzed, the surgeon will proceed with a specific treatment
plan and he or she will be able to execute it with a greater
degree of comfort and predictability.
187
■ PRINCIPLES OF SIMPLE
EXTRACTION
In the process of a simple extraction, the surgeon must exer-
cise a great deal of finesse and a certain degree of controlled
force to be able to deliver a simple tooth extraction. If the
surgeon finds himself or herself in a situation where they have
to exercise a lot of force to be able to deliver a certain tooth
extraction, they must stop and reassess the situation before
resuming.
As mentioned earlier, a simple extraction process involves
minor alveolar bone expansion, separation of the periodontal
ligament, and simple coronal forceps delivery of the tooth.
Successful extractions also depend on the surgeon’s thorough
and detailed understanding of the anatomy of the teeth
involved, the root form, angulation, their attachment to the
periodontal apparatus, and the bony structure underneath.
Experience will enhance the surgeon’s tactile sense. As the
tooth is being removed, the surgeon will be able to appreciate
the lateral forces applied on the tooth’s roots and their effect
on the alveolar bone. This will lead to avoidance of any exces-
sive forces that would produce root and alveolar bone
fracture.
The patient needs to be positioned in the dental chair to
allow for the surgeon’s optimal control and visibility. When
extractions are being performed in the lower arch, it is prefer-
able that the patient’s mandible is positioned in a parallel line
with the floor. Then the patient’s height should be adjusted
up and down to allow for the mandible to be positioned at the
same level at the surgeon’s elbow so that when the surgeon is
performing the extraction, the forearm is parallel with the
floor as well. When extracting a maxillary tooth, the patient’s
maxillary occlusal plane should fall at almost a 60° angle with
the floor.6
The surgeon’s position, relative to the patient’s position,
varies as well, depending on which tooth is being extracted.
It is also dependant on the surgeon’s dominant hand (Figure
11-1).
Using the appropriate specialized instrumentation facili-
tates the procedure and makes it more predictable. Typically
the surgeon will start by separating the superior portion of the
periodontal ligament, then subluxating with an elevator.
Choosing the right forceps is important to be able to grasp the
cervical portion of the tooth and position it as apically as
possible to try to shift the center of rotation toward the root.
This allows the most effective central bone expansion move-
ment and prevention of the fracture of roots or crown at the
same time. Sharp elevators and forceps are always more desir-
able to use because they will engage the tooth in a more firm
and predictable manner and prevent slippage and/or lack of
efficient delivery of force.
Pursuant to the separation of the periodontal ligament,
one must find an appropriate purchase point for the elevator,
try to position the elevator between the bony socket wall and
the tooth itself, and direct the elevator in an apical direction
188 SECTION II ■ Dentoalveolar Surgery

FIGURE 11-1. A, Controlled force is delivered most effec-

tively when a low, upright chair position is used for the extraction
of mandibular teeth. A higher, more reclined chair position is used
for the extraction of maxillary teeth. B, Most extraction instruments
are designed to be used from the right (or left) front chair location.
(From Pedersen GW: Uncomplicated extraction. In Oral surgery,
Philadelphia, 1998, WB Saunders.)

trying to subluxate the root and push it coronally. Most of

the time an effective elevation would prevent injury to the
adjacent teeth, maintain the integrity of the alveolar bony
structure, and make the forceps delivery extremely simple.
During the introduction of the elevator, the surgeon’s free
hand should, if possible, always hold the alveolar process with
the thumb on one side and the forefinger on the other side
and try to sense and direct the degree and direction of force
being applied to the alveolar process of the tooth (Figure
11-2).
When extracting one of the maxillary anterior lateral and
central incisors and/or mandibular premolars, the predomi-
nant extraction force is mainly rotational with the use of a
universal maxillary forceps #150 for the maxillary teeth and
an Asch forceps for the lower teeth (Figure 11-3). The maxil-
lary canines and the lower anterior teeth, however, seem to
have flatter roots and would require more lateral buccal and
lingual forces application in the process of the extraction first.
The maxillary premolars could have roots that are thin. A
maxillary universal forceps is typically used for these teeth to
be extracted. The forceps is positioned to grasp the crown FIGURE 11-2. The elevator is forcing the root upward and outward as its
portion of the tooth and seated as apically as possible. Lateral blade is being forced apically into the socket. As the surgeon’s experience
increases, such forces can be used to direct the tooth’s delivery. Note that the
force in a buccal fashion is applied first and then in the palatal
index finger is extended and can be used to control the forces required to
aspect with extreme care to prevent fracturing those thin
remove the root. (Modified from Peterson LJ, editor: Contemporary oral and
roots. Careful repetition of the same movement is done until maxillofacial surgery, ed 3, St Louis, 1998, Mosby.)
the tooth is subluxated. The alveolar bone is expanded, and
the tooth can then be delivered coronally (Figure 11-4).
A very similar technique is used for the maxillary molars
as well. Great attention must be paid not to cause excessive proximation of the handles of the forceps takes place. That
force, which could fracture the buccal plate. A variety of other process will luxate the tooth coronally, and then simple deliv-
maxillary forceps have been designed to allow for the beaks of ery of the tooth will follow. One must still pay great attention
the extraction forceps to enter in between the two buccal to prevent causing any damage to the soft tissue surrounding
roots, such as in a maxillary cowhorn (Figure 11-5). the extracted tooth (Figure 11-6).
Extraction of lower molars could be the most difficult Bone loss after tooth extraction without replacement is a
extraction in the mouth because of the density of the posterior well-documented phenomenon. A skilled surgeon should
mandible, the root form of lower molars, and proximity to avoid any traumatic extraction leading to further bone remod-
vital anatomic structures. A lower universal forceps #151 is eling and ultimately more bone resorption. Should the surgeon
best used. A variety of cowhorn forceps are used to allow for expect traumatic extraction, then the patient must be
the beaks to seat into the furca with very gentle digital pres- counseled for socket preservation and augmentation by the
sure. Once the cowhorn beaks are seated into the furca, gentle various grafting techniques available.
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth 189

B
FIGURE 11-3. A, Rotation is performed with a #1 forceps or a #150 (maxillary universal) forceps. The forceps is
seated against the tooth (A) and then forced apically. Continued apical pressure is applied, and buccal luxation begins
(B), followed by palatal luxation. Once some mobility is noted, the conical root of the anterior maxillary teeth allows rota-
tional forces to be used. The tooth is rotated distally (C) and then mesially (D). The process is repeated until the tooth
can be delivered from its socket (E and F). This technique can be used for the maxillary lateral incisor and the canine.
However, the canine often requires greater force and effort to remove it from its socket. B, The ideal forceps for the
removal of the mandibular premolar is the English/Asch forceps or the #151 (mandibular universal) forceps. All the
anterior mandibular teeth can be extracted similarly with this technique. The forceps are placed and seated apically (A),
and then light luxation is used to push the tooth buccally (B), followed closely by lingual movements (C). Rotational
movements can be used because the roots are frequently single and conical in nature (D and E). Care must be taken
when evaluating these teeth radiographically because they are in close proximity to the mental foramen. The foramen’s
location should be determined to prevent possible compression of the nerve.

FIGURE 11-4. The maxillary premolar has two

thin and slender roots. These can be easily fractured if
careful technique is not used. A #1 or #150 forceps
is preferred for this extraction. Initially the forceps
is seated and pushed apically (A). Then the tooth is
luxated buccally to begin alveolar expansion (B), and
then it is pushed palatally (C). This is repeated in a
careful and deliberate fashion. Occasionally, figure-
eight movements can be used until the tooth is removed
from its socket (D).
190 SECTION II ■ Dentoalveolar Surgery
■ SOCKET PRESERVATION AND
WOUND CLOSURE
In simple extractions, by definition, no surgical flaps are elevated
or required. Thus, simple wound closure is often unnecessary.
Ridge resorption after tooth extraction is a well-documented
phenomenon. Secondary to the extraction, the socket will
undergo partial bony filling and partial resorption in both the
horizontal and vertical dimensions. Extraction sites will
undergo about four times faster resorption than the regular
biologic rate in the first 12 months. Extraction sites that were
restored with removal prostheses will undergo much faster
FIGURE 11-5. The maxillary molars are commonly in close
proximity to the maxillary sinuses, and careful radiographic interpre-
tation can prevent possible antral involvement. These teeth are
removed with a #150 (maxillary universal), #210s, #53, or #88 L/R
forceps. Their three-rooted nature can make a relatively simple-
looking extraction more complex owing to root dilacerations or diver-
gence. The initial step is to seat the forceps and apply apical forces
(A) and then to apply slow and deliberate forces in the buccal and
palatal directions, allowing for initial expansion of the alveolus (B).
Because the maxillary bone is less compact, large initial forces can
result in buccal plate fractures and occasionally tuberosity fractures.
Larger forces and movements follow in a buccal and lingual direc-
tion, allowing for increased expansion of the bone (C and D). The
tooth is then carefully delivered out of the mouth buccally (E). If the
gingival begins to tear, stop the extraction so that the likely buccal
plate fracture causing it can be dissected free of the gingiva.
FIGURE 11-6. Mandibular molars are often the most difficult teeth to
remove owing to various factors, and they can have the most complications
because of anatomic considerations. They are best removed with #151 (uni-
versal) or #23 (cowhorn) forceps. Once the forceps is seated (A), heavy apical
pressure is applied. If a cowhorn forceps is being used, the tips of the beaks
should be wedged into the furca of the tooth by squeezing the handles of the
instrument and gently rocking the beaks into position (B and C). Once the
beaks are tightly seated around the crown, heavy luxation of the tooth occurs
in a buccal and lingual direction (D and E). When the tooth is adequately
mobile, a wiggling motion can be used to extract it from its socket. The
figure-eight technique is also used at this point, and all the while, apical
pressure is applied.
resorption as a result of nonphysiologic compression forces on
the alveolar bone surface.
In today’s practice, there is great emphasis on tooth replace-
ment that will meet a higher standard of function and
aesthetic outcome. Preserving the extraction sockets and
attempting to prevent the collapse of the soft and hard tissue
is the best first step toward achieving that goal.
Socket preservation techniques vary depending on the
long-term desired treatment plan. The surgeon must be well
aware of the various grafting techniques available, the bio-
compatibility of the grafting material, resorbability, turnover,
and handling.
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth
To minimize the resorptive phenomena and accelerate the
healing and bone filling process, it is best to isolate the deli-
cate environment inside the socket from the harsh elements
in the oral cavity. Grafting the site with the appropriate mate-
rial and/or using the appropriate membranes will help achieve
that goal. Whereas primary closure would be the most desir-
able environment for appropriate healing in the socket, it does
destroy the architecture and the anatomy of the soft tissue in
the area and, thus, should be avoided unless absolutely and
crucially necessary.6
Schlar described a technique of ridge preservation which
he termed “The Bio-Col Technique” using a combination of
Bio-Oss (Osteohealth Co. Shirley, NY 11967) in the socket
and a CollaPlug (SulzerMedica, Carlsbad, CA) wound dress-
ing to cover the Bio-Oss graft. This technique is not only
useful in preserving alveolar bone, but in maintaining soft
tissue architecture at the extraction site and provides the cli-
nician the benefit of maintaining the esthetic of the area. By
immediately supporting the soft tissues surrounding the socket,
the restorative dentist will be better able to create a pontic
that retains the appearance of a gingival margin and sulcus
resulting in a much more esthetic prosthesis.7
The surgeon, furthermore, must assess, after the extraction
process, the availability of bone volume height and width,
especially in an area that would receive an immediate implant
or one in the future, or have the pontic of a bridge in a cos-
metic zone. A good surgical practice would be to appropriately
diagnose and prudently inspect the bony defect before the
extraction process and have a prefabricated wax-up to the site
that would guide the surgeon to the amount of buildup needed
to achieve the desired results.8
However, if any papillae or margins were elevated during
the simple extraction process to gain access to purchase points
or better visibility, then this should be closed with minimal
tension, just enough to achieve the required hemostasis and
proximation of the anatomic structure to the preextraction
conditions. If removable prostheses are used to temporize the
site, they should be adjusted to avoid contact with the inci-
sion, if possible.
If implants are placed in the extraction socket at the same
time, then one should carefully assess the extraction socket
margins when placing the implant, accounting for some type
of remodeling. If immediate load is not indicated, then one
should preferably use a healing abutment on top of the implant
that would be flush with the gingival margins and allowed to
support the soft tissue architecture. If done correctly, the site
will have the best chance of achieving appropriate socket
filling around the implant, prevent soft tissue collapse, and
avoid any suturing to achieve appropriate hemostasis.
■ COMPLICATIONS
MILD BLEEDING
Moderate to mild bleeding is normal and expected after
extraction. However, it should be self-limited unless a com-
plicating medical history exists. A thorough medical history
should always be taken before the extraction to identify medi-
191
cations that could predispose the patient to excessive bleed-
ing, such as blood thinners (Coumadin, aspirin, Lovenox,
Plavix, etc.). Patients with bleeding disorders need to be iden-
tified before the extraction process and managed accordingly.
Management of the medical patient is discussed in a different
chapter. However, it is accepted practice for patients on blood
thinners to have minor oral surgery procedures without any
serious bleeding complications if a coagulation panel is within
therapeutic range. Should intraoperative and postoperative
bleeding persist, it could be managed easily with local mea-
sures, such as direct mild pressure with gauze and/or applying
hemostatic mediums (CollaPlug, surgical collatape, surgicoll,
etc.) and use of appropriate suturing technique.
■ SURGICAL EDEMA, DRY
SOCKETS, AND INFECTIONS
Surgical edema, dry sockets, and infections are not common
in simple extractions and will be discussed later in this chapter
in conjunction with surgical extractions and management of
third molars.
■ LIMITED MOUTH OPENING
If limited mouth opening is one of the postoperative compli-
cations, secondary to simple tooth extraction, one must dis-
tinguish between exacerbation of prior TMJ preexisting
condition versus trauma to the mastication muscles or facial
space infections. The most common is traumatic injury sec-
ondary to the introduction of the anesthetic through a syringe
and its associated needle, causing some degree of muscle tear.
The management of these two conditions is distinctly differ-
ent. An appropriate diagnosis should be made and managed
accordingly. Conservative TMJ therapy and physical therapy
for simple TMJ versus palliative therapy for muscle tear and
patient observation until appropriate healing takes place
versus incision and drainage of abscess are appropriate
considerations.
■ DAMAGE TO ADJACENT TEETH
The surgeon must be well aware of the surrounding structures
around the surgical field in which he or she is working. Careful
assessment must take place before the surgical extraction. A
thorough discussion with the patient must take place as well
if the potential exists for damaging adjacent teeth, especially
those with extensive decay and large restorations. Although
this complication is not common with simple tooth extrac-
tion, it is sometimes unavoidable.9,10
■ ORAL ANTRAL COMMUNICATION
In simple extraction of the first and second maxillary molar,
it is sometimes common that a communication between the
antrum and socket will exist at the extraction site. If the
opening is small (less than 2 mm), spontaneous healing will
usually take place without any further surgical correction and
with the appropriate medical management. If the opening is
more than 2 mm, additional suturing and placement of a
medium between the oral cavity and the antrum might be
necessary. The patients are to be given instructions to avoid
192 SECTION II ■ Dentoalveolar Surgery
any sudden change in the pressure/equilibrium, such as sucking
on straws or forceful sneezing.9,10
■ PAIN MANAGEMENT
Most of the time simple extractions do not necessitate any
extensive degree of pain management. Most simple extraction
patients would not require any further pain management than
over-the-counter medications, such as acetaminophen, ibu-
profen, or naproxen sodium. Nonsteroidal antiinflammatory
drugs have proven to be very effective in management of
postoperative discomfort following simple tooth extraction,
given that the medical history of the patient allows it. If
extensive surgical manipulation took place during the process,
then one could consider the combination of a narcotic drug
along with a nonsteroidal antiinflammatory when necessary.
The patient must be thoroughly instructed as to the side
effects of these medications, and the instructions of the admin-
istration of the drug should be very carefully reviewed. None-
theless, whatever management protocol is instituted, the best
outcome is always achieved by instructing the patient to start
the medications well before the expiration of the local anes-
thetic effect.
■ COMPLICATED EXODONTIA
Complicated exodontia involves techniques to remove teeth
other than by simple luxation of the tooth and forceps deliv-
ery. As all dentists are aware, not all extractions can be done
by simply grasping the tooth with forceps and expanding the
alveolar bone to deliver the tooth. Conditions, such as
advanced caries, abnormal root morphology, or difficult ana-
tomic locations, can make the extraction of a tooth compli-
cated and will necessitate a surgical extraction using specialized
techniques.
Experience has taught us that any planned simple extrac-
tion can develop complications that will lead to a surgical
extraction, and the oral surgeon must therefore be prepared
to routinely convert to using the specialized techniques that
will be discussed in this section. Although complicated surgi-
cal exodontia often emanate from attempts at simple forceps
extraction, it is best when surgical extractions are planned. In
most cases, proper diagnosis and careful surgical planning
before initiation of the procedure will save time, decrease
morbidity, and increase efficiency.
INDICATIONS
Common indications for surgical extractions are listed in Box
11-1.
■ GENERAL PRINCIPLES
Surgical extraction, like all other oral and maxillofacial surgery
procedures, must adhere to basic surgical principles of careful
planning, adequate surgical access and visibility, hemorrhage
control, meticulous handling of hard and soft tissues, mainte-
nance of good blood supply to flaps, good instrument mechan-
ics, cleanliness, and painstaking repair of the surgical
wound.
BOX 11-1 Indications of Surgical Extraction
Accidental fracture of the crown during simple extraction that leaves the root buried
in the socket
Retained roots
Severely carious teeth that will fracture with forceps extraction
Endodontically treated teeth
Teeth with internal resorption
Teeth with widely divergent roots
Teeth with dilacerated or greatly curved roots
Ectopic teeth in positions where forceps cannot be used
Teeth that are positioned close to vital anatomic structures
Unerupted teeth other than third molars
Hypercementosis
Ankylosed teeth
Mandibular third molar in the proximal segment of a fracture of the mandibular angle
region
Multirooted teeth located in areas of the jaw where bone preservation is critical for
implant placement.
Tooth that will be used for autotransplant
Surgical exodontia will usually involve three or more of the
following steps:
1. Elevation of a mucoperiosteal flap
2. Ostectomy
3. Sectioning of the tooth
4. Luxation and removal of the roots
5. Removal of radicular pathologic condition when
present
6. Débridement of the surgical field and the removal of
sharp bony edges
7. Wound closure
As is mandatory for simple extractions, good quality radio-
graphs to visualize decay, root morphology, intrabony patho-
logic conditions, and approximation to critical anatomic
structures are even more critical for surgical extractions. In
general the panoramic radiograph is the preferred imaging
modality for complex exodontia because it shows the entire
teeth-bearing areas, the full extent of any intrabony patho-
logic conditions that may be present, along with their rela-
tionship to vital anatomic structures. When periapical films
are used, they should be of good quality and show the entire
tooth along with close anatomic structures. For some unerupted
teeth, the panoramic film or the sole periapical radiograph will
not provide complete or accurate information as to tooth
position, and localizing films will be needed to properly deter-
mine their position.
■ FLAP DESIGN
In surgical exodontia, a “full thickness” mucoperiosteal flap
will be the type of flap used to facilitate the removal of the
desired tooth or root fragment. Reasons for reflecting the flap
are to:
1. Allow for complete visualization of the operative field.
2. Prevent unnecessary trauma to the adjacent soft tissue
when removing bone or teeth.
3. Provide an adequate working area that will allow for the
full removal of intrabony pathologic conditions when
present.
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth 193

Careful consideration must be given to the position of the releasing incision should never be placed on the facial aspect
incisions and to the type and shape of the flap. The following of the tooth in the midsulcular area because this frequently
are guidelines for flap design for surgical extractions: results in a periodontal defect.
• Incisions should be placed over bone not planned for When additional working access is necessary, the sulcular
removal. incision can be lengthened or a second vertical incision
• The incision should be long enough to allow for a flap tapered in the opposite direction may be added to convert the
that will give clear and adequate hard tissue visualization triangular flap into a trapezoidal flap (Figure 11-9).
and permit easy retraction without tearing.
• The base of the flap should be wider than the reflected ■ BONE REMOVAL
free margin to ensure a proper blood supply to the Sometimes it will be necessary to remove alveolar bone from
reflected soft tissue. the crown of the tooth or from the retained root to facilitate
• Avoid placing incisions over vital structures (mental its removal. This is most often done with a dental bur in a
foramen and lingual nerve). high-speed hand piece under constant irrigation. In some
The soft tissue flap configuration can be of three basic instances, a rongeur may be used. Alveolar bone removal must
designs: the envelope flap, the triangle flap, and the trapezoi- be as conservative as possible, removing only the amount of
dal flap. bone required to achieve the access that is needed to remove
The most common flap used in exodontia is possibly the the tooth or roots. The amount of bone removed will depend
envelope flap. The incision is made with a #15 blade around on the physical state of the crown or root and the level at
the necks of the teeth within the dental sulcus, including the
interdental papillae. The length of the incision usually involves
three to four teeth, but the length should be that which will
provide adequate access to the area of intervention without
the need for excessive retraction. Elevation of the flap is
started at the sulcular incision, where a sharp periosteal eleva-
tor is used to firmly lift the free gingival margins and the
incised dental papillae. The periosteum along with the supra-
periosteal structures are gently elevated from the bone (Figure
11-7).
Procedures that involve more than one tooth or where the
level of surgery is located beyond the apices of the tooth will
require vertical releasing incisions to improve the access. The
horizontal circumdental incision is made first; then the verti-
cal arm or arms are added in a fashion that allows a sufficient
quantity of the papilla to remain intact (Figure 11-8A, B). FIGURE 11-7. The envelope flap made with a periosteal elevator. (From
This intact papilla will serve as an anchoring point for sutures Costich ER, White RP: Fundamentals of oral surgery, Philadelphia, 1971, WB
and will have the least wound contraction upon closure. The Saunders.)

A B
FIGURE 11-8. A, A sulcular incision with a vertical release. The vertical release is done in the alveolar mucosa and
is tapered to provide a wide base for the flap that will be elevated from the bone. The vertical incision joins the sulcular
incision in such a way so as to save the interdental papilla. This fixed papilla will provide a stable point onto which the
repositioned flap may be anchored. B, A mucoperiosteal flap with an anteriorly based releasing incision. The base of the
flap is kept larger than the apex to ensure an adequate blood supply. (Part A from Dym H, Ogle OE: Atlas of minor oral
surgery, Philadelphia, 2001, WB Saunders. Part B from Costich ER, White RP: Fundamentals of oral surgery, Philadelphia,
1971, WB Saunders.)
194 SECTION II ■ Dentoalveolar Surgery

which the fracture of the root occurred. The ostectomy should
expose enough solid root structure to permit elevation without
crumbling. In general, buccal bone removal should be done
to expose 20% to 40% of the remaining root length. Bone can
also be removed within the socket to allow the introduction
of a narrow elevator (Figure 11-10A, B).
■ SECTIONING OF TEETH AND
REMOVAL
Any teeth that radiographically demonstrate abnormal root
morphology, which would impede its removal, or a tooth that
proves difficult to remove and requires excessive force to
elevate or luxate should be surgically sectioned so as to provide
a mechanical advantage. Sectioning the tooth into multiple
segments allows the surgeon to remove tooth fragments as
simple single-rooted teeth, improve leveraging, and minimize
the trauma to the adjacent bone.
When a multirooted tooth fractures at the cementoenamel
junction (CEJ) and leaves the roots joined, it should be sec-
tioned and then removed with either forceps or elevators.
FIGURE 11-9. A sulcular incision in the posterior mandible with vertical
releases anteriorly and posteriorly. The vertical release in the anterior should
be at the canine or lateral incisor area to prevent injury to the mental nerve.
(From Dym H, Ogle OE: Atlas of minor oral surgery, Philadelphia, 2001, WB
Saunders.)
There are several root tip forceps available for this purpose.
Sectioning of the mandibular molar tooth in a buccolingual
direction will allow easy removal in most instances (Figure
11-11). Sometimes it may be necessary to remove bone around
the roots as previously mentioned. In cases where the inter-
radicular bone is present, it may be eliminated to facilitate
root removal with an east/west, crane pick, or other types of
elevators (Figure 11-12). Purchase points directed toward the
root apex can also be placed with the drill to improve the
leveraging during elevation. A mandibular tooth with widely
divergent roots can be sectioned and extracted like two indi-
vidual premolars (Figure 11-13).
Like mandibular multirooted teeth, maxillary molars and
first premolars can also be sectioned into individual roots to
allow easier removal. Depending on the root morphology of
maxillary molars, their roots may be partitioned in a “T” or
“Y” configuration using a rotary instrument (Figure 11-14).
After the roots are separated, they can easily be removed with
a small straight elevator or a crane pick elevator (Figure 11-
15). The buccal roots should be removed first. Great care
should be taken to avoid pushing the roots into the maxillary
sinus. This risk is highest with maxillary second premolar, first
molar, and second molar teeth.
Compression of the buccal and lingual plates should be
minimal and should be avoided in orthodontic extractions
and potential implant sites. Aggressive removal of the inter-
septal or interradicular bone will lead to greater postoperative
bone resorption and should also be avoided.
At the termination of the procedure, the extraction socket
and the space under the soft tissue flap should be generously
irrigated to remove bone dust and tooth particles that may be
present. Leaving bone dust and clotted blood below the flap
could result in an infection. The surgeon should keep in mind
that the elevation of a flap and bone cutting will be additional

A B
FIGURE 11-10. A, Teeth often fracture during extraction leaving root fragments in alveolar bone. Adequate access
must first be established by either an envelope or three-cornered triangle flap. Buccal plate is removed with a bur to
expose root fragment. Space should be made to allow introduction of narrow elevator. B, Root is removed with elevator
wedged between root and alveolar bone. Controlled luxation is performed to prevent root displacement and soft tissue
injury. (From Dym H, Ogle OE: Atlas of minor oral surgery, Philadelphia, 2001, WB Saunders.)
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth 195

surgical trauma that will result in additional swelling and pos-
sibly an increase in postoperative pain and should make the
patient aware of these consequences.
■ IMPACTED TEETH OTHER THAN
THIRD MOLARS
Following mandibular third molars, the maxillary canines,
mandibular second premolars, and mandibular canines (in
order of frequency) are the impacted teeth most frequently
encountered in clinical practice. These impacted teeth may
be isolated, or they may be associated with other pathologic
entities, such as displacement or destruction of adjacent hard
tissue structures including teeth and bone, acute and chronic
inflammation or infection, and cystic or neoplastic diseases.
Treatment approaches to impacted canines and premolars will
be discussed in this section.
An important aspect in planning the removal or exposure
of these impacted teeth is the localization of the tooth, which

FIGURE 11-11. If lower molar tooth proves difficult to extract, it is sectioned through the furcation area, resulting
in two single-rooted teeth. (From Dym H, Ogle OE: Atlas of minor oral surgery, Philadelphia, 2001, WB Saunders.)

FIGURE 11-12. After one root of molar roots has been removed, the Cryer
elevator (east-west) is placed into empty mesial socket and turned with sharp
point engaging interseptal bone and root to elevate remaining distal root. (From
Dym H, Ogle OE: Atlas of minor oral surgery, Philadelphia, 2001, WB
Saunders.)
FIGURE 11-13. A mucoperiosteal flap exposes the buccal aspect of the
molar tooth requiring sectioning. The tooth is sectioned from the buccal to
lingual through the furcation. This allows removal of the tooth with simple ele-
vation and luxation. (From Archer WH, editor: Oral and maxillofacial surgery,
vol 1, ed 5, Philadelphia, 1975, WB Saunders.)

FIGURE 11-14. The maxillary molar is sectioned in a “Y”

fashion to allow for removal of each root in an individual fashion
(A-C ). (From Archer WH, editor: Oral and maxillofacial surgery,
vol 1, ed 5, 1975, Philadelphia, WB Saunders.)
196 SECTION II ■ Dentoalveolar Surgery
FIGURE 11-15. Buccal roots are then separated and delivered with
a straight elevator. (From Dym H, Ogle OE: Atlas of minor oral surgery,
Philadelphia, 2001, WB Saunders.)
may be located on the buccal aspect of the maxilla or mandi-
ble or on the palatal or lingual sides. To surgically expose or
remove the tooth, the surgeon must locate the crown because
the surgical approach will depend on its anatomic position.
The localization of the tooth is most often done by using two
periapical radiographs using the concept of parallax with a
shift in the horizontal plane. This is commonly referred to as
the rule of SLOB (same lingual-opposite buccal) or Clark’s
rule. This rule states that the tooth positioned posteriorly will
move in the same direction as the x-ray cone when a second
radiograph is taken and compared with the first radiograph.
■ CANINES
The permanent canines are the foundation of a functional
occlusion and an aesthetic smile and are the key component
of arch harmony and integrity. They provide lateral and pro-
trusive guidance, are an important element of an aesthetic
smile, and are often used as the primary anchorage for fixed
or removable prosthodontics.
Permanent maxillary canines are the second most fre-
quently impacted teeth with a prevalence of 1% to 2% in the
general population.11 It occurs twice as often in females than
males, has a high family association, and is five times more
common in Caucasians than Asians.12
For aesthetic and functional purposes, the impacted maxil-
lary canine should be treated in a manner that will facilitate
the recreation of this important foundation of the dental arch
and prevent a bony defect. The treatment of choice is indis-
putably surgical, and orthodontic restoration of the tooth and
several procedures exist for assisting eruption after surgical
exposure. As soon as delayed canine eruption and impaction
is confirmed, plans for exposure should be made and imple-
mented in conjunction with the orthodontist. Because success
rates are much lower after the late teenage years have passed,
FIGURE 11-16. Palatal flap reflected and nasopalatine duct exposed.
Impacted canine is now ready for exposure. Note envelope flap used with no
vertical releasing incision, though one can be used if treating physician is so
inclined. The neurovascular bundle is cut because this may be done with no
complications. The flap can be sutured to posterior teeth to aid in retraction.
(From Dym H, Ogle OE: Atlas of minor oral surgery, Philadelphia, 2001, WB
Saunders.)
early intervention is advisable. In some cases, with proper case
selection, interceptive orthodontics in the mixed dentition
stage have been able to obviate the need for surgical exposure.
However, when either protocol is impossible as a result of
anatomic limitations, patient-related contraindications, or
failure of assisted eruption, then surgical removal may be
necessary.
Eighty-five percent of impacted maxillary permanent
canines are palatal impactions, and 15% are labial.11,13
Whether for exposure and ligation or for removal, the pala-
tally positioned impactions are approached via a posteriorly
based palatal flap. The full-thickness mucoperiosteal flap is
developed from an intrasulcular incision around the palatal
aspects of the premolar or molar on the affected side and
extending to the contralateral central incisor or beyond. The
exact length of the incision will be determined by the amount
of desirable exposure. If bilateral canine exposure is to be
performed, then the incision will extend from the second
premolar to second premolar. The contents of the incisive
foramen can be transected without significant consequence
(Figure 11-16). A rotary instrument under constant irrigation
is used to expose the impacted crown without damaging its
enamel.
The following are suggested principles for surgical exposure
of the impacted canine: minimal exposure of the tooth, good
hemostasis and small attachment bonding, maintain the
integrity of the CEJ, and leave the undisturbed portion of the
follicle intact. After tooth exposure, the adjacent follicular
tissue is removed with a periodontal curette to minimize the
bleeding that will impede bonding; a vasoconstrictor is then
placed. When the area is relatively dry, the tooth is acid-
etched following the manufacturer’s directions and an orth-
odontic bracket bonded. Light-cured orthodontic bonding
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth 197

A B
FIGURE 11-17. A, Palatal flap retracted with bracket applied to cuspid crown and chain attached to orthodontic
arch wire. B, Palatal flap closed with interrupted 3-0 black sutures. Note gold chain is under flap and sutured to orth-
odontic arch wire. Make certain area is hemostatic before closure to prevent hematoma formation. (From Dym H, Ogle
OE: Atlas of minor oral surgery, Philadelphia, 2001, WB Saunders.)

composites offer significant advantages of speed and strength.
Before closing, the bonding should be tested for strength and
the gold chain tied to the arch wire with a suture (Figure
11-17).
If the tooth is to be extracted, bone is conservatively
removed from around the crown to clear the height of contour
and extend to near the level of the CEJ. The crown is sec-
tioned from the root and removed. Surgical sectioning of the
tooth must be done carefully to prevent damage to the adja-
cent roots or perforation into the nasal cavity. After delivery
of the crown, a purchase point is placed into the root surface
to allow a right-angled elevator to be engaged and remove the
root structure (Figure 11-18).
Maxillary labially impacted canines are approached via a
trapezoid flap. After exposure of the tooth, the flap may be
apically repositioned and treated via an open technique
(Figure 11-19). By repositioning the flap apically, attached
gingiva is placed at the level of the CEJ, and with eruption of
the tooth, the keratinized gingiva will be brought into the
arch. With the open technique, the orthodontic appliance
may be placed at a subsequent appointment. When the
impacted tooth is not in a position to allow repositioning of
the flap, a closed technique is used as previously described.
Extraction of labially impacted canines would follow the same
principles as previously described (Figure 11-20).
The mandibular impacted canine is most frequently located
on the labial position. The approach is dependent on the level
of the crown. Crowns that are within the alveolar bone are
approached via buccal envelope flap with an anterior release
or a trapezoid flap. The surgeon should be aware of the position
of the mental nerve and make significant effort to protect it
(Figure 11-21). Deeper impactions close to the inferior border
of the mandible are best approached via a genioplasty incision,
which would lead directly to the inferior portion of the man-
dible. Removal of the tooth is as described previously.
(The genioplasty incision is a gingivolabial sulcus incision, which
is made approximately 15 mm away from the mucobuccal fold
through the labial mucosa. A flap is developed below the labial
mucosa leaving an adequate cuff of mucosa along with some of the
orbicularis oris muscle superiorly. This dissection is taken toward
the labial aspect of the mandible at which point the periosteum is
incised and a subperiosteal dissection is carried out to the location
of the tooth.)
■ PREMOLARS
Following third molars and maxillary canines, the mandibular
second premolar is the next most frequently impacted tooth.
The vast majority will be on the lingual aspect of the mandible
and may either be adjacent to other erupted teeth or located
at a level below the apices of the erupted premolar. Premolars
that are located on the lateral aspect of the mandible should
be evaluated carefully for defensible indications to remove
them because risk of injuring the mental nerve is significant.
When the crown is located on the lingual aspect of the man-
dible, the surgical approach to remove this tooth will require
the elevation of an inferiorly based lingual mucoperiosteal
envelope flap. The soft tissue on the lingual alveolar region of
the mandible is very thin and not very easy to elevate without
tearing. To assist its elevation, local anesthetic may be injected
below the periosteum to hydrodissect the periosteum from the
bone.
The flap is started from an incision placed in the sulcus
around the necks of the teeth on the lingual. The incision
should be from the distal of the first molar to the lateral
incisor. The length, however, should be determined clinically
depending on the depth of the impaction and ease of retrac-
tion to provide adequate surgical access. The flap is reflected
medially to expose the area of the impacted premolar. A #6
round bur may be used to remove bone from around the clini-
cal crown starting from its occlusal aspect. A small straight
198 SECTION II ■ Dentoalveolar Surgery

FIGURE 11-18. A-I, A palatal impacted canine is exposed via a posteriorly based flap and conservative removal of
overlying bone. The crown is sectioned from the root, and a purchase point is placed on the root surface for elevation.
The tooth is elevated with a right-angled elevator, and the mucoperiosteal flap is returned to its original position. (From
Archer WH, editor: Oral and maxillofacial surgery, vol 1, ed 5, Philadelphia, 1975, WB Saunders.)

A B
FIGURE 11-19. A, Outlines trapezoidal incision used to expose underlying buccal impacted cuspid. Note how this
incision maintains attached gingiva, which is critical for periodontal long-term health of tooth. B, Shows how buccal flap
is vertically and apically repositioned and secured with interrupted 3-0 black sutures to maintain position and expose
cuspid crown. (From Dym H, Ogle OE: Atlas of minor oral surgery, Philadelphia, 2001, WB Saunders.)
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth 199

FIGURE 11-20. A labially impacted tooth is exposed via a mucoperiosteal flap with limited bone removal around
the crown. The crown is sectioned, a purchase point is removed, and the root is elevated and removed. Great care is
exercised to avoid adjacent tooth roots, the nasal floor, and the maxillary sinus during these procedures in the lateral
and anterior maxilla. (From Archer WH, editor: Oral and maxillofacial surgery, vol 1, ed 5, 1975, Philadelphia, WB
Saunders.)

elevator should be used to luxate the tooth to obtain some

FIGURE 11-21. The mandibular impacted cuspid is most frequently
located in the labial position. The treating physician should always be cognizant
of the mental foramen that may be present in the surgical field. The underlying
bone and cuspid are exposed through a vertical releasing incision and a pos-
terior release if access is found to be restricted with only the one anterior
release. The overlying bone is carefully removed and the crown sectioned.
(From Dym H, Ogle OE: Atlas of minor oral surgery, Philadelphia, 2001, WB
Saunders.)
initial movement of the roots. Once the crown is exposed, the
surgeon should make an effort to determine the angulation of
the tooth. Those that have a lingual angulation of the crown
can often be removed with small elevators placed into the
PDL space. A tooth that does not have a lingual inclination
where the path of delivery is impeded will require removal of
the crown and elevation of the root as previously described.
In situations where access is poor and it is difficult to elevate
the root, considerations must be given to leaving the root if
the crown and the dental follicle have been removed.
Following removal of the tooth, the area between the flap
and cortical bone should be thoroughly irrigated before repo-
sitioning of the flap.
Maxillary premolars are managed in a similar fashion. The
majority will have a palatal inclination. Very often they can
be removed by simple elevation with a small straight elevator.
Because there is usually crowding, care must be taken not to
loosen adjacent teeth (Figure 11-22).
200 SECTION II ■ Dentoalveolar Surgery

FIGURE 11-22. An impacted premolar is exposed via a posteriorly based palatal flap extending from the second
molar to the midline. The flap is reapproximated using interdental and interrupted sutures. (From Archer WH, editor: Oral
and maxillofacial surgery, vol 1, ed 5, Philadelphia, 1975, WB Saunders.)

■ TEETH LOCATED IN UNCOMMON
ANATOMIC POSITIONS
In rare instances, unerupted teeth may be found at the inferior
border of the mandible or high in the maxilla close to the
orbit. In almost every instance, these teeth can be removed
from an intraoral approach. For teeth located in the anterior
mandible, an incision made out in the lip and taken trans-
versely to the mandible will give the best access (Figure 11-
23). In the maxilla, a vestibular incision would be the best
approach.
In the posterior mandible, an incision lateral to the vesti-
bule, as used for sagittal split osteotomy, could be used. This
incision would permit wide lateral exposure, easy retraction,
and adequate isolation of the mental nerve. Like many surger-
ies in the head and neck, preservation of a named nerve is a
key to a successful operation. Mandible bone removal should
be very conservative. The tooth should be carefully sectioned
into multiple pieces to preserve bone structure, prevent frac-
ture, and to minimize the risk of damage to the inferior alveo-
lar nerve. The patient should be told of the possibility of jaw
fracture and that maxillomandibular fixation may be neces-
sary. If a fracture does occur, rigid fixation with miniplates
could be used to decrease the time of maxillomandibular fixa-
tion to 7 to 10 days or eliminate its need.
Teeth high up in the posterior maxilla require special con-
siderations because they are very risky to remove because of
the potential for displacing the tooth into a deeper anatomic
space or causing severe hemorrhage that may possibly require
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth 201

A B
FIGURE 11-23. A, An incision in the extended lip 5 to 7 mm from the lower vestibule. This incision is made through
the labial mucosa and extends to a depth of 2 to 3 mm into the orbicularis oris muscle. B, A flap is developed and
extended from the lip to the alveolus. On the buccal aspect of the mandible the periosteum is incised and elevated
occlusally to expose the area where the apex of the lower incisors would be located. (From Dym H, Ogle OE: Atlas of
minor oral surgery, Philadelphia, 2001, WB Saunders.)

vessel ligation. Further such an extraction may require an
extensive surgical procedure. In the majority of cases, it may
be prudent to leave the tooth and observe it for the develop-
ment of pathologic sequelae. When the tooth must be removed
because of a pathologic condition, it should be done in
the operating room under general anesthetic. If the tooth is
high and lateral (as determined from a CT scan), it may be
approached via a low vestibular incision with a subperiosteal
dissection along the tuberosity region to avoid the buccal fat
pad. When the tooth is located medial, a Le Fort I osteotomy
may be required to gain better access and safely remove the
tooth and associated abnormality.
■ WOUND CLOSURE
Wound closure will be the final step in a surgical extraction.
Before the flap is repositioned, the wound should be meticu-
lously examined for bone chips, bone dust, pieces of teeth, and
dental-related fragments—particularly amalgam particles.
The area between the soft tissue flap and bone should be
thoroughly irrigated with copious amounts of saline solution.
The flap is then replaced to as near the original position as
possible. Vertical releasing incisions are closed first so as to
maintain the correct length of the flap and to initially stabilize
it in its original position. Interrupted sutures are suitable for
most incisions within the mouth. Interrupted dental sutures
are used to secure tissue incisions made around the necks of
teeth. Passing the suture through the same interdental space
helps approximate the papillae better than passing it over the
contact point or around the tooth. Continuous, running
sutures may be used for longer incisions or where a “water-
tight” closure is desirable.
Most oral and maxillofacial surgeons prefer to use resorb-
able sutures. For intraoral procedures, the ideal resorbable
suture would be one that lasts 5 to 14 days, and at present
none of the commonly used materials appears to meet these
criteria. Clinical investigations to evaluate the longevity of
resorbable sutures in the oral environment found that the
median survival values were: gut—4 days, polyglycolic acid—
15 days, and polyglactin 910—28 days. Among the available
resorbable suture materials, polyglactin 910 (Vicryl) seems to
be one of the favorites in dental practice. Despite being
braded, it is resistant to traction and is easy to work with.
Clinical observations also show that the knots are secure, not
permitting the adhesion of plaque nor intense inflammatory
reactions around it. Thus, this suture is often selected for
complex exodontia, even when its removal is intended.
■ SURGICAL MANAGEMENT OF
IMPACTED THIRD MOLAR TEETH
The surgical removal of impacted third molar teeth is consid-
ered one of the most frequent procedures performed in oral
and maxillofacial surgery offices.
An impacted tooth is one that is erupted, partially erupted,
or unerupted and will not eventually assume a normal arch
relationship with the other teeth and tissues.14 Mandibular
third molars are the most frequently impacted teeth followed
by maxillary third molars and maxillary canines.
A study of 5000 army recruits found 10,979 impacted teeth
with only 212 of them not being third molars.15 The impacted
teeth fail to erupt normally into the dental arch for a variety
of possible reasons:
1. Inadequate space in the dental arch for eruption
2. Obstruction of tooth eruption as a result of the presence
of a cyst, supernumerary teeth, bone, or soft tissue lesions
or tumors
3. Angulations of teeth
202 SECTION II ■ Dentoalveolar Surgery
■ INDICATIONS FOR REMOVAL OF
IMPACTED THIRD MOLARS
The 1979 National Institutes of Health (NIH) consensus
development conference for the removal of third molars
developed guidelines and statements16 that provide guidance
to practitioners involved in oral and maxillofacial surgery
services. More recently, Third Molar Clinical Trials, a 7-year
study conducted under the auspices of the American Associa-
tion of Oral and Maxillofacial Surgery and the Oral and
Maxillofacial Surgery Foundation, has released new
data information and recommendations that are vital to
both the oral and maxillofacial surgeon and to the public at
large.
Symptomatic causes for extraction of third molar include:
1. Active/chronic infection at site (pericoronitis)
2. Cyst formation
3. Tumors
4. Caries
5. Preparation for orthognathic surgery
6. Preradiation therapy for head and neck cancer
7. Resorption of adjacent teeth
8. Persistent facial pain of unknown origin
9. Wisdom tooth in line of fracture
10. Active periodontal disease around distal of adjacent
teeth
The American Association of Oral and Maxillofacial
Surgery and the Oral Maxillofacial Surgery Foundation’s land-
mark 7-year study advise that most third molars, even those
that are asymptomatic and display no current sign of disease,
are at risk for chronic oral infectious disease, periodontal
pathologic conditions, and tooth decay and should be con-
sidered for removal in young adulthood. Those patients who
choose not to electively have them removed must be made
aware of their increased risks for systemic disease and the need
for monitoring for evaluation of future periodontal disease.17
Additional comments from the 1979 NIH consensus study
include:
1. The least morbidity associated with third molar removal
occurs when they are removed between the ages of 15
and 25 or when the roots are only two thirds formed.
This opinion is formed based on many reasons associated
with the anatomic development of wisdom teeth in
patients at this stage including:
a. Roots are generally straight and not curved.
b. Bone is softer and more pliant.
c. Inferior alveolar nerve is more distant from the root
apices.
d. Healing is more rapid.
2. Overwhelming clinical evidence clearly shows that
patients with impacted teeth who wait until symptoms
occur before seeking removal have greater morbidity
associated with their surgery. Clearly, early intervention
in the surgical removal of impacted third molars will
benefit most patients.
■ CONTRAINDICATIONS TO
REMOVAL OF IMPACTED TEETH
Elective removal of third molar teeth, like all surgical proce-
dures, should not be performed if the potential damage out-
weighs the benefits to be obtained. Clearly, patients with
significantly compromised and unstable medical conditions
are not candidates for elective third molar removal. It is also
the consensus of most surgeons that asymptomatic third molars
in the mature (over 50) adult population should not routinely
be removed, especially if no inflammation of periodontal
disease exists.18
■ INDICATIONS FOR REMOVAL
OF IMPACTED TEETH—
PERICORONITIS
A common finding in patients with lower third molar pain is
a clinical condition referred to as pericoronitis. In a study of
patients in Norway, the authors found that 43% of third molar
complaints in 1 year could be attributed to pericoronitis.19
Pericoronitis is an inflammation of the soft tissue surrounding
a partially erupted third molar and can be caused by multiple
factors.
1. Food debris that are often trapped under the soft tissue
flap overlying the impacted wisdom tooth and cannot
be effectively cleansed. As a result, bacteria (strepto-
cocci and a variety of anaerobic organisms) can invade
the site and initiate the infectious process.
2. The opposing maxillary third molar will often cause
constant occlusal trauma to the overlying soft tissue of
the lower third molar, which will result in a highly
swollen and inflamed tissue mass. This clinical condi-
tion is referred to as operculitis.
3. Pericoronitis can lead to a mild infection or a severe
fulminating infection requiring hospitalization and
aggressive surgical and medical treatment.
Mild to moderate acute pericoronitis can be best managed
by the removal of the impinging maxillary third molar, fol-
lowed by irrigation of the pericoronal tissues with saline,
hydrogen peroxide, or chlorhexidine solution, along with a
prescription for antiinfectives, such as penicillin or clindamy-
cin. It is the author’s opinion that it is best to avoid extraction
of the impacted mandibular molars if possible until resolution
of the acute pericoronitis phase to prevent spreading the
infection into deeper areas, although this is controversial with
some authors advocating their removal claiming the infection
will resolve more quickly.20
In some patients, pericoronitis can lead to serious systemic
illness that will usually have fever (greater than 101 °F)
malaise, trismus (inability to open greater than 20 mm), and
severe facial swelling.
Though removal of the overlying soft tissue (operculec-
tomy) has been advocated by some, rarely is it successful and
only delays the inevitable surgical extraction.
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth
TABLE 11-1 Basic Instruments for Third Molar Surgery
Technique
Cheek retraction and visualization of the surgical area incision
Flap development and reflection
Flap retraction
Bone Removal
Luxation and sectioning
Tooth Removal
Suture cutting, distal wedge excision, severing fibrotic tissue
Tying sutures, traction on follicle removing loose pieces of tooth
Suturing material
Curetting follicle or infection
Suctioning
Irrigation
■ ODONTOGENIC CYSTS
AND TUMORS
Impacted third molar teeth are often associated with cysts and
tumors, and screening panoramic x-rays are most helpful in
early diagnosis and detection. As the impacted teeth develop,
the surrounding follicular sac in most patients maintains its
original size, but in some cases may undergo cystic degenera-
tion and develop into a dentigerous cyst or keratocyst. As a
general guideline, if the follicular space around the crown of
the tooth is greater than 5 mm, a diagnosis of dentigerous cyst
can be made.
Similarly, odontogenic tumors can arise from the epithelial
cell lining within the dental follicle, and screening panoramic
x-rays are important in the thorough dental and medical eval-
uation of the patient.
■ CLASSIFICATION OF IMPACTED
THIRD MOLARS
Impacted maxillary and mandibular third molars can be clas-
sified by a variety of descriptive terms (Figure 11-24). The one
classification most commonly used refers to the tooth’s angula-
tions as compared with the long axis of the adjacent second
molar. The positions are referred to as mesioangular, distoan-
gular, and vertical and horizontal inclinations. Mesioangular,
tilted toward the second molar, is the most commonly seen
variety with 43% of impacted third molar mandibular teeth
and 63% of maxillary impacted third molars.21
The vertical impaction with its long axis parallel to the
second molar is the second most common type of impaction.
203
Instruments
Mouth mirror, wide retractor (Seldin #23, Minnesota) Scalpel handle with #15 blade
#9 periosteal elevator, Woodson, Molt
Wide retractor (Seldin #23, Minnesota)
Hand pieces: high-speed surgical hand piece (no air blown into the surgical field), two-
speed straight hand piece (using the higher speed), surgical straight hand piece (used by
many oral surgeons)
Burs: crosscut tapered fissure (702, 558), nontapered cross cut fissure, round (high-
speed burs should be surgical length) Straight elevators, such as the 301, and 34 or 34S
and Cryer East-West) elevators
Forceps, such as 150 and 151
Surgical scissors, such as Dean
Needle holder, such as Mayo-Hegar 6
4-0 or 3-0 silk or chromic gut suture with 3/8 circle reverse cutting needle
Surgical spoon curette
Surgical suction tip, preferably tapered, plastic or metal
Device: (1) through the hand piece or (2) with three-way syringe (irrigation medium from
a reservoir); (3) 15-30 mL irrigation syringe with a blunt irrigation needle; (4) bulb syringe;
or (5) plastic modeled irrigation syringe
Medium: sterile saline or sterile water
The distoangular impaction, with the crown facing distally or
posteriorly, is the most difficult of all to remove.
■ INSTRUMENTATION
Appropriate instrumentation is as critical to the successful
removal of impacted third molars as is good surgical tech-
nique. Before attempting any surgical third molar removal,
one should have the following instruments available (Table
11-1):
1. #15 blade
2. Periosteal elevator
3. Seldin retractor
4. Minnesota retractor
5. Elevators (thin and wide)
6. Bone files
7. Needle holder
8. Suture scissors
Rotary instruments for cutting both tooth and bone are
essential, whether they be air or nitrogen driven or electrical;
they must be autoclavable and not exhaust air into the surgical
field. Burs used are either round or fissured, and irrigation
during bone or tooth cutting must be available (sterile and tap
water).
■ SURGICAL TECHNIQUE—
MANDIBULAR THIRD MOLARS
Adequate visibility at the surgical site is essential to all good
surgical technique, and the surgical removal of impacted third
molar teeth is no exception. Incision design for the third
204 SECTION II ■ Dentoalveolar Surgery

a b

c d

a b

c d

B
FIGURE 11-24. Angulation classification of impacted teeth. A, Maxillary third molar impactions: mesioangular (a),
distoangular (b) vertical (c), and horizontal (d). B, Mandibular third molar impactions: mesioangular (a), distoangular (b),
vertical (c), and horizontal (d).
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth
General Principles for Surgical Technique of
BOX 11-2
Impaction Removal
1. Reflect mucoperiosteal flap to obtain good visual access.
2. Remove labial bone with high-speed surgical drill using round or crosscut
bur.
3. Expose crown of impaction up to CEJ and make room to allow for elevator
placement.
4. Attempt to gently evaluate for mobility with elevator (straight or angled).
5. Section crown (either horizontally or vertically depending on angulation of
impaction) with high-speed surgical hand piece. Be careful of lingual soft tissue
and depth of surgical cut.
6. Straight elevator should be used to separate crown from tooth.
7. Deliver roots with root tip elevators or crane pick. Be prepared to remove addi-
tional superior and labial bone and section roots if no mobility present.
8. Inspect bony crypt for loose debris and any bleeding problems and smooth bone
margins with bone file.
9. Carefully remove follicular soft tissue, and tease it out from surrounding
mucosa.
10. Copious irrigation of socket and beneath soft tissue flap before closure.
11. Reapproximate soft tissue flap and close with 3-0 or 4-0 chromic or black silk
sutures.
12. Consider intraoral injection of steroids if extensive bone surgery performed. Four
mg of dexamethasone (Decadron) can be injected into masseter muscle on
each side.
13. Evaluate for postsurgical bleeding before discharge.
molar surgery falls basically into two broad categories (Box
11-2 and Figure 11-25):
1. Envelope design
2. Triangular flap, an envelope flap design with a vertical
releasing incision
Obviously the degree of soft tissue reflection is dependent
on the type of impaction being removed and the quantity of
bone removal required. The ability to limit the amount of
mucoperiosteal flap retraction will certainly help decrease
postoperative pain and swelling, but should never be done at
the expense of compromising surgical technique or causing
the flap to tear because of poor or decreased visibility and
access.
The anterior border of the mandibular ascending ramus is
palpated with a finger to better appreciate the position of the
bone under the mucosa. A #15 blade then is used to make an
intrasulcular incision beginning from the distal of the lower
first molar and extending directly behind the second molar,
making certain to be always lateral to the midcrestal bone to
ensure that the lingual nerve is not damaged. This is because
the mandible flares laterally from the second molar position
toward the condyle. The lingual nerve can be found at or
above the crest of the alveolar ridge in 17% of the population,
but is usually found 0.2 mm inferior to the crest and 0.5 mm
lingual to the lingual cortex of the mandible in the third molar
region.22 The incision should always be done sharply so that
a full-thickness subperiosteal flap is developed without muscle
tearing to minimize annoying intraoperative oozing and post-
surgical edema. If greater visibility is required, a vertical releas-
ing incision can be added by incising the papilla and extending
it through the attached gingivae at the mesial of the second
molar. The vertical incision should be made at an angle so
205
that the bone of the flap is wider, thus ensuring a good blood
supply.
■ BONE REMOVAL AND TOOTH
SECTIONING
Bone removal before removal of impacted wisdom teeth is
almost always required, and careful attention to technique will
help decrease postoperative pain, swelling, and infection (Figs.
11-26 through 11-31). High-speed, low-torque surgical hand
pieces, those that do not blow air directly into the surgical
field, are most commonly used. Some oral and maxillofacial
surgeons prefer to use chisels, but this technique has greater
potential for possible complications in more inexperienced
hands. The type of burs used are operator dependent, but most
oral and maxillofacial surgeons use either #6 or #8 round burs
or straight crosscut fissured burs. The author prefers to use
straight cross cut fissure burs, but either can be used for bone
removal or tooth sectioning. Copious irrigation must always
be used to prevent thermal trauma to the bone and allow for
ease of sectioning and removal of bone and tooth debris.
Bone removal is carried out over the occlusal, buccal, and
distal aspects of the mandibular third molar to expose the
crown to its cervical height of contour in its buccal aspect.
After the crown is exposed on both its occlusal and buccal
aspect, a buccal trough and ditch is cut between the cortical
bone and the tooth. It is important for the trough to extend
into the cancellous bone and extend to the distal of the tooth.
Mesially the trough should be squared off in a right angle
fashion to allow a straight elevator to be introduced to attempt
to luxate or move the tooth slightly even before actually sec-
tioning the tooth.
Mandibular impactions usually require sectioning to remove
the tooth and help to preserve alveolar bone. When section-
ing teeth, one is careful not to completely drill through the
lingual aspect of the crown to mitigate the chances of causing
subsequent lingual nerve damage. Generally the tooth is sec-
tioned three-fourths of the way and then split with a straight
elevator.
Mesioangular impactions are the most common type and
range from easy to extremely difficult. Once the crown is
exposed and a trough developed, the crown is sectioned from
buccal to lingual along the buccal grove, extending into the
furcation. Fracture of the distal portion of the crown is accom-
plished, and then a straight elevator is placed on the mesial
aspect of the third molar beneath the cervical height of
contour to elevate the remaining portion of the tooth. The
tooth may still often require splitting the roots at the furcation
before elevating the remaining portion.
Distoangular impactions are the most difficult impacted
mandibular teeth to remove. This is because distal bone is
required to be removed and the tooth tends to be elevated
distally into the ramus portion of the mandible for its removal.
After making a trough and removing distal bone, the distal
portion of the crown is sectioned and fractured with an eleva-
tor and removed. The remaining crown and root fragments
are then removed with elevators. Vertical impactions require
206 SECTION II ■ Dentoalveolar Surgery

A B
FIGURE 11-25. A, The most important step in the removal of impacted mandibular third molars is a well-designed,
adequate mucoperiosteal flap to obtain appropriate access to the tooth. The anterior border of the mandibular ascending
ramus from the second molar is palpated with a finger to appreciate the position of the bone under the soft tissues. The
mandible flares laterally from the second molar position toward the condyle, and a straight incision behind the second
molar would fall off the mandible into the lingual soft tissues. Sharp incision of the periosteum provides for the develop-
ment of a more efficient subperiosteal flap for exposure of the third molar site. The blade is then placed behind the
second molar, and an incision is made in the gingival cuff around the distobuccal cusp of the tooth and released into
the buccal vestibule, stopping at the external oblique ridge to create a three-corner flap. If the third molar is partially
erupted, the incision should include the third molar buccal gingival cuff before progressing to the distobuccal aspect of
the second molar and the releasing incision. B, The most commonly advocated flap design is an envelope flap, with or
without a releasing incision into the buccal vestibule, that passes around the cervical gingival margin of the adjacent first
and second molars. The length of the flap and the number of teeth included are determined by the amount of exposure
necessary to gain visibility of the region and the experience of the practitioner. For a short envelope flap, the incision is
carried to the mesial aspect of the adjacent second molar. A longer envelope flap extends approximately to the mesial
line angle of the first molar.

the usual bone removal to expose the crown beneath its cervi-
cal height of contour. The crown is then sectioned and the
distal portion removed, and the remaining portion of the
tooth is then elevated in a distal occlusal direction. Some-
times the roots also require sectioning through the furcation,
followed by the removal of both distal and mesial halves.
Horizontal impactions can sometimes be quite difficult as
a result of the crown being tightly wedged deeply underneath
the height of contour of the second molar. As mentioned
previously, the overlying bone is removed and a buccal trough
developed, followed by sectioning of the crown from its roots.
Sometimes the crown must be sectioned into two portions
before its removal. Once the crown is removed, a purchase
point can be made in the remaining roots, and the roots are
then elevated forward with a crane pick or an east-west
elevator.
■ WOUND CLOSURE
Following removal of the impacted third molar mandibular
tooth, the socket is curetted out of any residual granulation
tissue and remaining dental follicle. The buccal alveolar plate
is bone filed and the socket copiously irrigated and sutured.
This is a vital step, which helps decrease postoperative patient
discomfort and possible infections. The flap is reapproximated
and closed with resorbable or nonresorbable suture depending
on the patient and surgeon’s requirements. The flap should
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth 207

FIGURE 11-26. The mesioangular impaction is sectioned after

exposure with a fissure bur from the buccal to lingual at the buccal
groove approximately two-thirds to three-quarters through the tooth
and extended to the furcation. A straight elevator is placed into the cut
and rotated to fracture the distal portion of the crown. The fracture
may remove only the distal portion of the crown or continue into the
bifurcation to include the distal root. Removal of the distal segment
without the root is all that is required for eventual complete removal
of the impacted tooth. Once the distal segment is removed, a straight
elevator is placed on the mesial aspect of the third molar below the
cervical height of the crown contour to elevate the remaining portion
of the tooth into the socket site. If it is difficult to insert an elevator
between the second and third molars, a purchase point can be cut
into the crown at the mesiobuccal line angle with a small round bur
or fissure bur. A Crane pick or a Cryer or Cogswell elevator is then
inserted into the purchase point and used to elevate the tooth from
the socket.

TABLE 11-2 Commonly Prescribed Analgesics

Drug Name Dosage Frequency
Tylenol No. 3 Codeine 30 mg and 300 mg acetaminophen q 4 hr-q 6 hr
Percodan Oxycodone 5 mg and 325 mg aspirin q 6 hr
Percocet Oxycodone 5 mg and 325 mg acetaminophen q 6 hr
Vicodin Hydrocodone 5 mg and 500 mg acetaminophen q 6 hr
Vicodin ES Hydrocodone 7.5 mg and 500 mg acetaminophen q 6 hr
Vicoprofen Hydrocodone 7.5 mg and 200 mg ibuprofen q 6 hr
Lortab (liquid) Hydrocodone and acetamino phen elixir 7.5 mg/500 mg per 15 mL q 6 hr
Motrin 600 mg ibuprofen q 6 hr
Ultracet Tramadol 37.5 mg/acetaminophen 325 mg q 4-6 hr

not be closed watertight with multiple sutures, but rather be
closed with two or three sutures to allow for limited
drainage.
■ IMPACTED MAXILLARY THIRD
MOLARS
The flap design for impacted maxillary third molars is similar
to mandibular third molars with the standard envelope flap
being used (see Figs. 11-27 through 11-29). It differs only in
that deeply impacted (very high) upper third molars will, in
the author’s opinion, require much more use of a vertical
releasing incision placed mesial to the second molar. The use
of a Minnesota retractor is most useful to help retract the
mucoperiosteal flap and to keep the cheek away to provide for
better visualization. The buccal maxillary bone is easily
removed with a sharp straight elevator followed by the use of
a Pott’s curved elevator to slowly expand the bone and elevate
the tooth.
■ PREOPERATIVE MANAGEMENT
OF THE IMPACTED THIRD MOLAR
PATIENT CONSULTATIVE VISIT
All patients scheduled for removal of impacted wisdom teeth
ideally should first be seen for a consultation visit. It is at this
time that diagnostic x-rays are taken, medical history reviewed,
and clinical exam performed (Box 11-3). Clinical teaching
aids (brochures, video, tapes, and drawings) can be used to
review and discuss the nature of the planned surgery and
review possible intraoperative and postsurgical complications;
it is also at this visit that a decision should be made as to the
type of anesthetic technique to be used during the actual surgi-
cal encounter. Although local anesthetic used appropriately
208 SECTION II ■ Dentoalveolar Surgery

FIGURE 11-27. Bone removal is accomplished, ensuring that

the buccal trough extends into the marrow space to clear the great-
est cervical contour of the crown. Distal bone of the ramus is
removed to completely expose the distal cusps and establish a
trough behind the tooth; the distal portion of the crown or the com-
plete crown should be sectioned, fractured with an elevator, and
removed. If possible it is helpful to keep part of the mesial aspect of
the crown attached to the mesial root to act as a handle and fulcrum
for removal of the mesial root. Frequently the mesial and distal roots
need to be sectioned from each other at the bifurcation and removed
independently.

BOX 11-3 Essentials of Third Molar Extraction
First Visit—Consultation
1. Thorough review of medical history.
2. Good quality diagnostic x-rays (panoramic x-ray views preferable).
3. Review all risks of procedures.
4. Review all postsurgical home care instructions.
5. Review surgical procedure using teaching aids.
6. Discuss and evaluate need for sedation.
7. Give patient prescriptions for analgesics and antibiotics.
8. Clarify all financial issues.
Surgical Visit
1. Have patient sign consent form.
2. Surgical hand piece available.
3. All surgical equipment readily available.
4. Suture material available and on surgical tray.
can provide a complete pain-free environment, many patients
will require some form of additional IV sedation to allow them
to calmly endure the surgical removal of multiple impactions.
The technique used is the surgeon’s preference, but whichever
method is chosen, intraoperative amnesia should be a desired
end result. Because the neurovascular canal carrying the infe-
rior alveolar nerve bundle is in close proximity to the apices
of the lower third molar teeth, a discussion of lower lip and
chin numbness or paraesthesia should take place. Though the
incidence of permanent paraesthesia (greater than 12 months
duration) is quite low, the patient should be made clearly
aware of this and other more commonly occurring postopera-
tive sequelae.
In many practices, the consultation visit is separate from
the surgical procedure, and the patients are given the consent
form to take home and return signed with them at the sched-
uled surgical visit. It is also at this consultation visit that all
prescriptions are dispensed and financial matters fully dis-
cussed. The wound infection rate after the removal of a third
molar is higher than that of a routine tooth extraction,23 with
the overall infection rate occurring in dentoalveolar extrac-
tions estimated at 1% to 5%.24 The prescribing of antibiotics
is an area of well-documented controversy with many
authors25,26 claiming that this has not been shown to be effec-
tive in decreasing postoperative infections and dry sockets,
and that overprescriptions of antiinfectives in noninfected
cases is inappropriate and may well lead to negative side effects
(resistant organisms, allergic reactions, drug toxicity). Never-
theless, the prophylactic use of antibiotics has been found to
have a significant effect on infection-related complications
after third molar surgery when used preoperatively but only in
bony impacted teeth.27 Patients are also given a prescription
for pain medication (opioid or nonopioid Table V) and told
to take 400 mg of ibuprofen 1 to 2 hours preoperatively because
this has been shown to help decrease the intensity of postsur-
gical pain.28 Additionally, patients are given a prescription for
an antiseptic mouth rinse (chlorhexidine 0.2%) so that they
can begin rinsing the day before because it has been reported
in some studies to be effective in the prevention of postopera-
tive infections.
■ POSTOPERATIVE INSTRUCTIONS
Before patient discharge following third molar removal, close
inspection of the surgical site should be performed to check
for hemostasis (Box 11-4). The patient should be given both
verbal and written postoperative instruction with a contact
number to access the treating physician in case of emergency.
Additional gauze pads should also be given along with appro-
priate prescriptions.
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth 209

A B
FIGURE 11-28. In the case of horizontal mandibular impactions, the crown is usually sectioned from the roots first. Following elevation of a mucoperiosteal
flap, bone removal exposes the greatest cervical contour of the buccal aspect of the crown and the distal root. The crown is removed, separating the crown at
the cervical aspect with a hand piece and completing the sectioning with a straight elevator. A, Another option is to remove the crown in two portions by making
an additional longitudinal division through the buccal and lingual segments of the tooth. B, Once the crown is removed, the roots should be elevated as a unit or
as separate root segments into the space created.

BOX 11-4 Sample Postoperative Instructions BOX 11-5 Dry-Socket Treatment Regimen
1. Bite down on gauze pad for 1 hr after leaving the clinic. 1. Confirm diagnosis.
2. Do not spit. Swallow your saliva continuously to keep your mouth dry. a. Continued presence of pain that begins to worsen on third or fourth postoperative
3. On arrival home, place ice bag on face for 20 min, take off for 20 min, but do day.
not freeze the skin. If too cold, place a thin towel on skin and apply ice bag on b. Fetid odor.
towel. c. Socket extremely painful upon light palpation.
4. Upon removal gauze pad may be stained pink. This does not mean there is d. Socket devoid of any clot or tissue upon close inspection.
bleeding—bite down on another clean gauze pad for 1 hr and repeat if neces- 2. Use irrigation syringe to flush loose debris from socket.
sary, but do not rinse. 3. Place socket dressing with dry-socket paste on ¼-inch gauze strip and pack to
5. For bleeding bite down on another clean gauze pad for 1 hr and repeat if neces- top of socket.
sary, but do not rinse. 4. See patient in 2 days for evaluation, and if pain persists, remove packing, irrigate,
6. Some swelling or discoloration may follow oral surgery and would cause no and replace packing.
concern. 5. Continue patient on appropriate pain medication while under treatment for dry
7. Do not rinse today. Tomorrow, rinse after meals, using ¼ teaspoon salt in a socket.
large glass of warm water. 6. Patient may benefit from a course of antibiotic therapy for an additional week if
8. Do not smoke for 48 hr. there are any systemic symptoms.
9. Diet: any soft food that you can mash with a fork (cold or warm, but not hot).
10. Brush all teeth carefully and gently, especially the teeth around the area of
operation. Use a soft toothbrush.
11. If you were given any prescriptions, take the medicine as directed.
12. Do not take aspirin if you have pain, take Tylenol or Advil.
13. If constipated, take a mild laxative tonight.
14. In case of emergency call the physician’s access number is.
210 SECTION II ■ Dentoalveolar Surgery
B spitting for 24 hours to prevent bleeding. Patients are also
FIGURE 11-29. A, Flap design for impacted maxillary third molars is
similar to that used to access mandibular third molars, except for obvious
anatomic differences. The envelope flap is most commonly used, with the distal
extent of the flap made with a scalpel blade immediately over the crest of the
ridge. The incision can be extended as far anteriorly around the second molar
as needed for sufficient access to the impacted tooth. B, In situations in which
the maxillary third molar impaction is relatively high, a releasing incision should
be made at the distobuccal line angle of the second molar to aid in visualizing
the tooth.
FIGURE 11-30. A vertical incision is extended mesial to the maxillary
second molar and then follows posteriorly around the sulcus. The incision then
extends backwards over the maxillary tuberosity to allow for better access. The
triangular flap is difficult, but an envelope can also be used for less complex
third molar impaction removals. (From Dym H, Ogle OE: Atlas of minor oral
surgery, Philadelphia, 2001, WB Saunders.)
FIGURE 11-31. Using a straight or contraangled elevator from the mesial
side, the tooth is then elevated out of its bony crypt in a distobuccal direction.
(From Dym H, Ogle OE: Atlas of minor oral surgery, Philadelphia, 2001, WB
Saunders.)
■ DIET AND ORAL HYGIENE
In the immediate postsurgical period (12 to 24 hours), the
patient should be advised to maintain a diet of soft foods and
avoid anything too hot. Patients should be told to avoid
brushing their teeth in the surgical site in the immediate
postoperative period and not perform any oral rinsing and
advised to limit vigorous exercise activity for the first 24 hours
following difficult impactions.
REFERENCES
1. Assael L: Indications for elective therapeutic third molar
removal: the evidence is in, J Oral Maxillofac Surg 63:1691-1692,
2005.
2. Weigner R, Axman-Kramer K, Loft C: Prognosis of conven-
tional root canal treatment reconsidered, Endodontic Dent
Traumatology 14:1-9, 1998.
3. Marx R: Biphosphonate induced exposed bone osteonecrosis/
osteopetrosis of the jaws. Risk factors, recognition, prevention
and treatment, J Oral Maxillofac Surg 63 (11):1567-1575,
2005.
4. Vallerand A, Heft M et al.: The effects of postoperative prepara-
tory information in the clinical course following 3rd molar extrac-
tion, J Oral Maxillofac Surg 52(11):1165-1170, 1994.
5. Saldanha J, Casati M et al.: Smoking may affect the alveolar
process dimensions and radiographic bone density in maxillary
extraction sites. A prospectus study in humans, J Oral Maxillofac
Surg 64(3):1359-1365, 2006.
6. Bath M, Prehavec JC: Basic exodontia. In Fonseca R, editor:
Textbook of oral and maxillofacial surgery, Philadelphia, vol I,
2000, Saunders.
7. Sklar A: Preserving alveolar ridge anatomy following tooth
removal in conjunction with immediate implant placement, In
Haug R, editor: Atlas of the oral and maxillofacial surgery clinics of
North America, Sep 1999, Elsevier.
 CHAPTER 11 • Basic and Complex Exodontia and Surgical Management of Impacted Teeth
8. Block M: Preserving alveolar ridge anatomy following tooth
removal in conjunction with delayed implant placement. In
Haug R, editor: Atlas of the oral and maxillofacial surgery clinics of
North America, Sep 1999, Elsevier.
9. Susarla S, Blaeser B, Magalnick D: Third molar surgery and
associated complications. Oral Maxillofac Surg Clin North Am
15(2):177-186, 2003.
10. Peterson LJ: Prevention and management of surgical complica-
tion. In Peterson LJ, Ellis E III, Hupp Jr E et al., editors: Con-
temporary oral and maxillofacial surgery, ed 3, New York, 1998,
Mosby.
11. Rayne J: The unerupted maxillary canine, Dent Pract Dent Rec
19:194-204, 1969.
12. Bishara SE: Impacted maxillary canines: a review, Am J Orthod
Dentofacial Orthop 101:159-171, 1992.
13. Stellzig A, Basdra EK, Komposch G: The etiology of canine
tooth impaction-a space analysis. Fortshcr Kieferothop 55(3):97-f,
1994.
14. Khanuja A, Powers MP: Surgical management of impacted
teeth. In Fonseca R, editor: Textbook of oral and maxillofacial
surgery, Philadelphia, vol I, 2000, Saunders.
15. Grover PS, Lorton L: The incidence of unerupted permanent
teeth and related clinical cases, Oral Surg Oral Med Oral Pathol
59:420-425, 1985.
16. NIH consensus development conference for removal of third
molars, J Oral Surg 38:235-236, 1980.
17. Assael L: Indications for elective therapeutic third molar
removal: the evidence is in, J Oral Maxillofac Surg 63:1691-1692,
2005.
18. Dym H: Management of impacted third molar teeth. In
Dym H, Ogle O, editors: Atlas of minor oral surgery, Philadelphia,
2000, Saunders.
19. Berge TI, Boe OE: Symptoms and lesions associated with retained
or partially erupted third molars, Acta Odontol Scand 51:115,
1993.
20. Martis C, Karabouta I, Cazaridis N: Extraction of impacted man-
dibular wisdom teeth in the presence of acute infection, Int J
Oral Surg 7:541-548, 1978.
21. Peterson LJ: Principles of management of impacted teeth. In
211
Peterson LJ et al., editors: Contemporary oral and maxillofacial
surgery, ed 3, St Louis, 1998, Mosby-Year Books.
22. Kiesselbach JE, Chamberlain JG: Clinical and anatomic observa-
tions on the relationship of the lingual nerve to the mandibular
third molar region, J Oral Maxillofac Surg 41:565, 1984.
23. Poeschl RW, Eckel D, Poeshel E: Postoperative prophylactic
antibiotic treatment in third molar surgery-a necessity, J Oral
Maxillofac Surg 62:3-8, 2004.
24. Loukota RA: The incidence of infection after third molar
removal, Br J Oral Maxillofac Surg 29:336, 1991.
25. Curran JB, Kenneth S, Young AR: An assessment of the use of
prophylactic antibiotics in third molar surgery, Int J Oral Surg
3:1, 1974.
26. MacGregor AJ: Reduction in morbidity in the surgery of the
third molar removal, Dent Update 17:411, 1990.
27. Piecuch JF, Arzadon J, Lieblich SE: Prophylactic antibiotics for
third molar surgery, J Oral Maxillofac Surg 53:53, 1995.
28. Schwartz S: Perioperative pain management. In Dym H, editor:
Perioperative management of the oral and maxillofacial surgery
patient, part II, Philadelphia, 2006, Saunders.
29. Jackson DC, Roszkowski MT, Moore PA: Management of post-
operative pain. In Fonseca RJ, editor: Oral and maxillofacial
surgery, Philadelphia, 2000, WB Saunders.
30. Haug RH et al.: The American Association of Oral and Maxil-
lofacial Surgeons-age-related-third molar study, J Oral Maxillofac
Surg 63:1106-1114, 2005.
31. Alling CC: Dysesthesia of the lingual and inferior alveolar
nerves following third molar surgery, J Oral Maxillofac Surg
44:454, 1986.
32. Pogrel MA: Complications of third molar surgery. In Kaban LB,
Pogrel MA, Perrott DH, editors: Complications in oral and maxil-
lofacial surgery, 1997, WB Saunders.
33. Meyer RA: Evaluation and management of neurologic complica-
tions. In Kaban LB, Pogrel MA, Perrott DH, editors: Complica-
tions in oral and maxillofacial surgery, Philadelphia, 1997, WB
Saunders.
34. Poeschl PW, Eckel D, Poeschl E: Postoperative prophylactic
antibiotic treatment in third molar surgery—a necessity, J Oral
Maxillofac Surg 62:3-8, 2004.
CHAPTER 12
COMPLICATIONS OF
Webster’s New World Medical Dictionary defines complication
as “an additional problem that arises following a procedure,
treatment or illness and is secondary to it. A complication
complicates the situation.”
Exodontia is the most common procedure performed by
oral maxillofacial surgeons. According to a report by the
Public Health Service, “. . . more than three-quarters of the
total cost of payments for oral surgery procedures were allo-
cated to removal of third molars.”1 It stands to reason that
most of the complications we see are related to exodontia.
These can be common or rare and can occur during or after
treatment. Nevertheless, with careful treatment planning and
adhering to good surgical techniques and principles, surgeons
can minimize the frequency of complications. In addition,
early recognition and proper management can help to improve
the outcome of procedures. Considering the fact that compli-
cations are a risk and potential sequelae of any surgery, it is
imperative that surgeons notify patients of them while obtain-
ing informed consent (Box 12-1). Complications can occur
even when the surgeon adheres to good surgical principles.
Variations in anatomy and the patient’s response to healing
can result in complications even when the surgeon executes
the surgical procedure within the standard of care.
Complications during exodontia:
1. Removal of the wrong tooth
2. Injuries to teeth and adjacent structures
3. Residual root remnants
4. Displacement of teeth or root tips
5. Soft tissue injuries
6. Oroantral communications
7. Swallowing or aspiration of teeth, fragments of teeth, or
restorations and crowns
8. Tissue emphysema
9. Sensory nerve injuries
Complications after exodontia:
1. Alveolar osteitis (dry socket)
2. Infection
3. Trismus, swelling, and pain
4. Temporomandibular joint problems
Complications that can occur during or after exodontia:
1. Hemorrhage
2. Injuries to osseous structures
212
DENTOALVEOLAR SURGERY
Gaetano G. Spinnato • Pamela L. Alberto
■ COMPLICATIONS DURING
EXODONTIA
REMOVAL OF THE WRONG TOOTH
One of the most frequent complications occurring during
exodontia is the wrongful extraction of teeth. Common causes
include: miscommunication between the referring dentist and
his office personnel with the specialist’s office, incorrectly
labeled radiographs or referral slips, and disagreement between
the dentist and the patient. A careful history with a review
of recent radiographs and a thorough clinical examination
is the best way to prevent this complication. In the event of
the inadvertent removal of the wrong tooth, if discovered at
the time of surgery, the tooth should be implanted immedi-
ately and stabilized if it is a healthy salvageable tooth. The
patient should be given antiinfectives and informed of the
event and instructed to return for follow-up care. If the patient
has a referring dentist, he or she should also be made aware
of what occurred. The event should be carefully documented
in the patient’s chart.
INJURIES TO TEETH OR ADJACENT STRUCTURES
Fractures and loosening of adjacent teeth and dislodging of
large restorations or crowns can accidentally occur during
exodontia. Careful evaluation of the surrounding dentition
and radiographs should be done before instituting treatment.
Often this complication is unavoidable because of loose
crowns or large restorations with recurrent decay under the
restoration. The patient should be made aware of the potential
for these events occurring (Figures 12-1 and 12-2). If teeth are
partially avulsed during removal of adjacent teeth, they should
be repositioned and stabilized. Any dislodged crowns from
teeth that do not show signs of decay can be permanently
recemented. Those teeth under crowns with decay should be
reinserted with temporary cement, and the general dentist
should be informed of the event. Adjacent teeth that are
fractured or that have large restorations dislodged should be
temporized. The patient should be referred back to their
general dentist for definitive treatment. The incident should
be well documented in the patient’s chart, and they should be
made aware of the problem.
 CHAPTER 12 •
BOX 12-1 Example of Informed Consent
CONSENT TO TREATMENT
CHRIS A.BROWN, D.D.S.
19 E.Center St. — Madison, WI 53701
608.123.4567
Date ________________
I was informed by the abovenamed doctor(s) of the risks,
possible alternative methods of treatment, and possible
consequences involved in the treatment by means of:
_______________________________________________
_______________________________________________
_______________________________________________
for the relief of ___________________________________
_______________________________________________
Understanding this,I hereby authorize the above named
doctor(s) or whomever s/he (they) may designate, to admin-
ister such treatment to
me (or _________________________________________)
Name of Patient if Minor
Signed ______________________________________
Patient or Person Authorized to Consent for Patient
Witness _____________________________________
Date ________________________________________
Form 4554 • 3/86SYCOM Madison, WI Printed in U.S.A.
FIGURE 12-1. Radiograph of roots with a crown in close proximity.
RESIDUAL ROOT REMNANTS
During exodontia, roots can fracture often in spite of good
surgical technique. Usually this occurs because the root is
dilacerated or divergent. If the remnant is a couple of milli-
meters in diameter and in close proximity to a vital structure,
such as a nerve or the sinus, risks versus benefits should be
considered. Usually a root remnant this size will be of no
consequence if not grossly infected. If a decision is made to
Complications of Dentoalveolar Surgery 213
FIGURE 12-2. Photograph of the roots with a crown in close proximity.
leave it, the patient should be informed, postoperative radio-
graphs should be taken, documentation should be entered in
the patient’s chart, and they should be evaluated periodically
both clinically and radiographically to ensure uneventful
healing.
DISPLACEMENT OF TEETH AND ROOT TIPS
Displacement of teeth and root tips is a rare occurrence.71-74
Some causative factors that have been implicated are the
inexperience of the surgeon, uncontrolled force, improper use
of instrumentation, and difficult access with poor visualization
and inadequate exposure.70-71 Variations in anatomy, such as
a thin lingual plate of bone in the mandibular molar area of
the maxillary sinus wall extending between the roots of the
maxillary molars, can increase the potential for the displace-
ment of teeth or root tips into the floor of the mouth or maxil-
lary sinus respectively.
The sites most frequently involved are the maxillary sinus,
the submandibular space, and the infratemporal fossa.70-80
Some reports describe an accidental displacement of a third
molar into the lateral pharyngeal space.71,78
Displacement of root tips or impacted teeth into the maxil-
lary sinus or infratemporal fossa usually occurs because of the
close proximity and thinness of the sinus floor or wall. In
removing a superiorly distally impacted third molar, adequate
bone removal, good visibility with careful elevation, and a
distal stop is a must. If inadvertently a tooth or root tip is dis-
lodged into the sinus, an attempt should made to retrieve it
through the extraction site with a suction tip. If the attempt
is unsuccessful, radiographs should be taken to localize the
tooth and a Caldwell Luc approach should be used to remove
it. When a third molar is displaced into the infratemporal
fossa, radiographs must be obtained to localize its position, the
incision should be extended posteriorly to the tonsillar fauces,
and with careful blunt dissection, an attempt should be made
to identify and remove it.70 Care must be taken to prevent
injury to the pterygoid plexus of veins, which can result in
brisk bleeding. If this happens, the procedure should be aborted
214 SECTION II ■ Dentoalveolar Surgery
and fibrosis should be allowed to develop around the tooth,
from several days104 to several weeks.17 An attempt can be
made to remove it by a hemicoronal or an intraoral approach
after CT analysis to determine its location. Some authors
recommend careful follow-up if the patient is asymptomatic.17
One report indicated no adverse affects after 15 months.17,105
Care should be taken in attempting to remove the distal roots
of third molars because the lingual cortex of the mandible
curves laterally and is thin in this area. When a root tip is
displaced into the sublingual space, an attempt should be
made to palpate it digitally and push it back into the socket.
If this is unsuccessful, a full flap should be raised on the lingual
and the mylohyoid muscle dissected free from its attachment
trying to keep the tip in position to prevent further displace-
ment and, thus, facilitate its removal. It is not often that a
root becomes displaced deep into the submandibular area. If
this should occur, fibrosis should be allowed to take place, and
if removal is necessary, an extraoral approach can be used to
retrieve it.
Infrequently, roots are pushed through thin cortical
plates in the maxillary bicuspid and molar areas. Usually, they
can be palpated subperiosteally and can be pushed back
through the socket, or an incision can be made below it to
remove it.
Some reports describe accidental displacement of third
molars into the lateral pharyngeal space.71,78 Care must be
taken with the use of surgical instruments to avoid such
untoward effects during exodontia.
SOFT TISSUE INJURIES
Soft tissue injuries can occur when performing exodontia. Soft
tissue injuries include laceration of the flap, burns, abrasions,
puncture wounds, and subcutaneous emphysema.
Lacerations of the flap can be caused by too small of a flap
and overretraction. These tears can increase the chance of
wound dehiscence and delay healing. If a tear does occur, the
margins should be reapproximated and carefully sutured.
Excising the edges before closure is indicated if the tear is
jagged. Designing larger flaps with releasing incisions and
using less retraction can prevent this complication.
Burns and abrasions are caused by rotary drills. Careful
attention is a must when using them. One must avoid catch-
ing the soft tissue with the shank of the bur and creating a
laceration. This usually occurs with the buccal mucosa and
the corner of the mouth. The use of a bur guard helps in pre-
venting this problem. These burns and/or abrasions are quite
painful and are slow to heal. Applying antiinfective ointment
or silver sulfadiazine treats these burns and/or abrasions. This
complication can be prevented by careful attention of the
assistant to the location of the shank of the bur when the
surgeon is cutting. Maintenance of the bur guard is important
to prevent its overheating, which can cause severe burns to
the lip.
Puncture wounds to the soft tissue can be the result of
uncontrolled forces with sharp instruments, such as a perios-
teal or a straight elevator. This can be prevented by using
FIGURE 12-3. Radiograph of maxillary molar with its roots in close
proximity of the sinus.
finger rest support from the opposite hand to protect the area
from potential slippage with an instrument. Small puncture
wounds should be left open and not sutured once hemostasis
is achieved. If hemostasis cannot be achieved, sutures may be
necessary. Because the instrument that punctured the soft
tissue could contain debris and bacteria, the patient should be
placed on antiinfectives.
OROANTRAL COMMUNICATION
Exposure of the maxillary sinus can occur while extracting
maxillary molars. Proper radiographic evaluation will usually
alert you to the fact that this may be a possibility. The mor-
phology of the roots should also be considered (Figure 12-3).
Widely divergent roots increase the chance that the sinus
floor could be removed along with the tooth. If the tooth roots
have close proximity to the sinus, less force should be used,
and division of the roots should be considered.
Oroantral communication is an important complication to
discuss with the patient when receiving an informed consent
for the removal of a maxillary molar. If this occurs, appropriate
treatment is necessary to prevent a postoperative maxillary
sinusitis and formation of a chronic oroantral fistula.
If the maxillary sinus is exposed during extraction, treat-
ment is determined by the size of the communication. Probing
the communication is not advised. This could further tear the
membrane. For small communication less than 2 mm, a col-
lagen plug can be placed in the socket. This will help maintain
a good blood clot. The patient needs special postoperative
sinus instructions advising them not to sneeze, smoke, rinse,
spit, suck on a straw, or blow their nose.
For moderate size communications (2 to 6 mm), a collagen
plug can be placed with figures-of-eight sutures over the socket
to prevent the plug from being dislodged. The patient should
be given the postoperative sinus instructions. A 1-week course
of antiinfectives, antihistamines, and nasal decongestants
should be given. Usually, Augmentin, clindamycin, or a ceph-
alosporin can be prescribed to decrease the possibility of a
maxillary sinusitis.
 CHAPTER 12 •
For a large communication (greater than 6 mm), the sinus
communication must be closed primarily using a flap proce-
dure. A buccal or lingual flap may be necessary to close these
large communications. Close follow-up is necessary for these
patients.
SWALLOWING OR ASPIRATION OF TEETH,
FRAGMENTS OF TEETH, OR RESTORATIONS
AND CROWNS
During exodontia, it is advisable to place an oral drape to
prevent swallowing or aspiration of loose teeth, dislodged
crowns or fragments of teeth, root tips, or dental restorations.
In the event of a foreign body being swallowed, the patient
should be sent to the hospital for radiographs to localize it.
The patient should then ensure passage. If a tooth, root tip,
or other foreign body is aspirated during surgery and it
becomes lodged in the trachea, methods used in Advanced
Cardiac Life Support, such as the abdominal thrusts, back
slaps, or the Heimlich maneuver, should be used in an attempt
to remove it.17 If the patient becomes unconscious, an attempt
should be made to remove it with a laryngoscope and a
McGill forceps, or an emergency coniotomy should be
attempted. In the event it passes the vocal cords, it will most
likely enter the right main stem bronchus or the right lung.
The patient should be transported to the hospital where an
emergency bronchoscopy can be performed to remove the
object. A detailed description of the event should be recorded
in the patient’s chart.
TISSUE EMPHYSEMA
Tissue emphysema is a complication that is seen less fre-
quently since the use of rotary instruments, such as the Hall
drill and electric hand pieces. It is caused by the inclusion of
air under pressure into the subcutaneous soft tissue. During
the removal of bone or the sectioning of teeth with an air
driven dental hand piece, air is forced subcutaneously result-
ing in a rapid onset of swelling. Other causes could be the use
of an air syringe and a patient coughing or sneezing when a
large flap is elevated.
FIGURE 12-4. Radiograph of a mesioangular impacted
third molar close to the canal.
Complications of Dentoalveolar Surgery 215
When palpated there is a feeling of crepitus and occasion-
ally some tenderness associated with it. Radiographs can show
air in the soft tissue adjacent to the surgical site. Extensive
subcutaneous emphysema can be life threatening or result in
an infection leading to meningitis or mediastinitis.
Treatment consists of ice application to the affected site,
systemic antiinfectives, and monitoring. The condition usually
resolves in several days; however, severe cases may require
hospitalization and IV antiinfectives.
SENSORY NERVE INJURIES
Sensory nerve injuries can occur with the removal of teeth
whose roots are close to the inferior alveolar nerve, lingual
nerve, and mental nerve. Temporary or permanent sensory
nerve disturbances can occur anywhere from 0.4% to 2% of
the time.106 It is important for the surgeon to obtain a detailed
informed consent from their patients concerning these com-
plications. The incidence of sensory nerve injuries from third
molar surgery is related to many factors. Tooth proximity to
the inferior alveolar nerve canal and variation in the ana-
tomic relation of the lingual nerve to the crown of the man-
dibular third molar are major factors that contribute to nerve
injuries.107
A higher incidence of nerve injuries occurs with the
removal of horizontally impacted teeth compared with mesio-
angular or distoangular impacted third molars107 (Figure 12-4).
The depth of the impaction, presence of completely devel-
oped roots, use of rotary instruments, and sectioning of teeth
can all contribute to nerve injuries. Division of the inferior
alveolar nerve is infrequent, but pressure and compression of
the nerve can take place during the removal of the third
molar. Neurosensory alteration of the inferior alveolar nerve
can occur when normal intraoperative and postoperative
hemorrhage occurs and extends into the mandibular canal.
Because this is a rigid osseous structure and the nerve is con-
fined within this canal, the accumulation of blood within the
canal can cause a compressing nerve injury. Usually the neu-
rosensory alteration will be temporary, but it can be perma-
nent. Injury to the lingual nerve occurs either during the
216 SECTION II ■ Dentoalveolar Surgery
FIGURE 12-5. Radiograph of a cyst close to the mental foramen.
reflection of the flap, fracture of the lingual cortical plate, or
perforation of the lingual cortical plate during sectioning of
the tooth. The path of the lingual nerve as it passes on the
lingual surface of the mandible near the mandibular third
molar is variable. In approximately 17% of cases, the nerve
lies above the crest of lingual bone and can be adherent to
the follicle of the third molar. Therefore in these cases, a
stretch injury or even a transection of the nerve can occur
when the surgeon has performed the extraction technique
within the standard of care.
The mental nerve can be injured during the removal of a
premolar or during flap development or retraction. In the
event of a high risk for nerve injury, the use of partial odon-
tectomy may be indicated (Figure 12-5). Seddon and Sunder-
land developed classifications for nerve injuries.108,109 The
Seddon classification is based on time from injury and degree
of recovery. It includes neurapraxia, axonotmesis, and neurot-
mesis. Sunderland expands his classification to include first
degree (neurapraxia), second degree (axonotmesis), third
degree, fourth degree, and fifth degree (neurotmesis).
Neuropraxis results from minor nerve compression or trac-
tion injury. Since there is no loss of axonal continuity usually
there is complete recovery within 2 months. Microsurgery is
not indicated. Axonotomesis is produced by blunt trauma,
crushing, or a severe traction injury. Continuity of the
axon is disrupted but not the epineurial sheath. Thus sensory
recovery can takes 2 to 6 months, though some cases have
taken 1 year. Microsurgery is not indicated unless a foreign
body is associated with it.
Sunderland’s third- and fourth-degree nerve injury is the
result of a compression, crush, or chemical injury. There can
be some spontaneous recovery but not completely with a pos-
sible poor outcome. Microsurgery may be indicated if there is
no improvement after 3 to 6 months. It should be emphasized
that as long as the patient is exhibiting signs of improvement,
microsurgery should be delayed.
Neurotmesis is the result of a complete transection of the
nerve. The prognosis for spontaneous recovery is poor. Micro-
surgery is indicated for these injuries. Neurosensory testing
should include two-point discrimination, light touch, brush
strokes, vibrational sense, pain stimuli, and thermal discrimi-
nation. This will help determine the injury classification and
recommended treatment. Nerve repairs should be performed
by surgeons proficient in microsurgery for the best results.
■ COMPLICATIONS AFTER
EXODONTIA
ALVEOLAR OSTEITIS (DRY SOCKET)
Dry socket, or alveolar osteitis, is one of the more common
surgical complications seen postoperatively. Some studies
have shown the incidence to be as low as 3% with all extrac-
tions.2-3,6-7 Other studies in the literature place the incidence
of dry socket in the removal of mandibular third molars as
high as 30%.4-7 Dry sockets rarely occur in the maxillary.
Although the cause is not known, data suggests that saliva
with a high bacterial count may be the etiologic factor in
causing destruction or malformation of the blood clot after
extractions.4 Other theories suggest fibrinolytic action as a
possible cause because the use of antifibrinolytic agents dem-
onstrated a decreased incidence of occurrence.4,10,11 Additional
factors that may be responsible for dry sockets occurring are
smoking,12 oral contraceptives,5 experience of the surgeon,13
complexity of the extraction,14 and poor oral hygiene.4
The symptoms of a dull throbbing pain usually present
themselves around the third to fifth day after surgery and are
often confused with an earache, headache, or pain from
another tooth with no evidence of pathologic condition. Nar-
cotic analgesics tend not to give relief as well as nonsteroidal
antiinflammatory drugs. Clinically the classical signs of infec-
tion are not present, but there is a fetid odor, and the extrac-
tion site is devoid of a clot or shows evidence of poor healing
with food debris. After irrigation and insertion of a medicated
dressing, relief is experienced within minutes. Commercially
prepared radiograph detectable dressings containing 20%
eugenol are available for use. Dry socket pastes containing
eugenol, guaiacol, chlorobutanol, and balsam of peru are also
available and can be impregnated onto radiograph detectable
filament gauze for use as a dressing. The dressings are usually
replaced every day or 2 after irrigation with normal saline. The
symptoms dissipate after several days; however, on occasion
they may persist longer. Beyond 3 weeks, radiographs should
be taken and reviewed, and the patient should be examined
clinically to rule out a different cause for the discomfort.
INFECTION
Signs and symptoms manifest within 3 to 4 days. They are
usually increased swelling, trismus, and tenderness along with
redness, an elevated temperature, general malaise, and many
times a purulent exudate.
Infections can occur postoperatively 3 to 4 days to several
weeks after surgery. Most of these develop in third molar
extraction sites, and the incidence has been reported to be
anywhere from 3% to 5%.14-15 Infection after dental extrac-
tions usually occurs in surgical cases requiring flap elevation
 CHAPTER 12 •
and bone removal.17 Patients who have poor oral hygiene,
periodontal disease, and are immunocompromised are more
susceptible to postoperative dental infections. Streptococci
species of bacteria appear to be the largest group of bacteria
causing postoperative oral infections, and studies have shown
these infections have an average of four different bacteria with
anaerobic outnumbering aerobic species.18 The most effective
treatment continues to be penicillin. However, because of the
increased recognition of anaerobic organisms in these infec-
tions, metronidazole or clindamycin can be substituted for
them.6,18,21 When given prophylactically to patients with
debilitating medical conditions or periodontal disease, antibi-
otics are thought to be of some value. Use of preoperative and
postoperative antibiotics is still a controversial topic.19,22-27
This practice may make treatment of subsequent infections
more difficult because of resistant strains of bacteria.23-27 There
are some reports of a bacteremia being associated with the
extraction of teeth.110,111 This is a rare occurrence. In addition
to antibiotic therapy, an incision and drainage should be per-
formed and cultures obtained for sensitivity testing. In severe
cases, consultation should be sought with infectious diseases.
Infection can be minimized by following good surgical tech-
niques with copious irrigation and adhering to principles of
asepsis. Infections following extractions can occur even when
the surgeon uses proper surgical techniques. The patient’s
local and systemic response to surgery, the virulence of the
bacteria on the area of the surgery, and the postoperative
compliance of the patient can place the patient at an increased
risk for infection.
BISPHOSPHONATE-RELATED
OSTEONECROSIS (BRON)
Oral bisphosphonates, such as Fosamax, Actonel, Boniva,
Didronel, and Skelid, are being used to treat osteoporosis,
osteopenia, Paget’s disease of bone, and osteogenesis imper-
fecta of childhood.28-31 The intravenous bisphosphonates,
pamidronate (Aredia), and zoledronic acid (Zometa) are
being used in the treatment and management of cancer-
related conditions.31 In 2003 and 2004, oral surgeons
published reports of nonhealing exposed bone in the maxil-
lofacial region in patients on intravenous bisphosphonates.
Subsequent to these reports, additional case series were pub-
lished.33-43 In 2004, health care professionals were notified by
the manufacturer of the complications with IV bisphospho-
nates, and in 2005 a broader class warning was released that
included the oral bisphosphonates.43-45 The American Asso-
ciation of Oral and Maxillofacial Surgeons (AAOMS) con-
siders a patient to have BRON if they have all three of the
following characteristics:
1. Current or previous treatment with a bisphosphonate
2. Exposed bone in the maxillofacial region that has per-
sisted for more than 8 weeks
3. No history of radiation therapy to the jaws
Currently the estimated cumulative incidence of BRON in
patients on IV bisphosphonates, which is based on retrospec-
tive studies with limited sample sizes, is from 0.8% to
Complications of Dentoalveolar Surgery 217
0.12%.31,46-54 Patients on oral bisphosphonate therapy are at a
much lower risk than those patients on IV therapy with the
estimated risk following extractions to be 0.09% to 0.34%;
however, the risk appears to increase if the duration of therapy
exceeds 3 years.31
In patients with a diagnosis of BRON, treatment should be
to eliminate pain, control infection, and prevent the progres-
sion or occurrence of osteonecrosis.31 Hyperbaric oxygen
therapy has not been proven to be effective in treatment of
these patients,31,56 and they do not respond as predictably to
surgical treatments that are used for osteomyelitis and osteo-
radionecrosis.34-36,41 In BRON, bony sequestra should be
removed or recontoured without exposing uninvolved bone.55
The AAOMS has proposed the staging and treatment
strategies listed in Table 12-1 for the treatment of patients
with BRON.31
It is recommended that any unsalvageable teeth be
extracted before any IV bisphosphonate therapy. It has also
been proposed that if systemic conditions permit that oral
bisphosphonates be discontinued for 3 months before and 3
months following extractions or waiting for 14 to 21 days for
the extraction site to mucosalize. No alteration or delay of
treatment is required for patients who are on oral bisphospho-
nates for less than 3 years and have no clinical risk factors. If
these patients have also been taking steroids, because this may
increase the risk of BRON, it is recommended that they take
a drug holiday for 3 months until osseous healing has occurred.
It is recommended that prescribing physicians be consulted
about discontinuing oral bisphosphonates in patients for 3
months before treatment if they have been taking them with
or without steroids. Therapy should not be restarted until
osseous healing is complete.31
OSTEORADIONECROSIS
Osteoradionecrosis (ORN) is an avascular necrosis of bone
caused by the three H (hypocellular, hypovascular, hypoxic)
tissue effects of radiotherapy. It can develop when teeth are
removed before radiotherapy but treatment is begun shortly
thereafter (early trauma induced-ORN) or when a tooth is
removed more than 3 years after therapy without HBO (late
trauma induced-ORN).57
TRISMUS, PAIN, AND SWELLING
Pain and swelling are a usual consequence of any surgical
insult to the body. Swelling and pain are the result of the
production of inflammatory mediators, such as leukotrienes,
prostaglandins, and thromboxane A2.17 Most swelling reaches
a peak in 24 to 48 hours then gradually plateaus off and begins
to dissipate over the next 48 to 72 hours. Some factors that
can contribute to increased swelling are complexity of the
extraction, excessive retraction, and length of the operating
time. The trismus that results is due to inflammation of the
muscles of mastication and is probably a protective mecha-
nism to limit function and further trauma. Either the surgical
procedure or the administration of the local anesthetic can
cause the trismus. Pain usually peaks several hours after
218 SECTION II ■ Dentoalveolar Surgery

TABLE 12-1 Staging and Treatment Strategies

BRONJ* Staging Treatment Strategies†
At risk category No apparent exposed/necrotic bone in patients who • No treatment indicated
have been treated with either oral or IV bisphosphonates • Patient education
Stage 1 Exposed/necrotic bone in patients who are asymptomatic • Antibacterial mouth rinse
and have no evidence of infection • Clinical follow-up on a quarterly basis
• Patient education and review of indications for continued bisphosphonate therapy
Stage 2 Exposed/necrotic bone associated with infection as • Symptomatic treatment with broad-spectrum oral antibiotics (e.g., penicillin,
evidenced by pain and erythema in the region of the exposed bone cephalexin, clindamycin, or first-generation fluoroquinolone)
with or without purulent drainage • Oral antibacterial mouth rinse
• Pain control
• Only superficial débridements to relieve soft tissue irritation
Stage 3 Exposed/necrotic bone in patients with pain, infection, and one • Antibacterial mouth rinse
or more of the following: pathologic fracture, extraoral fistula, or • Antibiotic therapy and pain control
osteolysis extending to the inferior border • Surgical débridement/resection for longer term palliation of infection and pain
*Exposed bone in the maxillofacial region without resolution in 8-12 wk in persons treated with a bisphosphonate who have not received radiation therapy to the jaws.
†
Regardless of the disease stage, mobile segments of bony sequestra should be removed without exposing uninvolved bone. The extraction of symptomatic teeth within exposed,
necrotic bone should be considered because it is unlikely that the extraction will exacerbate the established necrotic process.
Discontinuation of the IV bisphosphonates shows no short-term benefit. However, if systemic conditions permit, long-term discontinuation may be beneficial in stabilizing
established sites of BRONJ, reducing the risk of new site development and reducing clinical symptoms. The risks and benefits of continuing bisphosphonate therapy should be
made only by treating oncologist in consultation with the OMS and the patient.
Discontinuation of the oral bisphosphonate therapy in patients with BRONJ has been associated with gradual improvement in clinical disease. Based on the experience of two task
force members managing 50 BRONJ patients who were treated with oral bisphosphonates, discontinuation of oral bisphosphonates for 6-12 mo may result in either spontaneous
sequestration or resolution following débridement surgery. If systemic conditions permit, modification or cessation of oral bisphosphonate therapy should be done
in consultation with the treating physician and the patient.
American Association of Oral and Maxillofacial Surgeons: Position paper on bisphosphonate-related osteonecrosis of the jaws. Approved by the Board of Trustees Sept 25, 2006.

surgery. Fischer and his colleagues placed peak pain at 3 to 5
hours after surgery.63 Many studies have suggested the use of
steroids and nonsteroidal antiinflammatories to decrease swell-
ing and pain. Preoperative intravenous steroids, such as dexa-
methasone and betamethasone, have been shown to reduce
postoperative swelling and pain with third molar surgery.7,80-81
Narcotic combinations are used most frequently to control
postoperative pain, but long-acting local anesthetics have
been shown to be effective in reducing postoperative discom-
fort. The reasoning is believed to be that anesthetic lasts
longer than the peak pain period. Ice, which is advocated as
a method to limit postoperative swelling by many practitio-
ners, was not considered to be a considerable factor by Fors-
gren and his colleagues.82 Close attention to good surgical
techniques with copious irrigation is also believed to be effec-
tive in reducing postoperative pain.58,83-84
TEMPOROMANDIBULAR JOINT PROBLEMS
Trauma to the temporomandibular joint during mandibular
extractions is usually due to lack of support against lateral
forces during exodontia. These lateral forces can be counter-
acted by providing support to the mandible with the other
hand or the use of a bite block. Patients will usually complain
if too much force is being exerted during extractions.
It is very important to perform a thorough history and
physical exam to document a previous temporomandibular
joint problem. Certain studies have shown that 60% of the
population may suffer from some temporomandibular joint
dysfunction with an equal sex distribution.58,85 Patients without
a prior history of internal derangement of the temporoman-
dibular joint may develop symptoms from extraction forces.
Any history or signs of temporomandibular joint problems
should be documented in the patient’s chart before treatment.
During the consultation, the patient should be made aware of
this potential complication.
Surgical extractions may be indicated if the patient has a
previous temporomandibular joint dysfunction or if too much
force is being exerted. In the event the patient does develop
symptoms subsequent to exodontia, they should be placed on
a liquid or soft diet, instructed to limit their opening, apply
moist heat to the affected side several times a day, and be
prescribed nonsteroidal antiinflammatories and muscle relax-
ants for 2 weeks. Rarely will splint therapy be necessary in
these cases because the discomfort usually dissipates within a
week or 2. Most often if a patient requires splint therapy
because of persistent discomfort, it is probably because they
have a previous history of temporomandibular joint dysfunc-
tion. In an extremely rare situation, an MRI may be indicated
to rule out a disk displacement.
Dislocation of the condyle is a more acute problem if it
occurs during mandibular extractions. This can be prevented
by applying appropriate support during extraction. This com-
plication should be immediately corrected. Some surgeons
stand behind the patient and place downward pressure on the
external oblique ridge of the mandible with their thumbs to
reduce the dislocation, whereas others stand in front with the
patient lower and use similar maneuvers. The patient should
then be placed on analgesics and a soft diet.
 CHAPTER 12 • Complications of Dentoalveolar Surgery 219

■ COMPLICATIONS THAT CAN

OCCUR DURING OR AFTER
EXODONTIA

HEMORRHAGE
The majority of intraoperative or postoperative bleeding prob-
lems are not from coagulopathies but from local factors. Oral
fibrinolysis has been suggested as a possible cause of hemor-
rhage from extraction sites in patients who have a normal
bleeding profile and do not bleed after extraoral trauma.58-61
For the most part, if there is history of previous extractions
with no persistent hemorrhage, a local source should be iden-
tified and treated. It is wise to call patients to determine their
status the evening after surgery. If there is a complaint of
persistent bleeding, the patient should be instructed to remove
any excessive exophytic blot clot from the area, rinse with a FIGURE 12-6. Preoperative Panorex of an impacted third molar.
mixture of hydrogen peroxide and water, then salt water fol-
lowed by pressure with a moistened tea bag or a moistened
gauze pad. If bleeding continues for 30 to 60 minutes, the
patient should be seen. After the patient is anesthetized, any
clots should be removed by curetting the socket and an attempt
made to identify the source. Any remaining granulation tissue
should be removed. Bleeding from bone within the socket can
be controlled by crushing or burnishing of the source with an
instrument, placing bone wax, or cauterizing the site with a
bovie. If an arterial bleeder is identified, it should be ligated
or cauterized. The surgical site should be resutured, and any
persistent local oozing from the surgical site can be treated
with the application of hemostatic agents, such as absorbable
gelatin sponges (Gelfoam), oxidized regenerated cellulose
(Surgicel), microfibrillar collagen (Avitene), absorbable col-
lagen dressings (Collatape, CollaPlug), or topical thrombin
applied to some of these agents.
Occasionally, when administering a posterior superior alve- FIGURE 12-7. Fracture of the mandible secondary to the extraction of an
olar nerve block, swelling can develop rapidly in the area of impacted third molar.
the cheek. This is a hematoma that is usually caused by per-
forating the posterior superior alveolar artery or vessels in the
pterygoid plexus of veins. Treatment consists of immediate
application of topical pressure and ice packs. In patients who should be made to stabilize the tooth and segment with arch
are kept on anticoagulant therapy because of a potential of a bars.17 We have not had much success with this. Another
thromboembolic event occurring, local measures have been alternative to stabilization with arch bars would be orthodon-
used to control postoperative bleeding. These include Surgicel tic brackets and heavy wire or wire ligatures. If a decision is
and suturing. Other measures that have been used are a fibrin made to remove the tooth with its bony tuberosity, it must be
adhesive (Beriplast P, Centeon LTD, West Sussex, UK), carefully dissected free from the soft tissue and the tissue tear
tranexamic acid rinses, and an argon beam coagulator.86-102 closed. The site of the tear can be quite uncomfortable, and
in spite of a careful repair sloughing of the area can occur. The
INJURIES TO OSSEOUS STRUCTURES area usually heals and epithelializes by secondary intention.
Bony fractures can occur in many areas. Some common sites The bony segment can be used to graft the area.17 A primary
are the labial and buccal plate in the areas of the maxillary closure should be used to close the site, especially if the sinus
and mandibular canine, bicuspid, and molar teeth.62 An infre- was violated. When solitary teeth with a pronounced canine
quent bony fracture (0.00049%) can occur in the mandible or buccal eminence are to be removed, it is advisable to reflect
during the removal of third molars.6,103 On occasion with the mucosa and remove the tooth surgically to prevent a
removal of maxillary third molars, inadvertently the maxillary traumatic fracture and tissue tear. In the event of this happen-
tuberosity fractures and the palatal mucosa will tear. It has ing, an alveoloplasty should be performed and the tissue
been suggested that if the tooth is not carious, an attempt should be closed as judiciously as possible.
220 SECTION II ■ Dentoalveolar Surgery
FIGURE 12-8. A, Transoral open reduction of fractured mandible.
B, Osteoradionecrosis treatment.
During the removal of third molars, if a nondisplaced frac-
ture occurs, the fractured mandible should be treated imme-
diately with a closed reduction using either arch bars or
orthodontic brackets (Figures 12-6, 12-7, and 12-8). If a frac-
ture is severely displaced, arch bars or orthodontic brackets
and a transoral open reduction can be attempted to reduce it.
If this is unsuccessful, the patient should be hospitalized, and
an extraoral open reduction should be performed with internal
rigid fixation using a Risdon or a percutaneous approach.
REFERENCES
1. Freidman JW: Containing the cost of third molar extractions,
Public Health Rep 98:376-384, 1983.
2. Field EA et al.: Dry socket incidence compared after a 12 year
interval, Br J Oral Maxillofac Surg 23:419, 1985.
3. Heasman PA, Jacobs DJ: A clinical investigation into the inci-
dence of dry socket, Br J Oral Maxillofac Surg 22:115, 1984.
4. Larsen PE: Alveolar osteitis after surgical removal of impacted
mandibular third molars, Oral Surg Med Oral Pathol 73:393-397,
1992.
5. Catellani JE et al.: Effect of oral contraceptive cycle on dry
socket (localized alveolar osteitis) J Am Dent Assoc 101:777-
780, 1980.
6. Srinivas M et al.: Third molar surgery and associated complica-
tions, Oral Maxillofac Surg 15(2):177-186.
7. Pogrel MA: Complications of third molar surgery, Oral and
Maxillofac Surg Clin North Am 2:3, Aug 1993.
8. Awang MN: The aetiology of dry socket; a review, Int Dent J
39:236-240, 1989.
9. Berwick JE, Lessin ME: Effects of a chlorhexidine gluconate
oral rinse on the incidence of alveolar osteitis in mandibular
third molar surgery, J Oral Maxillofac Surg 48:444-448, 1990.
10. Julis LL et al.: Prevention of dry socket with local application
or terra-cortril in gelfoam, J Oral Maxillofac Surg 40:285,
1982.
11. Gersel-Pederson N: Fibrinolytic activity of blood and saliva
before and after oral surgery, Int J Oral Surg 10:114-121, 1981.
12. Sweet JB, Butler DP: The relationship of smoking to localized
osteitis, J Oral Surg 13:160, 1979.
13. Sisk AL et al.: Complications following removal of third molars:
the role of the experience of the surgeon, J Oral Maxillofac Surg
44:855-859, 1986.
14. Alling CL, Kerr DA: Trauma as a factor causing delayed repair
of dental extraction sites, J Oral Surg 15:3, 1957.
15. Osborn TP et al.: A prospective study of complications related
to mandibular third molar surgery, J Oral Maxillofac Surg 43:767-
769, 1985.
16. Goldberg MH, Nemarich AN, Marco II WP: Complications
after mandibular third molar surgery: a statistical analysis of 500
consecutive procedures in private practice, J Am Dent Assoc
111:277-279, 1985.
17. Fonseca RJ et al.: Complications of dentoalveolar surgery. In
Wells II DL, Capes JO, Powers MP, editors: Oral and maxillofa-
cial surgery, WB Saunders.
18. Quayle AA, Rossell C, Hearn B: Organisms isolated from sever
odontogenic soft tissue infections, Br J Oral Maxillofac Surg
25:34, 1987.
19. Bulut E et al.: The value of routine antibiotic prophylaxis in
mandibular third molar surgery; acute phase protein levels as
indicators of infection, J Oral Sci 43:117-122, 2001.
20. Sekhar CH, Naryanan V, Baig MF: Role of antimicrobials in
third molar surgery: prospective, double blind randomized,
placebo controlled clinical study, Br J Oral Maxillofac Surg
39:134-137, 2001.
21. Labrioza JD, Mascardo J, Alpert D: The microbiological flora
of oralfacial abscesses, J Oral Maxillofac Surg 41:711, 1983.
22. Pieluch JF, Arzadon J, Lieblish SE: Prophylactic antibiotics for
third molar surgery: a supportive opinion, J Oral Maxillofac Surg
53:53, 1955.
23. Curran JB, Kennett S, Young AR: An assessment of the use of
prophylactic antibiotics in third molar surgery, Int J Oral Surg
3:1, 1974.
24. Laskin DM: Prophylactic antibiotics: a problem or a panacea,
J Oral Surg 34:585, 1976.
25. Zeitler DL: Prophylactic antibiotics for third molar surgery: a
dissenting opinion, J Oral Maxillofac Surg 53:61, 1995.
26. Paterson JA, Cardon VA, Strategos GT: An examination of
antibiotic prophylaxis in oral and maxillofacial surgery, J Oral
Surg 28:753, 1970.
27. MacGregor AJ: Antiprophylactic antibiotics, J Oral Surg
34:1063, 1976.
28. Physician’s desk reference, ed 57, Montvale, NJ, 2003, Medical
Economics.
29. Delmas PD, Mevnier PJ: The management of Paget’s disease of
bone, N Engl J Med 336:558-566, 1997.
30. Letocha AD, Cintas HL, Troendle JF et al.: Controlled trial of
pamidronate in children with types II and IV osteogenesis
imperfecta, J Bone Miner Res 20:977-986, 2004.
31. American Association of Oral and Maxillofacial Surgery: Posi-
tion paper on bisphosphonate-related osteonecrosis of the jaws.
Available at www.AAOMS.org Accessed on March 17, 2005.
32. Bone HG et al.: Ten years experience with alendronate for
osteoporosis in postmenopausal women, N Engl J Med 350:1189-
1199, 2004.
33. Marx RE: Pamidronate (Aredia) and zoledronate (Zometa)
induced avascular necrosis of the jaws: a growing epidemic
[Letter], J Oral Maxillofac Surg 61:1115-1118, 2003.
34. Ruggiero SL: Osteonecrosis of the jaws associated with the use
of bisphosphonates: a review off 63 cases, J Oral Maxillofac Surg
62:527-534, 2004.
35. Estilo CL et al.: Osteonecrosis of the maxilla and mandible in
patients treated with bisphosphonates: a retrospective study, J
Clin Oncol Proc Am Soc Clin Oncol 22:8088, 2004.
36. Marx RE: Bisphosphonate-induced exposed bone (osteonecro-
sis/osteopetrosis) of the jaws: risk factors, recognition, preven-
tion and treatment, J Oral Maxillofac Surg 63:1567-1575, 2005.
 CHAPTER 12 •
37. Migliorati CA et al.: Bisphosphonate-associated osteonecrosis
of mandibular and maxillary bone: an emerging oral complica-
tion of supportive cancer therapy, Cancer 104:83-93, 2005.
38. Purcell PM, Boyd IW: Bisphosphonates and osteonecrosis of
the jaw, Med J Aust 1825:417-418, 2005.
39. Baga JV et al.: Jaw osteonecrosis associated with bisphonates;
multiple exposed areas and its relationship to teeth extractions.
Study of 20 cases [Letter], Oral Oncol 42:327-329, 2006.
40. Pires FR et al.: Oral avascular bone necrosis associated with
chemotherapy and bisphosphonate therapy, Oral Dis 11:365-
369, 2005.
41. Woo SB, Hellstein JW, Kalmar JR: Systematic review: bisphos-
phonates and osteonecrosis of the jaws, Ann Intern Med
144:753-761, 2006.
42. Woo SB, Hande K, Richardson PG: Osteonecrosis of the
jaws and bisphosphonates [Letter], N Engl J Med 353:100,
2005.
43. Hohnecker JA: Novartis “Dear Doctor” precautions added to
label of Aredia and Zometa. Sept 24, 2004.
44. United States Food and Drug Administration Oncologic Drugs
Advisory Committee: Combidex briefing information. Avail-
able at www.fda.gov/ohrms/dockets/ac/05/ briefing/2005-4096B1.
htm Accessed on March 17, 2005.
45. United States Food and Drug Administration Office of Drug
Safety: Postmarketing safety review. Available at: www.fda.
gov/ohrms/dockets/ac/05/briefing/2005-4095B2_03_04-FDA-
TAB3.pdf Accessed on May 6, 2004.
46. Durie BGM, Katz M, Crowley J: Osteonecrosis of the jaws and
bisphosphonates [Letter], N Engl J Med 353:99, 2005.
47. Bamias A et al.: Osteonecrosis of the jaw in cancer after treat-
ment with bisphosphonates: incidence and risk factors, J Clin
Oncol 23:8580-8587, 2005.
48. Dimopoulos MA et al.: Osteonecrosis of the jaw in patients
with multiple myeloma treated with bisphosphates; evidence of
increase risk after treatment with zoledronic acid, Haematolog-
ica 91 [Epub ahead of print], 2006.
49. Dimopoulos M et al.: The incidence of osteonecrosis of the jaw
in patients with multiple myeloma who receive bisphospho-
nates depends on the type of bisphosphonate, Blood 106:637,
2005.
50. Tosi P et al.: Bisphosphonates and osteonecrosis of the jaws:
incidence in a homogeneous series of patients with newly diag-
nosed multiple myeloma treated with zoledronic acid, Blood
106:3461, 2005.
51. Pozzi S et al.: Analysis of frequency and risk factors for develop-
ing bisphosphonate associated necrosis of the jaw, Blood
106:5057, 2005.
52. Cafro AM et al.: Osteonecrosis of the jaw associated with
chronic bisphosphonates therapy: an Italian experience, Blood
106:5152, 2005.
53. Zavras AI, Zhu S: Bisphosphonate are associated with increased
risk for jaw surgery in medical claims data; is it osteonecrosis?
J Oral Maxillofac Surg 64:917-923, 2006.
54. Hoff AO et al.: Osteonecrosis of the jaw in patients receiving
intravenous bisphosphonate therapy, J Clin Oncol 2006 ASCO
Annual Meeting Proceedings (post meeting edition) 24:
8528, 2006. Available at http://meeting.jco.org/cgi/content/
abstract/24/18_suppl/8528 (Accessed Jan 23, 2007).
55. Kademani D et al.: Primary surgical therapy for osteonecrosis
of the jaw secondary to bisphosphonate therapy, Mayo Clin Proc
81:1100-1103, 2006.
56. Chhoeu AH et al.: A case series of hyperbaric oxygen treatment
for non-radiation induced osteonecrosis of the jaw, J Oral Max-
illofac Surg 64(Suppl):80-81, 2006.
57. Marx RE, Stern D: Oral and maxillofacial pathology: a ratio-
nale for diagnosis and treatment, 2003, Quintessence Publish-
ing, 388-389.
Complications of Dentoalveolar Surgery 221
58. Pogrel MA: Surgical complications: complications of third
molar surgery. In Kaban LB, Pogrel MA, Perrott DH, editors:
Complications in oral maxillofacial surgery, Philadelphia, 1997,
WB Saunders.
59. Gilbe GV, Fellingham FP: Repeated postextraction hemor-
rhage, Br Dent J 125:385, 1968.
60. Bjorlin G: Local fibrinolysis in the oral cavity, Scand J Hematol
33:411, 1984.
61. Nilsson IM: Local fibrinolysis as a mechanism for hemorrhage,
Thromb Diath Haemorrh 34:623, 1975.
62. Peterson LJ: Postoperative patient management. In Peterson LJ
et al., editors: Contemporary oral and maxillofacial surgery, ed 3,
New York, 1998, Mosby.
63. Fisher SE et al.: Factors affecting the onset and severity of pain
following the surgical removal of unilateral impacted mandibu-
lar third molar teeth, Br Dent J 164:351, 1988.
64. Messer EJ, Keller JJ: The use of intraoral dexamethasone after
extraction of mandibular third molars, Oral Surg Oral Med Oral
Pathol 40:594, 1975.
65. Neuper EA et al.: Evaluation of dexamethasone for reduction
of post surgical sequelae of third molar removal, J Oral Maxil-
lofac Surg 50:1177-1182, 1992.
66. Hooley JR, Francis FH: Betamethasone in traumatic oral
surgery, J Oral Surg 27:398, 1969.
67. Forsgre H et al.: Effect of application of cold dressing on the
postoperative course in oral surgery, Int J Oral Surg 14:223,
1985.
68. Sweet JB, Butter DP, Drager JL: Effects of lavage techniques
with third molar surgery, Oral Surg 41:152, 1976.
69. Butter DP, Sweet JB: Effect of lavage on the incidence of local-
ized osteitis in mandibular third molar extraction sites, Oral
Surg 44:14, 1977.
70. Archer WH: Complications associated with oral surgery, Philadel-
phia, 1975, WB Saunders.
71. Kerim O et al.: Accidental displacement of impacted third
molar into lateral pharyngeal space, Turkish J Med Sci 32:431-
433, 2002.
72. Patel M, Down K: Accidental displacement of impacted maxil-
lary third molars, Br Dent J 177:57-59, 1994.
73. Oberman M, Horowitz I, Ramon Y: Accidental displacement
of impacted maxillary third molars, Int J Oral Maxillofac Surg
15:756-758, 1986.
74. Gay Escoda C, Berini-Aytes L, Pinera-Penalva M: Accidental
displacement of a lower third molar, Oral Surg Oral Med Oral
Pathol 76:159-160, 1993.
75. Laskin DM: Oral and maxillofacial surgery, St Louis, 1985, CV
Mosby.
76. Dormer BJ, Babett JA: Root section in the submaxillary space,
Oral Surg Oral Med Oral Pathol 35:876, 1973.
77. Mellor TK, Finch DL: Displaced third molar, Oral Surg Oral
Med Oral Pathol 64:131, 1987.
78. Pedlar J: Crown of a tooth in the lateral pharyngeal space, Br
Dent J 161:335-336, 1986.
79. Peterson LJ: Contemporary oral and maxillofacial surgery, ed 2, St
Louis, 1993, CV Mosby.
80. Skjelbred P, Lokken P: Post-operative pain and inflammatory
reaction reduced by injection of a corticosteroid. A controlled
trial in bilateral oral surgery, Eur J Clin Pharmacol 21:391,
1982.
81. El Hag M et al.: The inflammatory effect of dexamethasone and
therapeutic ultrasound in oral surgery, Br J Oral Maxillofac Surg
23:17, 1985.
82. Forsgren H et al.: Effect of application of cold dressings on the
postoperative course in oral surgery, Int J Oral Surg 14:223,
1985.
83. Sweet JB, Butler DP, Drager JL: Effects of lavage techniques
with third molar surgery, Oral Surg 41:152, 1976.
222 SECTION II ■ Dentoalveolar Surgery
84. Butler DP, Sweet JB: Effect of lavage on the incidence of local-
ized osteitis in mandibular third molar extraction sites, Oral
Surg 44:14, 1977.
85. Rieder CE, Martinoff JT, Wilcox SA: The prevalence of
mandibular dysfunction, J Prosthet Dent 50:81, 1983.
86. Halfpenny W et al.: Comparison of 2 hemostatic agents for
the prevention of postextraction hemorrhage in patients on
anticoagulants, Oral Surg Oral Med Oral Pathol 92(3):259.
87. Bailey BMW, Fordyce AM: Complications of dental extrac-
tions in patients receiving warfarin anticoagulant therapy: a
controlled clinical trial, Br Dent J 155:308-310, 1983.
88. Martinowitz U et al.: Dental extraction for patients on oral
anticoagulant therapy, Oral Surg Oral Med Oral Pathol 70:274-
277, 1990.
89. DeClerck D, Vinckier F, Vermylen J: Influence of anticoagula-
tion on blood loss following dental extractions, J Dent Res
71:387-390, 1992.
90. Sindet-Pederson S et al.: The effect of tranexamic acid mouth-
wash in anticoagulant treated patients undergoing oral surgery,
N Engl J Med 320:840-843, 1989.
91. Throndson RR, Walstaad WR: Use of the argon beam coagula-
tor for control of postoperative hemorrhage in an anticoagu-
lated patient, J Oral Maxillofac Surg 57:1367-1369, 1999.
92. Rose SM, Rosenbloom B: Continued anticoagulant in oral
surgery procedures, Oral Surg Oral Med Oral Pathol 40:448-457,
1975.
93. Donoff RB: Massachusetts General Hospital manual of oral and
maxillofacial surgery, St Louis, 1987, CV Mosby.
94. Madura JA, Rookstool M, Wease G: The management of
patients on chronic Coumadin therapy undergoing subsequent
surgical procedures, Am Surg 60:542-546, 1994.
95. Johnson WT, Leary JM: Management of dental patients with
bleeding disorders: review and update, Oral Surg Oral Med Oral
Pathol 66:297-303, 1998.
96. Mulligan R, Weitzel KG: Pretreatment management of the
patient receiving anticoagulant drugs, J Am Dent Assoc 117:479-
483, 1988.
97. Hirsh J, Levine M: Confusion over the therapeutic range for
monitoring anticoagulant therapy in North America, Thromb
Haemost 59:129-132, 1988.
98. Poller L, Taberner DA: Dose and control of oral anticoagulant
therapy and its control: an international collaborative survey,
Br J Haematol 51:479-485, 1982.
99. Poller L: Laboratory control of anticoagulant therapy, Semin
Thromb Hemost 12:9-13, 1986.
100. British Medical Association and Royal Pharmaceutical Society
of Great Britain: British national formulary, no 39, London,
2000, The Pharmaceutical Press.
101. Devani P, Lavery KM, Howell CJT: Dental extractions in
patients on warfarin: is alteration of anticoagulant regime nec-
essary? Br J Oral Maxillofac Surg 36:107-111, 1998.
102. Hilfenhaus J, Weidman E: Fibrin glue safety: inactivation of
potential viral contaminants by pasteurization of the plasma
components, Arzneimittelforschung 11:1617-1619, 1985.
103. Libersa P et al.: Immediate and late mandibular fractures after
third molar removal, J Oral Maxillofac Surg 60:163-165, 2002.
104. Gulbrandsen SR, Jackson IT, Turlington EG: Recovery of a
maxillary third molar from the infratemporal space via a hemi-
coronal approach, J Oral Maxillofac Surg 45:279, 1987.
105. Oberman M, Horowitz I, Ramon Y: Accidental displacement
of impacted maxillary third molars, Int J Oral Maxillofac Surg
15:756, 1986.
106. Ziccardi VB, Assael LA: Mechanisms of trigeminal nerve inju-
ries, Atlas Oral Maxillofac Surg Clin N Am 9:1-11, 2001.
107. Hill CM et al.: Nerve morbidity following wisdom tooth
removal under local and general anaesthesia, Br J Oral Maxil-
lofac Surg 39:423-428, 2001.
108. Seddon HJ: Three types of nerve injury, Brain 66:237-288,
1943.
109. Sunderland S: A classification of peripheral nerve injury pro-
ducing loss of function, Brain 74:491-516, 1951.
110. Rajasuo A et al.: Bacteremia following surgical dental extrac-
tion with an emphasis on anaerobic strains. Available at www.
pubmed.gov (Accessed Sept 24, 2007).
111. Okabe K, Nakagawa K, Yamamoto E: Factors affecting the
occurrence of bacteremia associated with tooth extraction, Int
J Oral Maxillofac Surg 24(3):239-242, June 1995.
112. Reynolds DC: Special considerations in exodontics. In Kruger
GO, editor: Textbook of oral and maxillofacial surgery, ed 5, St
Louis, 1979, CV Mosby.

SKELETAL ANCHORAGE FOR
Bernard J. Costello • Ramon L. Ruiz • Joseph FA Petrone
Orthodontists have always tried to develop ways to move
teeth while minimizing the unwanted reciprocal movement of
the teeth they pull against. This constant battle is more easily
won when ideal anchorage is in place to move teeth in an
efficient manner. Whereas dental implants were used as abso-
lute orthodontic anchorage in the past, they had not become
popular for a number of reasons, including cost, time of
sequencing for osseointegration, and their primary use for
dental restoration purposes, not orthodontic mechanics. These
concepts of skeletal anchorage are not new, but have gained
more attention in the literature as a result of a number of
innovations in design and technique. Even as this chapter is
being written, advances in materials and technique are poised
to change how these procedures are planned and performed
in the near future. The reader is encouraged to review the
literature regularly because the pace of change is currently
rapid.
The goals of orthodontic therapy include optimizing occlu-
sion, aesthetics, and facial balance. Traditional orthodontic
mechanics are very efficient at accomplishing these goals for
clinical scenarios that require mild to moderate compensa-
tion. However, those patients that have more significant dis-
crepancies require additional techniques. This is most evident
to the oral and maxillofacial surgeon when one examines
patients with moderate to severe skeletal discrepancies. Some
of these patients who are beyond the envelope of discrepancy
for standard orthodontic therapy can be compensated by using
growth modification and/or orthognathic surgery in combina-
tion with comprehensive orthodontic therapy. Now patients
with moderate discrepancies may benefit from skeletal anchor-
age devices to further compensate for malocclusions that were
not heretofore possible to treat with traditional orthodontic
mechanics. Additionally a whole host of problems encoun-
tered by the orthodontist on a regular basis are now more
efficiently treated with skeletal anchorage as an adjunct to
traditional mechanics.
This chapter discusses the basic concepts of skeletal anchor-
age devices of various types and reviews the current literature
on their success. A primer on orthodontic mechanics is
required to adequately treat patients with skeletal anchorage
devices, and the reader is encouraged to review principles of
orthodontic mechanics in conjunction with this chapter.
Much like the concepts introduced during the beginnings of
orthognathic dentofacial teams, treatment that uses skeletal
anchorage requires interdisciplinary collaboration and plan-
CHAPTER 13
ORTHODONTICS
ning with regular interaction, continuing education, and a
regular review of the literature. This constant communication
between orthodontist and oral and maxillofacial surgeon is
necessary to achieve superior results.
■ HISTORY OF SKELETAL
ANCHORAGE FOR
ORTHODONTICS
Recent attention has increased the interest in orthodontic
skeletal anchorage, although the concepts of using implant-
able devices for orthodontic anchorage have been present for
at least one half of a century.1-5 Only recently have innova-
tions in materials, new outcome data, and improved tech-
niques thrust this concept forward as a more mainstream
option for treatment. In the 1940s, Gainsforth and Higley
experimented with Vitallium screws and wires in the dog
ramus used for skeletal anchorage.6 This initial experiment
was not considered a success.6 Linkow used blade-type implants
in the posterior mandible to apply Class II elastics for retrac-
tion of maxillary incisors.7 This cross-arch technique was
apparently successful, but has the disadvantage of requiring a
blade implant placement and its osseointegration before use
as an anchor. Sherman used dental implants in dogs for
anchorage with marginal success.8 In 1979, Smith noted that
dental implants could act like ankylosed teeth during orth-
odontic movement.9 In 1988, Sharpiro and Kokich discussed
how dental implants could be used for orthodontic anchorage
before their prosthodontic use, and a number of practitioners
used this technique from this point forward.10 In 1995, Block
and Hoffman used a hydroxyapatite-coated onplant placed in
the midline palatal tissues for use with an orthodontic anchor
device. This was moderately successful, but required the
orthodontist to rethink anchorage in terms of palatal mechan-
ics instead of what was typically used with brackets and
bands.11 Costa used titanium miniscrews borrowed from plating
fixation systems for orthodontic anchorage with some success.12
In 1999, Umemori et al. described techniques for using a
modified rigid fixation plate for use as orthodontic anchorage.3
This was a particular leap in innovation because the plating
system could be easily placed and significant force could be
used without loosening of the device. This had been a major
drawback of screw systems in the past. Sugawara et al. and a
number of other groups worldwide subsequently described a
number of interesting compensation techniques for a variety
223
224 SECTION II ■ Dentoalveolar Surgery
of problems that traditionally would have required orthogna-
thic surgery to treat effectively, such as the anterior open bite
and significant Class III deformity.3,4,13-17
■ BASIC ORTHODONTIC
MECHANICS AND SKELETAL
ANCHORAGE
To understand the indications for skeletal anchorage, the
practitioner placing the devices must have a baseline under-
standing of orthodontic mechanics to ensure superior results.
Planning for a team approach to a skeletal anchorage case is
in many ways similar to planning for orthognathic surgery.
Issues that arise in the preoperative, intraoperative, and post-
operative phases of treatment concern both the orthodontist
and surgeon. As such, constant collaboration must occur to
ensure the best outcomes.
Anchorage is the resistance to unwanted tooth movement.
Orthodontic tooth movement obeys Newton’s third law that
states that for every action, there is an equal and opposite
reaction. For every movement of a tooth in one direction,
the force is distributed to the anchorage segment, thus poten-
tially affecting the position of those teeth within the anchor-
age segment. If an orthodontist wishes to move a canine
posteriorly (distally) but only one molar is present, then the
molar will have a tendency to drift towards the mesial if the
molar is used as an anchor for that movement. However, if
more anchorage is provided to that area, then the movement
can occur without unwanted mesial movement of the
molar.
Skeletal anchorage devices do not allow faster movement
of teeth or the ability to overcome exceptionally large
discrepancies—the devices have limitations. However, they
do provide absolute anchorage for orthodontic movement and
do so in a number of novel ways. They allow for more efficient
movement of teeth and address a number of anchorage problem
areas that previously were difficult or impossible to resolve
with traditional orthodontic mechanics alone.
Anchorage can be provided using intraoral or extraoral
techniques. Intraoral techniques commonly use tooth-borne
appliances to improve anchorage. This can be achieved by
increasing the number of teeth in the anchorage unit. For
example, teeth can be tied together with ligature wire to resist
unwanted tooth movement in another area. Another way of
increasing teeth in the anchorage segment is to use a transpala-
tal arch. A transpalatal arch can be fabricated to distribute
force to another segment of teeth across the arch. Alterna-
tively, elastic bands can be used between the opposing arches
to provide additional anchorage. This technique is commonly
used to close space after maxillary premolar extraction by
retracting the anterior dentition of the maxilla with elastic
bands bilaterally and attaching the elastic to the maxillary
posterior teeth. These Class II elastics also help to minimize
the unwanted mesial movement of the maxillary posterior
anchorage segments. This technique is based on compliance
and can be ineffective if the patient does not wear the elastics
regularly.
Another way to provide maximum anchorage to the pos-
terior teeth is to use a Nance button appliance that holds the
posterior molars in position with an acrylic button on the
anterior palate. Force can then be applied to the posterior
teeth to close premolar space, and the tendency for the molar
teeth to move mesially is resisted by the acrylic button on the
palate near the incisive foramen. These appliances may irri-
tate the tissue and become uncomfortable. Extraoral appli-
ances, such as headgear, can also be used to provide additional
anchorage, but are often subject to compliance issues and
rarely offer more than 6 to 10 hours of force per day. They are
also not readily accepted by some patients, particularly
adults.
Skeletal anchorage appliances provide anchorage that is
not tooth-borne, but rather based on stability within the bone.
These devices are advantageous for a number of reasons,
including:
• No or minimal reliance on existing dentition
• Patient compliance is not required
• Continuous rather than intermittent force may be
applied
• Surgical procedures are necessary, but they are simple in
most instances
• May be significantly less expensive than other surgical
options, such as orthognathic surgery
• Force may be applied very soon or immediately after
placement of the device
• The devices are easily removed
The anchorage applied may be considered direct or indirect.
Direct techniques are those that apply force directly from the
anchor to the segment that is to be moved. For example, maxil-
lary plates placed at the zygomatic buttresses may be designed
to provide intrusion force to the maxillary molars with the
intent of closing an anterior open bite. This would be a direct
technique because the force is applied from the anchor directly
to the molar teeth. Indirect techniques tie the anchor device
to the segment of teeth that requires more anchorage so that
more traditional mechanics can be used in the area. Rather
than an active, elastic connection between the anchor and the
archwire, indirect anchorage involves an inelastic or even rigid
connection between the anchor and the orthodontic appli-
ances. For example, if a maxillary anchor is tied by a steel
ligature to the anterior teeth to provide more anchorage to
that segment, a coil spring could be used on the archwire to
distalize the molar teeth. This would represent an indirect
technique because the force used is along the archwire via the
coil spring and represents a traditional type of mechanics in
orthodontics. The advantage to the indirect technique is
that most orthodontists already design their movements of
teeth based on traditional mechanics. Providing additional
anchorage via a skeletal device simply increases efficiency
without necessitating a new appliance design or vectors and
moments difficult to achieve in commonly used orthodontic
techniques. Either a direct or indirect technique can be used
in most situations, and each case requires careful planning to
ensure ideal placement of the anchor for these purposes.
 CHAPTER 13 •
Skeletal anchorage devices allow orthodontic movements
to be designed that were previously thought to be difficult, if
not impossible. Thus, compensation beyond the typical enve-
lope of discrepancy is possible for many clinical indications.
■ DEVICES FOR SKELETAL
ANCHORAGE
A number of devices have been used to provide additional
anchorage for orthodontic purposes. As mentioned earlier, the
early attempts that were successful used dental implants placed
with the intention of using them for total skeletal anchorage.
These had the significant drawback of requiring osseointegra-
tion before use in addition to the high cost. They also required
aggressive surgery for removal. Although some could be kept
in place for prosthetic use, it was often difficult to determine
the exact position required at the end of orthodontic treat-
ment when placing them for anchorage purposes before treat-
ing the malocclusion. Consequently, the implants were often
not in ideal position for the final crown or prosthesis, either
rendering them useless or requiring specialized prosthodontic
techniques to compensate for poor position.
Various dental implants, including miniature dental
implants, were used in a similar fashion and placed in the
retromolar region for anchorage purposes.8,18 These also
required osseointegration before use and surgical removal and,
thus, had the same types of drawbacks. Similar devices con-
tinue to be used in the palate, either in the midline or para-
sagittal to the midline. The anatomy in this region does not
support full bony integration of an implant in most instances.
Midline insertion into the septum may provide initial stabil-
ity, but may also create problems at the septum, such as septal
perforation, either at the time of placement or at the time of
removal. If the implants are placed parasagittally, a fistula may
result when the implant is removed as a result of the thin bone
in this region of the nasal floor and hard palate.
An attempt to get around these inadequacies of the endos-
seous implant approach was the onplant system with attach-
ments that would penetrate through the palatal tissues for
orthodontic anchorage. These onplants were coated with tita-
nium or hydroxyapatite in the hope of osseointegration after a
small palatal incision was made for a subperiosteal placement.
Long-term outcomes of this technique have not been reported,
and it has mostly been supplanted by single screws or plates at
other locations. As with any palatal implant, the additional
drawback of redesigning orthodontic mechanics around a
device positioned on the palate requires significant planning
by the orthodontist in a manner that is not conventional.
Placement of a bone screw for orthodontic mechanics has
been described using a number of different screw devices.10,14,19,20
Recently, there has been an explosion of these screws com-
mercially available for use. Originally, fixation screws used for
craniomaxillofacial surgery were placed and then attached to
the orthodontic appliance for use as additional anchorage.
Other screw systems used for alternative purposes, such as
maxillomandibular fixation, were modified for use as skeletal
anchorage. Eventually, screws specifically designed for use in
Skeletal Anchorage for Orthodontics 225
FIGURE 13-1. A maxillary anchor screw is used to provide anchorage to
the anterior dentition because of a lack of anchorage in the right posterior
maxilla. This will allow the orthodontist to distalize the premolars and canines
to treat the crowding of the anterior dentition while preserving the dental
midline. To view a color version of this illustration, refer to the color insert
section at the back of this book.
orthodontic skeletal anchorage were manufactured with ver-
satile orthodontic attachments to optimize their use (Figure
13-1). Both self-tapping and self-drilling systems are currently
available.
Screws are typically manufactured in multiple lengths for
a number of indications. Short screws can be used, but fail
more often as a result of minimal bone-to-screw interface.
Screws that engage cortical bone across the alveolus tend to
have more stability, and this technique requires longer screws
(8 to 12 mm). The thread pitch should also be ideal for the
type of bone in this area, and typically is approximately
0.6 mm. The attachments come in a variety of designs. We
prefer an attachment that allows for placement of a ligature,
elastomer chain, or wire. Although a number of entities man-
ufacture screws, it is very important to consider the quality of
the titanium used and the highly engineered aspects of the
screw. Poorly made devices are prone to fracture, and it is
recommended that surgeons use devices with proven use in
these indications. Devices should:
• Be designed for the purpose of skeletal orthodontic
anchorage
• Have a very high quality of manufacturing with stan-
dardized quality control
• Have an appropriate pitch thread to ideally engage bone
• Have the appropriate core and external diameter to
withstand orthodontic forces in maxillary and mandibu-
lar bone
• Be designed well at the runout and shaft-head interface
to prevent fracture
Screws that are smaller than 1.5 mm tend to fail much
more often and are not recommended for indications that
require significant force. Additionally, screws with bracketlike
head designs offer little advantage to more simple attach-
ments, which tend to be more versatile. Bracketlike
226 SECTION II ■ Dentoalveolar Surgery
FIGURE 13-2. A maxillary anchor plate is placed along the left maxillary
buttress. This allows placement of three or four monocortical screws away
from the tooth roots and placement of the orthodontic attachment in an ideal
position for intrusion of the maxillary molars. To view a color version of this
illustration, refer to the color insert section at the back of this book.
attachments require specialized custom bending of the orth-
odontic wire and often will fail with minimal torque or a force
that rotates the screw in the counterclockwise direction, thus
loosening it. The indications, success rates, and limitations of
screws used for skeletal anchorage are discussed later.
Plate systems were originally used by Sugawara and others
to provide additional three-dimensional stability and, thus,
increase the success rates over the long term. Originally, these
were modified fixation plates used for Le Fort osteotomies and
facial trauma repair.3,4 Eventually, custom-designed plating
systems specifically indicated for skeletal orthodontic anchor-
age were developed.4,13,21-25 Skeletal anchorage plates have the
advantage of increased stability, allowing the use of greater
force. They do not require osseointegration and can be loaded
immediately. The plates typically allow for placement of mul-
tiple small screws away from the tooth roots, thus preventing
injury (Figure 13-2). Skeletal anchorage plates are also easy
to remove, but require an additional incision and dissection.
CLINICAL INDICATIONS
Skeletal anchorage devices may be used in many different
applications to provide anchorage and optimize the efficiency
of tooth movement. The authors prefer plates over screws to
provide anchorage in an indirect manner when possible.
Direct anchorage techniques may also be helpful. Some exam-
ples of common uses of skeletal anchorage follow, and new
applications are being investigated on a regular basis.
■ MESIAL OR DISTAL MOVEMENT
OF TEETH WITH MAXIMAL
ANCHORAGE
The need to move posterior teeth in the mesial direction is
difficult because of a lack of anchorage from the anterior
FIGURE 13-3. A patient who has lost the lower primary first molars has
good position of the canines (Class I) and lacks enough anchorage posteriorly
to close the space without the unwanted distal movement of the canines. This
is a frequent problem for orthodontists who need to close space with maximum
anchorage. Anchorage plates or screws can provide absolute anchorage to
close the space efficiently without unwanted tooth movements.
segment.4,24,25 For example, when an overretained primary first
molar is extracted and the succedaneous permanent first bicus-
pid is missing, the orthodontist may choose to move the
remaining posterior tooth or teeth to the mesial to close the
space of the primary first molar (Figure 13-3). This is often
difficult because the anterior segment of teeth will have a
tendency to move to the posterior (distal) and subsequently
change the canine position to Class II. To maintain the posi-
tion of the anterior teeth including the Class I canine, a
skeletal anchor(s) may be placed to provide either indirect
anchorage with a rigid attachment to the anterior segment or
direct anchorage with an active attachment to the molar
segment. This will allow for more efficient movement of the
posterior molars to close the space, without losing the position
of the canine or disrupting the overbite and/or overjet rela-
tionship of the incisors. A variety of tooth movements are
possible, including distalizing the maxillary teeth to improve
a Class II relationship14,25 (Figures 13-4 and 13-5).
Alternatively, if a patient has a similar scenario but in Class
III, the orthodontist may choose to compensate by providing
maximum anchorage to the posterior teeth or distalize molar
teeth.26 This will allow the anterior dentition to be retracted
and close the space while providing maximum anchorage to
the distal (posterior) segment of teeth. Without skeletal
anchorage, this may be difficult to achieve because the poste-
rior teeth will have a tendency to move toward the mesial
using traditional mechanics (Figure 13-6).
It follows how this can be helpful after extraction of pre-
molars if the orthodontist wishes to close the space with
maximum anchorage in either segment. Although this is easily
done with traditional orthodontic mechanics, in certain
instances when anchorage is lacking or maximum anchorage
is desired, skeletal anchorage appliances can be used.
Text continued on p. 232
 CHAPTER 13 • Skeletal Anchorage for Orthodontics 227

A B

FIGURE 13-4. A patient with a significant Class II relationship who is unwilling to undergo orthognathic surgery
has upper first premolar extractions and lower second premolar extractions in preparation for orthodontic therapy. The
space in the maxilla is closed with the aid of anchor screws, which allow for closure of the space by bodily moving the
anterior centrals, laterals, and canines en masse. A-C, Preoperative occlusion photos. D, Preoperative lateral cephalo-
metric radiograph. E-G, Postoperative occlusion photos after 6 months of orthodontic therapy with closure of the space
and improvement of the Class II relationship. The force is generated at the optimized vector to allow for efficient
movement.
228 SECTION II ■ Dentoalveolar Surgery

A B

C
FIGURE 13-5. A patient with Noonan’s syndrome who has a skeletal Class II relationship. His behavioral issues
and bleeding disorder (both associated with his syndrome) make him a poor candidate for orthognathic or other cranio-
facial procedures. His Class II is compensated by distalizing the entire maxillary dentition with two skeletal anchors placed
in the posterior maxilla. Over time he develops a Class I relationship. At the time of the anchor placement, a genioplasty
is performed to balance his facial profile. A, B, Preoperative facial photographs. C, Cephalometric tracing showing a sig-
nificant Class II relationship that would typically be treated with orthognathic surgery.
 CHAPTER 13 • Skeletal Anchorage for Orthodontics 229

D E

F G

H I

FIGURE 13-5, cont’d. D, E, Photographs of the anchors in place after several weeks with minimal inflammation.
F, G, Photographs of the progression of treatment over 9 months as the Class II discrepancy improves. H, I, Posttreat-
ment facial photographs. To view a color version of this illustration, refer to the color insert section at the back
of this book.
230 SECTION II ■ Dentoalveolar Surgery

A B

D E

FIGURE 13-6. A 21-year-old female is shown with an asymmetric Class III relationship, but without significant
transverse discrepancy. She was unwilling to consider an orthognathic surgery treatment option, so one skeletal anchor
plate was placed in the posterior right mandible to bring the entire mandibular dentition to her right. This allowed for
distal movement of most of the mandibular arch of teeth and establishment of a Class I canine relationship. A-E, Pre-
treatment photographs. F, Mandibular anchor plate in place with orthodontic anchorage activated.
 CHAPTER 13 • Skeletal Anchorage for Orthodontics 231

H I

J K

FIGURE 13-6, cont’d. G-K, Posttreatment photographs.

232 SECTION II ■ Dentoalveolar Surgery
■ UPRIGHTING AND/OR INTRUDING
MOLAR TEETH
One of the more difficult movements in orthodontic treat-
ment is uprighting a molar tooth that has moved mesially into
an edentulous space. Most often this occurs in the adult
patient who has lost the first molar to caries, and the second
molar tips mesially over a period of time. Subsequent to this
event, if a patient presents for orthodontic treatment, it may
be very difficult to upright the second molar without extruding
the tooth and opening the patient’s bite.14,15,22 With the use
of a skeletal anchor, the tooth may be uprighted and intruded
in a much more efficient fashion.
Another difficult problem to remedy is the overerupted
maxillary or mandibular tooth that is in poor position as a
result of an edentulous space in the opposite arch. Intruding
teeth in this situation is exceptionally difficult using tradi-
tional orthodontic mechanics. However, the use of a skeletal
anchorage device(s) makes intrusion a relatively easy orth-
odontic movement.22 This technique may be used in the ante-
rior or posterior dentition. Patients who have a deep Class II
relationship with excessive overbite can have their anterior
maxillary dentition intruded and retropositioned to improve
the overbite and/or overjet relationship. Typically, this is
done with an intrusion arch or other traditional mechanics,
such as headgear. With skeletal anchorage devices, this is
made much more efficient and also requires very little compli-
ance from the patient.
■ CLOSURE OF ANTERIOR
OPEN BITE
There has been a great degree of excitement generated by the
initial reports of anterior open bite closure with orthodontic
anchorage appliances.* Typically, this is performed by placing
orthodontic plates or screws in the posterior maxilla apical to
the dentition. Force is then generated to intrude the posterior
molars and premolars as necessary to close the anterior open
bite. A number of case reports have shown this to be success-
ful. Excitement has grown in this area because of the difficulty
typically encountered with orthodontic-only closure of the
anterior open bite and the subsequent relapse that often
occurs. The alternative, of course, is orthognathic reposition-
ing with the presumed improvement in stability. Although it
is reported to be stable in case reports and a few case series
publications, there is no long-term database on stability of
these procedures as there has been for orthognathic surgery.
For this reason, the authors prefer to use this technique for
those patients who cannot or will not undergo orthognathic
surgery and for those patients who have minimal open bites.
Patients who have already failed orthodontic treatment for
closure of their open bites may be good candidates for this
procedure, but retreatment does come with additional risk,
such as root resorption. Patients should be cautioned regarding
*References 3, 4, 13, 16, 22, 27-29
the expectations of outcome over the long term. Hopefully,
more data will become available to assess the safety, efficacy,
and long-term stability of this treatment option.
■ ORTHOPEDIC GROWTH
MODIFICATION
An area of considerable controversy is the use of skeletal
anchorage to provide forces for orthopedic growth modifica-
tion in a manner similar to the use of headgear appliances.
This has been used in children during phase I orthodontic
therapy. For patients with a Class III skeletal pattern (midface
hypoplasia and/or mandibular prognathism), skeletal anchors
can be placed in the mandible to provide force to the maxilla
and encourage a more Class I relationship.30 This is similar to
reverse-pull headgear without the need for an external appli-
ance. Obviously, this would improve the mechanics by ensur-
ing constant force rather than relying on the patient to wear
the appliance only for a prescribed time.
Although the concept has been reported in the literature,
there is little evidence of its efficacy or safety. Practitioners
must be careful to avoid developing tooth structures and mini-
mize surgical procedures in this growing population so as to
not hamper tooth or bone growth and development. More
literature is necessary before practitioners can support the
widespread use of this technique.
SURGICAL PROCEDURES
The application of temporary anchorage devices for orthodon-
tic treatment usually requires only a minor surgical procedure.
The exact type of anchor (miniscrew or specialized anchor
plate), location, and angle of the device will be determined
by the orthodontic treatment plan. Preoperative planning
requires a careful clinical examination, panoramic radiograph,
and communication between the orthodontist and surgeon.
■ PLACEMENT OF SKELETAL
ANCHORAGE PLATES
Bone plates used for anchorage during orthodontic treatment
can be placed in a variety of anatomic locations within the
maxillary and mandibular arches. These devices typically
consist of a bone plate with holes for screw placement and a
transmucosal connecting arm, which extends from the plate
to a specialized working end. The working end of the appli-
ance allows for the attachment of wire, springs, elastics, and
other orthodontic constructs.
Within the maxillary arch, the anchor plate is typically
placed within one of the vertical buttresses of the midface
(e.g., zygomaticomaxillary buttress or piriform buttress) where
the bone thickness allows for adequate mechanical stability
using monocortical screws. The anterior maxillary wall is
avoided because of the thin cortical bone that is present
directly over the maxillary sinuses. These considerations are
reminiscent of the rationale applied when placing maxillary
bone plates within the piriform and zygomatic buttresses
during orthognathic surgery and the repair of midfacial
fractures.
 CHAPTER 13 •
A unattached tissues of the maxillary vestibule, increased irrita-
B In cases where the bone plate is positioned directly over the
C in combination with light conscious sedation may be prefera-
FIGURE 13-7. A-C, Maxillary anchor plate procedure. A small l-shaped
incision is used at the mucogingival junction to allow for placement of an
anchor plate. Three screws or more are placed with appropriate positioning for
the indicated orthodontic mechanics. Closure is achieved with resorbable
suture.
The procedure is easy to perform for most patients (Figures
13-7 and 13-8). First, a vertical incision, approximately 8 to
10 mm in length, is created from the mucogingival junction
superiorly into the maxillary vestibule. A small horizontal
releasing incision is often added along the mucogingival line
to improve direct visualization and minimize retraction-related
trauma to the soft tissues during anchor placement. A perios-
teal elevator is used to develop a full-thickness mucoperiosteal
Skeletal Anchorage for Orthodontics 233
flap exposing the underlying skeletal buttress. The anchor
device is carefully adapted so that the plate and connecting
bar closely follow the contour of the underlying cortical bone
of the zygomaticomaxillary or piriform buttress region. Care
should be taken to avoid any dead space or gaps between the
bone and the implanted portion of the device. Another criti-
cal technical consideration is the location of the connecting
bar as it exits the subperiosteal pocket and enters into the oral
cavity. The transmucosal position of the connecting bar
should be located at approximately the mucogingival junc-
tion. Nonkeratinized mucosal tissues should be avoided. When
the transmucosal location of the connecting bar is within the
tion, inflammation, infection, and soft tissue overgrowth may
result. Once the anchor has been appropriately contoured and
positioned, it is secured using self-drilling or self-tapping
monocortical screws. The incision is irrigated, and soft tissue
closure is carried out using resorbable suture material.
In contrast with the maxilla, the facial cortex of the man-
dible is composed of dense bone that allows for stable place-
ment of skeletal anchorage devices. Despite the favorable
cortical nature of the mandible, however, specific, key ana-
tomic structures including the mental foramen and nerve and
the mandibular canal must be avoided during placement.
Placement of anchors in the mandible is most frequently
carried out within the symphysis, posterior body, and ramus.
mandibular canal, monocortical screws should be used to
prevent injury to the inferior alveolar neurovascular bundle.
When skeletal anchorage plates are used, the bone plate
portion of the device is positioned away from the tooth root(s).
Even in certain cases where the bone plate must be placed in
closer proximity to the adjacent teeth, the risk of damage to
the underlying root structure remains very low. The use of
short bone screws that engage only the outer (facial) cortex
prevents damage to dental structures and allows for the orth-
odontic movement of teeth with minimal risk of hardware-
related impingement on the roots.
The placement of a skeletal anchorage plate is usually
carried out using local anesthesia. The use of local anesthesia
ble depending on the specific surgical plan, the number of
anchors being placed, and patient preference.
■ PLACEMENT OF MINISCREWS
FOR SKELETAL ANCHORAGE
Skeletal anchorage miniscrews are placed near or at the muco-
gingival junction and engage the cortical and cancellous bone
layers. Because the entire anchorage device is dependent on
the stability of the single screw, the longest length possible is
usually placed. In the maxillary arch, placement can be under-
taken at the buttresses (i.e., zygomatic or piriform), the hard
palate, or within the alveolar process in between tooth roots.
Within the mandible, placement can be undertaken along the
alveolar process at the mucogingival junction, the symphysis,
and within the retromolar pad region. Because the screws
234 SECTION II ■ Dentoalveolar Surgery

A
FIGURE 13-8. A-D, Mandibular anchor plate procedure. A small linear or l-
shaped incision is used to position the plate in a manner ideal for orthodontic
mechanics of the specific case. The incision is placed at or near the mucogingival
junction if possible to prevent inflammation. Closure is achieved with resorbable
B suture.

extend into the trabecular bone, the subsequent orthodontic
movement of tooth roots must be anticipated.
The surgical procedure for placement of miniscrews is min-
imally invasive and does not typically require the elevation of
a soft tissue flap. Local anesthesia is used and a simple infiltra-
tion is usually adequate for placement of a single bone screw.
In areas where a more pronounced tissue depth or thick fibrous
tissue is encountered, a small tissue punch or surgical blade
may be used to create a small puncture site for introduction.
A number of self-drilling screws are available, which allow for
placement of the anchor screw without the creation of a pilot
hole within the outer cortex of the maxilla. When anchor
screw placement is undertaken within the mandibular arch,
the use of self-drilling screws is generally avoided. The density
and thickness of the mandibular cortical plate may cause frac-
ture of the screw when a self-drilling anchor is used. Instead,
a pilot drill is made using the surgical hand piece, and a self-
tapping anchorage screw is placed.
POSTOPERATIVE REGIMEN
Postoperative radiographs should be obtained to confirm the
position of the skeletal anchorage devices relative to the sur-
rounding anatomic structures. A panoramic radiograph is
usually adequate. In cases where miniscrews are placed in
between teeth, periapical radiographs may be useful in exam-
ining the proximity of adjacent tooth roots.
Because the implants used for skeletal anchorage are trans-
mucosal and involve a portion of hardware that remains
 CHAPTER 13 •
exposed to the oral cavity, antiinfective coverage is employed
during the postoperative phase. Patients are given a 5-day
course of oral antiinfectives following surgical placement. The
most commonly used agents include penicillin, amoxicillin,
and clindamycin. In addition, meticulous oral hygiene and
chlorhexidine oral rinses during the first week after surgery
dramatically reduce the amount of soft tissue inflammation
and risk of infection.
Pain and discomfort following miniscrew placement is gen-
erally minimal. Patients undergoing anchor plate placement
may require a short course of analgesic coverage because the
procedure involves the creation of an incision and greater soft
tissue dissection. Patients may also report cheek irritation,
which tends to peak at approximately 10 days following surgery
before resolving.
Because temporary anchorage devices require primary
mechanical stability and not osseointegration, they may be
used for orthodontic treatment immediately following surgical
placement. Miniscrews may be activated immediately after
surgical placement. Application of full orthodontic force using
a skeletal anchorage plate is usually delayed for 7 to 10 days
following placement. This allows for adequate healing at the
site of the mucoperiosteal flap and at the soft tissue of the
mucogingival junction where the connecting bar is located.
■ OUTCOMES AND
COMPLICATIONS
Although, in general, the procedures described previously are
very successful, the overall success rate of screw and plate
systems warrant a special discussion. There is considerable
variation in the reported success of these techniques and a
number of opinions regarding the exact indications for the
choice of plates over screws in a given clinical situation.
Placement of a screw or plate system is associated with few
complications, but the surgeon must be aware of those rare
occurrences that can create issues for patients. Problems
related to skeletal orthodontic anchorage appliances are typi-
cally screw, patient, or operator related.
The overall success rates vary between devices rather dra-
matically. A number of reports have listed loosening or out-
right failure of orthodontic anchorage screws to be above
15%.* In some indications and anatomic locations, the rate
of loosening of the screw is higher than 30%. As might be
expected, the rate of failure of plates is considerably lower
with failure rates below 5%.4,23,24,27 It is important to recognize
that most of the data published are reported by the individuals
who placed and used the devices, and the definition of failure
may vary. There is an inherent self-reporting bias with such
literature. Plate systems obviously offer a greater degree of
three-dimensional stability and a higher integration with the
bone structure because of the multiple screws used for fixation.
Consequently the authors tend to use bone plates more often
than screws for cases that require longer treatment times and/
or greater forces. Many surgeons and orthodontists believe
*References 12, 14, 19, 20, 23, 31, 32, 33, 34
Skeletal Anchorage for Orthodontics 235
plates to be more stable, but they often are concerned regard-
ing the additional incision and dissection required for place-
ment despite the minor nature of the procedure.35
Complications related to the device itself can occur as a
result of device failure (fracture), loosening associated with a
design flaw, or infection. Most devices are made of a titanium
alloy that is of sufficient quality to prevent deformation of the
threads, breakage of the screw head or shaft, or fragmentation
of the metal during placement with the driver. Manufacturers
with experience manufacturing plates and screws rarely
encounter issues with material failure because of the extensive
experience with materials used in rigid internal fixation.
However, if the titanium is not sufficiently strong or the man-
ufacturing process for producing the screw has flaws, the screw
or plate may be more likely to break or fatigue quickly. This
can lead to device failure. Screws that are designed with
appropriate pitch thread for the soft bone of the maxilla may
also fail because of a lack of contact with cortical bone. This
is also true if the runout of the screw is particularly long
because the screw threads will not interface with adequate
cortical bone for stability. The screw will prematurely loosen
in this setting. Although infection is rare in this area, it does
occur in rare instances, and the devices should be sterilized
before insertion.
Operator-related complications can also occur for a variety
of reasons. Small screw systems require very careful placement,
and a fine tactile sense is necessary to avoid stripping the
bone-screw interface during placement. Overworking the
screw material can also lead to failure. Poor stability can also
occur as a result of a poor choice of placement, such as in the
midmaxillary antral sinus wall. Bone is not adequate in this
area to support fixation in most patients, and individual screws
or plates are prone to failure. Most screws and the working
attachments of plates should enter the oral cavity within
attached mucosa, if possible. Significant inflammation, pain,
and even infection may result if moveable mucosa surrounds
the screw head or working end of an anchor plate system.
The device must be placed in a location that is helpful for
the orthodontic mechanics required by the orthodontist. This
should be the case throughout the entire treatment period.
For example, if a screw is placed within alveolar bone to allow
for distal movement of teeth just anterior to that screw, the
eventual location of those teeth should be anticipated after
they are moved. Will the device be in the way of moving
teeth? Will it need to be replaced? Is it far enough away from
the point of attachment to allow for all of the movement
necessary throughout the case? All of these questions should
be addressed at the treatment planning stage before surgical
placement of the device to avoid the need for additional
surgery.
One area requiring special attention is that of root damage
from either placement of a screw or the drilling process. Sur-
geons who are comfortable with the anatomy of these regions
typically do not have issues with root damage, but this may
still occur as a result of anatomic variation or other causes.
Thankfully, roots have excellent recuperative power that
236 SECTION II ■ Dentoalveolar Surgery
allows for revascularization if a minimal insult occurs. If a
device has been placed and the screw is in contact with the
root of a viable tooth, then the patient typically will experi-
ence discomfort during mastication. Moving the root away
from the implant will typically relieve this discomfort, or the
device can be replaced in a new location.
A number of patient-related complications can occur.
Patients must have good quality bone to accept the devices
and have reasonable hygiene. Quality cortical bone is a neces-
sity for long-term stability of the anchors. Patients who have
systemic disorders that affect bone or mucosal healing are not
good candidates for these procedures. Likewise, those patients
who have undergone radiation therapy in the region or are
taking bisphosphonate medications are not good candidates.
Those patients that smoke are also prone to mucosal break-
down, infection, and failure of the devices.
■ SUMMARY
Skeletal anchorage devices allow orthodontic movements
that were previously thought to be difficult if not impossible.
The devices do not accelerate tooth movement, but do provide
more efficient mechanisms for moving teeth in a number of
situations. Additionally, unwanted reciprocal tooth move-
ments are minimized or prevented. An additional advantage
is the use of mechanics for which the success is not based on
compliance factors such as with headgear or elastic band
therapy that require patient placement and removal. Multiple
applications, devices, and technique innovations are evolving.
Caution is warranted for some applications because long-term
outcome data are not available at this time. Hopefully, addi-
tional outcome data will become prevalent and help us decide
how skeletal anchorage fits in best with our armamentarium
of treatment choices for significant skeletal and dental
discrepancies.
REFERENCES
1. Park HS, Kim JB: The use of titanium microscrew implant as
orthodontic anchorage, Keimyung Med J 18:509-515, 1999.
2. Park HS et al.: Microimplant anchorage for treatment of skeletal
class I bialveolar protrusion, J Clin Orthod 35:417-422, 2001.
3. Umemori M et al.: Skeletal anchorage system for open-bite cor-
rection, Am J Orthod Dentofacial Orthop 115:166-174, 1999.
4. Sugawara J: Dr. Junji Sugawara on the skeletal anchorage system,
J Clin Orthod 33:689-696, 1999.
5. Bae SM et al.: Clinical application of micro-implant anchorage,
J Clin Orthod 36:298-302, 2002.
6. Gainsforth BL, Higley LB: A study of orthodontic anchorage
possibilities in basal bone, Am J Orthod 31:406-417, 1945.
7. Linkow LI: The endosseous blade implant and its use in ortho-
dontics, J Orthod 18:149-154, 1969.
8. Sherman AJ: Bone reaction to orthodontic forces on vitreous
carbon dental implants, Am J Orthod 74:79-87, 1978.
9. Smith JR: Bone dynamics associated with the controlled loading
of bioglass-coated aluminum endosteal implants, Am J Orthod
76:618-636, 1979.
10. Shapiro PA, Kokich VG: Uses of implants in orthodontics, Dent
Clin North Am 32:539-550, 1988.
11. Block MS, Hoffman DR: A new device of absolute anchorage
for orthodontics, Am J Orthod Dentofacial Orthop 107:251-258,
1995.
12. Costa A, Raffini M, Melsen B: Microscrew as orthodontic
anchorage, Int J Adult Orthod Orthognath Surg 13:201-209,
1998.
13. Sherwood K: Closing anterior open bites by intruding molars
with titanium miniplate anchorage, Am J Orthod Dentofac Orthop
122:593-600, 2002.
14. Sung J et al.: Microimplants in orthodontics, Dentos Daegu, Korea,
2006, Needham Press.
15. Park HS, Kyung HM, Sung JH: A simple method of molar
uprighting with micro-implant anchorage, J Clin Orthod 36:592-
596, 2002.
16. Park HS: Clinical study of the success rate of microscrew implants
for orthodontic anchorage. Korean J Orthod 33:151-156, 2003.
17. Woo SS et al.: A clinical study of the skeletal anchorage system
using miniscrews, J Korean Oral Maxillofac Surg 29:102-107,
2003.
18. Roberts WE et al.: Osseous adaptation to continuous loading of
rigid endosseous implants, Am J Orthod 86:95-111, 1984.
19. Tseng YC et al.: The application of mini-implants for orthodon-
tic anchorage, Int J Oral Maxillofac Surg 35:704-707, 2006.
20. Cornelis MA, De Clerck HJ: Maxillary molar distalization with
miniplates assessed on digital models: a prospective clinical trial,
Am J Orthod Dentofac Orthop 132(3):373-377, 2007.
21. Jenner JD, Fitzpatrick BN: Skeletal anchorage utilising bone
plates, Aust Orthod J 9(2):231-233, 1985.
22. Sherwood K: Intrusion of supererupted molars with titanium
miniplate anchorage, Angle Orthod 73(5):597-601, 2003, 2002.
23. Cornelis MA et al.: Systematic review of the experimental use
of temporary skeletal anchorage devices in orthodontics, Am J
Orthod Dentofac Orthop 131(suppl 4):S52-528, 2007.
24. Cornelis MA, De Clerck HJ: Biomechanics of skeletal anchor-
age. Part 1. Class II extraction treatment, J Clin Orthod 40(4):261-
269, 2006.
25. De Clerck HJ, Cornelis MA: Biomechanics of skeletal anchor-
age. Part 2. Class II nonextraction treatment, J Clin Orthod
40(5):290-298, 2006.
26. Sugawara J, Daimaruya T, Umemori M: Distal movement of
mandibular molars in adult patients with the skeletal anchorage
system, Am J Orthod Dentofac Orthop 125(2):130-138, 2004.
27. Sugawara J: Treatment and posttreatment dentoalveolar changes
following intrusion of mandibular molars with application of a
skeletal anchorage (SAS) for open bite correction, Int J Adult
Orthod Orthognath Surg 17(4):243-253, 2002.
28. Kuroda S et al.: Treatment of severe anterior open bite with
skeletal anchorage in adults: comparison with orthognathic
surgery outcomes, Am J Orthod Dentofac Orthop 132(5):599-605,
2007.
29. Erverdi N, Keles A, Nanda R: The use of skeletal anchorage in
open bite treatment: a cephalometric evaluation, Angle Orthod
74(3):381-390, 2004.
30. Kircelli BH, Pektas ZO, Uckan S: Orthopedic protraction with
skeletal anchorage in a patient with maxillary hypoplasia and
hypodontia, Angle Orthod 76(1):156-163, 2006.
31. Miyawaki S et al.: Factors associated with the stability of titanium
screws placed in the posterior region for orthodontic anchorage,
Am J Orthod Dentofac Orthop 124(4):373-378, 2001.
32. Liou EJ, Pai BC, Lin JC: Do miniscrews remain stationary under
orthodontic forces? Am J Orthod Dentofac Orthop 126:42-47, 2004.
33. Favero L, Brollo P, Bressan E: Orthodontic anchorage with spe-
cific fixtures: related study analysis, Am J Orthod Dentofac Orthop
122(1):84-94, 2002.
34. Wilmes B et al.: Parameters affecting primary stability of
orthodontic mini-implants, J Orofac Orthop 67(3):162-174,
2006.
35. Cornelis MA et al.: Patients’ and orthodontists’ perceptions of
miniplates used for temporary skeletal anchorage: a prospective
study, Am J Orthod Dentofac Orthop 133(1):18-24, 2008.

LASERS IN ORAL AND MAXILLOFACIAL SURGERY
Mark F. Sosovicka
Lasers are currently used to perform a variety of procedures
and therapies within the practice of oral and maxillofacial
surgery. The laser offers many benefits over traditional surgical
procedures performed by traditional techniques of sharp dis-
section, and the use of the laser continues to expand in con-
junction with the advancement of laser technology. The use
of lasers within oral and maxillofacial surgery along with
potential benefits, drawbacks, and risks with certain proce-
dures will be reviewed along with the discussion of some newer
nontraditional applications of laser therapy.
■ LASER PHYSICS
A brief review of laser physics is essential to understand how
lasers work in regard to specific applications of their use for
surgical procedures. The physics of lasers is well known as
energy is transferred to an electron and then emitted to
produce laser energy based on Einstein’s quantum theory of
radiation hypothesis that atoms passing from a higher to a
lower energy state will emit energy or photons, representing
small units or quanta of electromagnetic waves.1 Electrons are
usually in a low energy orbit closest to the atomic nucleus,
and electrons can move to a higher energy level orbit by
absorbing external energy. Conversely, when the electrons
return to the original lower orbital level, the excess energy
previously absorbed is released as spontaneous emission in the
form of light or photons.
The laser production of energy is accomplished by the
transfer of energy to the electron of an atom. Normally the
low energy electron is excited through a photon striking
the atom and transferring energy to produce excitation of the
electron to a higher energy state, causing the electron to enter
another excitatory outer electron ring further away from the
nucleus of the atom through the absorption of energy. The
electron in the unstable higher energy state in an outer orbit
returns to the lower energy orbital ring of a resting state and
subsequently releases electromagnetic energy through sponta-
neous emission of radiation in the form of light. The stimu-
lated emission of radiation occurs when external energy of an
electrical, chemical, or optical source is used to initiate the
atomic photon emission as atoms produce stimulated emission
of radiation, which is used to generate laser energy.2
Maiman developed the acronym “laser” for light amplified
by the stimulated emission of radiation.3 Lasers are the devices
that rely on the stimulated emission of radiation to produce a
beam of light. Laser components include an energy source, a
CHAPTER 14
resonant chamber, and an active medium. The energy source
is usually electrical and flows through the laser medium. The
resonant chamber contains the laser medium and reflective
mirrors, one of which is highly reflective and another that is
only partially reflective, permitting some laser light to exit.
The active medium is the atom, molecule, or ion producing
the radiation. The type of medium commonly gives the laser
its name. Common mediums include the Nd : YAG laser,
which is a solid state laser composed of neodymium ions and
crystals of yttrium-aluminum-garnet. The CO2 laser is a gas
laser incorporating carbon dioxide, nitrogen, and helium. Dye
lasers are liquid lasers with fluorescent organic dyes injected
into a tube.
The components and design of a laser permit the efficient
production and emission of synchronized light. Initially, atoms
within the laser chamber absorb energy from the energy
source, in which atoms in the higher energy states spontane-
ously decay and give up energy. The released energy is absorbed
by other atoms and used to enter a higher energy state as a
so-called pumping phenomenon. Ultimately, a larger number
of atoms exist in a higher energy state called population inver-
sion. More and more atoms reach the higher energy state and
spontaneously decay releasing more energy, which results in
the emission of additional photons that travel within the laser
chamber as amplification of stimulated emission of radiation.
As pumping continues to maintain an ample population of
inversion with the resonant chamber, a beam of coherent light
is produced that is reflected and partially reflected by mirrors,
resulting in the emergence of a beam of bright, monochro-
matic, coherent light, or a laser beam.4
Lasers produce energy in the form of light, which is trans-
mitted to an object as the electron in the excited state is
bombarded with irradiation by photons of light as the electron
is returning to a more stable resting state. Two photons of
emitted light energy are produced and transmitted. The light
energy is amplified and emitted by radiation of the atom.
Emitted laser light is of the same monochromatic wavelength
in waves and remains collimated, or parallel, over long
distances or coherent versus other light that spreads over
distances.4
Lasers generate light in a similar manner through the exci-
tation of atoms by photons of light in a resonator or a cavity
through the use of a medium, and then the light strikes a fully
reflective and a partially reflective mirror, which releases
between 5% to 10% of the light. Different mediums will
237
238 SECTION II ■ Dentoalveolar Surgery
determine the wavelengths of light released. Gas, such as CO2,
is a common laser medium along with solid mediums, such as
garnet or ruby crystals, which release energy as they are elec-
trically charged to produce laser light energy.2
Laser light can be characterized by wavelength. The ultra-
violet range is 100 to 400 nm, visible range of 400 to 700 nm,
near-infrared range of 700 to 1400 nm, mid-infrared range of
1400 to 20,000 nm, and the far-infrared range of greater than
20,000 nm. Laser light can also be defined by other unique
properties. Laser light is monochromatic where all the photons
in a laser beam are of the same wavelength, allowing the laser
beam to attain a sufficient intensity to interact with tissues
based upon wavelength and the absorption, scattering, and
reflection properties of the target tissue. Laser light is also
coherent with all photons in the beam synchronized in time
and space, unlike the random photons of conventional light.
The laser beam is collimated with the beams parallel with the
ability of the beam to be focused on a small target area and
also allowing all the emitted laser energy to be captured and
delivered to a target site through a flexible fiber optical system
or with the use of mirrors.5
A multitude of factors can control the interaction of lasers
with tissues. Power density is the amount of power transmitted
per area of a cross-section of the laser beam in watts/cm2. It
also represents the power of the laser striking the targeted
tissue per unit area with the power density of a laser inversely
proportional to the square diameter of the focal target. The
spot size of the beam also determines the energy transmitted
by the laser because the spot size reflects the ability of the laser
to be focused, delivering more energy, or defocused as the
distance of the lens to the tissue is increased by the operator.
The vaporization threshold is the amount of energy in watts
necessary to vaporize the target tissue.5
The wavelength of the laser beam determines factors, such
as the degree of scattering, tissue penetration, and the amount
of energy absorbed by the tissues. The greater the degree of
scattering the less energy focused on the target tissue. Lasers
with less scatter are better used as a scalpel because the energy
is precisely delivered to a single spot of tissue, whereas a laser
with more scatter is better for photocoagulation5 (Figure 14-
1). Fluence is a term that describes the amount of energy
applied to a particular area of tissue. The overall delivery of
energy can be determined by computer-generated patterns to
maximize efficiency and minimize tissue damage.2
Exposure time is the amount of time the laser energy is
directed at the target tissue and can be varied by continuous,
pulsated, or other varied modes of delivery. Continuous or
nonpulsated delivery provides a continuous wave of laser
energy to the tissue over a time period determined by the
operator. The ability to pulsate the delivery of laser energy has
the effect of modifying the delivery of higher laser energy for
very short periods (e.g., 100 microseconds). The pulsation of
laser energy prevents deeper tissue penetration of the laser and
minimizes tissue heat buildup by allowing the thermal tissue
relaxation time for heat dissipation, allowing the tissue to
cool.6 The ability to control the heat buildup of the adjacent
Tissue
Laser light Laser light
shorter wave length longer wave length
FIGURE 14-1. Laser wavelength.
tissue with the use of the laser provides the operator with the
ability to control the interaction of the laser with the targeted
tissue and, ultimately, vary the effects of the laser on the
tissue.
The delivery of the energy by the laser can be modified to
produce optimal results depending on the desired tissue inter-
action. The pulsation of a laser provides a noncontinuous
delivery of energy to the target tissue. Pulsation rates are
measured in number of pulses per second and used to calculate
a pulse width, representing the time necessary for the pulse to
go from zero energy to maximum energy and return back to
zero energy. Superpulsation is another method to minimize
adjacent tissue damage by producing higher peak power per
pulse at shorter pulse width to allow for the precise cutting or
ablation of tissue with a laser.7 Ultrapulsation of the laser can
also be used by increasing the pulse speed, resulting in less
adjacent tissue damage. It has been useful in applications, such
as skin resurfacing.
The use of flashscanning can also be used to produce less
collateral tissue damage by limiting thermal damage. Flash-
scanning applies the use of a laser at continuous high energy
in a circular pattern through the use of rotating mirrors, which
limits the energy delivered to any specific area, allowing ade-
quate tissue relaxation. It has been used with skin resurfacing
procedures.8 Quality switching, or Q-switching, is another
method to limit damage of adjacent tissue with the use of a
laser. Q-switching provides the ability of the laser to produce
high-energy pulses of nanoseconds duration through the use
of an electromagnetic switch operating a shutter mechanism.9
Applications of the Q-switched laser have included treatment
of certain pigmented skin lesions and removal of tattoos. Ulti-
mately, the laser can be used for selective tissue destruction
while limiting the damage or undesirable effects to the adja-
cent tissue because the tissue relaxation time can be calcu-
lated for different tissues, such as skin, blood vessels, and
muscle.
 CHAPTER 14 • Lasers in Oral and Maxillofacial Surgery 239

Temperature Effects of Laser Energy on

■ LASERS AND TISSUE TABLE 14-1
Tissues
INTERACTIONS
Temperature °F Tissue effect
The effects of lasers on tissues can result in the energy of the 37-60 °F Tissue retraction and conformational protein changes
laser being reflected, transmitted, or absorbed. Energy absorbed >60 °F Protein denaturation and protein coagulation
within the tissue can be dissipated or converted to other forms 90-100 °F Tissue carbonization and tissue char
of energy, such as heat, shock waves, or chemical reactions. >100 °F Tissue ablation
The conversion of laser energy into heat by the tissue is
common with medical lasers interacting with molecular
compounds, such as water, melanin, or hemoglobin, within
the tissue called chromophores10 (Figure 14-2). The amount tissue, and absorption of the energy into tissue chromophores
of energy absorbed by the tissues is determined by the amount (Figure 14-3). Immediate reactions and delayed reactions
of chromophores within the tissue. The tissue reaction with take place once the laser reacts with the tissue through
the use of a laser is determined by the type of tissue exposed photochemical, photothermal, and photoablation reactions.
to the laser energy and the wavelength of the laser light Photochemical reactions can occur after lasers interact with
(Table 14-1). a photosensitizer, causing tissue necrosis.
Laser light results in one of four basic tissue reactions to Photothermal reactions result as the laser causes denatur-
the energy. The reactions include reflection off the tissue, ing of enzymes, coagulation, tissue necrosis, and vaporization.
scattering to the surrounding tissue, transmission through the Photoablation reactions of lasers can cause tissue disruption

Absorption Spectra of Water, HbO2, Melanin

Ultraviolet Visible Infrared
Ruby

Diode 940
Molar Absorption Coefficient

Water
Melanin
Hemoglobin
Diode 810

Neodymium

Holmium

Erbium
KTP

CO2

0.1 0.2 0.3 0.4 0.6 0 1 2 3 4 5 6 7 8 9 10

Wavelength (␮m)

FIGURE 14-2. Laser absorption chart.

Reflection Scattering Transmission Absorption

FIGURE 14-3. Tissue interactions.

240 SECTION II ■ Dentoalveolar Surgery

Invisible ionizing radiation Visible Invisible therma radiation

X-rays Ultraviolet Near infrared Mid infrared Far infrared

400 - 700 nm

200 nm 2000 nm 3000 nm

Argon Nd:YAG
514 nm 1064 nm
Argon Ho:YAG Er:YAG CO2
488 nm Diode 2120 nm 2940 nm 10.6 ␮m
830 nm 9.6 ␮m
HeNe Er.Cr:YSGG 9.3 ␮m
632 nm 2790 nm

FIGURE 14-4. The electromagnetic spectrum.

by thermal explosion or mechanical shock waves, causing

tissue disruption.5
Currently, there are multiple lasers for biomedical use, such
as the CO2, Nd : YAG, erbium : YAG, argon ion, and diode
lasers (Figure 14-4). The CO2 laser was developed in 1964 by
Patel at Bell Laboratories.11 CO2 lasers use a gas medium
composed primarily of CO2, which produces a laser beam with
wavelengths in the mid-infrared region of 10,600 nm. The
CO2 laser is commonly used in oral and maxillofacial surgery
and otolaryngology. The benefits of the CO2 laser include
minimal scatter, excellent water absorption, rapid soft tissue
vaporization, and negligible surrounding tissue damage. The
CO2 laser functions as an excellent scalpel and can focus pre-
cisely onto the target tissue, thus avoiding adjacent tissue
damage for hemostatic cutting as vessels below 0.5 mm are
coagulated.5 The CO2 laser previously had to be delivered
down an articulated arm by a series of mirrors, but is now
delivered through a flexible fiber, making the delivery more
versatile (Figures 14-5, 14-6, 14-7).
The Nd : YAG laser was also developed in 1960 at Bell
Laboratories by Geusic et al.12 The Nd : YAG laser is a solid
state laser and was the first laser developed. The Nd : YAG
laser produces a laser beam with wavelengths between 1064
and 1320 nm, and the beam itself is invisible requiring the use
of a helium-neon guide beam. The Nd : YAG laser is mini-
mally absorbed, but can deeply penetrate tissue up to depths
of 10 mm for deep tissue vasoconstriction of even vessels up FIGURE 14-5. Typical CO2 laser.
to 2 to 3 mm in diameter.13 There is also a greater amount of
adjacent tissue damage than the CO2 laser. Common maxil-
lofacial applications include coagulation of angiomas, vascular in decreased erythema, edema, and pain.14 The erbium : YAG
tumor resections, and arthroscopic surgery of the temporo- laser can also cut hard tissue, including both bone and enamel,
mandibular joint (TMJ). which makes it an obvious choice for oral and maxillofacial
The erbium : YAG laser produces a wavelength of 2940 nm surgical procedures where a combination surgery is performed
and is another laser that has excellent energy absorption by on both hard and soft tissue, such as crown elongation,
water, making it an ideal laser for intraoral use and for super- tooth exposure, and implant uncovering procedures. The
ficial skin resurfacing as a result of the limited depth of pene- erbium : YAG laser is used for operative dentistry and the
tration through skin with less adjacent tissue damage, resulting cutting of tooth structure.14
 CHAPTER 14 •
FIGURE 14-6. Close-up of typical CO2 laser.
FIGURE 14-7. Control panel.
The argon ion laser is a low wavelength laser of 488 to
514 nm that produces a blue-green color beam. The argon ion
laser is primarily used for photocoagulation of small vessels in
dermatology and ophthalmology.5
The Nd : YAGKTP laser is another available laser with a
wavelength of 0.32 μm through the use of a frequency-
Lasers in Oral and Maxillofacial Surgery 241
doubling potassium titanyl phosphate (KTP) crystal in the
green spectrum of light similar to the argon laser. The KTP
crystal halves or “doubles” the wavelength.13 Diode lasers are
another development that rely on the use of non-solid state
semiconductor technology. Diode lasers can attain higher
power around 0.81 μm with a power of 20 W, which has
applications similar to the Nd : YAG laser. Benefits of the
diode laser include a reduced size, reduced cost, and greater
versatility through the use of frequency-doubling crystals to
allow a variety of output wavelengths for applications ranging
from tissue excision, coagulation, periodontal surgery, or use
at lower wavelengths for the treatment of pain or to modulate
healing.15 There are also a multitude of low-level lasers pro-
duced that are used for a variety of nonsurgical therapeutic
treatments, which will be discussed in further detail later.
■ LASER EQUIPMENT REVIEW
The purchase of a laser represents a significant expense. Before
purchasing a laser, a review of available lasers should compare
certain practical characteristics of the laser unit. Primary con-
sideration should be given to the specific laser application or
intended function and the functional treatment range of the
laser along with the specifics of operation and considerations
of return on equity. Lasers are useful for a variety of procedures
for soft and hard tissue applications. Many practitioners want
a multifunctional laser with the ability to perform a variety of
surgical procedures. Therefore, any present and future applica-
tions of lasers should be considered before purchase. There are
also a number of lasers with multiple mediums available.
The length of service of a laser generally indicates that the
laser may be more reliable and has minimal operational break-
downs. Lasers that have been in service for extended periods
of time can indicate the laser has the ability to be used with
many diverse procedures and a greater professional accep-
tance, popularity, and reliability. Lasers with FDA clearance
for use on humans is paramount, although it is noted many
lasers and cosmetic procedures do not require FDA approval
when used for so called “nonsurgical treatments.”
The laser medium is usually crystal or gas and generates a
specific wavelength of laser energy for the desired application.
The name of the laser will often incorporate the type of
medium used. The type of medium will also dictate the overall
price of the laser. How long the laser medium will last is related
to the number of times the lasing medium expands itself over
time. Often the laser medium will require replacement after a
certain range of hours of use. The lifespan of the laser medium
should be considered in the purchase of a laser.
Laser wavelength will dictate the tissues’ response to the
absorption of the laser energy and the applicable use of the
laser. The emission mode of the laser will also vary from con-
tinuous to a pulsed mode. Continuous lasers will work more
rapidly, but also generate more heat and pain. Pulsed lasers
can provide less pain during the surgical procedure. Maximum
power as watts will determine the energy levels to affect dif-
ferent tissues, and the energy should be able to be modulated
depending on the application.
242 SECTION II ■ Dentoalveolar Surgery
Laser beam Ceramic
Tissue
Non-Contact Contact
laser delivery laser delivery
1. Handpieces 1. Ceramic tips
2. Microscopes 2. Crystal tips
3. Endoscopes
4. Microfibers
FIGURE 14-8. Laser delivery systems.
The laser delivery system should be versatile with easy
access in the oral cavity. Laser delivery systems can include
the hollow fiber, fiber with diffuser tips, bare fibers, and articu-
lating arm and hand piece.13 Hollow fiber delivery systems
have a perforated metal tip and require cooling by a nonflam-
mable gas, such as CO2, and are useful for coagulation in a
noncontact manner. Fibers with a diffuser tip are usually made
of sapphire and are used in a contact mode for cutting tissue.
Bare fibers are useful for use in confined cavities, such as the
TMJ, because of the small diameter and can coagulate or cut
tissue. The articulated arm and handpiece uses reflective
mirrors with the beam exiting through a handpiece to allow
both coagulation and cutting of tissue (Figure 14-8). Lasers
with hollow fibers or fibers alone will need periodic replace-
ment and result in higher operating costs than those with
articulating arms and hand pieces.16
Optional features of some lasers can include a cooling
system, such as a water spray, to protect the adjacent tissue
and remove debris during use of the laser. The beam and fiber
diameter is also important depending on the laser application.
Some lasers will require contact with the tissue, whereas
others operate in a noncontact mode at a variable distance
from the tissue. The noncontact lasers have a hand piece with
a lens along with a pointing blade or a HeNe target beam as
a visible guide. The sterilization cycle of the laser is also
important and may dictate the need for additional laser hand
pieces. Most lasers operate on 120 V power, although some
models require 220 V power and a separate electrical supply
within the office.16
Other factors to be considered in laser selection can include
size and portability of the laser unit. Appropriate training from
the manufacturer should be provided as part of the package
and should include training of the office staff. The laser war-
ranty should be evaluated because lasers can break down.
Consideration should be given to the time frame of the war-
ranty and if parts and labor are covered and if the laser can
be repaired on-site or has to be returned to the manufacturer.
Thorough research is advisable before obtaining a laser because
of the many available options, specific use limitations, and
large cost variations of available lasers.
Potential Laser Safety Issues for Patients and
BOX 14-1
Operating Personnel
Electrical source injury
Laser-ignited contact fire
Laser-ignited airway fire
Eye exposure injury
Laser plume inhalational injury
Inadvertent mucosal and skin burns
Enamel injury
FIGURE 14-9. Warning signs indicating the use of the laser and requiring
additional eyewear must be posted on the operatory doors while the laser is
being used.
■ LASER SAFETY
Laser safety is paramount to the use of lasers for oral and
maxillofacial surgical procedures. All laser equipment should
be thoroughly inspected and tested on an inert object, such
as a moistened tongue blade, before use to confirm proper
energy levels and safe operation of the laser. Adequate precau-
tions must be taken to prevent inadvertent exposure of operat-
ing room personnel and the patient to unintentional laser
energy not directed toward the therapeutic target tissue (Box
14-1). The laser should be inactivated before moving the laser
upon completion of the energy delivery to the operative site
to prevent inadvertent laser burns to the patient or operatory
personnel. The operatory room door must be closed during the
procedure, and warning signs indicating the use of the laser
and requiring additional eyewear must be placed on the opera-
tory doors while the laser is being used (Figures. 14-9 and
14-10).
Problems of inadvertent laser exposure can include corneal
or scleral scarring by direct exposure, making the use of safety
glasses with side shields mandatory. If the patient is receiving
laser therapy in the region of the eye, the use of metal corneal
shields with topical anesthetic and lubrication must be used,
otherwise the patient should have their eyes completely
covered with laser glasses or moistened towels17 (Figure 14-
11). Proper evacuation of the resultant laser plume via laser
vacuums with HEPA filters held near the operative field
should be used along with the use of viral filtering face
masks to prevent possible contamination of operating room
 CHAPTER 14 •
FIGURE 14-10. Operator eye glasses with side shields.
FIGURE 14-11. Corneal shields and laser glasses must be worn by
patients receiving laser therapy.
personnel with bacteria or viruses during laser procedures17
(Figures 14-12 and 14-13).
The use of nonflammable surgical skin preparations con-
taining no alcohol, such as Betadine or hexachlorophene,
should be followed by wiping with sterile water to prevent skin
color changes. The use of isopropyl alcohol or chlorhexidine
preparations containing alcohol should be avoided because of
potential flammability with pooling in facial crevices or poten-
tial flammability with vaporization of the alcohol after the
facial application.18 Nonflammable patient drapes for use with
lasers or moistened towels should also be used. The teeth must
also be protected with moistened gauze or commercial silicone
teeth protectors when using the laser around the mouth or
intraorally because enamel can be damaged by absorbed laser
energy along with possible thermal damage to pulpal tissue
from heat conduction.17 The need to protect adjacent oral
tissue from damage is also required, such as the use of wet
sponges, moistened tongue blades, and nonreflective ebonized
instruments, to prevent unintentional tissue damage.
The use of lasers in the presence of supplemental oxygen
requires the use of precautions to prevent inadvertent fires.
Patients under general anesthesia should use a commercial
metal-covered endotracheal tube specific for laser use or have
the tube wrapped with nonreflective foil to prevent a possible
fire in the endotracheal tube, with pressurized oxygen creating
a torchlike effect. The cuff should be inflated with normal
Lasers in Oral and Maxillofacial Surgery 243
FIGURE 14-12. Typical laser HEPA evacuator.
FIGURE 14-13. Evacuator control panel.
saline versus air, and the tube should additionally be protected
with wet sponges if exposed intraorally. If the patient is being
sedated and supplemental oxygen is used via a nasal cannula
or face mask, care must be used, and the oxygen delivery
cannula or mask can be wrapped in foil to prevent an airway
fire.18 The oxygen can be delivered through a nasopharyngeal
airway under low flow while packing off the posterior pharynx
with moistened gauze. The supplemental oxygen should be
used at a low flow or can be turned off while the laser is being
used. The use of facial drapes that can cause a high oxygen
concentration to accumulate under the drapes, possibly leading
to a fire, should be avoided. Saline or sterile water should also
be readily available to extinguish an airway fire if needed.
■ LASER USE FOR ORAL AND
MAXILLOFACIAL SURGERY
The use of a laser to perform oral and maxillofacial surgical
procedures has continued to evolve over the last 35 years.
Lasers have commonly been used to treat a variety of patho-
logic conditions, and the use of lasers for other modalities has
continued to grow. The laser has proven to be a useful tool
244 SECTION II ■ Dentoalveolar Surgery
FIGURE 14-14. Low-energy diode laser.
within the practice of oral and maxillofacial surgery for pro-
cedures, such as implant uncovering, gingival recontouring,
surgical exposure of teeth, laser-assisted arthroscopic TMJ
surgery, and treatment of oral pathologic conditions, such as
vascular lesions, and many other applications. The use of the
laser within oral and maxillofacial surgery continues to prog-
ress, especially with the newer low-level diode and other lasers
for newer applications to aid in bone healing, treatment of
periimplantitis, therapy for temporomandibular disorders
(TMD), and novel applications, such as navigational surgery
(Figure 14-14). Today, lasers are a common part of the arma-
mentarium of the oral and maxillofacial surgeon because the
laser equipment is readily available for office procedures with
the development of lasers that are multiversatile in use, easier
to operate, and more affordable in cost.
The use of lasers for oral and maxillofacial surgery was initi-
ated in 1970 by Polanyi with the use of a CO2 laser to incise
living tissue.19 Polanyi also developed a hand-held laser deliv-
ery system.19 The CO2 laser remains the most commonly used
laser for intraoral surgery as a result of the excellent absorption
of the infrared laser wavelengths of 10,600 nm by tissues with
high water content. A multitude of other lasers, such as argon,
holmium : YAG, and erbium : YAG, are also used for selected
applications in oral and maxillofacial surgery.14
The use of the CO2 laser for the surgical treatment of oral
mucosa stems from the excellent energy absorption because
oral mucosa has a 90% water composition making it ideal for
absorption of infrared energy.14 The laser energy results in
cellular disruption and vaporization of the oral mucosal tissue
by the CO2 laser.14 CO2 lasers also provide excellent coagula-
tion and hemostasis and decreased wound contraction and
scarring as a result of decreased fibrosis with healing.20 Other
benefits include decreased postoperative pain and edema with
intraoral surgery. The laser is also able to be used in areas of
limited exposure within the oral cavity where access with
conventional surgical scalpel blades or other means of dissec-
tion can be difficult, such as areas of moveable mucosa (e.g.,
the floor of the mouth, posterior pharynx, or soft palate).
Lasers do have some disadvantages, such as delayed wound
healing, possibly up to a 2- to 3-week period, versus conven-
tional surgical dissection techniques, which generally heal in
7 to 10 days because laser wounds are slow to epithelialize.21
■ INCISIONAL AND EXCISIONAL
LASER SOFT TISSUE
PROCEDURES
Laser soft tissue surgery is another common area where the
treatment can be well controlled with minimal adjacent tissue
damage and also provides excellent wound hemostasis. The
benefits of the CO2 laser are well documented for a variety of
intraoral soft tissue procedures because the procedures can be
completed with excellent hemostasis and less pain during the
procedure and postoperatively. The reduction of the associ-
ated bacteria is another benefit that results in improved wound
healing with a decrease in the rate of infection with surgery.22
The CO2 laser is set on a continuous wave in a range of 2 to
10 W for most excisional procedures with the smallest spot
size at the focal point of the laser to produce an incision of a
controlled depth and thin width.14 The laser can also be
defocused to permit coagulation of blood vessels to aid in
hemostasis.
A common example of a laser excision procedure would be
the excision of a labial or lingual frenum. The mucosa and the
underlying muscle are easily excised with the use of the laser.
Following the administration of local anesthesia, the frenum
attachments are separated and the surrounding tissue is pre-
served. The wound demonstrates complete hemostasis, and
suturing is usually not required. Following laser frenectomy
procedures, the wound heals slower than those done with
sharp dissection with a blade or scissors, although the patient
will usually experience less postoperative pain than with a
sharp dissection.
The laser-assisted excision of common benign mucosal
lesions is also commonly performed. For example, the laser
can be used to excise a fibroma of the lip or buccal mucosa by
excising the lesion in an elliptical manner with adequate soft
tissue margins usually extending 0.5 mm beyond the normal
margin for a scalpel excision to allow for a zone of lateral
necrosis within the specimen from the laser, which can be
difficult to interpret histologically.14 The specimen is sent for
routine histopathologic examination, and the subsequent
wound can be closed with sutures or left to granulate. Lesions
that can be excised with the laser include epulis fissurata,
mucoceles, or other mucus retention phenomenon with the
use of the CO2 laser on a continuous mode of 4 to 10 W
depending on the tissue to be incised and spot sizes of 0.1 to
0.5 mm.14 The entire mucocele lesion is outlined, excised, and
undermined. A ranula is treated with the laser by excising the
covering layer of mucosa at the periphery for marsupialization.
The laser will provide excellent hemostasis of the surgical site,
and the need for countertraction is negated as normally needed
for a scalpel blade excision with the use of the laser in the
 CHAPTER 14 •
floor of the mouth region. Suturing is generally not needed
with the use of the laser. Laser-assisted sialolith excision in
the floor of the mouth can also be performed by incision
through the mucosa and duct to the area of the stone with a
flash of light noted once the stone is encountered. The
sialolith is then removed, and the wound is left to granulate
without suturing to prevent stricture or obstruction of the
underlying duct.
Laser treatment of benign and premalignant oral lesions,
such as leukoplakia, erythroplakia, hyperkeratosis, lichen
planus, nicotine stomatitis, and other lesions, has been advo-
cated. All lesions should have a definitive clinical or histo-
logic diagnosis before laser treatment because laser vaporization
or ablation does provide tissue for biopsy after treatment.
Mucosal lesions and premalignant lesions can be adequately
managed with laser vaporization or ablation, and there is
no significant increase in the number of recurrences versus
traditional sharp dissection with a scalpel.14 Benefits of laser
treatment versus standard excision with a blade can include
decreased scarring, less potential to damage associated vital
structures, preservation of tissue elasticity, and decreased need
for reconstructive surgery, such as epithelial skin grafting,
which can alter the detection of recurrent tumors.22 Laser
treatment of mucosal lesions is also advocated for the treat-
ment of multifocal or diffuse lesions of the oral mucosa where
blade excision is impossible because of the inability to remove
large areas of mucosa. The laser treatment of diffuse or multi-
focal mucosal lesions allows the treatment of the area without
excision and produces minimal underlying or adjacent tissue
damage while minimizing pain, edema, and scarring.23 The
neomucosa of the treated wound behaves like normal mucosa
and permits additional laser treatment if the lesion would
reoccur.
Laser treatment of mucosal lesions also permits the abla-
tion or vaporization of tissue at controlled depths of less than
1 mm, preserving the submucosal tissue with the use of high-
power density at short application times to minimize heat
conduction and thermal tissue damage or burning. The laser
beam can be controlled by defocusing the beam to produce a
rapid bubbling of the epithelium and crackling noise as the
epithelium turns opalescent and leaves a light-colored base
with wiping of the char.22 The lesion is outlined and treated
by incomplete overlapping of the lased area with the use of a
vertical or horizontal “U” pattern to evenly treat the entire
lesion, and a second pass in a perpendicular direction using a
similar pattern can be performed if an inadequate depth was
obtained initially.14 The basal mucosal layers do not bleed
with ablation to the level of the basement membrane while
preserving submucosal structures, allowing reepithelialization
from the wound margins. Ablated areas of 1 cm2 or less will
generally reepithelialize in 2 to 3 weeks.24 As with any other
surgical treatment of mucosal lesions, the need for long-term
reevaluation must be performed.
Histologic studies of wound healing following laser treat-
ment have shown some carbonization, coagulation necrosis,
intercellular voids, and areas of cellular vaporization.25 The
Lasers in Oral and Maxillofacial Surgery 245
laser wound results in the presence of few myofibroblasts with
minimal contracture and scarring.23 The spread of cancerous
or precancerous cells is limited by the coagulation of adjacent
blood and lymphatic vessels.26 Laser wounds of the oral mucosa
are generally slow to heal by secondary intention because a
fibrous coagulum initially covers the wound and is slowly
replaced by epithelial migration.
The laser treatment of intraoral vascular lesions is an excel-
lent application because the laser energy is highly absorbed by
and coagulates hemoglobin, and the lateral thermal heat
damage produces vascular constriction by contraction of col-
lagen in the vessel wall. A variety of lasers can be used for the
treatment of intraoral vascular lesions, including the CO2,
argon, copper vapor, tunable dye, and Nd : YAG lasers.27 The
laser can be used to obliterate vessels of up to 500 μm in
diameter, allowing excision of small hemangiomas, telangiec-
tasias, and varicosities.21
■ LASER TREATMENT OF ORAL
PATHOLOGIC CONDITIONS
Lasers have been used as an adjunctive tool in oral medicine
to treat oral pathologic conditions, including ulcerations asso-
ciated with aphthous and herpetic stomatitis.28 The treatment
of aphthous stomatitis has responded well to diode laser
therapy with an overall reduction in pain and duration of the
lesions. Low-level laser therapy (LLLT) has also been used
with other pain entities, such as postherpetic neuralgia,
through biomodulation of inflammation and healing.
■ LASER USE WITH IMPLANT
SURGERY
The laser can be used with implant-related surgical procedures
as a result of many clinical advantages. Laser advantages
include excellent soft tissue cutting with hemostasis and
decreased pain and edema related to the surgical procedure.
Bone osteotomies can also be performed with a laser, also
resulting in decreased pain as a result of decreased mechanical
and thermal trauma to the adjacent tissue. The CO2 laser is
an excellent laser for periimplant surgery because the CO2
laser energy is not absorbed but reflected by titanium.14
The soft tissue flap for implant surgery can be incised with
the laser through cellular water vaporization with thermal
rupture producing thermal mechanical tissue ablation. The
thermal-mechanical tissue ablation results in minimal adja-
cent damage of the extracellular collagen matrix to 5 μm or
approximately 2 cell widths.29 Overall the laser incision of
soft tissue results in decreased postoperative pain and edema.
Scar formation is minimized, and minimal tissue shrinkage of
0.5 mm is encountered when compared with incision of soft
tissue with a blade of 3 mm. Overall healing time is also
decreased.29
Some selected areas of implant surgery where the use of a
laser has proven to be beneficial include sinus-lifting proce-
dures. The laser can be used to osteotomize the lateral sinus
wall with a decreased incidence of perforation of the sinus
membrane. The use of the YSGG (yttrium-scandium-gallium-
246 SECTION II ■ Dentoalveolar Surgery
garnet) laser with a 2780 nm wavelength has been used to
prevent iatrogenic perforation of the sinus membrane by use
of 3.5 W and a pulse of 140 microseconds for prevention of
cutting the membrane with the osteotomy or perforating the
membrane with initial flap elevation.29 The intact sinus mem-
brane eliminates the need for placement of a covering mem-
brane to prevent loss of grafted bone associated with dehiscence
of the sinus membrane. The need for additional tissue under-
mining and release of periosteum to facilitate closure is rare
with less postoperative pain and edema. The use of the YSGG
laser for osteotomy of ramal bone or symphyseal bone has been
described.30 The use of the laser decreases the amount of bone
necrosis from the donor site, and the laser osteotomy cuts have
a more narrow diameter than those from the use of a bur,
resulting in quicker and less painful postoperative healing.30
The laser can also be used for second stage implant un-
covering. The laser results in less overall tissue trauma, which
also preserves the amount of attached tissue adjacent to the
implants. The technique of laser exposure of implants can be
beneficial for optimal soft tissue preservation and mainte-
nance in the aesthetic zone.
Laser treatment of periimplantitis is another area that has
been investigated. Periimplantitis can be a difficult implant-
related complication, resulting in progressive loss of periim-
plant bone and potential loss of the implant with bacterial
contamination and penetration of the tissues. Common treat-
ment regimens have centered around antimicrobial therapy
through agents, such as chlorhexidine or citric acid, in
combination with surgical treatment to facilitate chemical or
mechanical débridement of the implant surface. The goal is
to decontaminate the implant and surrounding tissue to
promote regeneration of bone around the implant. Common
problems include limited effectiveness of systemic antibiotics
and possible damage to the implant with mechanical methods
of débridement, such as curettes or ultrasonic scalers.
Diode lasers have been proven to be beneficial for anti-
microbial decontamination of the implant and periimplant
tissue. Treatment of periimplantitis with the diode laser at
905 nm for 1 minute following the application of toluidine
blue to sensitize the bacterial cell membrane to the laser light
has been reported.31 The CO2 laser has also been used for the
treatment of periimplantitis with no alteration of the implant,
such as that encountered with the use of the Nd : YAG laser.31
Laser treatment of periimplantitis has been beneficial before
bone grafting of periimplant defects following removal of the
surrounding tissue and implant surface contamination. Care
should be taken when the implant energy is directed toward
the implant surface to prevent elevation of the implant-bone
interface above the 47 °C threshold of potential thermal-
related bone necrosis.14
■ USE OF LASERS FOR SURGICAL
TREATMENT OF THE
TEMPOROMANDIBULAR JOINT
The use of lasers for treatment of pathologic conditions of the
temporomandibular joint (TMJ) has developed over the last
15 years as both laser and arthroscopic technology has pro-
gressed. The use of the laser through less invasive arthroscopic
access to the TMJ represented a major development for TMJ
surgery by providing a less invasive form of treatment than
traditional open joint surgery.
Arthroscopic surgery of the TMJ was initiated by Ohnishi
et al. in 1975 and was further refined into the 1980s.32 McKain
and Sanders advanced the use of diagnostic and therapeutic
arthroscopic TMJ surgery within the United States in the mid-
1980s.33 Indresano et al. then initiated the use of laser-assisted
arthroscopic TMJ surgery to provide a means to access the
TMJ with better visualization of the joint and simultaneously
allow surgical manipulation of intraarticular tissues and patho-
logic conditions.34,35
Early difficulties with the use of laser-assisted arthroscopic
TMJ surgery included the inability to use a CO2 laser as a
result of the inflexible optical system and inability to transmit
laser waves through a liquid medium.35 The Nd : YAG laser
was difficult to control regarding adjacent tissue damage and
depth of the beam. The development of the holmium : YAG
laser in 1990 by Koslin for arthroscopic use in small joints was
a major achievement.35 The holmium : YAG laser is able to
transmit energy through a fluid medium with good absorption
and minimal thermal damage to the tissue within the TMJ.
The holmium : YAG laser was an excellent laser with good
adaptability for use with arthroscopic cannulae within the
TMJ for synovial repair, intrajoint hemostasis, synovectomy,
and disk repositioning procedures. Applications of the holmi-
um : YAG laser for TMJ surgery include synovectomy, release
of the anterior disk attachment for clicking or closed lock,
treatment of hypermobility as a result of instability of the
posterior attachment of the joint and disk, and recontouring
of perforated disks, allowing disk preservation.
Techniques of arthroscopic-assisted laser therapy of the
TMJ are fairly standard. The joint is accessed by traditional
arthroscopic techniques with the introduction of a second
cannula for insertion of the laser. Correct portal placement
through McCain’s techniques using anatomic measurements
and palpation allows adequate joint access while minimizing
potential complications of arthroscopic surgery.36 Triangula-
tion is used to position the laser for treatment of intraarticular
pathologic conditions. There is also the option of using a
double cannulae, developed by Ohnishi, which permits simul-
taneous and parallel positioning of the arthroscope and laser
with the joint.13
The holmium : YAG laser can be used arthroscopically for
the treatment of a variety of derangements of the TMJ as
expertly described and documented through the excellent
works of Koslin. Patients with anterior disk displacement with
pain and no improvement following conservative splint
or nonsurgical arthroscopic manipulation are candidates for
arthroscopic laser surgery. Nonsurgical treatment can rarely
decrease the popping, clicking, and other loud noises with
joint function.36 Painful anterior disk displacement with or
without closed locking is commonly treated with laser-assisted
arthroscopic surgery.
 CHAPTER 14 •
The laser-assisted surgery is performed by freeing the disk
by division of adhesions as an anterior-release procedure. The
anterior synovial tissue and disk attachment are divided to the
level of the lateral pterygoid muscle from a medial to lateral
position. The laser is used by lightly contacting the synovial
tissue at a power of 1 J and a setting of 8 pulses/sec, providing
simultaneous resection of the synovium and hemostasis.37 The
thickened anterior disk tissue acts as a ridge limiting condylar
movement and produces loud popping or clicking as the
condyle passes onto the disk. The thickened disk tissue is
thinned using the laser at 0.5 J and 14 pulses/sec.37 The disk
is mobilized from the anterior attachments with the laser and
is repositioned posteriorly with a blunt probe, and a suture is
placed through the posterior disk and synovial attachment
and retrieved through the accessory portal. The disk is repo-
sitioned posteriorly with the aid of the suture, and the ret-
rodisk synovial tissue is thinned also with the use of the laser.
Care is taken to prevent lasering of tissue at the oblique pro-
tuberance to prevent tethering and limited mobility of the
disk.37 The disk is now in a more posterior position and is
stabilized by the shrinkage of the posterior synovial tissue and
by tying the suture to the outside of the joint. The patient is
placed into physical therapy, and the goal of opening to
35 mm should be achieved.37 The patient is maintained on a
soft diet, and the use of a splint can be maintained to diminish
postoperative pain and residual joint noise over a 3-month
postsurgical recovery period.37
Joint adhesions at one time were thought to be a significant
contributor to TMJ dysfunction. Present literature and experi-
ence by Koslin has indicated that joint adhesions are not as
common as once thought and only result with severe inflam-
matory joint disease or trauma-induced intraarticular joint
bleeding.37 The adhesions are most commonly seen in the
anterior joint recess and can limit joint mobility and function.
The use of arthroscopic-aided lysis and lavage can be per-
formed to break the adhesions with irrigation to distend the
joint along with manipulation of the arthroscope or blunt
probe to sweep the joint. The use of the holmium : YAG laser
can also be used to break the synovial adhesions by ablation.
The laser ablates the adhesions at the point of attachment to
the fossae by using a 0.5-J setting at 14 pulses/sec.37
Hypermobility of the TMJ is exhibited by patients who
subluxate the condylar head anterior to the articular emi-
nence, resulting in the inability to reduce the joint or severe
pain with reduction. A variety of treatments, including emi-
nectomy, to allow the condyle to freely translate or blocking
procedures with osteotomies, bone grafts, or plating to limit
translation of the condyle have previously been used. The
option of laser therapy for TMJ hypermobility through coagu-
lation of the retrodisk tissue can be used to produce a contrac-
tile force to stabilize the disk in a new position and allow
fibrosis. Other treatment options include arthroscopic laser
scarification of the oblique protuberance combined with sutur-
ing of the posterior disk attachment for stabilization can also
be used. The holmium : YAG laser was used in conjunction
with triangulation and positioning through the helium-neon
Lasers in Oral and Maxillofacial Surgery 247
aiming beam and coagulation using 20 W power for 0.5
seconds.37 Joint hypermobility can also be treated with the use
of a holmium : YAG laser on redundant tissue of the medial
capsule to cause fibrosis and stabilization. The holmium : YAG
laser provides less tissue penetration than the Nd : YAG laser,
and the KTP laser also provides similar benefits. All of the
laser-assisted joint procedures reduce the anterior joint space
and overall mobility of the condyle within the joint. Unlike
other surgical joint procedures that use physical therapy to
increase joint mobility, the postoperative joint movement is
restricted in these patients to prevent immediate subluxation
of the joint. Ideally the joint opening should be restricted to
30 mm for a period of approximately 3 months to allow the
joint tissue to normalize, and the use of an occlusal splint is
not necessary.37
Arthroscopic laser treatment of the synovium can also be
performed for hyperplasia or hyperemia of the synovium as an
alternative to motorized shavers or electrocautery devices.37
Inflammatory joint disease is commonly a result of mobility or
dysfunctional problems associated with the TMJ. Patients can
also exhibit pain with no identifiable internal derangement
on imaging, possibly related to parafunctional habits, exces-
sive loading of the joint, or arthritides. Diagnosis of these
inflammatory conditions of the joint can be diagnosed by
arthroscopy and treated with the use of lasers. Laser-assisted
synovial surgery can target areas of synovial abnormality better
than rotary shavers or electrocautery and spare healthy adja-
cent tissue from thermal or direct mechanical damage.37 The
use of the laser is much more precise and controlled than
mechanical treatment of the synovial pathologic condition.
The technique uses a holmium : YAG laser from approximately
3 mm away from the synovium directed by a helium-neon
guide beam with 0.5 J and approximately 10 pulses/sec.37 The
synovium will slightly blanch from an erythematous state and
constrict with ideally no burning or scarring produced as the
areas of pathologic synovium are treated with the laser.
Selected steroid injection of the inflamed areas of synovium
can also be performed with Celestone before exiting the joint.
Physical therapy with a graduated goal of obtaining 40 mm of
opening is initiated along with the use of a soft diet and
occlusal splint therapy.37
TMJ disk perforations can also be treated with the use of
the arthroscope and laser versus traditional open-joint tech-
niques of disk repair or meniscectomy with or without replace-
ment. Ideally the condition of the bony condylar head should
be evaluated radiographically before any laser treatment of a
disk tear or perforation. Any bony changes of the condyle on
the articulating surface are a contraindication to any attempt
at a disk repair. Arthroscopic laser-assisted treatment of disk
perforations or tears can also be performed as an attempt to
allow disk preservation and prevent the need for disk replace-
ment procedures with grafting. Torn fragments of disk can be
smoothed, and the disk can be recontoured with the laser. The
use of the Nd : YAG laser on 0.5 to 1.0 J of energy and 14
pulses/sec can be used to remove and recontour fragmented
disk tissue through triangulation techniques.37 The reduction
248 SECTION II ■ Dentoalveolar Surgery
of any disk tears or fragments should permit the free function
of the condyle. The disk recontouring can also be combined
with a disk repositioning procedure through an anterior release
to relocate the area of the perforation away from the area of
condylar function.37 Physical therapy, soft diet, and the use of
a splint should also be used postoperatively to prevent the
development of disk adhesions immediately after surgery.
Meniscectomies can also be performed with the use of a laser
through an arthroscope as discussed by Mazzonetto and Spag-
noli with the use of a holmium : YAG laser to remove the disk
followed by rotary contouring of the condylar head and glenoid
fossa.38
Laser-assisted arthroscopic TMJ surgery can be associated
with certain risks. The risks include those similar for diagnos-
tic and surgical arthroscopy of the TMJ, such as facial nerve
injury, otic injuries including perforation of the tympanic
membrane, intracranial perforation, and instrument breakage,
resulting in a foreign body of the TMJ.40 The laser can actually
be beneficial in relation to some complications of standard
TMJ arthroscopy, such as intraoperative bleeding. The holmi-
um : YAG laser can be used for hemostasis of small vessels
during the arthroscopic procedures, although it is limited with
profuse bleeding from larger vessels.37
Low-level laser therapy (LLLT) has also been advocated
for the treatment of TMD. Commonly, TMD can have a
variety of clinical conditions involving the masticatory mus-
culature, TMJ, or both, with pathologic conditions of any
component resulting in TMD. The use of LLLT has been used
as another modality in the treatment of TMD for the muscu-
lature component of the condition in addition to conservative
therapies, such as the use of antiinflammatory medications,
soft diet, splints, and physical therapy.
Phototherapy LLLT devices for the treatment of TMD
have been used since the mid-1960s.41 Recent studies have
shown the effective use of LLLT for the treatment of muscu-
loskeletal and neurogenic pain pathologic conditions associ-
ated with TMD. LLLT has been proven to be beneficial on
pain fibers with applications, such as TMD and postherpetic
neuralgia. Recent studies by Cetiner et al. have demonstrated
that LLLT is an appropriate treatment for TMD and should
be considered as an alternative noninvasive therapy. The
study revealed that patients treated with LLLT for TMD,
including myogenic pain, limited mandibular mobility,
chewing difficulty, and joint tenderness, had statistically sig-
nificant improvement versus patients treated with a placebo
laser therapy. The study used a gallium-aluminum-arsenide
diode laser with a wavelength of 830 nm and a duration of
162 seconds and a dosage of 7 J/cm2 with application to the
overlying skin of the most tender areas for 10 sessions daily
for 10 weeks. Interestingly the LLLT improved TMJ mobility
by approximately 20% by comparison of maximal mouth
opening measurements for the patient test group.41
The effects of LLLT in TMD may be beneficial as a result
of both analgesic and antiinflammatory effects by increasing
the pain threshold, muscle stimulating effects, and alteration
of neural sensation. The immediate effects of LLLT with pain
reduction are possibly due to a direct effect on nerve cell
membranes producing a local anesthetic-like effect limiting
nerve conduction. The effects can last from days to weeks.
Prior studies have also shown the benefit of the use of LLLT
in patients with arthritides of the TMJ by Kuleckcioglu et al.42
The optimal application of LLLT in TMD needs further
refinement regarding duration, dosages, and wavelengths for
significant effects on TMD pathologic conditions. Studies by
Nunez et al. in 2006 have also shown that LLLT is more effec-
tive for the treatment of TMD than transcutaneous neural
stimulation (TENS) on mouth opening.43 Earlier studies by
Gray et al. in 1994 have also shown that LLLT, ultrasound,
and short-term diathermy are all beneficial for TMD treat-
ment.44 Therefore, LLLT can be an appropriate and alterna-
tive treatment of TMD as a result of the noninvasive nature
and ease of use for myogenic pain and other TMD-related
complaints. Currently, additional studies are being under-
taken regarding further use of LLLT for TMD that may prove
beneficial in the future.
■ LASER-ASSISTED SKIN
PROCEDURES OF THE FACE
Many oral and maxillofacial surgeons are involved in cosmetic
procedures for facial rejuvenation. Revision of facial scars is
another area often addressed by the oral and maxillofacial
surgeon. Laser treatment of the face is a common modality for
the treatment of aging, sun-related skin damage, and trau-
matic pathologic conditions of the face. Skin aging can be
from intrinsic or chronologic skin changes or from extrinsic
or sun-related photoaging.
Photoaging from environmental UV exposure results in
cosmetic defects, including drying, coarseness, and roughened
skin along with pigmentation, wrinkling, telangiectasias, and
actinic keratosis.45 Basal cell carcinoma, squamous cell carci-
noma, and melanoma can also develop from photoaging.
Intrinsic skin aging results in thin, fragile, finely wrinkled,
inelastic skin. Hemangiomas and seborrheic keratosis can also
develop.45
Skin cancer is associated with both aging and photoaging
with exposure to UVB radiation. Basal cell carcinomas, squa-
mous cell carcinomas, premalignant actinic keratoses, and
melanomas are all related to sun exposure. Treatment of pre-
malignant and malignant skin lesions is necessary for overall
health measures, unlike cosmetic-related skin procedures.
Skin damage can be quantitated by the use of scales proposed
by Griffiths or Glogau.46,47 The Glogau skin classification
provides specific criteria with five skin types based upon the
degree of skin wrinkling, photoaging, and acne scarring.47
Another recently developed skin classification was developed
by Obagi, which includes skin color, oiliness, thickness, laxity,
and fragility along with suitable skin rejuvenation procedures,
including preoperative and postoperative skin care recom-
mendations48 (Table 14-2).
A multitude of treatments are available for photoaging
including both topical treatments, such as retinoid vitamin A
derivatives, alpha hydroxy acids derived from fruit and dairy
 CHAPTER 14 •
TABLE 14-2 Comparison of Patient Evaluation Methods for Facial Laser Procedures
Facial skin classification Fitzpatrick
Criteria used Skin reactivity/skin color with UV radiation Wrinkles/photoaging
Classes I-VI
Evaluation outcome Potential hyperpigmentation/hypopigmentation
post-laser treatment
Drawbacks Specific skin problems (wrinkling/photodamage)
and procedure selection are not addressed
products, and antioxidants, such as vitamin C- and E-related
compounds.45 Rejuvenation procedures can include the use of
botulinum toxin injection, augmentation of soft tissues with
collagen or hyaluronic acid fillers, and resurfacing with peeling,
dermabrasion, or laser resurfacing. Soft tissue augmentation
by the injection of gel type of fillers to treat wrinkles, rhytids,
for lip enhancement, and to smooth facial contours are cur-
rently a temporary measure as a result of degradation, with the
need for repeat treatment through periodic maintenance.
Skin resurfacing is used for the treatment of photodamaged
skin by generalized controlled wounding, which stimulates
new skin growth. The new skin replaces the photodamaged
epidermal layers and tightens the dermal layers by shortening
existing collagen along with the production of new collagen,
improving the overall facial appearance.49 Resurfacing can be
accomplished through the use of chemical peels through con-
trolled injury, mechanical dermabrasion, and laser skin resur-
facing. All methods can be divided into superficial depth into
the stratum corneum and papillary dermis, middepth of the
upper reticular dermis, and deep wounding of the midreticular
dermis.45
Thorough evaluation of the patient, especially in regard to
skin condition, is needed to determine the most effective skin
resurfacing modality. Commonly, the depth of skin surface
irregularities correlates to the depth of injury needed by the
resurfacing. Consideration of scar formation must be discussed
along with other important aspects of overall facial health,
including any history of facial trauma, facial surgery, prior
rejuvenation or resurfacing procedures, radiation therapy, and
recurrent herpes viral infections.
Active herpes infection of the face is a contraindication
for resurfacing, and the procedure should be postponed until
complete resolution of the infection. The patient should be
started on prophylactic acyclovir at 400 mg b.i.d. starting 2
days before the procedure and maintained until 5 days after
the procedure or, alternatively, valacyclovir (Valtrex) 500 mg
b.i.d. with the same regimen.50 Additional attention should
be placed on the use of certain medications that affect facial
healing and possible hyperpigmentation, including isotreti-
noin, corticosteroids, and hormone replacement therapy. Skin
color based on the Fitzpatrick skin classification system, which
addresses the ability to tan or burn, should also be used to
screen patients.51 Patients with darker skin types are at a
greater risk for hypopigmentation with procedures extending
into the reticular dermis.
Lasers in Oral and Maxillofacial Surgery 249
Glogau Obagi
Skin variables (Color, oiliness,
hickness, laxity, fragility)
I-IV Skin types
Quantifies photodamage Correlates suitable procedures
and potential complications
Procedure selection is not addressed Extensive/complex classification
and treatment list
Antiinfective use with laser skin resurfacing for bacterial
prophylaxis is controversial with no conclusive literature sup-
porting the use of antiinfectives. Generally, antiinfectives
should be considered if occlusive skin dressings are used for
periods greater than 48 hours after laser skin resurfacing.
Extended use of occlusive dressings can place the patient at
risk for bacterial and fungal infections.50
The development of laser skin resurfacing has replaced the
use of dermabrasion procedures to correct superficial skin
imperfections. Laser resurfacing most commonly uses pulsed
CO2 lasers to produce controlled photothermal skin damage
of layers of the epidermis and outer dermis. Outer epidermal
layers are vaporized, and additional heat transfer produces
collagen shrinkage resulting in contraction of the dermis,
which eliminates superficial skin imperfections along with an
overall tightening of the face.
The use of the CO2 laser under various laser modalities,
such as limited dwell time, pulsation, and delivery time, can
limit overall thermal damage and obtain superior results. Pulse
duration can range from 600 microseconds to 1 ms.52 Laser-
delivered energy provides better control to the skin than the
use of chemical peels. CO2 lasers provide optimal treatment
of cutaneous photoaging, especially for lighter skin types.
Laser skin resurfacing is well known to be useful for treat-
ment of irregular pigmentation, acne scars, lentigines, fine
wrinkles, shallow rhytids, actinic keratosis, and other effects
of photodamaged skin. The treatment of deep rhytids with the
CO2 laser can result in suboptimal scarring and cutaneous
depigmentation. Care must be demonstrated with full-face
resurfacing because of possible hypopigmentation and ery-
thema, although the use of hydration under the topical anes-
thetic EMLA (eutectic mixture of local anesthetic) can limit
the incidence of thermal damage and injury producing subop-
timal results.53
The Er : YAG laser (erbium : yttrium-aluminum-garnet
laser) can be used for patients with dark skin color or pig-
mentation to limit thermal injury because the Er : YAG laser
energy is better absorbed by water than CO2 laser energy,
resulting in less thermal damage.45 The use of newer tech-
niques, such as nonablative laser resurfacing, has limited epi-
dermal damage while applying selective energy to the dermis.
The epidermis is spared by selective cooling. The overall
benefit is improved overall healing as a result of limited epi-
dermal damage, with less need for anesthesia of the skin and
simplifying overall wound care.53 This technique can be used
250 SECTION II ■ Dentoalveolar Surgery
for all skin types and is useful to treat fine skin lines and
shallow rhytids not associated with muscular movement,
although the nonablative treatments are less effective than
skin resurfacing.
The use of skin conditioners can improve overall laser skin
resurfacing results. The skin conditioners should be used pre-
operatively and postoperatively. The preoperative benefits of
skin conditioning include enhanced wound healing and limit-
ing pigmentation changes associated with the procedure.
Regimens include the use of tretinoin to normalize keratiniza-
tion, regulate skin depigmentation, and increase collagen
production for faster wound healing. Hydroquinone, as a skin
lightener, is used to decrease melanocyte activity to minimize
hyperpigmentation during healing. In general the epidermal
cell cycle time is 6 weeks to allow maturation of keratinocytes
for the basal layer to the stratum corneum, and the skin con-
ditioning program should be started, in general, for approxi-
mately 6 weeks before laser skin resurfacing.50 The program
should then be reinitiated after reepithelialization and healing
along with the use of sunblocks when exposed to outdoor
sun.
Wound healing after laser resurfacing can be improved
with the use of occlusive dressings and tretinoin. The overall
healing period lasts from 5 to 10 days depending on the depth
of resurfacing. Occlusive dressing, such as nonstick pads
(Telfa), silicone sheeting, and hydrogels, can promote faster
reepithelialization and decrease pain.50 The occlusive facial
dressings are generally used for the first 48-hour period follow-
ing laser treatment.50 The patient then is instructed to gently
cleanse their face twice daily and to apply emollients, such as
Aquaphor, petrolatum, Cetaphil, or Eucerin.45 The use of
compresses with water and mild acetic acid are used every 4
to 6 hours to decrease bacterial counts of the skin. The com-
presses are then followed by the reapplication of the emol-
lients. Sun exposure should be avoided for 3 to 6 months after
the facial laser treatment, and then a routine sun exposure
regimen should be initiated.45
Overall contraindications to laser skin resurfacing include
a multitude of conditions. Recent cosmetic facial procedures,
such as face-lifts, brow-lifts, or rhinoplasty, can interrupt lym-
phatic drainage and result in extensive edema after surgery.50
Medication use, such as steroids, retinoids, d-penicillamine,
and dilantin, is a contraindication to laser resurfacing.50 Psy-
chiatric disorders such as body dimorphic syndrome, prior
radiation treatment of the skin resulting in loss of adnexal
structures, and any history of keloid or hypertrophic scar for-
mation are all contraindications to laser skin resurfacing.
Active skin disorders, such as rosacea, acne, psoriasis, or ver-
rucae infections, are also contraindications to laser skin resur-
facing. Social factors, such as smoking, can also cause delayed
healing following laser resurfacing.50
Common complications of laser skin resurfacing can often
result from overaggressive treatment. The complications can
include persistent erythema beyond 2 to 3 months and hyper-
pigmentation, especially in patients with darker skin types,
such as Asians, Hispanics, and African-Americans.54 The
hyperpigmentation will usually resolve with time, sun expo-
sure protection, and possible treatment with topical steroids,
Retin-A, and hydroquinone. Hypopigmentation, as a result
of overtreatment, can be more serious because it can be per-
manent as a result of violation of melanocytes and will mani-
fest as a late complication months after treatment. Extreme
care should also be taken in patients with vitiligo because
the Koebner phenomenon can result in unmasking more
areas of vitiligo.19 There are no specific treatments for
hypopigmentation, and exposure to the sun will not fade the
area, making it very problematic. Hypertrophic scarring is
another complication of laser skin treatment and also results
from overaggressive treatment into the underlying deep
dermal layers of the skin, especially in the perioral region of
the face.55 Hypertrophic scarring can be difficult to predict,
although patients of dark skin types, such as African-Ameri-
cans or Asians, are more prone to this complication. Preven-
tion by limiting the laser energy and only treating the skin
to a chamois or champagne color to prevent overtreatment
into the dermis is advised by Niamtu.54 Treatment of hyper-
trophic scars can include traditional methods, such as steroid
scar injections, topical steroids, use of silicone sheets, or cus-
tomized elastomeric compression dressings, such as those used
for burns.
Scar revision for both traumatic and surgical scars is another
excellent indication for laser surgery. The ability to revise
scars through the use of a nonablative pulsed dye laser with
wavelengths of 585 nm has provided beneficial results with
decreased erythema and hypertrophy.56 The laser stimulates
collagen remodeling and production of new collagen along
with minimizing the fibroblast scar response. Multiple laser
scar treatments may be needed to achieve optimal clinical
results, and the laser scar revision therapy can be combined
with other treatments, such as steroid injections.
Blepharoplasty procedures have also been performed with
a variety of lasers, including the CO2, Nd : YAG, or KTP
lasers. The goal of blepharoplasty surgery is to create aesthetic
and functional eyelids with the removal of prolapsed fat and
redundant eyelid skin.57 The laser aids in providing excellent
hemostasis, allowing a clean dissection to minimize ecchymo-
sis and edema. Preparation includes the use of metal corneal
shielding. A standard scalpel blade incision through skin is
usually made, and the dissection is then continued with the
laser in a cutting focused mode to continue the dissection to
remove the excess skin and redundant orbicularis muscle. The
removal of the herniated fat pads is also performed with the
laser. The overall procedure results in better hemostasis with
the use of the laser than surgery with the use of blades and
electrocautery. The option of laser skin resurfacing is also
provided with the use of the laser if any skin redundancy exists
when a transconjunctival access is used.
Complications of laser-assisted blepharoplasty procedures
include potential damage to the globe, the associated perior-
bital skin and appendages such as lashes, and the lacrimal
apparatus. Complications associated with any other type of
blepharoplasty procedure including ectropion, entropion,
excessive scleral show, and wound infection or breakdown can
also be encountered with the use of the laser. The use of laser-
 CHAPTER 14 •
assisted blepharoplasty or laser skin resurfacing of the eyelids
should be performed with extreme caution in patients who
have had previous blepharoplasty procedures because these
patients are very prone to ectropion with additional proce-
dures.19 Laser skin resurfacing modalities can also be used
alone to treat skin wrinkles of the lower lid either in combina-
tion with a transconjunctival blepharoplasty procedure or
combined with a delayed blepharoplasty procedure using cuta-
neous incisions. The laser skin resurfacing of the lower lid is
performed with a CO2 laser as a single pass to treat fine skin
wrinkles.57
■ LASER TREATMENT OF
VASCULAR LESIONS OF
THE FACE
The laser-assisted treatment of vascular lesions of the face
provides the major benefit of not having to excise tissue with
the resultant scarring and cosmetic defects. The use of the
pulsed dye laser at 580 nm and short pulses of 450 microsec-
onds is the preferred treatment of vascular lesions, including
hemangiomas, vascular malformations, and ectasias.58 The
short pulse permits selective energy transfer to the targeted
blood vessels and hemoglobin while minimizing heat conduc-
tion and damage to adjacent tissue.
Hemangiomas are a common benign vascular lesion present
at birth or shortly after and with more than 80% appearing in
the head and neck region.58 The hemangiomas can be super-
ficial or deep and exhibit a growth phase of approximately 18
months followed by an involution phase of 3 to 10 years,
although the lesion may be cosmetically and socially unac-
ceptable.58 Vascular malformations are always present at birth,
vary in color, do not demonstrate a proliferation or involution
phase, and grow slowly in conjunction with the patient’s
overall growth. Ectasias are permanently dilated vessels in the
skin that are visible to the naked eye and do not exceed
1.0 mm in diameter.59 Telangiectasias are acquired and grow
with age and can be associated with intrinsic factors such as
cutaneous disorders, including rosacea, and systemic diseases,
including carcinomas, collagen vascular diseases, or preg-
nancy. Telangiectasias can also be associated with extrinsic
factors, such as alcohol or estrogen use and facial trauma.58
The pulsed dye laser has been used to treat the cutaneous
vascular lesions of the face, such as ectasias and port-wine
stains, with the laser energy focusing on the oxyhemoglobin
chromophore within the vasculature of the lesions while
sparing the adjacent normal tissue. Ectasias can often be
treated with a single session, whereas larger port-wine stains
require multiple sessions.58 Ectasias can often be treated with
a single session, whereas port-wine stains will usually require
multiple sessions.
■ LASER TREATMENT OF
CUTANEOUS PIGMENTED
LESIONS OR TATTOOS
Treatment of cutaneous pigmented lesions is another common
use for lasers with either ablation or resurfacing techniques.
The pigmented melanocytes allow the effective laser treat-
Lasers in Oral and Maxillofacial Surgery 251
ment and the type of laser used, and wavelength will depend
on the depth of the lesion. The need for accurate diagnosis of
cutaneous pigmented lesions is absolute, and a biopsy should
be performed before any laser treatment with the patient
being well informed about the possible need for additional
treatment depending on the final histologic diagnosis.
Ablative lasers, such as the CO2 and erbium : YAG, can be
used, but do not target any specific chromophore, therefore
careful removal of the lesion to prevent scarring must be
demonstrated.58 The need to establish the depth of the mela-
nocytes either into epidermis or deeper into the dermis must
be diagnosed because the deeper lesions cannot be superfi-
cially ablated. The use of noncontact Nd : YAG or the
Q-switched ruby laser has been useful to treat deeper pig-
mented lesions, including melanotic nevi, nevi of Ota, blue
nevi, and solar lentigines, because these lasers generate longer
wavelengths of high peak energy at rapid pulses, allowing
deeper tissue penetration without excess scarring or tissue
destruction.60
The use of the laser for removal of intentional or traumatic
tattoos is another commonly performed cosmetic procedure.
Removal of tattoos is often desired because the patient will
often perceive the tattoo as unaesthetic for a variety of reasons,
including fading of the ink, nonprofessionally produced
tattoos, or wanting to remove a symbol or letters after a period
of time. Tattoos were previously treated with the CO2 laser in
the 1990s, although the use of the CO2 laser for this purpose
has been replaced by other types of lasers specific for certain
tattoo colors specified by the wavelength emitted.61 The
removal of tattoos has been successful through the use of the
Q-switched ruby laser.58 Tattoo pigment within the dermis
selectively absorbs the laser waves and is fragmented into
small particles, which are able to be phagocytized by macro-
phages within the body to produce a gradual fading of the
tattoo over time without affecting the overlying epithelium.
Multiple laser removal sessions can be required for some
tattoos. Results are better than previously attempted methods,
such as dermabrasion or excision, because of a lower incidence
of hyperpigmentation or hypopigmentation and decreased
scarring.
■ LASER HAIR REMOVAL
Laser removal of unwanted hair or laser hair reduction is one
of the most commonly performed cosmetic procedures. Exces-
sive hair growth represented by either hirsutism, hair in
unusual places, or hypertrichosis, representing excessive non-
androgenic hair growth in men and women, which can be
localized or generalized throughout the body.62 The procedure
is regulated by the U.S. Food and Drug Administration guide-
lines, which require a 30% reduction of hair growth at 3
months following a single laser hair reduction treatment,
although the need for an additional three to five treatments
is not uncommon.62 Laser hair reduction is based on the affin-
ity of exogenous chromophores or melanin within the hair
shaft to laser waves with the heat production killing the hair
follicle. Ruby, alexandrite, and Nd : YAG lasers can be used
252 SECTION II ■ Dentoalveolar Surgery
for laser hair reduction with wavelengths of approximately
500 to 1000 nm at longer pulsations of greater than 100
microseconds used to destroy hair follicles while preserving
the epidermis.63 Laser hair reduction can only occur in the
telogen phase of the three phases of hair growth. During the
telogen phase, the follicle is preparing to grow new hair and
the chromophores are most sensitive to the laser energy. Laser
hair reduction may therefore require multiple intermittently
spaced laser treatments to increase the success of overall hair
reduction.
■ LASER TREATMENT OF SLEEP
APNEA AND SNORING
The use of the laser in the treatment of sleep apnea and
snoring is well documented. Obvious benefits of laser surgical
treatment of the soft palate and posterior airway include
excellent hemostasis, ease of use of the laser in the posterior
airway, and decreased postoperative pain and scarring.64 The
laser is commonly used to perform uvulopalatoplasties (UPP)
for the treatment of snoring and uvulopalatopharyngoplasties
(UPPP) for the treatment of mild sleep apnea. Overall, goals
of surgical therapy are aimed at an increase in the posterior
airway space and elimination of the need for multiple repeat
procedures for effectiveness because patients often refuse addi-
tional surgery following the initial procedure. The effective-
ness of the one-stage procedure for the UPPP is based on the
use of anatomic principles relying on the anatomy of the
palatal musculature with the goal of leaving the levator
muscles intact.65
The patient requires a thorough work-up with an accurate
diagnosis before any surgical treatment with an emphasis on
differentiation of snoring from sleep apnea.65 Snoring is often
a component of sleep apnea in combination with other clini-
cal symptoms, and patients with symptoms compatible with
sleep apnea should have a sleep study performed to confirm
the diagnosis. The work-up of a patient for sleep apnea centers
around differentiating if the sleep apnea is central or the result
of airway obstruction and centers around the use of a sleep
study or polysomnogram to correlate hypoxic events with
effects on the cardiovascular status of the patient. Additional
studies include cephalometric radiographic, MRI, or CT scan-
ning before treatment. A thorough evaluation of the upper
airway including nasopharyngoscopy with attention to certain
airway maneuvers, such as Mueller’s maneuver or a reverse
Valsalva with collapse during active inspiration with closure
of the mouth and nostrils, should be performed for a complete
airway evaluation.65
A polysomnogram and respiratory distress index (RDI) are
the gold standards in the diagnosis of sleep apnea based on
the number of hypopneas and apneas over a period of time,
including electroencephalographic data to correlate the stages
of sleep with the apneic events over time. The sleep study can
be performed in a sleep lab or at home through recording
devices or via continuous pulse oximetry with a recording over
the course of sleeping at night. Common clinical signs of sleep
apnea include daytime somnolence and cardiac and respira-
tory status changes. Laboratory studies will often show poly-
cythemia associated with sleep apnea. The ultimate goal is to
determine if the patient has sleep apnea or snoring and to treat
the patient appropriately because multiple surgical options are
available.66
Surgical treatment of snoring includes the treatment of
nasal obstruction and palatopharyngoplasty, whereas the
treatment of sleep apnea involves more aggressive protocols,
such as those of the Stanford protocol.67 This protocol involves
stage I procedures, such as palatopharyngoplasty, genioglossus
advancement, and nasal and hyoid surgeries, whereas stage II
involves maxillomandibular advancement surgery.67 The sur-
gical procedures have a better overall success rate as a result
of poor compliance issues with the use of methods, such as
continuous positive airway pressure (CPAP) or other devices
for jaw repositioning or more cosmetically acceptable proce-
dures than surgical tracheostomy.
Laser-assisted uvulopalatoplasty (LAUPP) has been used to
effectively treat snoring since the 1990s when the procedure
was developed by Kamani.68 Success rates with the LAUPP
are approximately 95%, which is similar to success rates of
the more aggressive laser-assisted uvulopalatopharyngoplasty
(LAUPPP).68 The LAUPP is based upon a circumferential
excision of the uvula and a portion of the soft palate that
produces scarring and contracture, which decreases the size of
the soft palate. Some studies have also indicated the LAUPP
can be beneficial for the treatment of mild sleep apnea.65
Limitations of the LAUPP and LAUPPP must be addressed
for the treatment of sleep apnea because inadequate lowering
of the RDI with these procedures alone can often result.
LAUPPP has proven to be beneficial for the treatment of
moderate to severe sleep apnea and is often combined with
other maxillofacial or skeletal procedures, such as genial
advancement or hyoid suspension. Major concerns with the
use of the LAUPP and LAUPPP are the possibility of velo-
pharyngeal incompetence postsurgically, although this is a
rare occurrence.64
LAUPP can be performed in an office setting with the
patient in an upright position under intravenous sedation and
local anesthesia, although patients with large tonsils or a
severe gag reflex should not be treated with LAUPP. The
patient is positioned upright to provide better access to the
soft palate and to allow use of the palatal backstop hand piece
with the palate positioned inferior and vertically away from
the posterior pharyngeal wall. Before introduction of local
anesthesia, the levator veli palatini muscle is located in the
area of the palatal dimple or folding and can be marked to
preserve the vertical palatal pull and prevent velopharyngeal
insufficiency.65
The procedure is performed with the backstop hand piece
in place to protect the posterior pharyngeal wall, and the laser
is set on a high power of 15 W with a 0.1- to 0.8-spot size and
is used with short continuous lasing to prevent excess thermal
conduction.64 The uvula, soft palate, and tonsils are resected
by the development of two vertical cuts, or trenches, in the
soft palate to a level inferior to the levator veli palatine
 CHAPTER 14 •
musculature.64 The vertical cuts are then connected horizon-
tally to remove the soft palate and uvula. The tonsillar pillars
are then excised in a superior to inferior direction, and addi-
tional soft palate in the lateral aspect can be removed if neces-
sary to improve the airway patency without compromising
palatal closure velopharyngeal competence.64 The wounds
heal by secondary intention, and suturing is usually not needed
because the laser provides excellent hemostasis.
LAUPPP can be performed to treat sleep apnea, often in
conjunction with other procedures to increase the overall
success rate. The LAUPPP can be performed in the office
under intravenous sedation and local anesthesia, although the
procedure is usually performed in the operating room because
other surgical procedures such as hyoid or genial advance-
ments can also be performed. The uvula, soft palate, and
anterior and posterior tonsillar pillars are removed, and the
lateral pharyngeal tissue is sutured to provide maximal airway
dilation. The patient should also have had any hypertrophic
tonsillar tissue removed to ensure maximal benefit of the
LAUPPP.
The LAUPPP is performed in a similar manner to the
LAUPP because vertical trenching incisions are made in
the soft palate as lateral as possible to remove tissue from the
anterior and posterior tonsillar pillars.64 A horizontal incision
is then made to connect the vertical incisions, and a triangular
section of palatal tissue is removed between the oral and nasal
aspects of the palatal mucosa. The posterior flap of nasal
mucosa is positioned forward and anterior and is sutured to
the anterior palatal oral mucosal flap to maximize the opening
of the airway.64
Complications of the LAUPP and LAUPPP can include
sore throat and difficulty swallowing. The patient is encour-
aged to maintain hydration, and a soft diet is maintained
along with supportive care with salt water rinses, the use of
anesthetic lozenges, humidified air, and analgesics. Patients
undergoing an LAUPPP are often monitored postoperatively
in the hospital for airway compromise or obstruction.64
Steroids should be used with the LAUPP to minimize edema.
Bleeding events are possible but rare because the laser pro-
vides excellent hemostasis with the procedure. Velopharyn-
geal incompetence, although rare, can also develop if the
levator muscles are violated, although the incompetence will
often resolve after a period of time.64 Infections are rare as a
result of the use of antiinfectives with the procedures. Excess
scarring is also possible and can cause velar insufficiency or
speech problems, although the incidence is rare if the laser is
used in a controlled manner to prevent thermal damage of
adjacent tissue.
The use of the LAUPP has been successful to treat prob-
lematic snoring, although the success of the LAUPPP alone
for the treatment of sleep apnea can be unsuccessful depend-
ing on the severity of the sleep apnea.69 Postsurgical sleep
studies should be performed to assess the effectiveness of
treatment if the LAUPPP alone is used for the treatment of
sleep apnea. Combined surgery of the LAUPPP and other
surgical procedures for airway advancement, such as hyoid
Lasers in Oral and Maxillofacial Surgery 253
or genial muscle advancement, is often needed to relieve
sleep apnea, and some cases will require maxillomandibular
advancement surgery to alleviate the sleep apnea in severe
cases.70
■ LOW-LEVEL LASERS
Low-level laser therapy (LLLT) uses a phototherapeutic
process through the use of low-level lasers with wavelengths
in the visible and invisible range of 400 to 800 nm and a low
power of 1 to 75 mW.71 The low-level lasers can be used
for phototherapy to deliver a small amount of energy to the
exposed living cells with minimal to no appreciable heat pro-
duction and beneficial cellular effects labeled as biomodula-
tion or biostimulation.72 The effects of LLLT are not recognized
in the United States as FDA-accepted therapy, and it is per-
mitted for use only as a clinical research tool, resulting in
“off-label” use by health care practitioners and others.71 The
LLLT produces no tissue damage or thermal changes, making
it relatively safe to use, and LLLT is classified as having no
significant associated medical risks with use by the FDA and
requires no specific precautions other than eye protection and
avoidance of use on cancerous tissues, the thyroid, reproduc-
tive organs, infected wounds, with pregnant patients, and
patients with cardiac pacemakers.71
The effects of LLLT are not completely understood, but
benefits on living tissues have been proposed as a result of
multiple mechanisms that include changes in microcircula-
tion, cell membrane potential, increased cellular metabolism,
activation of cellular enzymes, increased wound healing,
decreased inflammation, increased oxygen consumption, and
other changes.72 The changes produced by the LLLT results
in a photochemical effect on biologic molecules within cells
to affect the cell by altering the cellular reactions, membranes,
energy use, and metabolism to produce a therapeutic effect on
the tissues in the area of the therapy. LLLT may also stimulate
production of substances, such as prostaglandins, endorphins,
enkephalins, and other vasoactive or pain-modulating chemi-
cals, resulting in decreased pain, decreased inflammation, and
increased healing.73
■ LASERS AND WOUND HEALING
There have been many studies undertaken to associate the use
of LLLT with wound healing. The possible association of
LLLT with increased wound healing has been postulated
because of alteration of the fibroblast response and collagen
production to result in more efficient and faster wound
healing.74 The effects have been documented in animal studies,
and current beneficial applications include the possible use
with diabetic wounds, infections, and tissue grafting.
■ LASERS AND BONE HEALING
Laser irradiation of bone has been investigated to evaluate
possible enhanced bone healing. Multiple studies have shown
increased bone healing in animals when exposed to low-level
laser energy over short periods of time up to 2 weeks. Proposed
theories include a possible increase in the activation of
254 SECTION II ■ Dentoalveolar Surgery
cellular enzymes, increasing cellular energy, and release of
cellular calcium; increased cellular matrix production;
increased activity of bone marrow cells; or possible increased
differentiation of cells into osteocytes.75
The effect of LLLT on alveolar bone healing in rats was
also performed by Takeda in 1988.76 Results showed a more
rapid ossification of bone with irradiation. The study suggests
that low-level radiation with a laser may aid in fibroblast pro-
liferation along with the formation of trabecular osteoid tissue
formation. Another recent study by Weber et al. studied the
use of LLLT with autologous bone grafting in rats.75 The
results revealed qualitative and quantitative healing of bone
grafts with the use of LLLT, resulting in a positive biomodulat-
ing effect on the healing of autologous bone grafts. Additional
controlled studies are needed to evaluate the effects of LLLT
on bone healing involving clinical applications, such as
fracture healing, bone grafting, and implant healing and
integration.
■ EFFECTS OF LASERS ON
POSTOPERATIVE PAIN
AND SWELLING
The use of LLLT to modulate the pain response has also been
investigated and proven to be beneficial. LLLT has been
shown to modulate the pain response by producing an
analgesic-like effect, possibly by increasing the pain threshold
and modulating the pain response of nerves.77 The inflamma-
tory response to prostaglandins may also be altered to decrease
the amount of overall inflammation, edema, and pain associ-
ated with surgical procedures postoperatively.77 Overall results
have been somewhat inconsistent regarding the pain response
with LLLT following extraction or surgical removal of teeth.71
The use of LLLT with nerve paresthesias has also been evalu-
ated with patients reporting improved sensation and comfort
following the use of LLLT. Multiple studies have shown LLLT
to be beneficial in the treatment of paresthesias resulting in a
reduction in the severity and a decrease in the overall distribu-
tion of the sensory changes.78 The ability of LLLT to modulate
healing and pain responses postsurgically may need additional
investigation with controlled studies to determine the overall
benefits of LLLT with surgical pain and edema because optimal
laser energy levels, exposure times, and number of optimal
treatments should be evaluated (Box 14-2).
BOX 14-2 Effects of Low-Level Laser Therapy (LLLT)
Pain modulation
Increased microcirculation
Reduced tissue inflammation and edema
Accelerated wound healing
Muscle relaxation
Accelerated bone repair
Enhanced immune reactivity
Increased cellular ATP production
Increased cellular membrane transport
■ LASER APPLICATIONS FOR
GENERAL DENTISTRY
The application of lasers for general dental use continues to
grow with routine use for restorative dentistry, periodontal
care, orthodontics, and dental hygiene. The use of soft tissue
lasers is becoming increasingly popular for preprosthetic gin-
gival procedures. The benefit of hemostatic control with the
excision of gingival tissue can produce optimal restorative and
prosthetic results.79 Restorative and prosthetic treatment often
require the removal of gingival tissue to gain access for the
treatment of tooth structure below the gingival margin or for
gingival excision, required for moisture control with gingival
inflammation.
Gingival tissue can be removed by the use of a scalpel,
electrosurgery, or laser. The use of the scalpel has the disad-
vantage of eliciting bleeding, which is a major disadvantage
with subsequent restorative dental treatment. Electrosurgery
can also be used to remove gingival tissue with good hemo-
stasis, although excess heat can be generated, which can cause
irreversible recession of the soft tissue at the gingival margins
or possibly damage underlying alveolar bone.79 The recession
can possibly lead to exposure of restorative margins, resulting
in suboptimal aesthetics in the anterior zone of the mouth.
Lasers can offer a greater degree of control for the removal of
gingival tissue with minimal damage to the adjacent soft
tissue. Diode lasers offer the advantage of operating at wave-
lengths that are absorbed by gingival tissue and not by adja-
cent tooth structure.79
Aesthetic crown lengthening can be performed with the
use of a diode laser with 810 nm wavelengths.79 The use of the
diode laser provides greater operator control for the creation
of more precise gingival margins. Before the use of the diode
laser for gingival recontouring or crown lengthening, a thor-
ough periodontal evaluation should be performed with atten-
tion to the biologic width, indicating the amount of attached
gingival tissue and the location of crestal bone. The determi-
nation of the possible need for osseous contouring via flap
surgery versus soft tissue contouring alone can be determined.
The use of the diode laser also facilitates the placement of
final direct bonded or provisional prosthetic restorations as
hemostasis is achieved.
Diode lasers at a wavelength of 810 nm exhibit little or no
affinity for hard tooth structure, metal alloys, composites, or
porcelain.79 This benefit allows the laser to be used for soft
tissue recontouring procedures around tooth structure or
dental implants. The laser has little to no effect on cementum
or enamel and does not conduct or produce heat through the
tooth or existing metal tooth-related structures, thereby pre-
venting thermal pulpal injury.
The diode laser is used with the tip contacting or a few
millimeters away from the gingival soft tissue, with aiming
facilitated by a guide beam. The removal or contouring of
gingival tissue is performed along the tip of the laser with a
shallow tissue penetration producing a slower but more con-
trolled cutting of soft tissue than with an electrosurgical unit.
 CHAPTER 14 •
The diode laser is usually used in a pulsed mode to minimize
thermal conduction to adjacent tissue and to minimize car-
bonization and char formation. The development of an exter-
nal bevel to provide optimal gingival contour can be used with
hemostasis, providing increased patient comfort.
The use of the laser to aid in taking accurate impressions
can be performed for optimal prosthetic results. Exposure of
subgingival finish lines combined with good moisture control
through hemostasis can be obtained with the use of the diode
laser. This technique eliminates the need for a retraction cord
and produces minimal adjacent tissue necrosis to preserve and
allow complete regeneration of adjacent soft tissue with little
to no gingival recession as a result of the use of a pulsed mode
and air or water cooling with the laser.79
Lasers are increasingly being utilized for minor soft tissue
procedures related to orthodontic treatment.80 Lasers can be
used to treat gingival hyperplasia secondary to orthodontic
treatment as a result of poor oral hygiene measures. Aesthetic
tissue contouring with altered tooth eruption and soft tissue
exposure of unerupted teeth can be performed to provide
optimal orthodontic results. Often these laser soft tissue pro-
cedures can be performed by the treating orthodontist with
topical anesthesia alone.
The diode laser is an excellent tool for soft tissue recon-
touring procedures with no effect on the teeth and related
hard tissue components. The laser energy results in the pro-
duction of some heat, which vaporizes cells through a photo-
thermal effect called ablation when the tissue separates as an
incision and hemostasis occurs. The resultant soft tissue wound
heals faster with minimal pain because the wound is sealed,
sanitized, and protected by a biodressing.80
The creation of optimal aesthetics following orthodontic
treatment can be planned because ideal embrasures and gin-
gival contours can be achieved by the orthodontist. Delayed
passive eruption limiting crown exposure can be treated with
the diode laser to facilitate proper orthodontic bracket place-
ment. Proper bracket placement allows proper orientation and
alignment of the tooth with the use of preformed wires. The
diode laser can also be used to expose unerupted teeth for
orthodontic bonding. This technique facilitates the eruption
of teeth, allowing the completion of the orthodontic treat-
ment in a more timely manner. The unerupted tooth can be
exposed with excellent hemostasis to facilitate bonding of the
tooth at the time of the exposure during a single visit.
The diode laser can also be used to débride hyperplastic
tissue associated with inflammation as a result of poor oral
hygiene with orthodontic treatment.80 The diode laser removes
hyperplastic inflamed papillae and pseudopocketing to improve
the overall gingival health. It has become evident that the use
of the diode laser can be used to optimize the overall result of
orthodontic treatment through a variety of soft tissue proce-
dures ranging from the exposure of unerupted teeth to gingival
tissue modification and recontouring for optimal aesthetics.
The diode laser has also been used to perform crestal fiberoto-
mies to aid in the prevention of orthodontic relapse and to
assist in the rotation of teeth as a quick and bloodless proce-
Lasers in Oral and Maxillofacial Surgery 255
dure versus the use of a blade.80 Lasers are even being used by
orthodontists for hands-on treatment or by referral to other
dental specialists for aesthetic and functional laser surgical
procedures.
The diode laser has been recently used as an adjunct treat-
ment of periodontal disease in combination with scaling and
root planing (SRP). The adjunctive effects of the diode laser
with conventional SRP has been proven to be beneficial.81
The use of the diode laser with SRP was noted to decrease
postoperative pain. The microbiology of the periodontal
pocket revealed a decrease in the number of microbial colony
forming units in laser-treated sites following SRP, including
decreased levels of Actinobacillus actinomycetemcomitans, which
is associated with aggressive periodontal disease.81 The use of
the diode laser provided an alternative means of treatment of
A. actinomycetemcomitans with periodontal disease versus tra-
ditional treatment with antibiotic therapy.
The reduction in bacterial colony forming units and the
overall reduction in A. actinomycetemcomitans bacteria has
been postulated to be a result of the bacteria responding to
the diode laser energy of 810 nm at 0.8 W, although this has
not been confirmed.81 The diode laser has also been used to
alter soft tissue in tooth furcation areas as removal of tissue
for access to the furcation for periodontal maintenance. The
diode laser also results in faster wound healing with SRP,
resulting in increased comfort of the patient following the
periodontal surgery.
Overall the diode laser at a wavelength of 810 nm and
power of 0.8 W was equivalent to the treatment of chronic
periodontitis with SCP in regard to a reduction of subgingival
bacterial counts and a reduction in pocket depth, although
the use of the diode laser did not result in an increase in the
periodontal attachment levels.81 The diode laser treatment of
periodontal soft tissues has proven to be beneficial in conjunc-
tion with SRP versus SRP alone, although additional con-
trolled studies are needed.
The use of the diode laser has also been applied with peri-
odontal management techniques performed by dental hygien-
ists, although the use of the laser by dental auxiliaries can be
limited. The use of the diode laser for the treatment of peri-
odontal disease is based on the model that periodontal disease
is an inflammatory response of the periodontal tissue to bacte-
rial infection and the presence of a biofilm in the periodontal
pocket.82 The use of the diode laser has offered the dental
professional an alternative treatment for periodontal disease
as a result of the bactericidal effect of the laser in combination
with SRP.
The technique involves placement of the tip of the diode
laser in the periodontal pocket, and the laser is moved in a
sweeping motion from anterior to posterior to the base of the
pocket. The optical fiber system to deliver the laser energy is
only end-lasing, with the energy exiting at the end of the fibers
and not from the side wall. The laser is directed parallel to
the root surface and should not be used directly on the root
surface. The laser produces a stimulatory effect on the gingival
soft tissue while reducing pocket depth and resulting in faster
256 SECTION II ■ Dentoalveolar Surgery
and less painful healing. The laser energy is not used to remove
tissue. It is only focused on the tissue within the pocket to
produce a nonablative thermal event, which decontaminates
the periodontal pocket by reducing the number of bacteria
within the pocket along with a decrease in the exotoxins, such
as hyaluronidase and collagenase, which are responsible for
periodontal tissue destruction.82 The laser-assisted SRP proce-
dure provides the benefit of hemostasis with a less invasive
procedure than flap surgery.
The latest use of the diode laser for periodontal therapy
involves the use of a diode laser with initial pathologic pocket
formation as indicated by loss of clinical attachment, bleeding
on probing, the presence of inflammation, and loss of alveolar
bone height.82 The diode laser is used as a preventive measure
in combination with SRP before pocket formation. The use
of the diode laser to control periodontal disease through tissue
débridement and bacterial reduction has been performed.
Studies have assessed the effect of the laser to decrease bleed-
ing on probing when used in combination with SRP versus
SRP alone. The laser can also be used to palliate pericoronitis
through the excision of the operculum in patients unable to
have the third molar removed at the initial appointment with
the patient informed of the need for third molar removal at a
later date.
General dental treatments where the laser has been benefi-
cial include the use of lasers for power bleaching of teeth. The
application of lasers for tooth bleaching raises the temperature
of hydrogen peroxide to accelerate the chemical bleaching
process through the use of the diode laser.83
The use of the laser with operative dentistry includes the
use of lasers for tooth preparation. The Er : YAG laser has been
used for removal of both enamel, dentin, and nonmetallic
restorations.83 The treatment is based on the expansion of
hydroxyapatite by laser energy heating the water within the
hydroxyapatite structure and ablating the crystal structure.
The laser can be used to remove decay or sound tooth struc-
ture and decreases the need for local anesthetic use because
the friction and heat production with drilling is eliminated.
The use of the laser with endodontic treatment has been
established for débridement of infected tissue and associated
bacteria. The laser has been shown to be an excellent tool to
clean and sterilize the root canal system. Studies have shown
the laser energy to be superior for the removal of microorgan-
isms within the canal and smear layer of the surrounding
dentin of the canal versus chelating agents or chemical irrig-
ants, such as hypochlorite.84 The lasers also have a bactericidal
effect to sterilize the canal before obturation. The use of lasers
for endodontic treatment is becoming more common and has
known benefits over traditional rotary instrumentation of
canals, such as ease of use, decrease in the separation of instru-
ments, and decrease in the number of endodontic failures.
The use of lasers is becoming more common within general
dentistry because lasers have become more specific regarding
treatment options, especially for providing treatment using
the highest degree of technology to provide benefits, such as
decreased procedure times and decreased patient pain.
■ LASER-SCAN-BASED NAVIGATION
IN CRANIOMAXILLARY SURGERY
Studies of the use of laser-scan-based registration were used
for the treatment of patients with tumors, bone malforma-
tions, and foreign bodies of the head by Marmulla et al.85 The
laser scan uses the registration of complete areas and surfaces
instead of the use of single-point registration markers, produc-
ing a more accurate surgical navigation system. The laser-
scan-based surface registration can be used in cranial and
maxillofacial surgery. The laser scanner has been used to scan
about 200,000 measuring points on a patient’s face within
about 2 seconds, functioning as a surgical system navigator
(SSN).85 The laser-scan-based marker system was more
accurate than marker-based registration systems alone, and
radiation associated with some scanning systems, such as
computerized axial tomography (CAT scanning) and the need
for the placement of artificial markers, such as titanium pins
or screws, can be avoided.
SUMMARY
The use of lasers for oral and maxillofacial surgical procedures
and for surgical and nonsurgical treatment modalities within
both oral and maxillofacial surgery and dentistry have devel-
oped over the last 35 years. The development of specific lasers
for specific applications has improved overall patient treat-
ment by allowing the surgeon to perform surgery more
efficiently, with less pain, less edema, excellent control of
hemostasis, and greater overall patient satisfaction. The time
has come where the surgeon can no longer rely on the use of
a single laser for patient treatment. There is a need for con-
tinuing education regarding the technology and applications
of lasers within the specialty of oral and maxillofacial surgery
because the wave of technology continues to advance at a
rapid pace. The laser has been and will remain a valuable
component of the oral and maxillofacial surgeon’s armamen-
tarium because the laser can perform a wide range of proce-
dures for a wide range of conditions to provide optimal patient
care.
REFERENCES
1. Einstein A: On the quantum theory of radiation, Physikal Zeitschr
18:121, 1917.
2. Guttenberg SA, Emery RW: Laser physics and tissue interaction,
Oral Maxillofac Surg Clin North Am 16:143-145, 2004.
3. Maiman TH: Stimulated optic radiation in ruby, Nature 187:493-
494, 1960.
4. Boulnois JL: Photophysical process in recent medical laser devel-
opments: a review, Lasers Med Science 1:47, 1986.
5. Colt HG, Mathur PN: Basic principles of laser-tissue inter-
actions, UpToDate version 14.3:1-5, 2004. Available at
www.utdol.com, Accessed Sept. 21, 2007.
6. Walsh JT et al.: Pulsed CO2 laser tissue ablation: effects of tissue
type and pulse duration on thermal damage, Laser Surg Med
8:108-118, 1988.
7. Hobbs EH et al.: Superpulsed lasers: minimizing thermal damage
with short duration, high irradiance pulses, J Dermatologic Surg
Oncol 13:955-963, 1987.
 CHAPTER 14 •
8. Grevelink JM: Facial contouring using a flashscanner-enhanced
carbon dioxide laser, Facial Plast Surg Clin North Am 4:241-246,
1996.
9. Chan HH et al.: Recurrence of nevus of Ota after successful
treatment with Q-switched lasers, Arch Dermatol 136:1175-1176,
2000.
10. Boyen DK: A brief overview of noninvasive lasers in cosmetic
maxillofacial surgery, Oral Maxillofac Surg Clin North Am 16:231-
237, 2004.
11. Patel CK, McFarlane RA, Faust WL: Selective excitation
through vibrational energy and optical laser action in N2-CO2,
Phys Rev 13:617.
12. Geusic JE, Marcos HW, Van Uitert LG: Laser oscillation in
Nd-doped yttrium aluminum yttrium gallium and gadolinium
garnets, Appl Phys Lett 4:182, 1964.
13. Bradley PF: A review of the use of neodymium YAG laser in oral
and maxillofacial surgery, Br J Oral Maxillofac Surg 35:26-35,
1997.
14. Wlodawsky RN, Strauss RN: Intraoral laser surgery, Oral Maxil-
lofac Surg Clin North Am 16:149-163, 2004.
15. Niamtu J: The treatment of vascular and pigmented lesions in
oral and maxillofacial surgery, Oral Maxillofac Surg Clin North
Am 16:239-254, 2004.
16. Freedman G: Impact of lasers continues to grow: buyer’s guide
to dental lasers, Dent Today 25(12):130-139, 2006.
17. Brandon MS, Strauss RN: Complications of CO2 laser proce-
dures in oral and maxillofacial surgery, Oral Maxillofacial Surg
Clin North Am 16:289-299, 2004.
18. Guttneberg SA, Emery RW III: Laser cosmetic skin resurfacing:
superpulsed perspective, Oral Maxillofac Surg Clin North Am
16:197-213, 2004.
19. Polanyi TG, Bredemeier H, Davis T: A CO2 laser for surgical
research, Med Biol Eng 8:541-548, 1970.
20. Zeinoun T et al.: Myofibroblasts in healing laser excision wounds,
Lasers Surg Med 28(1):74-79, 2001.
21. Strauss RA: Lasers in oral and maxillofacial surgery, Dent Clin
North Am 44(4):851-873, 2000.
22. Kaminer R et al.: Bacteremia following laser and conventional
surgery in hamsters, J Oral Maxillofac Surg 48:45-48, 1990.
23. Clayman L: Management of mucosal pre-malignant lesions, Oral
Maxillofac Surg Clin North Am 6(4):431-441, 1994.
24. Carruth JA, Simpson JT: CO2 laser surgery of the oral cavity,
Year Book Otolaryngol 132, 1988.
25. Horch H, Gerlach KL, Schaefer H: CO2 laser surgery of oral
premalignant lesions, Int J Oral Maxillofac Surg 15:19, 1986.
26. Milhaski S et al.: Laser surgery in otolaryngology-interactions of
the CO2 laser and soft tissue, Ann NY Acad Sci 267:263, 1976.
27. Sexton J: Laser management of vascular and pigmented lesions.
In Catone G, Alling C, editors: Laser applications in oral & maxil-
lofacial surgery, ed 1, Philadelphia, 1997, WB Saunders.
28. Parkins F: Lasers in pediatric and adolescent dentistry, Dent
Clinics North Am 44(4):821-830, 2000.
29. Kusek ER: Use of the YSGG laser in dental implant surgery:
scientific rationale and case reports, Dent Today pp 98-102,
2007.
30. Lee CY: Procurement of autogenous bone from the mandibular
ramus with simultaneous third-molar removal for bone grafting
using the Er,Cr : YSGG laser: a preliminary report, J Oral Implan-
tol 31:32-38, 2005.
31. Romanos G: Point of care: Is there a role for lasers in the treat-
ment of peri-implantitis? J Can Dent Assoc 71(2):117-118,
2005.
32. Ohnishi M: Clinical applications of arthroscopy in temporoman-
dibular joint diseases, Bull Tokyo Med Dent Univ 27:141, 1980.
33. McCain JP et al.: Temporomandibular joint arthroscopy: a 6 year
multicenter retrospective study of 4831 joints, J Oral Maxillofac
Surg 50:926-930, 1992.
Lasers in Oral and Maxillofacial Surgery 257
34. Indresano AT: Surgical arthroscopy as the preferred treatment
for internal derangements of the temporomandibular joint,
J Oral Maxillofac Surg 59:308-312, 2001.
35. Koslin M: Laser applications in temporomandibular joint
arthroscopic surgery, Oral Maxillofac Surg Clin North Am 16:269-
275, 2004.
36. McCain JP, de la Rua H: Principles and practice of operative
arthroscopy of the human temporomandibular joint, J Oral Max-
illofac Surg 1:135-152, 1989.
37. Koslin M: Advanced arthroscopic surgery, Oral Maxillofac Surg
Clin North Am 18:329-343, 2006.
38. Mazzonetto R, Spagnoli D: Long term evaluation of arthroscopic
disckectomy of the temporomandibular joint using Holmium
YAG laser, J Oral Maxillofac Surg 59(9):1018-1023, 2001.
39. Dolwick MF, Armstrong JW: Complications of temporoman-
dibular joint surgery. In Kaban L, Pogrel A, Perrott D, editors:
Complications in oral and maxillofacial surgery, Philadelphia, 1997,
WB Saunders.
40. Cetiner S, Kahraman S, Yucetas S: Evaluation of low-level laser
therapy in the treatment of temporomandibular joint disorders,
Photomed and Laser Surg 24(5):637-641, 2006.
41. Kulekcioglu S et al.: Effectiveness of low-level laser therapy in
temporomandibular joint disorder, Scand J Rheumatol 32:114-
118, 2003.
42. Nunez SC et al.: Management of mouth opening in patients with
temporomandibular disorders through low-level laser therapy
and transcutaneous electrical neural stimulation, Photomed Laser
Surg 24:45-49, 2006.
43. Gray RJ et al.: Physiotherapy in the treatment of temporoman-
dibular disorders: a comparative study of four treatments methods,
Br Dent J 176:257-261, 1994.
44. Hegedus F et al.: Non-surgical treatment modalities of facial
photodamage: practical knowledge for the oral and maxillofacial
professional, Int J Oral Maxillofac Surg 35(5):389-398, 2006.
45. Griffiths C: The clinical identification and quantification of
photodamage, Br J Dermatol 127:37-42, 1992.
46. Glogau RG: Aesthetic and anatomic analysis of the aging skin,
Semin Cutan Med Surg 15(3):134-138, 1996.
47. Obagi ZE: Skin classification. In Obagi ZE, editor: Obagi
skin health restoration and rejuvenation, New York, 2000,
Springer-Verlag.
48. Weinstein C: Ultrapulse carbon dioxide laser rejuvenation of
facial wrinkles and scars, Am J Cosm Surg 14:3-10, 1997.
49. Obagi S: Pre- and postlaser skin care, Oral Maxillofac Surg Clin
North Am 16:181-187, 2004.
50. Fitzpatrick TB: The validity and practicality of sun reactive skin
types I through VI, Arch Dermatol 124:869-871, 1988.
51. Holck DE, Ng JD: Facial skin rejuvenation, Curr Opin Ophthal-
mol 14:246-252, 2003.
52. Airan LE, Hruza G: Current lasers in resurfacing, Facial Plast Surg
Clinic North Am 10:87-101, 2002.
53. Niamtu J: Common complications of laser resurfacing and their
treatment, Oral Maxillofac Surg Clin North Am 12(4):579-592,
2000.
54. Grover S, Apfelberg DB, Smoller B: Effects of varying density
patterns and passes on depth of penetration in facial skin utiliz-
ing the carbon dioxide laser with automated scanner, Plast
Reconstr Surg 104:2247, 1999.
55. Kilmer SL: Cutaneous lasers, Facial Plast Surg Clinic North Am
11:229-243, 2003.
56. Cook BE Jr, Lemke BN: Cosmetic blepharoplasty, Oral Maxillo-
fac Surg Clin North Am 12(4):673-687, 2000.
57. Weinstein C: Ultrapulse carbon dioxide laser rejuvenation of
facial wrinkles and scars, Am J Cosm Surg 14:3-111, 1997.
58. Niamtu J: The treatment of vascular and pigmented lesions in
oral and maxillofacial surgery, Oral Maxillofac Surg Clin North
Am 16:239-254, 2004.
258 SECTION II ■ Dentoalveolar Surgery
59. Costello BJ, Levin LM: Lasers in oral and maxillofacial surgery.
In Fonseca RJ et al., editors: Oral and maxillofacial surgery, vol I.
Saunders, 2000.
60. Chan HH et al.: Recurrence of nevus of Ota after successful
treatment with Q-switched lasers, Arch Dermatol 136:1175-1176,
2000.
61. Goldman MP, Fitzpatrick RE: Treatment of tattoos, Facial Plast
Surg Clin North Am 4(2):295-306, 1996.
62. Boyden DK: A brief overview of noninvasive lasers in cosmetic
maxillofacial surgery, Oral Maxillofac Surg Clin North Am 16:231-
237, 2004.
63. Dierickx CC: Hair removal by lasers and intense pulsed light
sources, Dermatol Clin 20:135-146, 2002.
64. Strauss RA: Lasers in the management of snoring and mild sleep
apnea, Oral Maxillofac Surg Clin North Am 16:255-267, 2004.
65. Dickson RI, Mintz DR: One-stage laser-assisted uvulopalato-
plasty, J Otolaryngol 25(3):1-13, 1996.
66. Strauss RA: Upper airway examination and nasopharyngoscopy,
J Oral Maxillofac Surg 54(8):12-13, 1996.
67. Riley RW, Powell NB, Guilleminault C: Obstructive sleep apnea
syndrome: a surgical protocol for dynamic upper airway recon-
struction, J Oral Maxillofac Surg 51:784-789, 1993.
68. Kamami YV: Laser CO2 for snoring: preliminary results, Acta
Otorhinolaryngol Belg 44:451-456, 1990.
69. Madani M: Surgical treatment of snoring and mild obstructive
sleep apnea, Oral Maxillofac Surg Clin North Am 14:333-350,
2002.
70. Waite PA, Vilos GA: Surgical changes of posterior airway space
in obstructive sleep apnea, Oral Maxillofac Surg Clin North Am
14:385-399, 2002.
71. Kahraman SA: Low-level laser therapy in oral and maxillofacial
surgery, Oral Maxillofac Surg Clin North Am 16:277-288, 2002.
72. Rosenshein JS: Laser biostimulation: photobioactivation, a mod-
ulation of biologic processes by low-intensity laser radiation. In
Clayman L, Kuo P, editors: Lasers in maxillofacial surgery and
dentistry, New York, 1997, Thieme.
73. Karasu HA: A study of the vascular response to low intensity
laser therapy (a dissertation), London, 1999, University of
London, Senate House.
74. Merado AR et al.: Influence of low level laser therapy on wound
healing and its biological effect on myofibroblasts, Laser Surg
Med 32:239-244, 2003.
75. Weber JB et al.: Laser therapy improves healing of bone defects
submitted to autologous bone graft, Photomed Laser Surg 24(1):38-
43, 2006.
76. Takeda Y: Irradiation effects of low-energy laser on alveolar bone
after tooth extraction: experimental study in rats, Int J Oral
Maxillofac Surg 17:388-391, 1988.
77. Roynesdal AK et al.: The effect of soft-laser application on
postoperative pain and swelling. A double-blind crossover study,
Int J Oral Maxillofac Surg 22:242-245, 1993.
78. Miloro M, Repasky M: Low-level laser effect on neurosensory
recovery after sagittal ramus osteotomy, Oral Surg Oral Med Oral
Pathol Oral Radiol Endodon 89(1):12-18, 2000.
79. Lee EA: Laser-assisted gingival tissue procedures in esthetic
dentistry. In Tarnow DP, editor: Applications of 810 nm diode
laser technology. A clinical forum, Mahwa, NJ, 2006, Montage
Media.
80. Sarver DM: Use of the 810 nm diode laser: soft tissue manage-
ment and orthodontic applications of innovative technology. In
Tarnow DP, editor: Applications of 810 nm diode laser technology.
A clinical forum, Mahwa, NJ, 2006, Montage Media.
81. Ciancio S: Wound healing of periodontal pockets using the
diode laser: an interview. In Tarnow DP, editor: Applications of
810 nm diode laser technology. A clinical forum, Mahwa, NJ, 2006,
Montage Media.
82. Press J: Effective use of the 810 nm diode laser with the wellness
model. In Tarnow DP, editor: Applications of 810 nm diode
laser technology. A clinical forum, Mahwa, NJ, 2006, Montage
Media.
83. Convissar RA: Lasers in general dentistry, Oral Maxillofac Surg
Clin North Am 16:165-179, 2004.
84. Takeda FH et al.: A comparative study of the removal of the
smear layer by three endodontic irrigants and two types of lasers,
Int Endodon J 32(1):32-39, 1999.
85. Marmulla R et al.: Laser-scan-based navigation in cranio-
maxillofacial surgery, J Craniomaxillofac Surg 31(5):267-277,
2003.

TREATMENT OF TRIGEMINAL NERVE INJURIES
John M. Gregg
The oral and maxillofacial surgeon who offers full-spectrum
treatment will likely experience nerve injuries during the
course of his or her career.1-4 Acute neurosensory symptoms in
lingual and inferior alveolar nerves (IANs) are present in as
many as 35% of patients 1 week after routine surgeries, such
as third molar removal. Although more than 90% will resolve
spontaneously by 3 weeks, an important patient subset of 15%
to 30% will retain abnormal sensations and impaired orofacial
functions for 3 months or more, and approximately 15% of
those injured will experience some level of persisting neuro-
pathic pain.5,6 Those patients with neuropathies persisting
more than 1 year after injury are considered permanent,
however, and may not be surgically reversible.
Some trigeminal nerve injuries may be unavoidable because
of anatomic variations and the nature of the deformities or
pathologic condition requiring treatment. Especially high
risks for injury to trigeminal nerves are inherent for patients
treated for orofacial trauma, developmental deformities,
reconstructive surgeries with endosseous implants, and, most
commonly, pathologic conditions associated with third molar
surgery. Unfortunately, nerve injury complications are still
perceived as evidence of surgical negligence by uninformed
patients.
There have been scientific advances in the diagnosis and
understanding of the causes and mechanisms of traumatic
neuropathies. We now have more than 2 decades of experi-
ence with surgical repairs that demonstrate satisfactory out-
comes for more than half of treated nerve injury patients.7 We
have learned that microsurgical repairs of lingual nerves are
more necessary and effective than inferior alveolar repairs.
Early aggressive medical and selective surgeries of acute nerve
injuries may prevent transition to chronic refractory neuropa-
thies and dysesthesias; therefore, it is recommended that
patients with dysfunctional sensory deficits and intractable
pain should be treated within 90 days of injury, if possible.
Results show that microsurgical repairs are likely to improve
deficient sensory functions, but less likely to eliminate chronic
neuropathic pain.8,9,10 Internal neurolysis procedures and
current nerve grafting procedures have yielded disappointing
outcomes, whereas microsurgical decompressions, with
neuroma resection and direct reanastomoses, have yielded the
most favorable results. The critical need for an effective allo-
plastic graft technique for use with cases of more extensive
nerve tissue loss remains a research challenge.
CHAPTER 15
This chapter offers six sections with information on: (1)
causes, classification of nerve injuries, and determinants of
nerve injury responses; (2) clinical measurement and diagno-
sis of trigeminal nerve injuries; (3) indications, contraindica-
tions, and techniques of surgical repair; (4) a survey of
outcomes of trigeminal repairs; (5) case-specific applications
for management of nerve injuries associated with facial trauma,
orthognathic, anesthetic, medicament, implant, third molar-
associated nerve injuries; and (6) current medicolegal issues
related to nerve injuries.
■ CAUSES, CLASSIFICATION,
AND DETERMINANTS OF
NERVE INJURIES
Trauma to the peripheral trigeminal nerves is a common
source of orofacial dysfunction, sensory loss, and neuropathic
pain.11,12 The most common causes are maxillomandibular
contusions and fractures, where the inferior alveolar and infra-
orbital nerves are almost always involved, and chronic impair-
ment persists in up to 35% to 50% of patients.13,14 Injuries to
inferior alveolar and lingual nerves also occur during third
molar surgery in approximately 1% to 4% of cases, and an
estimated 13% of those injured experience permanent neu-
ropathies.5,15,16,17 Endosseous implant surgery accounts for an
increasing number of cases of mandibular nerve impairment,
especially in those patients with more severe bony atrophy
and in those who undergo nerve repositioning surgeries.18,19,20
Chronic posttraumatic neuropathies from local anesthetic
injuries, although rare in comparison with the number of
injections carried out, can, nevertheless, be especially painful
and refractory to treatment.21,22 Similarly, nerves injured by
root canal instruments or surgical medicaments may display
sensory neurotoxicity that is difficult to treat.23,24 Orthogna-
thic surgery, particularly sagittal mandibular osteotomy, has a
high incidence of intraoperative nerve injuries, good levels of
early spontaneous recovery,25,26 but some degree of long-term
altered sensation in up to 50% of patients.27
A MECHANISTIC CLASSIFICATION OF
NERVE INJURIES
Sir Herbert Seddon and Sir Sydney Sunderland developed
nerve injury classifications that still provide a useful frame-
work for characterizing nerve injuries.28,29 Seddon’s hypothesis
was that increasing nerve damage results in greater permanent
259
260 SECTION II ■ Dentoalveolar Surgery

TABLE 15-1 Nerve injury Classification and Injury Responses

Injury Classification Causes Responses Recovery Microsurgery
Neurapraxia (Seddon) first- Minor nerve compression, Neuritis, paresthesias, Spontaneous recovery, Not indicated unless foreign body
degree injury (Sunderland) stretch, thermal, acute conduction block, no less than 2 mo preventing nerve recovery
infection structural damage
Axonotmesis (Seddon) Partial crush, traction, Intact epineurium, isolated Spontaneous recovery in Repair not indicated except
second-degree injury thermal, chemical injury, axon loss, episodic 2-4 mo Decompression if foreign body or
(Sunderland) hematoma, chronic infection dysesthesia perineural fibrosis
Third-degree injury Traction, crush, puncture, Wallerian axon loss, some Recovery crude senses, Decompression and repair if poor
(Sunderland) thermal, chemical injury internal fibrosis, peripheral >1 yr neuropathy, function, sustained pain at 3 mo
sensitization
Fourth-degree injury Full crush, extreme stretch, Neuroma-in-continuity, Permanent injury, Repair, neuroma resection if
(Sunderland) high thermal, direct hypoesthesia, and minimal spontaneous intolerable dysfunction pain after
chemical injury triggered hyperpathia recovery 3 mo
Neurotmesis (Seddon) Transection, tear, laceration, Amputation neuroma, Permanent injury, no Neuroma resection with
fifth-degree injury avulsion of nerve trunk anesthetic, evolving spontaneous recovery neurorrhaphy or graft if intolerable
(Sunderland) deafferentation pain dysfunction and intractable
neuropathic pain

loss of sensation. Sunderland’s scheme emphasized a progres-
sive destruction of nerve structures with Wallerian axon
degeneration and disruption of endoneurial, perineurial, and,
finally, epineurial tissues. The value of combining these two
classification schemes has been shown by quantitative sensory
testing (QST), which has verified that the depth of trigeminal
sensory loss correlates generally with increasing physical nerve
destruction.30,31 The Seddon-Sunderland linear injury scales
also correlate well with decreasing potential for spontaneous
nerve recovery, with increasing likelihood of dysfunctional
neuroma formation and with increasing need for surgical
repair interventions (Table 15-1).
Sunderland Type 1 (Seddon “neurapraxia”) injuries result
from ischemic effects of minor nerve trunk traction, mild
compression from edema, hematoma, or temporary increases
in local inflammation. Paraneural heat in the 48 °C to 54 °C
range, generated by rotating surgical instruments, may produce
Type 1 damage. The neurologic effects are primarily conduction
block, resulting in slowed stimulus responses. Although isolated
sites of neural demyelination may occur, Wallerian axon
degeneration is not expected, and there are no grossly visible
effects on the epineurium. Rapid spontaneous recovery toward
normal sensation and sensory functions is expected within
days to a few weeks. Microsurgery is not indicated, except for
the removal of compressive paraneural foreign bodies.
Sunderland Type 2 (Seddon “axonotmesis”) injuries result
from more forceful crush or abrupt nerve traction greater than
25 g.32 Partial compression from implants or displaced bone
may induce this level of injury. QST reveals deeper loss of
sensory responses, particularly for fine touch discrimination.
Some degree of axon degeneration may occur, but the endo-
neurium, perineurium, and epineurium remain intact. There-
fore axonal regeneration and sensory recovery is expected
within 2 to 4 months. Extraneural hematoma and secondary
scarification may be associated with this level of injury and
perpetuate mild neuropathy. In such cases, surgical decom-
pression may enhance recovery.
Type 3 Sunderland injuries are caused by more severe
mechanical crush, puncture, chemical, and thermal traumas
and result in Wallerian degeneration at the injury site and
some degree of cell loss in the trigeminal ganglion.33 The
endoneurium is also damaged, and some intraneural bleeding
and scarification may potentially interfere with complete axon
recovery. For this reason, this injury level may be associated
with permanent neurosensory disturbances. Painful burning
paresthesias and hyperphenomena may be seen within hours
of Type 2 and Type 3 injuries and may prompt surgical explor-
ation and repair if sensory test responses fail to show satisfac-
tory recovery within 3 months.
Type 4 Sunderland injuries result from extreme nerve
crush, thermal effects above 55 °C, intraneural local anes-
thetic injections, or caustic medicaments in contact with the
nerve. The epineurium is grossly intact, although contused,
and may be devascularized. Internal nerve structures are
damaged and replaced by disorganized scar tissue. Trigeminal
ganglion cell necrosis occurs, and central deafferentation
effects can be measured as high as thalamic levels, resulting
in centralized and spontaneous pain syndromes along with
severe peripheral sensory loss.34,35 QST reveals deep hypoes-
thesia to all stimuli, and percussion of the injury site may elicit
a hyperpathic aching pain and paresthesia. Neuroma-
in-continuity has formed in such cases, and microsurgical
resection and repair will be required if sensory reflex recovery
is to be improved.
Sunderland Type 5 (Seddon “neurotmesis”) is the most
extreme injury type, where there has been complete transec-
tion of the nerve trunk, loss of significant trigeminal cells with
centralized effects, and amputation neuromas forming at the
injury site. Patients who have sustained full-transection inju-
ries of intrabony IAN, yet have retained good nerve-end appo-
sition and support within the mandibular canal, may undergo
satisfactory levels of spontaneous recovery. Many Type 5
injured patients, however, will experience intractable pain
and poor orofacial functions and may benefit from repair. In
 CHAPTER 15 •
almost all Type 5 injuries to lingual and infraorbital nerves,
satisfactory spontaneous recovery will not occur and should
be microsurgically repaired as soon as the nature of the injury
is confirmed and sensory testing demonstrates anesthesia, with
or without dysesthesia (Table 15-1).
DETERMINANTS OF NERVE INJURY RESPONSES
A number of factors, both local and host-related, will deter-
mine the neurologic responses to injury. The type of injury
is a primary determinant of neurologic responses. Clean-
incision lacerations are less problematic than irregular or
avulsive lacerations.36 Injuries are clinically more disruptive
when they involve mixed nerve receptor types, such as com-
binations of somatosensory mechanoreceptors and taste
receptors, and somatosensory-autonomic fiber combinations,
such as maxillary nerve branches that contain postganglionic
parasympathetic fibers. Injuries that occur at proximal posi-
tions on the peripheral nerve are more significant than those
that occur at more distal sites because they are more likely
to result in loss of trigeminal ganglion cells and initiate
retrograde deafferentation effects into the central nervous
system. Multiple nerve injuries are also more significant
than isolated injuries because of accumulative central
deafferentation effects.37
Complete nerve lacerations or avulsions produce markedly
different responses than partial or incomplete nerve injuries
with regard to the effects on sensory perception and type of
dysesthesia that result. Paradoxically, lesser neurotrauma, as
seen with Sunderland Type 2 and 3 injuries and partial or
puncture injuries, are more likely to be associated with early
hyperesthesias, such as triggered pain, hyperalgesia, allodynia,
and immediate postinjury dysesthesias. Severe Type 4 internal
nerve damage and Type 5 complete laceration or avulsion
injuries, by contrast, are often not immediately painful, but
eventually lead to the formation of dysfunctional chronic
neuroma-in-continuity and amputation neuromas. These ini-
tially anesthetic lesions are more often associated with poor
orofacial function, referred and radiating forms of unpleasant
paresthesias, and spontaneous pain.31,38
Host factors are also significant determinants of the responses
to nerve injury. Increasing age negatively affects recovery from
all nerve injuries.39,40 Genetic factors, although inadequately
understood at this time, appear to be important determinants
through effects, such as increased intraneural collagenation,
extraneural scar, and autonomic derangements.41,42 The pres-
ence of nerve inflammation, bacterial infections, or herpes
simplex or zoster viral outbreaks in the nerve injury distribu-
tions can also interfere with the injury response and recovery
process.43,44 Even low-grade repetitive irritations of the injured
peripheral nerve or neuroma may induce a retrograde process
of central sensitization known as “windup.”34,45
Systemic influences also may influence nerve injury
responses; they include neurovascular diseases, such as chronic
arthritis, systemic lupus, and diabetic neuropathy. Exposure to
environmental neurotoxins, therapeutic medicaments, nico-
tinic acid, and nitrosamine components of tobacco may all
Treatment of Trigeminal Nerve Injuries 261
influence nerve injury responses by impairing Schwann cell
regenerative functions.46
■ CLINICAL MEASUREMENT
AND DIAGNOSIS
Clinical evaluation of patients with posttraumatic trigeminal
neuropathy requires quantitative assessments of: (1) impaired
global and orofacial functions, (2) pain and discomfort, and
(3) abnormal sensory stimulus responses. These assessments
are facilitated by the use of patient questionnaires, severity
scaling, QST, and pharmacologic analyses.
ASSESSING IMPAIRED FUNCTIONS
Trigeminal nerve injuries disrupt both orofacial and general
life functions. It is useful to ask that patients quantify their
perceived levels of dysfunction as a basis for treatment plan-
ning and for determining the effectiveness of treatments. A
suggested format for patient dysfunction scoring is presented
in Table 15-2. These same measures can be used at follow-up
patient visits to monitor progress in functions during recovery
from injury or surgery.
ASSESSING PATIENT DISCOMFORT AND PAIN
A questionnaire modified from the extensively tested McGill
Pain Inventory is useful for eliciting patient-perceived levels
of neurosensory discomfort and pain (Table 15-3).47 It includes
a linear scale on which patients are asked to focus on their
region of nerve injury and rate their “discomfort” on a global
TABLE 15-2 Function Impairment Assessment
Mark on the following scale your estimate of the amount of impairment or
disability that you are now experiencing as a result of your nerve injury
problem:
0 25 50 75 100%
none mild moderate severe complete
Please circle the functions that have been impaired by your current nerve
injury problem:
eating talking swallowing tasting tooth brushing dental care washing face
smelling smiling lovemaking sleeping working socializing other_______
TABLE 15-3 Pain and Discomfort Assessment
Mark on the following scale your estimate of the average daily level of
discomfort or pain:
0 25 50 75 100%
no discomfort mild pain moderate pain severe pain intolerable pain
discomfort
Please circle any words that describe your current sensation or pain
problems:
constant intermittent rhythmic steady brief triggered spontaneous
numb itching dry tickling tingling twitching wet rubbery
stretched swollen woody crawling moving quivering vibrating
cool warm cold hot burning pricking stinging electric cold hot burning
tender sore painful sore aching excruciating cramping shocking
bitter sweet sour salty tasteless
262 SECTION II ■ Dentoalveolar Surgery

Stimulus types

Level C Level B Level A

Hyperesthesia scale Noxious Crude touch/pressure Fine touch
⫹3

Response excess

Hyperalgesia

Hyperpathia
⫹2

Allodynia
Sensitization

⫹1

Normal responses
0 3
Deaffereatation
Response loss

A responses
⫺1 2

B responses
⫺2 1

C responses
⫺3 zero
Hypoesthesia scale Level C Level B Level A Recovery scale
Noxious Crude touch/pressure Fine touch

Stimulus types

FIGURE 15-1. Patient responses to three level stimuli, plotting noxious (C), crude pressure (B), and fine tactile (A)
responses. Hypoesthesia scale represents loss of sensory functions with deafferentation mechanisms. Hyperesthesia
scale represents mild, moderate, and severe overresponses to three level stimuli with sensitization mechanism. Recovery
scale ranges from anesthetic to normal control levels. (Modified from Rolke R et al: Quantitative sensory testing in the
German Research Network on neuropathic pain (DFSN): standardized protocol and reference values, Pain 123:231,
2006.51)

scale from zero (no discomfort) through 100% (“intolerable
pain”).
A listing of verbal descriptors is presented to patients to
elicit qualitative information about their neuropathy, and it
can be helpful in revealing underlying mechanisms of sensory
abnormality, pain, and dysfunction. Particular patterns of a
verbal descriptor may help the clinician discriminate between
different categories of pain.48,49 For example, certain forms of
neuropathic pain have been found to be strongly linked to
“tingling, hyperesthesia to touch, electric, and burning”
descriptors.50
A note of caution is given to clinicians interpreting verbal
descriptor complaints after nerve injury. All English-speaking
patients, when asked about altered sensation in their affected
nerve distributions, use the term “numbness.”6,31 However,
QST reveals that there is a wide range of objective sensory
loss among patients who use the term “numbness”; some
patients test severely hypoesthetic and even anesthetic,
whereas other “numb patients” may display near-normal stim-
ulus responses with objective testing. It is also important to
recognize this communication factor when final assessments
of the success of spontaneous recovery or surgical treatments
are made. Even in cases where there have been significant
improvements in objective functions and QST, some patients
may interpret their recovery responses as “unsuccessful”
because they still retain “numbness.”
CLINICAL NEUROSENSORY TESTING
Clinical neurosensory testing is done to determine the degree
of sensory impairments, detect neuropathic states, monitor
recovery, and determine whether trigeminal nerve repair is
indicated (Figure 15-1). Although a wide range of protocols
for experimental and clinical QST are currently being evalu-
ated, no single system is universally accepted.30,51 In standard
protocols, a range of stimuli from light mechanical to noxious
are presented to the patient’s region of nerve injury, and their
responses are compared quantitatively with responses from
contralateral uninjured tissues. The tests are designed to detect
and measure both negative responses (sensory deficits) and
positive responses (hyperesthetic reactions); this test scheme
also recognizes the possibility of normalcy in stimulus responses
(see Figure 15-1).
QST begins with the stimulation of large myelinated A-
alpha and A-beta nerve fibers associated with fine touch
discrimination, known as “Level A” testing. Level A stimulus
parameters include choices, such as two-point touch discrimi-
nation, static touch stimuli with light Frey’s hairs, or detec-
tion of brush or cotton-wisp stroking.30 The patient’s level
of correct detections in nerve-injured zones are compared
with normal control tissues, and the quantified results are
recorded or mapped on an orofacial drawing (Figure 15-2).
Level A testing may result in normal control levels of stimu-
lus detection, or it may reveal a full range of neural deficits
 CHAPTER 15 •
FIGURE 15-2. Format for anatomic mapping and data recording of quantitative sensory test responses. (Modified
from Zuniga JR et al: The accuracy of clinical neurosensory testing for nerve injury diagnosis, J Oral Maxillofac Surg
56:2, 1998.)
for fine-discriminative touch abilities (negative responses, see
Figure 15-1). The fine touch stimuli are also used simultane-
ously to expose abnormal sensory “overresponses” from
patients who report that the stimuli elicit paresthesias or, in
some cases, pain. Uncomfortable paresthesias and pain would
be recorded as a “positive” hyperesthesia (see Figure 15-1),
in this case allodynia, defined as “pain (or heightened pares-
thesia) due to a stimulus which does not normally provoke
pain.”52 If allodynia is exposed by Level A testing, patients
are asked to rank their abnormal responses as mild, moderate,
or severe (+1 to +3, see Figure 15-1). Because posttraumatic
neuropathic sensitization can be due to both peripheral and
central mechanisms, the finding of allodynia during QST
does not serve as an indication or contraindication to periph-
eral microsurgery.
Testing next turns to Level B evaluation of the patient’s
crude-touch detection abilities. More intense, blunt, and
crude forms of mechanical stimuli can be used, such as thicker
Frey’s filaments, nonnoxious light pin touching, and pressure
stimuli from an algometer. The stimulus intensities that
patients require to detect the stimuli are recorded and mapped
as with Level A. Patients who display deficits for (Level A)
fine discriminative stimuli, yet have good detection levels for
Treatment of Trigeminal Nerve Injuries 263
crude-touch Level B stimuli, are not usually candidates for
microsurgery because this is an acceptable functional level of
neurosensory recovery.
Hyperesthesias are also evaluated at Level B testing by
noting paresthesia and pain responses to the crude-touch,
compression, and percussion stimuli applied over the nerve
distributions. This may elicit the hyperphenomenon, known
as a pathologic Tinel’s sign or hyperpathia, defined as “a painful
syndrome characterized by an abnormal painful reaction to a
stimulus, especially a repetitive (mechanical) stimulus, as well
as increased threshold.”52 This “trigger response” is an indica-
tion of probable irritability of larger nociceptor A-delta fibers,
the likely presence of traumatic neuroma-in-continuity, and
is an anatomic target for nerve repair.
Level C examination presents noxious stimuli to the injured
nerve distribution, testing for the level of C fiber protective
abilities. Most common and convenient clinical stimuli are
deeper pin pressures, calibrated hemostat pinches, or instru-
ments heated to 48 °C to 50 °C. Patients who respond to
noxious stimulation by reporting pain well above that experi-
enced from stimulation of their control tissues are hyperalge-
sic. Hyperalgesia is defined as “an increased response to a
stimulus which is normally painful.”52 It represents another
264 SECTION II ■ Dentoalveolar Surgery
form of neural sensitization produced by both peripheral and
central nervous system mechanisms.34,35,53
Patients who fail testing at levels A and B but have retained
or regained basic detection of noxious stimuli are usually able
to protect their tissues from secondary traumas. However, they
more often have difficulties with orofacial functions, such as
mastication and speech, and are candidates for microsurgery
to improve on these functions. Patients who respond anes-
thetic to Level C noxious stimuli are obvious candidates for
surgical repair.
QUANTIFYING NEUROSENSORY RECOVERY
A final purpose of clinical QST is to rate the existing stage of
neurosensory recovery, using a suggested zero- to four-point
recovery scale (see Figure 15-1). Zero represents no measur-
able neurosensory recovery (anesthetic), #1 the recovery
range of Level C noxious detection functions, #2 the recovery
range of Level B crude-touch functions, #3 the recovery range
of Level A fine-tactile functions, and #4 full normal (control
level) functions.
PHARMACOLOGIC TESTING
Pharmacologic testing, using lidocaine in various forms, can
expand on information gained from clinical sensory testing
regarding neuropathy mechanisms. It can also help predict the
efficacy of treating patients with medical alternatives versus
nerve-repair surgery.
Local anesthetic blocks with lidocaine are made proximal
to the sites of nerve injury for patients with significant dis-
comfort or neuropathic pain. Positive and sustained pain relief
is often a reliable prediction that surgical repair will also
reduce pain levels. Conversely, failure in pain relief from a
successful block is a sign that irreversible centralized pain
sensitization exists and that surgical repair is unlikely to
improve pain levels.
Topical lidocaine and transcutaneous 12-hour release
patches are less predictive of efficacy of surgery, but are useful
for palliative pain management acutely after injury and during
recovery from nerve repair.54 For some patients, long-term
regular use of transcutaneous lidocaine is an acceptable alter-
native to surgery.
Intravenous lidocaine testing has been used successfully to
predict the efficacy of centrally acting medical therapies as
alternatives to surgery for patients with neuropathic pain.55
Lidocaine infusions at 1 mg/kg over a 5-minute time frame
may attenuate centrally sensitized neuropathic states without
inducing cognitive deficits. This may be helpful in directing
long-term medical therapies with centrally acting agents that
may be preferred by some patients over surgical repairs of
painful nerve injuries.
ASSESSING PATIENTS WITH TRAUMATIC
NEUROPATHIC PAIN
Previous studies of patients with trigeminal traumatic neural-
gias have combined information from verbal descriptors,
scaling scores, quantitative sensory and pharmacologic testing,
and nerve lesions observed at the time of surgical nerve repairs.
These studies have shown that patients whose complaints
center on dysesthesia or altered sensation with pain after
nerve injury cluster in two differing neuropathic clinical pro-
files: hypoesthetic pain and hyperesthetic pain.37,45,51 Patients
with a primarily hypoesthetic pattern complain immediately
after injury of “numbness” and often have minimal neuro-
pathic pain. When examined with QST, these patients are
deficient in neurosensory responses for all types and levels of
QST. Days to weeks after injury, however, patients gradually
report an intensifying pain perceived in the injured nerve
region and complain of “constant, dull, deep, crawling, and
burning” discomfort.31
When presented with Level B crude-touch stimuli, patients
with a hypoesthetic pattern experience intensified paresthe-
sias and burning hyperpathias. Studies have shown that
many of these patients have formed traumatic neuroma-in-
continuity from Sunderland Type 3 injury or amputation
neuroma from Type 4 injury. If identified within a few weeks
after nerve injury, these patients may respond favorably to
early surgical exploration and repair.
Unfortunately, studies have also demonstrated that with
longer postinjury time, many patients with hypoesthetic trau-
matic neuralgias experience further increases in constant,
spontaneous pain that does not respond to local anesthetic
blocks applied to the injured nerve trunks, suggesting both
central and peripheral sites of pain action.6,37 This pattern is
central deafferentation syndrome, or “anesthesia dolorosa,”
and is associated with severe nerve lesions, permanent loss of
trigeminal ganglion cells, and reduced afferent input to the
brainstem.56,67 It has been postulated that major deafferenta-
tion leads to “irritable foci” that develop electrophysiologi-
cally in the spinal cord and extend to thalamic and even
cortical levels.38 Deafferentation pain syndromes, if sustained
for weeks or months after nerve injury, become refractory to
both medical therapies and delayed microsurgical repairs.57
Patients with a primarily hyperesthetic pain pattern, in
contrast to those with hypoesthetic neuralgias, have more
severe early pain within hours to days of nerve injury. Their
primary verbal descriptors are “shocking, tingling, burning,
electric, and episodic.”6,45 Studies have shown that early,
intense responses more likely follow partial nerve injuries,
such as traction, compression, puncture, local anesthetic,
chemical, and burn injuries.31
A prime clinical feature of hyperesthetic posttraumatic
neuralgias is the presence of triggered paresthesias, allodynia,
and hyperalgesia, phenomena, which may be expressions of
both peripheral and central mechanisms.58,59,60 Local anes-
thetic nerve blocks produce a transient but complete
remission from allodynia and hyperalgesia. Patients with
hyperesthetic pain patterns are candidates for surgical decom-
pression and repair if their triggered pain and dysfunction are
intolerable or refractory to medical treatments.
It is also important that hyperesthetic neuralgia patients be
closely monitored through serial neurosensory examinations
after injury to detect signs of emerging central sensitization,
 CHAPTER 15 • Treatment of Trigeminal Nerve Injuries 265

Lingual, mental, infraorbital nerve injuries Inferior alveolar nerve injuries

Observed Unobserved Unobserved Observed

Nerve transection Partial injury Partial injury Nerve transection

(Type 5) (Type 1-4) (Type 1-4) (Type 5)

Acute medical/physical therapy (avulsed, unaligned,

Sensory reeducation bone unsupported,
Serial quantitative sensory testing foreign body)

Primary microsurgical Primary microsurgical

Decompression Functional sensory recovery Decompression
Neurorrhaphy Tolerable comfort level Neurorrhaphy
Graft repair 90 days post-injury Graft repair

Sensory reeducation Yes No Sensory reeducation

Secondary microsurgical
Supportive care/ Decompression Supportive care/
monitoring Neuroma resection monitoring
Neurorrhaphy
Graft repair

FIGURE 15-3. Treatment algorithm for trigeminal nerve injuries.

which is seen as a spread of the neuropathic nerve distribu-
tions (surround hyperalgesia) and new symptoms contralateral
to the nerve injury.61,62
Although the extreme forms of hyperesthetic and hypoes-
thetic neuralgia patterns are usually easy to differentiate
through patient study, it is also the case that patients may
have combined or mixed features. The decision to proceed
with surgical repairs becomes more challenging in such
cases.
■ NERVE REPAIR SURGERIES
(Figure 15-3)
PURPOSES AND PATIENT SELECTION
Neurosurgical interventions for patients who have sustained
trigeminal injuries have two purposes: to restore orofacial
sensory functions and to manage pain and discomfort. Repairs
are only done on sensory trigeminal branches; the motor root
is inaccessible except for major cranial-base procedures. The
sensory trigeminal nerves most commonly affected and ame-
nable to repair are the inferior alveolar, lingual, infraorbital
nerves, less frequently the supraorbital and supratrochlear
branches. The long buccal nerve is probably damaged with
great frequency during routine oral surgeries, but they are not
associated with significant levels of neuralgias or dysfunction
and therefore are not routinely treated. The auriculotemporal
nerves are also susceptible to injury during facial trauma and
surgeries for temporomandibular joint reconstruction and
parotidectomy. Although pain and dysfunction are described
for auriculotemporal injuries, there are no current microneu-
rosurgical treatments for these conditions.
Indications for surgical exploration and repairs of trigeminal
nerves are: (1) observed nerve injuries, (2) presence of para-
neural foreign bodies, (3) unchanging anesthesia or dysfunc-
tional hypoesthesia more than 2 months after injury, and (4)
medically intractable neuropathic pain. Additional clinical
indicators that are predictive of surgical success include pres-
ence of specific dysesthetic (hyperpathic) trigger points indi-
cating underlying traumatic neuroma and relief of pain and
paresthesia with local anesthetic nerve blocks.
Contraindications for trigeminal surgical exploration and
repair are: (1) signs of improving neurosensory functions based
on serial QST; (2) patient acceptance of existing impaired
function and discomfort levels; (3) signs of central sensitiza-
tion (spreading regional dysesthesia, secondary hyperalgesia);
(4) deafferentation pain unrelieved by local anesthetic nerve
blocks; (5) clinical signs of autonomic derangement (burning
sensations, erythema, swelling); (6) extremes of age, and
systemic or neuropathic disease; (7) excessive time since
original nerve injury; and (8) unrealistic patient expectations
(restoration of immediate, normal, or pain-free neurosensory
functions).
ACUTE NERVE INJURY PATIENT CARE
The primary goals of early nerve injury treatments are to
remove sources of ongoing or secondary nerve injury, to create
266 SECTION II ■ Dentoalveolar Surgery
a tissue environment for optimal nerve recovery, and to
prevent secondary neuropathic sensitization.
A soft diet is advised, hypermobile fractures should be sta-
bilized, and cryotherapy applied to the region. Injured nerves,
if visualized, should be freed of compressing foreign bodies,
bone or tooth fragments, toxic materials, or implant. Exposed
nerves should be cleansed with isotonic solution, gently
coapted and stabilized with temporary epineural sutures, if
possible, and barrier protected. Infection and inflammation
control, both locally and systemically, should be maximized.
Antiinflammatory, opiate analgesic, and psychosedative agents
for anxiety control and sleep promotion are used aggressively
to minimize CNS excitation. This may include use of local
anesthetic nerve blocks with long-acting agents. A course of
systemic corticosteroids, such as dexamethasone 8 to 12 mg/
day may minimize perineural inflammation during the first
postinjury week.63 Rapid-acting anticonvulsant agents, such
as clonazepam, given in divided doses at 2 to 10 mg daily may
further protect the CNS.64 Topical lidocaine can be delivered
either by p.r.n. lidocaine gels or through sustained 12-hour
release 5% transcutaneous lidocaine patch applications.54
A baseline examination with QST should be done and the
affected nerve distribution mapped. Patients should be coun-
seled regarding the nature of the nerve injury, the importance
of immediate and sustained observation and care, the possible
need for secondary consultation and microrepair, and the
probability of a protracted course of nerve recovery.
TIMING OF SURGERY
Surgeries are categorized according to the time of repair
relative to the injury dates. They are primary (immediate),
delayed primary, and secondary. Primary repairs are done in
those instances when the nerve has been exposed and the
injury observed, as is common during surgeries for trauma,
dentoalveolar pathologic conditions, orthognathic, implant-
reconstruction, and some third molar surgeries. Immediate
(primary) nerve surgeries, if technically possible, are the pre-
ferred time of repair from a biologic perspective. Axonal
regeneration is known to be optimal in earlier time frames,
within the first 3 weeks after injury, and before neuroma for-
mation and restrictive secondary scarring can occur. Limited
but effective primary repairs may be possible, even in office
settings. Surgical loupes can enable nerve decompression,
passive nerve apposition with or without epineural suturing,
and protection of the exposed nerve with inert alloplastic
barriers, such as Gelfoam or collagen tubule. Primary surgery
may then be followed by “delayed primary” repair if needed
and done within a few weeks of injury when regional tissues
have recovered from acute surgical effects and plans can be
made for more definitive nerve exposure and microsurgical
repair.
Unobserved trigeminal nerve injuries are the more common
circumstance and require secondary surgical repairs under
controlled conditions and after patients have met the surgical
indications’ criteria dictated by clinical conditions and serial
QST. The question of optimal timing for secondary surgeries
remains controversial and is the subject of ongoing research.65
There is much evidence that earlier surgical repairs, within 1
to a few weeks following injury, are preferred over longer
delays for three basic reasons: (1) optimal regenerative capac-
ity occurs within the first few weeks after injury, (2) early
intervention may prevent the development of traumatic neu-
romas and chronic neuropathic sensitization, and (3) ease of
technical repairs. With excessive delays, microsurgical repairs
become more difficult because of retraction and progressive
atrophy of nerve segments, increased extraneural and intra-
neural collagen deposition, and Schwann cell scarring.
Outcome analyses have shown that lingual nerve repairs done
within 90 days of injury can result in functional sensory recov-
ery (FSR) levels as high as 93% at the 1-year mark.66 This
same report showed, however, that FSR levels as high as 63%
can be gained for selected cases in which surgery occurred after
90 days, and other studies supported the conclusion that
there is no association between delayed repairs and sensory
outcomes.67,68
The timeline for soft tissue nerve injuries, such as lingual,
infraorbital, and mental nerves, is much shorter than for intra-
bony nerve injuries, such as inferior alveolar. This is due to
the very limited capacity for spontaneous regeneration of soft
tissue nerves as compared with intrabony branches, where the
mandibular canal can act as a natural conduit for nerve recov-
ery, given enough time.7
SURGICAL INSTRUMENTATION
Trigeminal nerve repairs require a quiet and controlled oper-
ating room environment. Surgical assistants familiar with the
goals and procedures of the microrepair are essential. The
microsurgical environment is more demanding of surgical
assistants because of the limited surgical field access, the extra
demands for stable retraction, hemorrhage control, and
delicate tissue management. Endotracheal intubation with
muscle relaxation is needed to prevent inadvertent patient
movements. Hemostasis can be enhanced with reverse Tren-
delenburg’s positioning and local anesthesia with vasocon-
strictor field blocking. Hypotensive general anesthesia may be
required to assist in hemorrhage control along with bipolar
electrocautery, used to prevent collateral injuries to the nerve
under repair. Although nerve access, nerve release, and
decompression can be accomplished with minimal magnifica-
tion, such as 3× to 6× surgical loupes, more detailed microre-
pairs are best done with an operating microscope with multiple
heads for assistant views of the operating field. Primary micro-
surgical instruments include a selection of small retractors,
vein and nerve hooks, varied length microforceps, locking
needle holders, and microscissors. Self-retaining flat vascular
spreaders and vascular clamps can be used in some circum-
stances. Preferred sutures are nonreactive nylon or proline, 7-0
through 9-0. Nonreflective background materials, such as
opaque foils, are helpful for visibility, tissue control, and to
assist in atraumatic microsuctioning. Inert and nontoxic bar-
riers, such as Gelfoam or biodegradable neurocuff materials,
should be available for nerve protection after repair. Their
 CHAPTER 15 •
purposes are to eliminate dead space, prevent paraneural
hematoma, collagen ingrowth, and secondary scarring at the
repair line and to minimize compression-ischemia.
The surgical principles for trigeminal microsurgery include
gentle atraumatic tissue management, hemostasis, removal
of paraneural foreign bodies and adhesive scar, excision of
dysfunctional neuroma segments, and alignment and anasto-
mosis of nerve segments with minimal tension. In those less
optimal circumstances when direct neurorrhaphy is not pos-
sible, the surgical goal is to create a microenvironment that
permits effective axonal down growth to nerve receptors,
either through interpositional grafting or sealed interposed
entubulation.
NERVE ACCESS AND
MICROSURGICAL TECHNIQUES
Most microsurgical repairs can be accomplished intraorally
with the exception of proximal injuries to infraorbital and
periorbital nerves and IANs injured posteriorly and inferiorly.
The primary steps in nerve repairs are: (1) decompression of
entrapped injured nerves with removal of foreign bodies and
release of paraneural compressing tissues or scars; (2) identifi-
cation of injury site, diagnosis, and excision of traumatic
neuroma; (3) microsuture repair with neurorrhaphy (direct
reanastomosis); and (4) interpositional graft repair if neuror-
rhaphy cannot be accomplished because of excessive nerve
tissue loss.
DECOMPRESSION
Also known as external neurolysis, decompression is the first
phase of all nerve repair procedures and involves a careful
release of the injured nerve from paraneural scarring and
removal of foreign bodies and impinging bone or tooth frag-
ments.69,70 The magnifying optics at 3× to 10× are used to free
the nerve while preserving its epineural vasculature. The
nerve injury site is then further inspected, observing for nerve
continuity, amputation neuroma, swellings, atrophy or opaque
nerve regions, signifying internal fibrosis or neuroma-in-
continuity. In those cases of Type 1 or 2 Sunderland nerve
injuries, and when high magnification nerve inspection fails
to reveal signs of neuroma, decompression may be the only
surgery required. In that case, a protective neural cuff entubu-
lation barrier may be placed before closure, using a protective
sheath such as the recently developed polyglycolic acid
(PGA)-collagen Neurocuffs.71,72,73 These alloplastic tubular
conduits have been associated with pain remissions among
patients with previously intractable neuropathic pain. There
are no reports available, however, of their efficacy for
treatment of trigeminal traumatic neuralgias.7,74
NEUROMA RESECTION
After decompression, the mobilized nerve is controlled for
repair by placing umbilical tapes proximal and distal to the
nerve injury site. The nerve is inspected for discontinuity and
amputation neuroma. In those cases where neuroma-
in-continuity deformity is identified, the level of lesion is
Treatment of Trigeminal Nerve Injuries 267
determined by high magnification inspection and transillumi-
nation of the nerve, noting nerve opacity and loss of surface
microvasculature and gently compressing the nerve with
microforceps to test for intraneural scarification.
When amputation or neuroma-in-continuity has been veri-
fied, the injury zone is sharply resected with a Beaver blade to
approximately 3 mm proximal and distal to the visibly neuro-
matous tissue and submitted for histologic study. Satisfactory
excision produces a normal herniation of intact fascicles from
the epineurial nerve endings. Adequacy of neuroma resection
can also be verified by submitting 1 mm cross-section biopsies
for frozen section histopathologic verification of normal nerve
fascicles. The tissue stumps are finally trimmed in preparation
for microsurgical nerve repair.
In those rare cases in which inspection reveals that nerve
repair is not possible, such as in the absence of the distal nerve
trunk, the residual proximal nerve trunk is engaged and
sutured into adjacent viable tissue, such as skeletal muscle.
This procedure is known as nerve redirection and is believed
to decrease the likelihood of reformation of active traumatic
neuroma at the nerve stump.75
INTERNAL NEUROLYSIS
A procedure used in the treatment of partial or neuroma-
in-continuity injuries of large spinal nerves, known as internal
neurolysis, has questionable utility for trigeminal nerve injury
management. In this procedure, saline is injected beneath the
epineurium in the nerve-injured zone. The fluid ballooned
region is then incised longitudinally, exposing the internal
nerve microstructure. When effective, this releases the inter-
nal nerve fibrosis and frees the nerve fascicles. Internal neu-
rolysis has primary application for cases of mild internal fibrosis
from Sunderland Type 2 and 3 injuries. If no release occurs,
however, and internal nerve fibrosis remains after injection,
the affected zone is excised as neuroma-in-continuity in prep-
aration for neurorrhaphy. Internal neurolysis has a long history
of successful use for treatment of spinal or digital nerves,
where there are larger fascicles and thicker perineuria.76
Similar techniques are less feasible for the trigeminal nerves
where distinctive fascicles and thicker perineurium does not
exist. There are no available convincing reports of internal
neurolysis being used effectively for trigeminal nerve repairs,
and this author’s patient outcomes have been poor after inter-
nal neurolysis was used as the primary treatment.77
NEURORRHAPHY
After neuroma resection, direct epineural microsurgical
reanastomosis (neurorrhaphy) is done using 6 to 12× magni-
fication, placing 7-0 to 9-0 nonreactive sutures usually at four
to six circumferential locations. Completed neurorrhaphies
should display no bulging or wrinkling between sutures, and
the nerve should lie passively when released. Minimal repair
line tension is significant because it has been shown that
tension across nerve microrepairs greater than 25 g may
produce gapping and inhibit axon down growth to the distal
nerve.32 At the completion of neurorrhaphy, the repair site is
268 SECTION II ■ Dentoalveolar Surgery
further protected from hematoma, fibrous tissue ingrowth, and
secondary neuroma formation by entubulating the nerve with
an alloplastic protective barrier, such as a biodegradable PGA-
collagen Neurocuff.71,72,73
NERVE GRAFTING (see Figure 15-8)
In more severe injury cases, direct neurorrhaphy repair may
not be feasible. Clinical experience has shown that nerve gaps
of greater than 15 to 20 mm cannot be routinely bridged by
direct neurorrhaphy without requiring excessive nerve dissec-
tion or producing excessive tension at the repair site. A range
of interpositional and entubulation graft procedures has been
used for more extreme injuries, including autologous nerve
grafts, interpositional grafting with muscle, interpositional
entubulation with veins or arteries, and alloplastic tubules.
Autologous Grafts
The primary donor nerves for trigeminal graft repairs are the
sural, greater auricular, and antebrachial cutaneous nerves.78,79,80
Each of these donor nerves is easily obtained with very ade-
quate tissue lengths of up to 6 cm. Grafts are attached with
minimal suturing as a result of graft tissue friability and are
ideally wrapped in a protective biodegradable barrier.
Problems with autologous grafts include numbness and
occasional neuroma formation at the donor sites. In the
case of the sural nerve, the lateral and posterior foot may display
deficits and difficulties with hyperesthesia from shoe contact
and ankle movements. Patients whose greater auricular nerves
have been harvested may complain of paresthesias over the
lateral neck and jaw angle, which is a problem for those patients
with adjacent trigeminal injury neuropathies. An added
problem with the greater auricular as a donor nerve is its vari-
able diameter, which is known to be in reciprocal relation with
the adjacent transverse cervical nerve branches.81
The greatest technical difficulty with autologous nerve
grafts is the incompatibility in shape, size, and fascicle numbers
between grafted nerves and trigeminal nerves. The lingual
nerve averages 3.2 mm in diameter and the IAN 2.4 mm, with
both nerves being generally cylindrical in shape. This
contrasts with the sural nerve at approximately 2.1 mm in
diameter and greater auricular at 1.5 mm; both are generally
flat in shape and with far fewer fascicles than the trigeminal
branches.82 Direct fascicular alignment from graft to trigemi-
nal nerve in the grafting procedure is therefore unlikely and
encourages disorganized axonal regeneration across the grafted
zone. Given the potential problems with autologous donor site
morbidities, the search for alternative grafting procedures
continues.83
Alternative Autografts
An alternative to nerve grafts with skeletal muscle plugs has
been tested for use in trigeminal repairs.84 There are no defini-
tive reports of the levels of neurosensory trigeminal recovery
that can be expected, however, after the use of muscle grafts.
Grafting with autologous harvested veins and arteries has
also been used clinically with mixed success.85,86 Vascular
FIGURE 15-4. Lingual nerve access and neurorrhaphy microrepair. To
view a color version of this illustration, refer to the color insert section
at the back of this book.
grafts are attractive donors because they are minimally inva-
sive and are readily available sources. Clinical use of vascular
entubulation grafts to date, however, has not resulted in
acceptable sensory recovery levels, perhaps because of the
collapse of grafted vessels and consequent interference with
axonal down growth.85
Alloplastic Grafts
Grafting with alloplastic conduits have been advocated with
the obvious advantages of graft availability and prevention of
donor site morbidities. Although biocompatible and effective
for short gap nerve repairs, tubules with PGA and GORE-TEX
materials have not produced satisfactory neurosensory recov-
ery outcomes for nerve gaps greater than 10 mm.87,88 Research
continues in the search for an effective alloplastic graft
alternative as biodegradable PGA-collagen tubular grafts
have shown promise in relieving chronic intractable traumatic
neuralgias in small patient series.71,72,73
LINGUAL NERVE REPAIRS
The lingual nerve can be approached either through a small
paralingual incision or through a wider lateral vestibular
incision (Figure 15-4). The paralingual approach is effective
if minimal dissection and simple decompression is anticipated.
It may be inadequate if there is a need for wider nerve release
for injuries higher on the nerve and for full neuroma resections
and repair. The paralingual incision may also be inadequate
if the nerve has been fully transected and has retracted into
proximal and distal spaces. The standard lateral vestibular
incision begins at the distobuccal aspect of the second molar,
and a full-thickness mucoperiosteal flap is elevated superolat-
erally over the external oblique ridge for approximately 2 cm.
A second full-thickness lingual mucoperiosteal flap is then
developed by first incising the lingual gingival papillae with a
#11 blade and carefully elevating a flap from the retromolar
pad and lingually to the first molar. The lingual flap elevation
 CHAPTER 15 • Treatment of Trigeminal Nerve Injuries 269

should be done carefully because the damaged lingual nerve

often is found entrapped superficially within the lingual flap
itself. The operating microscope is brought into place at 6× to
10× power, and the lingual nerve is identified and decom-
pressed from surrounding paraneural tissues using careful
microdissection. Once identified, the proximal portions of the
nerve are freed superiorly until normal appearing nerve trunk
is seen. Release then proceeds distally toward the nerve injury
site, identified by narrowing, loss of nerve continuity, and
presence of neuroma. Internal fibrous scarring may be revealed
by transilluminating the nerve and palpating gently with
microforceps. The nerve found distal to the injury site is
released into the floor of the mouth, avoiding exposure beyond
the crossing of the submandibular duct. It is important to
prevent direct damage to the epineurial surface proximal and
distal to the damaged tissue site. Typical exposure for repair
requires nerve release 5 to 7 mm proximal and distal to a given
FIGURE 15-5. Lingual nerve alloplastic (PGA-collagen) entubulation pro-
repair site.
tection of repair. To view a color version of this illustration, refer to the
The mobilized nerve is controlled by placing umbilical color insert section at the back of this book.
tapes proximal and distal to the nerve injury site and is then
inspected at high magnification to determine the nature of
nerve damage. When nerve discontinuity and amputation
neuroma are identified, the neuroma is resected with a Beaver
blade approximately 3 mm proximal and distal to the identifi-
able neuroma. Satisfactory excision produces a normal hernia-
tion of intact fascicles from the epineurial nerve endings.
Adequacy of neuroma resection can also be verified by submit-
ting 1- to 2-mm cross-section biopsies for frozen section his-
tologic verification of normal nerve fascicles. After neuroma
resection, epineural neurorrhaphy is accomplished with
progressive 7-0 to 9-0 sutures, placed typically at four to
six circumferential locations without tension. Completed
neurorrhaphies should display no “bulging” between sutures.
In those cases where a lingual neuroma-in-continuity is
identified, lesion excision is assisted by high magnification
inspection and transillumination of nerve and resection of FIGURE 15-6. Inferior alveolar nerve access via lateral nerve decortica-
3 mm proximal and distal into verified healthy nerve tion. To view a color version of this illustration, refer to the color insert
trunk. At the completion of neurorrhaphy, the repair site is section at the back of this book.
protected from hematoma, fibrous tissue ingrowth, and
secondary neuroma formation by entubulating the nerve with
an alloplastic barrier, such as a biodegradable PGA-collagen
Neurocuff (Figure 15-5).

INFERIOR ALVEOLAR NERVE REPAIRS

The surgical access to the inferior alveolar nerve is dictated
by the anatomic site and nature of the nerve injury (Figures
15-6, 15-7). For the mandibular midbody, superficial third
molar region, and distal IAN nerve injuries including those
near mental foramen, a buccal plate osteotomy exposure is
recommended.89 Lateral cuts are made vertically from the
alveolar crest to the inferior border 1.5 cm proximal and
distal to the targeted nerve injury site using a tapered fissure
diamond bur. A parasagittal superior bur cut then joins the
two vertical cuts. A final lateral scoring can be made at the FIGURE 15-7. Inferior alveolar nerve access via sagittal osteotomy. To
lateral-inferior border using the angled semilunar saw. The view a color version of this illustration, refer to the color insert section
rectangular buccal osteotomy is then completed by curved at the back of this book.
270 SECTION II ■ Dentoalveolar Surgery
FIGURE 15-8. Inferior alveolar autologous (sural) nerve graft. To view a
color version of this illustration, refer to the color insert section at the
back of this book.
small chisel release. Nerve decompression, neuroma resec-
tion, and neurorrhaphy with entubulation nerve wrap are
then carried out. At the completion of the nerve repair, the
medullary aspect of the bone plate is relieved to aid in the
nerve decompression, and the plate is finally replaced and
stabilized with percutaneous monocortical pins placed at
superior margins.
For more inferior and medially positioned mandibular
nerve injuries, where long nerve lesions are suspected, as with
endodontic paste injuries, and in the special cases related to
previous sagittal osteotomy orthognathic procedures, an expo-
sure through sagittal osteotomy is recommended (see Figure
15-7). The infrequent injuries to the IAN in the lateral
angular region require a submandibular Risdon incision
approach with lateral cortical window nerve exposure. Neu-
rorrhaphy repairs are very limited through this exposure,
however, because of the inability to mobilize nerve segments
after neuroma resection.
INFRAORBITAL NERVE REPAIRS
Distal infraorbital nerve injuries are approached through an
oral vestibular incision. Nerve decompression is accomplished
by diamond bur widening of the infraorbital foramen, relax-
ation of the nerve trunk inferiorly to permit neuroma resec-
tion, and neurorrhaphy repair of terminal branches as needed.
More proximal injuries from trauma to orbital floor are best
approached through a subconjunctival blepharoplasty inci-
sion. The decompression will require decortication of the
canal roof within the orbital floor and may require release at
the infraorbital rim before the repair is done. At the comple-
tion of proximal infraorbital repairs, an alloplastic graft barrier
is secured in the floor of the orbit.90
POSTOPERATIVE MANAGEMENT
Following acute nerve injuries and repairs, patient counseling
reinforces information about the expected course of recovery.
An expected period of anesthesia “numbness” of 6 weeks or
more is explained to patients, and a limited soft diet is recom-
mended for prevention of secondary accidental tissue trauma.
A restricted range of mandibular motion is also anticipated,
especially where lingual nerve repairs have been carried out,
and may require secondary temporomandibular (TM) physical
therapies for restoration of full joint functions.
Early postoperative medical support uses a 5- to 7-day
course of corticosteroids, such as tapering dexamethasone to
minimize paraneural edema.55 A short-acting anticonvulsant-
psychosedative agent, such as clonazepam (Klonopin) 0.5 mg
b.i.d., combined with titrated opiate analgesics are used to
prevent central neural sensitization.64
During intermediate and later stages of neurosensory recov-
ery and after surgery, transient episodes of hyperesthesia often
occur. Supportive medical therapy at these stages stresses use
of anticonvulsant, antidepressant, and analgesic lidocaine
therapies.91 Following inferior alveolar or infraorbital nerve
repairs, transcutaneous lidocaine patches may be applied to
hypersensitive tissues for 12-hour periods as needed.54,92 Anti-
convulsant therapy with gabapentin titrated from 900 to
3000 mg daily is often effective and well tolerated.93 The more
recently introduced agent, pregabalin (Lyrica), also has a very
favorable toxicity and side-effect profile, but has not under-
gone control study among trigeminal nerve–injured patients.94
Anticonvulsant drugs may be combined with nightly tricyclic
antidepressants if sleep dysfunction and depression are features
of the recovery period.95
SENSORY REEDUCATION AND
PATIENT FOLLOW-UP
The protocol for sensory reeducation should be explained
early in the postoperative recovery period, and active exercises
should be instituted within the first month, even before the
earliest signs of peripheral nerve transmission appear.96 Sensory
reeducation techniques, widely practiced and proven effective
for recovery of a wide range of neurotrauma conditions, have
recently been verified as an effective adjunct to trigeminal
nerve recovery.97 In these techniques, the intact somatosen-
sory cortex is believed to be “reeducated” through daily visual
and tactile stimulation of recovering sensory nerves and is
expected to enhance sensory perception over long recovery
periods.98
Patient counseling after nerve repair stresses the expected
gradual recovery of functions over a minimum of 1 year. The
surgeon schedules regular postoperative recall visits to rein-
force sensory reeducation efforts, monitor neurosensory recov-
ery using serial QST, measure evidence of recovering orofacial
functions, and offer palliative therapies as needed for residual
problems.
■ OUTCOMES OF
TRIGEMINAL REPAIRS
A large number of outcome analyses from all parts of the world
indicate generally significant improvements among repaired
nerve injury patients.7,9,66,99 This is in comparison with expec-
tations for patients with anesthesia or severe hypoesthesia that
 CHAPTER 15 •
has not been treated by 6 months postinjury; in those cases,
spontaneous recovery or significant recovery after 6 months is
“rare” and after one year “zero.”7,10,17,100
Outcomes of trigeminal surgeries for nerve injury are mea-
sured in terms of: (1) patient’s subjective perceptions of
improvements after surgery, (2) the extent to which patients
regain measurable orofacial and neurosensory functions, and
(3) improvements in orofacial neuropathic pain. Although it
is tempting to make direct comparisons of outcomes for the
alternative surgical repair procedures (decompression, neuror-
rhaphy, grafting), such comparisons are not usually valid
because each surgery is applied to differing types and severity
of neuropathologic conditions.
PATIENT PERCEPTIONS
Patient satisfaction with nerve repair treatment has been
shown to be tied mainly to perceived improvement in speech
and taste and reduction in triggered pain or paresthesias.101,102
Patient reports of satisfaction depend to considerable degree,
however, on the questions asked of them. If asked 1 year after
repair whether they have become “normal” in their neurosen-
sory perceptions and functions, the outcome would most often
be “no.” It is also the consensus gained from definitive outcome
studies that the attainment of completely “normal” or “perfect”
neurosensory perception and function after microsurgical
repair is “rare” or “unlikely.”7,10,67
When patients are asked about their global satisfaction
with their surgical outcomes, however, 55% rate their overall
satisfaction as good to excellent, and 45% have a negative
satisfaction rating of “fair to poor.”9,103 In another surgical
series, 82% of patients reported satisfaction scores of 5 or
better on a 10-point scale and negative outcomes in 20%.67 A
critical review of data from these outcome studies suggests that
negative patient-perceived outcomes are found more often
with older patients, where surgical injuries have been treated
with nerve grafting and among patients with dysesthesias of
longer duration.104,105
FUNCTION IMPROVEMENTS AND
SENSORY RECOVERY
The primary orofacial function impairments associated with
trigeminal nerve injuries relate to speech, chewing, swallow-
ing, and loss of protective reflexes, resulting in accidental
biting or sustaining secondary injuries to orofacial tissues. Few
outcome studies have specifically addressed these obvious con-
cerns, particularly speech, mastication, and swallowing. Avail-
able studies do show, however, that microsurgical nerve repairs
are highly effective in regaining C-fiber functions for avoid-
ance of lip and tongue biting and other secondary injuries. A
study that specifically addressed this level showed that patients
progressed from 34% preoperative awareness of a noxious pin
prick to 77% after surgery.67 Other studies have shown similar
gains in noxious and crude-touch functions after microsurgery
at 70% to 90% levels.8,106,107
Recovery of functional sensory improvements from micro-
surgery has been much better studied. Surgical repairs of Type
Treatment of Trigeminal Nerve Injuries 271
4 and 5 Sunderland injuries, a level of injury damage with
low expectations for spontaneous functional recovery, have
resulted in statistically significant improvements for both
protective and discriminative functions as determined by
QST.8,11,107,108
Overall functional sensory recovery rates for all sensory
modalities for repairs of mixed injury types range from 51% to
80%.67,66,108,106 Lingual nerve repairs are the most successful in
achieving functional recovery, even for modest levels of touch
discrimination.10,99,108 This may reflect the improved aware-
ness among oral and maxillofacial surgeons of timely referrals
of lingual injuries for early repairs.
Measurable improvements in taste perception after lingual
nerve repairs have been more modest, averaging 50%.67,101,109
In one report, 35% of patients studied 1 year or more after
repair rated their whole mouth taste as improved, whereas
82% of these same patients reported significant improvement
in their general somatosensory perceptual functions.110
As might be expected, results have been most favorable
when simple decompression (external neurolysis) surgeries
have been used as the sole procedure.69,70 Although favorable
outcomes have been reported for internal neurolysis and peri-
neurial fascicular repairs in spinal and motor nerves,75,76 there
are no reports of successful outcomes of similar internal neu-
rolysis repairs of trigeminal nerves. This author has noted no
significant improvements in QST among trigeminal nerve–
injured patients treated solely with internal neurolysis.77
Definitive clinical outcome comparisons between nerve
grafting and neurorrhaphy repairs are not available in the
current literature. Experimental animal studies and the limited
case series available have concluded, however, that functional
improvements after nerve grafting have also not reached the
levels attained by direct neurorrhaphy and remain at less than
50%.7,10,104 These outcomes almost certainly reflect a patient
population with greater severity of nerve defects leading to
the decision to graft.
Homologous cadaver grafts have also not produced
satisfactory outcomes after limited historical attempts, and
there are also no reports of efficacy of skeletal muscle nerve
gap grafts beyond isolated cases.84 Autologous grafting with
sural, greater auricular, and antebrachial cutaneous donor
tissues remains the gold standard, with improvement levels
expected at less than 50%. Unfortunately, there are no defini-
tive controlled studies available that exclusively measure
outcomes of standardized nerve grafts for discontinuity nerve
injuries.111
Alloplastic graft repairs have proven successful in treat-
ments of small numbers of patients and for bridging disconti-
nuity defects of less than 7 mm.87,88 This level of discontinuity,
however, is usually manageable with direct neurorrhaphy, and
the conclusion at this time is that a reliable alloplastic graft
for managing significant discontinuity trigeminal nerve inju-
ries does not exist.
Entubulation procedures with arterial and venous grafts
also have not demonstrated satisfactory improvement levels
among the small series that have been studied.85,86
272 SECTION II ■ Dentoalveolar Surgery
PAIN LEVEL IMPROVEMENTS
There remains a notable knowledge gap regarding the effec-
tiveness of neurosurgical repairs for patients with traumatic
dysesthesias.7 Available reports conclude that microsurgical
repairs do not induce new or additional forms of pain among
patients who were pain free before repair.10,67 More than half
of repaired patients report satisfaction with regard to pain
reduction, but more than 35% with pain are not improved by
surgery,7,9,10 suggesting that patient selection may be a prime
determinant for responses to surgery.
Alloplastic collagen tubule conduits, used for grafting or
wrap-protection of nerve repair sites, have shown promise for
reversing dysesthesias in a few spinal nerve–injured patients.71,73
Clinical trials demonstrating efficacy of the collagen alloplasts
for patients with trigeminal injury pain, however, are not cur-
rently available.
CONCLUSIONS
Outcome analyses of trigeminal nerve repairs lead to some
general conclusions. Those patients whose neuropathic pain
was significantly reduced after surgery appear to be those who
(1) had short-term hyperesthetic posttraumatic pain, (2) had
responded favorably to local anesthetic test blocks in the dis-
tribution of nerve injury, and (3) had sustained recent Sun-
derland Type 4 or 5 injury and displayed amputation or severe
neuroma-in-continuity at the time of surgical treatment.105
Unsatisfactory surgical outcomes for patients have been
found among patients with (1) long-standing deafferentation
pain in anesthetic or severely deficient nerve distributions, (2)
burning pain following local anesthetic or endodontic chemi-
cal injuries, and (3) patients who displayed clinical signs of
central or autonomic sensitization (spreading secondary
hyperalgesias, erythema, and swelling episodes).105
■ CASE APPLICATIONS
FACIAL TRAUMA NERVE INJURIES
There is surprisingly little reliable data regarding the preva-
lence and key clinical variables of nerve injuries associated
with facial trauma.112 A suspected high incidence of trigemi-
nal nerve injuries is likely underestimated in the literature
because trauma patients tend to not complain of sensory prob-
lems during acute stages of their injuries, and they are often
not available for long-term follow-up assessments. Surgeons
may also tend to focus on the fracture repair process to the
exclusion of documentation or treatment of the associated
neurosensory disorders.113
The best available information indicates that inferior
alveolar-mental nerve injuries occur acutely with 76% to 91%
of mandibular angle and body fractures.13,14 Immediately fol-
lowing fracture treatment, neuropathy may rise transiently to
as high as 91%, and permanent (1 year) incidence of neuro-
sensory disorder appears in 32% to 67% of patients.13,14,27
Infraorbital nerve injuries assessed by QST are found in
76% of patients with zygomatic-maxillary fractures and rises
to 100% among patients with orbital floor involvement.114
Permanent infraorbital neuropathy has been estimated to be
as high as 60%, with a range of 53% to 67% 1 year after treat-
ment.113,115 No studies are available that differentiate between
function impairments and chronic levels of dysesthesia after
facial trauma.
The main determinants of increased permanent neurosen-
sory deficits appear to be: (1) degree of fracture displacement,
(2) interval between injury and fracture repair, and (3) frac-
ture repair type.
Studies have shown that pretreatment sensory neuropa-
thies are found in 25% of nondisplaced mandibular fractures
and 73.5% of cases with greater than 5 mm pretreatment dis-
placement.13 Recent studies have also shown that there are
increases in sensory deficits between the pretreatment and
1 week posttreatment stages of mandibular fracture treat-
ments.116 Although this effect appears to be transient, it points
to the importance of prerepair neurosensory testing and
informing patients of possible sensory deterioration after treat-
ment. The interval between injury and fracture repair is also
significant, with neuropathies increased when there has been
more than 1 week delay.117
The type of fracture repair is a known variable, with rigid
fixations associated with more neuropathy than nonrigid113
and with long-term neuropathies more often found after open
reductions of mandibular fractures than closed.118 Interestingly
the reverse appears to be the case for zygomaticomaxillary
fracture repairs, where long-term infraorbital deficits are seen
more often when closed reductions or no treatments have
been done rather than open fixations.117
Acute nerve repair treatments in conjunction with fracture
repairs are recommended in the following circumstances: (1)
the nerve distribution tests anesthetic; (2) nerve transection
or major disruption is observed at surgery, and it is accessible
for repair; (3) the nerve-associated fracture is displaced greater
than 3 mm; and (4) the surgeon has the necessary skills,
instrumentation, and operative environment.
Secondary (delayed) microsurgical repair treatments are to
be considered for patients who (1) test anesthetic after 3 to 6
months, when nerve repair can be accomplished without
impairing bone healing and (2) patients continue with intol-
erable neuropathic pain and/or functionally disabling sensory
deficits.
It is recommended that clinicians discuss with patients the
risk-benefit features of open reduction treatment (more imme-
diate function) versus closed reductions (better neurosensory
recovery) and that they be informed of their increased risk for
worsening of neurosensory functions after treatment. Sensory
reeducation protocols should be engaged early during post-
treatment recovery, and patients should be followed for 1 year,
if possible, documenting their recovery with serial QST.
LOCAL ANESTHETIC INJECTION NERVE INJURIES
(Figure 15-9)
Acute trigeminal nerve symptoms after local anesthetic blocks
are common occurrences, with estimates that one in every 200
 CHAPTER 15 •
FIGURE 15-9. Dysesthesia with dysautonomia from local anesthetic
nerve injury.
mandibular blocks will be associated with a “traumatic episode”
of pain or paresthesia.119 A high majority, 80% to 88%, of
patients with these acute symptoms are known to have resolu-
tion within 1 week. However, approximately 10% to 15% will
have sustained or permanent neuropathy. Surveys have led to
estimates that permanent nerve injuries occur as a result of
mandibular block following one of every 26,000 to one in
800,000 mandibular blocks.21 These data suggest that any full-
time dental clinician will have at least one patient during his
or her career who has permanent nerve involvement resulting
from mandibular block.
The lingual nerve is the most commonly affected by anes-
thetic injuries. The lingual effects are also more incapacitat-
ing, with a much higher incidence of burning dysesthesias as
compared with injured IANs.21 The timeline for lingual anes-
thetic injury recovery also may be unique. If full recovery of
normal lingual neurosensory functions has not occurred by the
third week after injury, 86% will not recover further and are
considered permanent if neuropathy is present at 1 month.22
This is in direct contrast to the more common pattern of
recovery seen with partial mechanical injuries to lingual and
IANs, where gradual recovery of functions is expected to
continue for months following the injury.
There is also good evidence that needle contact with the
nerve during injection, producing “electric shock,” is not
likely a prime cause of nerve injury. Fewer than 50% of
patients who have sustained lingual injury report having expe-
rienced shocking paresthesias.21,22
The cause of anesthetic nerve injuries is largely unknown.
Two main mechanisms are theorized: intraneural mechanical
injury and indirect chemical neurotoxicity. Mechanical inju-
ries may occur from direct intrafascicular penetration or indi-
rect needle trauma from a barbed needle tip.120 Such injuries
could allow leakage of blood from a traumatized surface or
Treatment of Trigeminal Nerve Injuries 273
interfascicular vessels, resulting in intraneural hematoma with
potential compression ischemia or neurotoxicity from blood
contact with axons.121
There are almost no reports, however, of clear mechanical
nerve injury following injection alone based on observations
made at the time of secondary surgical exposure of the symp-
tomatic nerves. This author has observed only one case in
which the lingual nerve displayed Sunderland Type 4 injury
with demonstrable neuroma and significant internal derange-
ment. Neuroma resection and neurorrhaphy repair was carried
out in this case without successful recovery of sensation. In all
of this author’s remaining lingual nerve anesthetic injury
cases, and consistent with survey reports of microneurosur-
geons in the United States, surgical exposure of lingual
nerves injured during mandibular blocks have revealed little
objective evidence of mechanical injury. The typical appear-
ance of exposed nerves is of intact neurovascular bundles with
slight perineural fibrosis and loss of full nerve transparency
upon transillumination through the microscope. The nerves
otherwise display unremarkably normal appearance, even in
cases where patients have been severely debilitated and in
pain.122
These direct observations are among the strongest argu-
ments that chemical neurotoxicity, rather than mechanical
nerve damage, is the more likely cause of anesthetic neuropa-
thy. There is other support for the neurotoxicity theory: (1)
anesthetic injuries tend to involve the entire nerve distribu-
tion in contrast to the partial injury patterns often seen after
mechanical injuries from other sources, (2) a higher percent-
age of dysesthesia is seen among patients with anesthetic inju-
ries when compared with cases where the nerve was known
to be mechanically injured,21 and (3) direct nerve contact
during injection does not appear to be present in at least 50%
of cases.
The specific agent or concentration of local anesthetic used
may also be an etiologic factor in injection neuropathies.
Studies in Canada and Denmark reported significantly higher
rates of lingual and IAN nerve injuries associated with the
higher concentration anesthetics, 4% articaine and prilocaine,
after their introduction in 1985.22,123 Similar suspicions were
raised in the United States after articaine became available in
2000.124 However, Malamed has concluded that there is not a
significant difference in paresthesia rates between articaine
and lidocaine.125 Because of this lingering controversy, it is
recommended that 4% articaine or 4% prilocaine not be used
routinely for anesthetic nerve blocks, although these agents
are suitable for infiltration injections.126
There are no current anesthetic techniques or protocols
that absolutely prevent nerve injuries.127 There are certain
guidelines, however, that may minimize their severity: (1)
avoid purposeful stimulation of paresthesias during injection
to assist in localizing the nerve128; (2) minimize multiple injec-
tions into similar anatomic zones; (3) avoid bone contact with
needle tips, and replace the needle if a barb is detected at the
tip; and (4) if there are intraoperative signs of shocking-
burning pain, indicating that nerve contact may have been
274 SECTION II ■ Dentoalveolar Surgery
FIGURE 15-10. Mandibular canal spread of neurotoxic endodontic chem-
ical materials.
made, the needle should be retracted a few millimeters before
release of anesthetic solution.
There are isolated reports of clinical improvements after
early surgical exploration and external neurolysis of spinal
nerves injured by anesthetic injections.129 Most experience,
however, shows that local anesthetic neuropathies are highly
unresponsive to both medical therapies and surgical repairs, a
situation documented for both trigeminal and spinal nerves.128
Surgeries for patients with “burning” lingual neuropathies and
taste loss have been particularly disappointing. These experi-
ences and lack of objective clinical trials have lead to a general
consensus among oral and maxillofacial microneurosurgeons
that currently available surgical treatments of trigeminal
nerves traumatized by local anesthetic blocks are not strongly
advocated.123
Alternative nonsurgical therapies for chronic postinjection
neuropathies emphasize sensory reeducation and supportive
medical management.96 The primary agents are titrated
combinations of opiates and anticonvulsant-antidepressant
co-medicants.91,95,130
SURGICAL AND ENDODONTIC
MEDICAMENT INJURIES (Figure 15-10)
Trigeminal nerves are at risk for chemical neurotoxic injuries
from topical medicaments used in dentoalveolar and end-
odontic surgeries.131 Although there are adequate experimen-
tal animal studies of medicament effects on peripheral nerves,
there are few controlled epidemiologic studies or clinical trials
for these same agents.
Medicaments that may increase nerve injury risk are used
in dentoalveolar surgery for infection control, bony socket
hemostasis, topical analgesic treatments of postextraction
alveolar osteitis, and to prevent recurrence of cystic patho-
logic conditions.
Tetracycline antibiotic powders were advocated and in
widespread use in the 1960s for prevention and treatment of
third molar postextraction alveolar osteitis.132 However, studies
have shown that a chronic inflammatory foreign body response
may occur in response to tetracycline placed near IANs.133 An
experimental nerve injury model of epineural injury has shown
that tetracycline can significantly accentuate intrafascicular
inflammation when applied to the exposed nerve surface.134 In
spite of these findings, however, no direct correlation has been
proven between tetracycline use in dental sockets and increased
incidence of trigeminal neurosensory deficits.
Unacceptable levels of trigeminal neurotoxicity have been
demonstrated, however, for Carnoy’s solution, used for oral
hemostasis and prevention of mandibular cyst recurrence.135
Carnoy’s solution, consisting of chloroform, acetic acid, and
ethanol at a pH of 2.8, has been shown experimentally to
retard nerve conduction within 2 minutes of its contact with
the nerve and sustained these effects well beyond 2 weeks.136
Other studies have shown acceptable inferior alveolar tol-
erance of effects of intraalveolar liquid nitrogen used to
prevent recurrence of enucleated keratocysts.137 Bovine colla-
gen and bone wax used to control intrabony hemorrhage are
also well tolerated by peripheral nerves.138 In these same
studies, however, oxidized regenerated cellulose (Surgicel), at
pH of 2.8, produced transient decreases in neural function
immediately after contact with peripheral nerves, although
full conduction recovery was seen by 4 weeks. Gelatin
sponge was found to produce even longer sustained neuro-
pathy beyond 4 weeks.138 The overuse of these acidic agents
in contact with human peripheral nerves is therefore
discouraged.139
There are no definitive epidemiologic studies of trigeminal
injuries resulting from endodontic surgeries.131 Theorized
mechanisms of endodontic neuropathy include: (1) direct
nerve trauma from overinstrumentation with file and broaches,
(2) compression ischemia and intrabony inflammation inju-
ries from periapical overextension of filling materials, and (3)
chemical neurotoxicity from intracanal medicaments.
The endodontic medicaments most associated with chemi-
cal paresthesias are phenols, aldehydes, and halides, with
milder but significant effects also seen with the use of calcium
hydroxide, gutta percha, steroids, and antibiotics.131 The
primary determinants of nerve injury appear to be the amount
and concentration of foreign agents in contact with the nerve,
the duration of contact, the pH of the agent, and associated
epineural mechanical injury.140
Calcium hydroxide and gutta percha, although widely
used and safe in small intraalveolar quantities, are high in
alkalinity and are placed under pressure at high temperatures.
These agents may potentially enter and migrate within
the mandibular canal, resulting in extensive Wallerian dege-
neration.141,142,143,144 Such cases have been associated with
intractable burning neuropathic pain. Most cases of endodon-
tic neuropathies have been associated with inferior alveolar
injuries, with no available reports found to be associated with
maxillary endodontic procedures.
Microsurgical decompression surgeries are advocated for
patients with endodontic injuries as soon as the complications
are recognized. Injured nerves are exposed by lateral decortica-
tion of the mandibular canal, removal of chemical foreign
 CHAPTER 15 •
bodies, irrigation of the nerves with isotonic solution, and
placement of nerve barrier protections. Cases where there has
been extensive proximal spread of material in the mandibular
canal and neural destruction will require resection of necrotic
nerve segments and repair with neurorrhaphy or grafting. Sag-
ittal osteotomy may help achieve access to proximal portions
of the nerve.145
ORTHOGNATHIC NERVE INJURIES
Neurosensory disorder is a primary long-term complication of
orthognathic surgery, potentially involving inferior alveolar,
infraorbital, lingual infraorbital, and, occasionally, maxillary
nerve trunks.25,27
Injuries may result from direct instrument punctures,
lacerations, or stretches during osteotomy mobilizations and
punctures or nerve compression during placement of transos-
seous pin or plate fixation. After injury, orthognathic patients
display the full range of hypoesthesias, hyperesthesias, and
nonpainful and painful paresthesias. The greatest functional
difficulties and dissatisfaction, however, are associated with
triggered paresthesias and dysesthesias.146
Neurosensory disorder 1 week after bilateral sagittal split
osteotomy (BSSO) is nearly universal. Subjective analyses
and objective QST have found an IAN disorder in 97% of
BSSO patients 1 week after surgery.102 Acute lingual neuropa-
thy has been reported in 9% to 18% of patients.147 Six months
after orthognathic surgery, as many as 63% of a large patient
series reported abnormal spontaneous sensations, and 84%
had abnormality in response to tissue stimulations.102 These
data compare favorably with other studies where 73% of
patients had residual neurosensory abnormality at 6 months.147
One year postsurgical levels of inferior alveolar neurosensory
disorders have varied from 11.6% in one study,26 27%148 and
35% in others.25 The 1-year postoperative neuropathies, pre-
sumed to be permanent, were rated as “mild” by 32% and
“disturbing” by 3%.25 Other surveys have shown, fortunately,
that even permanent sensory complications do not serve as
the most significant determinant of patient satisfaction after
orthognathic surgery. Patients report that functional gains
and esthetic improvements outweigh residual neurosensory
disorder when asked about “quality of life” satisfaction after
surgery.26
The highest rates of neurosensory deficits have been found
among patients older than 35149 and are as high as 50% after
age 40.26 Long-term disorder is higher among women than
men, slightly higher when genioplasty is added to BSSO, and
with longer mandibular advancements.149,150 Other factors
increasing the risk of nerve injuries include a location of the
mandibular canal closer than 0.8 mm to the lateral mandibu-
lar cortex.151,152 Manipulation of soft tissues of the pterygo-
mandibular space immediately medial to the mandibular
lingula has been associated with higher levels of sensory
disorder.25
The IAN is also more likely injured if the rate of advance-
ment in distraction osteotomies is greater than 1 mm/day.153
Combining maxillary osteotomies with BSSO has not proven
Treatment of Trigeminal Nerve Injuries 275
to increase risk of neurosensory disorder (NSD).97,146 Nor has
the use of biodegradable screws and plates for transosseous
fixation been associated with higher levels of sensory
disturbances.148
Lingual nerves are also at risk for injury during orthogna-
thic surgery if unprotected from horizontal drilling during
bicortical pin fixation in the retromolar mandible and by
secondary nerve trauma if pins are overextended through the
medial cortex into the sublingual space. Lingual nerves injured
at the level of the mandibular lingula before or during the
medial osteotomy cut may be unrepairable in some cases
because of their inaccessible location.25
Sensory reeducation should be an integral part of postoste-
otomy patient care. Exercises should begin in the first week
after surgery and be conducted twice daily during the critical
early months after surgery. Recent research has shown that
sensory reeducation can significantly lessen the objectionable
impressions of sustained altered sensation after orthognathic
surgery.97
There are no published reports that specifically address
surgical treatments of orthognathic trigeminal injuries. It is
recommended, however, that direct neurorrhaphy be carried
out immediately if possible when nerve separation is observed
during orthognathic surgery. The specific technique will be
dictated by the site and nature of injury. When the IAN is
injured proximally at the point of entrapment in the medial
aspect of the distal osteotomy segment, it is necessary to com-
plete the osteotomy split to access the nerve for repair. In the
event of IAN injury during the vertical cut of lateral cortex,
the nerve may need to be freed and released peripherally to
the mental foramen by corticotomy. This is especially impor-
tant for mandibular advancement cases so that the nerve may
be repaired without tension.
IMPLANT NERVE INJURIES
Mandibular endosseous implant surgery carries a high inher-
ent risk of injury to inferior alveolar-mental and, to a lesser
degree, lingual nerves. Risks are amplified in cases of atrophic
posterior mandibular ridges, where direct manipulation of
nerves has been done among patients of middle or older ages
and those who use tobacco.154,155
The literature on the incidence of implant-related trau-
matic neuropathies is inconsistent because data collection
does not always distinguish between subjective patient reports
of sensory disorder and the results of QST. Because implant
injuries are more often Type 1 to 3 Sunderland in-continuity
lesions rather than Type 4 full-crush or Type 5 full-nerve
transections with the tissue loss defects found with other
types of trauma and surgery, the results of sensory testing tend
to be more favorable than levels of subjective patient
complaints.19
Acute injuries after mandibular implant placement are
reported as ranging from 0% to 44%, with average incidences
of 5% to 15%.19,20,156,157,158 Permanent (greater than 1 year)
neuropathies are reported at 0% to 19% with averages of
8.5%.18,159 Retrospective studies of patient outcomes where
276 SECTION II ■ Dentoalveolar Surgery
direct nerve manipulations (transposition and lateralization)
have been done found rates as high as 60% to 94% for 1 year
recovery of crude-touch detection abilities.160 Other studies,
however, report levels of permanent patient-reported sensory
abnormalities of 20% to 70%.161,162,163,164 The incidence of
permanent implant-induced trigeminal nerve injuries appears
to be decreasing over the past decade, possibly because of more
accurate presurgical planning and reduction in direct nerve
manipulation surgeries in favor of bone grafting and wider-
diameter implant techniques.
Implant nerve injuries appear to be caused by: (1) direct
mechanical trauma from drill or implant crush, (2) indirect
thermal drill trauma, (3) indirect mechanical injury from
collapse of bone into the mandibular canal, and (3) bleeding
into the mandibular canal and direct effect on nerve transmis-
sion or with potential for neurovascular “compartment
syndrome” ischemia.165,166
Injuries are most likely prevented if accurate presurgical
tomography and/or CT analyses have been used with drill-
length calculations that provide at least 2 mm of nerve clear-
ance. High-precision intraoperative navigation systems for
drill planning have been developed, but are not in widespread
use.167
When acute nerve injury has occurred and sensory testing
reveals objective sensory deficit more than 40 hours after
surgery, postoperative imaging assessment is done to deter-
mine the anatomic relation of the implant to the mandibular
canal. The neurovascular bundle is decompressed by removing
the implant and replacing it with a wider-diameter implant
or, alternatively, by elevating the implant from the canal and
retaining it in position to serve as a possible barrier to socket
bleeding and secondary nerve fibrosis.168 Medical support is
then provided with a 5-day corticosteroid series and aggressive
medical pain management.
Secondary microsurgical nerve exploration, decompres-
sion, and repair is indicated for patients who have sustained
implant nerve injuries and (1) demonstrate objective signs of
direct nerve injury verified through postimplant imaging, (2)
display anesthesia or functionally disabling hypoesthesia more
than 1 month following implant surgery, and (3) display medi-
cally intractable dysesthesia greater than 1 month.20,166
THIRD MOLAR NERVE INJURIES
Injury to inferior and lingual nerves is the most significant
frequent and potentially long-term complication associated
with the removal of impacted mandibular third molars. Classic
works by Alling and Kipp pointed to the potential problems
of impairments in speech, mastication, swallowing, social
functions, and sustained paresthesia and dysesthesia.5,169 The
IANs are injured more often than lingual nerves. However,
lingual nerve injuries are functionally more disabling and have
lower spontaneous recovery rates.1,2
In a recent survey of 535 oral and maxillofacial surgeons,
94.5% reported having patients with IAN injury over a
12-month period, and 53% had patients with lingual nerve
injury.4 Permanent injury of the IAN during the surgeons’
careers was reported by 78%, and 46% reported permanent
lingual nerve injuries. Rates of overall injury have been
calculated at one IAN injury per 2500 extractions and one
lingual nerve injury per 10,000 extractions. These data reveal
a higher occurrence of nerve injuries than predicted by the
earlier survey reports.1,2
The overall incidence of IAN injuries is reported as ranging
from 0.3% to 8.4% and lingual nerve injuries ranging from
1% to 22%.16,17,170 Most reports indicate that approximately
15% to 20% of patients who sustain nerve injury will
have residual and probably permanent effects 1 year after
injury.5,171,172 However, many of the epidemiologic studies of
nerve injury incidence are not comparable for several reasons:
Some studies are retrospective only; some are reports of only
subjective outcomes (i.e., are done by questionnaire only with
no objective sensory testing data); some reports give quanti-
fied levels of altered sensation (paresthesia), and very few
separate out incidence of dysesthesia (painful paresthesia);
some reports do not separate acute or short-term effects from
long-term or permanent injury effects; and the postinjury time
frames for study varies widely.
In the majority of cases of third molar lingual nerve inju-
ries, the cause of injury is reported by surgeons as unknown
(i.e., the nerve injury has not been observed).4 The IAN,
however, is more frequently exposed and visualized in extrac-
tion sockets. When the nerve has been exposed, there is a
20% risk of acute sensory alteration.17,170 Thirty percent of
those injured will retain altered sensation at 1 year, for an
overall 1-year sensory alteration of 6%. From a clinical stand-
point, the finding of an exposed, intact IAN bundle during
third molar surgery suggests that there is a 1 in 5 chance of
developing paresthesia and that patients with postoperative
paresthesia have a 1 in 4 chance of sensory alteration persist-
ing 1 year or more. The incidence of permanent deficit for
observed severe Type 4 or Type 5 transected trigeminal nerves
is not known. Extrapolation from studies of exposed but intact
nerves suggests a greater than 6% likelihood of permanent
IAN neuropathy.17,170
The likelihood and extent of third molar nerve injuries are
influenced by both preexisting patient factors and surgical
factors. Primary patient factors include: (1) patient age, (2)
depth and type of impaction, (3) preexisting regional patho-
logic conditions, and (4) local anatomy.
There are strong correlations between increasing patient
age and the incidence of IAN injuries.39,170 This is attributable
to both root formation and related pathologic conditions and
the known negative effects of age on recovery from all types
of nerve injuries and after repairs. Interestingly, there are no
similar proven age correlations for lingual nerve injuries.173
This may be due to the anatomic differences between the
nerves: the intrabony locus of the IAN versus the soft tissue
locus of the lingual nerve.
The depth and type of impaction is significant with respect
to inferior alveolar injuries; mesioangular and deeper horizon-
tal impactions are associated with the highest IAN rates and
with dysesthesia.15,170,174,175,176
 CHAPTER 15 •
Frequency of lingual nerve injuries has not been directly
correlated with the depth of impaction.173 Lingual nerve inju-
ries are more often “surprises” to the operating surgeon, and
many follow simple elevation of soft tissue impacted third
molars.4 This may be due to the important anatomic variation
in the proximity of the lingual nerve relative to the retromolar
lingual ridge crest. Cadaver and imaging studies have demon-
strated the high variability of lingual nerve position, with
approximately 20% of nerves lying above the lingual crest or
in direct contact with the lingual plate, a situation that pro-
vides little natural bony protection for the nerve.82,177,178 This
may also account for the occasional case reports of bilateral
lingual nerve transections.
Lingual nerve injuries are also increased in the presence of
preexisting pathologic conditions, especially erosion of the
lingual plate of bone by cyst or chronic infection. This may
increase the likelihood of injury to the exposed nerve from surgi-
cal instrument trauma or inadvertent nerve damage from over-
zealous socket curettage or extirpation of cyst remnants.40,179
The strongest predictor of IAN damage has been shown to
be the anatomic relationships between the nerve canal and
the dental roots as demonstrated on imaging signs.180 The
primary indicators are: (1) diversion and narrowing of the
mandibular canal, (2) darkening and deflection of the roots,
and (3) interruption of the white line of the canal.180,181,182,183
Studies have demonstrated that when one of these radio-
graphic predictors are present, there is a 16% occurrence of
nerve damage,181 and when two or more predictors are present,
the incidence is 30%.183 The highest predictors of true nerve-
root relations has been shown to be diversion or narrowing of
the canal, darkening of the roots, and interruption of the
radiopaque cortical line of the canal.181,182 It has been shown
that periapical radiography and conventional panoramic
methods are sufficient for identification of these key indicators
of root-nerve superimpositions.183 With the advent and
increasing availability of low-dose cone beam CT technology,
more accurate three-dimensional imaging may be indicated to
clarify the relationship between the IAN and the lower third
molar.180,183,184,185
Surgical factors that influence nerve damage include: (1)
experience of the surgeon,179,186 (2) anesthetic techniques, (3)
surgical techniques, and (4) nerve exposure during surgery.
IAN injuries have been shown to occur at markedly higher
rates when surgery has been done under general anesthesia as
compared with sedation or local anesthesia.187,188 This outcome,
however, more likely reflects general anesthesia case selection
for the highest degree of impaction difficulty rather than
factors inherent to the anesthetic itself. The highest levels of
inferior alveolar paresthesia and dysesthesia, in fact, have
been shown to result from ostectomy inferior and mesial to
horizontally impacted teeth.169,176,179
Surgical techniques that place the lingual nerve at greater
risk include placement of the opening incisions on the lingual
aspect of the retromolar ridge instead of over the external
oblique ridge in the lateral vestibule. Retromolar incisions
that follow the line of the posterior dental occlusion risk drop-
Treatment of Trigeminal Nerve Injuries 277
ping the blade directly into the pterygomandibular space
because of the lateral flare of the mandibular ascending ramus.
Ostectomy procedures carried out blindly posterior to the
impacted tooth carry the same risk of inadvertant lingual
nerve direct contact. The greatest single iatrogenic cause of
lingual nerve injury, however, appears to be lingual cortical
plate perforations or ostectomies carried out during tooth
sectioning.40,179,189
Prevention of nerve injuries is obviously of the highest
priority. Two particular preventive techniques, exposure and
instrument protection of lingual nerve and coronectomy for
prevention of root damage to IAN, may have value.
There is general agreement that the initial incision and flap
elevation for third molar access should be in the lateral buccal
vestibule.171,174,186 Some authors, however, have advocated
additional elevation of a lingual flap, used to identify the
nerve and allow placement of a subperiosteal retractor before
bone relief, tooth sectioning, or tooth elevation.190
Studies have shown that lingual flap elevation and nerve
identification is associated with higher 1-week postoperative
levels of paresthesias.39,179 However, recent meta-analysis and
controlled studies with more than 850 patients have shown
no difference in the incidence of permanent lingual nerve
injuries between standard buccal flap–only and both buccal
and lingual flap elevations.190,191,192,193 These data lead to the
conclusion that lingual flap elevation and nerve protection
may be a safe practice, particularly in cases where greater
access and visibility is needed. A key precaution is made,
particularly to the surgeon who might be tempted by lingual
flap exposure to carry out aggressive lingual bony plate ostec-
tomy or root sectioning.
Coronectomy, also called partial odontectomy or deliber-
ate root retention, has been advocated as a means of prevent-
ing root removal injuries to the IAN.194,195 This technique
is especially indicated if preoperative imaging indicates an
intimate relationship between the root of the tooth and the
IAN. The technique is not indicated for teeth or roots that
are mobile, where there is active root or apical infection, or
with horizontally impacted teeth in direct contact with the
nerve.196
The goal of coronectomy is to leave the part of the root in
direct contact with the nerve undisturbed and to not mobilize
the retained root. The crowns are transected with a narrow
fissure bur. Enough root is removed to permit bone to form
over the retained roots, usually at least 3 mm inferior to the
boney crest. Results of limited studies to date have been favor-
able with regard to prevention of IAN damage; one study
demonstrates no nerve injuries after successful coronectomy
when compared with 19% with conventional removal among
comparable risk patients.194
Other authors have expressed concerns, however, regard-
ing secondary risks of coronectomy from root migration, pulp
necrosis with apical infections and osteomyelitis, increased
antiinfective and radiography needs, and possible risk to
lingual nerves from bone perforation from this procedure.197,198
The current state of science regarding coronectomy suggests
278 SECTION II ■ Dentoalveolar Surgery
that clinicians consider it for patients whose IAN injury risks
appear extreme for complete removal of impacted roots.
Treatment of observed injuries to the IAN during third
molar surgery requires close observation and immediate inter-
vention. Osseous hemorrhage should be controlled with direct
bone pressure and bone wax as needed, avoiding direct pres-
sure on the nerve or collapsing bone pressure into the adjacent
mandibular canal. If observation of the nerve reveals the
nerve to be intact and supported by its boney floor and at least
one wall, then simple supportive care is carried out with mild
irrigation with isotonic saline to clean the nerve of foreign
particles and blood clot on the nerve. The nerve is then gently
overlaid by a biodegradable barrier, such as Gelfoam, before
closure. Similar protocol is used if the nerve is seen to have
been cleanly transected, but the nerve ends are passively
opposed, and it rests supported by the canal floor and one or
more wall. Ideally, a single superior or lateral 7-0 or 8-0 epi-
neural suture could be placed, if lateral access permits. For
damaged IANs that are not supported by bone and the seg-
ments are not passively aligned, delayed or secondary micro-
surgical repair may be required (see “Nerve Repair Surgeries”)
if unsatisfactory spontaneous recovery does not occur.
In the infrequent circumstance that lingual nerve separa-
tion (Type 5 injury) has been observed, definitive microsurgi-
cal repair is indicated as soon as it is practical199 (see “Nerve
Repair Surgeries, Lingual Nerve Repair”). In all cases of
acutely injured trigeminal nerves, supportive physical therapy
and medical care with analgesic, anticonvulsant, and anti-
inflammatory agents should be initiated (see “Postoperative
Management”). In the event that additional inflammatory or
infectious complications are active in the early postinjury or
postrepair time frame, the clinician should be careful with the
use of topical medicaments placed in the recovering third
molar socket (see “Medicament Injuries”). Delayed or second-
ary repairs of inferior alveolar and lingual nerves are carried
out after careful follow-up and when patients meet the prim-
ary criteria for microrepairs: sensory loss and intractable
dysesthesia.
■ MEDICOLEGAL ISSUES RELATED
TO NERVE INJURIES AND REPAIR
Iatrogenic trigeminal nerve injuries are among some of the
most common events leading to litigation. They are associated
with the highest dollar claims and awards reported by the
malpractice carrier (OMSNIC) that covers the greatest
number of oral and maxillofacial surgeons.200,201 Large surveys
have shown that nerve injuries are likely to occur during the
course of most oral and maxillofacial surgeons’ careers, both
nationally and internationally.1,2,3,4 Litigation complaints
alleging negligence regarding nerve injuries are still common
despite improvements in patient and surgeon risk education,
more careful surgical care, and informed testimony by experts
and defense teams.168,202,203 It is also established that some
injuries to trigeminal nerves may be inevitable and unprevent-
able because of preexisting patient variables. Increased risks
may be present from anatomic variation, developmental
anomalies, preexisting disease, and destructive local patho-
ses.15,176,177,178 It is also apparent that the operating surgeon can
often prevent troublesome litigation and failed defenses if
certain guidelines of patient communication, surgical care,
and documentation are followed.
THE PRESURGICAL EXAM AND
INFORMED CONSENT
The presurgical assessment and documentation should seek
out any history of preexisting sensory or neuropathic condi-
tions. Previous regional surgeries known to be associated with
potential nerve injuries should be documented, particularly
facial trauma and fractures, past surgeries for malignancy or
dentoosseous lesions, and orthognathic and implant surger-
ies.15,203 Systemic diseases that may have associated sensory
neuropathy, such as diabetes mellitus, rheumatoid arthritis,
herpes zoster, or recurrent herpes simplex, and exposure to
known neurotoxins should be investigated. Routine high-
quality diagnostic x-ray and appropriate additional imaging
should be available, if possible, before surgery, although CT
or MRI studies are not required as standard of care for nerve
injury prevention at this time.204 When the patient history is
suggestive of possible preexisting neuropathy, it is recom-
mended that baseline regional neurologic exam and quantita-
tive sensory test findings be documented in the record. A
thorough and patient-interactive informed consent process is
especially important regarding nerve injuries. Patients should
have a clear understanding of the medical reasons for the
proposed surgery, the relative benefits of that surgery balanced
against the possibility of nerve injury, and reasonable alterna-
tives to the surgery. The consent discussion should clarify to
patients that “nerve injury” does not refer to motor deficits,
but that “possible permanent effects” on sensory functions
could occur. The possibility of injury from local anesthetic
injections or chemicals should also be indicated during the
consent process.205 The consent process needs to be conducted
without language barriers, done in the presence of witnesses,
such as family and clinical staff, and should be completed with
signatures. The informed consent form regarding nerve inju-
ries developed by OMSNIC is recommended.
DOCUMENTATION
Typed operative note entries with detailed operative notes are
the standard of care for hospital or surgical center operating
room surgeries. This level of documentation is not required
for routine office surgeries. Chart documentation, neverthe-
less, should be legible and include some notation regarding
the basic surgical approach used. Depending on the specific
surgery, entries might include brief notes of location and
design of incisions, whether the approach was extraoral or
intraoral, if bone relief or tooth-root sectioning was done, the
type of bone screws or plating done, the specific locations and
sizes of endosseous implants placed, whether nerve transposi-
tions were done, and whether biopsies were incisional or exci-
sional. The record should also reflect any unusual procedures
that were required during surgery, such as incomplete removal
 CHAPTER 15 •
of a lesion, and the decision to retain root tips or foreign
bodies, such as broken instruments or burs, whose removal
could endanger adjacent nerves. The operative record should
note unusual intraoperative observations, such as brisk peri-
neural bleeding, observed nerve exposure, whether there is
complete or partial laceration, whether the nerve ends are
passively aligned, and whether the nerve is supported or
unsupported. If immediate nerve suture or entubulation
support has been carried out, this should obviously be docu-
mented in detail.
WHEN NERVE INJURY HAS OCCURRED
When surgical observations indicate nerve injury or postsurgi-
cal patient symptoms suggest that nerve injury has occurred,
certain steps should be taken. The patient’s subjective com-
plaint should be recorded in their language (“numb, burning,
stabbing, shocking”) using modified McGill Inventory terms
if needed. The patient’s estimated pain severity level (0 to
10), and any specific function problems (tongue biting, speech,
or chewing difficulties) should be recorded as baselines for
comparison with future recovery and treatment responses. A
full clinical examination with baseline QST of injured and
adjacent nerve distributions is very important and should
include a rating of sensory deficits measured (zero to four,
anesthetic to normal) and a description or drawing of the
anatomic features of the neuropathic regions. Based on these
and follow-up examinations, a specific neurologic diagnosis
should be established (anesthesia, dysesthesia, hypoesthesia,
or hyperesthesia) in the record and explained to the patient
in lay terms. Follow-up QST is used to plot signs of spontane-
ous neurosensory recovery or lack of recovery. The surgeon
should share his diagnosis with patient and family, stating
expectations for recovery, treatments that may be required,
and the possibility that secondary consultation referrals may
be needed. No retrospective changes should be made in the
clinical record following nerve injury, although supplemental
recalled findings can be entered into the follow-up record if
signed and appropriately dated. There is evidence from medical
risk-management research that litigation problems can be pre-
vented or minimized if the clinician indicates to the patient
that error(s) occurred during the patient’s care and led to an
unfavorable outcome and that the physician has sincere
concern and wishes to help in the patient’s recovery.206 There
may be specific cases of poor nerve injury outcomes related to
“honest and unavoidable mistakes” where the surgeon consid-
ers this strategy after consultation with the insurance carrier’s
risk management staff.
WHEN REFERRAL FOR SECONDARY NERVE
INJURY CARE IS CONSIDERED
Referral to a subspecialist in nerve injury management should
be considered on an individual patient basis as soon as the
criteria and indications for surgery are met, ideally within 3
months of the nerve injury (see “Purposes and Patient Selec-
tion”). Patient acceptance for surgery is based on objective
and subjective signs of failing nerve recovery and/or refractory
Treatment of Trigeminal Nerve Injuries 279
dysesthesia. The decision to refer may also be influenced
by patient preference and practical considerations, such as
unavailability of trained specialists.204 In those cases where
secondary nerve repair is being considered, both the referring
primary surgeon and the secondary repair surgeon should com-
municate key expectations to the patient. Patients should be
informed that nerve repair, no matter how technically well
it is performed, (1) is not likely to restore “full normal” or
“perfect” subjective sensation or complete functional recov-
ery; (2) some nerve injuries are not repairable, a fact that
cannot be discovered until the injured nerve has been exposed
at the time of secondary surgery; (3) surgical repair may not
improve existing pain levels, especially when there are signs
of central nervous sensitization; (4) recovery of sensory reflexes
is not immediate after nerve repair, rather that gradual recov-
ery is expected during a 6- to 18-month time frame, with crude
senses returning earliest; and (5) a program of sensory reeduca-
tion will need to be followed by the patient after repair surgery,
and return office visits will be required for 1 to 2 years after
surgery to test for signs of neurosensory recovery.
REFERENCES
1. Schwartz LJ: Lingual anesthesia following mandibular odontec-
tomy, J Oral Surg 31:918, 1973.
2. Fielding AF, Raschiele DP, Frazier G: Lingual nerve paresthesia
following third molar surgery: a retrospective clinical study,
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 84(4):345,
1997.
3. Lydiatt DD: Litigation and the lingual nerve, J Oral Maxillofac
Surg 61:197, 2003.
4. Robert RC, Bacchetti P, Pogrel MA: Frequency of trigeminal
nerve injuries following third molar removal, J Oral Maxillofac
Surg 63(6):732, 2005.
5. Alling CC: Dysesthesia of the lingual and inferior alveolar
nerves following third molar surgery, J Oral Maxillofac Surg
44:454, 1986.
6. Gregg JM: Abnormal responses to trigeminal nerve injury, Oral
Maxillofac Surg Clin North Am 4:339, 1992.
7. Gregg JM, Zuniga JR: An outcome analysis of clinical trials of
the surgical treatment of traumatic trigeminal sensory neuropa-
thy, Oral Maxillofac Surg Clin North Am 13(2):377, 2001.
8. Rutner TW, Zaccardi VB, Janal MN: Long-term outcome
assessment for lingual nerve microsurgery, J Oral Maxillofac Surg
63(8)1145-1149, 2005.
9. Lam NP et al.: Patient satisfaction after trigeminal nerve repair,
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 95(5):538,
2003.
10. Pogrel MA: The results of microsurgery of the inferior alveolar
and lingual nerve, J Oral Maxillofac Surg 60(5):485, 2002.
11. Hillerup S: Iatrogenic injury to oral branches of the trigeminal
nerve: records of 449 cases, Clin Oral Invest 11(2):133, 2006.
12. Walter JM, Gregg JM: Analysis of post-surgical neurologic
alteration in the trigeminal nerve, J Oral Surg 37:410, 1979.
13. Ibizuka T, Lindquist C: Sensory disturbance associated with
rigid internal fixation of mandibular fractures, J Oral Maxillofac
Surg 49:1264, 1991.
14. Marchena JM, Padwa BL, Kaban LB: Sensory abnormalities
associated with mandibular fractures: incidence and natural
history, J Oral Maxillofac Surg 56:822, 1998.
15. Susarla SM, Blaeser BF, Magalnick D: Third molar surgery and
associated complications, Oral Maxillofac Surg Clin North Am
15:177, 2003.
280 SECTION II ■ Dentoalveolar Surgery
16. Haug RH et al.: The American Association of Oral and
Maxillofacial Surgeons age-related third molar study, J Oral
Maxillofac Surg 63(8):1106, 2005.
17. Jeries W et al.: Permanent sensory impairment following third
molar surgery: a prospective study, Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 102(4):1, 2006.
18. Bartling R, Freeman K, Kraut RA: The incidence of altered
sensation of the mental nerve after mandibular implant place-
ment, J Oral Maxillofac Surg 57:1408, 1999.
19. Ellies LG: The incidence of altered sensation of the mental
nerve after mandibular implant placement, J Oral Maxillofac
Surg 57:1410, 1999.
20. Gregg JM: Neuropathic complications of mandibular implant
surgery: review and case presentations, Ann Roy Australas Coll
Dent Surg 15:176, 2000.
21. Pogrel MA, Thamby S: Permanent nerve involvement result-
ing from inferior alveolar nerve blocks, J Am Dent Assoc
131:901, 2004.
22. Hillerup S, Jensen R: Nerve injury caused by mandibular block
analgesia, Int J Oral Maxillofac Surg 35(5):437, 2006.
23. Grotz KA et al.: Treatment of injuries of the inferior alveolar
nerve after endodontic procedures, Clin Oral Invest 2(2):73,
1998.
24. Poveda R et al.: Mental nerve paresthesia associated with end-
odontic paste within the mandibular canal: report of a case,
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 102(5):46,
2006.
25. Panula K, Finne K, Oikarinen K: Incidence of complications
and problems related to orthognathic surgery: a review of 655
patients, J Oral Maxillofac Surg 59(10):1128, 2001.
26. Al-Bishri A, Rosenquist J, Sunzel B: On neurosensory distur-
bance after sagittal split osteotomy, J Oral Maxillofac Surg
62(12):1472, 2004.
27. Westermark A, Bystedt H, von Konow L: Inferior alveolar
nerve function after sagittal split osteotomy of the mandible:
correlation with degree of intraoperative nerve encounter and
other variables in 496 operations, Br J Oral Maxillofac Surg
36:492, 1998.
28. Seddon HJ: Three types of nerve injury, Brain 66:237, 1943.
29. Sunderland S: A classification of peripheral nerve injuries pro-
ducing loss of function, Brain 74:491, 1951.
30. Zuniga JR et al.: The accuracy of clinical neurosensory testing
for nerve injury diagnosis, J Oral Maxillofac Surg 56:2,
1998.
31. Jaaskelainen SK, Teerjoke-Oksa T, Forssell H: Neurophysio-
logic and quantitative sensory testing in the diagnosis of tri-
geminal neuropathy and neuropathic pain, Pain 117(3):349,
2005.
32. Terzis J, Faibisoff B, Williams HB: The nerve gap: suture under
tension versus graft, Plast Reconstr Surg 56:166, 1975.
33. Eriksson L et al.: Traumatic changes of the inferior alveolar
nerve and Gasserian ganglion after removal of a mandibular
third molar: report of a case, J Oral Maxillofac Surg 64:1821,
2006.
34. Dubner R, Ren K: Brainstem mechanisms of persistent pain
following injury, J Orofac Pain 18(4):299-305, 2004.
35. Sessle BJ et al.: Properties and plasticity of the primate somato-
sensory and motor cortex related to orofacial sensorimotor
function, Clin Exp Pharmacol Physiol 32(1-2):109, 2005.
36. Pogrel MA, Le H: Etiology of lingual nerve injuries in the third
molar region: a cadaver and histologic study, J Oral Maxillofac
Surg 64:1790-1794, 2006.
37. Gregg JM: Studies of traumatic neuralgias in the maxillofacial
region: surgical pathology and neural mechanisms, J Oral
Maxillofac Surg 48:228, 1990.
38. Rasmussen PV et al.: Symptoms and signs in patients with sus-
pected neuropathic pain, Pain 110:461, 2004.
39. Bruce RA, Frederickson GC, Small GS: Age of patients and
morbidity associated with mandibular third molar surgery, J Am
Dent Assoc 101:240, 1980.
40. Valmaseda-Castellon E, Berini-Aytes L, Gay-Escoda C:
Lingual nerve damage after third molar surgical extraction,
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 90:567,
2000.
41. Mailis A, Wade J: Profile of Caucasian women with possible
genetic predisposition to reflex sympathetic dystrophy: a pilot,
Clin J Pain 10:210, 1994.
42. Devor M, del Canho S, Raber P: Heritability of symptoms in
the neuroma model of neuropathic pain: replication and com-
plementation analysis, Pain 116:294, 2005.
43. Goldberg MH: Frequency of trigeminal nerve injuries following
third molar removal, J Oral Maxillofac Surg 63(12):1783,
2005.
44. Nurmikko TJ, Rasanan A, Hakkinen V: Clinical and neuro-
physiological observations on acute herpes zoster, Clin J Pain
6:284, 1990.
45. Jensen TS, Baron R: Translation of symptoms and signs into
mechanisms in neuropathic pain, Pain 102:1-8, 2003.
46. Diatchenko L et al.: Idiopathic pain disorders-pathways of vul-
nerability, Pain 123:226, 2006.
47. Boureau F, Doubrere JF, Luu M: Study of verbal descriptors in
neuropathic pain, Pain 42:145, 1990.
48. Galer BS, Jensen MP: Development and preliminary validation
of a pain measure specific to neuropathic pain: the neuropathic
pain scale, Neurology 48:332, 1997.
49. Krause SJ, Backonja MM: Development of a neuropathic pain
questionnaire, Clin J Pain 19:306, 2003.
50. Bennett M: The LANSS pain scale: the Leeds assessment of
neuropathic symptoms and signs, Pain 92:147, 2001.
51. Rolke R et al.: Quantitative sensory testing in the German
Research Network on neuropathic pain (DFSN): standardized
protocol and reference values, Pain 123:231, 2006.
52. Merskey H, Bogduk N, editors: Classification of chronic pain:
descriptions of chronic pain syndromes and definitions of pain terms,
ed 2, Seattle, 1994, IASP Press.
53. Robinson PP et al.: Peripheral mechanisms for the initiation of
pain following trigeminal nerve injury, J Orofac Pain 18(4):287,
2004.
54. Rowbotham MC et al.: Lidocaine patch: double-blind con-
trolled study of a new treatment method for postherpetic neu-
ralgia, Pain 65:39, 1996.
55. Mao J, Chen LL: Systemic lidocaine for neuropathic pain relief,
Pain 87:7, 2000.
56. Rawlings CE, Wilkins RH: Treatment of the deafferentation
pain syndromes of the trigeminal system, Adv Pain Res Therap
19:291, 1991.
57. Friedman AH: Treatment of deafferentation pains following
peripheral nerve injury, Adv Pain Res Therap 19:321-330,
1991.
58. Xie Y et al.: Functional changes in dorsal root ganglion cells
after chronic nerve constriction, J Neurophysiol 73:1811,
1995.
59. Woolf CJ, Salter MW: Neuronal plasticity: increasing the gain
in pain, Science 288:1765, 2000.
60. Ikeda R: NMDA receptor-independent synaptic plasticity in
the central amygdala in the rat model of neuropathic pain, Pain
127:161, 2007.
61. Essick GK, Patel S, Trulsson M: Mechanosensory and thermo-
sensory changes across the border of impaired sensitivity to
pinprick after mandibular nerve injury, J Oral Maxillofac Surg
60(11):1250, 2002.
62. Xu M et al.: NMDA receptor-mediated activation of medullary
pro-nociceptive neurons is required for secondary thermal
hyperalgesia, Pain 127:253, 2007.
 CHAPTER 15 •
63. Seo K et al.: Efficacy of steroid treatment for sensory impair-
ment after orthognathic surgery, J Oral Maxillofac Surg 62:1193,
2004.
64. Bartusch SL et al.: Clonazepam for the treatment of lancinating
phantom pain, Clin J Pain 12:59, 1996.
65. Susarla SM et al.: Does early repair of lingual nerve injuries
improve functional sensory recovery? J Oral Maxillofac Surg
65:1070, 2007.
66. Susarla SM et al.: Functional sensory recovery after trigeminal
nerve repairs, J Oral Maxillofac Surg 65:60, 2007.
67. Robinson PP, Loescher AR, Smith KG: A prospective, quan-
titative study on the clinical outcome of lingual nerve repair,
Br J Oral Maxillofac Surg 38(4):255, 2000.
68. Robinson PP, Smith KG: A study on the efficacy of late lingual
nerve repair, Br J Oral Maxillofac Surg 34:96, 1996.
69. Joshi A, Rood JP: External neurolysis of the lingual nerve, Int
J Oral Maxillofac Surg 31:40, 2002.
70. Greenwood M, Corbett IP: Observations on the exploration
and external neurolysis of injured inferior alveolar nerves, Int J
Oral Maxillofac Surg 34(3):252, 2005.
71. Nakamura T: Clinical application of nerve conduits consisting
of a polyglycolic acid (PGA)-collagen composite tube filled
with collagen sponge, Connect Tissue 35:53, 2003.
72. Inada Y et al.: Human peripheral nerve regeneration across the
sensory nerve gap bridged by a polyglycolic acid tube filled with
collagen sponge, J Joint Surg 22:89, 2003.
73. Inada Y et al.: Surgical relief of causalgia with an artificial nerve
guide tube: successful treatment of causalgia (complex regional
pain syndrome type II) by in situ tissue engineering with a
polyglycolic acid-collagen tube, Pain 117:251, 2005.
74. Dodson TB, Kaban LB: Recommendations for management of
trigeminal nerve defects based on a critical appraisal of the
literature, J Oral Maxillofac Surg 55:1380, 1997.
75. Dellon AL, Mackinnon SE, Pestronk A: Implantation of sensory
nerve into muscle. Preliminary clinical and experimental obser-
vations on neuroma formation, Ann Plast Surg 12:30, 1984.
76. Mackinnon SE, Dellon AL (Eds): Internal neurolysis. In Surgery
of the peripheral nerve, New York, 1988, Thieme.
77. Gregg JM: The efficacy of internal microneurolysis for treat-
ment of traumatic trigeminal neuroma-in-continuity lesions.
(Unpublished, 2007).
78. Brammer JP, Epker BN: Anatomic-histologic survey of the sural
nerve: implications for inferior alveolar nerve grafting, J Oral
Maxillofac Surg 46:111, 1988.
79. Eppley BL, Snyders RV: Microanatomic analysis of the trigemi-
nal nerve and potential nerve graft donor sites, J Oral Maxillofac
Surg 49:612, 1991.
80. McCormick SU et al.: Microanatomic analysis of the medial
antebrachial nerve as a potential donor nerve in maxillofacial
grafting, J Oral Maxillofac Surg 52:1022, 1994.
81. Takasaki Y et al.: Reconstruction of the inferior alveolar nerve
by autologous graft: a retrospective study of 20 cases examining
donor nerve length, Bull Tokyo Dent Coll 44(2):29, 2003.
82. Pogrel MA et al.: The relationship of the lingual nerve in the
third molar region. An anatomic study, J Oral Maxillofac Surg
53:1778, 1995.
83. Miloro M, Stoner JA: Subjective outcomes after sural nerve
harvest, J Oral Maxillofac Surg 63(8):1150, 2005.
84. Rath EM: Skeletal muscle autograft for repair of the human
inferior alveolar nerve: a case report, J Oral Maxillofac Surg
60(3):330, 2002.
85. Pogrel MA, Maghen A: The use of autogenous vein grafts
for inferior alveolar and lingual nerve reconstruction, J Oral
Maxillofac Surg 59:985, 2002.
86. Miloro M: The use of autogenous vein grafts for inferior alveo-
lar and lingual nerve reconstruction, J Oral Maxillofac Surg
59:988, 2001.
Treatment of Trigeminal Nerve Injuries 281
87. Pitta MC et al.: Use of Gore-Tex tubing as a conduit for inferior
alveolar and lingual nerve repair: experience with 6 cases,
J Oral Maxillofac Surg 59:493, 2001.
88. Pogrel MA, McDonald AR, Kaban LB: Gore-Tex tubing as a
conduit for repair of lingual and inferior alveolar nerve continu-
ity defects: a preliminary report, J Oral Maxillofac Surg 56:319,
1998.
89. Miloro M: Surgical access for inferior alveolar nerve repair,
J Oral Maxillofac Surg 53:1224, 1995.
90. Epker BN, Gregg JM: Surgical management of maxillary nerve
injuries, Oral Maxillofac Surg Clin North Am 4(2):439, 1992.
91. Gregg JM: Medical management of traumatic neuropathies,
Oral Maxillofac Surg Clin North Am 13:343, 2001.
92. Devers A, Galer BS: Topical lidocaine patch relieves a variety
of neuropathic pain conditions: an open-label study, Clin J Pain
16:205, 2000.
93. Levendoglu F et al.: Gabapentin is a first line drug for the treat-
ment of spinal cord injury, Spine 29:743, 2004.
94. Dworkin RH, Corbin AE, Young JP: Pregabalin for the
treatment of post-herpetic Neuralgia, Neurology 60:1274,
2003.
95. Max MB: Antidepressants as analgesics. In Fields HL,
Liebeskind JC, editors: Progress in pain research and management,
vol 1 Seattle, 1994, IASP Press.
96. Meyer RA, Rath EM: Sensory rehabilitation after trigeminal
nerve injury or nerve repair, Oral Maxillofac Surg Clin North Am
13(2):365, 2001.
97. Phillips C et al.: Sensory retraining after orthognathic surgery:
effect on patients’ perception of altered perception, J Oral
Maxillofac Surg 65:1162, 2007.
98. Florence SL et al.: Sensory enrichment after peripheral nerve
injury restores cortical, not thalamic, receptive field organiza-
tion, Eur J Neurosci 13:1755, 2001.
99. Renton T: Lingual nerve assessment and repair outcomes, Ann
Roy Australas Coll Dent Surg 16:113, 2002.
100. Strauss ER, Ziccardi VB, Janal MN: Outcome assessment of
inferior alveolar nerve microsurgery: a retrospective review,
J Oral Maxillofac Surg 64:1767, 2006.
101. Zuniga JR, Chen N, Phillips CL: Chemosensory and somato-
sensory regeneration after lingual nerve repairs in humans,
J Oral Maxillofac Surg 55:2, 1997.
102. Phillips C et al.: Relationship between patients’ perceptions of
post-surgical sequelae and altered sensations after bilateral sag-
ittal split osteotomy, J Oral Maxillofac Surg 65:579, 2007.
103. Susarla SM et al.: A comparison of patient satisfaction and
objective assessment of neurosensory function after trigeminal
nerve repair, J Oral Maxillofac Surg 63(8):1138, 2005.
104. Smith KG, Robinson PP: An experimental study of three
methods of lingual nerve defect repair, J Oral Maxillofac Surg
53:1052, 1995.
105. Gregg JM: Studies of traumatic neuralgia in the maxillofacial
region: symptom complexes and response to microsurgery,
J Oral Maxillofac Surg 48:135, 1990.
106. LaBanc JP, Gregg JM: Trigeminal nerve injuries: basic prob-
lems, historical perspectives, early successes and remaining
challenges, Oral Maxillofac Surg Clin North Am 4:277, 1992.
107. Strauss ER, Ziccardi VB, Janal MN: Outcome assessment of
inferior alveolar nerve microscopy: a retrospective review,
J Oral Maxillofac Surg 64:1767, 2006.
108. Hillerup S: Neurosensory recovery after microsurgical suture of
lingual nerve lesions, Int J Oral Maxillofac Surg 32:S77, 2003.
109. Hillerup S, Hjorting-Hansen E, Reumert T: Repair of the
lingual nerve after iatrogenic injury: a follow-up study of
return of sensation and taste, J Oral Maxillofac Surg 52:1028,
1994.
110. Scriviani SJ et al.: Taste perception after lingual nerve repair,
J Oral Maxillofac Surg 58(1):3, 2000.
282 SECTION II ■ Dentoalveolar Surgery
111. Dodson TB, Kaban LB: Recommendations for management of
trigeminal defects based on a critical appraisal of the literature,
J Oral Maxillofac Surg 55:1380, 1997.
112. Thurmuller P, Dodson TB, Kaban LB: Nerve injuries associated
with facial trauma. Natural history, management and outcomes
of repair, Oral Maxillofac Surg Clin North Am 13(2):283-293,
2001.
113. Schultze-Mosgau S et al.: Prospective study on post-traumatic
sensory disturbances of the inferior alveolar and infraorbital
nerve in mandibular and midfacial fractures, J Craniomaxillofac
Surg 27:86, 1999.
114. Fogaca WC, Fereirra MC, Dellon AL: Infraorbital nerve injury
associated with zygoma fractures: documentation with neuro-
sensory testing, Plast Reconstr Surg 113(3):834, 2004.
115. Taicher S et al.: Recovery of the infraorbital nerve after zygo-
matic complex fractures: a preliminary study of different treat-
ment methods, Int J Oral Maxillofac Surg 22:339, 1993.
116. Halpern LR, Kaban LB, Dodson TB: Perioperative neurosen-
sory charges associated with treatment of mandibular fractures,
J Oral Maxillofac Surg 62(5):576, 2004.
117. Vriens JPM, Moos KJ: Morbidity of the infraorbital nerve fol-
lowing orbitozygomatic complex fractures, J Craniomaxillofac
Surg 23:363, 1995.
118. Ibizuka T, Lindquist C: Rigid internal fixation of fractures of
the angular region of the mandible: an analysis of features
contributing to different complications, Plast Reconstr Surg
91:265-271, 1993.
119. Harn SD, Durham TM: Incidence of lingual nerve trauma and
postinjection complications in conventional mandibular block
anesthesia, J Am Dent Assoc 121:519, 1990.
120. Stacy GC, Hajjar G: Barbed needle and explicable paresthesias
and trismus after dental regional anaesthesia, Oral Surg Oral
Med Oral Pathol Oral Radiol Endod 77:585, 1994.
121. Rayan GM et al.: Histologic and electrophysiologic changes
following subepineurial hematoma induction in rat sciatic
nerve, Clin Orthop 229:257, 1988.
122. Pogrel MA, Schmidt BL: Trigeminal nerve chemical neuro-
trauma from injectable materials, Oral Maxillofac Surg Clin
North Am 13(2):247, 2001.
123. Haas DA, Lennon D: A 21-year retrospective study of reports
of paresthesia following local anesthetic administration, J Can
Dent Assoc 61:319, 1995.
124. Dower JS: A review of paresthesia in association with admin-
istration of local anesthesia, Dent Today 22:64, 2003.
125. Malamed SF: Nerve injury caused by mandibular block analge-
sia, Int J Oral Maxillofac Surg 35(9):876, 2006.
126. Yagiela JA: Recent developments in local anesthesia and seda-
tion, Compendium 25(9):697, 2004.
127. Smith MH, Lung KE: Nerve injuries after dental injection: a
review of the literature, J Can Dent Assoc 72(6):559, 2006.
128. Kaufman BR et al.: Debilitating chronic pain syndromes after
presumed intraneural injections, Pain 85:283, 2000.
129. Yaffe B, Pri-Chen S, Lin E: Peripheral nerve injection injury:
an experimental pilot study of treatment modalities, J Reconstr
Microsurg 3(1):33, 1986.
130. Sharav Y et al.: The analgesic effect of amitriptyline on facial
pain, Pain 31:199, 1987.
131. Conrad SM: Neurosensory disturbances as a result of chemical
injury to the inferior alveolar nerve, Oral Maxillofac Surg Clin
North Am 13(2):255, 2001.
132. Quinley JF, Riyer RQ, Gores RJ: “Dry socket” after mandibular
odontectomy and use of soluble tetracycline hydrochloride,
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 13:38,
1960.
133. Moore JW, Brekke JH: Foreign body giant cell reaction related
to placement of tetracycline-treated polylactic acid: report of
18 cases, J Oral Maxillofac Surg 43:767, 1985.
134. Leist JC et al.: Experimental topical tetracycline-induced neu-
ritis in the rat, J Oral Maxillofac Surg 53:427, 1995.
135. Stoelinga PJ: Long-term follow-up on keratocysts treated
according to a defined protocol, Int J Oral Maxillofac Surg 30:14,
2001.
136. Loescher AR, Robinson PP: The effect of surgical medicaments
on peripheral nerve function, Brit J Oral Maxillofac Surg 36:327,
1998.
137. Schmidt BL, Pogrel MA: Neurosensory changes after
liquid nitrogen cryotherapy, J Oral Maxillofac Surg 62:1183,
2004.
138. Alkan A et al.: The effects of hemostatic agents on peripheral
nerve function: an experimental study, J Oral Maxillofac Surg
65:630, 2007.
139. Olson RAJ, Roberts DL, Osbon DB: A comparative study of
polylactic acid, Gelfoam, and surgical in healing extraction
sites, Oral Surg Oral Med Oral Pathol 53:441, 1992.
140. Grotz KA et al.: Treatment of injuries of the inferior alveolar
nerve after endodontic procedures, Clin Oral Invest 2(2):73,
1998.
141. Fanibunda K, Whitworth J, Stele J: The management of
thermomechanically compacted gutta percha extrusion in the
inferior dental canal, Br Dent J 184:330, 1998.
142. Ahlaren FK, Johannessen AC, Hellem S: Displaced calcium
hydroxide paste causing inferior alveolar nerve paresthesia:
report of a case, Oral Surg Oral Med Oral Pathol Oral Radiol
Endod 96(6):734, 2003.
143. Yatsuhashi T et al.: Inferior alveolar nerve paresthesia relieved
by microscopic endodontic treatment, Bull Tokyo Dent Coll
44(4):209, 2003.
144. Poveda R et al.: Mental nerve paresthesia associated with end-
odontic paste within the mandibular canal: report of a case,
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 102(5):46,
2006.
145. Scolozzi P, Lombardi T, Jaques B: Successful inferior alveolar
nerve decompression for dysesthesia following endodontic
treatment: report of 4 cases treated by mandibular sagittal oste-
otomy, Oral Surg Oral Med Oral Pathol Oral Radiol Endod
97(5):625, 2004.
146. Phillips C et al.: Qualitative descriptors used by patients fol-
lowing orthognathic surgery to portray altered sensation, J Oral
Maxillofac Surg 64:1751, 2006.
147. Cunningham LL et al.: A comparison of questionnaire
versus monofilament assessment of neurosensory deficit, J Oral
Maxillofac Surg 54:454, 1996.
148. Kallela I et al.: Assessment of material- and technique-related
complications following sagittal split osteotomies stabilized by
biodegradable polylactic screws, Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 99(1):4-10, 2005.
149. Van Sickels JE et al.: Effects of age, amount of advancement,
and genioplasty on neurosensory disturbance after a bilateral
sagittal split osteotomy, J Oral Maxillofac Surg 60(9):1012,
2002.
150. Ylikontiola L, Kinnunen J, Oikarinen K: Factors affecting neu-
rosensory disturbance after mandibular bilateral sagittal split
osteotomy, J Oral Maxillofac Surg 58:1234, 2000.
151. Yamamoto R et al.: Relationship of the mandibular canal
to the lateral cortex of the mandibular ramus as a factor in
the development of neurosensory disturbance after bilateral
sagittal split osteotomy, J Oral Maxillofac Surg 60(5):490,
2002.
152. Levine MH, Goddard AL, Dodson TB: Inferior alveolar nerve
canal position: a clinical and radiographic study, J Oral
Maxillofac Surg 65:470, 2007.
153. Hu J et al.: Changes in the inferior alveolar nerve after man-
dibular lengthening with different rates of distraction, J Oral
Maxillofac Surg 59:1041, 2001.
 CHAPTER 15 •
154. Meyer RA: Microsurgical repair of nerve injuries associated
with dental implants, J Oral Implantol 22(1):42, 1996.
155. Ruskin JD: Inferior alveolar nerve considerations. In Block MS,
Kent JN, editors: Endosseous implants for maxillofacial reconstruc-
tion, Philadelphia, 1995, WB Saunders.
156. Zarb GA, Schmitt A: The longitudinal clinical effectiveness of
osseointegrated dental implants. The Toronto Study. Part III.
Problems and complications encountered, J Prosthet Dent 5:272,
1990.
157. Higuchi KW, Folmer T, Kultje C: Implant survival rates in
partially edentulous patients, J Oral Maxillofac Surg 53:264,
1995.
158. Kiyak HA et al.: The psychological impact of osseointegrated
dental implants, Int J Oral Maxillofac Implants 5:272, 1990.
159. Hirsch JM, Branemark PI: Fixture stability and nerve function
after transposition and lateralization of the inferior alveolar
nerve and fixture installation, Br J Oral Maxillofac Surg 33:276,
1995.
160. Rosenquist B: Implant placement in combination with nerve
repositioning: experiences with the first 100 cases, Int J Oral
Maxillofac Implants 9:522, 1994.
161. Haers PE, Sailer HF: Neurosensory function after lateralization
of the inferior alveolar nerve and simultaneous insertion of
implants, Oral Maxillofac Surg Clin North Am 7:707, 1994.
162. Kan JY et al.: Endosseous implant placement in conjunction
with inferior alveolar nerve transposition: an evaluation of neu-
rosensory disturbance, Int J Oral Maxillofac Implants 12:463,
1997.
163. Chiarot M: Assessment of mental nerve function after inferior
alveolar nerve (IAN) transposition, J Oral Maxillofac Surg
58:40, 2000.
164. Ferrigno N, Laureti M, Fanali S: Inferior alveolar transposition
in conjunction with implant placement, Int J Oral Maxillofac
Implants 20(4):610, 2005.
165. Ziccardi VB, Assael LA: Mechanisms of trigeminal nerve inju-
ries. Microneurosurgery of the trigeminal nerve, Atlas Oral
Maxillofac Surg Clin North Am 9(2):1, 2001.
166. Hegedus F, Diecidue RJ: Trigeminal nerve injuries after man-
dibular implant placement-practical knowledge for clinicians,
Int J Oral Maxillofac Implants 21(1):111, 2006.
167. Gaggl A, Schultes G, Karcher H: Navigational precision
of drilling tools preventing damage to the mandibular canal,
J Craniomaxillofac Surg 29(5):271, 2001.
168. Caissie R et al.: Iatrogenic paresthesia in the third division of
the trigeminal nerve: 12 years of clinical experience, J Can Dent
Assoc 71(3):185, 2005.
169. Kipp DP, Goldstein BH, Weiss Jr WW: Dysesthesia after
mandibular third molar surgery. A retrospective study and
analysis of 1,377 surgical procedures, J Am Dent Assoc 100:185,
1980.
170. Valmaseda-Castellon E, Berini-Aytes L, Gay-Escoda C: Inferior
alveolar nerve damage after lower third molar surgical extrac-
tion: a prospective study of 1117 surgical extractions, Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 92(4):377, 2001.
171. Ziccardi VB, Zuniga JR: Nerve injuries after third molar
removal, Oral Maxillofac Surg Clin North Am 19:105, 2007.
172. Goldberg MH: Frequency of trigeminal nerve injuries following
third molar removal, J Oral Maxillofac Surg 63(12):1783,
2005.
173. Black CG: Sensory impairment following lower third molar
surgery: a prospective study in New Zealand, N Z Dent J 93:68,
1997.
174. Peterson LJ et al.: Contemporary oral and maxillofacial surgery,
St Louis, 1993, Mosby.
175. Hill CM et al.: Nerve morbidity following wisdom tooth
removal under local and general anesthesia, Br J Oral Maxillofac
Surg 39:423, 2001.
Treatment of Trigeminal Nerve Injuries 283
176. Carmichael FA, McGowan DA: Incidence of nerve damage
following third molar removal. West of Scotland Oral Surgery
Research Group study, Br J Oral Maxillofac Surg 30:78, 1992.
177. Kiesselback JE, Chamberlain JG: Clinical and anatomic obser-
vations on the relationship of the lingual nerve to the man-
dibular third molar region, J Oral Maxillofac Surg 42:565,
1984.
178. Miloro M et al.: Assessment of the lingual nerve in the third
molar region using magnetic resonance imaging, J Oral Maxil-
lofac Surg 55:134, 1997.
179. Renton T, McGurk M: Evaluation of factors predictive of
lingual nerve injury in third molar surgery, Br J Oral Maxillofac
Surg 39:423, 2001.
180. Rood JP, Shehab BA: The radiological prediction of inferior
alveolar nerve injury during third molar surgery, Br J Oral
Maxillofac Surg 28(1):20, 1990.
181. Blaeser BF et al.: Panoramic radiographic risk factors for inferior
alveolar nerve injury after third molar extractions, J Oral
Maxillofac Surg 61(4):417, 2003.
182. Sedaghatfar M, August MA, Dodson TB: Panoramic radio-
graphic findings as predictors of inferior alveolar nerve exposure
following third molar extraction, J Oral Maxillofac Surg 63(1):3,
2005.
183. Monaco G et al.: Reliability of panoramic radiography in evalu-
ating the topographic relationship between the mandibular
canal and impacted third molars, J Am Dent Assoc 135:312,
2004.
184. Nakagawa Y et al.: Preoperative application of limited cone
beam computerized tomography as an assessment tool before
minor oral surgery, Int J Oral Maxillofac Surg 31(3):322,
2002.
185. Pawelzik J et al.: A comparison of conventional computed
tomography images in the preoperative assessment of impacted
mandibular third molars, J Oral Maxillofac Surg 60(9):979,
2002.
186. Bataineh AB: Sensory nerve impairment following mandibular
third molar surgery, J Oral Maxillofac Surg 59:1012, 2001.
187. Brann CR, Brickley MR, Shepherd JP: Factors influencing
nerve damage during lower third molar surgery, Br Dent J
186:514, 1999.
188. Hill CM et al.: Nerve morbidity following wisdom tooth
removal under local and general anesthesia, Br J Oral Maxillofac
Surg 39:423, 2001.
189. Rood JP: Permanent damage to inferior alveolar and lingual
nerves during removal of impacted mandibular third molars:
comparison of two methods of bone removal, Br Dent J
172(3):108, 1992.
190. Pogrel MA, Goldman KE: Lingual flap retraction for third
molar removal, J Oral Maxillofac Surg 62(9):1125-1113,
2004.
191. Pichler JW, Beirne OR: Lingual flap retraction and prevention
of lingual nerve damage associated with third molar surgery: a
systematic review of the literature, Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 91:395, 2001.
192. Gargallo-Albiol J, Buenechea-Imaz R, Gay-Escoda C: Lingual
nerve protection during surgical removal of lower third molars.
A prospective randomized study, Int J Oral Maxillofac Surg
29:268, 2000.
193. Chossegros C et al.: Is lingual nerve protection necessary for
lower third molar germectomy? A prospective study of 300
procedures, Int J Oral Maxillofac Surg 31(6):620, 2002.
194. Renton T et al.: A randomized controlled clinical trial to
compare the incidence of injury to the inferior alveolar nerve
as a result of coronectomy and removal of mandibular third
molars, Br J Oral Maxillofac Surg 43(1):7, 2005.
195. Pogrel MA: Partial odontectomy, Oral Maxillofac Surg Clin
North Am 9:85-91, 2007.
284 SECTION II ■ Dentoalveolar Surgery
196. Pogrel MA, Lee JS, Muff DF: Coronectomy: a technique to
protect the inferior alveolar nerve, J Oral Maxillofac Surg
62:1447, 2004.
197. Assael LA: Coronectomy: a time to ponder or a time to act?
J Oral Maxillofac Surg 62:1445, 2004.
198. Garcia-Garcia A: Is coronectomy really preferable to extrac-
tion? Br J Oral Maxillofac Surg 44:75, 2006.
199. Yachouh J et al.: Lingual nerve injury during removal of
the lower third molar: importance of early intervention, Rev
Stomatol Chir Maxillofac 107(5):393, 2006.
200. Hupp JR: Legal implications of third molar removal, Oral Max-
illofac Surg Clin North Am 19:129, 2007.
201. Estabrooks L: Litigation and the lingual nerve, J Oral Maxillofac
Surg 61:200, 2003.
202. Venta I, Lindquist C, Ylipaavalniemi P: Malpractice claims for
permanent nerve injuries related to third molar removals, Acta
Odont Scand 56:193, 1998.
203. Chaushu G et al.: Medicolegal aspects of altered sensation fol-
lowing implant placement in the mandible, Int J Oral Maxillofac
Implants 17:413, 2002.
204. Assael LA: The nerve under the microscope, J Oral Maxillofac
Surg 60:483, 2002.
205. Orr DL, Curtis WJ: Obtaining written informed consent for the
administration of local anesthetic in dentistry, J Am Dent Assoc
136:1568, 2005.
206. Lazare A: Apology in medical practice: an emerging clinical
skill, JAMA 296(11):1401-1404, 2006.
 S E C T I O N III •
ORAL AND MAXILLOFACIAL SURGERY—
OFFICE MANAGEMENT
Franklin T. Walker • David E. Frost
■ THE OMS PRACTICE IS A
SURGICAL BUSINESS
Oral and maxillofacial surgeons are trained to competently
deliver health care and typically receive a dearth of business
training as they matriculate through dental school, residency,
and other postdoctoral training. The vast majority of oral and
maxillofacial surgery (OMS) practices are multimillion dollar
businesses. To succeed in today’s practice environment, high-
quality OMS care must exist in juxtaposition with a high level
of business acumen. These two principles are not mutually
exclusive and must be present in every facet of the OMS
practice: in the office, at the emergency department, in the
hospital or surgical center, or dealing with real estate ventures.
The practice environment has changed drastically over the
past several decades. Health care is one of the most regulated
of business environments, which necessitates a fully engaged
surgeon on the “business side” of the practice. In this chapter,
we will introduce the most important subjects that an oral and
maxillofacial surgeon needs to have basic knowledge of to be
successful:
1. Legal entities
2. Practice advisors
3. Evaluating the practice
4. Organizational styles
5. Human resources
6. Financial management
7. Legal documents
8. Risk management
9. Information technology
JOINING OR STARTING A PRACTICE
A surgeon leaving residency, a military obligation, or an aca-
demic position typically begins a new practice from the ground
floor up or enters an existing practice. There are benefits to
both; however, establishing a new practice can be a daunting
proposition because of the necessity to establish the opera-
tional and the business aspects simultaneously. There are,
however, a number of common aspects to both scenarios: the
Practice Management
CHAPTER 16
selection of business advisors, acquiring licensure and certifi-
cation necessary to practice, learning how to manage time and
money, and planning for the future.
Establishing a solo surgical practice begins with an analysis
of the general geographic area of interest. Specific details of
the area that influence the decision process include hospital
support location, population and demographics, socioeconom-
ics, referral practices to existing oral and maxillofacial surgeon
ratio, patient to surgeon ratio, and real estate availability.
There are a number of firms that can do a very detailed analy-
sis and comparisons. Some of the information that they can
provide include: population and traffic flow analysis, income
statistics, general dentist referral patterns, building and over-
head projections, and long-range economic forecasts for spe-
cific geographic locations.
■ LEGAL ENTITIES
Practices may take the form of several legal entities. Each
of these present various advantages and disadvantages. Tax
implications and personal liability are two of the most impor-
tant differences between each of these. Possible practice struc-
tures include sole proprietorship (SP), general partnership
(GP), limited partnership (LP), limited liability company
(LLC), C corporations, or S corporations.
Unincorporated entities include SP, GP, limited liability
partnership (LLP), and LLCs. For the oral and maxillofacial
surgeon that does not plan to work in a group practice, the
SP is a very convenient way to organize a practice. The
surgeon-owner signs all contracts and collects revenues in his
or her name. The surgeon-owner is also liable for all obliga-
tions of the practice, and personal assets could be attached if
there is a settlement against the practice.
Each of the unincorporated partnerships generally have the
following characteristics: There are two or more persons or
entities in a business for profit, and any income or loss flows
through to the partners for income tax purposes. The partner-
ships are therefore not taxable entities.
The GP is also a convenient entity to establish when there
are a limited number of surgeons in the group. Typically,
285
286 SECTION III ■ Practice Management

TABLE 16-1 Comparison of Legal Entities

Issue Corporation (C Corp and S Corp)
Definition Corporation for profit organized
under the state corporations act S
corporation designation under federal
Internal Revenue Code
Designation of owners Shareholders
Liability of owners in organization Shareholders generally not personally
liable for debts of corporation, but
liable for own acts
Management Directors and officers
Persons in position to bind organization Officers
Governing documents Articles of incorporation, bylaws and
shareholders agreement
Type and number of owners No limits on type or number in C
corp. S corp. limited to 75 persons.
Ownership classes Different stock classes allowed in C
corp. S corp. is limited to one class
of stock.
Tax treatment As a C corp. unless S corp. election
is selected for income tax purposes
Partnership
An association of two or more
persons to carry on, as co-
owners, a business for profit
Partners
Partners are jointly liable for the
obligations of the partnership
Partners
Partners
Partnership agreement
No limit on type. Must have at
least two partners.
Any financial arrangement
between partners allowed
Almost always as a partnership
for federal tax purposes
Limited Liability Company (LLC)
Hybrid. An LLC formed under state
LLC statute.
Members
Members and managers are not
liable for any debt, obligation, or
liability of the LLC
Members or managers
Members or managers
Articles of organization, operating
agreement
No limits, although individual
managers and members must be 18.
Can have as few as one member in
many states.
Any financial arrangement allowed. In
absence of agreement, interests are
proportional based upon level of
contribution/capital account balance.
Generally, as a partnership for federal
tax purposes

partners share equally in the profit and loss of the partnership,
or, by proxy, alternative methods for revenue and expense
sharing can be established. The personal assets of all partners
are at potential legal risk, and all can be responsible for obliga-
tions incurred by other partners.
An LLP typically consists of at least one general partner
and one limited partner. The general partner(s) can be liable
for all obligations of the partnership, whereas the limited
partner receives some shielding from debts and obligations of
the partnership.
An LLC has characteristics of both a partnership and a
corporation, and ownership may consist of multiple persons.
Members of an LLC are not responsible for the debts and
obligations of the LLC. Earnings pass through to the owners
for tax purposes.
C and S corporations provide shielding from debt and other
obligations for the shareholders. A C corporation is managed
through a board of directors selected by the shareholders. The
board of directors elects officers who are responsible for exe-
cuting the policies. The C corporation is subject to double
taxation because taxable income is subject to corporate income
tax earnings, and funds distributed to the shareholders are
individually taxed. S corporation earnings, on the other hand,
flow through to the shareholders for federal and state income
purposes (Table 16-1).
■ PRACTICE ADVISORS
No individual can possess all of the comprehensive knowledge
base that is necessary to establish and maintain a successful
practice. A surgeon should surround himself or herself with a
team of professional advisors, which include accountants,
attorneys, bankers, insurance brokers, retirement plan admin-
istrators, other practitioners, an office manager, and in larger
practices, a practice administrator.
ACCOUNTANT
An accountant who has achieved the licensure of a certified
public accountant (CPA), generally has a college degree or
completed significant course work in accounting, has success-
fully completed a comprehensive examination, and practiced
with an accounting firm for 2 years. Individual states may have
specific licensure requirements. Typically a CPA can provide
services including bookkeeping, creating a financial statement
with analysis, and tax return preparation. A person or firm
that has previous health care experience can give invaluable
advice regarding every financial decision. The CPA should be
proactive communicating to the management team with
advice regarding decreasing overhead, improving cash flow,
and increasing revenue. It is also important that they are
aware of changes in the tax codes germane to the practice.
ATTORNEY
The attorney or firm selected by the practice should have a
comprehensive working knowledge of health care law, includ-
ing malpractice, contract and corporate law, and tax and
estate planning.
The attorney drafts legal documents pertaining to practice
entity formation and other ownership entities, such as real
estate or life insurance policies. Employment and buy-sell
agreements are of particular importance to a group OMS prac-
tice to facilitate a smooth transition from the associate posi-
tion to ownership and eventually to retirement. The quality
 CHAPTER 16 • Oral and Maxillofacial Surgery—Office Management
of these agreements becomes particularly important should
a dispute arise between partners, associates, or heirs. For the
surgeon contemplating joining an existing practice, he or she
should hire their own attorney to review and make recom-
mendations regarding any contracts.
BANKER
A lender is selected before the inception of the OMS practice
to establish guidelines for the financing of capital equipment,
computers, or the purchase of office space. Discussion should
include the possibility of a cash flow shortfall. Many banks
offer special service lines that are tailored to health care orga-
nizations and surgical practices.
INSURANCE BROKER OR REPRESENTATIVE
The insurance professional is an integral part of the profes-
sional organization’s advisor team. This person can assist with
decisions concerning buy-sell agreements for both the business
and property and the insurance funding that may be necessary
to protect these investments. Other important areas include
key person insurance, retirement planning, group insurance,
and personal insurance for the surgeon-owner.
Selection of an insurance representative is based on educa-
tion, health care experience, and their access to a variety of
insurance options. Various professional designations include
chartered life underwriter, chartered financial consultant, cer-
tified financial planner, Master of Business Administration,
and others.
RETIREMENT PLAN ADMINISTRATOR
The professional life of an OMS surgeon can easily extend to
30 years or more, which enables the individual to potentially
accumulate substantial retirement assets. A retirement plan
administrator should provide two services: plan administra-
tion and investment advice. Plan administration includes
drafting of documents, accounting for participants’ account
balances, and filing annual tax returns. As firms are inter-
viewed, several factors should be taken into consideration:
fees for administering the plan, timely reporting, and invest-
ment selection. Options for the calculation of service fees
include a percentage of the total assets, a per participant fee
and/or charges to carry out the testing of the plan. The pro-
spective administrator should provide cost projections and be
prepared to discuss each facet. Once a plan administrator is
selected, a 3- to 5-year timeline is established to achieve the
investment objectives of the practice. There are multiple plan
options, including, but not limited to 401(k)s, self-employed
pension plans (SEPs), Individual Retirement Accounts
(IRAs), pension plans, and defined benefit plans. The type of
investments selected for the retirement plan(s) will be driven
by the risk tolerance and investment goals of the practice and
its shareholders.
PRACTICE ADMINISTRATOR
The practice administrator is an integral part of the manage-
ment team and has the responsibility for ensuring that the
287
practice functions in a seamless manner. If the employee
charged with the direct oversight of the practice business and
nonclinical areas does not have the core competencies, educa-
tion, or experience required to manage a practice, ultimately
a myriad of difficulties can develop. There are several organi-
zations that candidates can be gleaned from: American College
of Health Care Executives (ACHE), American College
of Medical Practice Executives (ACMPE), and the Medical
Group Management Association (MGMA). Competent
administrators will be well versed in finance, accounting,
human resources, compliance/risk management, governance,
information systems, and strategic planning.
MARKETING AND PUBLIC RELATIONS
An OMS surgical practice is referral driven; therefore, the
importance of marketing and public relations cannot be
understated. Communication on multiple levels with the
referral base is the cornerstone to a marketing strategy. Because
each practice is unique, it is impossible to list or diagram a
marketing scheme that fits all situations. Every level of the
practice from reception, surgical nurses, and administrators to
the surgeon needs to take an active role in developing and
implementing a strategic plan. The surgeon owners of the
practice ultimately are responsible for the content and review
process, but the daily functions can be delegated to the admin-
istrative staff.
■ PRACTICE EVALUATION
Custom designed surveys that are completed by patients and
referrals are of great value to evaluate the health of a practice.
Surveys may be distributed in many venues: over lunch, in the
office, via mail, or the Internet. Samples of both a referral and
patient survey are noted in Exhibit 2 and 3. In these, responses
are graded from 0 to 5, 0 being nonapplicable, 1 indicating
they strongly disagree, and 5 that they strongly agree.
The questions in the referral survey (Table 16-2) are proba-
tive in nature as to the underlying relationship that exists
between the OMS practice and the referral practice. Analysis
of responses may necessitate additional query of the respon-
dent if there are negative results.
The questions contained in the patient survey (Table 16-3)
are weighted toward the administrative aspect of the OMS
practice. Despite the fact that the patient was referred for a
clinical procedure, they are typically in a better position to
judge their experience in the administrative arena than their
clinical experience. Questions 24 to 27 refer to an OMS prac-
tices’ website. Interactive computer-based contact with the
patient and referral sources are being used increasingly to
obtain practice information and register for appointments. A
well-designed website is paramount to an overall efficient
practice.
NEW PROCEDURES
Communication with referral offices and patients regarding
the scope of procedures and services that a practice offers is
an excellent way to highlight new innovations or techniques.
288 SECTION III ■ Practice Management

TABLE 16-2 Referral Survey

The physicians and staff at X, Y, and Z strive to deliver the highest quality service to our referral offices.
Satisfaction surveys give constructive criticism that helps to identify ways to better serve our referral offices (you) and continuously improve our service. Your
feedback will help us see how our office policies, employees, and attention to detail can be improved. We welcome your compliments, comments, and
criticisms. Please feel free to complete this survey anonymously.
Please take a few minutes to complete this form and return it in the enclosed self-addressed, stamped envelope.
Thank you!
Name: _________________________________
E-mail address: _________________________________
Years practicing: _________________________________
Years practicing in area: _________________________________
Years referring to OMSA: _________________________________
0 Not applicable 3 No opinion
1 Strongly disagree 4 Somewhat agree
2 Somewhat disagree 5 Strongly agree
For each question below, please indicate your agreement with the statement in question by circling the number to the right that best fits your
opinion. Use the scale above to match your opinion. Please feel free to add any comments in the space provided.
SCHEDULING
QUESTION SCALE
1. Making a referral to OMSA was easy. 0 1 2 3 4 5
Comment:
2. My patients are able to make a consultation appointment within a reasonable time frame. 0 1 2 3 4 5
Comment:
3. My patients are seen for surgery in a timely fashion. 0 1 2 3 4 5
Comment:
4. Emergency patients are seen in a timely manner. 0 1 2 3 4 5
Comment:
5. OMSA’s policy of seeing patients for a consultation before scheduling surgery is made clear. 0 1 2 3 4 5
Comment:
COMMUNICATION
QUESTION SCALE
6. When my office called OMSA, the person answering the phone was courteous. 0 1 2 3 4 5
Comment:
7. I receive appropriate correspondence after my patients are seen at OMSA (i.e., letters, surgery date notice, 0 1 2 3 4 5
pathology reports, etc.).
Comment:
8. Letters from the physicians regarding patient treatment plans are helpful. 0 1 2 3 4 5
Comment:
9. I would like more correspondence. 0 1 2 3 4 5
Comment:
10. I have been able to find one of your physicians when I wanted to talk to him or her. 0 1 2 3 4 5
Comment:
11. Radiographs were returned to my office in a timely manner. 0 1 2 3 4 5
Comment:

This may be accomplished through direct mailing, newslet-
ters, waiting room audiovisual equipment, brochures, web-
sites, and media presentations.
■ ORGANIZATIONAL STYLES
SOLO PRACTICE
The primary advantage that a solo practitioner possesses is the
ability to set his or her own schedule and make all decisions.
A solo practitioner normally has an independent personality,
has a high energy level, and is not hesitant to simultaneously
tackle the administrative and clinical challenges.
Overhead and staffing issues are far less complex in an SP
situation.
Unless the surgeon hires outside expertise, it will be neces-
sary to manage multiple tasks that in group practice may be
shared, such as computer repair, insurance coding, human
resources, or accounts payable management.
 CHAPTER 16 • Oral and Maxillofacial Surgery—Office Management 289

TABLE 16-3 Patient Survey

Note: Questions are set up so that the respondent will indicate agreement on a 0-5 scale (0 N/A, 1 Strongly disagree, 5 Strongly agree).
1. I came to this practice for: (Check ALL that apply)
[ ] Third molar surgery (wisdom teeth)
[ ] Tooth extraction surgery
[ ] Corrective jaw surgery (orthognathic)
[ ] TMJ/Facial pain management
[ ] Facial aesthetic surgery
[ ] Infection treatment
[ ] Dental implants
[ ] Nonmalignant pathologic condition
[ ] Cancer screening
[ ] Tooth exposure bracket
[ ] Orthodontic anchorage screws or plates
SCHEDULING OF CONSULTATION
2. Making an appointment with X, Y, or Z was easy.
3. I was able to schedule an appointment within a reasonable time frame.
4. I was able to be seen at the office location I requested.
5. X’s, Y’s, or Z’s policy of seeing patients for a consultation appointment before scheduling surgery was made clear.
6. When I scheduled my consultation, I was appropriately informed of what I needed to bring (e.g., x-ray, referral slip, insurance information) to my
appointment.
7. When I scheduled my consultation, I was appropriately informed of what I would need to pay.
8. Directions to the office were clearly explained and easy to follow.
CONSULTATION
9. When I arrived at OMSA for my appointment, my interaction with the reception desk personnel was pleasant and professional.
10. The overall atmosphere in the office was inviting and organized.
11. I was seen by the physician in a reasonable amount of time after my arrival.
12. I found the nursing staff to be courteous and knowledgeable.
13. My physician’s explanation of the treatment plan was clear and thorough.
14. Preoperative instructions led me to be well prepared for the surgical experience.
CHECKOUT/PAYMENT POLICIES
15. My wait to check out was reasonable.
16. My interaction with the staff upon checkout was excellent.
17. I was scheduled for surgery within an acceptable time frame.
18. The explanation of my financial obligation and payment schedule was clearly explained to me so that I understood it.
SURGERY
19. After surgery, my recovery room experience was excellent.
20. The written postoperative instructions were clearly written and easy to understand.
21. The verbal postoperative explanations by the recovery nurse were very helpful.
22. If I needed to call the physician after office hours, my call was returned promptly.
WEBSITE
23. Have you visited our website? (Yes/No) If no, please skip to the next section.
What was your main motivation to visit the site? (More information on procedure / Learn about our physicians / Request a consultation / Download patient
forms / Learn about our payment policies / Office hours / Phone number / Locations and directions / Other [please list]) (Indicate agreement below)
24. It was easy to find the information I needed.
25. My overall impression of the website was that it was helpful and informative.
COMMUNICATION
26. When I arrived at OMSA, the people I interacted with were polite, understanding, and helpful.
27. Office policies were explained to me so that I understood them.
28. When I called OMSA, the person answering the phone was well informed and helpful.
29. If I called about my account, my concerns were handled with prompt, courteous attention.
30. If I called the Ask-a-Nurse line, I was helped in a timely manner.
MISCELLANEOUS
31. Courtesy filing of my insurance was processed in an accurate and timely manner.
32. If “limited” weekend office hours were available, I would definitely select weekend appointments.
OVERALL SATISFACTION
33. Based on my experience, this practice will be recommended to my family and friends with high regard.
290 SECTION III ■ Practice Management

GROUP PRACTICE ■ HUMAN RESOURCES

Four possible advantages inherent in a group practice include Oversight of human resources is a difficult and unpredictable
sharing after-hour call coverage, the potential leverage during aspect of the practice and carries with it the risk of potential
managed care contracting and purchasing, and having col- legal ramifications from employees or government agencies.
leagues to discuss various clinical issues, such as diagnosis and Problems can be minimized with detailed documentation
treatment planning. and clear communication as to each employee’s job descrip-
As a group practice grows, it is possible to have a division of tion, expectations, and areas of responsibility and lines of
labor between the surgeons. Surgeons tend to gravitate toward supervision.
a specific area of interest in the management arenas, such as
marketing, staff education, or the financial aspects of practice POLICY MANUAL
management. Regardless of personal preferences, each member Office policy manuals are an excellent format to communicate
of a group practice must have an overall knowledge of the with staff members. Regular performance reviews also allow
clinical and administrative aspects of the practice. the staff member and physician to communicate, document
A managing partner is the initial liaison with the practice expectations and achievements, and work toward a team
administrator or office manager. A managing partner should concept.
be a shareholder, be elected by the other shareholders, and be The manual includes job performance and expectations
compensated for his or her additional responsibilities. A senior for the employee not only in the office setting but also offsite
partner with practice experience is ideal for this position. As marketing during business-related functions, continuing edu-
a group grows, it becomes increasingly difficult for a managing cation, hospital-based surgery, or any venue where profes-
partner to provide the comprehensive supervision necessary. sional decorum or discussion of the practice may take place
Larger groups can form committees with one or more of the (Box 16-1).
surgeons as chairperson. Templates are available from many sources that can be
Finance—retirement plan administration, review of finan- modified to reflect the individual practice. The contents of
cial statements and decisions regarding capital investments the manual should be reviewed regularly by the shareholders,
and buy-sell arrangements. practice administrator, human resource manager (in larger
Human resources—continuing education, compensation, practices), and the corporate attorney.
and benefits.
Quality assurance and risk management—review of morbidity
and mortality, infection rates, chart review, and site
accreditation. BOX 16-1 Policy Manual
Compliance—radiology regulatory issues, Occupational Mission and Vision Statement
Safety and Health Administration (OSHA), and Health Qualifications for Employment
Insurance Portability and Accountability Act (HIPAA). Education
Probationary periods
Information systems—hardware and software, imaging, and CPR/ACLS/PALS/ATLS
electronic health records (EHR). Other certifications
Define full- and part-time employees
ASSOCIATE OR SALARIED POSITION Pay period
Office hours
Following the completion of a long process through under- Pro Bono surgical benefits
graduate education, dental school, and residency, the indi- Dress Code
Clinical dress code
vidual is often faced with a significant debt. For this reason, a Administrative dress code
salaried associate without any additional financial responsi- Leave Policy
bilities may be attractive. An existing practice can offer a Maternity
Sick leave
potential associate a trial period of 1 to 2 years. The time Leave with and without pay
period selected allows both the associate and the owners an Insurance Plans
opportunity to evaluate each other’s working style, personal- Health insurance
Disability insurance
ity, and personal goals. For the surgeon nearing the end of a Life insurance
career, an associate position may enable them to step away Cafeteria Plan
from some of the responsibilities typically tied to practice and Flex spending accounts
Child care
partnership. Holidays
Advantages of an associate position include a guaranteed Continuing Education
salary and benefits with few administrative responsibilities Retirement Plan Participation Requirements
Office Financial Policy
and a limited debt exposure. Disadvantages include limited Infection Control
involvement in practice decisions, no incentive for increased Sterilization
income with increased production, and no control of the Immunization requirements
Performance Evaluations
benefits received.
 CHAPTER 16 • Oral and Maxillofacial Surgery—Office Management 291

TABLE 16-4 Pay Ranges in a Group Practice

BENEFIT PLANS
Administrative Grade 85% Midpoint 115%
The type of benefits offered to employees will vary between
Administrative director A 16.57 19.49 22.41
practices, based on size, geographic region, cost, and the pref-
AP/AR manager B 14.57 17.14 19.71
erence of the shareholders. A well-conceived benefit package
Insurance manager C 11.26 13.25 15.24
is extremely important to long-term employee retention. The
Front office supervisor D 12.89 15.16 17.43
cost of hiring and training a new employee far exceeds the
Business projects coordinator E 10.63 12.5 14.38
costs of a well-conceived benefit package that retains staff. A
Patient coordinator F 12.31 14.48 16.65
cafeteria plan benefit package may be less expensive in certain
Receptionists (I-III) G 11.76 13.84 15.92
circumstances. A cafeteria plan specifies a specific dollar
Administrative assistant H 8.50 10 11.50
amount that an employee may spend on a menu of benefits.
Clinical
Some examples of employee choices include health, life,
Implant coordinator I 14.73 17.33 19.93
disability or dental insurance, child care and educational
Clinical supervisor J 15.48 18.21 20.94
expenses, uniforms expenses, etc. An employee may also elect
OR surgical assistant K 15.02 17.67 20.32
to take some of the allocated monies as salary in lieu of
Surgical assistant L 13.74 16.17 18.60
benefit(s) or put additional pretax salary toward benefits.
Chief recovery nurse (RN) M 15.77 18.55 21.33
There are increased costs to a practice if an employee receives
Recovery nurse (RN/LPN) N 13.68 16.09 18.50
salary in lieu of a benefit as a result of FICA matching
requirements. Sterilization tech O 10.55 12.41 14.27
Transport P 10.82 12.73 14.64
ORGANIZATION OF LABOR AND COMPENSATION
The labor pool in a practice is split into two general divisions:
administrative and clinical. In a solo practice, employees may behavior and those that require modification. Comments need
be tasked with both administrative and clinical duties. The to be specific with an agreed-upon plan and timeline for cor-
job titles will reflect their areas of influence and responsibility. rection, if there is to be any behavior modification.
Administrative duties include scheduling, check in and check
out, accounts receivable and payable, medical records, and JOB DESCRIPTIONS
insurance. Clinical duties include surgical assisting, recovery Each position within the practice should have a job descrip-
room, radiology, implant coordination, supply management, tion (Tables 16-6 and 16-7), which clearly and concisely
housekeeping, and drug compliance. states minimal education and experience required, reporting
Pay ranges for particular job descriptions can be established responsibilities, duties, and physical and computer knowledge
using data from the American Association of Oral & Maxil- expected. After the employee reviews their performance
lofacial Surgeons (AAOMS), ACHE, MGMA, and other assessment, there may be questions that need to be addressed.
practices within a similar geographic region. The example in When consensus is established, the employee and reviewer
(Table 16-4) is a group practice with multiple surgeons and signs and dates the document.
offices. Job titles and descriptions are established and, using
market data, a midpoint salary range is identified. A thirty ■ FINANCIAL MANAGEMENT
percentage point range is used, with 85% of the midpoint for Unfortunately, dental school and OMS residency training
the low end and 115% of the midpoint to establish the top of curriculum has little to no financial management content.
the salary range. Salaries noted in this example are hourly for This places the new practitioner in a position that they must
full-time employees. At the discretion of the practice, part- rely on other professionals to provide advice and guidance in
time employees may have a higher base salary but fewer the early stages.
benefits.
BUDGETING
PERFORMANCE EVALUATIONS A budget is an essential part of the planning process for the
Employees should be evaluated on a regular basis. Most prac- practice and includes 1-, 3-, and 5-year projections. By com-
tices will find that an annual review is sufficient, unless there paring projected production, net revenue, and expenses against
is disciplinary action at some other time in the year. This actual numbers, a variance can be derived. At any point in
process should include the shareholders, the practice admin- time over the fiscal year, it is possible to make decisions and
istrator, applicable managers, and the employee. Performance adjustments based on performance compared with projections.
evaluation documents can take many forms, but should, at Table 16-8 is an example of a monthly budget variance report.
some point, become specifically modified to take into account The budgeted amounts for production, revenues, and costs are
goals for the particular OMS practice. Note that the example listed in column A. The actual amounts are listed in column
above (Table 16-5) has an area for technical excellence and B. The dollar variance amounts, budget minus (−) actual, are
four categories where a supervisor may grade the employee. listed in column C. Comments lists the reason(s) for the
There is also opportunity for comments regarding both good associate variances. Budget variances should be reviewed
292 SECTION III ■ Practice Management

TABLE 16-5 Performance Evaluation

Drs. X, Y, and Z OMS Practice
Performance Evaluation
Technical Excellence:
䊐 䊐
Unsatisfactory
Demonstrated job knowledge and
understanding is not sufficient to meet
the quality, safety, and technical goals
and standards established for the
position. Decisions are rarely sound or
practical.
Specific Examples and/or Comments:
Includes the technical skills and expertise that enable an employee to make sound technical judgments, to
provide or support quality care, and to otherwise successfully perform the position.
䊐 䊐
Needs Improvement Achieves Expectations Exceeds Expectations
Demonstrated job knowledge Demonstrated job Demonstrated job knowledge and
and understanding is not knowledge and understanding is exceptional. Employee’s
consistently sufficient to meet understanding is sufficient decisions are consistently sound, practical, and
the quality, safety, and to meet the quality, safety, based on thorough analysis.
technical goals and standards and technical goals and
established for the position. standards established for
Decisions are not consistently the position. Employee’s
sound or practical. decisions are consistently
sound and practical.

Customer Service Orientation: Includes teamwork, attitude, behavior, interpersonal skills, and problem-solving skills that enable an employee to
respond to internal and external customer needs and expectations in a positive manner.

䊐 䊐
Unsatisfactory
Poor service orientation. Does little to
contribute to the satisfaction,
productivity and development of others,
including new employees and/or
students. Unresponsive to employee or
supervisor suggestions for service
improvement.
Specific Examples and/or Comments:
Needs Improvement
Positive, but inconsistent
service orientation. Occasionally
contributes to the satisfaction,
productivity and development of
others, including new
employees and/or students. Not
consistently responsive to
employee or supervisor
suggestions for service
improvement.
䊐 䊐
Achieves Expectations
Positive service orientation.
Readily contributes to the
satisfaction, productivity
and development of others,
including new employees
and/or students.
Responsive to employee
and supervisor suggestions
for service improvement.
Exceeds Expectations
Exceptional service orientation. Makes
extraordinary effort to contribute to the
satisfaction, productivity and development of
others, including new employees and/or
students. Initiates and implements suggestions
for service improvement.

Adaptability:
䊐 䊐
Unsatisfactory
Demonstrates very little independent
thinking in addressing problems.
Resists accepting new tasks and
reacts negatively to change. Rarely
contributes to departmental needs.
May require corrective action.
Specific Examples and/or Comments:
Includes initiative and flexibility to accept and master changes in function, equipment, technology and/or
departmental needs, and the dependability to adhere to attendance and other OMSA policies.
䊐 䊐
Needs Improvement Achieves Expectations Exceeds Expectations
Demonstrates some Consistently demonstrates Consistently demonstrates initiative and
independence in addressing independence in independence in addressing problems.
problems, accepting new tasks addressing problems, Assumes formal/informal leadership role in
and adjusting to changing work accepting new tasks and adapting to new tasks or changing work
conditions—but is inconsistent. adjusting to changing work conditions. Demonstrates exceptional initiative
Occasionally initiates conditions. Consistently in seeking opportunities to contribute to
opportunities to contribute to initiates opportunities to departmental needs.
departmental needs. May contribute to departmental
require corrective action. needs.
 CHAPTER 16 • Oral and Maxillofacial Surgery—Office Management 293

TABLE 16-6 Job Description: Administrative Director

Drs. X,Y, and Z OMS Practice
Title: Administrative Director
Job Category: Administrative
Job Division: Director
Reports to: CEO
Location: Durham (primary), Chapel Hill & Sanford (as needed)
Work Schedule: Full time
Schedule Code: 1
Minimum Education Required: High school diploma/GED
Minimum Experience Required: Previous supervisory experience
Preferred Qualifications: Continued education (technical school, community college, university)
Previous administrative experience
Previous dental/medical office experience
Previous data processing/computer entry experience
Duties—Primary: Hire and train front office staff in all offices
Coordinate front office staffing
Verify weekly payroll/transmission to accountant
Maintain human resources records
Coordinate physician’s schedules for all offices
Transmit on-call physician information to hospital/ER call service
Fill in for front office staff in all areas when necessary
Duties—Secondary: Assist front office staff with troubleshooting of patient accounts
Assist front office staff with patient scheduling
Assist in AR reporting
Required Physical/Mental Skills: Friendly attitude toward patients and co-workers
Appropriate office attire
Accurate record-keeping skills
Accurate data entry and computer skills
Continued learning of changing scheduling adjustments
Continued learning of insurance requirements
Continued education in management skills
Continued education in human resource administration
Ability to administer continuous CPR
FLSA: Nonexempt
Pay Grade: A
Last Updated: 2/22/2007
Note: This job description is not intended to be all-inclusive. Employee may be expected to perform other related duties to meet the ongoing needs of the
organization.
I have read the Administrative Director job description and understand the functions and objectives of the position at this practice.
Employee’s Signature Date

monthly to determine reasons for revenue and cost differences

from the projected amounts. REVENUE CYCLE AND FINANCIAL POLICY
There are nine steps in the revenue cycle as the patient enters
ACCOUNTING the practice and continues through to the completion of
OMS practice accounting involves two areas: the revenue and treatment:
the expense. Revenue is driven by the production of the physi- 1. Scheduling
cians within the practice, which in turn is based on patient 2. Registration
visits, surgical procedures, and managed care contracts. A 3. Financial counseling
typical OMS patient cycle is outlined as follows: 4. Capture of charges
1. Patient referral 5. Coding
2. Patient consultation, data gathering, diagnostic appoint- 6. Claims processing
ments, and treatment planning 7. Denial management
3. Patient surgical or treatment appointments 8. Account resolution
4. Patient postoperative appointments 9. Payment posting
294 SECTION III ■ Practice Management

TABLE 16-7 Job Description: Clinical Supervisor

Drs. X, Y, and Z OMS Practice
Title: Clinical Supervisor
Job Category: Clinical
Job Division: Supervisor
Reports to: 1. CEO
2. Administrative Director
Location: Durham or Chapel Hill
Work Schedule: Full time
Schedule Code: 1
Minimum Education Required: High school diploma/GED
OMAAP Certification
Minimum Experience Required: Previous experience as an OMS surgical assistant
Preferred Qualifications: Certified Dental Assistant
Previous experience with purchasing OMS supplies
Previous supervisory experience
Duties—Primary: All surgical assistant duties
Coordinate administration of surgical assistants
Coordinate HR information for clinical staff with Administrative Director
Train clinical staff
Purchase surgical supplies
Duties—Secondary: All recovery room duties
All scrub tech duties
Required Physical/Mental Skills: Friendly attitude toward patients and co-workers
Appropriate office attire
Punctuality and attendance at work
Accurate record-keeping skills
Continued education in OMS surgical assisting
Continued education in management skills
Ability to administer continuous CPR
FLSA: Nonexempt
Pay Grade: J
Last Updated: 2/22/2007
Note: This job description is not intended to be all-inclusive. Employee may be expected to perform other related duties to meet the ongoing needs of the
organization.
I have read the Clinical Supervisor job description and understand the functions and objectives of the position at this practice.
Employee’s Signature Date

TABLE 16-8 A Monthly Budget Variance Report

A B C Comments
Budget Actual Variance
Feb Feb
Production 307352 462613 155261 Increased physician days
Total Revenue 304278 380926 76648
Refunds 18257 20919 2662
Net Revenue 286022 401448 115426
Operating Expense 191635 219756 28121 Increased retirement funding
Fixed OH 35000 28611 −6389
Office Expense 20022 13535 −6487 Less computer costs
Surgical Supplies 24312 20156 −4156
Travel Expense 6006 14592 8586 Increased meeting expense
Taxes/Licenses 2288 0 −2288
Miscellaneous 5148 6540 1392
Total Expense 284411 303190 18779
Net Operating Revenue 1611 56817 55206
 CHAPTER 16 • Oral and Maxillofacial Surgery—Office Management 295

Revenue cycle performance is one of the most critical ele- TABLE 16-9 Balance Sheet
ments in the practice’s financial status and must be monitored
ASSETS
regularly. In many instances, it may be 60 to 90 days until all Current Assets
of the fees are collected. Each step in the revenue cycle is
Cash 47561
dependent on the next for timely reimbursement. Practices
A/R OMSNIC Stock 1914
typically fall into two categories: fee for service and those that
A/R Eastowne LLC 51108
participate with managed care plans. Practices that are fee for
Total Current Assets 100583
service are able to set their own financial policy. This could
Property and Equipment
include the collection of a portion or all of the surgical fees
Furniture and Fixtures 440044
at the time of service, leaving any unpaid portion to be billed
Dental Equipment 540122
to the patient. A fee-for-service practice is able to generate
Professional Library 4969
considerable cash flow on the front end of the revenue cycle.
Computer Software 66803
A practice that participates in a managed care plan will typi-
Less Accumulated Depreciation −980800
cally collect the appropriate co-payment at the time of service,
Net Property and Equipment 71138
file the insurance claim, and wait for reimbursements. If the
Total Assets 171721
claim is not filed accurately and needs to be refiled, there are
LIABILITIES
added days until the funds are collected.
Current Liabilities
FINANCIAL POLICY 401(k) Plan Payable 10500
Payroll Taxes Payable 12768
The practice’s financial policy describes expectations for
Current Long-Term Debt 28600
patient and third-party payment and includes fees, a timeline
Total Current Liabilities 51868
for expected payment, interest charges for delay of payment,
Long-Term Liabilities
collection costs, allowable discounts, and any relationship
Long-Term Note Shareholders 58909
with third-party payers. When a patient is initially scheduled,
Long-Term Debt 146400
fees are quoted for the consultation, data gathering, diagnostic
Total Long-Term Liabilities 205309
records, and treatment planning aspects. After the consulta-
Total Liabilities 257177
tion is completed, fees and the financial obligations for the
STOCKHOLDER’S EQUITY
treatment are discussed with the patient. An agreement is Retained Earnings −22499
signed by the patient acknowledging their understanding, Treasury Stock −62957
which then forms the basis of a contractual relationship. The Total Stockholder’s Equity −85456
structure of the policy and the manner in which it is presented Total Liabilities and Stockholder’s Equity 171721
forms one of the most important impressions that patients and
families form of any practice.
The financial arrangements may vary if the treatment is
provided on the same day as the surgery. The overall goal in
all policy objectives is to minimize the time that accounts are assets and liabilities at one point in time and consists of three
unpaid and to maximize the practice’s cash flow. categories: assets, liabilities, and owner’s equity. Assets include
The following examples illustrate the financial effect with cash, equipment, office furnishings, accounts receivable, com-
two different practice philosophies. In both scenarios, the fee puters, and other tangible items. Liabilities include the finan-
for service is $1200. In practice A, the patient is required to cial obligations of the practice: notes, leases, and accounts
pay one third of the fee at the time of treatment. This is fol- payable to vendors and for tax obligations. The excess of assets
lowed by a second one third payment within 30 days and the minus liabilities equals the owner’s equity in the practice.
balance within 60 days. Practice B requires half of the payment There must be a balance in the equation: assets = liabilities +
at the time of surgery and the balance within 60 days. stockholder’s equity.
By collecting $400 at the time of treatment, practice A has The P&L statement (Table 16-10) is a summary of reve-
$800 of its fee at risk, whereas Practice B has only $600 at nues and expenses for a certain time period. A statement
risk. Practice A therefore has 16.6% more money at risk for should be generated monthly and include an overall summa-
noncollection. The risks for noncollection decrease with a tion for the fiscal year.
higher percentage of insurance coverage. Local trends within
the medical and dental community regarding payment for FINANCIAL STATEMENT TREND ANALYSIS
services may need to be taken into account. A useful financial tool is a trend analysis of the P&L state-
ment, which includes revenue production. The following
FINANCIAL STATEMENTS P&L statement represents a multiple office practice with six
There are two components to surgical practice financial state- providers. It has been modified to include a line for total pro-
ments: a balance sheet and a profit and loss statement (P&L). duction and a year-versus-preceding year comparison, using a
The balance sheet (Table 16-9) is a listing of the practice’s dollar and a percentage change.
296 SECTION III ■ Practice Management

TABLE 16-10 Profit and Loss Statement

2006 2005 $ Change % Change % of NR
PRODUCTION 386153 368417 17736 0.05
REVENUES
Office A 194112 219132 −25020 −0.11
Office B 142362 119744 22618 0.19
Office C 60307 39828 20479 0.51
Other Income 500 0
Less Refunds −29862 −28044 −1818 0.06
Net Revenue 367419 350660 16759 0.05
OPERATING EXPENSES
Staff Salaries 104408 74432 29976 0.40
Physician Salary 98434 127133 −28699 −0.23
Retirement 5667 15481 −9814 −0.63
Medical Reimbursement 0 0 0 0.00
Health & Life Ins 16674 12988 3686 0.28
Disability Ins 3742 2664 1078 0.40
Mileage Re 439 636 −197 −0.31
Typist 5865 5200 665 0.13
Payroll Tax 8476 6779 1697 0.25
Uniforms 2195 0 2195 0.00
Subtotal 245900 245313 587 0.00 0.67
FIXED OVERHEAD
Office Rent 27060 21520 5540 0.26
Office Utilities 2162 1745 417 0.24
Cleaning & Maintenance 1454 1257 197 0.16
Equip Rental 10682 926 9756 10.54
General Insurance 3536 1554 1982 0.56
Malpractice Insurance 0 0 0 0.00
Cell phone 105 142 −37 −0.26
Telephone 3391 3046 345 0.11
Subtotal 48390 30190 18200 0.60 0.13
OFFICE EXPENSES
Advertising 1457 2524 −1067 −0.42
Business Gifts 0 0 0 0.00
Collection Expense 1096 1010 86 0.09
Bank Service Charges 3175 3087 88 0.03
Dues & Publications 12470 11559 911 0.08
Grounds Maintenance 1094 807 287 0.36
Accounting 1696 946 750 0.79
Legal 2080 0 2080 0.00
Library Upkeep 939 1250 −311 −0.25
Computer Maintenance 146 1000 −854 −0.85
Office Supplies 3804 1563 2241 1.43
Pagers 231 113 118 1.04
Postage 246 441 −195 −0.44
Repairs & Maintenance 476 1162 −686 −0.59
Stationery & Printing 3111 1427 1684 1.18
Subtotal 32021 26889 5132 0.19 0.09
 CHAPTER 16 • Oral and Maxillofacial Surgery—Office Management 297

TABLE 16-10 Profit and Loss Statement—cont’d

Surgical Supplies 2006 2005 $ Change % Change % of NR
Drugs & Medications 1881 91 1790 0.95
Film Developing 0 0 0 0.00
Laundry 0 0 0 0.00
Lab Expenses 0 3510 −3510 −1.00
Dental & Surgical Supplies 30544 20720 9824 0.47
Subtotal 32425 24321 8104 0.33 0.09
TRAVEL CME EXPENSE
Airfare 1366 1497 −131 −0.09
Taxi/Rental Car/Parking 446 422 24 0.06
Medical Education −516 1445 −1961 −1.36
Business Meals 1479 888 591 0.67
Hotels/Lodging 7504 2603 4901 1.88
Tour Packages 4680 1435 3245 1.00
Travel Advances 347 210 137 0.65
Subtotal 15306 8500 6806 0.80 0.04
TAXES & LICENSES
Licenses & Permits 1769 390 1379 0.28
Income Tax expense 0 0 0 0.00
Taxes: Property 0 1345 −1345 −1.00
Taxes: Real Estate 0 880 −880 −1.00
Taxes: Sales 0 0 0 0.00
Subtotal 1769 2615 −846 -0.32 0.00
MISCELLANEOUS
General Depreciation 4805 4805 0 0.00
Contributions 0 25 −25 −1.00
Interest Expense 1127 527 600 1.14
Christmas Party 0 0 0 0.00
Professional Consultants 0 0 0 0.00
Nondeductible Expenses 0 0 0 0.00
Casual labor 0 0 0 0.00
Bad Debts 0 0 0 0.00
Alarm Monitoring 325 0 325 1.00
Alarm Maint/Repair 0 0 0 0.00
Profit Sharing Admin 1631 1455 176 0.11
Flex Plan Admin Fees 81 0 81 1.00
Miscellaneous Unclassified 0 0 0 0.00
Subtotal 7969 6812 1157 0.17 0.022
Total Operating Expense 383780 344643 39137 0.11
Profit/Loss −16361 6018 −22379 1.45
Operating Margin −0.045 0.017 −0.062 1.39

FINANCIAL REPORTING
Through trend analysis, a practice is able to identify changes
in costs over time: month to month and year to year. A posi-
tive variance indicates a lowering of costs. Although costs
typically rise over time, it is the rate of change that is most
relevant. If revenues do not keep pace with costs, then profit-
ability decreases.
Ratio analysis of the financial statements provides an
ongoing assessment of the financial health of a practice. Com-
monly used ratios include gross collection ratio, net collection
ratio, overhead ratio, and accounts receivable turnover.
Gross Collection Ratio
Cross collection ratio = cash collections/gross charges
The gross collection ratio is a measure of payment for services
rendered over a specific time. It is affected by the practice’s
fee schedule, the patient financial policy, the prevalence of
managed care plans and payer mix, and the manner in which
the revenues are collected. If gross charges for a month are
$600,000 and the cash collections are $480,000, then the
gross collection ratio is 80%. The 20% not collected typically
would result in contractual adjustments required by the
298 SECTION III ■ Practice Management

TABLE 16-11 Equal Share Model

Dr. X Dr. Y Dr. Z Total
Gross charges $745,000 $600,000 $540,000 $1,885,000
Collection percentage ×0.80 ×0.80 ×0.80 ×0.80
Cash collections $596,000 $480,000 $432,000 $1,508,000
Percent of total 40 32 28 100
EQUAL SHARE DISTRIBUTION COMPENSATION FORMULA
Collections allocated $502,667 $502,667 $502,667 $1,508,001
(−) Overhead costs (50%) $251,333 $251,333 $251,333 $754,000
Compensation $251,333 $251,333 $251,333 $754,000
Compensation as % of collections 42% 52% 58%
PRODUCTION-BASED COMPENSATION FORMULA
Collections by surgeon $596,000 $480,000 $432,000 $1,508,000
(−) Overhead costs (50%) $298,000 $240,000 $216,000 $754,000
Compensation $297,000 $240,000 $216,000 $754,000
Compensation as % of collections 50% 50% 50% 50%

managed care contracts under force with the practice. For
example, if a practice has a contract with a payer that states
that the payer will reimburse 80% of the usual and customary
charges, then there will be a 20% contractual adjustment.
Net Collection Ratio
Net collection ratio = cash collections/net charges
The net collection ratio measures collections after allowing
for managed care contractual write-offs. It reflects the effec-
tiveness of the collection process in place.
Overhead Ratio
Overhead ratio = overhead expense/cash collections
The overhead ratio demonstrates the percentage of income
that currently is used to operate the practice. Physician’s com-
pensation and benefits are normally not included in the over-
head costs.
Accounts Receivable Turnover
Accounts receivable turnover =
accounts receivable/monthly production
The accounts receivable turnover ratio indicates how long
monthly production typically spends in accounts receivable
and will vary depending upon payer mix, structure of managed
care contracts, patient financial policy, and effectiveness of
the collection process.
Financial reporting is normally done monthly.
COMPENSATION PLANS
Compensation plans assume a variety of forms and complex-
ity. In a solo practice, a surgeon is compensated the net of
revenues minus all expenses. In a multiple-surgeon practice,
the calculation of compensation may take the form of equal
shares, a production-based formula, or a hybrid of both.
Designing a fair compensation plan takes into account differ-
ences in practice style, production, and possibly other duties
beyond treating the patients. As the size of a group increases,
the possibility of disproportionate production also increases.
The basic formula for physician compensation, whether in
solo or group practice, is:
Net revenue − overhead costs (fixed, variable, and direct) =
surgeon compensation
Defining Terms of Formula
Practice net revenue is total revenues (after contractual
adjustments) minus any refunds that are due to patients or
insurance companies for overpayment. Fixed costs are expenses
that stay flat over a period of time, such as office rents. Vari-
able costs increase or decrease, such as surgical supplies. Direct
costs are attributed to expenses by surgeons, such as travel and
continuing education.
EQUAL SHARE MODEL
In an equal share model, the surgeon compensation is split
equally among the shareholders. Table 16-11 illustrates how
each surgeon receives identical compensation, despite differ-
ent production levels. An equal share compensation model
works well when providers have a similar range of production
and do similar surgical procedures.
PRODUCTION-BASED MODEL
In a production-based model, compensation is based upon the
individual surgeon’s collections and is useful if there are varied
production levels. A potential disadvantage exists if there is
competition for patient referrals within the same group.
HYBRID OR BASE PLUS BONUS MODEL
A base plus bonus model achieves a middle ground between
the equal shares and production model(s). A base salary is
established, which is not affected by production. It may be
necessary to adjust the base from time to time to ensure that
 CHAPTER 16 • Oral and Maxillofacial Surgery—Office Management 299

TABLE 16-12 Hybrid or Base Plus Bonus Model

Dr. X Dr. Y Dr. Z Total
Gross charges $62,500 $58,400 $56,100 $177,000
Amount exceeding B/E $12,500 $8,400 $6,100 $27,000
Collection ratio 0.90 0.90 0.90 0.90
Cash collections $56,250 $52,560 $50,490 $159,300
Percent of total gross charges 35% 33% 32% 100%
Overhead (50%) $26,550 $26,550 $26,550 $79,300
Base salary $20,000 $20,000 $20,000 $60,000
Amount available for bonus $20,000
Bonus $7,000 $6,600 $6,400 $20,000

it is below the break-even point (B/E). In Table 16-12, the
calculated B/E point is $50,000 in total monthly gross charges,
and the amount that each surgeon exceeds the base is bonus
collections. A 50% overhead is illustrated in this example,
which is allocated equally, and the predetermined base salary
is $20,000 per month. The collection percentage for the prac-
tice month is 90% of gross charges. The overhead costs and
the base salary are subtracted from the collected amount,
which leaves $20,000 for bonuses.
Distribution of the bonus is based upon his or her produc-
tion percentage of gross charges.
Compensation plans are not a governance tool, but a
mechanism to equitably distribute the net revenue of the
practice to the surgeons. Annual or semiannual reviews allow
for adjustments. Modifiers to compensation can be added if
there are additional duties that the individual surgeon carries
out.
■ LEGAL DOCUMENTS
Basic legal document requirements of an OMS practice include
articles of incorporation and/or operating agreement, employ-
ment agreements, buy-sell agreements, lease agreements, and
third-party payer contracts. The number and complexity will
vary greatly depending upon the legal structure of the practice,
local and state requirements, and advice from attorneys and
other professionals.
ARTICLES OF INCORPORATION/OPERATING
AGREEMENT
The operating agreement specifies and formalizes how the
entity shall run, whether a C or S corporation, LLC, or GP,
and includes formation, election of officers, ownership, how
reporting should take place, meetings, and dissolution.
EMPLOYMENT AGREEMENT
Employment agreements describe the terms of employment
for shareholders in the practice, associate physicians, and
other key employees. These agreements should define the
capacity in which the employee serves, compensation, bene-
fits, termination, covenant not to compete, and future owner-
ship. Table 16-13 is an example of a physician employment
agreement, but should not be construed as all inclusive. Varia-
tions will depend on the will and intent of the shareholders
(given legal constraints) to provide an equitable work envi-
ronment for those employed under these agreements.
BUY-SELL AGREEMENTS
Buy-sell agreements are the legal documents that cover a
change in practice ownership and include provisions for sur-
geons entering and leaving the practice. Ownership should be
considered a mutually agreeable arrangement between the
surgeons and not a right or obligation.
Whether being bought out of or buying into a practice, the
method of valuing the practice must be clearly spelled out.
Practice valuation is typically based on several factors: hard
assets, accounts receivable, and goodwill. Hard assets include
equipment, such as computers, radiology equipment, surgical
chairs, and other office furnishings. Accounts receivable
includes monies owed the practice from patients and payers
and should be discounted to the net collection rate of the
practice. If the accounts receivable is $600,000 and the net
collection rate is 95%, then the valuation of accounts receiv-
able would be $570,000. Goodwill is often the most difficult
asset to determine and will vary considerably in different geo-
graphic and socioeconomic situations. Using a professional
firm experienced in practice valuation can be a valuable
resource.
Practice valuation of a five-shareholder OMS practice:
Hard assets $450,000
Accounts receivable $570,000
Goodwill $620,000
Total practice value $1,640,000/5 shareholders
Per share value $328,000
In a multiple-physician practice, the ideal scenario would
be equal valuation of a buy in and a buyout. Variables in this
formula revolve around the length of payment in or out and
interest or other fees. In the previous example, a surgeon
buying into the practice would pay a total of $328,000 over 5
years ($65,600 annually or $5,666 monthly). In the case of a
surgeon being bought out, the practice could reimburse the
partner over an extended time period so that the cash flow is
not adversely affected. Table 16-14 is an outline of a sample
buy-sell agreement. Because tax laws are constantly changing,
the ramifications of the practice’s buy-sell agreements should
300 SECTION III ■ Practice Management

TABLE 16-13 Surgeon Employment Agreement Outline

I. Duration of the Contract
A. Length of the contract
1. Option: annual with automatic renewal
B. Effective date of the contract
II. Conditions Under Which Contract Can Be Terminated
A. Voluntary termination by employee or employer with thirty (30) days’ written notice
B. Death of employee
C. Suspension, revocation, or cancellation of employee’s right to practice medicine or dentistry in the state of (state)
D. Employee loses privileges to any hospital at which the practice regularly maintains admission privileges
E. Employee fails or refuses to follow reasonable policies or directives established by the practice
F. Employee commits acts amounting to gross negligence or willful misconduct to the detriment of the practice or its patients
G. Employee is convicted of a crime involving moral turpitude, including fraud, theft, or embezzlement
H. Employee breaches terms of the employment contract
I. Employee becomes and remains disabled in excess of three (3) consecutive months
III. Compensation
A. Amount of annual salary
B. Incentive bonus, calculated as follows: (formula)
C. Determine amount and duration surgeon will be paid during a period of disability
IV. Benefits
A. Health insurance
B. Retirement plan contribution
C. Malpractice insurance and tail-end premium
D. Dues, books, and periodicals
E. Licenses
F. CME expenses
1. Annual allowance of $ (dollar amount)
G. Entertainment
H. Automobile
I. Relocation
J. Vacation leave
K. Sick leave
L. Life and disability insurance
M. Cellular phone
N. Pager
O. Other
V. Outside Income
A. Decide on the type of outside income the surgeon can retain and the type of outside income earned by the surgeon that the practice will be entitled to
retain.
B. At the same time as (A), discuss the surgeon’s restrictions on outside employment.
VI. Surgeon’s Duties
A. Required work hours
B. Required on-call schedule
C. Discuss any restrictions on the acceptance of new patients by the surgeon.
D. Discuss any provision if the surgeon is called to jury duty or other duty, such as military reserves.
VII. Termination Compensation
A. Determine how much the surgeon will be paid if employment is terminated.
VIII. Opportunity to Buy into Practice Ownership
A. How long after joining the practice?
B. What exactly will the physician be allowed to buy into?
1. Accounts receivable
2. Hard assets of the practice
3. Goodwill
C. How will the assets be valued?
1. By independent appraiser
2. By fixed formula
D. If applicable, how will accounts receivable be valued?
E. How will fixed assets be valued?
F. How will the buy-in price be paid for?
IX. Reasonableness of Covenant Not to Compete
What is the duration of noncompletion?
What is the geographic area of noncompetition?
What are the prospective penalties and/or compensatory damages?
Is there a buyout clause?
Is the covenant too restrictive?
Tinsley R: The practice management handbook, New York, 2002, Aspen.
 CHAPTER 16 •
TABLE 16-14 Buy-Sell Agreement Checklist
• Buyout events:
Death
Disability
Retirement
Voluntary and involuntary termination
• Agreement specifies details of buyout in the event of a disability.
• Agreement specifies any age restrictions for retirement (withdrawal before age 62 is voluntary and carries tax implications).
• Specify notification requirements for voluntary withdrawal.
• In the case of a voluntary withdrawal, agreement specifies whether there will be penalties to the buyout price if the owner forms a competing practice,
joins a competing practice, or violates the employment contract.
• Vote requirements to admit a new surgeon into the practice.
• Periodic review of buyout calculations and methodology of payments.
• Qualifications of firm used for any appraisals.
• Routine review of tax consequences for the practice and surgeons for buy in and buyout.
• The buyout amount has been calculated for each owner using the current formula in the agreement.
• Periodic shareholders review of all contracts.
Tinsley R: The practice management handbook, New York, 2002, Aspen.
be regularly reviewed by the accountant, attorney, and
shareholders.
If a solo practitioner is selling his or her practice, the
process of purchasing shares may be different than in a group
situation. The selling surgeon must agree upon a price with
the prospective buying surgeon. The buyer can work in the
seller’s practice for a specified period of time, which generates
revenues that an agreed-upon portion can be used toward the
purchase. During this time, the purchasing surgeon also has
an opportunity to gain vast knowledge regarding the overall
operation and administration of the business.
LEASE AGREEMENTS
The practice and/or shareholders may own or lease the office
space they occupy. There are a multitude of possible owner-
ship entities, including a sole ownership, LLC ownership,
leasing from outside sources, or shared arrangements with
other professional organizations. The decision is based on tax
implications, geographic limitations, and other legal obliga-
tions. A contract is required, which has parameters including
liability, duration of the agreement, shared responsibilities,
and the financial obligations between the parties. Lease docu-
ments include rental rate per square foot, liability, duration of
lease, leasehold improvements, and responsible party for utili-
ties, repairs, and maintenance.
MANAGED CARE CONTRACTING
In many areas of the country, there are companies that have
employees enrolled in capitation insurance plans. Because of
the large potential patient pool, it becomes a financial neces-
sity for the OMS practice to consider participating in these
plans. The ability for the practice to competently negotiate
with third-party payers is a key factor in their financial success.
Box 16-2 outlines the steps of a typical third-party payer
contractual negotiation. The terms of reimbursement and
the contractual language must be scrutinized carefully. If the
surgeon is not familiar with these negotiations, then a consul-
tant should be involved. Third-party payer contracts may also
Oral and Maxillofacial Surgery—Office Management 301
spell out terms for: patient scheduling, emergency call, profes-
sional liability, assignment of court costs in case of a lawsuit,
all factors that may weigh heavily on the overall operations
of the practice.
■ RISK MANAGEMENT
Risk management encompasses both the clinical and admin-
istrative aspects of the practice. Federal laws and guidelines
will dictate many of the practices’ protocols, whereas share-
holder prerogatives guide others. Risk management in an
OMS practice includes the following areas: informed consent,
quality assurance, treatment protocols, collection protocols,
OSHA and HIPAA compliance, and insurance coverage.
The AAOMS provides information and continuing educa-
tion opportunities on the topic of risk management. OMS
National Insurance Company (OMSNIC) is OMS surgeon
owned and provides professional liability insurance for OMS
providers, and they have regular seminars and online formats
for their clients.
INFORMED CONSENT
The informed consent process begins with the first contact
that the surgeon makes with the patient. All discussions and
decisions must be documented in writing in the clinic note
and then ultimately on a consent form specifically designed
for the process. Some procedures will require a more lengthy
and detailed educational process before obtaining a signed
consent form. This process can take the form of printed mate-
rials or brochures, audiovisual presentations, or one-on-one
discussion with the surgeon and/or designated staff members.
It is important that the patient and family have been given
adequate opportunity to ask questions regarding their treat-
ment plan, and that all alternatives have been presented. The
age at which a patient can legally give their consent is gener-
ally 18 years. Exceptions may exist when a patient is emanci-
pated from their parental control or if they are married earlier
than 18 years of age. It is advisable that every practice verify
with their attorney what their state laws are. In the event that
302 SECTION III ■ Practice Management
Managed Care Contract
BOX 16-2
Negotiation Checklist
Steps for Managed Care Contract Negotiation/Renegotiation
• Obtain copy of payer’s existing contract.
• Obtain payer’s existing reimbursement schedule for the related contract.
• Assess antitrust concerns; consult legal counsel if necessary.
• If reimbursement schedule is not based on RBRVS, then compare with current
Medicare rates and determine percent of Medicare being reimbursed.
• Obtain CPT frequency report.
• Draft contracting questionnaire and submit to client for completion. (Purpose:
Determine and assess practice leverage position with payer.)
• Obtain contact information (phone number, physical address, e-mail address) for
the provider representative and the manager for the provider representative that
handles contract issues for practice. Also, obtain same information for the execu-
tive director.
• Develop contracting strategy.
• Decide most favorable way to initially contact the payer (e.g. letter, meeting,
telephone, e-mail).
• Contact payer and make contract proposal. Negotiate!
• Maintain strict follow-up schedule.
• Obtain payer’s response to the proposal.
• Review and analyze the payer’s response and decide whether to accept or offer
a counterproposal.
Acceptance
• If decision is made to accept, submit to physician for review and acceptance.
• If the surgeon accepts the terms, notify payer and document.
• Obtain written contract change and execute.
• Make certain future reimbursement agrees with new contracted rates.
Counterproposal
• If the decision is a counterproposal, adjust counterproposal appropriately (Coun-
terproposal may be our original proposal). Submit to payer.
• Maintain strict follow-up schedule.
• If necessary, communicate with payer contact’s superiors.
• Obtain payer’s final response to counterproposal.
• Review and analyze payer’s response and decide whether to accept or reject.
Discuss proposal with surgeon.
• If the surgeon accepts, notify payer and document.
• Obtain written contract change and execute.
• Make certain future reimbursement agrees with new contracted rates.
• If the surgeon rejects, decide whether or not to terminate payer contract.
• Analyze potential financial impact as a result of termination.
• If the surgeon decides not to terminate, negotiation ends.
• If the surgeon decides to terminate, assess antitrust issues. Confer with legal
counsel if necessary.
• Have the surgeon submit termination notice to payer.
• Recontact payer and determine if they are willing to reconsider their position.
• Assist the surgeon with patient notification.
Tinsley R: The practice management handbook, New York, 2002, Aspen.
the patient is incapacitated, it is necessary to carry out the
entire presurgical discussion with the power of attorney and
get their signature. Obtaining a signed consent form does not
eliminate the possibility of legal action but having good
patient rapport, adequate discussion, and a well-documented
patient record prevents many possible future problems.
QUALITY ASSURANCE
Much like a hospital or surgical center requires certification
and documentation of quality assurance, it is incumbent upon
every OMS practice to be vigilant regarding every aspect of
patient care provided in their facility. Periodic chart reviews
can identify deficiencies that would otherwise go unnoticed.
Patient complaints should be assessed, and an action plan
established to prevent repeating a problem. If there have been
any staff injuries or complaints, they need to be documented
along with any remedial action taken. Treatment protocols
are helpful when there are complex procedures anticipated.
This protocol, which may be as simple as the route and type
of drug used for subacute bacterial endocarditis prophylaxis or
as complex as the work-up for an orthognathic or implant
surgery, provides a road map for the treating team to follow.
COLLECTION PROTOCOL
Patient financial policy and the associated counseling is the
initial component of the collection protocol. As discussed in
the revenue cycle section of this chapter, the practices’ deci-
sion regarding what to collect at the initial visit (in a fee-for-
service practice) is important in determining what will be “at
risk.” In practices that primarily participate with third-party
payers, the decision is far less critical. The contract will deter-
mine the co-payment and subsequent reimbursement. The
office policy needs to include a plan to manage delinquent
payments. There are vendors that can externally act as col-
lection agencies for the practice. There are state and federal
guidelines pursuant to the collection of delinquent accounts.
OSHA COMPLIANCE
The Occupational Safety and Health Act (1973) was estab-
lished to prevent work-related injuries, illnesses, and deaths
by issuing and enforcing standards for workplace safety and
health. In an OMS practice, the standards for employee safety
include immunization requirements, guidelines for the steril-
ization of instruments and cleaning of operatories, needle stick
management, fire safety, handling of hazardous materials
(material and safety data sheets), working with blood-borne
pathogens, and universal precautions. An OSHA officer for
the practice should be designated and preferably should be a
physician. The OSHA officer is responsible for all documenta-
tion, including the initial and annual training of all personnel.
In addition, there are specific OSHA posting requirements
that vary somewhat in each state. There are a number of
sources that can be used to assist in the initial design of the
office policy, including the American Dental Association and
the AAOMS.
HIPAA COMPLIANCE
The Health Insurance Portability and Accountability Act
(1996) protect health insurance coverage for workers when
they lose or change their jobs. It also provides standards that
ensure the privacy of a patient’s health care information, par-
ticularly in electronic media.
INSURANCE COVERAGE
There are several types of insurance coverage that an OMS
practice should consider having for both surgeons and the
practice, including professional negligence-malpractice, life
and disability, loss of business, buyout insurance, premises, and
worker’s compensation. Professional negligence-malpractice
insurance protects the surgeon from claims of breaching the
 CHAPTER 16 • Oral and Maxillofacial Surgery—Office Management
standard of care while caring for a patient. Malpractice insur-
ance is mandatory. Life insurance provides coverage for loss
of life, and disability insurance provides coverage for the
surgeon should he or she become disabled and not be able to
perform the duties customarily associated with his or her posi-
tion. Loss of business insurance protects the business from loss
as a result of flood, hurricanes, and tornadoes, typically classi-
fied as “acts of God.” Buyout insurance is life insurance that
can be taken out to insure the life of a surgeon partner. The
insurance policy would be such that it would accrue value over
time while providing a death benefit should the partner die.
If the partner does not expire before his or her retirement, the
insurance policy can be surrendered for the cash value at the
time and used to supplement the cash buyout payment from
the practice to the retiring partner. Premises insurance pro-
vides coverage for the office and office contents: equipment,
computers, medical records, etc. Worker’s compensation
insurance will provide supplemental income for a worker
should they become hurt or disabled on the job and not be
able to perform their duties either in the short or long term.
■ INFORMATION TECHNOLOGY
Information technology (IT) is paramount in the delivery
of health care and can improve your practice in three signifi-
cant areas: patient care, communications, and practice
management.
By implementing electronic health records, the paper
patient chart is eliminated, thus enabling the records to be
accessed from any computer terminal in any office or off-site
location, which is very beneficial in the case of a practice with
multiple physicians and offices. Digital imaging systems are
now the standard for new office set-ups, and many existing
practices are converting to digital systems. Digital imaging
systems eliminate the need for a dark room and film while
providing easy access to images in all areas of the office by
computer or tablet. It is also possible to manipulate digital
images to enhance the information obtained from them.
E-prescribing facilitates communication between surgeons,
pharmacies, and health plans so that all parties can submit
prescriptions and check eligibility and benefits immediately.
This also decreases the possibility of prescription forgery and
decreases patient time waiting in the pharmacy.
Communications have been improved through the adop-
tion of e-mail systems for inner office, and with patients and
303
referral sources. Inner office e-mail provides the staff a method
for confidential, secure communication that can be tracked
for verification and audit. Through web-based or e-mail–based
office systems, patients may register for appointments, receive
appointment confirmations, billing and insurance informa-
tion, and directions to the office location. Referral sources
have the ability to send digital radiographs as an e-mail attach-
ment, eliminating postage and the possibility of loss of
material in transit.
There are a number of office management systems available
on the market. Some are designed specifically for the OMS
practice, whereas others are either a dental- or medical-based
system. The basic requirements include accounts receivable
and payment, scheduling, word processing, and financial
tracking. Recent editions of practice management systems
have features that assist with managing insurance claims,
reducing the possibility of incomplete claims being filed. Min-
imizing denials ultimately improves the revenue cycle. This
ultimately improves practice cash flow and profitability.
Management of an OMS practice can be challenging
regardless of the number of surgeons, employees, or offices. It
is improbable that one person can carry out all the aspects of
business that are required each day. Surrounding oneself with
an experienced team is the first step to success but maintaining
a daily active role will solidify the future.
REFERENCES AND
SUGGESTED READINGS
Keagy B, Thomas M: Essentials of physician practice management, San
Francisco, 2004, Jossey-Bass.
Lutz S: Physician group management at the crossroads, New York, 1999,
McGraw-Hill.
Pavlock E: Financial management for medical groups, Englewood, CO,
2000, MGMA.
Price C, Novak A: How to evaluate employees, Englewood, CO, 2002,
MGMA.
Satinsky M: Handbook for medical practice management in the 21st
century, London, 2007, Radcliffe.
Schryver D: An assessment manual for medical groups, Englewood, CO,
2002, MGMA.
Tinsley R: The practice management handbook, New York, 2002,
Aspen.
Weatherington T, Perry R: Office management. In Fonseca RJ,
editor: Oral and maxillofacial surgery, vol 1, St Louis, 1999,
Saunders.
Wolper L: Physician practice management-essential operational and
financial knowledge, Great Neck, NY, 2005, Jones and Bartlett.
CHAPTER 17
ACCREDITATION
The history of oral and maxillofacial surgery is synonymous
with outpatient anesthesia and surgery. Oral and maxillofacial
surgeons have historically been leaders in this area of health
care delivery. In recent years, there has been a trend in the
medical community toward operating out of licensed and
accredited surgicenters. Surgicenters can be state licensed,
Medicare approved, and/or accredited by the Accreditation
Association for Ambulatory Healthcare (AAAHC) or the
Joint Commission (formerly the Joint Commission on Accred-
itation of Healthcare Organizations [JCAHO]).1 The experi-
ence of operating in an accredited surgicenter is very rewarding
for a number of reasons:
1. Surgicenters make delivery of care better. There are
numerous checks and balances for infection control,
incident reporting, and adverse reactions that often go
unnoticed in an ordinary OMS practice.
2. The general public views accredited surgicenters as
being state of the art. In this competitive world, patients
have more confidence in their surgeons if they operate
in an accredited surgicenter. An accredited surgicenter
serves to unify the practice. The physicians and staff
develop pride in their operating facility, knowing that
they are practicing at the very highest level.
3. With the support of anesthesiologists coming into an
oral and maxillofacial surgicenter, more sophisticated
cases are being done on an outpatient basis. Some of the
cases performed are cosmetic surgery, orthognathic
surgery, and cancer and reconstructive surgery. Fre-
quently, cases that were traditionally completed in a
hospital setting are now being safely performed in an
outpatient surgicenter. This is also easier for the
patient.
4. Surgicenters can be viewed as a profit center. Patients
are accustomed to paying hospitals a facility fee. This
facility fee can be paid to the surgicenter, and in some
cases, insurance companies will pay facility fees. It is
always more economical to perform a case in a surgicen-
ter than a traditional hospital setting. People who have
made a commitment to operating under the very best
conditions choose certified surgicenters. In the coming
years, certified surgicenters will become more common
and very possibly the standard of care.
There are many different accreditation organizations. His-
torically, OMS practices are accredited by the following
agencies:
304
OF SURGICENTERS
John O. Akers
1. State and Medicare licensure. Individual states have
unique requirements. Some states allow AAAHC and
JCAHO accreditation to satisfy state requirements. In
23 states, AAAHC certification satisfies state licensing
requirements.
2. AAAHC, Accreditation Association for Ambulatory
Healthcare. This organization was formed in 1979
and has accredited more than 3000 organizations
throughout the ambulatory health care environment
(Table 17-1).
3. JCAHO, Joint Commission on Accreditation of Health-
care Organizations formed in 1951. It has evaluated
and accredited 16,000 health care organizations in the
United States, 195 oral and maxillofacial surgery offices,
both military and civilian.
4. AAAHC and JCAHO both require compliance with
industry standards, such as the Occupational Safety and
Health Administration (OSHA) and state standards for
licensure. These standards address patient rights, patient
treatment, risk management, performance improve-
ment, staff and patient education, and infection
control.
In the future, accreditation may become the gold standard
that all states require. In general, accreditation standards tend
to be higher than the state regulations. In addition, accredita-
tion surveyors have the experience of examining facilities all
over the United States. This experience helps surveyors
to bring new ideas into the facility. This shared experience
benefits everyone—patients, physicians, and staff.
Accreditation provides the leaders with the tools and disci-
plines they need to organize and build an effective team, cre-
ate projects and meet the challenges of improving care. It also
gives them feedback systems to constantly monitor all aspects
of quality more efficiently, thus allowing them to design and
build safer systems to eliminate the destructive practice of in-
dividual blame. Accreditation aims to address problems, not
people. Competent professionals can make mistakes, but with
good leadership, consistence in place, the chance of harm is
minimized. A motivated leader seeking the goal of increased
happiness for his or her patients and for himself, is a tipping
point to improving the quality of care provided. This is true no
matter what the size of the organization or the practice setting.
The goal of the accreditation process is to arm those leaders
with a philosophy and the tools that have stood the test of
time. Accreditation standards lay out the common denomi-
nators found in high quality clinical practices on a national
level. Its purpose is to show the efficiency of planned actions
 CHAPTER 17 • Accreditation of Surgicenters 305

TABLE 17-1 Ambulatory Accreditation Comparison3

Accreditation Association for Ambulatory Health Care, Inc. Joint Commission on Accreditation of Healthcare Organizations
3201 Old Glenview Road, Ste 300 One Renaissance Blvd.
Wilmette, IL 60091-2992 Oakbrook Terrace, IL 60181
847/853-6060, www.aaahc.org 630/792-5000, www.jcaho.org
Cost $2990 Cost: $3975
Length of accreditation: 3 years Length of accreditation: 3 years
Emphasizes constructive consultation and education On-site education and consultation by surveyors throughout the survey
Accreditation based on self-assessment, survey, and committee review Accreditation based on compliance with JCAHO standards and continuous efforts to improve
the care and service provided
Survey Content Comparison
SURVEY ACCREDITATION STATE
JCAHO, AAAHC Licensure, Medicare
Compliance Varies by state Mandatory
Emphasis Evaluation and education Inspection
Frequency Triennial Annual
Notice Announced (preponderantly) 5% unannounced Unannounced and announced
Funding Provider fees Tax dollars
Expectations Achievable standards Minimum expectations
Scoring Systems and processes Individual deficiencies
Value Improvement Enforcement
Process Survey compares performance against standards Survey compares performance against regulations
Approach Education/consultation Sanctions/penalties/fines
Findings Recommendations for improvement Citations
Award Accreditation Licensure or certification
Survey Results JCAHO notified immediately
AAAHC 60 days
Courtesy of Primary Resources, Inc. for Practice Management Notes, 2002.

TABLE 17-2 Comparison of JCAHO with AAAHC

Requirements JCAHO AAAHC Comment
State license required If required by state If required by state Federal & state guideline must be
addressed
Some states recognize AAAHC & JCAHO in
lieu of certain licensing requirements
Application fees $1700 deposit fee $610 nonrefundable
Cost of survey Determined by number of physicians and Determined by size & complexity of JCAHO spreads cost of survey over the 3
volume organization years requiring an annual fee
Survey time One surveyor for 2 days 1-1½ days with one surveyor May be longer if high volume
Length of accreditation 3 years 6 months, 1 year, or 3 years Based on compliance with standards
Surveyor Paid employee Volunteer
Recognized by third-party state & federal Yes Yes Recognized but not guaranteed facility fees
agencies and professional liability carriers Should be negotiable
Unannounced surveys First survey announced Only if requiring Medicare survey AAAHC provides 30-day window for
unannounced survey
Resurvey unannounced Medicare requires unannounced
surveys
Reporting requirements during Yes No JCAHO: For partial or noncompliant
accreditation time frame elements of performance, periodic reports
are due
Sentinel events and 12 months after
survey a requirement to participate in an
evaluation of standards compliance along
with a plan of action
Notification of accreditation status on Yes No
survey date Information collected during survey
is presented to a committee to be
A final written report will follow within 6-7 Evaluated, and the decision is based
weeks on comparative organizations
Written report 10-12 weeks
306 SECTION III ■ Practice Management
and how that can create a synergy that will improve present
practices and generate new ideas. The strength of a common
objective to improve the quality of care will motivate all in-
volved to excel and grow. Accreditation can also facilitate a
healthy workplace. It creates an environment in which indi-
viduals know what is expected of them and why it is impor-
tant to the mission. A satisfied worker (professional) is usually
more productive and less likely to wander. New employees are
indoctrinated with a plan of how we do it here. In addition,
worker satisfaction improves when they feel they are part of
something that makes a difference. Accreditation can help de-
velop these good habits and provide the framework that fosters
this end.2
The accreditation process is an ongoing self-analysis, peer
review, and consultation. An accredited office should con-
tinue to improve with each year of participation (Table 17-2).
Once the decision is made to become accredited, the decision
must be made as to which agency will be used. A copy of
the standards required should be requested from that agency,
and the self-evaluation and preparations should begin. There
should be a minimum 4-month (preferably 6 to 8 months)
history of compliance with the guidelines. Once the standards
have been received, a meeting should be held with all staff
members and physicians of the center. Team leaders should
be chosen, and each leader should be delegated a chapter or
portion of the guidelines to review for compliance. Weekly
meetings should be held with team leaders to determine com-
pliance, and open discussions should be held regarding the
necessary changes that should be initiated. Policies and pro-
cedures need to be updated and approved for any areas of
deficiency. During a survey, expect to be asked by the surveyor
to show a policy and procedure for a specific situation. An
internal survey should be held when all areas have been
addressed. It needs to be understood that full compliance
needs to be achieved before the survey is scheduled. Too many
organizations rush the process and cause much undue stress
and frustration to both physicians and staff. Once all steps
have been taken, the call can be made to schedule the survey.
All agencies have a time frame in which the survey needs to
be done after application has been made. Preparation and
planning is the key to every successful survey and business.
REFERENCES
1. AAAHC—Accreditation Association for Ambulatory
Healthcare
JCAHO—Joint Commission on Accreditation of Healthcare
Organizations
2. DiPlacido F, DMD, FACD
3. American Association of Oral and Maxillofacial Surgeons, 2003.
Available at www.aaoms.org (accessed Jan 8, 2007).

CREDENTIALING AND HOSPITAL PRIVILEGING
David P. Kretzschmar
In 1981 the Joint Commission, formerly known as the Joint
Commission on the Accreditation of Healthcare Organiza-
tions (JCAHO), recognized the training and subsequent com-
petency of oral and maxillofacial surgeons (OMSs) to perform
routine history and physical examinations (H & P). Before
this change, the admission and presurgical H & Ps of an OMS
necessitated a counter signature of a physician, usually the
patient’s family physician, the emergency room physician, or
the anesthesiologist performing the presurgical review. This
change lifted a significant barrier for the oral surgeons within
the hospital arena, and it was a significant step forward in
gaining autonomy with our surgical colleagues.
A survey of the membership of the American Association
of Oral and Maxillofacial Surgeons (AAOMS) in 1993 indi-
cated that 18% of the respondents were denied H & P privi-
leges at one or more hospitals. These denials were almost
exclusively based on restrictions outlined in the bylaws of the
medical institutions. Of those respondents who were granted
H & P privileges, 56% said that a change in the bylaws of the
institution was necessary before they could perform histories
and physical examinations.1 According to the Committee on
Hospital Affairs of AAOMS, until 1996 the most common
request for assistance on medical issues and disputes was
regarding credentialing to perform the H & P exam. Since
that time, inquiries regarding the privileging of cosmetic
surgery procedures have moved to the forefront.2 Of course,
there will always be “territorial” struggles at many institutions
between the facial trauma specialists, certain cosmetic and
aesthetic surgery disciplines, and protective providers who feel
threatened by competition.
An OMS cannot be denied privileges to practice the spe-
cialty as it is known and defined, as long as the surgeon can
document certification of training from an accredited resi-
dency program, demonstrate competency in the requested
privileges, and be an individual of sound character and high
ethical standards. The depth of this credentialing and privi-
leging process will now be explored and reviewed.
■ BACKGROUND
The majority of OMSs practice their specialty under the aus-
pices of a state license in dentistry. There are also many
“double-degree” individuals who are licensed to practice by
both the dental and medical boards of their states. A few sur-
geons will choose to practice solely under medical licensure.
CHAPTER 18
The day-to-day office practice of oral and maxillofacial surgery
in the private outpatient setting requires only a current state
license to practice, a valid sedation certificate, and a state
permit to operate a small business. When an individual applies
for admitting and surgical privileges at hospitals and ancillary
surgery centers, there will certainly be applications to process,
increased levels of background review, and provider scrutiny
by the hospital credentialing committee. This, in itself, can
be an arduous and frustrating task.
Hospitals and medical centers vary in the structure of their
medical staff membership. Some institutions will have a
Department of Dentistry in addition to a Department of
Surgery, and the question always exists as to which depart-
ment the OMS really belongs. Teaching hospitals that have
an active oral and maxillofacial surgery residency program
usually position the OMS program as a division of the Depart-
ment of Surgery. University medical centers that have associ-
ated schools of dentistry will often place the OMS training
program under the guidance of the dental school’s graduate
education programs. Nevertheless, the hospital side of the
equation must have the members of the medical staff conform
to the bylaws, rules, and regulations of the institution for cre-
dentialing and granting of hospital privileges.
The oral surgeons who practice under their dental license
will be categorized in a group of nonphysician licensed inde-
pendent practitioners (LIP). This group includes dentists,
podiatrists, optometrists, and clinical psychologists. Another
group, limited licensed practitioners (LLP), is made up of
individuals who can only practice under the supervision of a
physician or by proscription; this group includes physician
assistants, nurse practitioners, nurse anesthetists, midwives,
physical therapists, and others. The oral surgeons are usually
listed in the LIP grouping and should not be included in
the LLP. The Joint Commission defines a licensed indepen-
dent practitioner as “any individual permitted by law and
by the hospital to provide patient care services without
direction or supervision, within the scope of the individual’s
license and consistent with individually granted clinical
privileges.”3
The medical staff membership of surgery centers and hos-
pitals may be organized into preferred provider organizations
(PPO) or independent practitioner associations (IPA) that are
organized as medical corporations. Often times these struc-
tured organizations may attempt to control staff membership
and may attempt to control voting rights for certain nonphysi-
307
308 SECTION III ■ Practice Management
cian individuals. OMSs must always be aware of these situa-
tions and must always confront obstacles to equal staff
membership, including equal access to providing appropriate
patient care and receiving equal reimbursement for services
rendered.
■ THE SPECIALTY
The scope of practice of the OMS is certainly broad, and there
is a wide range of procedures, many of which overlap with
other dental and medical specialties. OMSs, however, are the
only LIPs with verified competency in physical diagnosis, as
recognized by the Joint Commission in its 1997 medical staff
standard MS.6.2.1. It states that “qualified oral and maxillo-
facial surgeons may perform the medical history and physical
examination, if they have such privileges, in order to assess
the medical, surgical, and anesthetic risks of the proposed
operative and other procedures.”3 In addition, the Joint Com-
mission continues and defines a qualified OMS as “an indi-
vidual who has successfully completed a postgraduate program
in oral and maxillofacial surgery accredited by a nationally
recognized accrediting body approved by the United States
Department of Education. As determined by the medical staff,
the individual is also currently competent to perform a com-
plete history and physical examination in order to assess the
medical, surgical, and anesthetic risks of the proposed opera-
tive and other procedures.”3
In January of 2005, the Centers for Medicare and Medicaid
Services (CMS) proposed rule changes that affected the list
of practitioners eligible to perform the history and physical
examination, authenticate verbal orders, secure medications,
and complete postanesthesia evaluations. The wording of the
existing list of practitioners with these privileges had been
replaced with the term “physician” as defined by the Social
Security Act. At the time of this proposed change, an alert
was issued to the AAOMS membership, which elicited more
than 175 comments to the H & P changes. In response to
these comments, the CMS issued a statement saying “it was
not our intent for this revised language to lead to a reduction
in the pool of professionals who are qualified to perform the
H & P. For clarification in this final rule, the specific reference
to oromaxillofacial surgeons has been retained. However,
based on hospital policy and State law, the pool of other quali-
fied individuals can be restricted.”4 The AAOMS issued a
second member alert message in December 2006, notifying the
membership that the final revision of the CMS retains the
reference to OMSs as being eligible to perform the complete
H & P. This was another significant victory for the specialty
of OMS and a credit to AAOMS working for its
membership.
The specialty of oral and maxillofacial surgery is recognized
by the American Dental Association (ADA). Oral and maxil-
lofacial surgery advanced training programs are accredited by
the Commission on Dental Accreditation (CODA),5 which
is a funded, albeit independent, organization of the ADA.
CODA is recognized and accredited by the U.S. Department
of Education and the Commission on Postsecondary Educa-
tion. Similarly the other surgical specialties are organized
under the umbrella of the American Board of Medical Spe-
cialties (ABMS) or the American Osteopathic Association
(AOA). These surgical specialties are accredited by the
Accreditation Committee for Graduate Medical Education
and similar accrediting bodies for osteopathy and podiatry.
The reliability and respectability of the specialty dental
boards are embraced by the existence and validity of CODA.
Although voluntary, CODA is accredited by the Department
of Education and the Council on Postsecondary Education.
The process involved in receiving these accreditations ensures
that the oversight of advanced training is valid and valuable.
Of the 29 members of CODA, four are appointed by the
ADA, four are appointed by the American Association of
Dental Schools, and four are appointed by the American
Association of Dental Examiners. There are four public
members, one dental student, one dental hygienist, one dental
laboratory technician, and one member appointed by each of
the eight recognized dental specialties. This structure of checks
and balances ensures impartial oversight and excellent quality
in the specialty education programs. Contrary to this struc-
tured process of specialty oversight, there are also unrecog-
nized boards in medicine and dentistry, such as the American
Board of Cosmetic Surgery and the American Board of Implant
Dentistry.
The Joint Commission recognizes that specialty “board cer-
tification is an excellent benchmark and is considered when
delineating clinical privileges” (1997 MS.5.15.2). The Ameri-
can Board of Oral and Maxillofacial Surgery (ABOMS) is the
equivalent specialty board for oral surgeons as the member
boards of the American Board of Medical Specialties are to
their respective specialties. The ADA is to the ABOMS as
the ABMS is to the medical specialty boards. There should
not be any justification for denial of hospital privileges, cre-
dentials, or staff membership based on the uniqueness of the
fact that ABOMS does not belong to the ABMS organization.
The ABOMS examination process is a very intense, thorough,
and all-encompassing evaluation of the knowledge base of its
applicants, and recognition of board certification is indeed an
accomplishment. The ABOMS examination process can defi-
nitely stand shoulder to shoulder with any surgical specialty
examination process. Several years ago the ABOMS board of
directors voted to offer and require a recertification examina-
tion every 10 years for those members attaining board certifi-
cation after the year 1990. This change was made to ensure
that the ABOMS membership continues to stay abreast of the
current knowledge base and scope of practice of the specialty
of oral and maxillofacial surgery.
■ ACCREDITATION AND
CERTIFICATION
The majority of OMSs perform their routine daily procedures
in an office clinic environment or other similar outpatient
ambulatory setting. Many practitioners have even incorpo-
rated outpatient operating rooms, capable of supporting
general anesthesia surgical cases, within the walls of their
 CHAPTER 18 •
clinical structure. In 1997 Medicare granted approval status
to several accrediting agencies for ambulatory surgical centers.
Therefore, the ambulatory care manuals published by agen-
cies, such as the Joint Commission and the American Associa-
tion for Ambulatory Health Care, may prove helpful to OMSs
operating in their offices or similar outpatient facilities.6 The
offices of OMSs and other surgical specialists can be accred-
ited by either of these organizations as single practices, group
practices, or outpatient surgery centers. Providers, at their
own initiative, can request a survey and apply for facility
accreditation.
An OMS who possesses a medical degree is eligible for fel-
lowship status in the American College of Surgeons (ACS);
however, there is no specialty section within ACS for those
who do qualify. Even though most OMSs perform facial plastic
surgery, they likewise are not eligible for membership in the
American Academy of Facial Plastic and Reconstructive
Surgery, unless they hold a medical degree. The same restric-
tion is true for the two societies representing head and neck
surgeons. There is an American Board of Facial Plastic and
Reconstructive Surgery that is not recognized by ABMS, but
is usually given equivalent status to ABMS member boards.
Again, certification is only available to the medical-degreed
oral surgeon. There is one cosmetic surgery organization that
has welcomed membership from surgical specialists of diverse
backgrounds, and that is the American Academy of Cosmetic
Surgery. This group does not make any distinction between
the “single-degree” and the “double-degree” OMS and will
invite all who meet the qualifications for membership and
fellowship status.
The Joint Commission recognizes that there are many
paths for obtaining and maintaining “training, competency,
and ability.”3 The Joint Commission, the American Medical
Association (AMA), the ACS, and the American College of
Physicians all recognize the overlap among specialties as
acceptable and even advantageous. The American Society of
Cosmetic Surgeons has embraced the policies of these profes-
sional organizations and concurs that overlap of specialties
performing cosmetic surgical procedures is in the best interest
of the patients.
California enacted legislation in 1997 to require accredita-
tion of all facilities where any form of parenteral sedation or
anesthesia is administered that has the probability of inducing
a loss of the patient’s protective reflexes. If a provider has a
current permit to administer general anesthesia or conscious
sedation from the state board of dental examiners, the dental
office is exempt from this requirement. The majority of states
now require a valid sedation permit for dentists and OMSs
who perform light sedation, deep sedation, and/or general
anesthesia in an office or hospital setting. There are several
requirements to fulfill when applying for a sedation permit:
show documentation of appropriate anesthesia education and
training; hold a current basic life support certification and, in
most instances, proof of advanced cardiac life support training;
and pass an inspection of the facility, including the use of
available emergency equipment. In many states, part of the
Credentialing and Hospital Privileging 309
office inspection process will include a practical application
of an anesthesia technique on a routine dental and/or surgical
procedure in the presence of the evaluator. These anesthesia
permits are usually renewable on a 1- to 3-year basis, with the
office reinspection varying between 5 to 10 years.
As of this writing, the ADA’s Council on Dental Educa-
tion and Licensure (CDEL) and the Committee on Anesthe-
sia have proposed changes to the published anesthesia
guidelines and policy statement.7 The emphasis is, as always,
on patient safety, and the proposed changes refocus the guide-
lines based on the anesthetic’s effects on the central nervous
system and not on the route of administration. In addition,
an important change is the ability to rescue a patient from an
unintended deeper level of sedation. Such training is not
included in the standard dental school curriculum and cannot
adequately be taught in a continuing education program. Fur-
thermore, AAOMS issued a letter of support stating that such
knowledge and skill can only be acquired in a postdoctoral
training program that requires competency in the administra-
tion of anesthesia as part of the residency training curriculum.8
OMS graduates of accredited residency training programs defi-
nitely fulfill the above requirements. However, providers
always need to be cognizant of state policies and the guidelines
of accrediting agencies when pursuing credentials and privi-
leges in anesthetic techniques.
■ DEFINITIONS AND RESOURCES
OMSs should familiarize themselves with the definitions of
both dentistry and the specialty of oral and maxillofacial
surgery. In 1997, the House of Delegates of the ADA recog-
nized the need for a national standard and, for the first time,
defined the practice of dentistry. Resolution 33H establishes
the definition of dentistry as “the evaluation, diagnosis, pre-
vention and/or treatment (non-surgical, surgical or related
procedures) of diseases, disorders and/or conditions of the oral
cavity, maxillofacial area and/or the adjacent and associated
structures and their impact on the human body; provided by
a dentist, within the scope of his/her education, training and
experience, in accordance with the ethics of the profession
and applicable law.” Each individual state has a Dental Prac-
tice Act (DPA), and the definition of dentistry does vary from
state to state. The most favorable language for a DPA defini-
tion is similar to the state of Maryland, which includes any
procedures “in the curricula of an accredited dental school or
in an approved dental residency program of an accredited
hospital or teaching institution.” Table 18-1 provides the lan-
guage of the states and their respective definitions of dentistry
and/or activities of the dentist.9
Regarding the specialty of OMS, the definition has been
in place for more than 25 years by the ADA. “Oral and maxil-
lofacial surgery is the specialty of surgery which involves the
diagnosis, surgery and adjunctive treatment of diseases and
defects involving both the functional and aesthetic aspects of
the hard and soft tissues of the oral and maxillofacial region.”
It is very important for providers to know and understand the
wording of their respective DPAs when responding to ques-
310 SECTION III ■ Practice Management

TABLE 18-1 Dental Practice Act Definitions of a Dentist or Dentistry

State Relevant Language
Alabama To diagnose, treat, prescribe, or operate for any disease, pain, deformity, deficiency, injury, or physical condition of the teeth or jaws
or adjacent structures
Alaska Diagnoses, treats, operates on, corrects, attempts to correct, or prescribes for a disease, lesion, pain, injury, deficiency, deformity, or
physical condition, malocclusion or malposition of the human teeth, alveolar process, gingiva, maxilla, mandible, or associated tissues
Arizona With specific reference and application to the teeth, gums, jaws, oral cavity, or tissue adjacent thereto in living persons
Arkansas Examination, diagnosis, treatment, repair, prescription and/or surgery of or for any disease, disorder, deficiency, deformity, condition,
lesion, injury, or pain of the human oral cavity, teeth, gingiva, and soft tissues and the diagnosis, the surgical adjunctive treatment of
the diseases, injuries, and defects of the human jaws and associated structures
California Diagnosis and treatment, by surgery or other method, of diseases and lesions and the correction of malpositions of the human teeth,
alveolar process, gums, jaws, or associated structures; such diagnosis or treatment may include all necessary related procedures
and the use of drugs, anesthetic agents, and physical evaluation
Colorado Performs or attempts or professes to perform any dental operation or oral surgery . . . diagnoses or professes to diagnose, prescribes
for or professes to prescribe for, treats or professes to treat disease, pain, deformity, deficiency, injury, or physical condition of the
human teeth or jaws or adjacent structures
Connecticut Performs any operation in or makes examination of, with intent of performing or causing to be performed any operation in the mouth
and surrounding and associated structures . . . who diagnoses and treats diseases or lesions of the mouth and surrounding and
associated structures
Delaware Diagnoses or treats diseases or lesions of human teeth, jaws, or oral tissues mechanically, medicinally, or surgically or by the use of
radiograms, x-rays, or fluoroscopic methods, or attempts to correct malposition thereof
District of Columbia Diagnosis, treatment, operation, or prescription for any disease, disorder, pain, deformity, injury, deficiency, defect, or other physical
condition of the human teeth, gums, alveolar process, jaws, maxilla, mandible, or adjacent tissues or structures
Florida Examination, diagnosis, treatment planning, and care of conditions within the human oral cavity and its adjacent tissues and
structures. It includes the performance or attempted performance of any dental operation or oral or oral maxillofacial surgery and any
procedure adjunct thereto
Georgia Examines any human oral cavity, teeth, gingiva, alveolar process, maxilla, mandible, or associated structures . . . Undertakes to do or
perform any physical evaluation of a patient . . . before, incident to, and appropriate to the performance of any dental services or oral
or maxillofacial surgery
Hawaii Diagnosis, prevention, and treatment of diseases of the teeth, oral cavity, and associated structures
Idaho With respect to the teeth, gums, alveolar process, jaws, or adjacent tissues of another person
Illinois Diagnoses, treats, prescribes, or operates for any disease, pain, deformity, deficiency, injury, or physical condition of the human
teeth, alveolar process, gums, or jaw
Indiana Offers to diagnose or professes to diagnose or treat or professes to treat any of the lesions or diseases of the human oral cavity,
teeth, gums, or maxillary or mandibular structures; extracts human teeth or corrects malpositions of the teeth or jaws
Iowa Persons who treat or attempt to correct by any medicine appliance or method any disorder, lesion, injury, deformity, or defect of the
oral cavity, teeth, gums, or maxillary bones of the human being
Kansas Diagnoses or professes to diagnose, prescribe for or professes to prescribe for, treats or professes to treat, disease, pain, deformity,
deficiency, injury, or physical condition of the human teeth or jaws, or adjacent structure
Kentucky Diagnoses or treats diseases or lesions of human teeth or jaws, or attempts to correct malpositions thereof, or who diagnoses or
treats disorders or deficiencies of the oral cavity and adjacent associated structures
Louisiana Diagnose, treat, correct, operate, prescribe for any disease, pain, injury, deficiency, deformity, or physical condition of the human
teeth, alveolar process, gums, jaws, or associated parts
Maine Diagnoses or professes to diagnose, prescribes for or professes to prescribe for, treats or professes to treat, disease, pain, deformity,
deficiency, injury, or physical condition of the human teeth or jaws or adjacent structures
Maryland Diagnose, treat, or attempt to diagnose or treat any disease, injury, malocclusion, or malposition of a tooth, gum, jaw, or structures
associated with a tooth, gum, or jaw if the service, operation, or procedure is included in the curricula of an accredited dental school
or in an approved dental residency program of an accredited hospital or teaching institution
Massachusetts Diagnose, treat, operate, or prescribe for any disease, pain, injury, deficiency, deformity, or other condition of the human teeth,
alveolar process, gums, jaws, and associated parts
Michigan Diagnosis, treatment, prescription, or operation for a disease, pain, deformity, deficiency, injury, or physical condition of the human
tooth, teeth, alveolar process, gums, jaws, or their dependent tissues
Minnesota Diagnose, treat, prescribe, or operate for any disease, pain, deformity, deficiency, injury, or physical condition of the human tooth,
teeth, alveolar process, gums, jaw, or associated structures
Mississippi Diagnose or profess to diagnose or examine or contract for the treatment of or treat or profess to treat or hold himself out as treating
any of the diseases or disorders or lesions of the oral cavity, teeth, gingivae, or maxillary bones, or who shall extact teeth, repair or
fill cavities in human teeth, correct malposition or irregularities of the teeth or jaws, practice surgery of the head or neck incident to
the practice of oral surgery
Missouri Diagnoses or professes to diagnose, prescribes for or professes to prescribe for, treats or professes to treat diseases, pain,
deformity, deficiency, injury, or physical condition of human teeth or adjacent structures
 CHAPTER 18 • Credentialing and Hospital Privileging 311

TABLE 18-1 Dental Practice Act Definitions of a Dentist or Dentistry—cont’d

State Relevant Language
Montana Diagnoses, professes to diagnose, prescribes for or professes to prescribe for, treats or professes to treat diseases, pain, deformity,
deficiency, injury, or physical condition of human teeth, jaws, or adjacent structures
Nebraska Diagnoses or professes to diagnose, prescribes for, or professes to prescribe for, treats or professes to treat diseases, pain,
deformity, deficiency, injury, or physical condition of human teeth or jaws or adjacent structures
Nevada Diagnoses, professes to diagnose or treats or professes to treat any of the diseases or lesions of the oral cavity, teeth, gums, or the
maxillary bones
New Hampshire Diagnose or profess to diagnose or to treat or to profess to treat or prescribe or professes to prescribe for any of the lesions,
diseases, disorders, or deficiencies of the human oral cavity, teeth, gums, maxilla, mandible, or associated structures
New Jersey Diagnose, treat, prescribe, or operate for any disease, pain, deformity, deficiency, injury, or physical condition of the human tooth,
teeth, alveolar process, gums, cheek, jaws, oral cavity, and associated structures
New Mexico Diagnosis, treatment, correction, change, relief, prevention, prescription of remedy or surgical operation for any disease, pain,
deformity, deficiency, injury, lesion, or other physical condition of human teeth, gums, jaws, oral cavity, or adjacent tissues
New York Diagnosing, treating, operating, or prescribing for any disease, pain, injury, deficiency, deformity, or physical condition of the human
mouth, including the teeth, alveolar process, gums, jaws, and adjacent tissues
North Carolina Diagnoses, treats, or prescribes for any disease, disorder, pain, deformity, injury, deficiency, defect, or other physical condition of the
human teeth, gums, alveolar process, jaws, maxilla, mandible, or adjacent tissues or structures of the oral cavity
North Dakota Examination, diagnosis, treatment, repair, administration of local or general anesthetics, prescriptions, or surgery of or for any
disease, disorder, deficiency, deformity, condition, lesion, injury, or pain of the human oral cavity, teeth, gingivae, and soft tissues
and the diagnosis and the surgical and adjunctive treatment of the diseases, injuries, and defects of the human jaw and associated
structures
Ohio Performs, advertises to perform dental operations of any kind ... diagnoses or treats diseases or lesions of human teeth or jaws or
associated structures or attempts to correct malpositions thereof
Oklahoma Treating any of the diseases or disorders or lesions of the oral cavity, teeth, gums, maxillary bones, and associated structures; . . .
shall treat deformities of the jaws and adjacent structures
Oregon Examination, diagnosis, treatment planning, care, and prevention of conditions, which shall include, but not be limited to, the cutting,
altering, repairing, removing, replacing, or repositioning of hard and soft tissues within the human oral cavity and its adjacent or
related tissues and structures
Pennsylvania Diagnoses, treats, operates on, or prescribes for any disease, pain, or injury or regulates any deformity or physical condition of the
human teeth, jaws, or associated structures
Puerto Rico Perform operations on or make examinations of human teeth, maxillary bones, gums, oral cavities, or adjacent tissues with the intent
of performing or causing to be performed any operation thereon
Rhode Island To diagnose or profess to diagnose or to treat or profess to treat or to prescribe or profess to prescribe for any of the lesions,
diseases, disorders, or deficiencies of the human oral cavity, teeth, gums, maxilla, mandible, and/or associated structures
South Carolina Diagnose or treat or profess to diagnose or treat any diseases or lesions or conditions of the oral cavity and associated adjacent
structures
South Dakota Examination, diagnosis, treatment planning, and care of conditions within the human oral cavity and its adjacent tissues and
structures
Tennessee Diagnoses, prescribes for or treats any disease, pain, deformity, deficiency, injury, or physical condition of the human teeth, jaws, or
associated structures, and such diagnosis and treatment may include the use of a complete or limited physical examination of
patients by a board eligible or board certified oral surgeon or resident in an approved oral surgery program so long as such oral
surgeon or resident is practicing in a hospital setting
Texas Diagnose, treat, remove stains or concretions from teeth, provide surgical and adjunctive treatment for any disease, pain, injury,
deficiency, deformity, or physical condition of the human teeth, oral cavity, alveolar process, gums, jaws, or directly related and
adjacent masticatory structures
Utah Diagnose, treat, operate, or prescribe for any disease, pain, injury, deficiency, deformity, or physical condition of the human teeth,
alveolar process, gums, jaws, or adjacent structures in the maxillofacial region
Vermont Diagnose or profess to diagnose, to treat or profess to treat or to prescribe for or profess to prescribe for any lesions, diseases,
disorders, or deficiencies of the human oral cavity, teeth, gums, maxilla, mandible, or adjacent associated structures
Virginia Diagnoses, treats, or professes to diagnose or treat any of the diseases or lesions of the oral cavity, its contents or contiguous
structures
Washington Diagnose, treat, remove stains and concretions from teeth, operate or prescribe for any disease, pain, injury, deficiency, deformity, or
physical condition of the human teeth, alveolar process, gums, or jaws
West Virginia To diagnose or profess to diagnose or to treat or profess to treat or to prescribe or profess to prescribe for any of the lesions,
diseases, disorders, or deficiencies of the human oral cavity, teeth, gums, maxilla, mandible, and/or (adjacent) associated structures
Wisconsin Diagnoses or professes to diagnose or treats or professes to treat or prescribes or professes to prescribe for any of the lesions,
diseases, disorders, or deficiencies of the human oral cavity, teeth, investing tissues, maxilla, mandible, or adjacent associated
structures
Wyoming Diagnoses or professes to diagnose, prescribes for or professes to prescribe for, treats or professes to treat diseases, pain,
deformity, deficiency, injury, or physical condition of human teeth, jaws, or adjacent structures
312 SECTION III ■ Practice Management

TABLE 18-2 Sample Privilege List for Oral and Maxillofacial Surgeons
REHABILITATION OF DENTAL ARCHES
_____ Oral prosthesis for malformation of the face, jaws, and mouth _____ Scar revision
_____ Fabrication of implant, cribs, meshes, wires, stents, splints, and _____ Cyst and tumor removal
facial prosthesis FRACTURES AND RECONSTRUCTIVE SURGERY
_____ Fabrication and application of custom obturators _____ Maxillary and mandibular dentoalveolar fractures
_____ Occlusal adjustment and equilibration _____ Repair of avulsed and luxated teeth and segments
_____ Treatment of temporomandibular joint pain dysfunction _____ Placement and removal of dental and skeletal wiring
_____ Treatment of myofascial pain _____ Maxillofacial fractures—closed and open reduction
_____ Appliance therapy for clenching of bruxism _____ Grafting of mucosa, bone, and bone substitutes
_____ Implantation or reimplantation of teeth _____ Osteotomies, intraoral and extraoral, complete or segmental,
INTRAORAL SURGERY maxillary and mandibular
_____ Mucogingival surgery _____ Nerve repair, resection, repositioning, or reattachment
_____ Tissue grafting, including harvesting and placement _____ Temporomandibular joint manipulation, arthroscopic, and open
_____ Guided tissue regeneration surgery
_____ Root resection and hemisection _____ Nasal fractures
_____ Periapical surgery and retrograde obturation _____ Zygomatico-maxillary fractures
_____ Single uncomplicated extractions _____ Naso-orbital-ethmoid complex fractures
_____ Multiple uncomplicated extractions ESTHETIC AND COSMETIC SURGERY
_____ Surgical removal of impacted teeth _____ Rhinoplasty
_____ Surgical removal of imbedded teeth _____ Blepharoplasty
_____ Apicoectomy _____ Lip revision
_____ Alveolectomy _____ Brow lift
_____ Alveoloplasty _____ Endoscopic surgery
_____ Root resections _____ Rhytidectomy—modified
_____ Removal of torus palatinus _____ Rhytidectomy—SMAS
_____ Removal of torus mandibularis _____ Otoplasty
_____ Repair of minor and severe lacerations OTHER
_____ Biopsy _____ H & P
_____ Removal of benign tumors _____ Conscious sedation
_____ Cystectomies from hard and soft tissues _____ Anterior and posterior iliac bone graft harvest
_____ Incision and drainage of minor infections _____ Costochondral bone harvest
_____ Incision and drainage of major infections _____ Cranial bone harvest
_____ Salivary gland surgery _____ Skin graft harvest
_____ Salivary duct surgery _____ Forensic identification
_____ Ranula and mucocele surgery _____ (Additional requests)
_____ Plastic repairs, including bone grafting to alveolar and palatal Agreement
defects I agree with the above delineation of privileges and will under ordinary
_____ Maxillary sinus surgery circumstances practice under these conditions as outlined. However, under
_____ Transplantation and reimplantation of teeth cases of emergency or qualified circumstances, it may be necessary to
_____ Frenulectomy perform procedures outside of these parameters. Also when new techniques
_____ Sequestrectomy and skills are mastered, I shall request the executive committee to approve
_____ Preprosthetic surgery, including vestibuloplasty modifications of my privileges.
_____ Surgical placement or removal of dental implants ______________________, D.D.S., M.S., M.D. Date _____
EXTRAORAL SURGERY Approved: Yes ____ No ____ Comment: _________________
_____ Incision and drainage of infections _______________________________________________________
_____ Lip surgery—pathologic ______________________, (Section chief) Date _____
_____ Lip surgery—traumatic ______________________, (Chair, executive committee) Date _____
_____ Lip surgery—cosmetic ______________________, (Chief, professional services) Date _____
_____ Biopsy

tions about credentialing or scope of practice issues. The
offices of the state boards of dental examiners and the state
societies of OMSs would always be knowledgeable contacts
for helpful information on these topics.
The AAOMS has many resources available to the surgeons
concerning hospital staff issues. These include the AAOMS
Committee on Hospital Affairs, the Committee on State and
Intergovernmental Affairs, and the Committee on Residency
Education and Training. The ABOMS and the ADA’s
Council on Preventive and Inter-Professional Relations may
also be helpful for guidance regarding hospital staff issues. The
Guidelines for Hospital Dental Services was revised by the
ADA in 1992. These guidelines address topics, such as depart-
mental organization, medical staff bylaws, clinical privileges,
hospital admission, and management of patients, just to name
a few.
An example of a privilege list for OMSs is in Table 18-2,
and the AAOMS also has a similar sample privilege list avail-
able for review and use as needed. A privilege list is part of
the applicant’s credentialing process, and most hospitals and
medical centers have a list on file from the AMA’s Hospital
Medical Staff Section.10 Helpful resources are also available
 CHAPTER 18 •
from the AAOMS; these include the Oral and Maxillofacial
Surgery Parameters of Care, the Statement on History and Physi-
cal Examination, the Guidelines to Hospital Credentialing in Oral
and Maxillofacial Surgery Procedures, and the AAOMS Model
Medical and Dental Staff Bylaws and Procedures. In 1991, the
ABOMS and AAOMS combined forces and published the
Joint Statement on the Training and Practice of Oral and Maxil-
lofacial Surgery.11 These documents are very good references
for the oral surgeons and for the medical centers concerning
background information and medical staff issues.
The AAOMS has gone even further to assist its member-
ship by developing the Guidelines on the Equivalency of Surgical
Procedures in 1996. This reference guide was prepared in an
effort to group and equate surgical procedures based on related
knowledge and skills. The guidelines have seven categories
ranging from the upper face to the neck and pharynx region,
to autologous grafting procedures, and to credentials for
technologically specific intervention, such as endoscopic,
laser, and microsurgical procedures. These guidelines allow
the surgeon to demonstrate ongoing maintenance of compe-
tency and ability based on a wide variety of procedures that
require a common base of knowledge and experience. They
also allow divisions, departments, and training programs to
evaluate the level and range of specialty procedures performed
at their institution.
■ CREDENTIALING AND
PRIVILEGING
The OMS must become familiar with the bylaws of the medical
institution for which he or she is seeking credentialing and
privileging. The bylaws are usually written in accordance with
Joint Commission hospital accreditation standards and indi-
vidual state medical society guidelines. Furthermore the Joint
Commission (Figure 18-1)12 advises medical staffs to evaluate
their privileging process by answering the following
questions:13
• Is the process defined?
• Are all independent practitioners included?
• Are responsibilities defined, understood, and fulfilled?
• Are privileges hospital specific?
• Is licensure verified?
• Can questions of training and experience be verified?
• Are peer recommendations received and considered?
• Can questions of a practitioner’s competence be
verified?
• Can the medical center support the requested
privileges?
• Can the success of the process be verified?
Surgeons who are intent on applying for privileges would
be served well to verify that the hospital can adequately
answer the above questions. Familiarization with the previ-
ously mentioned documents from the ADA, AAOMS, and
ABOMS would also be helpful. In preparing this chapter, five
different hospitals of various sizes in three different states were
surveyed regarding their respective bylaws and their creden-
tialing and privileging processes. The systems and processes
Credentialing and Hospital Privileging 313
for each of these institutions were very similar in format,
wording, requirements, and notification.
The summarized preamble to an average medical staff
general bylaws document would read as follows:
* WHEREAS, ______ Medical Center is a nonprofit cor-
poration organized under the laws of the state of ______,
and
* WHEREAS, its purpose is to serve as a general hospital
providing patient care, medical education, and research, and
* WHEREAS, it is recognized that the medical-dental staff
is responsible for the quality of medical care in the hospital
and must accept and discharge this responsibility, subject to
the ultimate authority of the board of trustees of ______
Medical Center (governing body), and that the cooperative
efforts of the medical-dental staff, the chief executive officer,
and the governing body are necessary to fulfill the hospital’s
obligations to its patients
* THEREFORE the physicians and dentists practicing in
this hospital hereby organize themselves into a medical-dental
staff in conformity with these bylaws. Also it shall be the
policy of the organized medical staff, as set forth in these
bylaws, not to discriminate on the basis of race, sex, creed,
age, disability, and/or national origin.
Four of the five hospitals surveyed listed the Division of
Surgery to include sections of General Surgery, Urology, Neu-
rosurgery, Thoracic Surgery, Ophthalmology, Otolaryngology,
Oral and Maxillofacial Surgery, Plastic Surgery, and Dentistry.
The fifth hospital listed the section of oral surgery under a
separate Division of Dentistry, because this institution has a
rather large dental department with several specialties of den-
tistry represented. A clause will exist within the medical
center bylaws for the establishment of new sections or the
discontinuance of existing sections, as needed, based upon the
recommendations and approval of the executive committee.
Credentialing is “the process of determining whether a
physician may be admitted to membership in the organized
medical staff of a hospital.” Privileging is “the process of grant-
ing the right to perform certain activities within the institu-
tion.”14 The primary responsibility for both of these functions
rests on the medical staff; however, input and approval from
the hospital through its executive committee and board of
directors is also required. The Joint Commission recommends
that objective criteria for awarding privileges be in place
before evaluating an applicant for a given privilege. It main-
tains that these criteria must “pertain to, at the least, evidence
of current licensure, relevant training and/or experience,
current competence, and health status.”15
The medical staff is responsible for:
• Initial assessment of applicants for privileges
• Ongoing monitoring of the performance of the medical
staff members
• Periodic reevaluation and renewal of privileges
• Specific delineation of clinical privileges
• Assessing and monitoring compliance with privileges16
The medical staff must perform these functions without
prejudice and in agreement with the procedures and protocols
314 SECTION III ■ Practice Management

Does the organization

No have or plan to have the Yes
resources necessary to
support the privilege?

Has the credential verification

No process established that the applicant
has the licensure, training, education
and ability to perform the privilege?

Yes

Grant privilege with Does the applicant currently

No
focused professional perform the privilege sought
practice evaluation at the organization?

Yes

Does data collected through the

ongoing professional practice
No evaluation validate competency?

Initiate focused
professional practice
evaluation

Yes

Does focused professional

practice evaluation
validate competence? Yes

Retain privilege and continue to

validate competence via ongoing
No professional practice evaluation

Privilege is Privilege is restricted

not granted or revoked

FIGURE 18-1. Process for hospital privileging and reprivileging.

delineated in its bylaws. The Joint Commission outlines the ■ APPOINTMENT

required components of granting privileges as: (1) an individ-
ual’s documented experience in categories of treatment areas
or procedures, (2) the results of treatment, and (3) the conclu-
sions drawn from quality assessment and improvement activi-
ties, when available.17 There is no mention of specific routes
of training or board certification. Additionally, note that
privileges should be granted based on “categories” of treat-
ment areas and not specific procedures.
The AAOMS Guidelines to Hospital Credentialing describes
different levels of training and experience as it relates to clini-
cal privilege eligibility (Table 18-3).
Both didactic and clinical education, training, and experi-
ence are all important in determining the level of competence
an applicant may possess. To further assess a provider’s perfor-
mance, the hospital can use any and all of the following
methods:
 CHAPTER 18 •
Levels of Training Applicable to
TABLE 18-3
Hospital Privileges
Level Description
1 Literature review, videotape review, and appropriate textbook
acquisition
2 Continuing medical education credits in accredited didactic
course work, to include pure subject-specific courses
3 Continuing medical education credits in accredited didactic/
dissection courses (surgical skills workshops with hands-on
experience)
4 Completion of observational training programs that are formally
recognized by an appropriate association
5 Assistant surgeon experience
6 Primary surgeon experience under supervision or proctorship
(highest level for residents)
7 Primary surgeon without supervision, outpatient free-standing
facility
8 Primary surgeon without supervision, hospital
• Direct observation and review
• Medical record review
• Computer simulations
• Patient simulators
• Effect of continuing education
• Utilization review
• Patient satisfaction surveys
• Cognitive tests
• Decision analysis
• Technical skills assessment
• Interpersonal skills assessment
• Malpractice claims or risk management
• Outcomes of diagnosis and treatment18
The bylaws of the hospital have more recently been viewed
as contracts between the hospital and medical staff that estab-
lish the member’s procedural and substantive protections.
Privileges are just that, and denial of hospital privileges has
been held to be valid only when based on patient care con-
siderations. During the past several years, the courts have also
begun to consider medical staff bylaws as contracts, and denial
of membership or privileges has been viewed as a wrongful
termination case.19
As mentioned previously, the preparation of this chapter
included review of the medical staff bylaws from five medical
centers. Under the heading of “Appointment to the Medical
Staff” one institution’s bylaws summarized it well for all of
them. Under the heading of general qualifications, the
“appointment to the medical staff is a privilege which shall be
extended only to professionally competent individuals who
continuously meet the qualifications, standards, and require-
ments set forth in this policy and in such policies as are
adopted from time to time by the Board. All individuals prac-
ticing medicine and oral surgery in the hospital unless excepted
by specific provisions of this policy, must first have been
appointed to the medical staff.”20
Credentialing and Hospital Privileging 315
The preceding statement is followed by a clause that only
physicians and dentists who satisfy the following conditions
shall be qualified for appointment to the medical staff:
• Are currently licensed to practice in this state.
• Are located (office and residence) within the geographic
service area of the hospital as defined by the hospital,
close enough to provide timely care for their patients.
• Possess current, valid professional liability insurance
covered from an insurance company licensed or approved
to do business in this state, in the amount of 1 million
to 3 million dollars, unless the board of trustees specifies
otherwise.
• Completion of a program that renders the person eligible
for board certification by an ABMS member board,
AOA, or ABOMS. For those appointed to the medical
staff after January 1, 2001, certification must be achieved
within 4 years of appointment.
• Can document their: (1) background, experience, train-
ing, and current clinical competence; (2) adherence to
the ethics of their profession; (3) good reputation and
character, including physical health and mental and
emotional stability; and (4) ability to work harmoni-
ously with others sufficiently to convince the hospital
that all patients treated by them at the hospital will
receive quality care.20
Initial appointment to a medical staff is usually granted on
a provisional basis for a period of 6 to 12 months and then
followed by a regular appointment for a period not to exceed
2 years. Reappointment to the medical staff is generally
granted at 2-year intervals. There are certain obligations for
practitioners when they accept an appointment to a medical
staff. Of the medical centers surveyed, one of them outlines
these obligations as follows: (1) to abide strictly by the gener-
ally recognized Principles of Medical Ethics of the American
Medical Association or by the Code of Ethics of the American
Dental Association; (2) to comply with the medical staff’s
bylaws, rules, and regulations; department requirements; and
all hospital policies, procedures, and requirements, in addition
to all applicable federal and state laws and regulations; (3) to
provide patients with continuous care and supervision consis-
tent with accepted standards of practice; (4) to accept com-
mittee and consultation assignments and perform such medical
staff, committee, department, or hospital functions for which
the practitioner is responsible by appointment, election, or
otherwise; (5) to provide emergency services, take calls, and
provide consultations in accordance with department require-
ments unless specifically exempted; (6) to consider as part of
the practitioner’s responsibilities the education of medical
students, house staff, nurses, and allied health personnel.21
■ ADVERSE ACTION
Whenever the activities or the professional conduct of a cre-
dentialed practitioner are considered to be lower than the
standards of the medical staff, or are disruptive to the routine
and normal operations of the hospital, corrective action may
be taken. All complaints against a practitioner and requests
316 SECTION III ■ Practice Management
for corrective action are normally submitted in writing to the
chief of professional services of the institution. Of course,
there must also be substantial evidence included to support
such a complaint, and then the case is reviewed by the officers
of the medical staff. After investigation, further action may
include dismissal if the complaint is without merit, corrective
action, or disciplinary action, if warranted. Any recommenda-
tions for reduction, suspension, or revocation of clinical privi-
leges or for suspension or expulsion from the medical staff
entitles the affected practitioner to the procedural rights pro-
vided within the bylaws of the medical staff.
If a surgeon is denied privileges with his or her initial
application, the medical staff board will notify the individual
in writing of the decision. Usually the board will cite voids
and deficiencies of the provider’s application and make recom-
mendations for improvement and timely resubmission of the
application. If a surgeon has been decredentialed as a result of
some adverse activity, he is entitled to challenge the decision
and receive fairness of review under the bylaws of the institu-
tion. This is often called “due process.” Legal courts will not
usually involve themselves in hospital internal affairs unless
there is a suit involving actions deemed to be arbitrary, capri-
cious, out of compliance with bylaws, unfair, in bad faith,
unfairly discriminatory, or bias on the part of a committee or
individual members.19
The basic element of due process is impartiality. The
surgeon in question has the responsibility to obtain a review
of the charges and substantiate that there has been noncom-
pliance with the bylaws of the hospital. Without using legal
threats, the surgeon should challenge the committee’s deci-
sion and clarify that he or she is only asking for equal treat-
ment under the bylaws. In dealing with hospitals and medical
staffs, attorney Arthur Chenen recommends following these
guidelines:22
• Do not underact. Seemingly minor adverse actions may
be reported to state boards or the National Practitioner
Data Bank and be interpreted more harshly by other
hospitals, institutions, or agencies.
• Know your hospital bylaws. This cannot be emphasized
enough.
• If you have made a mistake, admit it.
• Get an objective opinion. Find an unbiased educated
individual to evaluate the facts before you initiate legal
action. This means a surgeon, not a lawyer.
• Know when to compromise. Make sure that legal action
is worthwhile for more than just egotistical reasons.
• Consult a lawyer early, but do not litigate early.
• Do not start a fight that you cannot finish. Due process
and bias cases are the financial responsibility of the
individual. Participants should have a reasonable esti-
mate of the costs of entering litigation and an under-
standing of individual responsibilities and liabilities. Do
not forget to count nonmonetary costs: possible adverse
publicity, lost productivity as a result of time away from
the office, loss of referrals, and personal time and
stress.
Court cases in the medical staff area generally deal with
either the reasons a hospital may use to exclude or terminate
a practitioner from the medical staff or the procedures used to
accomplish the exclusion or termination. Cases also address
whether the hospital may be liable for credentialing of prac-
titioners or for the actions of medical staff members.23 Depend-
ing on state law, there may be immunity for hospitals and
medical staffs for credentialing and other peer review activi-
ties. Generally, this immunity is limited to authorized actions
taken in the course of peer review and requires that the actions
have been taken in good faith, in the absence of malice.
At the federal level, the primary law dealing with peer
review is the Health Care Quality Improvement Act
(HCQIA). This law was intended to provide immunity for
participants in the peer review process. The HCQIA also
established the National Practitioner Data Bank for collection
of the professional review actions involving physicians and
other health care providers and for periodic disbursement of
this data to querying hospitals and agencies.
■ SUMMARY
OMSs play an important role in the delivery of comprehen-
sive medical care in the hospital environment. The heritage
of oral and maxillofacial surgery is based on the pursuit of
those strong, talented, and high-spirited leaders of the past.
“They sought knowledge and skill beyond the dental doctor-
ate and built the science-art surgical base in academic and
hospital training programs. Every year of our history has
brought challenge and change . . . (and) . . . hundreds of sur-
geons . . . and administrative associates have contributed to
the planting and nurturing of our specialty.”23 The unique
situation of the OMS raises special issues with regard to
medical staff membership and privileges. Success in this arena
requires thorough knowledge of all the rules and regulations;
demonstration of “training, competency, and ability” within
the specialty; and equality with medical colleagues.
It is certainly appropriate to be thankful to those who have
persevered before us in advancing the specialty of oral and
maxillofacial surgery. It is also appropriate for the current
membership to persevere for those who are to follow. Quoting
the words of President Theodore Roosevelt, “every man owes
a portion of his time to the betterment of the profession to
which he belongs.”24
REFERENCES
1. Donlon WC: A right to the privilege, AAOMS Forum 36:2-9,
1992.
2. Kethley Jr JR: Credentialing in maxillofacial trauma: establish-
ing a full scope practice in the hospital and office (AAOMS
annual session, Seattle, Sept 1997), J Oral Maxillofac Surg
55(suppl):5, 1997.
3. Joint Commission on Accreditation of Healthcare Organiza-
tions: Medical staff. In 1994 Accreditation manual for hospitals,
Oak Brook Terrace, IL, 1994, JCAHO Department of
Publications.
4. AAOMS Member Alert: CoP final rule retains OMS H&P
reference, AAOMS Publications and Communications, Dec
2006.
 CHAPTER 18 •
5. Commission on Dental Accreditation: Standards for advanced
specialty education programs in oral and maxillofacial surgery,
Chicago, 1993, CODA.
6. Joint Commission on Accreditation of Healthcare Organiza-
tions: 1998-99 Comprehensive accreditation manual for ambulatory
care, Oak Brook Terrace, IL, 1998, JCAHO Department of
Publications.
7. American Dental Association, Council on Dental Education
and Licensure, Committee on Anesthesia: Guidelines for use of
sedation and general anesthesia by dentists (draft proposal), Chicago,
IL, 2006, ADA.
8. AAOMS Correspondence to Council on Dental Education and
Licensure, Feb 2007, American Dental Association.
9. Donlon WC: Credentialing and privileging for oral and maxil-
lofacial surgeons. In Fonseca RJ, Marciani RD, Turvey TA,
editors: Oral and maxillofacial surgery, vol 1, New York, 1998,
WB Saunders.
10. American Medical Association: Statements on delineation of hos-
pital privileges, Chicago, 1991, AMA Department of Hospital
Medical Staff Services.
11. AAOMS/ABOMS: Statement on the training and practice of oral
and maxillofacial surgery, Rosemont, IL, 1991 AAOMS.
12. Joint Commission on Accreditation of Healthcare Organiza-
tions: Comprehensive accreditation manual for hospitals: the official
handbook, Oak Brook Terrace, IL, 2007, JCAHO Department of
Publications.
13. Roberts JS: The JCAHO credentialing process. In Langsley DG,
Stubblefield B, editors: Hospital privileges and specialty medicine,
ed 2, Evanston, IL, 1992, ABMS.
14. Ball JR: Credentialing, privileging and performance: view from
the 90s. In Langley DG, Stubblefield B, editors: Hospital privileges
and specialty medicine, ed 2, 1992, Evanston, IL, ABMS.
Credentialing and Hospital Privileging 317
15. Harpster MH, Veach MS: Risk management handbook for health
care facilities, Oak Brook Terrace, IL, 1992, JCAHO Department
of Publications.
16. Jessee WF: Assessing, monitoring, and improving medical prac-
tice in the hospital. In Langsley DG, Stubblefield B, editors:
Hospital privileges and specialty medicine, ed 2, Evanston, IL, 1992,
ABMS.
17. Joint Commission on Accreditation of Healthcare Organiza-
tions: Comprehensive accreditation manual for hospitals: the official
handbook, Oak Brook Terrace, IL, 2007, JCAHO Department of
Publications.
18. Langsley DG: The use of specialty and subspecialty credentials
for hospital privileges. In Langsley DG, Stubblefield B, editors:
Hospital privileges and specialty medicine, ed 2, Evanston, IL, 1992,
ABMS.
19. Fraiche DD: Legal aspects of clinical privileges delineation.
In Langsley DG, Stubblefield B, editors: Hospital privileges and
specialty medicine, ed 2, Evanston, IL, 1992, ABMS.
20. Forsyth Medical Center: General bylaws of the medical-dental
staff: appointment, re-appointment, and clinical privileges,
Winston Salem, NC, 2005.
21. Wake Forest University Baptist Medical Center: Bylaws of the
medical staff: obligations of appointment, Winston Salem, NC,
2006.
22. Chenen AR: Hospital privileges: speak softly, but carry a big
lawyer, Conn Med 50:541, 1986.
23. Hopkins JP: Medical staff law and important legal cases. In
Cassiot CA, Searcy VL, Giles CW, editors: The Medical staff
services handbook: fundamentals and beyond, Boston, 2007, Jones
and Bartlett.
24. Alling CC et al: Building of the specialty of oral and maxillofa-
cial surgery, J Oral Maxillofac Surg 47(10):foreword, 1989.
CHAPTER 19
MARKETING THE
About 8 years ago, the author had the honor to author a
chapter on marketing the oral and maxillofacial surgery
(OMS) practice in Dr. Fonseca’s text series. He considers it a
further honor to once again be asked to update this marketing
chapter. Believe it or not, a lot has changed since the original
writing of this chapter. Huge paradigm shifts have occurred in
our profession.
• At the time of the original writing, most oral and maxil-
lofacial surgeons were slaves to referring dentists; now
many referrals are a virtue of participating (or lack
thereof) in insurance plans, HMOs, PPOs, etc.
• Eight years ago, most oral and maxillofacial surgeons were
involved in the considerable practice of orthognathic
and temporomandibular joint (TMJ) surgery, and now
(for various reasons) many of us shun these procedures.
• Eight years ago, most oral and maxillofacial surgeons
took on-call duties at local hospitals, and now (unfortu-
nately) many oral and maxillofacial surgeons have aban-
doned this responsibility and privilege.
• Eight years ago, dental implants were popular, but now
they represent a virtual “new age” in our profession.
• Eight years ago, this author practiced full-scope OMS,
and now his practice is limited to cosmetic facial
surgery.
• Eight years ago, having a website was a cute means of
having some identity. Today it is not only the main way
that society communicates and seeks information, it is
essential for marketing, patient education, and registra-
tion and is expected by the public.
• Eight years ago, the Yellow Pages were the mainstay of
marketing; today the Internet has displaced telephone
book advertising. We have gone from “let your FINGERS
do the walking” to “let your FINGER do the walking.”
• Eight years ago, mailing panoramic radiographs to and
from referring sources was the standard; today digital
imaging and electronic transfer of images is replacing
hard copy transfer.
• Eight years ago, cellular telephones were an upper class
luxury; today one must post “turn off your cell phone”
signs in the office so as not to be continually
interrupted.
• Eight years ago, this chapter discussed mailing newslet-
ters to referring sources, and today an e-mail blast is a
more popular option.
318
ORAL AND MAXILLOFACIAL
SURGERY PRACTICE
Joseph Niamtu III
Considering all of these changes, there is a new spin on
some parts of marketing our wonderful profession. This chapter
will have a lot of repeat from the previous chapter because
some of this material is timeless. Other information has been
updated, changed, or refuted to reflect the contemporary
changes of oral and maxillofacial surgeons.
To devote a chapter to marketing in such a comprehensive
oral and maxillofacial textbook is indicative of progress. This
progression has been made on many fronts. First and foremost
is the progress made within our profession.
Whether in the military or in sports, the first rule of com-
petitive strategy is to know your adversary. In the consider-
ation of marketing the OMS practice, we too must realize the
adversarial barriers.
OMS occupies a realm in the public perception interposed
somewhere between that of dentistry and medicine. This fact
has shrouded our identity and services with an air of ambiguity
from the onset of the recognition of OMS as a specialty. This
ambiguity of services rendered and the public’s lack of aware-
ness of our training and education presents a further market-
ing barrier. Finally the voracious and aggressive increase of
our scope of practice and procedures has increased exponen-
tially, leaving the consumer confused about what exactly we
do or used to do.
The aforementioned situations cumulatively have held us
back in the marketing and public awareness arena. Ask the
man on the street what a plastic surgeon does and he will
likely give you an accurate description. That same question
posed to the same person about OMS will more than likely
not be representative of the scope of services we perform. This
public appreciation of scope has, in the author’s opinion, not
increased proportionately, even though our national organiza-
tion has made great strides to publicly convey our training.
Entering this discussion with these principles in mind
facilitates and obviates the barriers we face and the direction
we, as a specialty, must pursue.
■ WHAT IS IN A NAME?
The majority of dentists graduating today receive a DDS
degree, which implies surgical expertise to the public. The
more descriptive DMD degree is of progressive thinking and
public understanding. The specialty of OMS was in line for a
name change for a long time. As a result of the politics
of teaching institutions, many reputable OMS residency-
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
training programs were forced to pursue nondentoalveolar
procedures in a surreptitious manner. As a result of our excel-
lent training in general anesthesia, many programs were able
to perform some of the advanced procedures within their own
clinic because of fear that other competing surgical specialties
may protest. This proved, and in some programs still proves,
to be a double-edge sword. On one hand, we were being
trained in trauma, cosmetics, etc., but on the other hand, this
secretive approach breeds the mind-set that propagates ano-
nymity. For years we would not mention the word cosmetic
because of fear of noncoverage by third-party carriers or criti-
cism from other surgical specialties.
Some very progressive leaders in our national organization
foresaw the need to change these preconceived limitations
and levied for a name change within our specialty. Unbeliev-
ably, they met with resistance; however, history led us into
the new profession of OMS.
The good news of the name change was that it was cer-
tainly more descriptive of our scope and gave us pride in pursu-
ing procedures and techniques that were sometimes done in
the after-hours clinic. The bad news is that the term maxillo-
facial is not understood by the general public and, in the
author’s opinion, has further masked what exactly it is that
we do. The author predicts a name change by our specialty to
“oral and facial surgery” within the next decade.
On top of this, our public perception is further hampered
by the fact that much of what we do is painful, inconvenient,
expensive, and without a tangible physical appreciation for
the patient. Third molar surgery would be a perfect example
of this concept.
■ ACADEMIC MARKETING
Marketing is a popular major for many college students, and
in the first-year courses, they learn the basics of the profession.
Because much confusion seems to exist among health care
providers on what exactly is the difference between market-
ing, selling, and advertising, it is appropriate to review the
textbook definitions in Marketing 101.
Selling is concerned with the plans and tactics of trying to
get the customer to exchange what they have (money) for
what you have (goods and services).
Marketing is primarily concerned with the much more
sophisticated strategy of trying to have what the customer or
patients want.
By these definitions, one can clearly see that selling focuses
on the need of the seller, whereas marketing focuses on the
need of the buyer. Selling is concerned with the seller’s need
to convert their product or service to cash, whereas marketing
is satisfying the needs of the customer.
A marketing-oriented office provides value-satisfying
service that patients want. It also provides not only the generic
product (in our case, surgery), but also important is how the
service is made available. Extended hours, payment plans,
patient insurance assistance, modern facility, state of the art
procedures, and painless treatment are just a few of the ways
this service is made better.
319
■ LEARNING FROM BIG BUSINESS
In the nineteenth century, the United States became a
production-oriented economy and, over the past century, has
shifted to a consumption economy. The energy and thoughts
of the business community were once devoted to developing
and improving ways of manufacturing. We now take our
ability to manufacture for granted; the emphasis has shifted to
a marketing orientation, and the energy and thought start
with the customer (or in our case, the patient).
After the end of World War II, the General Electric Co.
pioneered the marketing concept in industry. The marketing
concept is described as “a way of life in which all resources of
an organization are mobilized to create, stimulate and satisfy
the customer and profit for the owner.” If one truly under-
stands this paragraph, they can begin to understand what
marketing is really all about.
Corporations speak of the four Ps of marketing. They are
product, price, promotion, and place. Product refers to making
sure that the product is the right one and of superior quality.
Price refers to establishing a price that makes the product as
attractive as possible and still maintains a profit. Promotion is
simply communicating with one’s clients or potential clients.
Place refers to putting the product where it can be most effec-
tively used.
The correct analysis and mix of the four Ps are important,
and marketing experts further maintain that a marketing
leader must:
1. Determine the nature of changes in the market.
2. Identify and cultivate customers for the company’s
existing or potential services.
3. Meet the needs and wants of customers or potential
customers.
4. Maintain a profitable position.
All of these factors are applicable to our profession. One
merely needs to supplement the word patient for customer or
client.
Number two in the above list is very often overlooked.
Historically, there have been many changes in the fee-for-
service practice in medicine and dentistry. Before insurance
coverage, the patient understood their obligation for respon-
sibility for health care costs. With the advent of health insur-
ance plans, the burden of responsibility, at least in the mind
of the patient, became the responsibility of the doctor. With
the advent of exponentially increasing medical technology,
the price of health care soared and became beyond the reach
of most self-pay patients. Physician’s and hospital’s fees became
obtrusive, and cost-cutting measures were instituted with
shifts toward less hospital time and generalized cost contain-
ment. Managed care then entered the scene and has caused
profound changes in our profession. There is now a shift to
having primary care physicians triage patients, and surgeons
are looking for ways to provide their services without the time
and monetary expense of hospitals.
Physicians who had the ability to see these trend shifts were
able to adjust their marketing and business strategies to meet
320 SECTION III ■ Practice Management
the current need. Those who do not adapt may fail to thrive
in this managed market.
Anyone who has read about corporate marketing is familiar
with the concept of paradigm shifts. A paradigm is a model,
and the paradigm for marketing OMS practices has been the
same for years. Be a good physician, PR your referring sources,
and one would prosper. We are now in the midst of a paradigm
shift. With managed care, larger practices with multiple
locations have positioned themselves to be attractive to the
managed care plan of large companies. Now many patients are
referred to a given surgeon, not because the general dentist
wanted to send the patient, but rather because they had to use
a participating specialist. Those surgeons who refuse to explore
managed care options may be driven out of business because
they have not anticipated this paradigm shift.
A commonly used example of the loss of business domina-
tion from paradigm shifts is the Swiss watch-making industry.
For hundreds of years, the Swiss dominated the making of
watches and timepieces throughout the world. The paradigm
for success was a mechanical product that was made from
complex mechanical manufacturing and assembly of labor-
intense intricacy. The Rolex chronometer wristwatch is an
example of the fine product produced under this paradigm.
The Swiss prospered and literally controlled the world produc-
tion of wristwatches. In 1968 the Swiss controlled 65% of the
world market in timepieces. They reaped 80% of the profit in
the timepiece industry and employed 65,000 employees.
Around 1968 a Swiss company invented the liquid crystal
watch and set up a booth at the 1968 World Watch Congress
in Switzerland and introduced their new technology. This
concept was staggering. The watch had no moving parts, did
not require movement or winding to function, and delivered
accuracy 1000 times that of the finest Swiss timepieces.
Although this timepiece technology was astounding, the
major Swiss watchmakers were indifferent and did not even
patent their own invention. Why? Because it did not fit their
paradigm for what a wristwatch should be. Two companies,
Seiko and Texas Instruments, did take notice, however, and
saw the old paradigm for timepieces go out the door. They
realized the potential of this new product and were able to
move with this new paradigm. The rest is, of course, history.
The Swiss workforce lost 50,000 employees and dropped from
80% of the market share to 10%. Today the Japanese domi-
nate the world timepiece market; they had virtually no market
share in 1968.
The point is that what works in marketing today may not
be effective in the future, and the ability to predict and adapt
is critical. Marketing is dynamic, not static.
Staying abreast of current technology is also important in
the paradigm model. The bread and butter of our profession
was once the extraction of carious teeth. It was only several
decades ago that multiple full-mouth extractions were common
on the office schedule of most oral and maxillofacial surgeons.
Today because of fluoridation and education, full-mouth
extractions have diminished rapidly to the point that some
dental schools have trouble finding denture patients. Having
four difficult impacted third molars removed simultaneously
was not common 40 or 50 years ago. With the advent of high-
speed drills, effective ambulatory anesthesia, and antibiotics,
this procedure has become the mainstay of most OMS prac-
tices. Anytime a single procedure dominates the well-being of
any business, its obsolescence could doom the business. The
insurance coverage of third molars may fall into disfavor or be
otherwise manipulated by insurance companies. We must, as
a profession, be aware of this possible paradigm shift for what
constitutes OMS.
Fortunately, our leaders have seen these caveats, and many
of our ranks are entering the arenas of implant surgery, cos-
metic surgery and other nontraditional OMS procedures.
All of the above underline the predictive thought for
medical marketing. It is not uncommon to find physicians who
are very averse to marketing in the form of advertising. These
physicians say that they do not market. This is such a fallacy;
we all present an image, and this is marketing. Some physi-
cians are actually doing negative marketing by having poor
staff and lack of policy while condemning an office committed
to excellence.
■ MARKETING THE ORAL
AND MAXILLOFACIAL
SURGERY PRACTICE
The author enjoys a mix of private practice and academic
environments. The phrase “Always be a teacher and always
be a student” drives many of our ranks to excel in both venues.
The author has written and lectured extensively on the subject
of marketing the OMS practice, and regardless of the com-
munity, state, or country, many physicians are in search of the
“secrets of marketing.” The delusion of these individuals con-
founds the author time and time again. Practitioners want to
know “what to do to get referrals.” Sometimes, despite a well-
prepared and well-presented course on marketing, participants
will confront the author at the end of the lecture and say, “all
of that is fine and well, but what is it that you really do to get
patients? Do you give holiday presents? Do you do lunches?
Do you need fancy imaging, etc.” These physicians have
missed the entire point. The correct answer is all of these and
none of these.
Marketing is not the act of giving something to receive a
patient on a one-to-one basis. Marketing is more of a mind-set
and a practice lifestyle. There are many successful practices
that spend tens of thousands of dollars on marketing events
and gifts, and there are just as many practices that thrive
without spending a dime on parties, gifts, etc. The latter prac-
tice focuses on two things: superlative patient care and simply
knowing how to say thank you.
In addition to the above examples, there are physicians
that do all the correct marketing, even employing professional
firms, yet have stagnant practices. These practices go through
the motions, but have poor leadership principles and staffs
that negate their marketing investment.
Successful marketing, as stated earlier, is a grass-roots level
of excellence that starts before the patient ever gets a foot in
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
the door. The bane of existence of any specialist in any disci-
pline is the reliance upon others for referrals. It is rare that a
patient sees a sign for OMS and drops in, whereas a Family
and Cosmetic Dentistry sign may cause people to walk in and
begin a relationship. If one follows a thriving practice, they
will see a constant trend of patients referred from sources other
than general dentists. If an OMS office provides a warm,
loving, and caring environment, patients of record and reputa-
tion will bring in as many or more patients than do primary
referral sources. It is usually at this point that a physician really
begins to feel and enjoy independence.
Getting to this point usually takes a number of years, but
can be greatly accelerated by attention to basic communica-
tion skills and common sense.
The grass-roots level, of which we spoke, must literally
permeate every aspect of one’s practice, and it must be stressed
that the staff is far more important in the spectrum of market-
ing than the physician. Most offices that are stressful and
unprofitable suffer from poor leadership. Most physicians have
no experience at human resource management and have accu-
mulated what knowledge they have from hard knocks. It is
shocking but correct to say that most employee problems are
the fault of the employer and not the employee. Leadership is
essential to make any team of individuals with a common goal
cohesive and effective. In the author’s opinion, 98% of the
problems that make practitioners dislike their jobs stem from
poor hiring and firing practices and the lack of leadership.
There can be only one leader in an office and that must be
the physician. Leadership cannot be confused with manage-
ment. One can delegate management and hire managers, but
again there can only be one leader, and leadership cannot be
delegated.
For the sake of comparison, let us envision two separate
practices. One practice is a thriving, progressive, profitable
practice that continues to grow. This office always seems to
be on the forefront of the profession, and when you walk into
this office, you are overcome with the energy of the staff. The
environment is modern, clean, bright, and friendly and
employs the latest technology. The physician and staff are
aesthetically presentable, and smiles and warmth abound.
When in the office for awhile, it becomes evident that the
office represents the leader. It is if he or she is “working at
home.” It is also evident that the physician has a passion for
his or her profession, and practice is a joy and a privilege. The
staff is cohesive; their careers seem enjoyable, and they work
as if it is fun. This office presents an image, and that image is
impressed upon the patients that are exposed to this environ-
ment. It seems to rub off on the patients, and they leave with
an enthusiasm for this staff. They sense the energy and the
warm, friendly treatment and are impressed enough to
comment to their friends and neighbors. Although they do
not look forward to surgery, they do not mind and may even
enjoy visiting the office. They enjoy being part of the energy
and enjoy the special attention that seems so rare in this fast-
moving technological era. The referring physicians and their
staffs have the same feelings about this office and are confident
321
that when referring a patient they will be thanked for sending
the patient to such a compassionate office. If a patient goes
back to a referring dentist and says that the OMS was expen-
sive and the surgery made them sore and the recovery was
extended but thanks for sending them to such a warm, caring,
and compassionate specialist, megamarketing has been accom-
plished. This is never a coincidence; it is the finality of great
effort and attention and detail. It is a result of the pursuit of
excellence, based on the principles of leadership and policy.
Let us now contrast this office with one of mediocrity. This
office may be right next door to our previous example, but
always seems to be “chasing its tail.” The office does not glow
and is unkempt. The staff is stressed and bickering. The physi-
cian and the staff do not convey an aesthetic image and seem
to have a goal of reaching 5:00 pm. Confusion and happen-
stance seem to rule, and there is an obvious lack of organiza-
tion. The general atmosphere seems tense and rushed, and fun
seems to be the last thing that anyone is having. The entire
experience is reminiscent of old-fashioned dentistry. The staff
turnover is high, and the future of health care seems pessimis-
tic to these folks.
Although the above contrasting examples are fictitious, we
all can probably relate to a real-life example of each scenario.
We must ask ourselves what exactly it is that makes such a
difference. Knowing the answer to this question illuminates
the principles of successful marketing. These are again leader-
ship and human resource skills.
■ WHAT IS YOUR VISION?
The very first principle to discuss is vision. There are very few
successful people in any walk who achieved success by chance.
Virtually everyone who has achieved success and professional
contentment is a visionary. A person must have a clear idea
of their goals and a plan for approaching them. Without this,
chaos will rule. If asked, any oral and maxillofacial surgeon
should be able to state their vision or guiding principles and
their end point. This should also be second nature to the staff;
after all if you as a leader do not have a vision, then how can
you expect your staff to have clarity on where you are going
as an office? This vision must be communicated with the staff
and constantly reinforced. If this is not done, a cohesive team
cannot be built. It sounds trivial, but it is the single most
important factor in beginning a journey to excellence. It is
said that excellence is a journey, not a destination. In other
words, there is no finish line; improvement and superlative
patient care and the love of what you do are the dividends. If
while reading this text you cannot immediately stop and write
down your particular vision, then you should stop reading
(and start writing your vision) because it is the first rung of
the ladder to excellence. By the same token, if you and your
staff are not in the pursuit of excellence, then you should send
your patients elsewhere so that they may receive the best care
available. Obviously, this sounds drastic, but underlines the
point.
A vision must be practical, ethical, and attainable; have a
time frame; and be modifiable to bend with the curves of life.
322 SECTION III ■ Practice Management
The vision of the author has been to: (1) build a large group
practice that is enjoyable to both owners and staff and to serve
patients with a warm, loving, and compassionate environ-
ment; (2) pursue technical excellence and to stay abreast of
the forefront of our specialty; (3) become financially indepen-
dent and serve those less fortunate with the ability to obtain
our services through community work; (4) become a well-
known entity for going out of the way to better provide for
patients and referring offices; and (5) to have fun in the
pursuit of excellence in OMS.
After one develops a clear vision, the next critical step is
to assemble a team of individuals capable of carrying out this
vision. In any major team sport, tryouts are given, and the
leaders search for certain critical attributes to best serve the
effort. The vision is clear; it is to win. Can you imagine a team
that merely selected its players without tryouts? They would
never win because the right person for the right position
would be all too random. With this in mind, it becomes
obvious why some practices fail to win; the selection process
is random.
Selecting the proper employees is a skill and can evade
even the largest of businesses. There are scientific statistical
methods for selecting the proper person for a job; however,
the real answers are simple when applied to real life. For the
sake of comparison, we will call a perfect employee a 10 on a
1 to 10 scale. In most progressive practices, a 7 or less is unac-
ceptable. If a physician can surround themselves with 9s and
10s, marketing can be as easy as showing up for work. Because
the caliber of employee is paramount and usually directly
proportional to the success and stress level of any practice, the
importance is obvious.
■ HIRING AND FIRING
Anyone who thinks that this topic is inappropriate in a mar-
keting chapter already has serious misconceptions. Inevitably,
when one closely examines the details of a successful OMS
practice, exemplary hiring and firing practices exist. The con-
verse is true for poorly run or unsuccessful stress-ridden prac-
tices. For the sake of comparison, the author will continually
compare the details of two practices. One practice is profit-
able, user friendly, energetic, and sets new standards for the
community and has a physician and staff that enjoy their
careers.
The other practice withers on profit, has a frustrated staff
and physician, does not experience sufficient growth, has high
staff turnover, and just is not fun to work for.
By contrasting the factors that differentiate these two prac-
tices, we can gain tremendous insight to some of the most
common marketing problems. It is not going out on a limb to
make two important statements. Most problems that are
encountered in a practice concerning marketing and commu-
nication can in some way be directly attributable to the hiring
and termination policies of the practice. Statement number
two is the fact that the extent of the leadership of the physi-
cian will directly affect the policies or lack thereof in the office
and will contribute to the employee relations problems. Most
employee relation problems are the fault of the employer, not
the employee.
One of the inherent problems that have, for a long time,
affected professionals in all branches of health care is the
dearth of business courses offered to the physician in his or
her preprofessional training. One of the thrusts of today’s
medical and dental school curricula is the inclusion of busi-
ness and practice management courses. Even in the most
progressive didactic environments, this topic is usually too
little too late.
A compounding modifier to the above is the fact that
medical and dental practices have traditionally evolved as
independent, closed-circuited, small business models that
have been resistant to outside consultation or change of struc-
tural and managerial paradigm. This has created a very inbred
system of strong independence, but little thrust toward inter-
dependence. Although there certainly are positive points
associated with this structure, it fails to adapt to changing
paradigms, and because of this, physician’s offices tend to be
trapped in a whirlpool of poor management, communications,
and lack of adaptability. Inflexibility in this arena, in the
author’s mind, has led to our inability to predict the current
managed care crisis. Cost containment and efficiency issues
should have been predicted and dealt with a decade ago,
instead of now. The ability to foresee and adapt to change
is essential to succeed in any facet of business, including
medicine.
The other component that has crippled the business of
private practice surgery, in the author’s opinion, is the failure
to pay attention to the trends of corporate America. We
have been so steeped in autonomy that we simply have
ignored the changing trends of big business. Corporate
America approaches management strategies with the same
statistical scientific scrutiny that we afford our surgical litera-
ture. There exists a wealth of knowledge on human resources
and marketing that has basically been ignored by health care
providers. It is usually only through consultants that we gain
exposure to this information. Because of this, we are currently
reinventing the wheel, which increases stress levels and
decreases efficiency. It is a safe bet that the successful prac-
tices that we contrast already have an understanding of the
above.
■ PROFESSIONAL CONSULTATION
The term consultant has been mentioned several times already,
and this is an appropriate time to expound on this now. We
all seek advice from outside sources, especially in situations
where that person has a higher level of knowledge pursuant
to what we are doing. Most oral and maxillofacial surgeons
would not take apart their own engines if their car stops
running nor would they consider taking the transistors out of
their TV if it falls into disrepair. This example can be carried
out ad nauseam, but underlines that our lives revolve around
professional advice. Therefore, it is difficult to believe that so
many physicians are resistant to obtaining outside consulta-
tion. Our autonomy sometimes gets in the way. Anyone that
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
runs a practice has very strong emotions and opinions about
the way the practice runs. When you add partners to the
scheme, these emotions and opinions increase logistically. It
is very difficult to make prudent decisions in the face of emo-
tional issues. Anyone who has made decisions to institutional-
ize a parent, euthanize a pet, terminate a marital relationship,
or deal with similar issues will testify that it is very hard to
make these decisions because emotions cloud the clarity of the
issue. In these instances, we usually turn to those we trust to
separate the issue from the emotions.
This emotional attachment to our practices often causes
warped perceptions of the way the practice runs. To make
rational decisions, one must have the big picture. A good
metaphor of this situation would be a person enjoying a scenic
boat ride along a beautiful river. The person in the boat is
overcome with the beauty of the trees, water, and wildlife.
The boat ride is absolutely wonderful, except there is some-
thing very ominous happening. There is a person in an air-
plane that is flying over this boat, and they can see more of
the picture. The person in the airplane can see that 10 miles
downriver is a huge waterfall that will kill everyone currently
enjoying the boat ride. The person in the boat is disadvan-
taged by not seeing the entire picture, and the person in the
airplane can avert disaster by alerting the captain of the boat
to the impending danger. This metaphor illustrates the role
that a consultant can play in your practice. Given the level
of quality that we all seek in everyday life, it is unfathomable
that so many physicians are resistant to these ideas. The
author has experienced, in numerous practices, the awakening
of the entire office by qualified consultants. Adapting an old
adage, a physician who refuses to seek business advice has a
fool for an advisor. Another pitfall that the author experiences
is “pseudoconsultation.” This involves taking advice from the
wrong people. Frequently, surgeons turn to accountants or
attorneys for this type of advice because these individuals are
familiar with the practice. Most of these professionals have
little practice management experience and often prove to be
poor advisors. A frequent excuse for not seeking outside assis-
tance is cost. Some physicians say that they quite simply
cannot afford it. The author is on record as saying that you
quite simply can afford it.
Successful general dental practices have multiple hygienists
doing recall visits. The dentist may pay these hygienists $200
per day. This can be a significant expense. These physicians
may make a clear profit of $1000 per day after paying the
hygienist. Many dentists never hire a hygienist because they
“can’t afford one.” Again how can they afford not to? A quali-
fied practice management may cost up to $10,000 for several
days of work. If these people can institute changes that increase
your accounts receivable, billing, coding, and staff relations
by several percentage points, the payoff in profit and stress
reduction may be tenfold. Yet why are so many physicians
resistant to this concept? If a physician is truly interested in
excellence, he or she must take the first step. For many people,
they cannot ever commit to take that step. As stated earlier,
if someone is not about excellence, then they should send
323
their patients to another oral and maxillofacial surgeon so
they can have the best care.
■ EMPLOYEE RELATIONS
Because many new practitioners will be reading this chapter,
the author will begin at an elementary level and progress. The
basis of the chapter is paramount to all employers, regardless
of the time in practice.
There exist universal situations that enhance or detract
from any business, and choosing the correct employees is para-
mount, regardless of the type of business. This applies espe-
cially to all of the service-oriented businesses, of which health
care happens to be one. Unfortunately, many physicians never
grasp the concept that their business is based around service
and therefore struggle and endure unnecessary stress, whereas
their colleagues who do understand the concept have fulfilling
and profitable practices.
In any service-related industry, it is usually the level of
service that sets businesses apart. For instance, if you had to
ship one of your most prized possessions somewhere overnight
and were ultimately concerned about its safe and timely
arrival, would you choose Federal Express or the U.S. Postal
Service? Most people would choose Federal Express because
of the perceived level of customer service on behalf of Federal
Express and the lackadaisical attitude often attributed to gov-
ernment employees. Service of one’s customer or patient base
is the key to success. A physician may be a genius and the best
surgeon in a given area, but if the staff is abusing patients, the
practice will not prosper. On the other hand, a very mediocre
physician can be elevated to hero status by a staff that nurtures
their patients. Most physicians are clueless on correct hiring
and firing concepts, and the ones with experience have often
earned their knowledge through hard knocks. When the
author lectures to large groups of physicians in any locality,
employee relations always occupies one of the top three
enumerations of practice stress.
In the past, poor hiring and termination practices may have
only meant increased employee turnover and physician stress.
In today’s litigious environment, improper human resource
skills frequently lead to lawsuits. Wrongful discharge, sexual
harassment, discrimination, and other employment-related
litigation is on the rise. For a suit-prone employee, the ability
to win a hugely unreasonable settlement holds much better
odds than a lottery ticket. Sexual harassment suits have been
settled for millions of dollars for innocently intended gestures
or actions. This is a frank reality of modern employment law
and circumstances. This is the wrong arena in which to learn
by mistake. Suits for sexual harassment are not covered by
malpractice or umbrella insurance and are the responsibility
of the defendant. Guilty or not, subsequent publicity can be
very damaging to the morale and reputation and pocketbook
of the physician. Because most OMS offices involve a male
physician with a female staff, the author strongly advises all
new practitioners to thoroughly gain information about local
and local employment laws.
324 SECTION III ■ Practice Management
Initially a new oral and maxillofacial surgeon will more
than likely require a staff of at least three employees. The
American Association of Oral and Maxillofacial Surgeons
(AAOMS) recommends that two employees assist at surgery,
and someone needs to tend to the front desk and clerical
duties. Some new physicians may economize by using two
employees and placing the telephones on a recorder during
surgery; however, availability to your referring physicians is
compromised. There is no doubt that as soon as a physician
can afford adequate staff, he or she will enjoy a safer and more
efficient practice.
The easiest positions to fill are surgical assistants. There
exists a strong pool of dental assistants, nurses, surgical techs,
etc. As with any business, previous experience is preferable.
A seasoned assistant can actually teach many things to a new
physician. It is also preferable to hire an assistant who can also
obtain hospital assisting privileges. As with all positions,
a friendly, compassionate, presentable, mature assistant is
optimal. One potential problem of hiring new employees is
the age and experience levels of the applicant pool. This pay
and experience level is filled with young, inexperienced
females. Many of these people have little experience, and
their reliability and maturity levels may be insufficient to suit
one’s needs. In addition, this segment of potential employees
is often transient as a result of schooling, relationships, and
childbearing. The author has taken pride in hiring this type
of employee and watching them grow into an excellent staff
member. This, however, has been in the presence of superla-
tive staff members who had the opportunity to mold the new
employee into a polished employee. Hiring this type of person
without nurturing can lead to many employee-employer
difficulties.
The job of practice receptionist is a much more challenging
situation. This employee is literally the ambassador of the
practice and, more than any other employee, can add or
detract from the practice. This person is usually the first person
that gives an impression of the spirit of your practice. In many
cases, perspective patients call the office and are confronted
by many barriers. Pain, expense, inconvenience, apprehen-
sion, third parties, and lack of appreciation of services are just
some of the common barriers between physicians and their
patients. Many of these patients are “shopping around” to find
a caring and reassuring environment or the ability to tailor
finances. An exceptional receptionist will act like a magnet
bringing these patients to fruition, whereas a rude or noncom-
passionate person may distance them even more. This posi-
tion calls for multitasking, especially for the new physician
with a small staff. Besides the receptionist’s duties, this
employee must assist in coding, billing, insurance, accounts
receivable, and collections. All of these functions are as vital
to the success of the practice as the skill of the physician. This
position begs for a mature, experienced individual and will
command a higher salary. This is money well spent because
this person can literally help shape the future of the
practice.
WHERE TO FIND GOOD EMPLOYEES
This is a question posed by all businessmen and business-
women. Experience is very important, and the optimal situa-
tion is to hire someone that has worked in an OMS practice.
The author warns against hiring an employee from a col-
league’s office, unless it is discussed upfront with the neighbor-
ing physician. A new physician can count on intimidating
existing practitioners, and there is no need to start off in a
deeper hole.
Local dental societies usually have newsletters with
employment sections that can prove useful. The want ads in
the local area are a traditional means of finding help. The
author warns about placing anyone’s home telephone number
in the ad for applicants. It is not unusual to have many,
many calls at all hours of the day and night. The author,
instead, suggests a neutral address or P.O. Box to which
applicants can send résumés. If the new physician does not
have hiring experience, it is suggested that a qualified party
assist in the interview process. It is important to hire someone
with the correct “fit,” who will augment the personality of
the physician. Many employment situations are a roll of the
dice, but the author cautions hiring someone that conveys
feelings of suspicion. This is no place for a demure introvert.
Hire someone with good eye contact, a good smile, and an
enthusiastic attitude. An employee that “glows” is a keeper
and will infect the other employees and patients with that
glow.
As the practice prospers, additional employees will be
added. It is not unusual for an OMS practice to have three to
six employees per physician. As we will allude to later in this
section, many offices believe that they are understaffed, when,
in reality, they are actually overstaffed.
New physicians are frequently at a quandary about starting
salaries. By surveying colleagues in the general dental com-
munity, one can establish a scale for given positions in a given
community. Additionally, many of the “throwaway” dental
periodicals offer yearly regional staff salaries and regional
fees.
One of the major incentives to work for many people is to
obtain insurance benefits. In health care professions, it is
pretty much a given to offer health insurance as a benefit.
Although there are many means of doing this, some of the
most common are as follows:
Many companies offer group health plans at a substantial
savings, whereas other employers give their staff a monetary
sum for the employee to use for the plan of their choice.
Because many employees may have coverage from spouses,
they may not need all the benefits that another employee
would. So-called “cafeteria plans” present a menu of options
that employees may choose from and are a popular option.
Other benefits include sick leave, holidays, uniform allow-
ance, and retirement benefits. Most physicians have pension
and profit sharing plans and therefore are required to match
funds for employees. This is a tremendous benefit and is often
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
overlooked. An employee with longevity can save thousands
of dollars in 401(k) plans or similar vehicles. This benefit must
be fully explained to be appreciated and extends the gift of
ownership to one’s staff.
Let us now direct our attention to the actual art and science
of hiring and firing. If there is one element of running a busi-
ness for which most physicians are unprepared, it is finding,
keeping, and terminating employees. Almost every seasoned
practitioner bears some emotional scar from improper han-
dling of employee issues. Many in our ranks have been parties
to lawsuits for violating the most basic tenets of employment
procedures. Enumerating several commandments of hiring, it
is important to discuss some absolute basics. Many of these
principles probably existed in the marketplaces of ancient
Rome, yet millions of bosses make these mistakes 2000 years
later.
The author strongly believes that it is an absolute infrac-
tion to hire spouses or family members as employees. Nepo-
tism will at some time cause employee problems. The author
has lectured all over the country on this subject and is often
met with resentment for stating this opinion. It never fails
that at the end of a lecture a physician or spouse will confront
the author in stern disagreement. The author’s response is that
there are always exceptions to the rule, but he is aware of
countless problems involving family. This is especially difficult
for partners or other employees because preferential treatment
may be perceived. In addition, the spouse may have the
“coach’s son syndrome” and apply stresses that are unneces-
sary. There is no doubt that it is difficult for a partner or
manager to reprimand one’s spouse, and if push comes to
shove, it is rarely the other person who must leave the prac-
tice. The author has observed many state of the art practices
over the past 20 years, and it is rare to find an exceptional
practice with family members as employees. Two exceptions
that exist are having family help in the very inception of the
practice as a cost-savings issue or casual summer employment
for odd jobs.
On the subject of nepotism, it is also an unwise practice
to hire relatives of current staff. The same pitfalls apply, and
many embezzlement schemes have involved this type of
situation.
Although it appears painfully obvious, professional
physician-employee relationships should stay just that. In this
era of sexual harassment, even the most benign of gestures can
be grounds for a successful suit. The author is aware of multiple
cases throughout the country, involving very expensive and
embarrassing outcomes for a surgeon. The author is aware of
suits brought for telling off-color jokes, inappropriate body
contact that was a “back rub,” and commenting on an employ-
ee’s attire or physical traits.
Another common violation is the temptation to manipu-
late monetary funds. Some physicians may pocket cash that
comes across the front desk and believe that it is untraceable.
Always remember that if a staff member witnesses a physician
evading taxes or doing anything illegal, he now has a partner.
325
If the physician can steal cash and no one knows, then why
should not the employee also steal?
A physician spends as much or more time with staff than
they do with his or her family, and there exists a temptation
to bare one’s soul. The author cannot stress enough the need
to always keep some distance from the physician’s private life
and what the employee knows or hears. The author is familiar
with several exceptional surgeons who were dragged through
the mud by a terminated and disgruntled employee. Never
underestimate the diabolic nature of a scorned employee. Like
a nasty divorce, they will use any weapon of destruction, so
do not provide them with ammunition.
Let us get back to hiring and discuss the interview process.
There is a true art in being a good interviewer. This involves
the art of listening. Listening not only to what the employee
says, but being able to read between the lines as to what the
employee represents. We will elaborate on this later.
First of all, the dress and demeanor of an interviewee is
important. Given the fact that most people are at their best
in dress and behavior at an interview, it is usually safe to
assume that what you see is the best you will ever see. If dress
or demeanor is inappropriate at an interview, it will only go
downhill.
The author believes strongly in hiring bubbly, enthusiastic
employees, and if an applicant does not smile and show strong
eye contact, they are usually a poor choice.
An additional caveat is an applicant that speaks negatively
of previous employers. This should be a severe warning, espe-
cially for individuals who claim to be “victims.” There is little
doubt that you will be the next bad guy on their list.
As stated earlier, experience should be high on the list of
employment attributes. Training someone to do a job is okay,
but for a new physician, it merely adds additional stresses. It
is better to hire a “teacher” than a “student” for the new physi-
cian. Interviews need not be exhaustive and should be stan-
dardized. In short you have two people sizing each other up.
Do not forget that the applicant is also interviewing you as a
boss, and when an employee resigns, they are effectively firing
you as a boss. It is a two-way street. One good question to ask
is what the applicant liked or disliked about their previous job.
This can extract key information about how they may inter-
face in your office. It is important to know if they can meet
your standards in terms of overtime and Saturdays, etc.
The next most important thing is to be able to relate your
vision and the goals of your practice. You must actually present
written documentation of who you are, where you are going,
and how you plan to have this applicant assist your journey.
Many physicians do not have these guiding principles in
writing. How can an employee relate to goals that are nonex-
istent? Again you should provide this applicant with his or
her job description and discuss it in detail. If you desire an
exceptional practice, you need to employ exceptional people.
If you do not have written job descriptions, you must settle
for mediocrity. The author suggests that the physician make
an audiotape or videotape containing the guiding principles
326 SECTION III ■ Practice Management
and visions of the practice. This will standardize the interview
process and simplify this task.
If you have properly defined your goals and visions, you can
effectively ask the employee if they want to play on your team
and follow your rules. If you have not defined the rules of the
game, then how can you possibly expect the employee to play?
The author has presented the rules of the game to applicants,
and they stated that they could not comply with our expecta-
tions. This employee has done both of us a tremendous service
because it may have been months of frustration before the
employee quit or was terminated. The point is that if we did
not have the job description and rules of the game defined,
then we could not have gained this information.
Employee references can be very patronizing or very signifi-
cant as to hiring. Unfortunately, legal precedents have been
set, and it can be grounds for a suit. Many employers are very
happy to get rid of a problematic employee and do not want
to have any backlash from a bad reference, so their word may
not be accurate. On the other hand, an employer may be
afraid to give an accurate reference because of concern about
legal recourse. It probably requires speaking to several indi-
viduals to actually obtain an accurate base. To simplify this
process, it is important to ask the previous employer if he or
she would hire that employee again. It is also prudent to ask
them if the applicant possessed the attributes or lack thereof
that we are about to discuss. This gives some standardization
to the referral process and allows the new employer to find out
the applicant’s ability to fit into their office. Any employer
must be extremely careful about providing a negative refer-
ence. If an applicant can prove that you have prevented them
from employment, you may be liable. Million dollar lawsuits
have been awarded to employees who were able to prove defa-
mation. The author severely cautions any employer against
giving a verbal or written negative reference, especially to a
stranger. Many large companies will only verify employment
history, the date an employee was hired, and the period of
time that the employee worked. These companies refuse to
comment on subjective questions. If an employer wants to
provide a negative reference without jeopardizing himself, the
statement “I cannot comment on this employee under advice
from my attorney” should make the point without creating
liability.
There is no doubt that hiring the incorrect employee can
cost thousands of dollars. The cost of training, the loss of effi-
ciency, and the negative impact are immeasurable.
The author believes that there are eight attributes that
make a perfect employee. For the sake of measurement, we
will refer to a perfect employee as a “10.” What we desire is
to be able to screen for employees that are a “7” or above. The
following attributes will greatly assist this evaluation process
(Box 19-1). The author owes Howard Rochesti of the Mercer
Corp. in Santa Barbara, CA, for his ability to distill this valu-
able information into simple categories.
1. Competency and presentation
2. Unconditionally committed
3. Givers or takers
Key Interview Points to Consider When
BOX 19-1
Interviewing Potential Employees
1. Competency and presentation
2. Unconditionally committed
3. Givers or takers
4. Offensive or defensive
5. Superstar or team player
6. Joyous
7. Self-managing
8. Learner
4. Offensive or defensive
5. Superstar or team player
6. Joyous
7. Self-managing
8. Learner
1. Competency and presentation
Competency is the foremost attribute required in the
consideration. Again in any service-oriented business cus-
tomers or patients expect and seek a certain level of care
and service. When a person goes to a nice restaurant, they
know in advance that it will be expensive. For that expense,
they expect a high level of service (e.g., prompt seating,
polite treatment, accurate ordering, fast service, and atten-
tion to detail). A waiter that cannot meet those expecta-
tions is incompetent. If you order a rare steak and salad
with dressing on the side and get a well-done steak and a
salad drenched in dressing, that is incompetence. This
incompetence will, across the board, cause unhappy cus-
tomers and invariably harm the reputation of the owner.
What is frustrating here is that the restaurant owner may
really have paid attention to detail. He may have a beauti-
ful facility with ample parking. He may purchase only the
finest ingredients, and he may have hired the best chef in
the area. Despite all the attention to detail, a single incom-
petent employee may shatter his dream of having a fine
restaurant by negating his attention to detail. There is a
difference between inexperience and incompetence. If our
waiter had a badge that said “waiter in training,” we may
expect a lesser level of service. This employee may become
an excellent waiter, but should not be turned loose on the
public without someone supervising. Presentation is also a
very important factor to consider in our business. The dis-
cipline of OMS involves cosmetics, aesthetics, and health.
One of your most powerful marketing principles is the
appearance of the physician and staff. Slovenly, out-of-
shape staff with yellow teeth or fingers from smoking or
excessive body piercings or tattoos is not the image that
we are trying to convey. An obese employee that is bubbly
and neat may be an asset, but someone with cellulite
bulging from dingy polyester white scrubs does not assist
your marketing efforts.
2. Unconditional commitment
Unconditionally committed is defined as commitment
with the lack of conditions. The closest example that the
author can find is a resident in a training program. As resi-
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
dents, we could not allow anything to take precedence over
our work. None of us would have dreamed of telling our
respective program chairman that we could not meet a
deadline because we ate lunch and did not have time. We
were in an environment where lunch was not a priority,
and our work took precedence. When we are called to the
ER in the middle of the night, we cannot say, “it’s late, call
me in the morning.” These are examples of unconditional
commitment.
Owners of businesses have much more impetus to be
unconditionally committed because they reap more of the
benefits or failures than the employees. For this reason, it
is rare to find this level of commitment in an employee.
One thing about any society is that people identify and
bond with cohesive organizational units that convey a
common goal. Fraternities, sororities, social clubs, sports
fans, bowling leagues, scouting, and church groups are
examples of situations where people unite and develop
sometimes extreme loyalties. There is usually little mone-
tary incentive in these groups, and the point is that we are
social animals and will extend great effort for “the cause.”
This same socialism extends into office settings, and when
employees bond and identify, they will put forth great
effort for the good of the practice. When you have a good
leader, clear-cut goals, and the correct employees, the
ensuing business is a beautiful machine. Physicians that
have exceptional and profitable practices probably are good
leaders and have exceptional employees with a well-defined
common goal.
An unconditionally committed employee will perform
within reason to accomplish the task at hand. An applicant
that will not work overtime or on Saturdays or follow your
rules of the game is only conditionally committed and does
not meet our criteria.
Finally an employee may be unconditionally committed
to you and not your vision. If an employee is only commit-
ted to you and you come into work with a poor attitude,
then they will take on your attitude. If the employee is,
however, committed to your vision, then they will pull you
aside and remind you of your commitment to excellence
and point out that your attitude that particular day is not
what our goals define.
3. Givers vs. takers
Someone is either a giver or a taker. A giver is a loving,
compassionate person who truly enjoys giving of them-
selves. These people understand the win-win concept and
fully realize that the more they give the more they will
receive in return. These people exude a generosity that is
not measured in physical gifts, but more importantly in the
subjective sense. These people give gifts of advice, time,
compassion, empathy, and service. You should, by now, be
getting a picture of what it is that we want in an
employee.
A taker, on the other hand, operates in the win-lose
environment in that for them to win, someone else must
look bad or lose. This was the person that reminded the
327
teacher that they did not collect the homework assign-
ments in school. Their means were not to serve as a
reminder, but rather to look good at the expense of others.
This is a malignant personality trait and is manifested in
all sections of culture. An oral and maxillofacial surgeon
that refers to other ORL and maxillofacial surgeons as
competitors instead of colleagues is another example of a
taker. Any person that speaks negatively about anything
to enhance their own identity is a taker. A giver would
compliment the other person on their efforts and then
focus on those of their own. Although it is impossible to
screen for this attribute in an interview, this behavior must
be identified and these people removed from your staff.
One bad apple can spoil the whole bunch. If, as an employer,
you ever come across the “what’s in it for me?” attitude,
you must take action. If an employee must have someone
lose for them to win, guess who will be losing? The losers
are the boss, the other staff, and the patients.
4. Offensive and defensive employees
By this categorization, we are referring to one’s ability
to accept change. Change is the basis for all molecular
structure and all of life. Everything from the subcellular
level on up involves motion, change, and energy. If
you examine successful people and successful practices,
you will see that they thrive on change. Change should
breed excitement, but for many people, it breeds fear
and insecurity. If physicians are truly interested in
approaching excellence, then they must continually
change all aspects of their practice to increase efficiency
and service. The author challenges and rewards his staff
for changing. We look at our forms, our policies, our fur-
nishings, and so on and brainstorm, as a group, on how
to improve. Accepted employee suggestions are validated
by monetary rewards.
Some employees are intimated by change and take the
“if it ain’t broke, don’t fix it” attitude. This is poison in a
motivated practice. Employees that encourage and accept
change are termed offensive, whereas those employees that
fear and resist change are termed defensive.
The author recently made significant changes to the
current charting system in his office. These changes meant
altering the status quo of everyone’s interaction to the
structure and handling of the office charts. It was truly
enlightening as an employer to witness the offensive staff
immediately recognize the potential for increased efficiency
and service, whereas the defensive staff members could
only see problems. For these defensive staff, this meant
doing things differently, and even though it was actually
less work on their part, they resisted as a result of their
personality trait.
It is appropriate for staff to challenge change. When the
author proposed the charting system changes, he did not
consider some shortcomings and was enlightened by chal-
lenge from the offensive staff. It was interesting that the
pitfalls put forth by the defensive staff were less amenable
to improving anything.
328 SECTION III ■ Practice Management
We all like change because it counters boredom. If we
all wore the same clothes every day and ate the same food
at every meal, life would not be as interesting. The same
holds true in the workplace. A valid leader understands
that all change may not be effective and must concede to
their staff that a given plan was not working. It is alright
to make mistakes and not dwell on them, but rather to
move foreward and, by trial and error, enhance the service
to your patients. Successful practices have offensive
players.
5. Superstars vs. team players
The term superstar is not a positive adjective in the
sense we are using it. A superstar is that type of employee
that can do it all. Although this might be appropriate or
even desirable for your first employee, you will have prob-
lems when you begin adding staff. The superstar manipu-
lates situations so that all the attention swirls around them.
It is not about winning the game; it is about how many
points they scored. The superstar believes that for their
previous experience or superior intellect they can “do
better.” They feel superior and are often overprotective of
the physician and the practice. Their attitude is that they
must “save” the practice from the incompetent hands of
the other employees. These employees may take some time
to recognize because they seem so dedicated on the surface.
If one examines the attitudes of their co-workers, it will
become evident if they are respected leaders and role
models or self-servingly critical.
There are tricks to ferret out this personality type. They
frequently place themselves in situations that “no one else
can do.” For instance, they are the only ones that can back
up the computer or the only ones that do the payroll, etc.
They thrive on being needed for important functions. They
frequently do this to become indispensable. They may
cause many employee problems and realize that the other
employee will be fired because the practice cannot run
without the efforts of the superstar. You cannot fire these
employees because no one else can perform the vital func-
tions, such as backup or payroll. The key to neutralizing
superstar status is cross-training. Give several staff respon-
sibility for critical functions. This is good business sense
and lessens the chance of fraud and embezzlement. Cross-
training prevents superstardom.
The above examples do not mean that one person
should not have responsibility. The difference is in the
person. Although the superstar wanted other staff kept in
the dark, the team player would have communicated the
important responsibilities to the other staff so that the
office would function in his or her absence. Look for, hire,
and reward team players; they will make your life and
practice less stressful.
Although OMS is not physically challenging, many
physicians go home at night exhausted and stressed. They
are not exhausted from doing surgery; they are exhausted
from having to constantly manipulate staff members to
keep peace. Superstars embezzle from the practice. They do
not steal money; they steal energy. They are like sponges,
and they steal the energy and excitement from the other
staff or even patients. To counter this type of behavior in
these “indispensable” staff, the physician must constantly
be manipulating situations and environment. This is what
becomes stressful and exhausting. Surround yourself with
team players and you will be energized. Synergy occurs
when the total is greater than the sum of the parts. Team
players, offensive staff, and givers blend harmoniously to
create synergy.
6. Enthusiasm, joy, and energy
Knowing that we spend a significant part of our time
with our staff, it makes sense to seek enthusiastic, joyous,
and energetic people. Happiness and enthusiasm are con-
tagious and are self-perpetuating. Friendly people with high
energy levels are a welcome addition to any group of people.
If you truly believe that there are no dress rehearsals in life,
then you should make the most out of every waking second.
For movers and shakers, there is no room for pessimism.
The form of OMS is not particularly exciting for the
patient, but an enthusiastic, joyous, energetic staff member
can greatly enhance the service and happiness level of
patients through attitude. Surround yourself with enthusi-
astic, joyous, energetic employees, with the other previ-
ously mentioned attributes, and your practice will
prosper.
7. Self-managing
Once you have found staff with these positive attributes,
you need to make sure that they are self-managing. There
exist employees that know just what to do, but will not
perform unless directly supervised. This is a drain because
you need two people to do the job of one. There is nothing
wrong with the concept of a manager, but if you must liter-
ally stand over someone to ensure progress, you have an
employee that is not self-managing. Self-managing employ-
ees are a pleasure to work with and take all the effort out
of management.
TERMINATION
If the author could highlight a single entity that holds back
progress and perpetuates turmoil, it would be the ignorance
and hesitancy of physicians to terminate an employee. One
must make a decision to run a practice or an employee repair
service. There is no doubt that terminating an employee is a
decision that is wrought with emotional and legal ramifica-
tions. Firing someone or being fired can provoke so many
emotions in both parties that many physicians procrastinate
or endure years of unnecessary stress because they cannot
bring themselves to “pull the trigger.”
In this situation, we again ignore the tenets of big business.
In the corporate world, termination and the factors leading
to it are clearly defined, and it is not uncommon for an
employee to be terminated in the presence of co-workers
while a company security guard hands them a box in which
to place their belongings, then escorts them to the door. It
is very traumatic for an employee to be terminated because
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
it signifies failure and humiliation. It is even worse when the
employee believes that they were unfairly terminated. If an
employee is terminated for being tardy and has the retort that
“Mary Ann is always late,” your credibility is lost, and you
may open yourself up for a wrongful termination suit. The
best way to prevent termination is to use correct hiring prin-
ciples. This sounds so trite, but in most offices hiring is such
a haphazard event that it becomes a roll of the dice. The
author is constantly amazed in his travels at the lack of atten-
tion to basic human resources policy. Time after time, well-
established offices do not have written job descriptions, policy
manuals, employee documentation files, and other basic
information. Every office should have a written policy on
exactly what it takes to be an excellent employee and
what it takes to be terminated. In addition to this, employers
must be consistent with these policies with every employee.
If an employee does not know the goals of the practice,
the day-to-day policies, and what is expected of them, how
can they be expected to perform? Without structure one has
chaos. Unfortunately, many practices function in a chaotic
state.
For all the above reasons, every practice needs a map and
a compass. The map is the policy manual, and the compass is
the leader of the practice, the physician. No one can get from
point A to point B in unfamiliar territory or inclement weather
without navigational aids. Can you imagine an NFL team with
no one designated as the quarterback? If there was no leader
and anyone could call any play at any time, chaos would rule,
and the team would never advance. Similarly, if the team had
a quarterback who knew all the plays but there was no play-
book for the rest of the team, the same chaos would rule. Any
successful team must have a leader and a playbook, and any
pilot must have a map and a compass. Similarly, every office
must have a leader and rules of the game, which we will
enumerate later.
When the performance of an employee begins to falter, the
leader must conscientiously ask himself or herself if it is an
employee or employer problem. Often, as we have pointed
out, the perceived employee problem is actually a leadership
problem. If it is truly an employee problem and the employee
can be salvaged, then a written warning and a second chance
may be extended for a probationary period. If the employer
believes that the employee is not catching on or is unsalvage-
able, then it is better to approach the inevitable ASAP. It is
also important to document employee shortcomings and proof
of counseling of the employee. This is critical in terms of
defending a wrongful discharge suit or an unemployment
claim.
DOING THE DEED
If the proper pretermination steps have been carried out, the
actual task of termination need not be complicated. The
single most important point is to have the entire script well
prepared and clear in your mind. This is no time to ad lib or
fumble around; absolute clarity is essential. It is also important
to realize that if you are unhappy with the performance of a
329
staff member, they are probably aware of this; they are also
probably unhappy, and sometimes the termination of employ-
ment is actually a relief on the part of both parties. The author
always terminates an employment relationship on a Friday
afternoon, unless a significant infraction, such as theft or sub-
stance abuse, has transpired. It is important to have a private
environment away from other employees, and it is mandatory
to have an employee, preferably of the opposite sex, present
to document and witness. The author very simply tells the
employee that the employment relationship is not working.
He further tells the employee he believes that they are a fine
person, but they are just not a good fit for the practice. The
author states that he has a certain vision and direction for
the practice; the employee is not moving toward the goals of
the practice, and again it is not a good fit. The author prefers
not to delve into specifics because it opens the door for argu-
ment or comparison with other employees. If the employee
pushes in that direction, the author takes control of the situ-
ation and reiterates that the topic is not open for discussion
and moves on. It is imperative not to insult the employee and
leave them with self-esteem. If the situation is applicable, the
author offers the employee the ability to resign with severance
benefits or be terminated with no benefits. The author enters
the interview with two predrafted letters, one for resignation
and one for termination, and gives the employee a choice. If
the author believes that there may be legal implications or
retribution, he has the practice attorney present. It is accept-
able to have a manager or attorney do the actual firing, as long
as the proper channels are followed. In fact it may be wise for
the physician to distance himself or herself from these pro-
ceedings. This author has eight partners and more than 50
employees. As a result of this size, we have an administrator
with medical group management experience and a trained and
experienced human resources manager. Hiring and firing is an
ongoing occurrence and is beyond the scope and training of
the physicians.
Although it may seem cold, it is an absolute necessity to
obtain any keys, credit cards, or any other practice possessions
immediately. There are many cases of documented sabotage
involving the violation of this. An even greater temptation
for sabotage is to terminate an employee with 2 weeks’ notice.
This is a perfect invitation for this person to be unproductive
or diabolic within your office. A prudent employer will already
have a replacement lined up to step right into the position.
The author stated earlier that some physicians will commit
serious errors in judgment by taking money from the front
desk, having affairs with staff, or allowing staff to know per-
sonal or family information. It is after firing an employee that
they become disgruntled and expose any deceit or retribution.
This is a real and all too common situation; do not fall
victim.
■ INITIATING A MARKETING PLAN
Although the author has until now downplayed the specifics
of a marketing plan, they are very important. Their impor-
tance is only relevant after a physician and staff is committed
330 SECTION III ■ Practice Management
to understanding the theory and mind-set of excellence and
patient-centered care.
We, as physicians, have a dual commitment that is nonex-
istent in most other businesses. We have taken an oath and
are expected to sacrifice for the well-being of our fellow man.
Going to the ER in the middle of the night to treat a patient
without funds is a good example of some of the problems that
set us aside from other profitable businesses. In addition, what
we do is expensive, and traditionally, people have a low prior-
ity for paying physician’s bills. No one would think of going
to a restaurant and ordering a meal and be shocked to receive
a bill and have to pay on the spot. This mentality has, in the
past, not carried over to physicians because the general public
considers health care a right and not a privilege. Things are
quite simply different today, and we must again adapt to be
profitable. Most physicians are compassionate and realize that
their profession assists many people who may not have the
ability to pay. On the other hand, without sufficient profit,
the business will not thrive to a point to provide that service.
We literally walk a tightrope, with patient care and medical
ethics on one side and the need for aggressively structured
business on the other side. An improper mix can detract from
our humanity or force us out of business.
This is an opportune time to discuss profit. When lecturing
on the subject, some physicians find the mere mention of
profit objectionable or unprofessional. This is a capitalistic
society, and our economic thrust is on profit. Profit is not a
four-letter word, but loss is. There are few businessmen or
businesswomen who do not desire the amenities that society
offers. Having a profitable business allows one to pursue their
careers in a more content manner, in addition to offsetting
the mix of indigent treatment. Many of the frustrated prac-
titioners in OMS are frustrated because of their lack of profit.
Their poor hiring and firing practices and lack of formal
policy and leadership are impeding their profitability and
enjoyment, and this is all tied together in the marketing
equation.
We have stressed the leadership concept and the impor-
tance of the staff to the success of the office. Let us now
examine the role of the physician in the image of the office
because, after all, image and marketing are inseparable.
Most successful practitioners have a passion for their pro-
fession. In this day and age it is difficult to find time, but a
marketing plan starts with clinical excellence. A physician
needs to be well read and attend continuing education, con-
cerning what is current and contemporary. By doing this, he
or she is satisfying a public thirst, which is a thirst for what is
new. People are constantly intrigued by newer and better ways
to accomplish mundane tasks. The mere incorporation of
lasers, advanced implant technology, advanced imaging,
minor cosmetic procedures, and advanced practice manage-
ment systems will enhance the image of the practice. This
advancement will only occur if your patients and referral base
know about the advances. This lack of communication is a
pitfall for many physicians. You may be the most advanced
surgeon in the area, but if your referral base and patients are
not aware of it, you have sacrificed valuable marketing
opportunities.
Communication is the essential measure for a successful
practice and, in this age of computers, has never been easier.
The author believes that a physician should view his or her
practice as a team, a family, and a center. This center is the
nucleus for what is current and best serves the patient. Gen-
eralists will list the lack of specialist’s communication high on
their list of complaints. The generalist relationship is such
that they see a given patient and their family several times
each year for many years and develop a special communica-
tion with these patients. The specialist may see most patients
for two or three visits and be faced with the barriers of pain,
expense, and fear. It is definitely more difficult to develop this
level of communication experienced by the general dentist in
several visits. We therefore must work harder and be more
impressive. When a general dentist refers a patient to a spe-
cialist, he or she may not see that patient for months. If the
oral and maxillofacial surgeon failed to send a referral letter
detailing the surgery, it is very embarrassing for the dentist
because they are ultimately responsible for the global care of
their patients. A smart specialist would realize that anytime
they could communicate with their referring physician it is
free marketing. Each time your letterhead crosses the desk of
a referring source, it makes a subliminal marketing impression.
Communicate in writing with personalized stationary and,
when possible, handwritten personalized notes (Figure 19-1).
An astute surgeon will continually search for ways to
communicate.
The previous areas of discussion are primarily philosophi-
cal, but, nonetheless, paramount to the understanding of the
global nature of marketing. We will now focus on some basics
that may actually be applied to one’s individual practice. It is
important to mention that these ideas expressed by the author
are by no means exhaustive. They only scratch the surface as
to some important guidelines. The author once participated
in an AAOMS seminar in which five practitioners presented
a slide show of a patient’s journey through their office. This
FIGURE 19-1. A personalized note card used by the author to commu-
nicate with referral sources and patients.
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
lecture focused on each physician’s image, physical plant,
referral and marketing strategies, patient care, etc. There
were many simple but thought-provoking ideas presented.
The point is that satisfying a patient is an inexhaustible
process, and there are endless means, some big, some little, of
improving service and thanking referral sources.
When considering the basics of a marketing plan, try to
imagine your favorite restaurant. What is it that you like about
it? They probably have a clean environment with friendly and
accommodating staff. Their service is probably excellent, and
their food is unparalleled in presentation and taste. The res-
taurant probably has reasonable prices and has amenities, such
as staff that remember the patrons, easy parking, and a way of
always making you feel that you are their only customer, even
on their busiest nights. Try to apply this thought process to
all the details of your practice. No matter how busy, we should
attempt to make each patient feel that they are the only
patient in our practice. Concierge care is all the rage in
medical practices, but astute physicians have been providing
concierge care free of charge all along.
IMAGE AND LOGO
The most basic of basics in marketing is identity. The first
thing that you need to do is to be remembered. Can you
imagine if one of the most famous soft drink companies did
not stress their logo? All people would remember is “that”
company with the good taste. The cola wars are a Madison
Avenue example of how essential image is. These companies
spend billions of dollars making sure that society remembers
their name. Some image marketing is so effective that a
product name becomes the moniker for all products of that
type. When you hear someone ask for Scotch tape or a Xerox,
they probably are speaking in a generic sense. This psychology
applies to health care marketing, and without a logo, it is
much more difficult to gain an identity.
There are many ways to create a logo. One can consult with
a graphic artist or marketing firm or make it a project with
your staff to do it internally. The logo should represent the
physician and the practice. If sailing is the passion of the
physician, a tasteful logo centered around a sailboat makes a
point and is fun. Once decided, you should obtain a service
mark for the logo to protect its unlawful usage. The logo
should be distinctive and colorful and should be used when-
ever possible. The author uses his logo on prescription forms,
all stationary, newsletters, invitations, and virtually anything
that represents the practice, including scrubs (Figure 19-2).
When people see this logo, they think of our practice. If
the logo is not distinctive, it is not as effective. The author
believes that the commonly used logo of a retrognathic and
prognathic profile and a normal profile has been overused in
our profession. It is also effective to have a slogan to compli-
ment one’s logo. It should say it all in a nutshell.
UNIFORMITY
In the author’s opinion, one of the beneficial aspects of the
stringent Occupational Safety and Health Administration
331
FIGURE 19-2. Wearing personalized scrubs with the practice logo is a
good way to promote the practice.
(OSHA) requirements was the widespread acceptance of sur-
gical scrubs in the office. In the author’s opinion, having
freshly laundered scrubs with the practice logo and the name
of the employee embroidered on the scrub top is a functional
and professional look and also designates the players of the
team to the patients. The office is one place that you should
be able to tell the players without a program. Going back to
the sports metaphor, all teams have uniforms. The issue of
name tags for employees is also important (Figure 19-2). When
a patient is placed in the unfamiliar environment of an OMS
office, he or she can become very intimidated. The unusual
sights, sounds, and smells coupled with the fear of surgery and
pain does not exactly present a relaxing environment. The
patient, in this situation, looks for any vestige of warmth,
friendliness, or compassion and will bond with these people,
thus mitigating these fears. When you can call someone by
his or her name, this automatically puts a person one step
closer to a bond. When one examines the habits of very suc-
cessful people, they inevitably are quick to remember a new
name and use it frequently in a conversation. People like to
hear their name in conversation. Many physicians write the
first name of a patient on the chart in very large letters that
may be seen across the room so that the entire staff may refer
to the patient by name. Some offices use a chalkboard with
“welcome Bill Smith” inside the treatment rooms. In any
event, it is very helpful and should be mandatory for all
employees to have some sort of name tag. If for no other
reason, it will allow a patient to be specific when they compli-
ment or criticize an employee’s performance.
THE ART OF THE EVALUATION
Breaking the Ice
The anxiety associated with visiting a physician is sometimes
palpable. Some people become diaphoretic and obviously
stressed. There are many subtle tricks that most seasoned
practitioners employ to place patients at ease and make it a
positive experience. First and foremost is to avoid isolation.
In busy practices, the patient is often whisked into the
treatment room and left alone while the team is seeing
other patients. Leaving a patient alone in a room is negative
332 SECTION III ■ Practice Management

FIGURE 19-3. Engaging patients in casual conversation before “getting FIGURE 19-4. Wide screen TVs in the evaluation suite can be used for
down to business” helps relax the patient. teaching and continuing education.

marketing. A staff member should always accompany a waiting

patient and engage them in relaxing not medical conversation
(Figure 19-3). This author has made a nominal investment in
large screen television sets in the main treatment and surgery
rooms (Figures 19-4 and 19-5). It is okay to leave a patient
unattended if he or she has something to do, and handing
them a remote for the big screen TV can bide time and miti-
gate the feeling of waiting.
Nothing is more important than a smile. As a result of the
stress associated with our career, we must sometimes force a
smile, but no physician or employee should ever enter a treat-
ment room without a smile. No other body language is as
reassuring. In addition to smiling, patients like to be touched.
Classic medicine from thousands of years ago talks of “the
laying of the hands.” There is something about appropriate
compassionate touching that helps the physician-patient rela- FIGURE 19-5. Wide screen TVs in the surgery suites provide diversion
tionship. A hand shake or a pat on the shoulder is sometimes for the patient.
all that is necessary. Unhappy patients that feel rushed through
one’s office will frequently say, “The doctor didn’t even touch their horses, it really makes the patient feel appreciated and
me.” There is an art of making people wait for your services the surgeon seem impressive.
while making them believe that they did not wait excessively. Some patients are difficult to warm up, and complimenting
In other words, if you can keep them engaged and occupied, them is a nice way to begin a conversation. The color of a
they will not realize the length of the wait. dress, the smell of perfume, a piece of jewelry, or the patient’s
Posture is also important when speaking to apprehensive children are all easy compliments. Complimenting on the
patients or any patient. Again no matter how rushed a physi- great work of the patient’s dentist serves to reinforce the
cian is, they should always sit down sometime during the patient’s faith in their dentist, and they frequently repeat this
patient conversation. It is better to be eye level with the fact the next time they visit the dentist, which has a positive
patient; this shows that you are “into the patient.” marketing appeal for you.
Masters of communication will always begin a professional There are many times that we are truly rushed in trying
visit by making small talk with the patient. People are to accommodate overbooking, emergencies, and all the other
impressed by the fact that a busy physician would ask about problems with a busy schedule, but by paying attention to the
their hobbies, families, vocation, etc. Again taking 30 seconds above details, it can change the perception of the patient. In
to informally chat with a patient can lessen the appearance of addition, if a staff member precedes the physician and does
being too busy. A patient is really impressed when you remem- the same type of communicating, a cumulative effect results.
ber a personal fact months later, and astute communicators Every physician and staff member should always ask if there
will make a notation on the chart “Patient likes riding horses,” are any questions before discharging the patient. With posi-
etc. When the patient returns months later and you ask about tive communications, one can accomplish in 5 minutes what
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
may take others 25 minutes. Providing a variety of high-class
and informative material on the physician, the staff, and the
office will also help pass the time in a constructive manor and
assist your marketing.
THE ART OF WAITING
Waiting is one thing that patients hate. This is one reason
we refer to the lobby as a reception room and not a waiting
room. Industries, such as fast-food companies, banks, and
retail stores, have done many studies on waiting. Fast-food
chains have found that people do not mind waiting as much
if their order is taken immediately, even if there is a significant
wait afterword. In addition, people that cannot wait are served
first. Drive-thru windows take precedence over the counter
customers. Retail businesses have found that customers pay
less attention to time if they have something free. This may
be a bowl of candy or a self-serve coffee station. We, as physi-
cians, can take advantage of this type of psychology. In addi-
tion, if a patient is going to experience a long wait, they will
do much better if they are informed. A progressive office will
update the patients on the status of the wait and offer anyone
the opportunity to use the telephone to adjust their other
business or reschedule the appointment. People become quite
agitated when held in limbo. Again, if you are truly interested
in marketing, make these patients comfortable, provide them
with useful information about your office and services, and
give them something to do.
The author always apologizes to patients for an unreason-
able wait and tells the patient that their time is just as valuable
as his own. In addition, the author will often adjust the fee in
the interest of patient relations. We further explain to the
angry patient that we devoted our time to a patient with an
emergency, and if it were the angry patient who needed our
services, we would be there for them, and others would have
to wait. Our office also sends an apology letter to patients that
have experienced substantial waits.
Running behind on a schedule is a fact of life in many
offices, but some common sense and special attention can
mitigate this factor, which causes patient dissatisfaction. This
is marketing in its purest form.
PHYSICAL PLANT
In the institution of a marketing plan, few things are as impor-
tant as the home base. Although the first impression of one’s
office usually begins before the patient arrives at the office,
the first 5 minutes in the reception room probably defines
much of the patient’s attitude. It is important to remember
that our profession is about well-being and aesthetics, and our
offices must represent this. From time to time, the author will
sit in his reception room during business hours and just
observe. It is interesting to see how people interact with one’s
office and to make observations yourself. There are many
intimidating and offensive things that occur in our offices.
When walking through our own office, we are sometimes
oblivious to these factors because of our accommodation.
When we walk through the fragrance department of a large
333
department store, we are usually impressed by the mix of fra-
grances; however, the employees behind the perfume counter
do not notice the smell. In this case the smell is a positive
factor, but the smell of burning flesh from a cautery, strong
disinfectants or medications, burning dentin, etc., are cer-
tainly not palatable to your patients, even though you and
your staff do not notice them. The same thing can be said
about noise. There are few things more offensive to anyone
than the sound of a drill or the shriek of a patient in pain.
Couple this with the sound of a patient with airway problems
or anesthetic gagging, and you are subjecting your patients in
the reception area to a cacophony of scary and unwelcome
sounds. How are they supposed to feel if they are next to be
treated or if it is their family member in surgery? All noxious
sounds do not come from patients. In a professional environ-
ment, we must be very careful about staff and physician con-
versations being audible to patients. In the Capitol building
in Washington, D.C., there is a popular attraction that illus-
trates the peculiarities of acoustics. If one stands in a certain
spot in one of the large rooms adjacent to the rotunda
and whispers, the conversation may be heard with clarity in
another area some 60 feet away. It is astounding that the
acoustics carry a whisper that far.
This same acoustical situation can and does exist in offices.
There are many well-documented situations where patients
have overheard remarks from the staff or physician, personal
telephone calls, or employee bickering. Also, patients may
misinterpret what they think they heard. In many offices,
receptionists make collection calls or speak with patients
about sensitive financial or health information. The wrong
conversations can provoke ill will or even legal problems.
The author always recommends sound attenuation tech-
niques for the reception room, the surgical suite, and the phy-
sician’s private office. In addition, it is important to keep a
professional decorum at all times in the company of patients.
An office need not be elegant to make a good impression.
Practice management experts will attest that cleanliness is one
of the biggest factors that affect the thoughts of patients. In
this day and age of potentially fatal communicable diseases,
sterility and cleanliness are paramount. Many practitioners
have signs posted throughout their office extolling their extra
attention to sterilization and the like. This is pure marketing.
This is a good point to bring attention to another important
point of marketing. If you go out of your way to improve
service for someone, it is imperative to let them know. When
we send cleaning to a dry cleaner and we get a shirt or blouse
back with a sign attached to a button informing us that the
cleaners saw that the button was missing and replaced it, we
realize extra service. Just think how frustrated you would be if
you packed that shirt or blouse for an important out of town
meeting and getting dressed before the meeting you had no
button. In this case the dry cleaner was showing exemplary
service, and you only realized it because they pointed out their
extra effort. Had you unpacked the clothing for the meeting
and did not have a sign on the button, you would have never
realized the extra effort. When you go above and beyond the
334 SECTION III ■ Practice Management
call of duty to extend service, let your patients know of your
efforts or they may go unappreciated. As consumers, some-
times we pay in excess for a superior product. We have all
purchased something that was more expensive than usual, but
we purchased it because it was explained to us that only the
best parts were used and the guarantee is exceptional. People
will pay more money for goods or services that they deem to
be exceptional. If your office is exceptional, you need to point
it out in every respect to your staff and patients.
It is a great promotion to have the staff compliment the
physician and vice versa. Many times patients make telephone
rounds with multiple offices to find the one that “feels” best.
By a receptionist saying to a patient “Oh you will love our
doctor, he or she is so gentle and friendly; you will just love
them,” he or she really goes out of their way to make sure you
have as pleasant an experience as possible. As a practitioner,
the author is absolutely positive that many patients who were
riding the fence or telephone shopping came to the office
because of the complimentary nature of the staff. In return it
also says a lot about a physician who compliments his or her
staff in front of a patient. Most of us are probably very appre-
ciative of our staff, but fall way short of expressing thanks. By
complimenting a staff person in the presence of a patient, you
sincerely elevate the morale of the employee and reinforce the
cohesive nature of the team to your patient. If there is one
fault that we all are guilty of as employers, it is having an
employee that does 99% of things correctly and we jump on
them for the 1% they do wrong. The world needs more
compliments.
It pays to take a weekly stroll through your entire office
when there are no patients present to visually inspect the state
of your facility. Some subtle details will jump out that may
not be noticeable in “the heat of battle.” Outdated or wrinkled
periodicals, dirty carpeting, unhealthy plants or flowers, messy
aquariums, outdated or worn furniture, dirty windows, and
crooked pictures are just a few things that should be inspected
by the staff and physician on a regular basis. The clinical areas
must be clear of difficult to notice objects, such as wire, impres-
sion material, bits of suture, etc.
The author strongly recommends redecorating the entire
office every 5 years, whether you think it needs it or not. First
of all, it probably does need renovation, and secondly, it is
amazing how little things, such as paint, wallpaper, and furni-
ture, can increase morale. Many of us spend as much or more
time in the office than at home. For this reason alone, it
should be nice and represent you and your interests. Although
unfinished or pine furniture was once popular, it now portrays
a yard sale image.
IDENTIFYING A TARGET MARKET
Again, image and marketing are inseparable. Every business-
person struggles for a way to identify their target market and
spread the word of their goods or services. There is no disput-
ing that word of mouth is a very effective means of marketing,
but it is also the slowest. There are many means by which to
mass market, and we will discuss them later.
Identifying the target market for any business is very chal-
lenging. It may cost several hundred thousand dollars to find
out that Pepsi drinkers are 23-year-old Republican college
graduates. Fortunately, for our profession, our target market is
obvious. For the vast majority of us, the general dentist or
dental specialists are the funnel for our business. When the
author speaks to new practitioners, he makes the point that
10 general dentists could support an oral and maxillofacial
surgeon if they were prudent practitioners and properly
screened their patients. The problem for most of us is that we
are not the only show in town. There are usually many choices
for a dentist, so why choose our given practice?
An entire text can be devoted to this question alone. Ini-
tially, many established referral relationships begin when a
practitioner enters practice, and, if the service is appropriate,
continue as habit. Why did this dentist originally begin refer-
ring to a new surgeon in the first place? Age distribution has
an influence in that many dentists refer to specialists of com-
parable age. They may know each other or at least both relate.
Many established physicians may refer to a new physician
because they have empathy for the new practice, or simply
because the physician is just new and different. Perhaps they
believe that the new physician has skill in the latest tech-
niques. There are many reasons why an established general
dentist may stop sending patients to an established practice
and begin sending them to a newer or different practice. The
biggest problem, however, is that it has to do with a change
in service.
When a practitioner first enters the practice, he or she is
usually enthusiastic and hungry for business. As a result of this,
new practitioners do all the right things. They see any patient
at any time, they work until the job is done, they are quick to
express their gratefulness for referrals, they are very friendly
to patients and referring dentists, and will bend over backward
to get new business. They are humble but confident and are
usually excited if not supercharged about OMS.
With this willingness and attitude in mind, it is easy to
deduce that not only new physicians get patients, but also why
experienced physicians may lose patients. Obviously, most of
us lose some of the vigor we once had, but too many physicians
fall into a false sense of strength as a specialist and assume that
a decade-old referral relationship will continue out of habit.
This could not be further from the truth. If physicians con-
tinually decrease their level of service, they are literally invit-
ing competition into their referral area. When considering a
marketing plan, remember to try and do as many of the things
that made you successful, and never, never let your guard
down out of overconfidence. It requires much less energy to
maintain a favorable referral relationship than to try to reenter
one.
PREENTRY MATERIALS
The best time to market is always. Many physicians are under
the impression that they need not concentrate on marketing
patients until the patient contacts the office. This is not true.
First, many physicians mount tasteful and effective media
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
marketing campaigns, and we will discuss these specifics later.
More importantly is the ability to obtain a favorable position
with the gatekeepers of your target market (e.g., the general
dentist, dental specialists, local physicians, ERs, pharmacies,
etc.) A busy general dentist is very similar to a busy ER physi-
cian in that they need to get problem patients out of their
office to stay on schedule. They will take the path of least
resistance to get the patient to another caregiver, usually a
specialist. If your office is easy to get a patient into, you
are in the most favorable position; if your line is busy or your
receptionist makes the general dentist’s staff jump through
hoops, then you are in an unfavorable position. A prudent
specialist will constantly adapt their office to make it easy to
make an appointment. If you are unsure of how hard or easy
it is to make an appointment at your own office, have a friend
call monthly to make sham appointments with different sce-
narios. Example scenarios would include an emergency
appointment, a pushy patient, a handicapped patient, etc. It
is quite a learning experience to do this. It is also useful to use
the “secret shopper” scenario. This involves having an anony-
mous patient (that not even the physician knows) make an
appointment with the practice for an evaluation. The secret
shopper should document all aspects of care, conversations,
office observations, waiting times, staff and physician
demeanor, etc. Then this is filed in a report and shared with
the staff. This author has done this multiple times, and it
always serves to point out deficiencies.
There are many techniques to facilitate a favorable referral
position. Many physicians supply the referral base with referral
pamphlets with pictures of the physician and staff and perti-
nent information about the surgical experience. These bro-
chures often have a map to the specialist’s office and important
telephone numbers. Some practitioners include some promo-
tional gifts with the brochure, such as refrigerator magnets,
fast-food coupons, discounts for surgical evaluation, adoles-
cent-oriented coupons, etc. A presurgical packet makes a nice
presentation for a patient to receive and helps the patient
identify with the specialty office before they ever walk through
the door. The author has found this to be a very efficient and
timesaving method, which allows the office to schedule more
patients, who will experience less waiting. In addition, we
have found the patients to be more accurate when they can
fill out forms at their leisure. Any marketing, business, and
promotion should involve the Internet. Many offices now
employ online patient registration and appointment ability.
Having a professional website that details all aspects of the
practice and offers advanced registration is employed by con-
temporary practices. Not having a website in this day and age
is an obvious deficiency that makes a practice stand out in a
negative way. Just having a website is not enough, it must be
aesthetic and informative. Contemporary patients seek
information.
MAKING IT EASY
Because most general dental offices have panoramic radio-
graphs on their patients, they usually send them to the oral
335
and maxillofacial surgeon for the patient’s appointment.
Sending the referring office a self-addressed stamped Panorex
envelope greatly facilitates this process and puts that office in
a more favorable position. Using electronic transfer of digital
radiographs is even better, assuming one’s referral sources are
as advanced. There are hundreds of ideas being used by suc-
cessful offices. The challenge for us all is to constantly think
of service-oriented ideas to better serve our referral bases and
patients. It is fun and rewarding to challenge your staff to liter-
ally dissect everything that constitutes your office and try to
reassemble it for better patient service.
SYNERGY IN MARKETING
Synergy occurs when the whole is greater than the sum of its
parts. This can be applied to marketing only when the physi-
cian involves his or her staff. A physician can have the best
marketing mind in the world, but be tremendously reduced in
effectiveness if the staff is not involved. McDonald’s fast-food
chain has a policy of training their managers and franchise
owners. They require these executives to literally begin at the
bottom. Managerial trainees must flip burgers on the grill, run
the French fryer, and make milkshakes for several weeks before
putting on their white-collar clothes. Many businesses take
this grass roots approach because it brings home an enormous
point. A manager is more effective if he or she understands
everyone else’s job. In addition, this experience will stimulate
the innovative mind to find a more efficient and profitable
way to get the job done. It is shameful that, as physicians, we
do not spend one day of the year as a receptionist or surgical
assistant. We would gain much insight into our practices. Our
staff hears, sees, and feels things that elude the physician.
If a physician has the right staff (if you do not, you are
negative marketing), they will exponentially compliment the
marketing experience. It is essential to communicate and for-
mally launch a marketing campaign. It is very effective to refer
to this as a patient-service enhancement campaign. The
author recommends canceling patients and having a half-day
meeting. The purpose of this meeting is to point out to the
staff the importance of patient-centered care and to explain
the benefit of superlative service. Each staff position should
have a specific job description, and it is imperative to chal-
lenge the staff to be innovative and try to improve each detail
of the patient’s experience. The physician must be prepared
to reward the staff with some type of incentive for their con-
tribution. This is a win-win situation because when the staff
wins, the physician wins more. Once you have challenged the
staff and they respond to the challenge, an energy level is
created that is almost palpable. The ensuing enthusiasm serves
to further fuel the synergy engine and draws the entire team
to a common goal: superior patient service. The author is
continually amazed with the endless ideas submitted by the
staff and frequently asks, “Why didn’t I think of that?”
The author requires each employee to submit at least two
ideas and rewards them with a monetary bonus. An employee
that does not submit two ideas cannot be reviewed until this
is completed, and no review means no raise. An employee
336 SECTION III ■ Practice Management
The 1995 American Society for Quality
BOX 19-2 Survey on the Reasons for Customers
Switching Service Providers
• Death: 1%
• Moved away: 3%
• Influenced by friends: 5%
• Lured away by competition: 9%
• Dissatisfied with work: 14%
• Attitude of indifference on the part of an employee: 68%
without an idea on how to improve patient service has no
place in an office in pursuit of excellence.
Failure to enlist your staff in the marketing of your practice
will deprive you of your most effective and most economical
asset.
In 1995, the American Society for Quality conducted a
survey on the reasons for customers switching service provid-
ers. The interesting results are as follows (Box 19-2):
• Death: 1%
• Moved away: 3%
• Influenced by friends: 5%
• Lured away by competition: 9%
• Dissatisfied with work: 14%
• Attitude of indifference on the part of an employee:
68%
This survey most probably applies to every type of business
on the planet. Most of us can relate to a restaurant that has
great food but mediocre service; one rude waiter or waitress
can ruin the best of products or service.
PATIENT SURVEYS
The quintessential marketing question is “What is it that I
can do to better serve my patients, staff, and referral base?”
This also translates into “How can I be more profitable?”
Individuals spend thousands of dollars to find this answer
when it is actually right under their noses. Ask your patients,
staff, and referring physicians what they want and how you
can better serve them, and they will tell you for free. Place a
two-dollar bill in the return envelope with the survey as an
extra incentive for return of information.
The survey need not be exhaustive, and the more to the
point it is, the more participation you will probably have.
There are several schools of thought on how to execute this
type of polling process. Many physicians believe that anonym-
ity is important to obtain true and unbiased input. Some
physicians will use a professional marketing firm to do this,
although the author believes that this is unnecessary. If one
believes that bias is a possibility, a neutral return address and
P.O. Box can be used. The author is familiar with practitioners
that rent a P.O. Box and have envelopes and stationery
printed with a fictitious company, such as “Martin Market
Research.” The survey contains a cover letter that states that
they are a market research company conducting a survey for
Dr. X’s practice. Proponents of this type of approach believe
that referring offices may be more candid with a third-party
firm than they would be with the known office.
The author has experience with multiple methods or refer-
ral surveys and still prefers performing surveys from his own
office on his own letterhead. The experience has been that
referrals are very candid and specific and frequently sign the
survey. The author gives the responder the option to sign or
remain anonymous.
In this day and age of business and the state of junk mail,
it is difficult to get people to fill out a treatise. The survey
should be 10 to 15 yes or no questions followed by an open-
ended area asking for any specific input on how we can
improve our office.
Some of the basic questions asked are as follows:
• Is it easy to refer patients to our office?
• Are our hours of operation convenient?
• Is it easy to reach us for emergency patients?
• Is our after-hours answering service polite and
effective?
• Do your patients generally relate a positive experience
when returning from our office?
• Do our insurance and billing personnel serve your
patients well?
• Is our office efficient in communicating about your refer-
rals and prompt in returning your referral records?
• Does your office enjoy our educational and social
functions?
• Do you have any suggestions for future social or educa-
tional functions?
• Please list any positive comments you have about our
office.
• Please list any negative comments you have concerning
our office.
• Please list any additional comments that may assist our
office in serving your staff and patients.
The above are merely examples of meat and potatoes survey
questions. It is less important what you ask than the fact you
care about asking. An office that does not take advantage of
this powerful tool on a regular basis has surely missed the
marketing boat.
If a given referral source makes a negative or interrogatory
comment and signs the survey, it is important to respond in
writing as soon as possible. Failure to do this may be ignoring
the truthful critique of that physician and taken as
offensive.
It is possible to oversurvey a referral base. This task should
be done every 2 years. The author also uses what he refers to
as precision surveys. This is a very specific survey, concentrat-
ing on a single subject or procedure. An additional precision
survey used by the author is one that is mailed only to referral
staff and not intended as a physician survey. These can be
even more accurate because it is often the staff that actually
makes a referral. The general dentist may simply tell the assis-
tant or hygienist to “send this patient to the oral surgeon for
their wisdom teeth.” From that point on, it is the staff of the
dentist that deals with the patient and the specialist. In the
consideration of a marketing plan, never, never overlook
referring staff because they may be your greatest allies.
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
Although a referral survey is an integral instrument for an
office interested in excellence and patient-centered care, it
only tells half of the story. To really discover how to better
serve your patients, ask them, too.
The author has gained tremendous insight into the percep-
tion of patients from random patient surveys. The operative
word here is random. There are obviously multiple phases of
the surgical experience, and, depending in what phase you
catch a given patient, the survey may or may not be accurate.
For instance, a patient who has been to the office for an evalu-
ation may be very pleased, whereas a patient with a dry socket
and a postoperative nerve dysesthesia may be disgruntled at
that given point in time. By the same token, a patient may
have had an excellent experience all the way through the
office; however, 3 months later they become unhappy about
their lack of insurance coverage and resultant balance owed
to the office.
As a result of the temporal differences, one would not gain
a representative sampling of the true global office experience
unless all sectors are queried. The author recommends a sug-
gestion box in the reception area and a monthly random
sampling of patients in various phases of their surgical experi-
ence. It is also significant to reinforce the need for statistically
significant responses. Sending out 10 surveys may be futile,
although any input is better than wondering, and this is espe-
cially important for negative criticisms.
The next link in the survey triad is your own staff. As we
have eluded to time and time again, the staff is your most
powerful marketing tool. They work closely with patients in
ways that we as physicians never see. Your staff has input that
is vital to achieving excellence and a patient-centered office.
Ask them, listen to them, and reward them for making things
better. Once you have input from the survey and begin to
institute changes, you will begin to notice a difference. It is
also at this point that your patients will notice a difference.
When this whole process gains momentum, a beautiful thing
happens; it is called marketing. You can actually see and feel
it. It is no coincidence, and it can and will work for anyone
willing to take some time and follow some basic steps.
LUNCHES AND MARKETING
If there were a time-honored PR entity, it surely would be the
business lunch. Many big deals have been negotiated over a
restaurant table, and many referring physicians have been
courted over the same table.
This is one area that this author believes is minimally effec-
tive as a PR tool, with notable exceptions. It seems that our
lives have continued to become more and more hectic and
that people have accommodated in a variety of ways. Many
people that sat around the breakfast table with the family as
a child are now gulping down breakfast in the car on the way
to work. Lunch for many businesspeople is a time to return
telephone calls or catch up on the morning’s work. It is safe
to assume that most medical and dental offices run behind
schedule. Trying to force a harried luncheon date of a social
nature into a tight schedule can make a usually pleasant expe-
337
rience undesirable. By the time two people drive to a destina-
tion and order food, it is already time to leave. Instead of
enlightening a referring physician, a rushed lunch may actu-
ally be an imposition. Exceptions to this are extended lunch
hours that would allow both parties time to relax or if the
referring physician is a good friend. In the case of a strong
existing friendship, there is much less social strain to court the
other physician. Another problem with lunches is that many
specialists pursue referring physicians, and they sometimes are
“lunched to death.” A referring physician may actually be put
off by the thought of a long lunch, but be embarrassed to turn
you down. It is perhaps best to schedule a dinner or a weekend
event that is not so bound by time constraints. Obviously,
these matters are personal and do not apply to every situation;
nonetheless, the subject warrants consideration.
It is sometimes wise to leave a referral relationship strictly
the way it is. It is human nature to try to become close to
someone who is sending you business. The referring office is
probably sending you patients because you and your staff treat
their patients well. Sometimes the best thing to do is to con-
centrate on the treatment and not the social value. A referring
physician need not become your best friend, but you do need
to find a means of thanking them. Really successful offices are
those that know how to say thank you. Once you figure out
how to do this by different means on a consistent basis, you
have figured out marketing.
OBTAINING OUTSIDE CONSULTATION
We have touched on the importance of this strategy in the
beginning of this chapter, and additional discussion is war-
ranted because it relates to the topics at hand.
Oral and maxillofacial surgeons are leaders by virtue of
what they have achieved. Their ranks hold a most impressive
array of talented men and women. The author is always
impressed when attending our annual meeting by the caliber
of their membership. Many have entered this specialty to be
independent, and it is sometimes difficult to look to others for
assistance. One of the most beneficial things that the author
has done to benefit his practice is the use of outside consul-
tants. Again, for many OMS practices, it would be unthink-
able for them to consider a consultant because they believe
that they know their practices or cannot justify the expense.
With the proper consultant, this is so very far from the truth.
We all believe that we know our practices, but we are blinded
by a subjective factor, and that factor is referred to as emotion.
All practitioners truly desire their practice to prosper, but
unnecessary stress and inefficiency burden many physicians.
These physicians assume that the practice has to represent this
drudgery and are destined to tolerate it for the sake of their
careers. These physicians have cheated themselves and given
in to the cop-out that OMS “is not what it used to be” and
cannot be enjoyed. They believe that they have an intimate
knowledge of their practice and community, but they cannot
see the burden that their emotion has created.
This same situation exists in our practice because a trained
professional can see and appreciate things that we cannot. “A
338 SECTION III ■ Practice Management
fish cannot see water because he is in it all the time” sums up
the need for outside consultation. The author has found this
to be a constant breath of fresh air and change. It has been
especially effective for partner relations, managerial selection,
associate buy-in, employee relations, and plotting the course
for the future. To spend $10,000 or $12,000 to make 5 to 10
times that in profitability seems a no brainer, yet so many
physicians wish to do it themselves. The monetary gains are
probably overridden by the gain in efficiency and decrease in
stress.
It is not only problematic or inefficient practices that
require professional consultation. Thriving, prosperous prac-
tices also need preventive maintenance. It is always wise to
change the oil before the engine blows up.
Often the product of a consultation visit leads to gross
changes. Closing or opening satellites, terminating senior staff
or associates, changing fee structures, and altering buy-in and
buy-out policies are a few of the changes that the author has
experienced, but these have all been retrospectively beneficial
for the entire practice.
Where does one find a qualified consultant? Many times
professional associations maintain lists of consultants recom-
mended by the membership. One caveat is that just because
a consultant calls himself or herself qualified, does not mean
that he or she can carry the load. The field of health care is
replete with “consultants,” and a former dental hygienist may
not have the professional background to make hard business
and accounting decisions. Another beneficial source is
the Medical Group Management Association (MGMA). This
professional organization is a nationwide entity with very
valuable health care resources. Any practice with a manager
should require membership with this group. They have publi-
cations, multispecialty practice figures and forecasts, employ-
ment opportunities, and a vast network of printed material
available. This organization can recommend a list of qualified
consultants.
When considering a given consultant, always ask for refer-
ences and check them thoroughly. Good people come highly
recommended. Maintain a reasonable expectation of any con-
sultant. Most mature practices have problems that took years
to occur and cannot be fixed overnight. A good consultant
will be able to focus on the main areas of weakness and initiate
short- and long-term goals for the practice. The author would
no more consider practicing without a consultant than he
would without malpractice insurance.
COMMUNITY SERVICE
It has been said that what one gives to his or her community,
they will get back tenfold. The author truly believes that this
applies to OMS. There are many positives about being an
active participant in community service programs. First of all,
it gives a local physician a means of paying back and thanking
the community. There is never a community where someone
cannot afford our services, but is in great need. This type of
charity work really brings a good feeling to the caregiver, and
inevitably the community will notice. A caring physician
donating his or her services to those in need is an impression
that sticks in the mind of the citizenry and frequently gener-
ates publicity that further reinforces the giving role. The
author and his partners have had much experience with
a multitude of community service projects, and everyone
involved becomes a winner. It is a powerful means of assisting
the less fortunate and building a reputation for compassion.
PROCEDURE-SPECIFIC MARKETING
There are procedures we perform as physicians that provide
more clinical and economic satisfaction than the removal of
carious teeth. It is these rewarding operations that most physi-
cians wish to proliferate in their practices. It probably can be
safely stated that the best means of marketing dentoalveolar
procedures is to market to the general dental offices. Although
this certainly holds true with such expanded procedures as
implants, temporomandibular disorders (TMD), surgical
orthodontics, and cosmetics, the general dental office in itself
may not be the optimal marketing target. For one thing,
certain referring dentists may not do or believe in such areas
of surgery as TMD or implants. There are practitioners that
have a captive audience of possible implant or TMD patients,
but because of previous bad experiences or failure of the
dentist to stay current, their patients may be told on a daily
basis that “implants don’t work” or “TMJ surgery is ineffec-
tive” or “cosmetic surgery can only be provided by plastic
surgeons.” Obviously, this caliber of referring dentist is beyond
the casual “go see the oral surgeon” mentality that more fre-
quently exists. It is for reasons like this and the broader markets
available that procedure-specific marketing can greatly
enhance one’s patient base.
The first and foremost factor in subspecialty marketing is
clinical excellence. Unless a physician is on the cutting edge
of education in a given area, he or she cannot profess excel-
lence. Being on top of continuing education allows one to
possess information that may be disseminated to referring col-
leagues. It sets one apart as an expert and opens the door for
preferred referral and confidence. Equally important is the
need for OMS to achieve good treatment results. Nothing
succeeds like success, and this certainly applies to specialty
marketing. Once this type of relationship is established, it is
not uncommon for a given referral source to continue to send
patients to another oral and maxillofacial surgeon but send
the procedure-specific cases to you because of your efforts and
results. In many cases, this allows one to “get a foot in the
door” to obtain all the patients referred from a given office.
Without technical excellence it is much more difficult to
market to referring physicians or the public because they may
be more informed than the treating physician. A specialist
preaching antiquated techniques will soon lose the confidence
of referrals.
Another reason that general dentists may not be an ade-
quate target for procedure-specific marketing is that cosmetic
surgery is beyond their training or interest, or they are simply
uninformed. This brings us to the second important point in
procedure-specific marketing and that is educating your target
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
market. It is absolutely imperative that your primary market-
ing target, which is the referring dentists, is knowledgeable
and aware of your services. The key is to educate this group
to be aware of indications for the techniques that you offer.
Given the emphasis on aesthetic dentistry, there exists a
fertile market and opportunity to present literature and discuss
one’s given level of interest.
The specialist with these goals in mind needs to prepare
information packets for referring dentists to give to patients
and an educational experience to inform the dentist and their
staff.
The second half of the successful equation for procedure-
specific marketing is the dissemination of information to the
secondary target market, which is the public. We will discuss
this specifically in the following text.
As the oral and maxillofacial surgeon matures in practice,
he or she will find areas of the specialty that are more person-
ally and financially rewarding, and most will desire to
“subspecialize” or, in some cases, limit one’s practice to these
specific techniques. This author began the pursuit of cosmetic
facial surgery over a decade ago and progressively began doing
more and more cosmetic surgery each year. This became a
passion and eventually led to limiting his practice solely to
cosmetic facial surgery. At first this was met with some skepti-
cism from the local dental community, but after publishing
more than 150 articles on the subject and lecturing interna-
tionally on the subject, the naysayers warmed up and are quite
supportive.
INTERNAL MARKETING
This is the most overlooked marketing tool in our profession.
We are in somewhat of a unique situation in that our recep-
tion rooms hold a captive audience. We, on a daily basis, have
patients escorted to our offices by individuals of varying ages.
These patients sometimes require a significant wait and
are frequently bored. Many people bring books or trust that
physician’s offices have magazines. The latest issue of People
magazine will do little to promote your procedure-specific
marketing efforts.
If a surgeon is truly interested in cultivating given areas of
practice, then every person that walks in and out of that office
becomes a prospective patient or referral source. It is shameful
that many of our colleagues are doing truly dramatic expanded
OMS procedures on the other side of the door, yet the major-
ity of potential patients a few yards away remain unaware.
With multiple advances in personal computers, it is truly
easy to make excellent display and educational materials that
only 5 years ago would have required expensive professional
assistance. Now anyone with a PC, desktop publishing soft-
ware, and a color inkjet printer can make high-grade, quality
pictures, pamphlets, newsletters, and a multitude of other
promotional material. It is quite simple to make a Microsoft®
PowerPoint® presentation of one’s given clinical passion and
display this in the reception room and other treatment rooms.
The choice is yours; a patient can wallow in boredom or pass
time by looking at before-and-after photos, case presentations,
339
FIGURE 19-6. Looping PowerPoint presentations detailing the scope of
the OMS practice can provide the patient with interesting information while
waiting and simultaneously market the practice.
educational videos, and interactive CD ROMs (Figure 19-6).
People thrive on information and, especially in that environ-
ment, will read or look at anything put before them. The
author has not only found this to be an effective marketing
tool, but has also created a broad area of interest for staff
members to develop and become involved. This enhances the
team concept because it makes the staff believe that they are
truly contributing more directly.
One’s reception room can have Norman Rockwell pictures
or posters of functional and cosmetic patients in the preopera-
tive and postoperative stages. If the surgeon is a contributor
to the professional or media literature, it is very effective to
display these articles in the reception room. Anything that
shows the public one’s expertise or interest in specific expanded
procedures is of great marketing advantage (Figure 19-7).
Although the patient can gain much information from a
well-displayed reception room, it is imperative to give them
information to take home. Brochure racks with informational
and educational procedure-specific pamphlets are very popular
with patients. Physicians that pursue the powerful potential
of internal marketing will attest that many patients comment,
“I didn’t realize that oral surgeons did that.” If a surgeon
believes that it is too aggressive to place pictures, etc., on the
wall, then tasteful coffee table photo albums can serve the
same purpose. If you have a clinical passion, brag about it, and
the patients will become interested.
In all considerations of marketing, one must constantly ask
the question “How can I spread the word about these proce-
dures that I enjoy doing?” The answer is to take everything to
the next step. If you are making promotional media for your
own office, how about distributing it to the offices of your
known referral sources? A tastefully prepared album demon-
strating the given procedure or procedures may well be a
welcome addition to the reception rooms of your referring
dentists.
340 SECTION III ■ Practice Management
FIGURE 19-7. Displaying articles published by the surgeon or media
featuring the surgeon can serve to instill confidence in patients.
Finally, and it may sound trite, the author strongly recom-
mends actually telling patients that one has expertise or
enjoyment for given procedures. It is amazing how much
people talk, and word of mouth is and always will be the
ultimate marketing tool.
Offering wireless Internet service in your reception room
or having a PC that is always online is also a welcome con-
venience for patients.
NEWSLETTERS AND MEDIA PACKS
As is true to all marketing, informing a target referral or a
target patient market of one’s services is key. We assume that
most general dentists and patients are well acquainted with
our professional capabilities. It has always amazed the author
that even newly graduating dental students are frequently
mis-informed about our capabilities.
Newsletters have become very trendy, and many of them
are probably discarded without being read. The key to effec-
tive use of this powerful marketing tool is presentation and
content. A Xerox copy of a newsletter on a folded white
8.5 × 11 piece of paper just does not get attention. In addition,
a recipe for summer punch is not relevant. One can literally
spend thousands of dollars in the development of a profes-
sional newsletter, but it can be done for almost nothing with
a PC and a copy center.
First, people like reading news. It does not even have to be
news that relates directly to your specific procedure. Almost
everyone will listen to health-related news. Articles from the
New England Journal of Medicine or the vast array of health
news and studies available on the World Wide Web serve as
good filler. If one is truly pursuing excellence in a specific
procedure, chances are that they are well acquainted with the
current literature. Great articles can be built around scientific
journal literature. Anything new, controversial, or of interest
is likely to draw attention.
In most referral circles, referring offices are well acquainted
with the specialty office, and some personal information may
be of interest. Interoffice news, such as courses attended by
the physicians, articles published, awards of physicians and
staff, and other “gossip,” may hold interest. There are many
things that can be disseminated through newsletters. Office
hours, new staff, seminars, insurance and coding information,
and the like are very relevant. Pictures, graphs, tables, and
color all enhance such a publication.
In the employment of a newsletter, the author warns of
several pitfalls. To be effective, the newsletter must be con-
sistent. Many offices begin with a very energetic newsletter
and a commitment to continue, only to fizzle out after one or
two issues. A well-constructed newsletter is work intensive,
and setting realistic goals is paramount. It is far more effective
to have a quality quarterly newsletter than a mediocre monthly
publication. The author suggests finishing the future issue
before the present issue is released. This forces the office to
have issues “in the can” for future uses. The other important
point is to involve everyone in the practice. If each employee
and physician is responsible for a given duty, the workload is
dispersed and organized.
If one is serious about a referring office appreciating the
newsletter, the quality and quantity cannot be overlooked. If
you are truly providing useful information, chances are that
your referring offices may wish to keep the publications. A
personalized three-ring notebook with your office name and
logo will give the physicians somewhere to store your newsl-
etter and enhance the perceived value of your medium.
Obviously, also offering the newsletter via e-mail is
advantageous.
A media pack is the equivalent of a fragmented newsletter
intended for one’s referring offices. An example may include
brochures of your office, scientific article reprints, promotional
freebies for the referring physician, actual case presentations
of aesthetic or functional results, medical emergency tips, per-
sonalized pens, magnets, Post-it notes, etc. This marketing
tool is intended as a promotional “care package,” and its con-
tents can be innovatively constructed with the efforts of your
staff (Figure 19-8).
While on the subject of marketing for referrals, there is an
imperative link that is missed by many offices, and that is the
referring staff. As we have pointed out various times, it is fre-
quently the general dentist’s assistant, hygienist, or reception-
ist that actually makes the referrals. It is very uncommon that
these individuals receive a direct thank you from referring
offices, and, once done, it leaves a serious impression. Never
underestimate the power of ancillary referring staff. Our prac-
tice has numerous CME activities, specifically for referring
physicians and staff (Figure 19-9). This is typically done on a
Friday (a bad time for an oral and maxillofacial surgeon to
miss work, but a common day for the general dentist and spe-
cialist). These seminars discuss common OMS procedures and
those that may be very relevant for the dental practice. ACLS,
office emergencies, cosmetic facial surgery, advances in dental
implants, and antibiotic and medication updates are popular
subjects. Our practice makes this a fun day and raffles some
gifts, such as an iPod, Botox injection coupons, and other
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
FIGURE 19-8. Everyone likes something for free, and patients appreciate
a welcome to the practice gift. Cosmetic samples, personalized bottled water,
pens, magnets, and informational brochures are provided for all new
patients.
FIGURE 19-9. Offering all-day CME programs for referring physicians
and staff is an excellent way to promote the practice while providing a
service.
goodies. In addition, the staff and physicians receive continu-
ing education credit for these meetings.
MEDIA NETWORKING
Our nation and the world have made the planet smaller by
the ability to report news events as they unfold. In 1864, it
took weeks for some rural people to find out about the assas-
341
sination of President Lincoln. Most of us, on the other hand,
observed the events of Operation Desert Storm live. There
are many sources of news and informational services, includ-
ing satellite, cable TV, network TV, local TV stations, maga-
zines, newspapers, and other printed material on national and
local levels. With all these sources of news, these companies
have the constant need to report anything of interest. Editors
literally scramble to find anything that might provide interest
to sell their respective media.
This need for news coupled with the rapid advances in our
specialty provide a fertile situation for newsworthy material.
The baby boomers are now into their 50s, and we have as
health conscious a society as ever. People want to know and
understand their health and disease. It is not unusual to turn
on the television set and see an actual surgical operation.
Virtually every form of media has a health news section, and
as oral and maxillofacial surgeons, we need to take advantage
of this.
Many of the procedures we perform produce dramatic
results and are therefore newsworthy. In addition, we are
doing many new procedures that are even more interesting to
the general public. Even such simple operations as dentoal-
veolar surgery hold interest to the public because they and
their families will undergo many of these experiences.
There is a multitude of ways to gain this type of exposure.
In some cases, editors will call local physicians to inquire
about specific procedures. This is a hit-and-miss situation.
Some physicians employ professional marketing firms to initi-
ate a media campaign and usually obtain adequate results at a
significant expense. The methods used by professional agen-
cies are basically saturating any and all media sources. This
requires the compilation of press releases and distributing
them to the usual sources. This basically is a simple procedure
and requires little more than the ability to write and some
mailings.
Instead of spending serious money on professional services,
the average practitioner can do this in-house. A press release
is no more than a short story with an interesting headline.
“Teeth in One Day” or “Weekend Face-Lift” would be typical
headlines followed by a several paragraph description. It is
important to keep these releases informational and not pro-
motional and to focus on the operation and not the physician.
Generally, the author will be quoted, and the marketing
is in the name association with the technique. Sometimes,
depending upon the topic, the editor may do an in-depth
article, and a subliminal promotion is usually appreciated by
the public. It is important to remain accurate and quote
average success rates, etc. Sensationalism or fictitious infor-
mation can severely reflect on the credibility of the editor
and the company.
It is important for anyone who begins this type of media
promotion to understand that the return may be one hit in 50
releases and not become discouraged with the ratio. It is per-
sistence that frequently wins out. In addition, many health
editors file away this type of information, only to use it months
later when a related topic or article surfaces. It definitely helps
342 SECTION III ■ Practice Management
FIGURE 19-10. Having a close relationship with local media can serve
as public education and distinguish a surgeon in the community.
to have a working relationship with local newspapers, televi-
sion, and radio news or health editors (Figure 19-10).
FINANCES
Many practitioners fail to see payment options as a significant
marketing tool. This can be a true practice builder. Our
country has been built by making it possible for people to
purchase goods and services without paying for them at the
time of purchase. Department stores established this concept
years ago and issued charge cards. This has existed in our
society for many years from the corner store to the biggest of
businesses.
The thrust of insurance coverage will shift to significant
patient responsibility, whereas many patients may be left
without any coverage. All of this accentuates the need for a
financial program. For most patients, what we do is a middle
class luxury, and we are a low priority for payment. It is not
uncommon for a patient not to realize that they have impacted
third molars until their dentist points them out. They are then
referred for removal and undergo inconvenience, discomfort,
and expense without any real perceived appreciation. People
do not mind paying for something they perceive as important,
but are quicker to default on items or services without per-
ceived value.
If one extends payment plan options, they must inform
the target market to turn this into a marketing tool. Obvi-
ously, a sensible ratio exists for each practice, and one does
not want an excessive amount of payment plans. One must
keep in mind that when we extend someone credit, we are
actually giving them an interest-free loan. Most physicians
do not want to be in the banking business, but those with
true business sense realize that a vast potential exists.
Although there are many honest individuals that will be
compliant, payment options must be set up with the non-
compliant patient in mind. Payment options must be strin-
gent and have signed contracts as to what happens in the
case of default. Most us are used to paying home or auto
loans, and if we were to default, we would face consequences.
The same must be instituted when formulating a payment
plan. First, one must determine the credit risk of a patient.
The author, like many practices, maintains a modem con-
nection with the credit bureau and can check on the record
of a patient. It is interesting to see a given credit history
because it is not uncommon for people to have good credit
with banks, but multiple infractions with health care provid-
ers. Needless to say, a patient in this category is a poor risk.
If a patient defaults on a payment plan, the balance is due
immediately and will go to collections with the signed patient
agreement. The agreement also states that it is the patient
who is responsible for the attorney’s fees. If default conse-
quences are not explained upfront, the plan is ineffective. In
the author’s office, there are certain requirements to qualify
for credit, and a credit report is filed. Some patients remain
ineligible, but the majority of applicants do qualify. There is
a down payment required at the time of surgery, and experi-
ence has shown that those patients unable or resistant to this
will have a high default rate. If a surgical procedure has a
$1000 fee, we require one-third of the amount on the day of
service and extend the remaining balance for 3 to 6 equal
payments. The patient is issued a computer-generated coupon
book similar to car loan coupons and an expected payment
schedule. As stated earlier, if payments are tardy or missed, the
account may be turned over to collections.
Many offices charge a reasonable interest rate on their
loans, and this can be a profitable situation. It also takes some
of the sting out of lending money.
There are corporations, such as Care Credit (www.care-
credit.com) that greatly automate and simplify credit opera-
tions, and many offices have shifted most credit situations to
this type of service.
YELLOW PAGES ADVERTISING
In the previous edition of this text and chapter, much verbiage
was dedicated to this subject. Since the first printing, the
Internet has overtaken the telephone book as a primary infor-
mation source. Many practices have significantly backed down
their emphasis on Yellow Pages advertising. It may still be
important to have a presence here, but a generic ad that lists
services and locations will probably suffice, and the other
money is better spent on Web services.
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
COSMETIC SURGERY MARKETING
In the past 30 years, we have witnessed an explosion in the
scope of our profession. We have advanced from dentoalveolar
and trauma specialists into orthognathic surgery, which
increased our aesthetic awareness and opened the door for
progression into the facial cosmetic arena. This says a lot
about the aggressiveness and ability of our ranks.
Although at the current time, full-blown cosmetic prac-
tices constitute a mere fraction of our membership, this area
promises great excitement and growth potential. Aesthetic
surgery is especially attractive to the oral and maxillofacial
surgeon for a variety of factors. First of all, we have been doing
cosmetic and nasal surgery with our osteotomies for some
time. We have an excellent understanding of the face and are
enthusiastic about providing surgical techniques that someone
actually wants or looks forward to. Our ability to perform
outpatient ambulatory surgery allows us a cost-effective forum,
and, finally, with the current state of managed care, all special-
ties are looking for noninsurance reimbursement. This under-
lines the point we have eluded to several times that people
will spend money on something that they perceive to be
adding value to their lives. With the aging baby boomers,
there is a more fertile market than ever before. The door is
wide open for our specialty, providing we make cosmetic
surgery part of our grass roots training. Most residency pro-
grams teach cosmetic facial surgery procedures; it is part of the
OMS board exam and is covered by OMS malpractice insur-
ance. It represents part of the evolving contemporary scope of
our profession.
For those of us already in practice, the challenge to keep
up exists along with the ability to expand our practices.
Someday in the future, people may well wander into an OMS
office and ask for a face-lift. For now, however, we must
elevate the public’s awareness of what it is that we do.
We are very lucky because we have a captive audience in
our reception rooms on a daily basis. All of us who have done
osteotomies and genioplasties should have enough before-
and-after pictures to construct an interesting display in the
reception and evaluation areas. As stated so many times
earlier, to successfully market a technique, one must possess
expert status and have significant experience with the tech-
nique and its complications. For this reason, one should tread
lightly and not overmarket commensurate to experience. The
author believes that skin care, genioplasty, facial liposuction,
facial mole and lesion removal, repair of split earlobes from
pierced ears, chemical facial peels, lip and wrinkle enhance-
ment with injectable fillers, and Botox injection are proce-
dures that can be performed in the office and are easily within
the capabilities of most oral and maxillofacial surgeons. With
a basis of these procedures, one can build a cosmetic surgery
base with little expense. Some physicians may be satisfied with
only these procedures, whereas others will progress to laser
resurfacing, eyelid, nasal, and face-lift procedures. These obvi-
ously will take a significant commitment on the part of the
physician and on our specialty as a whole. Fortunately, there
343
exist many worthwhile courses to enhance our education. A
potential drawback may be the dental practice acts in some
states. Most of us practice under the auspices of the dental
laws, and they need to be constantly updated to remain current
with our progression and advancement. It is imperative that
our political ranks pursue this in all states.
A much simpler means of expanding one’s practice into
the cosmetic arena is to hire an associate with the expanded
training. This associate can kick off the introduction of the
procedures and teach the other partners how to perform these
procedures.
Most cosmetic surgery practices cater to an affluent patient
base. For most patients, aesthetic surgery is a luxury, and these
patients are used to luxurious environments. An office dedi-
cated to cosmetic surgical procedures cannot project the
proper image with unfinished pine furniture and NASCAR
magazines. These offices must look as nice as the living room
of the clients seeking your consultation. Formal furniture with
a professional decoration scheme is of utmost importance in
the mind of the author. Most patients seeking facial cosmetic
procedures are female, and this is an important statistic to
keep in mind and tailor the office to.
Confidentiality in cosmetic surgery is an entirely different
ballgame, and neighbors or acquaintances do not necessarily
want to be seen in this environment. In addition, the recep-
tion room is not the place for a prospective laser patient to
view a 48-hour postoperative laser patient. Private entrances
and cubicles can assist this situation immensely.
Cosmetic surgeons are very keyed into informational
sources and have a vast array of informational and skin care
products available for their patients (Figure 19-11). A
cosmetic-oriented practice should be well stocked with litera-
ture explaining various procedures and techniques because
these frequently open the door for various procedures (Figure
19-12). When performing chemical peels or laser resurfacing,
there are many products that may be sold through the office
that will assist the patient and income stream of the practice.
FIGURE 19-11. Offering skin care products provides a service and is an
introduction to further cosmetic procedures.
344 SECTION III ■ Practice Management
FIGURE 19-12. There should never be a bored patient in the reception
room. Providing educational and marketing materials promote the practice and
are appreciated by patients.
In addition, there is an added convenience for the patient to
be able to purchase their required products without going
somewhere else. Many plastic surgery practices have ancillary
staff that generate significant income from consultation and
sales of pretreatment, posttreatment, and maintenance prod-
ucts. This should not be overlooked, but the staff must be well
trained.
There are many avenues available to market the cosmetic
practice. This is easy lecturing because of the level of public
interest associated with this topic. As stated earlier, many
social clubs and organizations exist that actively seek patients.
This is grass roots marketing and will interest male and female
members. To truly tap the perspective market, one must gain
exposure to female clientele. Many women’s clubs exist, and
speaking to a group like this can be a tremendous marketing
experience. If one thinks about the habits of cosmetically
inclined individuals, then beauty shops, makeup counters, and
clothing stores are good marketing sources when tastefully
done. Ear piercing kiosks at malls, tanning salons, and health
clubs are also excellent sources of prospective patients. Provid-
ing referring dentists and OB-GYN offices with personalized
informational brochures on cosmetic procedures can also be
effective, although many physicians may not display such
material. Some practitioners publicize the fact that they offer
significant discounts to staff of medical or dental offices. The
strong testimonial from a satisfied medical staff person can
provide powerful marketing.
Internal marketing is a good way to inform prospective
patients and stay under the radar screen of competing special-
ists, who may go to unbelievable lengths to limit one’s scope
of practice. External marketing is effective, but will more
likely bring on the wrath of the competition. Professional
marketing firms are established in all cities and can initiate
personalized marketing plans commensurate with given
budgets. This author spends a significant amount of time and
money on cosmetic surgery marketing. It is more of a lifestyle
than a task. Being extremely involved in publishing and lec-
turing says a lot about any surgeon and is a great asset when
the public is informed. The dissemination of advertising in
our practice includes television, radio, newspapers, local
“throwaway” papers, websites, seminars, sponsoring of local
events and charities, donating goods or services to local events,
and performing pro bono cosmetic surgery on needy patients.
This author believes that it is important to segregate the cos-
metic side of the practice from the dentoalveolar side because
the competition has done its best to confuse the public about
having cosmetic surgery from a “dentist.” The author is proud
of his profession, but the difference between cosmetic surgery
and dentoalveolar surgery is less confusing than segregating
the two. Some practitioners physically segregate the facility,
and others see only cosmetic patients on certain times
or days.
The cosmetic patient must be marketed from the first visit
and continually thereafter. A welcome gift is provided for
each patient and contains various marketing and informa-
tional materials, cosmetic sample product brochures, bottled
water, magnets, pens, and sometimes discount or promotional
coupons. In addition, each patient is sent a personal letter
after their evaluation appointment thanking them for choos-
ing our office. This author does not charge for cosmetic evalu-
ations and believes that it is a barrier that can deter even
wealthy patients. Many times patients have been seen for a
free cosmetic evaluation that have also been seen by compet-
ing specialists and end up choosing our office because they saw
how special we are. In addition, offering same-day procedures
(same day as the evaluation), such as Botox, mole or spider
vein removal, etc., can build patient loyalty. This author has
performed many face-lifts on patients that wandered into the
office for a Botox injection. Discount coupons are sometimes
used that provide a free Botox injection; after nine injections,
the tenth treatment is free. Alternatively, if a patient brings
a friend for Botox or filler injection, they each receive a dis-
count. Some physicians do not feel comfortable with this type
of marketing, but all patients love it.
If the physician or a staff member is an interesting public
speaker, many venues lay waiting for cosmetic presentations.
Salons, spas, health clubs, and women’s groups are excellent
marketing opportunities (Figure 19-13).
Considering all possible marketing strategies, nothing can
replace compassion and availability. The author gives his cell
phone number and e-mail to all cosmetic patients, and this
level of availability is priceless for marketing. Calling postop-
erative patients (not only cosmetic surgery patients, but all
postoperative patients) is also an unexpected and appreciated
service.
 CHAPTER 19 •
FIGURE 19-13. Public information seminars of targeted groups, such as
women’s clubs, are effective in generating interest and referrals on cosmetic
surgery or other aspects of OMS.
Most of the marketing techniques applicable to procedure-
specific marketing, as discussed in an earlier part of this
chapter, are effective in the cosmetic arena. The use of a pro-
fessional and educational website is invaluable. This author
has treated many patients from out of town and even out of
the country solely from Internet exposure. Most of our patients
truly study the Web pages before making an appointment and
by the time of the evaluation are already well educated.
Any physician who is serious about marketing needs to
have a good camera and use it constantly. If one physician
performed 100 procedures with no documentation, whereas
another physician performed 10 procedures with great follow-
up images and statistics, the second physician can better
market because of these valuable tools. Many times the one
who better tells the story wins the prize. Digital imaging has
changed the paradigm for taking and archiving images and has
made this a much simpler task. Preoperative and postoperative
images of cosmetic surgery (or any procedure) are invaluable
for marketing, medicolegal considerations, and the patient
record.
CALL-ON-HOLD
One can promote his or her practice with call-on-hold devices.
In a well-run office, patients on hold will be minimal. Few
things put patients off more than a long hold, especially for
those calling for an initial appointment. The receptionist
should take a number and return the call within 5 minutes,
rather than put the patient off. A long hold on the telephone
is basically telling the patient that they are not a priority.
All offices will experience holding telephone patients, and
the recorded promotional messages can be helpful. One thing
the author cautions is to make a script that stands out from
others because these devices are very popular, and many seem
to have similar dialogs. These devices may be purchased inex-
Marketing the Oral and Maxillofacial Surgery Practice 345
pensively from communication companies or telephone stores,
or for a larger price, a professional company will take care of
the hardware and scripting. We live in the information age,
and patients want information.
CALLING POSTOPERATIVE PATIENTS
In the author’s opinion, this is the single most important PR
technique that a physician can do. No other type of marketing
can do so much for so little investment.
Many oral and maxillofacial surgeons call their patients in
the evening to check on their status. These “phone rounds”
are quite rare in the medical world, and many patients are
literally taken aback by the fact that their surgeon took the
time to personally call. The author has, many times, had
patients say that the reason that they returned to the office or
sent another patient was the exemplary fact that the physician
called them after surgery.
If the physician cannot call the patient, then the surgical
assistant should call, or the receptionist can dial up the patient
the following day to have the physician say hello. The impact,
however, is much more significant when the physician person-
ally calls the patient the night of the surgery. If a surgeon did
no other PR, he or she would get a lot of mileage out of this
technique.
ACTIVITY SPONSORSHIP
Marketing is recognition, and community sponsorship directly
relates to recognition and helping individuals. The author and
his partners are active in many community groups, including,
Big Brothers Big Sisters, area mentally-disabled citizens groups,
scouting, Rotary Club, YMCA, minority groups, athletic
teams, charity groups, etc. Some of this activity includes direct
participation or speaking, whereas other involvement includes
sponsorship or buying uniforms with our name and logo or
placing ads in athletic programs or posters. Most aggressive
marketing offices follow the tenet “every little bit helps.”
MANAGED CARE AND MARKETING
The fee-for-service environment along with the laws of supply
and demand have set the stage for referral favoritism for a
century. We are now in the midst of a managed care revolu-
tion, and many rules are rapidly changing. Although no one
likes the fact that we are doing more and being paid less, we
must learn to adapt to a thin environment. With all the nega-
tive talk, one positive is that managed care has made many of
us better businessmen and businesswomen. Physicians have
been notorious for being remiss in many business functions,
but as a result of the previous profitability, could afford to be
sloppy with their business practices. The ensuing changes
have forced many physicians to take a hard look at their
coding, billing, collection, purchasing, and other business line
items to control costs and raise profitability. Some physicians
have actually found that the attention to business detail will
make them more profitable than before.
Because managed care companies recruit closed groups of
participating physicians and specialists, there may be no
346 SECTION III ■ Practice Management
choice as to specialists. In other words, we may have a captive
audience of general dentists that has no choice but to refer
patients to our office because of contractual participation.
This negates many of the previous referral tactics that have
been traditionally used to gain preference. There is still no
substitute for superlative patient care, but depending how long
managed care stays popular, the traditional specialist market-
ing may become much less of an issue.
DO YOU KNOW WHAT IS HAPPENING AT YOUR
FRONT DESK?
As we have stated so many times preciously, your staff is your
greatest or worst marketing asset. Because the physician is
usually far away from the front desk, many of us are unaware
of what is truly going on. The author (as stated earlier) has
sent “sham” patients to make appointments and progress,
unknown to all staff and physicians, through the office. The
office administrator or consultant are the only individuals that
know the identity. At the next staff meeting, the “mystery
patient” comes and presents their input and observations.
This has served to be quite informative, in addition to keeping
everyone on his or her toes. The author also has individuals
call to make appointments to check on the courtesy and con-
sistency of the staff. It is also interesting to drop a $20 bill in
one’s petty cash to see what happens with the monthly
reconciliation.
An exceptional receptionist is the keystone of a successful
office. This person can bond with prospective patients or drive
them away in hoards. The key to being busy is to make it easy
to make an appointment at your office. As stated earlier, there
are many barriers to OMS. It hurts; it is expensive; insurance
is complicated; it adds inconvenience; it causes apprehension;
and many of the procedures performed have little perceived
value by patients. A great receptionist will work on these bar-
riers with the prospective patient and turn an inquiry tele-
phone call into an appointment. When a patient calls and has
obvious fear, a good receptionist will brag on how good the
physician is and how gentle and painless the surgery is. If a
patient calls and is concerned about finances, an astute recep-
tionist will bring the patient in for a complimentary consult
and explain to them that the practice has payment options.
If a patient calls and is concerned about insurance hassles, the
proficient receptionist will tell them the name of their per-
sonal insurance person in the practice that will process their
insurance. If a prospective patient is concerned about incon-
venience, a good receptionist will work the patient into the
schedule to suit them. Many patients call various offices to
shop for price or just a general feel of office demeanor. A
smiling, energetic, enthusiastic receptionist will “attack” these
patients with kindness and service and win them over. We
use the word ‘smile’; although you cannot see a smile on the
telephone, you can certainly sense it. All of our offices have
signs at the front desk that say, “always answer the phone with
a smile.” This is truly the first rule of service. We all have bad
days from time to time, but they must stop when the telephone
rings. It is absolutely imperative to treat every telephone call
as if it was your best friend. Remember that the patient is our
boss. The author has some very trusted and competent employ-
ees, but we do not allow them to answer the telephone because
of their rough edges when dealing with the public.
There are many simple tricks that an excellent receptionist
can use. When a new patient comes to the front desk, and the
receptionist asks, “Have you ever been a patient here before?”
this can be very negative. This patient may have a purged
chart, been a patient several years, and had a $15,000 osteot-
omy and we are asking them if they have ever been here. This
is an insult; the appropriate greeting is “When is the last time
you have been to our office?” At worse, they will say “Never.”
When a patient of record calls, the staff should act obviously
excited and engage in a minor conversation. People adore
being remembered or being recognized. In this harsh world of
automated answering, a smiling, friendly voice is a rare find.
This is paramount when any referring physician calls. If your
front desk people do not know something personal about your
referring physicians, then you have the wrong staff. “Dr.
Niamtu, it is so good to hear your voice, how have you been,
are you still making people beautiful?” is much better than
“How do you spell that name?” Making contributions to some-
one’s office and not being recognized is a real turn off. Even
new employees must act like referring physicians and patients
are old friends.
One thing that occurs in all offices is cancellations. Most
offices have patients that make appointments, but fall through
the cracks for various reasons, usually finances, time, or fear.
An excellent receptionist will reschedule a broken appoint-
ment before the patient hangs up. If the appointment is can-
celled, this patient should be placed on a list and be called
multiple times to reappoint. Staying busy involves working
broken, missed, or cancelled appointments.
These same characteristics need to carry over to the clini-
cal staff also. These clinical and clerical positions are usually
distinctly different, and if communication is lacking between
“the front” and “the back,” the office cannot be efficient. If
one examines successful, happy, profitable offices, they invari-
ably find a harmony between clerical and clinical employees.
The key to this communication is cross-training. It is impos-
sible for someone to truly appreciate someone’s job unless they
have done it themselves. We earlier alluded to the policy of
fast-food chains, requiring their managers to spend time on
the grill and French fryer as part of their training. The author,
during a citywide blizzard, assisted in answering the telephones
and from that day on gained ultimate respect for the ability
to manage multiple telephone lines and maintain a smile. If
an office stresses cross-training, then every employee will
know the rigors of each other’s job. If your receptionist cannot
take a Panorex or assist in surgery or if your assistant cannot
make appointments, then you are short changing your patients,
your staff, and yourself.
The clinical staff also has very special requirements involv-
ing patient service. A good assistant is a buffer between a busy
physician and apprehensive patients. On the evaluation, these
employees can assist in filling in the blanks that the physician
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
has not expressed. They can assist in patient treatment
decisions and can quite often sway a patient toward a given
treatment plan. Compassion is essential for these staff
members. The ability to calm apprehensive patients and hold
the hand of a preanesthetic patient can truly mold the entire
surgical experience. This is no place for a gruff employee.
PUTTING IT ALL TOGETHER
THROUGH COMMUNICATION
The author has outlined many theories and techniques related
to marketing and patient service. We have used the term
“content, happy, and profitable practice” many times through-
out this chapter. Anyone who has built this type of office will
testify that it is a task of significant proportions, and the
pursuit of excellence is never ending. It is said that excellence
is a journey, not a destination, because there is no finish line.
If someone is truly dedicated to their profession and practicing
with enjoyment and profitability, they will peruse the follow-
ing tenets:
• Hire and maintain the correct staff.
• Provide leadership and enthusiasm.
• Make clear what is expected through a policy manual.
• Train the staff to be patient-centered service
providers.
• Reward them for their efforts.
• Pursue excellence in all facets of your practice.
• Know when to terminate an employee.
• Constantly improve the level of training and
communication.
• Always be a teacher and a student.
These tenets are key to set the stage for organized market-
ing. Without these, there is no marketing, unless it is negative
marketing. A common misconception is that marketing
merely involves the physical techniques mentioned earlier. A
surgeon cannot market alone, and an uninformed or under-
trained staff cannot market at all. Constant communication
and consultation are paramount in keeping the team sharp.
No football team would ever reach the Super Bowl without
practice. For the oral and maxillofacial surgeon, this practice
involves staff communication. Any progressive practice has
regular meetings with the physicians and managers and the
staff. Even though one’s staff may know what to do and what
to say, it has to be continually stressed to stay aware and sharp.
Enthusiasm is contagious, and the same may be said of the
lack thereof. This team spirit must be perpetuated. The author
has monthly staff meetings with the partners and manager,
quarterly staff meetings with everyone included, and an annual
retreat for staff focused on communication, patient service,
and continuing education. In addition to this, the manager
has regular meetings with various locations. One does not
need to have a group to do this; it is actually much easier with
a smaller office. Regardless of size, everything in this chapter
applies to all offices.
To enhance optimal communication, one must have policy
and consistency in all positions. The author and his partners
have used a set of communication principles that is referred
347
to as “the rules of the game.” This is an excellent list from
which to build and a valuable tool to show a prospective
employee that you are contemplating hiring.
As stated so many times earlier, every game has rules and
to win one must be acutely aware of all the rules to prevent a
disqualification. The winners in OMS are happy, profitable
practices, and the losers are those who go home exhausted and
frustrated and dislike what they do for a living.
The following principles are referred to as the “rules of the
game” and in the author’s office take precedence over all other
forms of communication. All partners, managers, and employ-
ees are aware of the rules, and they are posted throughout the
office in bright Day-Glo laminated frames. The author believes
that it is very important for each and every person in the
practice to have intimate knowledge of the rules, and like
referees in sports, the owners and managers must have even
greater understanding. We will examine each rule and its
implication as it relates to OMS.
Rule 1. Be willing to support our missions, values, and guiding
principles.
This rule, although very obvious, is the most often over-
looked. The author is amazed and confounded by how many
OMS practices do not have a written policy manual with
distinct job descriptions and a clear outline of the vision or
goals of the practice. If you do not communicate these with
an employee, how can you possibly expect them to support
them?
Rule 2. Speak with good purpose.
Gossip among physicians and employees is one of the
most destructive forces in an office. This involves speaking
about someone without his or her presence. This is done by
idle, unchallenged employees and can literally undermine
your entire staff and effort. This should be grounds for ter-
mination and strictly prohibited. This also applies to those
who say one thing and do another. A leader must truly
practice what they preach. Like your mom said, “If you can’t
say anything nice, don’t say anything!” This especially
holds true for pessimists.
Rule 3. Be open and honest in your communication with each
other.
Actually expressing one’s true feelings is sometimes very
difficult. We are often afraid to hurt someone’s feelings,
rock the boat, or cause friction, so often it is easier to agree
with someone or support their improper behavior because
you may be intimidated to express the truth. This is one of
the most difficult things for some people to do, but if this
rule is not followed, the others are meaningless. One must
be able to look partners, managers, and employees in the
eye and tell them exactly how one feels. If this is done with
consistency, a person will be respected. For this to work, all
individuals must take a pledge to be open and honest. This
breaks the ice and paves the way for open-ended commu-
nication. Failure to do this will perpetuate the problems of
communication that plague many practices.
Rule 4. Complete agreements and be responsible to others and
yourself.
348 SECTION III ■ Practice Management
When people sit down to iron out problems, it is human
nature for everyone to want to jump on the bandwagon and
to volunteer to take responsibility to make a change. This
frequently involves a task, behavior change, or a sacrifice.
All too often, those that are enthusiastic starters often lose
their vigor or neglect to follow through on the task or the
behavior that they promised. This is common and is one
huge reason why some practices never get out of the hole.
It is imperative that when someone says that they will
do something that they take the responsibility to follow
through and that the leader of the practice take the respon-
sibility to coach them through their stated work and insist
on its timely completion. A person must realize that when
they fail to follow through on a task, they let themselves
down and the practice.
a. Make only agreements that you are willing and intend to
keep.
b. Clear up any broken or potentially broken agreements at
the first appropriate time with the appropriate person.
This is especially important. If one sees that they are
missing their promise or timeline, then it is important to
discuss this with the correct person at the correct time. The
immediate leader for this staff position must be made aware
of the possible lack of follow-through, and it should be
expressed immediately. Complaining to the incorrect person
may be gossip, and failing to notify the leader immediately
will compound the problem by procrastination.
c. Do not commit to others unless there is agreement.
Because a given individual believes that he or she has
the correct idea or action does not make it correct. This
must be clearly communicated to the group, and a positive
response must ensue, which requires rule number 3.
Rule 5. If a problem arises, look first at the system, not the
people, then make the correction.
If there is one thing that many employers are guilty of it
is this. We stated earlier that most employee problems are
the result of the employer, not the employee. This is usually
true. Employees often take the brunt of criticism when the
employer is guilty for being a poor leader. If there is no
policy manual, no job descriptions, no vision or goals, then
whatever occurs is happenstance or coincidence. Your
chances of having an enjoyable, profitable practice then fall
into the odds of winning the lottery. Virtually any employee
problem can be traced to improper leadership. Next time
you are disappointed with an employee, stop and look in
the mirror and ask yourself as a leader, “Did I do everything
possible to make the rules and goals known and set clear
standards to be followed in this case?” It takes a big person,
but so often a leader cannot answer this in the affirmative.
A true leader will admit the shortcoming and do better; a
poor leader will continue to be a blamer.
Rule 6. Do not be a blamer.
No one likes taking criticism or being wrong, but blaming
others for one’s failure or shortcomings will only perpetuate
mediocrity. The three hardest words to say are “I was
wrong.” Once a person can speak with honesty and admit
this, they will be respected and open the door to other
individuals to exhibit this honesty. For this environment to
exist, the other staff must be supportive and accept an
apology and honesty and not persecute the individual or
dwell on the admission.
Rule 7. Commit to add value by making more out of less.
For any business to thrive, each person must add value.
It is when staff or physicians detract value that stress and
waste occur. The key to operating a successful business in
this day of managed care and business is to be lean, eco-
nomical, innovative, and value conscious. This is not only
in physical spending, but also on decisions and the entire
aura of the practice. Waste in policy or expenditures will
severely affect the ability for some physicians to enjoy their
work and make a profit. Each and every staff member should
constantly challenge each other and the practice to do
more with less, and when a suggestion is valid, that employee
should be rewarded.
Rule 8. Have the willingness to win and allow others to
win.
In a win-win situation, the attitude is if I allow others
to win, then I win also. With an employer, the win is even
bigger. This is a competitive world, and many people are
used to winning to be promoted or to advance. Unfortu-
nately, many of these people believe that they can only win
if someone else loses. This creates a backstabbing environ-
ment, and for the person to win, someone must lose. If this
person is your employee, then the practice will ultimately
lose. These people are very goal oriented and are difficult
to control. A win-win person, on the other hand, progresses
and advances just as fast, and with fewer waves, because
they realize that by allowing others to win, they will win
and may win bigger. It is this type of employee that portrays
altruism and is a valuable asset to any practice. The world
needs more winners.
Rule 9. Focus on what works, retreat on what does not.
Many times the best intentions are put forth with ideas
or policies, only to have them fail or fall short of the
intended benefit. A progressive leader will realize that some
ideas, no matter how good they seem, are not feasible.
These leaders will admit the shortcoming, regroup, and
attack the problem from another angle. A poor or resistant
leader will not admit to the shortcoming and beat a dead
horse, even though it is not in the best interest of the prac-
tice. Some leaders remain hardheaded and will propagate
poor policy just because they cannot admit to being incor-
rect. No matter how good it sounded, if it does not work,
move on. What is also important here is not to focus too
much on the past. If one is surrounded by individuals that
will not forget a mistake and continually reflect on what
did not work, the proper environment is not being fostered
to admit a mistake. Do not dwell on the past; learn from
mistakes and move on.
Rule 10. Encourage the risk of innovation.
One must focus on the very best communication for the
staff and the best service and care for the patients. To do
 CHAPTER 19 • Marketing the Oral and Maxillofacial Surgery Practice
FIGURE 19-14. A small change in the way we handle emergencies led
to a huge change in after-hours nuisance calls.
this often requires going outside of the usual parameters
for practice and service. If one follows the usual details for
running a practice, then one will have a usual practice.
To have an exceptional practice, one must constantly chal-
lenge the leaders and the staff to think of innovative means
to better the communication and patient service and care.
Sometimes staffs are shy or hesitant to provide input. Some-
times those who provide input are ridiculed or ignored or
worse yet go unrewarded. Big business learned decades ago
that it pays to have good ideas, and one should pay for good
ideas. If someone makes a suggestion that makes a differ-
ence, they deserve reward. They win, you win bigger, and
your patients win biggest.
An example is how our practice decreased after-hour
calls by 90%. No one loves being on call, and we all get
nuisance calls. Many or most of the after-hours calls involve
medications. Some are warranted, and many are drug
seeking. Our practice simply put a message on our after-
hour recorder that “No prescriptions are filled after-hours
or on weekends.” We also posted these signs throughout the
office (Figure 19-14). We initially feared that we may offend
legitimate patients in pain, but we were wrong. Legitimate
patients called during office hours, and drug seekers called
someone else. We literally decreased our emergency calls
by 90%.
Rule 11. Do not shoot the messenger.
Upon hearing bad news, the king would kill the mes-
senger or so the story goes.
None of us want to hear bad things about our practice,
but to ignore them, only makes things worse. “Ignorance is
bliss” is only for someone that wants to work in a stressful
and nonprofitable environment. A good leader must demand
to know what is good and what is bad and must liberate the
staff, patients, and referring physicians to have unencum-
bered input. If you make it hard for someone to tell you
negative things, you will never hear them. This is not
reality. Sometimes it requires a negative to make a positive.
True leaders have an open-door policy for constructive
349
criticism and will act accordingly. Before criticizing
someone, first try to understand the principles of the policy
and always offer criticism in a positive and constructive
manner, as stated in rule number 3. Encourage critique.
Rule 12. Raise the “red flag” when overloaded.
Leadership requires energy, and sometimes, with the best
of intentions, we put too much responsibility and burden
on ourselves. Even though we think we can handle it, we
become overloaded and begin to break rule number 4. This,
although with good intentions, actually encumbers the
practice and skews all the above rules. We all have limits
of responsibility that we can handle and must maintain a
good mix of relaxation and outside activities. If one becomes
overloaded in trying to make something better, they may
actually make it worse. We all tend to multitask, and some-
times, instead of advancing a few prime goals, we wallow in
stagnation. This leads to inefficiency and burnout. In addi-
tion, if our managers “raise the flag,” we can appreciate their
honesty, instead of admonishing them months later when
we see that the projects are not done. It is far more advanta-
geous to admit overload and ask for help to keep the prac-
tice on track. Never be afraid to ask for assistance, and
never create an environment where this is frowned upon.
Rule 13. Always maintain a sense of humor.
Life is a short ride, and we all have only so many heart-
beats to enjoy it. Sometimes we take things way too seri-
ously. There is a time for seriousness and a time for levity.
Most influential and successful people that the author has
had the pleasure of being associated with always find humor
in life and make the best out of all situations. As oral and
maxillofacial surgeons, we live in a high-stress environment
and face sometimes grave decisions on a daily basis. No
matter how bad things seem in a given crisis, history tells
us that they will pass and improve. Optimism is a virtue and
is contagious. Try to smile every second and try to find
humor and laughter in life. There are no dress rehearsals in
life. How would you treat people tomorrow if you knew it
was your last day on earth? The button that fell off your
shirt or the flat tire would carry much less aggravation.
■ SUMMARY
The author has attempted to illustrate that marketing is not
a specific task, but rather a lifestyle. If one examines very suc-
cessful practices, they will invariably find an excited, energetic
leader with an enthusiastic and caring staff that enjoys what
they do for a living. Marketing, as we have illustrated, goes
far beyond the bounds of a gift or party and is a total commit-
ment to excellence and the desire to share this with one’s
patients, referring physicians, and the public. Marketing, like
underwear, is very personal, and the same techniques will not
work for every physician or locale. Each one of us needs to
find his or her own comfort level and do as much possible as
they can with what they have. Marketing need not be adver-
tising or yelling and screaming. Subtly informing target
patients of your services can be accomplished in many ways.
Oral and maxillofacial surgeons are very innovative individu-
350 SECTION III ■ Practice Management
als, and the author could not possibly cover all the various
strategies of marketing. We have attempted to dissect the
theoretical aspects of marketing and to present various options
as viewed by the author. “The customer is always right,” “Do
unto others as you would have done unto you,” “Offer an
excellent product at an affordable price,” and “Always be a
teacher and always be a student” are phrases that may be
centuries old. Certain common-sense factors in how one pres-
ents his or her product or service will have an enormous
impact on the success of their business and their happiness in
their profession. Whether an office consists of multiple physi-
cians and locations or a one-physician, five-employee single
office, the theories and techniques presented apply across the
board.
REFERENCES
Mandell DB, O’Dell JM: Tips on selling your medical practice,
Nephrol News Issues (3):51-52, 2008.
Baker M: Risk management programs: a means to lower premiums,
Bull Am Coll Surg 93(3):24-6, 2008.
Frank EK: Why my cash-only practice failed, Med Econ 85(5):54, 57,
2008.
Rudolph J: Bond with patients when time is scarce, Med Econ
85(5):50, 53, 2008.
Weiss GG: Use marketing to draw in more patients, Med Econ
85(5):29-30, 33-4, 37, 2008.
Weiss GG: When patients cancel, you’re on the line, Med Econ
85(5):22-4, 28, 2008.
Gendusa J: Marketing that pulls, Mark Health Serv 28(1):18-21,
2008.
Swerdlick M: Everything matters to marketers, Mark Health Serv
28(1):12, 2008.
Seymour J: How to keep the lawyers away. Protecting business and
personal assets from lawsuits, MGMA Connex 6(2):29-30, 2006.
Finley M: Is solo simpler? Minn Med 91(2):10-1, 2008.
Kasinec DT: How does your output grow? Measuring billing depart-
ment productivity, MGMA Connex 6(2):26-7, 2006.
Lowes R: Smarter scheduling puts you in control, Med Econ
18;85(2):50-2, 54, 56-7, 2008.
Guglielmo WJ: Job sharing: flexibility has a price, Med Econ 85(2):40-
3, 2008.
Weiss GG: Employed? What your boss wants from you, Med Econ
85(2):25-6, 30, 33, 2008.
Master MA, Eveloff SH: How to prevent employee fraud, Med Econ
85(4):63-5, 2008.

OFFICE DESIGN AND ERGONOMICS
Richard F. Scott
■ OFFICE DESIGN OVERVIEW
DEFINING GOALS
Successful office design is the product of many factors. These
include the practitioner’s goals and expectations and the
resources, both financial and material, available to that prac-
titioner. These, of course, will vary tremendously for different
oral and maxillofacial surgeons. Nevertheless, there are some
general guidelines that are useful when considering the cre-
ation of a new facility in which to practice oral and maxillo-
facial surgery or in the remodeling or renovation of an existing
one. If you consider this process as a journey, then these
guidelines serve as a road map to take you from your current
position to your desired one.
Before beginning your journey, it is paramount that you
enumerate your reasons for making the trip. You may be a
recent graduate of a training program and establishing a new
office. You may have practiced for many years and wish to
relocate or renovate. The reasons for this may be many. You
may be dissatisfied with the quality of the existing physical
plant or its location. The treatment rooms may be too small.
There may be a lack of storage or insufficient parking. You
may desire to own, rather than lease, or wish to establish a
satellite office to enhance your referral base.
The point is that your first step should be to establish a list
of what you hope to accomplish. What are your goals? These
goals should be further divided into short-term and long-term.
What do you want your practice to be like in 1 year, 5 years,
or 10 years? How do these goals impact upon office location
and design?
Time should be taken to develop a worksheet that defines
your specific goals and prioritizes them. Completion of this
first step is absolutely critical to ensure a successful outcome.
Once your goals and objectives are established, you must
ask how to position yourself to accomplish these objectives.
CREATING A ROAD MAP
The first steps taken to achieve objectives often involve the
factors of location, new construction versus existing construc-
tion, square footage required, and lease versus own. If you are
considering renovating existing office space, you must ask
whether this will satisfy your stated objectives. Can you work
within the existing space limitations or acquire adjacent
CHAPTER 20
square footage? Can you achieve better office efficiency and
patient flow? Are you satisfied with current parking and neigh-
boring businesses? Are the expenditures of renovation offset
by the gains made in personal satisfaction? What is the pro-
jected downtime for the renovation, and how will that impact
your cash flow and referrals?
If you are relocating versus renovating, you must gather
demographic information about suitable options. Much infor-
mation can be obtained from local governmental agencies and
community organizations. Information regarding population
growth, age of residents, and income statistics should be con-
sidered in addition to zoning regulations, projected highway
development, trends in new building construction, and avail-
ability or occupancy of office space. Certainly, the potential
referral sources in the geographic area should be considered.
Once this information is obtained, you must see how it fits
with the objectives you have set.
The decision to lease or to own your office space must be
considered. This is perhaps most impacted by the current
amount of funding available to you and by your short- and
long-term goals. Advantages and disadvantages of each should
be enumerated. Input from your CPA, lawyer, and financial
advisor should be sought. Legal advice with regard to lease
negotiations should be used.
In conjunction with decisions about location, you need to
develop a plan addressing what you require in square footage.
This can be approached by listing each room or component
you anticipate, for example, waiting room, business office,
operatories, etc., and then list a projected size in square footage
for each room. Included must be hallways, wall build-out
requirements, and mechanical room requirements. You must
also allow for handicapped square footage and code require-
ments for your particular location.
At this point, you should be able to arrive at an
approximate amount of square footage required to satisfy
your current and future objectives for your practice. How
does this figure work with the space available in the locations
you are considering? Can you make a match? You must also
ask if it fits in with certain requirements you might have.
For example, northern natural light, the need for a separate
personnel entrance, and a separate patient exit different from
the reception room entrance and exit. Have you included
adequate storage facilities, or does the building have a
basement?
351
352 SECTION III ■ Practice Management
FINANCIAL PROJECTIONS AND FEASIBILITY
As you combine thinking about location and overall square
footage requirements, you must add financial projections to
the mix. Financial projections will include cost per square
foot, property taxes, common area maintenance costs, utili-
ties, equipment costs, surgical supplies, business office equip-
ment, and office furniture. It is usually possible to obtain an
estimate of build-out cost per square foot for your geographic
area. A good source for this information is your local dental-
surgical equipment supplier or salesperson. Other sources
are local builders and lending officers from local banks.
Equipment and surgical supply cost can be obtained from
your local suppliers. You should ask several vendors to supply
you with competitive bids for your business. The same should
be done with suppliers of office furniture and office
equipment.
A financial summary and feasibility document must now
be assembled. It should include the financial projections noted
above, but also include such business overhead projections as
monthly rent or, if owning, monthly mortgage payments, pro-
jected monthly utility expenses, anticipated payroll expenses,
insurance expenses, and local, state, and federal taxes. For
example, it is extremely important to include sales tax when
working on projections of equipment, surgical supplies, and
business office furniture and equipment. Offsetting these pro-
jections of expenditures will be projections of anticipated
gross revenue. Responsible financial planning will be expected
of you as you approach potential lenders for funding. This will
most likely be a bank and will, again, most likely be a long-
term relationship. Choose your bank wisely and engage your
accountant in the decision. How much money can you borrow?
What is the best interest rate available? Should it be a variable
or fixed rate? Can you defer principal payment? What best fits
your financial projections?
At this point, you have established a statement of your
goals and what you wish to accomplish. You have selected a
location for your facility. You have determined an overall size
for the physical plant of your facility. You have projected the
financial expenditures necessary to build and equip your facil-
ity. You have established projections of anticipated gross
revenue generation and anticipated overhead. You have iden-
tified a lender willing to provide you with the capital necessary
to achieve your goals. It is now time to . . . STOP. Are you
being realistic? How does your personal lifestyle and personal
expenditures impact on the scenario generated? Are they
compatible? Have you accounted for, as much as possible, the
unexpected? Are you comfortable with the degree of risk you
are undertaking? Reassessment before moving forward should
be part of the overall plan for success. It is a good time to
review your plans with your accountant, attorney, banker, and
other trusted persons whose opinions you respect and value.
Once reassessment is satisfactorily completed, it is time for
moving forward.
Let us look at some of these issues in more detail.
■ OFFICE DESIGN:
OVERALL FLOOR PLAN
The typical oral and maxillofacial surgery office must accom-
modate areas of space dedicated to the accomplishment of
certain tasks. These can be listed as:
• Surgical treatment area
• Pretreatment area (consultation, radiology, conference)
• Posttreatment area (recovery)
• Sterilization and infection control area
• Patient reception, waiting area, checkout, and exit area
• Business office area
• Restrooms
• Physician’s office area
• Laboratory area
• Lunchroom area
• Staff office area
These areas designated to a specific task should also be
arranged in a pattern that will provide for efficient patient,
staff, and surgeon traffic flow. The patient reception area,
waiting room, checkout area, and patient exit should be iso-
lated from the surgical treatment and posttreatment areas.
The pretreatment area should be located between the patient
reception or business office area and the surgical treatment
area. It should be possible for a patient to enter the office,
be received by the business office personnel, be escorted to
the radiology suite, then to the consultation room, and back
to a checkout area of the business office without physically or
visually encountering the surgical treatment area or posttreat-
ment area.
This is important for minimizing patient anxiety, protect-
ing patient privacy, and for infection control purposes. It is
strongly recommended that a separate exit be provided for
patients who have had surgical procedures and that this exit
is located away from the reception area. The surgical treat-
ment area and posttreatment area and the sterilization and
infection control area should be centrally located. Traffic flow
within this area should not impinge on traffic flow in the pre-
treatment area.
The private areas of the office, consisting of the physician’s
office area, staff office area, laboratory area, lunchroom, staff
locker room, and restrooms, will have no patient flow and be
located the farthest away from the reception room area. A
separate entrance for staff located close to the locker room
should be strongly considered, and a private entrance for the
physician’s office area is also beneficial.
Surgical treatment area: This area drives not only the
practice but also the office design. It is where the surgeon will
spend the bulk of his or her time while in the office. When
designing this space, the number of surgeons that will be
working at the office, the type of surgery that will be done,
the type of anesthesia that will be used, and whether or not
the surgeon will be seated or standing should all be included
in the design process. These factors will all impact on the
number of surgical operatories that will be required and the
 CHAPTER 20 •
FIGURE 20-1. An uncluttered surgical treatment room decreases patient
anxiety and enhances traffic flow.
size of each. Two operatories and a consult area should be
considered for each surgeon. This will be impacted by the type
of surgery being provided. It is a good rule of thumb for prac-
tices weighted toward dentoalveolar procedures. Other surgery,
such as cosmetic, implant, or orthognathic or distraction, may
require designated and modified operatories. These operatories
require additional space for anesthesia machines, lasers, addi-
tional Mayo stands, personnel, etc.
Space for a standard operatory should approximate 144
square feet. Special procedure operatories may require 300 to
400 square feet. In the standard operatory, two sinks for hand
washing should be considered: one sink for the surgeon and
one for the assistant. They are not expensive to install if
included in the original floor plan and can save 2 to 3 minutes
per patient encounter. If the surgeon sees 20 patients per day,
this can free up to 3 to 5 hours per week.
If designated surgical areas are required, a separate scrub
sink area is necessary. The operatory should be as uncluttered
as possible, and cables and cords should be kept off the floor.
An uncluttered appearance is also less intimidating to the
patient. Designating the wall behind the long axis of the
seated patient for the delivery system and monitoring equip-
ment is a good way of accomplishing this. It should also be
remembered that operatories should be of sufficient size and
design to accommodate a crash cart and resuscitative efforts
(Figure 20-1).
Office Design and Ergonomics 353
FIGURE 20-2. The consultation room is a modified, warmer version of
a surgical treatment room.
Pretreatment area: The pretreatment area consists of the
consultation and examination room, radiology suite, and con-
ference room.
Consultation room: This room is a modified version of the
operatory. It contains a patient chair and track lighting, but
no delivery system is required. Only one sink area is required.
It can be smaller than the operatories, but must be able to
accommodate at least two seated persons (e.g., the parents of
the patient and the surgeon and patient) (Figure 20-2).
A minimum space of 100 square feet is required for this
room. This room should be:
• Located close to the radiology area
• Equipped with intraoral radiology capabilities
• Soundproof
• Close to the business office
• Isolated from the surgical area
It should be remembered that this room will be part of the
patient’s first impression of your office and practice. It should
be decorated and furnished accordingly.
Radiology suite: A transition in design of this area is
ongoing as a result of advances in technology. The standard
radiology techniques are being replaced by digital radiology
techniques and cone beam 3-D imaging. This technology
should be included in the design, if not for immediate imple-
mentation, then for future transition. A minimum space of
100 to 144 square feet should be provided for this area. This
space should provide for easy wheelchair maneuverability. It
should be located close to the consultation room and business
office. It will also form one of the first impressions your patient
has of the office and should be designed accordingly. If con-
ventional radiography techniques are being used, a separate
darkroom area with a deep well sink will be required. This can
generally be 20 square feet in dimension. When designing this
space, however, you may wish to consider possible future use
of this space if film developing will not be required in the
future. For example, you may wish to make it large enough for
a future recovery room or storage area.
354 SECTION III ■ Practice Management

personnel and should be located close to the operatories to

minimize transport time.
Sterilization and infection control area:

FIGURE 20-3. The conference room should be designed to accommo-

date a number of purposes. It should be uncluttered and comfortable.

Conference room: A separate conference room can serve FIGURE 20-4. View of the nonsterile side of the sterilization and infection
many purposes. It can be an area to discuss treatment plans control area. Note the below-the-counter commercial trash compactor,
with patient and family outside the consultation room. It may in-counter sharps disposal, in-counter ultrasonic cleaner, and deep well sink
with faucet knee activation. The flow is from the right to left, where autoclave
be used as an area for business office personnel to discuss
units receive clean instruments.
financial arrangements with patients. It can be used as an area
for staff to review postoperative care with caregivers before
discharge of patients who have undergone sedation. It can be
used as an area for clinic supervisors to meet with sales repre-
sentatives without disturbing the patient flow. This room need
only consist of a table with chairs. It should be located near
the consultation room and business office and out of the
busiest patient flow area. It should be soundproof and requires
85 to 100 square feet (Figure 20-3).
This entire pretreatment area should be located close to
the business office and reception area and away from the surgi-
cal treatment area. Patient flow should be designed to accom-
modate patients entering the reception area, interacting with
the business office staff, being escorted to radiology, then to
the consultation room, and back to the business office and
reception area without encountering the surgical area or FIGURE 20-5. View of the sterile side of the sterilization and infection
recovery area. This is important for minimizing patient anxiety control area. The flow is right to left. Instrument packs have been removed
and for infection control. A patient restroom located in or from the autoclave units, allowed to dry, and stacked for future use. Note
near this pretreatment area should be considered. It must be undercounter locking refrigerator. Undercabinet lighting has been provided.
handicapped accessible and will require 50 to 70 square feet.
Posttreatment area: This is the recovery area for patients
receiving general anesthesia or sedation. The number of The sterilization area should be centrally located in regard
recovery rooms depends on the number of surgeons and the to the surgical treatment rooms. It will be one of the busiest
number and type of anesthetic procedures performed. Provid- areas in the office and, consequently, have a busy traffic flow.
ing two recovery areas for each surgeon is a good rule of A natural flow of traffic will exist within the sterilization area
thumb. If short-acting sedative techniques are used and excel- from contaminated to sterile. It should be laid out in a logical
lent scheduling principles used (e.g., alternating sedation pro- fashion to accommodate this flow. High usage of cabinets and
cedures with those requiring local anesthesia only, or consults), drawers in this area dictates high-quality cabinetry built for
patients may be recovered in the operatories and discharged durability and flexibility. High-volume practices should con-
directly from there. Recovery areas must be equipped with sider a commercial grade trash compactor in this area. The
suction, oxygen, and monitoring equipment. Patients in the clean or sterile side of this area often houses storage of drugs
recovery room area require continuous monitoring by trained used in patient treatment. Duel locking cabinetry is required.
 CHAPTER 20 • Office Design and Ergonomics 355

FIGURE 20-6. The patient waiting area should project the image that
you want for your practice. Cluster seating; indirect lighting; high-quality, FIGURE 20-7. Entrance foyer with coat rack and stone flooring for use
comfortable furnishings; and floor covering should be considered. in cold or rainy weather.

A small refrigerator is also located in this area for storage of

drugs, film, etc. Sterile surgical packs and trays and anesthesia
tray set-ups are often stored in this area.
Although the surgeon typically spends little time during
the day in this area, his staff may spend a large part of their
day here. It should be designed to accommodate this fact. A
squared U shape provides for open flow in this area. A ten-
dency to design this space with too little square footage is a
common mistake. For a busy practice with two surgeons and
six operatories, 125 to 150 square feet should be allocated for
this space. This helps in traffic flow and aids in satisfying
infection control principles.
Patient reception and waiting area: This is an area of the
facility that the surgeon may not enter during the entire week.
However, it is perhaps the busiest area of the facility and one
of the things your patients or their families will remember
most. It should be designed and furnished with this in mind FIGURE 20-8. The reception desk of the business office. The 4-foot wide
(Figure 20-6). wall behind the desk conceals rotating, locking patient chart filing cabinets.
Patient numbers and the number of surgeons working must
be considered in designing this space. Because many patients
are sedated or receive general anesthesia during their visit, facility with six surgical treatment rooms, the patient recep-
they will be accompanied by one or two others. Thus, for each tion and waiting area should occupy 350 to 400 square feet.
patient seated in an operatory, you should plan on 2 to 2½ Business office area: The business office should be located
seats in the waiting room. You must also consider space for adjacent to the reception and waiting room area. There should
end tables, coffee tables, planters, art work, etc. Efforts to be a designated area for greeting patients and a separate area
decrease patient apprehension should be considered in the for patient checkout. Depending on the size of the practice,
design and color choices of the waiting area. This can be done more than one checkout area should be considered. At least
by sets of cluster seating rather than perimeter-only seating, one of these should be handicapped accessible (Figures 20-8
recessed incandescent lighting, rounded walls, soft color wall and 20-9).
paint or covering coordinated with good carpeting, and appro- Keep patient privacy in mind when designing check-in and
priate music through ceiling speakers. In geographic locations check-out areas. The design of the business office must be
that experience cool or winter weather, an entrance foyer with done in conjunction with your information technology (IT)
a coat rack and umbrella stand should be provided. This coordinator and telephone system coordinator. Work stations
should have easily cleanable flooring, such as stone or tile, and or docking stations for computer terminals, network servers,
floor mats that can be cleaned (Figure 20-7). telephone lines, fax lines, patient pay credit card machine,
If such options in the building exist, natural outdoor light- and electrical outlets must be included in the design process
ing via windows should be incorporated in the design. In a for this area. Consider mounting keyboards on retractable
356 SECTION III ■ Practice Management
FIGURE 20-9. A separate checkout area located away from the reception
desk. It is handicapped accessible and provides privacy.
trays beneath the counters at the computer work stations.
Cabinetry and storage for supplies, forms, and other paper
products will be required. There will typically need to be space
for patient records; however, this is an area, like radiology,
that is changing with technology. More and more new office
designs will consider a “paperless” approach. It is unclear how
much space this will actually save. These issues should be
discussed with your software professional during the design
process. The number of work stations will depend on the size
of the practice. For each surgeon, there should be at least two
work stations. One of these stations can also be used for either
the reception station or patient exit station. An estimate of
90 to 100 square feet per employee in this area is reasonable.
If you anticipate having a business office staff of four persons,
then your space requirement will be in the 350- to 400-square
feet range. Estimate 9 lineal feet of counter space for each
front desk staff person.
Restrooms: The number of restrooms will vary according
to personal preference. However, there will typically be des-
ignated restrooms for the physicians, staff, and patients and
their families. Even if your building has public restrooms in
an adjacent foyer, atrium, or hallway, it is a good idea to have
a patient restroom within your facility. This should be located
near the junction of the “front” and “back” portions of your
office. The reference to the “front” portion of the office refers
to the reception and waiting room area, business office, con-
sultation room, radiology suite, and conference room. The
reference to the “back” portion of the office refers to the ster-
ilization area, operatories, and recovery area.
Generally, all restrooms, including staff and physicians,
will be required to be handicapped accessible, providing hand-
rails and wheelchair maneuverability. Your contractor will be
knowledgeable in this area. You should be aware of local
interpretations of the Americans with Disabilities Act and
plan on 60 to 65 square feet for each restroom. Depending on
overall office image concepts, you may wish to upgrade fea-
tures in the patient’s restroom. This may include upgrading
FIGURE 20-10. Patient restroom that is upgraded and handicapped
accessible.
the floor and wall covering, lighting, sink and faucets, etc.
(Figure 20-10).
Physician’s office: The inclusion and design of a private
physician’s office is a personal preference and will vary greatly.
The surgeon will spend the majority of his or her time outside
of this space. However, there are times when privacy is
required, and work space that ensures privacy is desired. There
are also times when the physician may be at the office outside
of normal business hours to work on business matters that
cannot be accomplished during the day or week because of
patient demands. A personal office is ideal for this. The office
should be able to accommodate seating for two other persons
for private meetings with staff, business advisors, sales repre-
sentatives, etc. Consideration for a private entrance directly
into the physician’s office should be made. This allows for
evening and weekend access without opening the entire office.
A separate alarm zone for the physician’s office allows access
to this area without disarming the rest of the office. The phy-
sician’s office will generally have a separate restroom and
closet. If multiple physicians are present, this can be an open
space with appropriate desk numbers, or individual offices can
be considered (Figures 20-11 and 20-12).
Laboratory: The amount of space required for a laboratory
is dependent on the type of surgery being done. The area
should accommodate the anticipated number of persons using
it at a given time. It will typically require countertop space,
 CHAPTER 20 • Office Design and Ergonomics 357

FIGURE 20-11. Physician’s private office with natural lighting, private

entrance and exit to outside of the building, and a desktop large enough to
accommodate a flat screen computer monitor, telephone, printer, and in and
out trays.

FIGURE 20-13. A comfortable, cheerful lunchroom provides a quiet

environment for staff to enjoy their lunch on premises. This kitchen is equipped
with a microwave, refrigerator, dishwasher, garbage disposal, microwave-safe
dishes, and silverware. The individual carpet squares under the table easily
peel up for convenient replacement if soiled.

FIGURE 20-12. Additional physician’s private office with natural lighting,

private bathroom, and intraoffice digital communication screen within easy
reach.

a deep base sink and plaster trap, a lathe, and model grinder.
It should be in an area of the facility remote from the front
area and as far from the operatories as possible and, if possible,
be soundproof. If only one person will be in the lab at a time,
then a space of 70 to 100 square feet should be adequate.
Lunchroom: This area can add greatly to staff job satisfac-
tion. Soliciting staff input into its design can add to this. It
should be large enough to accommodate your number of
employees and be away from the flow of the office. It will
typically house a microwave, sink with garbage disposal,
dishwasher and refrigerator, and a table and chairs for staff
(Figure 20-13).
If you anticipate a table with six chairs, allow 160 to 180
square feet. The staff restroom can be located off the lunch-
room. You also may wish to include a changing or locker room
for staff in this area. If so, allow an additional 60 square feet
for this purpose.
FIGURE 20-14. The surgical staff office is located within view of the
surgical treatment flow so that surgical assistants working at their desk can
monitor any special or emergent needs.
Staff office: Strong consideration should be given to a staff
office for the surgical staff. This should be located in the surgi-
cal area of the office. It should contain desk space for computer
terminals, telephones, and allowance for shelving for surgical
supply books, surgical protocol manuals, and Health Insurance
Portability and Accountability Act (HIPAA) and Occupa-
tional Safety and Health Administration (OSHA) compli-
ance records (Figure 20-14).
It is an area where patient notes can be entered regard-
ing postoperative surgical calls and patient postoperative
358 SECTION III ■ Practice Management
FIGURE 20-15. The use of curved walls is a pleasing transition from the
pretreatment area to the surgical area. Sound control is an added benefit of
the curved wall.
telephone calls answered. It is unlikely that all surgical staff
will be in this area at any given time, so desk space can be
shared. Depending on staff numbers, a space of 100 to 165
square feet should be allocated.
Additional space requirements: During the initial phase
of office design, it is important to remember incidentals, such
as hallway space, biohazard space, tank room, mechanical
room, and storage. Hallways will be 4 or 5 feet in width. Hall-
ways can serve purposes other than traffic flow. They can add
significantly to the image of the office. Using curvature in the
design is pleasing to the eye and can aid in sound control and
alter line of sight. Varying the composition of walls (e.g., using
glass or glass block) can enhance aesthetics, as can indirect
lighting and varying floor covering near exits (Figures 20-15
and 20-16).
Walls will typically be 5 inches in width, but may be 7
inches in width to provide additional sound installation. A
vented biohazard closet should be included in the design. This
will require approximately 15 square feet.
Space will be required for a medical tank room to house
oxygen and nitrous oxide tanks and possibly nitrogen tanks.
Local codes will dictate the size of this room. A 4 × 4 foot
space is usually adequate. It will generally require ventilation.
If a basement is available in the building that has easy access,
this is an excellent area for a tank room. The basement is also
an excellent area for the suction and/or compressor. If located
within the floor plan on a single floor design, the compressor
should be in an area away from traffic, and a sound-insulated
room will be required. An area of 3 × 5 feet will accommodate
FIGURE 20-16. Glass or glass block is aesthetically pleasing and
enhances natural light. The stone used in the exit and entrance foyers provides
easy maintenance, accommodating heavy traffic flow and inclement weather.
the compressor. If a single-level floor plan is in effect, space
will also be required for the heating and cooling system and
hot water heater. Approximately 40 square feet will be required
to house these components and to allow access to them for
maintenance.
Storage space seems to disappear inversely to the number
of years in the facility. It is wise to plan for several storage
areas within the facility. One should be in the business office
area and be sufficient to store business forms, copy paper, sta-
tionary, envelopes, ring binders, etc. One should be in the
surgical area and be adequate to store several weeks of dispos-
able surgical and anesthetic supplies. A storage area in the exit
foyer should be considered. This is a good place to temporarily
store deliveries that cannot immediately be unboxed and put
away by staff.
An additional storage area for the crash cart and back-up
mobile oxygen, back-up suction device, and wheelchairs
should be considered (Figures 20-17 and 20-18).
These can be recessed in an open space off a hallway in the
surgical area. It keeps them out of the way and out of direct
patient view, but readily accessible. A 7 × 3 foot recess is suit-
able for this purpose.
■ EQUIPPING AND
FURNISHING THE OFFICE
A more detailed look at equipment and furniture for the office
is required. A worksheet for equipment should be developed.
 CHAPTER 20 •
FIGURE 20-17. The crash cart, wheelchairs, oxygen, etc., should be
easily accessible.
FIGURE 20-18. Recessed bays to house the crash cart, wheelchairs,
etc., keep them out of the traffic flow in the surgical area, but are quickly and
easily accessible.
HARD EQUIPMENT
Computers and net server: There should be one work station
or docking station for each front desk personnel, one for each
physician, and one for every two surgical assistants in the staff
office. You may wish to consider an additional work or docking
station in the conference room. If digital radiology techniques
are employed or “paperless” office principles used, then you
must be able to access such information in each operatory and
in the consultation room. It is important to identify an IT
representative and software technology representative early in
the planning process so that all necessary wiring, cables, inter-
net access, and electrical outlets can be included in the archi-
tectural blue prints before beginning construction. The net
server should be located in or near the business office, but out
of the flow of daily traffic. Sufficient electrical outlets for print-
ers and calculators should also be part of this planning
process.
Telephone system: This also is an area that is undergoing
transition as technology evolves. Your IT representative
Office Design and Ergonomics 359
FIGURE 20-19. The intraoffice digital communication system screen
allows two-way communication, keeping all staff personnel apprised of office
patient flow, telephone calls, emergency situations, etc.
should be able to assist you in this area. You should consider
employing mobile wireless headsets for business office person-
nel to provide mobility and multitasking capabilities. The
number of lines required and the location of all telephone
jacks required should be incorporated in preconstruction plan-
ning. The control panels for your telephone system should be
in an area away from traffic flow, but easily accessible for
servicing.
A separate closet that houses the net server, telephone
system, alarm system, music system, and intraoffice communi-
cation system is an excellent idea. A 3 × 5 foot space is ade-
quate with appropriate wall mountings.
Intraoffice communication system: A system of intraoffice
communication is mandatory within the facility to manage
and direct physician, staff, and patient flow. Recessed, in-wall
mounted digital readout screens located throughout the facil-
ity and controlled by the front desk personnel, but allowing
station input, is an example of such a system (Figure 20-19).
The screens should be located, as much as possible, out of
direct view of the patient (e.g., behind the patient on the
delivery system wall in the operatories). They can digitally
alert personnel of when patients are ready for seating and dis-
charge, direct physician and staff to appropriate areas, alert
personnel of incoming calls, and alarm if an office emergency
is in progress. Use a system that allows you to customize direc-
tions and alerts according to the needs of your practice. Your
equipment representative will be able to advise you of your
options in regard to this system. Wireless technologies may
develop in this area.
Security system: Some wiring for the office security system
will be required, and plans should be finalized before construc-
tion. Considerations for zones within the office and control
pad locations should be made. You may wish to look at keyless
entry systems, which allow you to monitor and record person-
nel accessing the office and time of entry.
Radiology equipment: Careful planning is required here to
allow for advancements in technology. Traditionally a pan/
ceph machine, either conventional or digital, will be required,
360 SECTION III ■ Practice Management
in addition to a periapical-intraoral unit. Consider a second,
wall-mounted periapical unit in the consultation room. Three-
dimensional cone beam units may be considered or at least
provided for in the future.
If a darkroom is to be used, it will require a deep sink,
autoprocessor, duplicator, safe light, ventilation and/or exhaust
fan, and floor drain.
Sterilization room equipment: Hard equipment, in this
area, includes deep sink, ultrasonic cleaner, cold sterilization
unit, two or more autoclave units, undercounter refrigerator
(with lock), and possibly a commercial grade trash
compactor.
Consider recessing the ultrasonic cleaner into the counter-
top. Also, consider mounting the autoclaves on retractable
drawers so that they are off the counter, but accessible. Also,
consider recessed undercounter sharps and biohazard
disposal.
Laboratory equipment: This area will vary according to
the type of surgery being done in the office. It will traditionally
require a model trimmer, lathe, laboratory hand piece, deep
sink with plaster trap, dust collector, model vibrator, and
plaster bin.
Surgical and/or dental chairs: This is a large-expense item,
and care should be taken in the selection of the surgical and/or
dental chairs that best suit the physician using them. Their
design may vary according to whether the surgeon sits or
stands or is left- or right-handed. It is best to visit showrooms
and experiment with different models. Once a decision is
made, it is best to have uniformity throughout the treatment
rooms. Designated rooms for specialized procedures may
require a different surgical chair. The number of chairs required
will equal the number of operatories plus the consult room
and possibly the radiology suite.
Surgical track lighting: This will be required in each oper-
atory and in the consultation area. Consider lighting that can
be turned on and off via sensors so that you do not have to
physically throw a switch.
Delivery system (i.e., nitrous oxide, oxygen, suction,
nitrogen, compressor): Careful planning of the delivery
system requirements will involve your equipment sales repre-
sentative. This will impact on future plumbing and electrical
requirements and must be completed and incorporated into
the architectural plans before the initiation of construction.
Delivery systems are typically mounted on the wall behind the
long axis of the seated patient. They will be required in each
operatory, and suction and oxygen should be supplied in the
recovery areas in each recovery bay (Figure 20-20).
Anesthesia machines: These may be only nitrous oxide
delivery units (one for each physician) or may be general
anesthetic machines depending on the anticipated types of
surgery to be performed.
Monitoring device: Monitors will be required in each
operatory. In an effort to keep as much as possible up off the
floors, you should consider mounting the monitors on the
same wall as the delivery system on adjustable wall mounts.
This allows easy operator visualization and keeps all leads and
FIGURE 20-20. The delivery system is located behind and out of view
of the seated patient. The intraoffice digital communication system screen is
in easy view and reach of the physician and surgical assistant.
cords behind the patient. Pulse oximetry and blood pressure
monitoring should also be available in the recovery bays.
View boxes: If standard film radiology is employed, then
each operatory and consultation room will require a wall-
mounted view box.
Heating, ventilation, air conditioning (HVAC): Tem-
perature control within the office is important for patient
comfort and for the comfort of those working in the facility.
Temperature requirements will vary throughout the facility.
For example, temperatures in the surgical area will typically
be lower than those in the business office or reception area.
Temperatures in the sterilization and infection control area,
which contains heat generated from autoclave units, will
often be kept lower than that in the surgical areas. HVAC
design should provide for separate temperature zones through-
out the office.
COMPUTER SOFTWARE
A number of computer software programs, designed specifi-
cally for the oral and maxillofacial surgery practice, are avail-
able. When considering the purchase of such software, you
should seek out offices currently using the software and ask
their opinion regarding strengths and weaknesses. Purchase of
computer hardware must be coordinated with software pro-
grams. Software should be chosen wisely because they can be
great timesavers or great sources of frustration. It is not wise
to try to save money here by buying less expensive systems.
You should also evaluate the amount of computer software
support available to you and understand how upgrades and
add-ons are managed. Make sure that adequate on-site soft-
ware training for the entire staff is part of your software
package. Reliable back-up systems are paramount and should
be easy for business office personnel to perform.
SURGICAL SUPPLIES
Tray set-up for each procedure (i.e., surgical instruments
required on each tray): During start-up, it is easy to purchase
too many or too few surgical instruments. One way to deter-
 CHAPTER 20 •
mine the number and type of instruments required is to list
the instruments that should be on a standard third molar tray,
biopsy tray, fracture tray, or implant tray, etc. Then estimate
the number of trays that will be required during a workday,
allowing for sterilization turnaround time. These lists may
vary from surgeon to surgeon, but standardization within an
office should take precedence.
Number of trays required: Once the number of such trays
required is determined, multiply the list of instruments required
for each type of tray by the number of trays desired to ascertain
the number of each kind of instrument to be ordered.
Additional instruments: A number of instruments do not
need to be included in each tray, but should be available on
a case-by-case basis (e.g., certain forceps, different scissors,
skin hooks, etc.). Smaller numbers of these will be required,
and they can be centrally stored.
Mayo stands: Plan on 1 to 1½ Mayo stands per
operatory.
BUSINESS OFFICE EQUIPMENT
Copy, fax, and credit card transaction machines: If a large
amount of copying is anticipated, consider high-quality copiers
with sorting capabilities. You may also wish to have a separate
copy machine in the staff office area.
Shredders: All security-sensitive documents should be
shredded before disposal. Consider several shredders through-
out the office.
Postage machine: These machines are often rented or
leased.
Filing cabinets: Various space-saving designs are available,
such as revolving core cabinets. Some can be added as the
need arises. Consider cabinets that can be locked for patient
confidentiality and office security.
OFFICE FURNITURE
• Waiting room
• Business office
• Physician’s office
• Staff office
• Lunchroom
• Conference room
• Recovery area
Some general comments about office furniture should
suffice. High-quality furnishing will outlast and outperform
low-quality furnishing. The increase in the initial outlay of
capital to acquire high-quality commercial furniture is offset
by its durability and aesthetic qualities over time. This should
especially be considered when furnishing the waiting room
and reception area, business office, conference room, consulta-
tion room, and even patient bathroom.
This is a good time to discuss the use of a qualified, licensed,
interior design specialist. They will be able to supply you with
information on many options, involving floor covering (vinyl,
wood, tile, carpet), wall covering (environment friendly
paints, wall papers, faux painting), ceiling material, lighting
schemes (recessed, accent, work space, fixtures), window
Office Design and Ergonomics 361
dressings, and furniture options. The interior design specialist
will be able to advise you on quality, durability, maintenance,
and cost in regard to these options. They will also present
color schemes for various work spaces, effectively coordinating
wall and floor coloring with ceiling, lighting, and furniture to
present the kind of image that you wish to portray to your
patients. They will be able to interact directly with the con-
struction supervisor and should be on-site at various points of
construction to ensure successful outcomes. Commercial
interior design personnel should be an integral part of your
team.
■ THE PROJECT
CONSULTANT TEAM
The project consultants have been referred to previously, but
will briefly expand the discussion here.
In addition to the commercial interior designer, an archi-
tect, general contractor, accountant, attorney, banker, IT-
management consultant, and dental-medical equipment
consultant will all form the project team, and each plays a
pivotal role. Assembling an experienced team that you trust
and can easily work with will help to ensure success and
decrease the overall stress of the process. Each plays a pivotal
role at various points in the process.
It should be noted that there are a number of companies
that specialize in medical-dental office construction and offer
to organize and oversee the entire process of design and con-
struction. They have a preassembled team of experienced con-
sultants that take you through the entire process. Those who
use these companies often relate a decrease in the stress and
time commitment involved in such a project. There is a strong
sense of centralization and of turning everything over to an
experienced team. Potential disadvantages to this approach
are added cost, not developing relations with local and com-
munity experts, and often working with out-of-state personnel
in a long-distance fashion. The decision to use one of these
companies is a personal one and should, obviously, be decided
upon at the outset.
If you do not employ such a company to manage your entire
project for you, then the various consultants who will make
up your project management team should be selected care-
fully. You may already have a strong professional relationship
with a CPA, attorney, banker, and financial planner. If you
are currently in an existing facility, you will probably have a
working relationship with a medical-dental equipment sales
representative. It is likely that these individuals will have been
involved in similar projects and may offer suggestions as to
experienced and reliable contractors, architects, and IT per-
sonnel. All will interact with other members of the team on
numerous occasions.
Fees for these specialists must be included in your cost
projections, in addition to permit and inspection costs.
■ ERGONOMICS
When designing the various working stations within your
office, whether it is in the surgical areas or business office, it
362 SECTION III ■ Practice Management
is important to incorporate ergonomics. The word ergonomics
comes from the Greek words ergos (meaning work), and
nomos (referring to natural law or system). The study of ergo-
nomics involves looking at how the human body interacts
with the work environment and designing that environment
to improve the overall efficiency and well-being of the indi-
vidual and the organization.
Ergonomically designed work environments decrease the
risk of repetitive strain injuries (RSIs). These may involve
muscles, nerves, tendons, joints, or spinal disks. They may
manifest as pain and fatigue. RSIs are often associated with
awkward working positions. Examples include a computer
monitor placed too high or too low, poor wrist positioning,
inadequate or improperly directed lighting, and seating with
inadequate back support. Poor design of the work areas not
only increases the risk of RSIs, but also leads to a decrease in
office efficiency and productivity.
It is wise to use sound ergonomic principles when designing
work stations. Examples include proper countertop height,
telephones within easy reach of the dominant hand, computer
screens at eye level, adjustable seating with lumbar support,
and nonglare lighting. Attention should be paid to noise and
temperature control. Accessory equipment, such as document
holders, footrests, and palm and/or wrist supports when using
the keyboard or mouse, should be considered.
Members of your project consultant team should be able to
assist you in designing an ergonomically sound facility.
■ FINANCING THE PROJECT
At this point, you have identified a location, ascertained space
requirements, developed a design for office layout, and received
build-out projections, projected equipment costs, and interior
design costs. It is now time to secure funding for your project.
Two types of loans will be required: a construction or build-
out loan and an equipment loan. They will be depreciated
over different periods of time. Your cost projections should be
divided accordingly.
The more organized you are in assembling information to
present to prospective lenders, the smoother the process will
be. Prepare in advance a portfolio that you can give to the
lender. This portfolio should be divided and labeled by cate-
gory. An efficient system is to prepare several of these portfo-
lios that will be ready to present to prospective lenders as they
are identified. Always keep a master portfolio for your records,
which should include a list of the institutions that were given
a copy. Because this information is highly confidential and
contains personal information, consider keeping it in the
security of your home during this transition period. It should
include:
• A curriculum vitae
• Current net worth, both personal and business
• Recent tax returns, both personal and business
• Current year and previous years practice financial
statements
• Projected annual gross and net revenue
• Indebtedness, personal and business
• Credit references
• Anticipated construction costs, itemized by builder
• An itemized projection of equipment costs
• Architectural blueprints of the building and the office
space
You may also wish to have available a list of, and informa-
tion about, previous construction projects your builder has
completed. If you are leasing space that will be built according
to your office design, the landlord will often provide a certain
dollar amount per square foot for build-out expenses. This is
often a negotiable amount and should be included in lease
negotiations. This build-out allowance will be included in
your financial projections presented to your lender. If leasing,
a copy of the lease should be included in the portfolio.
You should consider presenting your information to several
lenders; a well-designed and thought out project with a high
probability of successful outcome will be attractive to lenders,
and they will often compete for your business. Remember that
you will be entering into a long-term relationship with your
lender and one that may be a source of future capital for future
projects. Therefore, develop the relationship carefully.
■ CONSTRUCTION PHASE
Initiation of construction is begun with the development of
a timeline, specifying when various phases of construction
will occur. This timeline should be distributed to all project
consultants. The contractor will also note on the timeline
when construction draws, and the amount he will require for
the draw, are due. Different consultants will be required to
be on-site at the project during different phases of the project
to ensure that details of the design are successfully transferred
from blueprint to reality. For example, medical-dental equip-
ment supply representatives should be present while plumb-
ing for equipment lines are being installed. IT personnel
should be present while in-wall wiring is being installed
before drywall installation. Interior designers should be
present while special lighting requirements, or any upgraded
features, are being installed. It is important that project con-
sultants communicate with one another as the timeline pro-
gresses. It is likely that the physician will be required to
ensure that this communication is happening. The physician
should plan on visiting the site on a regular basis. If the
physician is not available for this, then a project manager
must be designated who will ensure that such communication
and site visitation occurs.
A definite completion date must be agreed upon at the
beginning of the project. If moving from an existing office to
a new one, downtime will occur in which the old office is
closed and the new office is not yet open. Equipment suppliers
will need to transport equipment that is being transferred from
the old office to the new one. Business office equipment, sup-
plies, and patient records will also need to be transferred. This
downtime must be minimized, and an accurate timeline will
be critical to accomplishing this. A 2-week downtime is real-
istic. The physician should be present and on-site during this
downtime. The physician must also communicate clearly to
 CHAPTER 20 •
his staff how the work schedule, any time off, or vacation time
should be handled during the downtime transition.
New letterhead, business cards, billing statement, referral
pads, website information, etc. should be updated during the
construction phase and be ready to be placed into effect at
time of move in. All referring physicians and their staff should
be notified of your new office location. Patients should be
informed of the move and should clearly understand if they
will see the physician at the old location or the new location
if scheduled during the transition from old office to new
office.
A final walk-through should be completed before moving
in. This should be planned with the general contractor, and
they should be present at the walk-through. All local and state
inspections and a certificate of occupancy should be com-
pleted before moving in.
■ SUMMARY
The journey from a current practice environment to a new
facility is complex, challenging, exciting, and rewarding. It
begins with a well-conceived and defined destination in mind.
It is achieved by sequential steps, each building upon the
previous one, and with continuous reference to the road map
to ensure that you remain on course.
It will more than likely take some time after moving into
your new facility before you have finalized all details regarding
Office Design and Ergonomics 363
construction, equipment, and decoration. At that point, your
staff will be comfortable with their new environment, having
established an efficient workflow using all the advantages of
your newly designed and well-equipped office. Additionally,
you will be more confident about the decision you made to
take on the substantial responsibility of designing and financ-
ing this venture.
After this settling-in period, an open house reception for
your referring physicians and their staff and potential referring
physicians in the area is a good idea. It presents an opportunity
for a celebration that allows you and your office staff to show-
case your new workplace. If you have changed your location,
it helps referring physicians and their staff to know where your
new office is located. You may be surprised how many of your
open house guests are considering this type of project and will
seek out your advice.
BIBLIOGRAPHY
1. American Association of Oral and Maxillofacial Surgeons: Office
design and construction for the oral and maxillofacial surgeon,
9700 W Bryn Mawr Ave, Rosemont, Ill.
2. American Association of Oral and Maxillofacial Surgeons: Prac-
tice management notes, AAOMS Today Newsletter, July/August
2007.
3. Diecidue RJ, Streck Jr P: Practice management, Oral Maxillofac
Clin North Am 2(3):377-504, 1999.
CHAPTER 21
CODING, INSURANCE,
It is a fact of life that the oral and maxillofacial surgeon must
perform complicated surgical procedures, including surgical
orthognathic, temporomandibular joint surgeries, cosmetic
procedures, and trauma procedures, in addition to extractions,
third molar surgery, implants, and other surgical procedures,
which make up a practicing scope of oral and maxillofacial
surgery. Each and every surgeon would like to perform what
they are able to do on any given day and not have to be
bothered with the everyday business decisions of practice.
However, there is a business side of practice, which every
surgeon needs to become very familiar with to practice effi-
ciently and ethically and to be reimbursed properly for the
procedures that they perform. In this chapter, the topics that
will be discussed will focus on the parts of practice that will
lead to a successful career within the specialty.
■ CODING
HISTORY OF CODING
It appears that the listing of causes of death in the London
Bills of Mortality in the late seventeenth century was the first
attempt to determine what different diseases were responsible
for death in live births who died by the age of 6.1 From this
early study of deaths, there developed statistical study of all
diseases that were linked to the death of a patient. As diag-
nosis and types of diseases matured over time, with the
advances in medicine and science, there was a need to include
diseases that, although not fatal, were causes of disability and
sickness. This was called the International Lists of the Causes of
Death. Since this first listing, there were five revisions of the
established list. In 1948, the first World Health Organization
(WHO) updated a sixth revision of the list and published it
as The International Classification of Diseases (ICD). Two addi-
tional revisions occurred in the 1950s and 1960s. In 1977,
ICD-9-CM was published with wide acceptance by the inter-
national medical community.2
DIAGNOSTIC CODING
A major revision of the ICD Code usually occurs in 10-year
cycles and becomes the accepted official code set. However,
revisions within the official code set can occur on a yearly
basis.
The Centers of Medicare and Medicaid Services (CMS)
previous to 2005 allowed a 90-day grace period for practitio-
ners to use revised, deleted, and new codes in the submission
364
AND THIRD-PARTY PAYERS
Charles Lynum Cuttino III
of codes for reimbursement for services performed. Now
CMS does not allow a grace period, and practitioners are
required to use the current codes, which become effective on
October 1 of each year.
ICD-9-CM is a numeric code set, which is composed of
three to five numerals. The three-digit codes indicate a cate-
gory of a disease. For example, 524 is that category of dento-
facial abnormalities, including malocclusion. The fourth digit
is preceded by a decimal point and indicates a subcategory of
the section. The code for temporomandibular joint disorders
is 524.6. The fifth number is specific for the diagnosed disor-
der (e.g., 524.63 is articular disk disorder [reducing or
nonreducing]).
To find appropriate codes to describe clinical situations,
you must use both the alphabetic index and the tabular list
found in category 1 of ICD-9-CM. To find the proper diag-
nostic code, look up the main term of the diagnosis (e.g., a
patient who has a right preauricular swelling with a history
that the swelling has been present for 5 days and is painful
while eating). The clinical diagnosis is parotitis of the parotid
gland. The alphabetic index indicates a code of 527 (diseases
of the salivary glands). In a tabular list, subcategories of this
section indicate specific salivary gland diseases. For sialoadeni-
tis (parotitis), the proper code is 527.2.
Cross-references are listed under the main code, in addition
to any exclusion terms that appear with the main code describ-
ing the condition.
Any code selected must be supported by proper documen-
tation within the clinical chart.
There has been an initiative carried out by third-party
payers to add a significant number of dental ICD-9-CM codes
in the past several years. These new diagnostic codes, which
impact dentists, are mainly in the 520 to 529 ranges. This is
an attempt to be prepared for the possible mandate that all
dental claims submitted will require diagnostic codes for sub-
mission on the dental claim form. This will also be a mecha-
nism by which the third-party payer may judge that the
procedure code submitted is compatible with the diagnostic
code for the treatment to be considered for reimbursement.
INTERNATIONAL CLASSIFICATION OF
DISEASES—ICD-10
The next revision of the code is ICD-10, which was endorsed
by the WHO in 1990 and has been used in some countries
since 1994. The United States began studying the Code in
 CHAPTER 21 •
1999 to develop ICD-10-CM. During 2000, there were 23
countries using ICD-10.3 The U. S. Department of Health and
Human Services (HHS) has approved the use of ICD-10 by
2010, unless another date is determined. The date of use will
occur when the date is filed in the Federal Register 2 years
before implementation.
Other diagnostic code systems, which have been listed as
possibilities for the future, are the Systemized Nomenclature
of Dentistry (SNODENT) and Systemized Nomenclature of
Medicine (SNOMED). SNODENT and SNOMED were both
developed by the College of American Pathology as a descrip-
tive code set, which would be used in an electronic chart
environment. SNODENT contains 6000+ terms and 4000
codes, which are highly specific as to physical findings that,
in many instances, are not related to specific disease processes.
For a diagnosis of caries, the dental record would be supple-
mented with codes defining diabetes, hypertension, or obesity.
At the present time, there has been no field testing on use in
a clinical situation. The use of the codes is cumbersome and,
at the present time, requires a professional individual to input
the codes for a complete chart and cannot be easily delegated
to a staff individual for input into the chart.
CURRENT PROCEDURAL TERMINOLOGY (CPT)
CPT codes that are used to record specific medical, surgical,
and diagnostic procedures are maintained by the American
Medical Association under a CPT editorial board. The revi-
sions occur yearly and become effective January 1 of each
year.
A CPT code contains five numerals, which are specific for
a medical or surgical procedure and are mandated by law to
be used in the submission of Medicare and Medicaid medical
claims. They are required by most commercial carriers to adju-
dicate claims that fall under health policies. These codes
provide a definition of the specific procedure.
CPT codes are divided into eight sections, including:
Evaluation and management 99201 to 99499
Anesthesiology 00100 to 01999,
99100 to 99140
Surgery 10021 to 69990
Radiology 70010 to 79999
Pathology and laboratory 80048 to 89356
Medicine 90281 to 99199,
99500 to 99602
Category II performance 001F to 4018F
management
Category III emerging technology 03T to 0140T
CPT codes are not specialty specific and may be used by
any provider. Where indicated the specific code may have a
modifier attached to add additional information.
Modifiers for surgical procedures performed by oral and
maxillofacial surgeons may include:
-22 Unusual procedural services—Use where procedures
are greater than usually required to perform the surgery.
Usually used when there are complications associated
with the procedure. Use of -22 should be carefully con-
Coding, Insurance, and Third-Party Payers 365
sidered because the procedures should be significantly
unusual and more extensive than normally performed.
-23 Unusual anesthesia—Use when a procedure usually
performed with local anesthesia must be done under
general anesthesia.
-47 Anesthesia by surgeon—Use when regional or general
anesthesia is provided by the operating surgeon.
-50 Bilateral procedures—Use when the same procedure
is provided bilaterally. It is not used when “unilateral or
bilateral” is stated in the definition of the code. If a code
depicts that it is bilateral and is performed only on one
side, use the HCPC level II modifier -LT for the left side
and -RT for the right side.
-51 Multiple procedures—Use when multiple procedures
are carried out by the same provider on the same day at
the same session. Use to identify surgical procedures
performed in combination. The primary procedure is
reported, and all subsequent procedures have the -51
modifier appended.
-53 Discontinued procedure—Use when a procedure is
terminated for various reasons. The modifier is used
when the procedure is stopped before the desired result
is obtained. It is not used when the procedure is stopped
before anesthesia induction.
-62 Two surgeons—Use to report two surgeons operating
as primary surgeons on the same patient at the same
session. It should not be used if one surgeon is operating
as an assistant surgeon.
-80, -81, or -82 Assistant surgeons—May be used for an
assistant surgeon, a minimal assistant surgeon, or when
a qualified resident is not available.
Other modifiers are indicated as explanations of specific
codes.4,5
For example, an 18-year-old male has been evaluated for
a surgical orthognathic defect and was diagnosed as having a
vertical maxillary hyperplasia and a skeletal retrognathia. His
surgical plan was to include a Le Fort I maxillary osteotomy
with intrusion and separated into three parts and a bilateral
saggital osteotomy. This was accomplished by surgeon A and
an assistant surgeon, surgeon B. The ICD-9-CM codes are
524.01 and 524.04. The surgical reconstruction is coded as
21143 and 21195. Surgeon A submits these codes for reim-
bursement. Surgeon B submits 21143-80 and 21195-80 as the
assistant. The reason the bilateral sagittal osteotomy is not
reported with the modifier -50 is because the definition of
21195 contains the word rami, meaning two.
EVALUATION AND MANAGEMENT CODES (E/M)
These codes are probably the most misunderstood of all the
codes in CPT and require the documentation of multiple
levels of evaluation to be used.
There is a need to establish if the patient is a new patient
or an established one. The definition of a new patient is a
patient who has not been seen by the physician servicing the
patient or by any other physicians within the same practice
and in the same specialty for 3 years. An established patient
366 SECTION III ■ Practice Management
is one who has received services from the physician who is
providing services or received services from another physician
in the same practice and the same specialty within 3 years.
There is no difference if the patient is seen in the emer-
gency department. E/M services in the emergency department
are treated in the same manner, whether a new or established
patient.6
Levels of Service
There are three to five levels of E/M within each code. The
most important levels are medical history, physical examina-
tion, and medical decision-making process and are considered
the key elements of all the E/M codes. All of the E/M codes
carry the requirement to have a chief complaint noted in the
documentation of an encounter.
History
The medical history can be classed as problem focused,
expanded focused, detailed history, and comprehensive
history. Each category has specific subcategories, which have
increasing values.
History of Present Illness (HPI)
The HPI includes the location of the signs or symptoms, such
as what are the signs of pain or swellings; how significant are
the signs; how long have the symptoms been present; what
caused the symptoms; what makes it better or worse; and are
there any other signs that go along with the presenting signs.
A brief HPI would include from one to three of the above
signs. An expanded HPI would include at least four or more
signs or symptoms.
A detailed history includes the chief complaint (CC),
expanded HPI, a problem-focused system review (a review of
the system that contains the CC, such as the head and neck),
and pertinent past and family history that applies to the
patient’s complaints.
A comprehensive history includes the CC, expanded HPI,
pertinent past and family history that applies to the patient’s
complaints, and a comprehensive review of systems.
Examination
Examination can be classified as a problem-focused, expanded-
focused, detailed, or comprehensive examination.
Examinations can be classified into two types. The first is
a single organ system, which is specifically related to the
patient’s symptoms and the judgment of the examiner as to
the scope of the examination.
The second type of examination is a general multiple
system examination, which examines multiple organ or body
systems.
CPT classifies the organ systems as:
1. Eyes
2. Ears, nose, mouth, and throat
3. Cardiovascular
4. Respiratory
5. Gastrointestinal
6. Genitourinary
7. Musculoskeletal
8. Skin
9. Neurologic
10. Psychiatric
11. Hematologic, lymphatic, immunologic7
A problem-focused examination includes the area of the
chief complaints.
Expanded problem-focused examinations include an exam-
ination of the affected area and any other organ systems that
may be symptomatic.
A detailed examination includes an extended examination
of the symptomatic area and other symptomatic systems.
A comprehensive examination is a complete examination
of multiple organ systems.
Medical Decision Making
Decision making deals with three major decision points,
which have to be considered to determine the complexity of
the decisions. The first is the number of potential diagnoses
that could apply, the second deals with the amount and com-
plexity of data necessary for the review, and the third is the
risk of complications, morbidity, or mortality.
Each of these classifications can be subclassified into
straightforward, low complexity, moderate complexity, and
high complexity. Each of these subclassifications can be
identified as minimal, limited multiple, or extensive.
There is a difference in the code description between the
new or established patients in the requirements for satisfying
the conditions of correct coding.
Time
CPT in establishing the E/M codes has included time frames,
which should be considered in choosing the correct code. The
times include work done before the consult, during the consult,
and after the consult. The time frames vary for new patients
from 10, 20, 30, or 45 to 60 minutes for codes 99201 to 99205.
For established patients, the time frames vary from 5, 10, 15,
25, or 40 minutes for codes 99211 to 99215.
Counseling during Consultations
When consultations or coordination of care are mainly a dis-
cussion with the patient or family and occur for a 25-minute
time frame, the code used should be 99214. The amount of
time should be recorded in the chart, with start and finish
times listed in the chart, and 50% of the time documented
should be face-to-face counseling.
Emergency Department Evaluations
Only one provider can report an emergency department
service on any given encounter. If the emergency room physi-
cian reports the emergency encounter using CPT codes 99281
to 99285, the requested oral and maxillofacial consultation
should be one of the office or other outpatient visits, new or
established patient, codes 99201 to 99205 or 99211 to
99215.
 CHAPTER 21 •
If the oral and maxillofacial surgeon requests a patient to
go to a specific emergency department for after-hours evalua-
tion, it should be reported as a new or established patient
encounter, office or other outpatient visit, codes 99201 to
99205 or 99211 to 99215.
INPATIENT CONSULTATIONS
Hospital consults have to satisfy certain requirements. The
request for the consultation must be documented in the
patient’s chart and state the requested consultant and
the reason for the consultation. To write in the chart “Refer
to Doctor X for evaluation” is not appropriate.
There can be only one consultation per hospital admission.
If there is subsequent care, they should be documented using
subsequent hospital care (99231 to 99233).
The consultant must report the CC, an HPI, previous
medical history as it applies to the CC, and the examination.
Also incorporated is any laboratory or radiographic tests
that are indicated and the proposed treatment plan with
follow-up. There is no distinction made between new or
established patients in these cases. In coding for these
procedures, the same levels of complexity of the parameters
of the codes apply in the same way that they do for other E/M
codes.8
RADIOGRAPHIC CODING
There are two components for radiographic coding in CPT.
The first component is the technical component, which
encompasses material, equipment, and technical staff. The
second is the professional component, which includes the
professional supervision, reading of the study, and preparing
the report. It is reported with a -26 modifier, indicating the
professional component of the study. An oral and maxillofa-
cial surgeon may also report the interpretation of a radio-
graphic study if he or she evaluates the material and determines
that the findings are different for what the clinical situation
indicates and are different from the previous evaluation by the
radiologist (e.g., an MRI of the temporomandibular joints
indicates that the study is within normal limits and the clini-
cal examination indicates that the patient suffers from a closed
lock). The surgeon’s reread of the study and interpretation of
the MRI indicates an anterior displaced disk, which is nonre-
ducing. The surgeon must definitively document in the chart
the findings that document the differences in the interpreta-
tions from the initial report. This should be reported as 70330-
26 with the additional modifier of -77 (repeat procedure by
another physician).9
ANESTHESIA
The rules for providing anesthesia are established by each
state. These rules differ from state to state; therefore, each
practitioner must be familiar with all statutes and rules estab-
lished by the state board of dentistry in the state where they
practice. As an example, the rules to administer sedation and
general anesthesia in Virginia can be found at www.dhp.vir-
ginia.gov/dentistry.10
Coding, Insurance, and Third-Party Payers 367
Anesthesia Codes
One rule of anesthesia, which is incorporated in all proce-
dures, is that local anesthesia is inclusive for all procedures
listed in CPT and CDT codes. In those cases where there is
a mandated need for control of pain, an anesthesia code is
adjunctive to the procedure.
The anesthesia CPT codes are divided into sections, which
are anatomically listed. The codes used by oral and maxillo-
facial surgeons (OMS) are those found under the listing of
“Head” and “Neck.” The codes under this heading are descrip-
tor specific for the procedure being used.
In 2006, CPT established six new codes for moderate seda-
tion (99143 to 99150). Moderate sedation is defined as a
drug-induced depression of consciousness, where patients
respond purposefully to verbal commands and/or light tactile
stimulation. There is maintenance of the airway by the patient,
and there is spontaneous ventilation. Moderate codes do not
include minimal sedation, deep sedation, and monitored anes-
thesia codes (00100 to 01999). The codes are divided into two
categories. One where the surgeon performing the surgery also
provides moderate conscious sedation. The codes used range
from 99143 to 99145. When a doctor other than the surgeon
administers the moderate conscious sedation the codes range
from 99148 to 99150.11,12
Anesthesia is administered in time blocks, usually in 15-
minute increments. The time when the CPT code begins is
when the individual providing the anesthesia starts preparing
the patient and ends when the patient is safely under the care
of the recovery room personnel. There are modifying units,
which are added to the primary anesthesia code. They relate
to the physical status of the patient and range from P1 (normal
healthy patient) to P6 (a declared brain-dead patient whose
organs are being removed for donation).
CDT codes for anesthesia are found in the adjunctive general
services in the CDT 2007-2008 book. For CDT anesthesia
codes, the time begins when the physician administering the
anesthetic agents initiates the appropriate anesthesia and mon-
itoring protocol and remains with the patient until the physi-
cian may safely leave the room to attend to other patients.13
OTHER CPT CATEGORIES
CPT also contains category II and category III code sections.
Category II codes are intended as tracking performance pro-
cedures within the clinical chart. The codes are composed of
four digits followed by the letter F. These codes are not
intended to replace category I CPT codes.14
Category III codes are temporary codes, which designate
new or emerging technology or procedures. These codes are
archived after 5 years. These codes may be used, if listed,
instead of using “unlisted” codes.15
Current Dental Terminology (CDT)
The CDT (the code) was first published in 1969 as a way to
record what procedures were accomplished for the dental
patient. In 1986, the first dental code procedure manual was
published by the American Dental Association (ADA). The
368 SECTION III ■ Practice Management
revisions and maintenance of the code set is under the direc-
tion of the ADA Council on Dental Benefit Programs through
a subcommittee on the code. In 2001, the maintenance of the
code came under the direction of the code revision committee
(CRC) of the council.
The CRC is made up of equal representation of the payer
community and ADA representatives. Requests for additions,
deletions, or modifications to the code set may be submitted
by any interested party.
The proper manners for submissions for changes to the
code are specific and require a format that will enhance the
acceptance by the CRC. If an OMS wishes to submit a request
for a revision, it would be beneficial to contact the American
Association of Oral and Maxillofacial Surgeons (AAOMS)
for help in preparing the submissions.
All submissions received by the code committee are
reviewed by the CRC committee and voted on for their value
to the code and express current accepted techniques and treat-
ments. The revision process begins on odd-numbered years,
with a specific calendar of timelines over 2 years for the sub-
mission of code requests and action on three different batches
of submissions. The CRC may approve, deny, or table submis-
sions for further study as they are submitted.
The code is published in its revised state every 2 years. It
becomes effective on January 1 of odd-numbered years. All
code submissions to third-party payers must be the codes listed
in the latest version of CDT. The latest version is CDT 2007-
2008, sixth edition. The next edition will become effective
in 2009.16
The CDT is divided into twelve sections, which cover the
different classifications within the profession of dentistry. The
sections are not specialty specific and may be used by any
practitioner of dentistry.
I Diagnostic D0100 to D0999
II Preventive D1000 to D1999
III Restorative D2000 to D2999
IV Endodontics D3000 to D3999
V Periodontics D4000 to D4999
VI Prosthodontics, removable D5000 to D5899
VII Maxillofacial prosthetics D5900 to D5999
VIII Implant services D6000 to D6199
IX Prosthodontics, fixed D6200 to D6999
X Oral and maxillofacial surgery D7000 to D7999
XI Orthodontics D8000 to D8999
XII Adjunctive general services D9000 to D9999
The code is alphanumeric and begins with the letter D,
designating it as a dental code. The following four digits des-
ignate the section of the code; D7240 (removal of impacted
tooth—complete bony) is an oral and maxillofacial code.17
The nomenclature is the definition of the specific code
number. The descriptor is a narrative, which enhances the
nomenclature to clarify the usage of the code.
CDT is a national standard coding system in the Health-
care Common Procedure Coding System (HCPCS Level II).
The code is required to be used in the submission of billing
claims for all dental procedures.
The ADA dental claim form has been updated and became
effective on January 1, 2007. The claim form is maintained
and modified by the ADA and is used when modifications
have been made.
Having a code listed in CPT and CDT is not a guarantee
that the code is reimbursable. Third-party companies have the
leeway to cover or not cover certain procedures.
■ CHART DOCUMENTATION
Documentation within the medical or dental record is
extremely important, whether it is to support what was per-
formed for medical and/or legal reasons or for developing data
to support the filing of claims for reimbursement for the benefit
of the patient. This also applies to documentation of third-
party facilities, such as hospital charts. There is an adage that
states, “If it is not in the chart, it did not happen.”
Documentation allows you, the practitioner, to remember
what was actually performed on a given day many months
after the procedure was accomplished. It allows trained coders
to accurately report what is needed to file a legitimate claim
for reimbursement.
Charting has to be legible to anyone who reads a chart. In
the future, there will be paperless charting with the advance-
ment of the computerization of the practice of oral and maxil-
lofacial surgery. At the present time, many surgeons are
recording information on paper charts by hand for all
entries.
The most logical way to record notes in a chart is by printed
material; handwritten, legible notes; or by electronic entries.
The use of checklists on charts leaves concerns about whether
the procedures were actually performed.
When you address a case of third molars, the office record
should document what was actually performed. The office
notes should be as complete as any hospital note included in
a hospital chart. A note concerning the removal of an impacted
tooth should state at a minimum, “#17-Hockey stick incision,
full thickness buccal flap, tooth 80% bone covered, bone
removal, tooth sectioned and removed by elevation, follicular
sac removed, closure with 3-0 chromic.” This would give a
complete documentation of what was performed to remove
tooth #17 and what the classification of the impaction was
from a clinical perspective. Many times reimbursement is
based on the radiographic analysis by a consultant of a third-
party payer, which may not be accurate from a clinical
standpoint.
Abbreviations have now become standardized for hospital
charting and should be carried over to clinical charting in the
practice. Obtain the standard abbreviations from your hospital
that are currently used in documenting hospital notes and
physician’s orders.
■ INSURANCE
CLAIMS SUBMISSION
Claim submission is based on what is documented within the
medical or dental chart. You should not submit claims that
 CHAPTER 21 •
lack definitive documentation, which will support the code
submitted. Claims submissions may be submitted on CMS
1500 forms or on the ADA dental claim form, depending on
whether the benefits of the patient are medical or dental
related.
For all submissions, the highest valued code should be
listed on the first line of the form. Most third-party payers will
reimburse the highest valued code at 100% and any subse-
quent code submitted at the highest value at 50% of their
value.
For CPT codes, you must provide an ICD-9-CM code in
conjunction with the procedure code. This allows the third-
party payer to determine if the submitted procedure is appro-
priate for the diagnostic code.
Dental claim submissions are not required to submit a diag-
nostic code at the present time. Presently, however, there is
influence bearing on the use of diagnostic coding for dental
claims. It is anticipated that diagnostic coding and dental
modifiers will be mandated in the future, especially as elec-
tronic transmission of claims increases.
CORRECT CODING INITIATIVE
In 1994, CMS contracted with a Medicare carrier to deter-
mine which codes were not to be used in combination with
other procedure codes performed on the same day or during
the same encounter. These codes are divided into two sec-
tions. Component codes are those codes that are considered
as an integral part of another code and should not be billed
together. If component codes are submitted, only the highest
relative value unit (RVU) procedure will be reimbursed, and
the other code will be denied. Some codes can be filed on the
same day of service if the procedure is distinct or independent
from other services or involves a different anatomic site or
organ system by using the modifier -59.18
Mutually exclusive codes are those procedure codes that
are not likely to be performed on the same encounter. If these
exclusive codes are reported, only the code with the least
RVU value will be reimbursed, and the higher valued code
will be denied.
The National Correct Coding Initiatives Edits for specific
codes may be found on www.cms.hhs.gov/NationalCorrect-
CodInited/NCCIEP/list.asp. Current coding updates may be
purchased on a quarterly basis.19
■ THIRD-PARTY COMPANIES
PARTICIPATION CONTRACTS
All individuals participating in health care plans require
signing of a participating contract. A contract is a legal docu-
ment, which is enforceable by the participant or the company
providing health care services. All OMSs must read and
understand the components of a contract before signing, with
emphasis on small-print sections. They should evaluate the
conditions that are being placed on them by the contract. The
penalties stated in the contract should be evaluated and
accepted, such as resigning from participating in the plan.
Coding, Insurance, and Third-Party Payers 369
In evaluating whether to participate with a specific
company, you should research the company and its policies
on the Internet. The ADA provides a free service for evaluat-
ing contracts if they are submitted for evaluation through a
state dental association. The ADA will evaluate the contract
in strict legal terms and will not provide advice as to whether
to participate or not in a specific contract. There is a fee for
this evaluation if it is submitted by an individual and not a
state dental association. Another mechanism of evaluating
contracts is to contact an attorney who is well versed in health
care contracts.20
Also, evaluate how participation will impact your current
practice and accounting system. Analyze whether or not the
demographics of the plan’s subscribers will fit into the way
that you practice. Look at the reimbursement schedules and
determine if the amount of reimbursement will cover your
overhead and allow a profit.
Be particularly cautious about audits that are prescribed in
the contract. If you are advised by a third-party payer that an
audit is pending, you should be aware of what will be included
in the audit and the timing of an audit. Determine the number
of charts that will be included in the audit and what parame-
ters will be covered. Some carriers, for example, will request
that 10 to 20 charts be evaluated. If any violations of fre-
quency of use or standards of care are discovered, there will
be an estimate of the total number of charts in the practice,
and the monetary penalty will be multiplied by the practice
number. This could lead to thousands of dollars in fines. The
demand of repayment could be immediate, with no grace
period. Most important, never allow an auditor to evaluate
patients’ charts that are not serviced by the company perform-
ing the audit. A nonparticipating provider does not have to
submit for an audit. Should you have questions about an audit,
you should seek legal advice.
Some contracts may have silent or rental network PPO
provisions. These provisions would allow a plan to market the
provider’s agreed-upon fee schedule to a network broker.
When a claim is submitted to a particular company, they will
submit it to a network broker, who will evaluate its database
and determine the greatest discount fee for that provider that
is listed for a specific procedure. The provider will then receive
a reimbursement, which is much lower than the negotiated
amount.
Practices should run frequent internal audits to determine
if they are receiving reimbursements that are routinely less
than the contracted fee amounts. The American Medical
Association model managed care contract specifically defines
a payer, which makes it clear that a managed care plan cannot
rent or lease the terms of agreement to other entities.21
CLAIMS SUBMISSIONS
Medicare has strict rules pertaining to the submission of
claims. All OMSs who are participating or nonparticipating
(with the exception of those who have opted out of Medicare)
are required to submit claims for Medicare-covered services.
For those procedures that are excluded from Medicare bene-
370 SECTION III ■ Practice Management
fits, the provider may be required to submit claims if the
patient requests that a claim be submitted or if they desire to
obtain a denial for the procedure. The areas that are excluded
from Medicare benefits are any procedure dealing with cos-
metics and dental care, including dental prosthesis.
It is necessary to have the patient sign an advanced benefi-
ciary notice (ABN) when there is a possibility that a proce-
dure is not a covered procedure. This must be done before the
procedure is performed. If it is not signed or is signed after the
procedure, the provider will not be able to bill the patient and
will receive no reimbursement from Medicare. A notice of
exclusion from Medicare benefits (NEMB) is signed before
instituting a procedure when it is known by the provider to
be a noncovered procedure, such as extraction of teeth.22 After
the ABN is signed, the code for the procedure should have
one of the following modifiers appended:
-GA—waiver of liability statement on file
-GY—item or service statutorily excluded or does not meet
the definition of any Medicare benefit (used when patient
insists that a claim be filed)
-GZ—Item or service expected to be denied as not reason-
able and necessary (used when the patient refuses to sign
the ABN). The patient may not be held responsible for
charges that are deemed to not be medically necessary
unless they have been given advance notice that Medi-
care may not approve the service.23,24
NATIONAL PROVIDER IDENTIFIER (NPI)
The Health Insurance Portability and Accountability Act
(HIPAA) of 1996 required that all providers obtain a unique
provider number, which is required to be on all claims submit-
ted by May 23, 2007, including all dental claims and CMS
1500 claims. NPI is a government issued 10-digit number for
an individual provider, which does not include identification
of the place of practice or the locality where the provider
practices. The NPI will replace the identification codes previ-
ously used, such as a unique physician identification number
(UPIN), and will be the uniform identifier for all third-payer
companies.25
■ CLAIMS ADJUDICATION
Third-party payers have developed internal rules in their adju-
dication process, which are generally unknown to the pro-
vider. These rules allow the payers to bundle submissions for
multiple reasons. One such rule would bundle the removal of
a dentigerous cyst in conjunction with the removal of a com-
plete, bony, impacted third molar. The reason for this is that
many of the submissions have been determined to be fraudu-
lent. As a general rule, if a claim is denied or only one of the
procedures is benefited, the claim should be appealed with
documentation, which includes the size of the lesion and the
submission of a pathology report. Many times the practitioner
is unaware of what the resulting adjudication of a claim has
been, and therefore there is a need for an appeal. The practice
business office should be acutely aware of reimbursements and
have the ability to understand that codes have been bundled
on a reimbursement. The practice accounting system should
be able to report on a quarterly or yearly basis the amount of
reimbursement by code for individual third payers as it relates
to the practice overhead.
In appealing a reimbursement, a letter should be sent to
the third-party payer stating the reasons for the appeal along
with documentation. The letter of appeal should always be
signed by the practitioner and not by a staff individual.
When submitting claims for biopsy or excision of a lesion,
it is proper to withhold the submission of a claim until there
is a pathologic diagnosis for the lesion. This will prevent a
possible diagnosis, rather than a final diagnosis, from being
incorporated incorrectly in the chart.
■ MEDICARE FEES
In 1992, Medicare established the Medicare fee schedule for
reimbursement for submitted procedures. Payment is based on
a Resource Based Relative Value Scale (RBRVS). There are
three components of the RBRVS, which play a part in estab-
lishing a fee schedule.
RVUs are assigned to each CPT and HCPCS level II
codes.
1. Work RVU—the provider effort and skill required to
provide the service
2. Practice expense RVU—practice overhead, includes
rent, supplies, and salaries
3. Malpractice RVU—the cost of malpractice and liability
insurance
GEOGRAPHIC PRACTICE COST INDEX (GPCI)
Each of the RVU categories is given weighted index values
known as the Geographic Practice Cost Index (GPCI). The
GPCI creates a local index, which is an adjustment of a
national average.
For CPT Code 21141, reconstruction midface, Le Fort I,
single piece, segment movement in any direction (e.g., for
long face syndrome) without bone graft in Virginia, the values
are as follows:
Work RVU = 19.27
Expense RVU = 13.16
Insurance RVU = 2.36
Total RVU = 34.79
The RVU is multiplied by the GPIC.
Work RVU (19.27) × GPCI Work (1.00) = 19.27
Expense RUV (13.16) × GPCI Expense (0.942) = 12.39672
Insurance RUV (2.36) × GPCI Insurance (0.569) = 1.34284
Total RVU is the sum of the individual values =
33.00956.
CMS establishes the conversion factor, which measurers
the RVU in terms of dollars per RVU and publishes it in the
Federal Register each year. Congress has the ability to change
the value of an RVU before its implementation. For 2007, the
conversion factor is $37.8975. This number is multiplied by
the total RVUs. $37.8975 × 33.00956 = $1251.00. This is the
fee by Medicare to a Le Fort I one piece osteotomy.26
 CHAPTER 21 •
■ FRAUD AND ABUSE
The HIPAA of 1996 established a comprehensive program to
combat fraud against all health plans, both public and private.
The statute required the establishment of a national Health
Care Fraud and Abuse Control Program (HCFAC) under the
direction of the U.S. Attorney General and the Secretary of
HHS. The Office of Inspector General (OIG/HHS) along
with the Department of Justice (DOJ) and the Federal Bureau
of Investigation (FBI) under the direction of the Attorney
General or the Secretary of Health and Human Services are
the investigative arms who are required to work with federal,
state, and local authorities in determining if fraud has occurred
with health care agencies, whether from the provider side or
the insurance industry.27
Fraudulent health care claim submissions have caused an
increase in the premium cost of individuals of approximately
$1800 per year. Most health care providers attempt to record
and report legitimate claims for their patients. There are some
providers, however, who have attempted to commit fraud with
Medicare, Medicaid, and private insurance companies by
developing illegal schemes.
These schemes have included billing for procedures that
were not provided, double billing of codes, unbundling, upcod-
ing procedures to more complex codes, and miscoding.
Although the OIG and FBI are not as concerned by an occa-
sional miscoding, it does become a concern if frequently
repeated (e.g., coding all simple extractions as surgical extrac-
tions). Third-party payers develop profiles on all submitters of
claims and when there are variations in what is routinely
submitted, it will raise questions about the provider.
Claims of fraud and abuse can be submitted by individuals
who are allowed to bring suit on behalf of the government,
known as qui tam cases (whistle-blowers). If the claims are
successfully prosecuted, the whistle-blower will receive 15%
to 30% of the award or fine.28
The prosecution of abuse and fraud cases can lead to both
criminal and civic penalties. Criminal penalties are based on
knowingly or willfully intending to defraud Medicare, Medic-
aid, or any other type of federal health care benefit plan. These
may include prison terms up to 5 years and penalties up to
$250,000 per claim. There can also be an exclusion from
Medicare and Medicaid plans for 5 years. If a provider has
three exclusions, they will be permanently excluded.
Civil cases will be deemed guilty if a provider knowingly
submitted a claim that he or she knew or should have known
was false or incorrect. These penalties may be up to $10,000
per item that is incorrectly submitted. In addition, they will
have up to treble the fines of the amount that was improperly
submitted.29
■ PRACTICE CONSIDERATIONS
The business of the practice of oral and maxillofacial surgery
has become complex for today’s practitioner. It is extremely
important to have a well-trained staff to be able to identify
inappropriate reimbursement, prevent inappropriate submis-
Coding, Insurance, and Third-Party Payers 371
sions, and advocate for the practice and patients with third-
party payers.
Coding is an integral part of obtaining proper and honest
reimbursement for what is provided for our patients. It is rec-
ommended that all surgeons should take advantage of coding
courses, which are provided by both the ADA and the
AAOMS. It is a great benefit to the practice to include key
employees in these courses.
All providers and staff should know the primary coding
volumes of CDT, CPT, and ICD-9-CM.
The ADA provides coding courses on CDT, by request,
from ADA constituent and component societies. Requests
are made to the ADA council on dental benefit programs.
AAOMS provides three coding courses. The introduction
course is Basic Online. This course requires registration and
is designed for professionals and staff who have never had a
coding course. Beyond the basics is a participation seminar,
which is given four times a year in various sections of the
country. Registration is made through AAOMS. A third
course is Advanced Coding Online, which is an Internet-
based course through AAOMS.
REFERENCES
1. History of the development of the ICD, www.who.int/entity/
classifications/icd/en/HistoryOfICD.pdf (accessed Sep 7, 2006).
2. Beacon health solutions, www.beaconllc.com/hcref/cclookup/
icddescription.htm (accessed Sep 18, 2006).
3. World Health Organization, www.who.int/Classification/icd/en
(accessed Jan 3, 2007).
4. CPT plus, Los Angeles, 2006, Practice Management Information
Corp.
5. Beyond the basics coding course, 2005, American Association
of Oral and Maxillofacial Surgeons, www.aaoms.org. (accessed
Jan 20, 2007).
6. CPT 2007, ed 4, revised, 2006, American Medical Association.
7. CPT 2007, ed 4, revised, 2006, American Medical Association.
8. Personal communication, Heather Mays, Richmond, VA, Com-
monwealth Oral and Facial Surgery.
9. Personal communication, Paula Kantas, Rosemont, IL, Ameri-
can Association of Oral and Maxillofacial Surgeons, Senior
Associate, Coding and Reimbursement.
10. Virginia Board of Dentistry, rules and regulations, www.dhp.
virginia.gov/dentistry (accessed Feb 1, 2007).
11. CPT 2007, ed 4, revised, 2006, American Medical Association.
12. Six new moderate sedation codes in CPT 2006, www.aaoms.
org/practice_mgmt.php (accessed Jan 11, 2007).
13. Current dental terminology, CDT 2007-2008, Chicago, American
Dental Association.
14. CPT 2007, ed 4, revised, 2006, American Medical Association.
15. CPT 2007, ed 4, revised, 2006, American Medical Association.
16. Current dental terminology CDT 2007-2008, Chicago, American
Dental Association.
17. C L Cuttino, AAOMS consultant to the CDT code.
18. Modifier -59 article, www.cms.hhs.gov/NationalcorrectcodInited/
(accessed Feb 17, 2007).
19. NCCI edits, www.cms.hhs.gov/NationalCorrectCodInited/
NCCIEP/list.asp (accessed Feb 17, 2007).
20. Alexander HC, Cuttino CL: Coding and practice management,
fair and just reimbursement for your honest services, Lecture,
Richmond, VA, 2006, 14th Annual Women in Science, Den-
tistry, Osteopathy and Medicine.
372 SECTION III ■ Practice Management
21. Silent and Rental Network PPOs: Identification and prevention,
American Association of Oral and Maxillofacial Surgeons, www.
aaoms.org/practice_mgmt.php (accessed Jan 11, 2007).
22. Medicare form CMS-2007.
23. Beyond the basics coding course, 2005, American Association
of Oral and Maxillofacial Surgeons, www.aaoms.org. (accessed
Jan 29 2007).
24. Medicare beneficiary notice: ABN or NEMB, American Asso-
ciation of Oral and Maxillofacial Surgeons, www.aaoms.org/prac-
tice_mgmt.php (accessed Jan 1, 2007).
25. National provider identifier, CMS, www.cms.hhs.gov (accessed
Feb 18, 2007).
26. Physician fee schedule, www.cms.hhs.gov/physicianfeesched
(accessed Feb 18, 2007).
27. Health care fraud and abuse control program report (HCFAC),
HHS Office of Inspector General, http://oig.hhs.gov/publications/
(accessed Feb 17, 2007).
28. Federal register 71(161), www.oig.hhs.gov/authorities/docs/06/
waisgate.pdf (accessed Feb 20, 2007).
29. Beyond the basics coding course, 2005, American Association
of Oral and Maxillofacial Surgeons, www.aaoms.org (accessed
Jan 20, 2007).

RISK MANAGEMENT IN ORAL
MAXILLOFACIAL SURGERY
Steven M. Holmes • Debra K. Udey
■ RISK MANAGEMENT—AN
OVERVIEW
Risk management in medical and dental practice begins with
the golden rule. Treat patients the way you would want to
be treated or the way you would want your spouse, parents,
or children to be treated. We all want to receive the highest
quality of care in medicine and dentistry. We want our physi-
cians and dentists to listen to our symptoms and concerns,
evaluate us appropriately through a complete examination
and appropriate diagnostic tests, obtain outside consultation
when appropriate, consider treatment options, and then
discuss those options with us objectively so that we can
choose our course of treatment. We want to understand the
risks, benefits, and possible complications of our treatment
options, including no treatment. We want the process to be
legibly documented in our medical and dental records so that
it can be reviewed to possibly help with additional challenges
that we might face. The concept certainly sounds good and
seems to be attainable. Why are so many malpractice claims
filed against physicians and dentists? How does the oral and
maxillofacial surgeon accomplish the task of minimizing
risk?
OMS National Insurance Company (OMSNIC) insures
approximately 83% of the practicing oral and maxillofacial
surgeons in the United States. OMSNIC’s statistics show that
15% to 17% of oral and maxillofacial surgeons have at least
one claim filed against them every year. Every 7 years the
practicing oral and maxillofacial surgeon can expect to have
one of his or her patients make a written request for compen-
sation or actually file a lawsuit for an injury or a perceived
injury. The good news is that the frequency of claims has
drifted downward over the past few years. Unfortunately, the
bad news is that the severity of verdict awards and settlements
is continuing to escalate. Million dollar verdicts are common-
place, which affects the amounts paid in settlements by
increasing them. Some very sobering news is that plaintiff’s
attorneys are winning more often than they did in the past.
This has happened as a result of legislation favorable to their
efforts, the ongoing education of plaintiff’s attorneys on how
to successfully sue physicians, and a decrease in the number
of frivolous lawsuits being filed.
By far the most common claims are related to the proce-
dures performed in the oral and maxillofacial surgeon’s office
on a daily basis. These are the extractions, removal of impacted
CHAPTER 22
AND
teeth, placement of dental implants, biopsies, etc. Of OMS-
NIC’s 6346 closed claims through 2005, 78% stem from these
“routine” procedures. The costs of defense and indemnity pay-
ments of these claims accounts for 68% of all expenditures
through 2005. More than $9 million has been paid in wrong
tooth extraction claims alone.
Many of the factors involved in a patient bringing a lawsuit
against an oral and maxillofacial surgeon are under the control
of the surgeon. Modifying behavior and establishing office
systems to protect against a claim are the primary tools avail-
able to reduce the risks of a lawsuit. Unfortunately, oral and
maxillofacial surgeons are hesitant to accept their responsibil-
ity to help protect themselves from a patient’s claim of negli-
gence. Minimal improvements in loss prevention could
prevent many potential claims from being brought.
The records of physicians and dentists are one of the biggest
problems in the defense of claims. Surgeons seem to be far
more interested in treating the next patient than taking the
time to clearly document the current patient’s chart. Millions
of dollars are needlessly paid on defensible claims that are
settled or lost in court as a result of inadequate records.
Physicians and dentists in this country practice in a liti-
gious climate. They are no longer looked upon as community
leaders, and the medical and dental professions have been
changed politically. Medicine and dentistry are looked upon
as businesses more than learned professions. In the environ-
ment of managed care (i.e., more patient visits per day and
less face-to-face physician-patient time), patients frequently
fear that physicians are more interested in making money than
providing good patient care. There are many factors that have
led to changes in patients’ attitudes toward instituting legal
action against physicians and dentists.
A second major problem leading to claims and lawsuits is
the lack of rapport. Not infrequently, patients begin legal
proceedings against their health care providers because their
physician did not take the time to talk to them to give them
a reasonable explanation or any information about their situ-
ation and their perceived injury. A plaintiff’s attorney can
supply them with a simple explanation using understandable
medical and dental science, leading the patient to believe that
their physician treated them in a negligent manner. The phy-
sician will likely come too late to the conclusion that a few
more minutes spent with the patient answering their questions
honestly and compassionately could have prevented a claim,
but that opportunity has been lost.
373
374 SECTION III ■ Practice Management
We also live in a society with increasing personal debt and
decreasing personal savings. Monetary demands on individu-
als are an ever-increasing concern. Instant gratification and
more sophisticated marketing efforts encourage us all to have
the latest and most sophisticated personal items. This has
brought more people to the brink of personal bankruptcy.
These same monetary demands affect the oral and maxillofa-
cial surgeon and their patients. What happens when the
patient has an infection or prolonged recovery from a proce-
dure and unexpectedly misses work or has unanticipated addi-
tional medical or dental expenses? They often become angry
toward the health care provider. The chances of winning a
lawsuit are much better than winning the lottery, and, in a
situation like the earlier one, a patient may be much more
willing to take such a chance.
Taking risk management issues seriously before being sued
can make an oral surgeon’s practice life easier. Unfortunately,
many will not take the simple necessary steps to help limit the
chances of litigation until after experiencing an emotionally
painful, time-consuming lawsuit.
■ BACKGROUND INFORMATION
State legislatures develop laws—medical and dental practice
acts—that define how physicians and dentists may practice.
They also make the laws governing how patients may bring
lawsuits against physicians. State departments of public regu-
lation and state boards of dentistry and medicine also dissemi-
nate rules and regulations that further dictate and control how
physicians must practice.
Malpractice claims are usually filed under state tort systems.
These are civil actions that allow a patient with an alleged
injury to seek monetary damages from the caregiver who alleg-
edly caused the injury. Malpractice is defined as the failure to
meet the duty of care and/or a breach of accepted standards
of care as established by the profession. Lawsuits can occur
when the failure or breach results in injury and damage to the
patient.
The patient is labeled the plaintiff, and the physician is
labeled the defendant in a legal action. Each is usually
represented by an attorney. In most cases, the plaintiff’s
attorney will only recover expenses and receive a financial
reward if the plaintiff “wins.” Their financial reward is
known as a contingency fee, a percentage of the indemnity
payment (usually 30% to 40%). The indemnity payment is
the settlement amount or verdict amount. The defense attor-
ney usually is paid on an hourly basis by the defendant’s mal-
practice liability insurance carrier or, if uninsured, the
defendant.
“Standards of care” are usually national and are based upon
the duty of the physician to use the care and skill ordinarily
used by reputable members of the profession practicing under
similar circumstances. In most jurisdictions, the plaintiff must
have an expert witness substantiate the failure to meet the
standard of care. The defense will also use expert witness
review to demonstrate that the care received by the patient
was within the standard of care. In a case that goes to trial,
the jury will use the expert witness’s testimony to decide if
there was a breach of the standard of care.
To “win” in a malpractice case, the plaintiff must prove
what is known as the A, B, C, Ds of litigation.
A. A physician-patient relationship must exist between the
patient and the physician. This is defined by state law.
Acceptance implies a duty of care. The plaintiff must prove
the physician-patient relationship. The physician must
have accepted the patient as a patient of record in the
practice. Every patient is not accepted for treatment—
this is a decision made by the physician. Once past the
examination and consultation phase, the court will likely
determine that a physician-patient relationship was
established.
B. The physician must have breached the standard of care.
Expert witnesses on both sides will testify as to whether
the defendant has met the standard of care. Posttrial jury
interviews have established that jurors evaluate defendant
physicians to decide whether they would receive appropri-
ate care if they were the physician’s patient. Expert wit-
nesses that come from many states away or from the “ivory
tower” of the university centers are not as believable to
jurors as a “wet-fingered” oral and maxillofacial surgeon
from the local community. Jurors wonder why the plaintiff
or defendant could not find a local oral and maxillofacial
surgeon to testify about the care rendered to the
plaintiff.
Some states require that an expert witness be from the
same specialty as the defendant. This is the most level
playing field. Unfortunately, there are still states where the
tort laws have not been updated, and the experts can be
from another specialty, such as a general dentist or a
physician.
Occasionally, the plaintiff is able to avoid proving that
the defendant’s care breached the standard of care by the
use of res ipsa loquitur (the thing speaks for itself). Negli-
gence is inferred in the absence of actual proof. The defen-
dant must explain the alleged injury instead of the plaintiff
proving the negligence. Such cases include foreign bodies
left in a patient without the patient’s knowledge (e.g.,
broken instruments, burs, or packing material). Three con-
ditions must exist for the plaintiff to apply res ipsa
loquitur:
1. The defendant was the only health care provider that
could have caused the injury to the plaintiff.
2. The patient was not responsible and did not contribute
to the injury.
3. The injury would not have occurred unless the defen-
dant was careless or negligent.
C. The patient’s injury must have been caused by the
defendant’s breach of the standard of care. No other
intervening causes or events contributed to the injury. The
plaintiff’s expert witness testimony will attempt to show
that the defendant’s actions were the proximate cause of
the injury. Actions by staff contributing to the injury are
often assigned to the defendant physician. Certain states
 CHAPTER 22 • Risk Management in Oral and Maxillofacial Surgery
have a legal “captain of the ship” doctrine, where all sub-
sequent injuries or complications occurring to the patient,
caused by others, after the initial event are assigned to the
defendant.
D. The patient must have suffered damages associated
with the defendant’s actions. If damages are proved, the
plaintiff is compensated with a monetary award. There are
three types of damages that plaintiff’s attorneys can
claim:
1. General damages are related to the pain and suffering
caused by the injury to the patient. These can be both
physical and emotional. Loss of consortium claims is
general damages.
2. Special damages are the actual monetary costs that the
patient has paid for treatment or care of the alleged
injury. These are both current and future monetary
losses to the patient for physician’s bills, hospital costs,
loss of income, psychological counseling, rehabilita-
tion, etc.
3. Punitive damages can be assigned if the plaintiff’s attor-
ney can prove that the patient’s damages were caused
by the defendant’s deliberate actions that were substan-
tially below the standard of care. Attempting to do such
things as hiding the cause of the injury from the patient,
concealing facts about the case, altering the patient’s
records, or providing care while intoxicated could result
in punitive damages. Such damages are meant to punish
the physician for the substandard care or illegal acts.
Once these types of circumstances are discovered by
the defendant’s malpractice insurance company, the
case is usually settled rather than risk the defendant’s
personal assets in a court case. Punitive damages are
usually not covered under a professional liability insur-
ance policy.
■ INCIDENTS AND CLAIMS
An incident is any injury or untoward event that occurs to a
patient that may cause a patient to seek compensation from
the physician. Included in liability insurance contracts is the
provision that the physician has the obligation to report any
and all incidents in a timely manner to the insurance company.
A lower molar extraction patient with a significant paresthe-
sia, an anesthesia following removal of a lower third molar
tooth, a bur guard burn to a lip, an infection following an
elective surgery requiring hospitalization and loss of income
to the patient, or a fracture following removal of a lower third
molar are all examples of incidents that could lead to a lawsuit.
Any event causing a patient to be transported to an emer-
gency room or hospital for evaluation or care is a reportable
event. Significant incidents often require a self-report be filed
with the state’s department of professional regulation (DPR),
medical board, and/or dental board.
Incident reporting allows the insurance company’s claims
handlers to help the physician manage the potential risk
involved with the incident. Liability carriers have extensive
experience with these injuries and can offer a vast amount of
375
help and support to the insured physician. Incidents do not
affect the underwriting of the insured, nor do they change the
premium charged for future insurance policies.
Each state has a statute of limitations that specifies how long
a patient has to file a lawsuit after the incident occurs. These
laws vary by state, but are generally 2 or 3 years from when a
reasonable patient knew or should have known about the
injury. The time in which a minor can file a lawsuit often
begins when the minor has reached the age of majority, but
this also varies by state.
The determination of whether a patient has filed a claim
within the statute of limitations is one instance in which
documentation of the clinical chart is particularly important.
If the chart clearly reflects the discussions with the patient
about the injury, it limits the patient’s ability to claim that he
or she did not know about the injury to potentially extend the
statute. In addition, the oral and maxillofacial surgeon who
does not document in the patient’s record mapping and testing
for an alleged paresthesia may be surprised by the size of the
affected area alleged by the patient, once an attorney is
involved on the plaintiff’s side.
It should be recognized that statutes of limitation are
frequently tolled or waived by plaintiff-oriented judges. This
occurs frequently in cases of fraud or retained foreign bodies
that were not disclosed to the patient. The retained root tip,
broken instrument, or end of a broken bur must be disclosed
to the patient and the disclosure documented clearly in the
patient’s record.
Claims arise from a specific action by the patient or when
a serious event affecting the patient has occurred. These must
be reported to the liability insurance carrier immediately.
1. A written request for compensation from the patient or
their attorney. This can range from a request to cover
expenses to repair an accidentally chipped tooth during
an extraction procedure to a request for $1 million to
compensate for the pain and suffering associated with
hospitalization and surgery for treatment of an infection
following surgery.
2. A lawsuit can be filed against the physician. The first
notice of this action may be the receipt of a summons
and complaint. This legal document requires prompt
action to defend the physician.
3. Savvy plaintiff’s attorneys or an angry patient can file a
complaint with the DPR and/or board of dentistry or
medicine about a physician. These DPR claims allege a
violation of the state dental or medical practice act.
Oral and maxillofacial surgeons should be aware of their
state practice acts. A portion of state licensure proce-
dures involves passing a test concerning these require-
ments. The board’s duty is to protect the public, and
certain states have very aggressive boards that investi-
gate physicians with a passion. The results of investiga-
tions by state boards may be admissible in a malpractice
lawsuit. Therefore most liability insurance companies
find it appropriate to defend their insured physicians in
these cases.
376 SECTION III ■ Practice Management
The lack of clarity and detail in the patient’s record is
often the reason these claims are filed by the plaintiff’s attor-
ney. Plaintiff’s attorneys will do anything to annoy the physi-
cian and hopefully influence him or her to pressure their
insurance company to settle a claim. Not having patient
prescriptions listed in the patient’s record in the “legal”
manner prescribed by the law is a common violation that
triggers a DPR complaint. This will require hours of the
physician’s time to defend and expenses for the insurance
carrier. A patient who believes that he or she was wronged
by the physician and cannot find an attorney to sue the
physician will often turn to the DPR with an inadequate
care complaint to attack the physician.
4. If the insurance company believes that the potential
liability associated with a reported incident is very
serious, they will begin an open investigation claim. Cases
involving very serious situations, such as a patient who
suffers a stroke or MI during or after an office or hospital
surgery leading to death or a debilitated state of life, will
likely be seen as serious enough to begin an investiga-
tion of the facts of the case. Insurance companies will
do this to allow them to set aside money (reserves) for
a potential payment on the claim and report the claim
to their reinsurer. Gathering early information can often
prevent claims or lessen the cost of the resulting
claim.
Every practicing oral and maxillofacial surgeon will receive
an occasional request for records from an attorney. This is
usually the first written document, indicating that a patient is
attempting to find an attorney to file a lawsuit against the
physician. It is crucial that an oral and maxillofacial surgeon
resist the temptation to review the patient’s records and add
additional comments or clarification to existing notes before
forwarding the copies to the attorney. Any alteration of the
records, once discovered, will automatically cause settlement
of the case, no matter how defensible it is.
The plaintiff’s attorney will conduct an investigation to see
if the case has merit.
The patient must sign a release, which will accompany the
request for records. Upon receiving a request for records and
the signed release, the physician must contact his or her liabil-
ity carrier immediately. Copies of the requested records must
be released to the attorney in a timely manner. Reasonable
copying fees can be charged for the production of the copies
of the patient’s chart, radiographs, and any other records.
Frequently, state law dictates the amount that can be charged
for the copies. Original records should never be released to
anyone. You are under no obligation to provide anything to
the plaintiff’s attorney other than true copies of the patient’s
records.
If the plaintiff’s attorney requests anything else (e.g., a
treatment summary), the request should be reported to your
claims handler, and you will likely be advised not to honor
the request. If your handwriting is illegible, providing a ver-
batim transcript of your records without any additional
comment is appropriate. The copies of the patient’s records
must be forwarded to the patient’s attorney, even if the
patient’s account is not paid in full.
■ THE LAWSUIT PROCESS
Certain states, in an effort to limit frivolous lawsuits, now
require that the plaintiff’s attorney submit an affidavit or cer-
tificate of merit before an actual lawsuit can be filed. The
affidavit or certificate is a statement by a similar specialist
licensed to practice in the state who: (1) provides similar
patient services, (2) has reviewed the available patient records
and other pertinent information (the patient’s unsworn state-
ment about the negligent care), and (3) attests to the negli-
gent care provided by the defendant physician or dentist. The
physician providing the affidavit or certificate of merit is paid
by the plaintiff’s attorney to review the records and to sign
and provide the document. In states not requiring an affidavit
or certificate of merit, the first notice of a lawsuit received
by the defendant physician will be a summons and
complaint.
There is a very short time period for the defendant to
respond once a defendant receives an affidavit, certificate, or
the summons and complaint. This is usually 30 days, but can
vary by state. When either of these documents is the first
notification received by the physician about a patient’s alleged
injury, the physician must contact their insurance company
immediately. To not report receipt of these documents can
actually jeopardize coverage.
The clock is ticking. A copy of all of the patient’s records
must be forwarded to the insurance carrier immediately. The
insurance company will assign counsel to respond to the alle-
gations within the required time period. The court requires a
formal response to the affidavit, certificate, or summons and
complaint by the defense attorney within the specified period
of time, or there are severe consequences.
If the court does not receive a response within the required
time period, a default judgment will be issued against the physi-
cian. This holds him or her negligent on all counts involving
the alleged injury without any opportunity to defend the
actions. The court will decide the monetary amount of damages
to compensate the plaintiff without a trial.
Plaintiff’s attorneys will often exaggerate and embellish the
allegations. This is designed to increase the anticipated emo-
tional response of the defendant in the hopes that he or she
will want to settle the case instead of fighting it. The assigned
defense counsel and the insurance company’s claims handler
will discuss the allegations with the defendant.
Once the formal complaint or a request for compensation
has been received, the defendant physician can only discuss
the case with the assigned attorney and the insurance company.
These are privileged communications and do not need to be
shared with the plaintiff’s attorney. Any other discussions are
discoverable by the plaintiff’s attorney. The surgeon must not
discuss the claim with colleagues. The plaintiff’s attorney will
ask the defendant with whom he or she has discussed the case.
If such a discussion has been held, the colleague will be
deposed to obtain information casually disclosed. The oral and
 CHAPTER 22 • Risk Management in Oral and Maxillofacial Surgery
maxillofacial surgeon will need to spend time away from prac-
tice and family working on the defense of the allegations.
The beginning of a lawsuit involves both sides gathering
information and evidence. This is called discovery. It takes the
form of the collection of records from other physicians and
dentists, written questions from each side, interrogatories that
must be answered, unsworn statements from the plaintiff and
defendant, and sworn statements. Depositions are the sworn
statements taken in front of the defendant’s attorney, plain-
tiff’s attorney, and a court reporter. The expert witnesses will
evaluate all of the pertinent records and documents and make
their assessment regarding the appropriateness of the care
provided to the patient.
As the process continues, the claims handler at the insur-
ance company and assigned defense attorney will discuss the
defensibility of the claim. The defense attorney will discuss
the claim with the defendant to develop the defense strategy.
An insurance company may also have a “claims committee”
of physicians to review the information and make recommen-
dations to the defense attorney.
As discovery progresses, a determination is made to defend
or settle the case. In cases of clear liability or those where a
determination is made that the case cannot be won in court,
the claims handler will attempt to effect a settlement. In most
cases, settlements can be reached. However, in a small number
of cases, plaintiffs are unwilling to settle for an amount that
is reasonable, and the case must be tried to allow a jury to
award a reasonable amount.
Cases that are clearly defensible are most often tried. The
lawsuit process can be arduous and uncomfortable, but the
claims handlers and the defense counsel do all they can to
assist and support the defendant physician. The court system
is capricious at best, and it is impossible to predict that every-
thing outlined above will go along as planned. But when the
defense team (the attorney, claims handler, and physician)
works well together, there is often a good result.
INSURANCE
All forms of insurance involve the sharing of risk. The cost of
insurance is determined by the anticipated costs involved with
paying and defending claims. The concept is the same for
homeowners, automobile, and liability insurance. Most home-
owners do not experience a loss every year, most of us do not
have an automobile accident each year, and “only” 15% of
oral and maxillofacial surgeons have a malpractice claim every
year. So we can pay a “small” amount each year that is pooled
to pay the costs for the few individuals who do have a claim.
Premiums are actuarially determined on a state or regional
basis. These rates vary by territory as a result of the differences
in the costs of claims in that area. A loss ratio is determined
by the actuary for a specific state or region. This is the total
premium divided by the indemnity payments and the cost of
providing the defense. Areas that are much more litigious
have higher premiums than areas with fewer claims.
There are two types of malpractice insurance. Claims made
policies are more prevalent than occurrence policies. Claims
377
made insurance logs the lawsuit into the year that the insur-
ance company first became aware of the incident or claim.
Occurrence policies log the claim into the year when the
injury occurred. An occurrence policy, under certain circum-
stances, can receive a claim many years after the event actu-
ally occurred. This makes accurate pricing of an occurrence
policy more difficult. When a physician who has a claims
made policy stops practicing, there is no need for current
coverage, but there is a need for tail coverage to cover any
claims that are made after the physician’s retirement date.
Most insurance companies offer free tail coverage if the physi-
cian has been insured with the company for 5 years.
REDUCING RISK
If there were fewer claims, there would be less money
spent on both the costs of indemnity payments and the costs
associated with the defense of claims, and the cost of liability
insurance would go down. There are many common factors
that help prevent claims from being filed or lead to a successful
defense of a case. The same factors can account for the need
to settle defensible claims. Liability insurance company’s
risk managers have learned that the best way to decrease the
frequency of claims is to have a very aggressive risk manage-
ment education process. The process includes face-to-face risk
management seminars, online risk management seminars, the
formation of appropriate forms for the use of their insured
physicians, and help with government mandated issues. This
follows the age old rule: An ounce of prevention is worth
a pound of cure. Of course, there is no substitute for sound
clinical practice.
If physicians understand why malpractice claims are filed
and how to avoid the common pitfalls leading to a claim, an
actual decrease in the cost of liability insurance can be
attained. Changing practice policies and procedures to reduce
the common factors involved in oral and maxillofacial surgery
claims can achieve positive results. The number one factor
causing claims against all physicians is the loss of rapport with
the patient. Most lawsuits occur because of a lack of or per-
ceived lack of communication or an attitude problem with the
physician. The office staff and the facility can also contribute
to a lawsuit. When a patient waits in the reception area for
more than an hour, the staff person mispronounces their
name, the trash can is overflowing in the operatory, there are
blood splatters on the light, and/or the physician seems rushed
and does not seem to listen to the patient, the circumstances
are optimal for a misunderstanding and subsequent anger over
a problem.
Anger is a real problem in all types of lawsuits. It is usually
at the base of lawsuits filed over automobile accidents, slip and
fall injuries, divorces, business deals gone bad, and medical
malpractice. People do not sue someone who they like and
trust. They sue someone when they are angry with that person
over a perceived injury or injustice.
Another issue we must deal with is the patient’s lack of
personal responsibility. The patient who has neglected a
problem for a period of time or refused to seek care when
378 SECTION III ■ Practice Management
referred (often multiple times for a potential problem) and
then suffers an infection or requires a more complex proce-
dure, will often blame a health care provider.
Communication and rapport are the main focus when a
patient develops a complication. Oral and maxillofacial sur-
geons will have patients who will have a paresthesia or anes-
thesia or develop an infection following treatment. Although
the surgeon is not liable for the inherent risks of treatment
that occur in the absence of negligence, the better informed
the patient is about the associated risks and possible complica-
tions of a planned procedure, the less the chances of a claim
arising if a complication does occur. Thorough consultation
discussions help patients to have reasonable expectations and
to understand that treatment outcomes are not guaranteed. A
detailed, well-documented informed consent discussion and
an appropriate, signed informed consent form along with com-
passionate care can help prevent a lawsuit from occurring.
Maintaining good rapport with patients and their families is
paramount in getting the patient through difficult times
following a complication.
■ PATIENT RAPPORT
Teaching rapport is difficult. Like good record keeping, the
importance of rapport with patients is undeniable. How this
is approached in training programs varies. Taking the time to
keep detailed records and deal with patient nuances is just not
attractive to health care providers. With the demands of
today’s practice environment of managed care, less face-to-
face patient time, and less reimbursement, we tend to move
on to the next patient as rapidly as possible. Oral and maxil-
lofacial surgeons choose the dental profession because of per-
sonality traits and professional desires that often do not make
for wonderful record keepers and good listeners. Dentists are
logical, scientific, skillful with their hands, and independent
workers. Oral and maxillofacial surgeons thrive on performing
surgery with precise skill. The unexciting chores of record
keeping and communicating with patients at the patient’s
educational level are difficult for the oral and maxillofacial
surgeon, yet it is these two factors that lead to most malprac-
tice claims.
As a result of the nature of oral and maxillofacial surgery
practice, there is little time spent with the patient. The patient
may be seen for a consultation, return for a surgical procedure,
and then be seen for a postoperative follow-up visit. A number
of patients are seen for their consultation and surgery on the
same day, frequently a busy day. Many patients are sedated or
asleep for their surgery. There is little time to develop
rapport.
Oral and maxillofacial surgeons must constantly train staff
and work on their own techniques to provide the appropriate
quality of care. Staff must understand that they have to
respond to patients in the same manner that they themselves
would like to be treated. Positive attitudes and treating patients
with respect will help prevent claims. Office systems that (1)
ensure that the oral and maxillofacial surgeon reads, initials,
and dates every pathology and laboratory report, (2) docu-
ment how and when recall patients are contacted, and (3)
eliminate billing errors and never refer to collection patients
who have encountered surgical complications can go far to
reducing claims.
The oral and maxillofacial surgeon should periodically go
and sit in the reception area for a period of time at the end of
a usual office workday. Is the carpet dirty, is the paint stained
or peeling, and are the magazines torn and a month old; what
image do patients perceive even before they enter the office?
Sit in the consultation room on the patient’s side. Have your
staff go through the routine they do with a patient. Is it how
you would want to be treated? When a patient is a no-show
for a surgical appointment, have your staff seat you for the
surgical procedure. Are the light handles clean? Is the light
shield spotted with blood? Is the surgical table clean and
covered appropriately? Pick up the instruments; are there par-
ticles of bone or tooth on the elevators or forceps? Are the
implant drills free of debris? These are all items that patients
see and do look for. If the quality of the environment is less
than acceptable, what will their conclusion be about the
quality of the surgery?
Patients have no way to evaluate the surgical skills of an
oral and maxillofacial surgeon. They can receive recommen-
dations and maybe talk to a previous patient, but they really
cannot evaluate the quality of a surgeon. So they evaluate the
things that mean something to them. They remember how
they were greeted by the receptionist over the telephone and
when they came into the office. Was the staff having a good
day or a bad day? Was the office clean? Did there seem to be
any problems with sterile technique? Did the staff or physician
seem rushed? Was the physician arrogant? When a complica-
tion does occur, these are the items that the patient will
remember and use to make their determination about the
cause of the problem.
There are any number of things that one can do to increase
rapport with patients. A number of simple communication
devices can easily be used. The first and most important is to
sit down and talk to the patient. Look the patient in the eye,
instead of looking at the chart or writing the entire time. Talk
to the patient on the same level, both physically (sit down
with the patient) and verbally (use simple language and avoid
the use of jargon or acronyms).
When a patient speaks to you, do not interrupt him or her.
Aside from steering the conversation away from something
you might need to know, it is just plain rude. Do not anticipate
what a patient is trying to say if he is not being clear. Ask him
to rephrase the question or repeat it back to him so that you
are both sure the right question is being answered.
One of the most crucial times for an oral and maxillofacial
surgeon to be available to a patient is when a complication or
untoward event occurs. Taking the time to sit down with the
patient to explain exactly what happened and what the future
course will be is critical. Give patients enough time to digest
the information, allow them to ask questions, and be available
for any additional questions they may have. An empathetic
and reassuring voice can go a long way to ensuring that the
 CHAPTER 22 • Risk Management in Oral and Maxillofacial Surgery
patient remains satisfied with his or her care. Giving a patient
the information they need does much to keep them from
becoming angry and turning to an attorney to obtain the
information that they should be obtaining from you.
■ INFORMED CONSENT
Patients have the right to determine their course of treatment,
including the choice of no treatment. Historically, informed
consent comes from the legal principles of battery. Battery, a
criminal act, is the intentional, unwanted touching of another
person without consent or permission. The Schloendorff v.
Society of New York Hospitals5 court decision in 1914 stated:
“Every human being of adult years and sound mind has a right
to determine what shall be done with his own body . . . and a
surgeon who operates without the patient’s consent commits
an assault for which he is liable in damages.”
When OMSNIC began as AAOMS Mutual Insurance
Company in 1988, one of the first projects was to educate the
policyholders about the importance of informed consent for
surgical procedures. Informed consent is a process, not just a
signed form. The process consists of educating the patient
about all of the informed consent elements to develop realistic
expectations before treatment. The process must be docu-
mented through progress notes and informed consent forms.
Procedure-specific consent forms were developed to aid the
oral and maxillofacial surgeon in documenting the informed
consent process.
Today the oral and maxillofacial surgeon is required to
disclose the material risks and benefits of a proposed procedure
that a reasonable person would want to understand to decide
whether or not to undergo a procedure. This includes any
alternatives that are available to the patient even if provided
by another health care professional. Disclosure of possible
complications of all of the alternative treatments is necessary
for a patient to make an informed choice of treatments. Docu-
mentation in the patient’s record of the informed consent
discussion is imperative in the prevention of malpractice
activity. There are specific elements of the informed consent
process that should be included in the informed consent form
or the documentation in the progress notes:
1. The specific medical necessity and diagnosis for the pro-
posed treatment.
2. The anticipated benefit of the proposed treatment.
3. The nature of the proposed treatment and alternatives.
What is involved with the proposed procedure?
4. The expected outcome of the proposed procedure and
the outcomes from alternative treatments.
5. The risks associated with no treatment.
6. No guaranteed outcomes or results.
7. Documentation of the patient’s opportunity to ask
questions.
8. Offering the patient the opportunity to seek a second
opinion before proceeding with treatment.
Patients want to understand the risks, benefits, and the
possible complications associated with treatment of a medical
or dental situation. Informed consent is the process that edu-
379
cates patients about these things so that they develop realistic
expectations before treatment. Patients with realistic expecta-
tions who are supported through a complication or prolonged
healing course are less likely to turn to an attorney to file a
lawsuit against their health care provider.
Educational materials are becoming more available. There
are many means of disseminating informed consent informa-
tion, including Internet-based patient interactive education,
where every keystroke is recorded and admissible; informed
consent DVDs; informed consent videos; and printed bro-
chures and pamphlets. All of these methods supplement the
informed consent discussion between the oral and maxillofa-
cial surgeon and the patient and/or guardian. If the use of
these materials is not documented in the patient’s chart, it
cannot be used in the defense of a claim. Oral and maxillofa-
cial surgeons can significantly help to decrease claim frequency
and increase the defensibility of claims by having appropriate
documentation. If it is written in the patient’s record, the
plaintiff’s attorney will be less likely to file a lawsuit, and if
the case is pursued, the jury will most often believe that the
record is accurate.
Consent is the legal obligation of the health care provider
that provides the service. Practices with multiple physicians
need to beware that the law, in most states, requires the oper-
ating surgeon to be the one who obtains the patient’s or
guardian’s consent. The educational process of obtaining
informed consent cannot be delegated to staff. The consent
process must be conducted on a level appropriate to the under-
standing of the patient and/or guardian. The use of lay lan-
guage and appropriate translation is essential to obtaining
informed consent. If translation is provided to the patient or
guardian, the translator needs to be identified in the patient’s
record. Many insurance companies provide translations of the
most common consent documents in Spanish.
Documentation of the informed consent discussion in the
patient’s progress notes is essential. A signed informed consent
document alone will not provide sufficient evidence of the
patient’s consent. If the plaintiff’s attorney does not file an
allegation of “lack of informed consent” as part of a lawsuit,
the attorney may be able to have the judge rule that the signed
informed consent document be withheld from the jury. The
patient’s progress notes cannot be withheld from the jury and
can clearly document the discussion with the patient and/or
guardian.
As a result of the educational process undertaken by
OMSNIC, the frequency of lack of informed consent claims has
dropped dramatically, resulting in a significant reduction in
the premiums for liability insurance paid by oral and maxillo-
facial surgeons. That success is remarkable and worthwhile,
but the process continues.
■ DOCUMENTATION AND
LEGIBLE RECORDS
In a typical oral and maxillofacial surgeon’s day, the need to
move on to the next waiting patient leaves little time to
record legible and detailed chart notes or dictate a compre-
380 SECTION III ■ Practice Management
hensive note. Developing practice patterns that allow for
adequate time for documentation can be the factor that pre-
vents a plaintiff’s attorney from accepting a dissatisfied patient
as a client.
Approximately one-third of claims are deemed to be inde-
fensible by claims handlers and defense attorneys as a result
of a lack of appropriate chart notes. Malpractice insurance
carriers are forced to settle far too many defensible claims
because of poor records. Most training programs teach resi-
dents to document hospital and clinic patient records in a
SOAP format. Unfortunately, once training is completed and
surgeons are in their own practice, this habit seems to disap-
pear far too frequently. There is no better manner to docu-
ment every patient visit than the SOAP format.
State dental and medical practice acts specify record
keeping standards. The basic concept is that any other similar
physician or dentist should be able to read the patient’s records
and describe the following:
1. The patient’s complaints and symptoms
2. The findings and results of the patient’s examination
3. The diagnostic tests and their results
4. The discussion about the diagnosis and treatment
options given to the patient
5. The risks, benefits, and possible complications and the
options and likely consequences of no treatment
This applies to every patient visit, from the initial consulta-
tion to the last postoperative visit. If the oral and maxillofacial
surgeon’s records do not meet these requirements, the records
are not up to the legal standards. Brief and inadequately
recorded chart notes allows the plaintiff’s attorney to “paint”
a picture of the patient’s care that implies substandard treat-
ment, equivalent to the chart notes.
SOAP charting helps prevent claims when used for all
patient visits.
The subjective patient’s complaints and concerns are listed.
Listening to the patient, making eye contact, and then noting
the patient’s statements helps establish rapport. Noting these
comments in the record will allow a picture of the ongoing
care to be “seen” far more clearly.
The objective findings are documented. These should be
both positive and negative findings. The lack of swelling,
redness, or drainage can be an important factor in defense of
a claim. The presence of signs with objective descriptions (i.e.,
size, length, induration, color, etc.) limits the latitude afforded
the plaintiff’s attorney in his or her descriptions of the alleged
injury.
The oral and maxillofacial surgeon’s assessment of the
situation is documented. This is the one most common factor
left missing from charts. Understanding the thought process
that led to the decision making is very important. Trying to
remember the patient and how decisions were made after
months or years is often difficult. Jury interviews show that
jurors believe that if it is written down in the record, it is likely
to be the truth. A patient can suffer a less than ideal result.
This may lead to ongoing treatment that causes additional
problems. When the patient’s chart is devoid of any documen-
tation about how the oral and maxillofacial surgeon made the
ongoing treatment decisions for the patient, it allows the
plaintiff’s attorney to use his or her experts to fill in the blanks
to describe a negligent pattern of behavior. The factors that
led to the decisions are then left to debate in the courtroom
or settlement discussions.
The plan for the patient’s care is written down. Not only
will the surgeon who treated the patient know what was
planned, but a partner or subsequent treating surgeon will also
know the plan. This again limits the “playing field” for the
plaintiff’s attorney.
Frequently the patient’s record is short and cryptic, with
little or no clinical information. This is especially true for
cases that seem to be “simple” or “routine.” In training, the
oral and maxillofacial surgery resident was taught to document
patients’ charts so that if a different resident saw the patient
at subsequent visits, he or she would know the patient’s diag-
nosis and ongoing treatment plan. Residents learn how to
dictate a detailed operative report for all cases performed in
the main hospital operating room. Any other oral and maxil-
lofacial surgeon could read the dictated report and discuss
unusual anatomy, how the surgery was performed, any prob-
lems encountered, and complications that occurred.
An orthognathic operative report would precisely describe
where incisions were made, how the flaps were reflected,
where bone was cut, the amount of the movements in all
directions, what type of fixation was used, how the flaps were
reapproximated, and the type of sutures that were used. An
implant and bone grafting operative report would describe the
incisions, the bone defects, density of the bone encountered,
how the preparations for implant placement or bone graft
insertion were done, what implants were placed, any bone
grafting or soft tissue grafting performed, donor sites, growth
factor use, location and type of membranes placement, and
how the tissues were closed. Even extraction cases had detailed
operative reports.
Legally, we have the same requirements for our office notes.
Another oral and maxillofacial surgeon should be able to read
our office notes and describe how the patient’s surgery was
accomplished. At follow-up visits, the patient’s condition
should be understood. This includes extractions, removal of
impacted teeth, placement of dental implants, bone and/or
soft tissue grafting procedures, cosmetic surgeries, in essence,
every surgery or procedure done in the oral and maxillofacial
surgeon’s offices.
When a claim occurs and the record is lacking clinical
details, defensible claims are frequently lost. It becomes a liars’
contest in the courtroom. Add a believable patient and an
arrogant physician to the mix, and the defensibility of a lawsuit
is even more difficult. A little effort in documenting the
patient’s condition and the thought process that led to the
decisions can easily make the difference between a costly set-
tlement and an appropriate dismissal.
There are many ways to make legible, descriptive records
easier to accomplish. Many suppliers make appropriately sized
(8½ × 11 inch) patient charts and forms. Certainly, medical
 CHAPTER 22 • Risk Management in Oral and Maxillofacial Surgery
and dental practice is past the time of the 5 × 8-inch card
patient record. Many liability insurance companies offer
various forms, including informed consent documents, health
history forms, anesthesia records, discharge criteria, prescrip-
tion logs, etc. for their insured physicians to use. Some offices
are now “paperless,” with the entire patient record kept on
the computer hard drive. No matter how records are kept,
legal requirements must be met. Patient records must be kept
for the time period required by state law.
State law requires that the patient’s record be legible. Dic-
tated and transcribed records are obviously the most legible
and the best manner in which patient records can be kept.
Voice-activated computer transcription systems for medical
and dental records are becoming commonplace. Many physi-
cians still use handwritten charts. During discovery, at the
beginning of the claims handling process, the insurance
company will usually ask an insured with a difficult to read
chart to transcribe the patient’s record. Frequently, the insured
cannot read his or her handwriting and abbreviations. The
oral and maxillofacial surgeon can develop a list of abbrevia-
tions that are used in patient’s charts. The list should contain
all abbreviations used in the office and should be forwarded
to the insurance carrier with subpoenaed records.
All chart entries must be dated and initialed. Some prac-
tices have staff write everything in the patient’s chart. Other
practices allow staff to write in the patient’s record along with
notes written by the physician. Either way, staff entries are
more problematic. The staff person may not completely under-
stand the patient’s or the physician’s comments. The staff
person may write what they thought the patient meant or
what the physician meant and accidentally get the informa-
tion wrong. The staff entry may be not as detailed as desired
in an effort to save time.
Every chart entry must be initialed by the person making
the entry. All staff entries must be read and countersigned by
the oral and maxillofacial surgeon. Any corrections or addi-
tions to the note must be made by the physician in a following
note properly dated and initialed. A list of all employees’ ini-
tials should be kept in the office and updated quarterly. When
an insured cannot identify who wrote in the patient’s chart,
defense is more difficult. The plaintiff’s attorney will embar-
rass the oral and maxillofacial surgeon in questioning about
the unidentified person who was allowed to write in the
patient’s record.
It is best that the physician make all entries in the patient’s
record regarding the clinical care and discussions with other
health care providers. Front office and clinical staff can make
notations about receipt of the items of importance to the
patient’s care (e.g., pathology reports, referring physician’s
letters, implant surgical guides, radiographs, scans, models,
etc.) and appointment issues. A clear contemporaneous rep-
resentation of the activity in the office involving patient care
will not only aid in the defense of a claim, but may make a
plaintiff’s attorney shy away from taking the case.
Every page must contain the patient’s name. All entries
must be in chronologic order. Additions and clarifications can
381
be added to a record, but the addition must be a new entry,
dated when added, and labeled as an addition for the date of
the clarification. Never try to “squeeze” additional notes next
to an already completed note or write in the margin of the
form.
SOAP format notes for all patient visits are the best way
to maintain appropriate patient records. Plaintiff’s attorneys
love to obtain the patient’s physician’s or a subsequent treat-
er’s dictated and transcribed chart notes to compare with the
oral and maxillofacial surgeon’s scribbled, cryptic chart notes.
When enlarged to 2 × 3 feet in size and presented to the jury
on easels, the plaintiff’s attorney will use the comparison of
the chart notes to make the oral and maxillofacial surgeon
seem far less attentive and caring than the patient’s physician
or the subsequent treater.
Plaintiff’s attorneys are masters at dissecting patient records
and using every hole or void to support their case to prove
malpractice. They will fill every blank spot and every less than
complete entry with their own description of the situation
that shows carelessness and negligence. Given a complete,
legible record that documents the patient’s care, frequently
the plaintiff’s attorney will not take a potential case because
of the work required to prove the negligence. Remember that
the plaintiff’s attorney’s possible paycheck is 30% to 40% of
the settlement or verdict. This amount is decreased by the
legal fees that the attorney has expended (unless they are
charged to the plaintiff). But if the plaintiff’s attorney “loses,”
there is no paycheck, and the attorney is out all of the expenses.
Plaintiff’s attorneys would prefer to take the easier cases, with
poor records, where the possibility of “winning” is high and
leave behind the more difficult cases when the records are
documented properly.
Record alterations are illegal. In some states, altering a
patient’s record is a felony. An alteration of a patient’s record
is a premeditated act. A claim where there is even the slightest
possibility of an altered patient chart cannot go to court. The
plaintiff will win the case, and the physician may be subject
to criminal penalties. The insurance company will have to
settle the claim, frequently for much more than the claim is
worth, to protect the oral and maxillofacial surgeon who has
committed the illegal act. The physician could be liable for
criminal charges, in addition to the civil malpractice case.
The defense of criminal charges is not covered under malprac-
tice liability insurance. If the alteration was discovered by the
plaintiff’s attorney, punitive damages could also be claimed.
Punitive damages are not covered by most liability carriers.
Plaintiff’s attorneys are very good at finding even minor addi-
tions added to patient records at a later date. Handwriting
experts can testify to the likelihood that an entry is an addi-
tion as a result of the difference in ink, spacing, slant, etc.
A recurring example of this involves the patient who has
a complication following treatment. The patient enlists an
attorney to make a claim against the oral and maxillofacial
surgeon. The surgeon’s records are subpoenaed. Before copying
the records, the surgeon reviews the patient’s chart and notices
that the consultation note does not mention the specific com-
382 SECTION III ■ Practice Management
plication that the patient experienced. The surgeon “remem-
bers” that this complication was discussed and adds a notation
of it. When the copied records are received, the claims handler
notices that the notations in the chart are made on every
other line with regularity. But where there should be a blank
line, there is a notation about the exact complication experi-
enced by the patient. This is very incriminating. Can anyone
prove when the notation was placed in the chart? Even discus-
sion about the timing of this note will cost the surgeon credi-
bility. Resist the temptation to jeopardize the defense of a
claim. Defense attorneys are specialists in working through
and presenting the missing items in a patient’s record. Let the
defense attorney tackle the situation, rather than make a
claim indefensible.
Diagnostic tests are conducted in oral and maxillofacial
surgeons’ offices, patients are sent to other facilities for diag-
nostic tests and/or consultation, and pathology specimens are
sent for diagnosis. The reports of all these items must be noted
by the surgeon and kept in the patient’s chart.
All radiographs obtained in the oral and maxillofacial sur-
geon’s facility must be dated, read, and noted in the patient’s
record. These include periapical, occlusal, panoramic, cepha-
lometric, skull, sinus, cone beam computerized tomography,
etc. Maxillofacial computerized tomographic units are becom-
ing more commonplace in the surgeon’s office. These scans
may reveal areas of the head and neck that may be outside of
the oral and maxillofacial surgeon’s training. Reading these
scans may present an obstacle for the surgeon. The surgeon
has the same liability for a pathologic condition that is evident
on any film taken in the office, be it a panoramic film or a
computerized tomographic scan. If the oral and maxillofacial
surgeon is not comfortable reading the radiographs taken in
the office, an outside service should be contracted to review
the radiographs and provide a written report. A patient can
not sign a waiver relieving the oral and maxillofacial surgeon
of liability for any pathologic condition that was evident on
a radiograph or scan but not recognized by the surgeon.
Once a specimen has been obtained from a patient, there
is the responsibility to make sure that the laboratory receives
it and that the result is received back in the office in an
appropriate time period. All pathology and laboratory speci-
mens must be logged out and the reports logged in. These
reports must be reviewed, initialed, and dated by the oral and
maxillofacial surgeon. A good practice is for the surgeon to
also make an entry in the patient’s progress notes regarding
the diagnosis or findings. The chart must also have a notation
of the patient receiving the information about the diagnostic
test.
There must be office practices in place that absolutely
prevent possible catastrophic events from occurring, such as a
biopsy specimen being lost or a report from the laboratory not
being received. Pathology reports can be lost in the mail or
“lost” electronically as a facsimile transmission. If the report
is not available at the patient’s postoperative visit, neither the
patient nor the surgeon knows the result. If the chart is filed
after the patient’s postoperative visit, a disaster can occur.
Often patients will assume that everything is okay when they
do not receive a call from the office.
If a patient fails their postoperative appointment and the
pathology report is filed in the chart without discussing the
diagnosis with the patient, a disaster can occur. Front office
staff filing the patient records remaining on the reception
desk at the end of a busy day in the office could result in a
pathology report being placed in a clinical chart without
having been reviewed. Office practices and fail-safe proce-
dures must be in place to prevent laboratory or pathology
reports from slipping through a crack in the system. It is very
difficult to defend the plaintiff’s attorney’s question: “Doctor,
if you thought it important enough to have a biopsy speci-
men or laboratory specimen taken, wasn’t it important
enough to obtain the result and notify the patient?” Failure
to diagnose cancer lawsuits are often very ugly, painful, and
costly cases for both the patient and oral and maxillofacial
surgeon.
Diagnostic testing for hospitalized patients is frequently
ordered according to standardized formats. It is important for
the surgeon to know the results of these tests. It is easy to
assume that the result is normal if the surgeon is not contacted
with an abnormal result. Currently, many oral surgical proce-
dures are performed as outpatient surgeries, and it is possible
for the results of certain preoperative testing not to be posted
to the patient’s hospital record until after the patient has been
discharged. The surgeon can assume that the anesthesiologist
or preoperative nurse has reviewed the test results, but the oral
and maxillofacial surgeon’s office protocols must make sure
that all test results are received in the office. These reports
must be reviewed by the surgeon, initialed, and dated before
being filed in the patient’s office record, even if they are
received after the patient’s surgery. The surgeon will be held
liable for any abnormal test result that has been ordered on
his or her patient.
State dental and medical practice acts require that all pre-
scriptions be recorded in the patient’s chart in the legal
manner. That requires the full name of the drug, the strength,
the amount, how the drug is to be taken, and any refills.
Common serious side effects discussed with the patient should
also be recorded on the progress notes. It is best to have a
medication flow sheet in the patient’s chart where all prescrip-
tions and sample medications are logged “in the legal manner.”
The recording of prescriptions can be accomplished in a
number of ways to satisfy the state requirements. Many office
computer systems print prescriptions with duplicate copies for
the patient’s chart, or staff can record the prescription infor-
mation on the progress notes. The best way to keep prescrip-
tion information in patients’ charts is a dedicated prescription
log. Having every prescription listed in one location allows
the surgeon, partner, or staff to have the information about
all of the drugs that have been prescribed for the patient avail-
able with little effort. This can help prevent cases involving
drug addiction and the overprescribing of narcotic medica-
tions. It can also help prevent a DPR complaint against the
surgeon.
 CHAPTER 22 • Risk Management in Oral and Maxillofacial Surgery
It would seem that properly documenting a patient’s record
is a laborious, time-consuming effort. Yet with the proper
forms and only a few minutes of time, the quality of every
patient’s chart notes could improve tremendously. When
involved in a lawsuit that is difficult to defend because of the
lack of legible, detailed chart notes, the surgeon will usually
change his or her attitude toward the importance of good
documentation. Risk managers try to convince their insured
physicians that a few minutes spent documenting patients’
charts on a daily basis is a tremendous investment compared
with the hours that are required to be spent away from family
and out of practice once involved in a lawsuit.
■ DISCHARGING PATIENTS FROM
YOUR PRACTICE
All health care providers have discretion in choosing the
patients they accept for treatment, with certain limitations.
Physicians do not have a duty to accept all patients for care,
though one must be careful in certain situations. For instance,
the Americans with Disabilities Act prohibits withholding
care “due to discrimination” for individuals covered by the act,
and managed care agreements may obligate a provider to
provide treatment for all patients covered under the contract.
Hospital emergency room commitments or the “on-call”
schedule may limit a provider’s ability to decline to care for a
patient.
Establishing a physician-patient relationship obligates the
physician to the duty of continuing care for the patient until
one of several situations exist: (1) the patient no longer
requires care, (2) the health care provider and the patient
mutually agree that the care should be continued elsewhere,
or (3) the relationship is terminated by the physician or the
patient. Providing ongoing care to patients that are uncoop-
erative, refuse to follow instructions, and are generally non-
compliant is a potential liability that the oral and maxillofacial
surgeon does not have to accept. This type of patient can be
discharged from care following the legal requirements of the
state law. The reason for withdrawing from the patient’s care
does not need to be disclosed to the patient unless required
by state law. Discussing the situation with the liability insur-
ance company’s claims handler or a local attorney is recom-
mended so that all of the state requirements are met.
To discharge a patient from care, the surgeon must be
certain that the patient’s condition is stable. Once that has
been established, the surgeon must send the patient a letter
stating that the surgeon is withdrawing from the patient’s care.
The letter must give the patient a means to locate a new pro-
vider. This is easily done by providing the name and tele-
phone number of the local dental society. The letter must
include the offer to provide continuing care or emergent care
for the period of time stated in the state law. It is also a good
idea to offer a copy of the patient’s records to the subsequent
treater with an appropriately signed release. This letter must
be sent by certified mail, return receipt requested, and by
regular mail. The letter should be marked at the top—sent by
certified mail, return receipt requested, and regular mail.
383
Managed care contracts should be reviewed for the terms
under which a patient may be discharged from care. The
problems caused by the patient leading to the decision to
withdraw from care must be thoroughly documented in the
patient’s record. Abandonment is an uncommon claim, and
discharging patients from care is a serious decision. Seek
counsel from the insurance company’s claims staff for situa-
tions that could possibly be termed abandonment.
■ AMERICANS WITH
DISABILITIES ACT
In 1990, the United States Congress passed the Americans
with Disabilities Act1 (ADA). This is one of the nation’s most
comprehensive civil rights statutes. The intention of this law
was to help prevent discrimination, make “auxiliary aids and
services” available for effective communication, and make
health care facilities physically accessible and usable by
patients with disabilities. There are significant implications
for even the smallest oral and maxillofacial surgery practice.
Covered persons include those that are positive for human
immunodeficiency virus (HIV) infection and acquired immu-
nodeficiency syndrome (AIDS), diabetes, hypertension,
obesity, short stature, chronic fatigue syndrome, alcoholism,
migraine headache, post myocardial infarction, hearing loss,
and sensitivity to smoke, and many more “disabilities.” The
definition of disability is very broad.
The ADA prohibits health care providers from using the
“disability” of the covered individuals as a means to refuse
needed care. One of the biggest concerns faced by oral and
maxillofacial surgeons is the direct questioning on health
history forms of the HIV status of a prospective patient. Some
state laws prohibit directly asking this question or any ques-
tion that might lead patients to believe that their civil rights
have been violated. Some states do not prohibit the question,
and some local jurisdictions allow the question, whereas the
rest of the state does not. It is therefore important to know
the laws of your city and state. Questions on health history
forms asking about treatment for mental illness or alcoholism
are other examples of “disabilities” that are covered by the
ADA. Asking the patient if there are any health issues that
they wish to discuss in private may be more comfortable for
the patient. Certain information may be important in the
health care of a patient; the manner in which the information
is obtained is the potential liability. Questions about having
a compromised immune system would seem to be acceptable.
Once a physician-patient relationship is established and the
patient has been accepted for care, direct questions regarding
HIV status and treatment for mental illness are not considered
discriminatory because the answers will not prevent patient
care.
The ADA imposes obligations upon health care providers
to provide “auxiliary aids and services” so that disabled
persons can benefit from the services provided in the office.
This includes a range of things from simple assistance with
movement from a wheelchair to an examination table to
providing “qualified” interpreters for deaf patients. If a
384 SECTION III ■ Practice Management
hearing impaired patient asks for a qualified interpreter, the
oral and maxillofacial surgery practice must provide the inter-
preter as an expense to the practice and cannot seek reim-
bursement from the patient. In some cases, a family member
or friend may qualify to be the interpreter. Exercise caution
in using family members as a qualified interpreter. Emotional
or personal involvement or the patient’s inability to share
information with others may render a family member unable
to interpret “effectively, accurately, and impartially.” It is
recommended that the interpreter sign a “translator’s state-
ment.” Refusal to provide an interpreter or an attempt to
transfer the expense to the patient will likely result in a
claim of discrimination.
■ HIPAA PRIVACY AND SECURITY
The Health Insurance Portability and Accountability Act of
1996 (HIPAA),2 also known as the Kennedy-Kassebaum Act,
has significant implications to the oral and maxillofacial
surgery practice. The public has grown increasingly concerned
about disclosures of confidential health information. A portion
of HIPAA was enacted to protect confidential health
information.
Health care practices are permitted by the privacy portions
of the law to use protected health care information (PHI) for
purposes of “treatment, payment, and health care operations.”
A “notice of privacy practices” signed by the patient acknowl-
edges that the practice may use the patient’s information to
conduct regular business, as noted earlier. Any additional dis-
closures of the protected information require separate consent.
To comply with HIPAA regulations, the oral and maxillofa-
cial surgery practice must:
1. Keep a notice of privacy practices posted in a prominent
place in the office and on their website, if applicable.
2. Have each patient sign a notice of privacy practices that
acknowledges the practice’s ability to use the patient’s
health information to conduct normal business
practices.
3. Ensure that all business associates who have access to
PHI sign a business associate agreement acknowledging
that they cannot use or disclose the information in any
manner that would not be permissible for you or your
practice under the HIPAA privacy regulations.
4. Employ HIPAA-approved authorizations for release of
PHI.
5. Educate all staff about privacy and confidentiality rules
and regulations.
HIPAA security regulations cover PHI and information
that is maintained or transmitted in an electronic form (EPHI).
The practice must protect the “confidentiality, integrity, and
availability” of the EPHI that it creates, stores, maintains,
and/or transmits. This means that the privacy is ensured, that
the information is not altered or destroyed, and that it is
accessible and usable by authorized persons.
The HIPAA security regulations also mandate that all
EPHI must be protected by recipients of the information. An
addendum was added to the business associate agreement to
ensure that business associates who receive PHI electronically
(such as billing companies, etc.) agree to keep the information
confidential. They are also responsible for ensuring that any
“downstream” recipients of the PHI will also agree to keep the
information confidential.
■ RELEASE OF RECORDS
A specific court order may command release of copies of a
patient’s record without a signed release from the patient. This
order is labeled a subpoena duces tecum and requires that the
original records be brought for copying, or that exact copies
of the records be delivered to the court or the attorney who
obtained the court order. Certain states require that the physi-
cian notify the patient of the subpoena to allow the patient
to object to the release of their chart and/or radiographs. It is
appropriate to notify the patient of the subpoena if the patient
may be unaware of the court order.
A patient may sign a release ordering that copies of their
records be delivered to anyone that they designate. Such
releases must be HIPAA compliant; if they are not, a HIPAA
compliant form must be substituted and properly signed. This
includes an attorney representing the patient in a motor
vehicle accident, a slip-and-fall injury, or an action against
an insurance company. Reasonable copying charges may be
assessed and received before release of the patient’s records.
Records must be released, even if the patient has not paid
for the services rendered by the oral and maxillofacial
surgeon.
A patient is entitled to a copy of his or her own chart.
Patients need to sign a release when requesting that a copy of
their records be forwarded to any other health care provider
or themselves. Remember that dissatisfied patients may direct
that another health care provider receive a copy of their
records and then obtain a copy from that health care provider.
Patients find ways to obtain copies of their records without
the oral and maxillofacial surgeon suspecting they are maneu-
vering to file a lawsuit. Although one should never alter a
patient’s chart, this is one more reason not to. Patients may
obtain copies of their charts in a roundabout manner, without
your knowledge.
■ LIMITED ENGLISH PROFICIENCY
Title VI of the Civil Rights Act of 19643 prohibits discrimina-
tion on the basis of race, color, or national origin by an entity
that receives federal financial assistance. It has been deter-
mined that individuals with limited English proficiency (LEP)
are also protected under this law. This means that the oral
and maxillofacial surgeon is required to ensure that LEP
patients can “meaningfully” access programs and services.
This applies to patients receiving Medicaid and Medicare
assistance.
The requirements are based upon the number of LEP
patients treated by the practice:
1. If the LEP group of patients is fewer than 100 persons,
the LEP patients must be provided written notice in the
primary language of the LEP language group of their
 CHAPTER 22 • Risk Management in Oral and Maxillofacial Surgery
right to receive competent oral translation of written
materials.
2. If the LEP group of patients is 5% of the practice or 1000
patients, whichever is less, the LEP patients must be
provided translations for vital documents for patient
interactions.
3. If the LEP group of patients is 10% of the practice or
3000 patients, whichever is less, the LEP patients must
be provided translated written materials to include vital
documents in the primary language of the LEP language
group.
If a practice falls under these guidelines, rules apply to serve
the LEP patient population. A comprehensive written lan-
guage assistance program is required. Employing a consultant
is often the best way to address these requirements. It is illegal
for a health care practice to encourage or require minority
language patients to provide their own interpreters. The prac-
tice must maintain bilingual employees or interpreters. The
patient may be reluctant to disclose certain important medical
information or intimate details of a personal nature to a family
member or child acting as an interpreter. Additionally, a
family member or a friend has no obligation to maintain con-
fidentiality. Violations of these statutes can lead to a claim.
■ EMTALA
The Emergency Medical Treatment and Active Labor Act4
(EMTALA) was enacted to prevent hospitals from withhold-
ing emergent or urgent treatment to indigent patients or from
transferring indigent patients to other health care facilities
before such patients’ conditions are stabilized. This applies to
the oral and maxillofacial surgeon who is “on-call” for the
emergency room. EMTALA does not apply to patients who
are seen at the emergency room and then sent to an oral and
maxillofacial surgeon’s office. The law requires that a patient
who has not been stabilized may not be sent out of the facility
before being stabilized. A patient who can leave the hospital
to go to an oral and maxillofacial surgeon’s office under his or
her own power is stable, and the law does not apply.
■ THE FUTURE
TELEMEDICINE
With ever-increasing technology and ability to see informa-
tion remotely, the possibilities for medical practices are bound-
less. However, before one considers doing consultations
online, there are issues to consider. One main issue is jurisdic-
tional rules regarding where patients can be seen. In some
states, it is a crime to treat a patient from another state. This
can be extremely problematic for practitioners who read
patient films from other states. In some medical specialties,
some practitioners are advertising to patients via websites that
encourage consultations online. Medical advice is dispensed
via the website, which, in some jurisdictions, could constitute
a physician-patient relationship. If that relationship involves
parties from two different states, it could run afoul of state
laws.
385
Some uses of technology can certainly be used to the phy-
sician’s advantage, such as reviewing his or her own patient’s
films remotely. Physicians need to be well aware of state and
local rules and regulations before entering into situations
where online “work” is considered.
■ ONLINE COMMUNICATION
Online communication with patients can be a boon to the
busy oral and maxillofacial surgeon. Playing games of phone
tag with patients who have questions can waste an inordinate
amount of time. Being able to communicate with them at a
time that is convenient can make the communication process
so much more effective. There are several policies to put in
place before beginning such communications. First and fore-
most, it is very important to outline the boundaries of online
communications. They should not be used for urgent matters.
Whereas this is obvious to the surgeons and office staff, all
patients need to be aware of it. An office should consider
obtaining a patient’s formal consent before communicating
with him or her by e-mail.
Prescribed turnaround times should be established. If the
physician is not available to check the e-mail, someone from
the office must do it so that the e-mails do not sit unanswered.
The office could also set up an automatic reply to patient e-
mails to acknowledge their receipt and give a time frame in
which they will be answered. Discreet subject headers should
be used for confidentiality purposes. When composing e-mail
responses to patients, assume that they will not be seen only
by the patient, and choose your words accordingly.
It is important to make copies of all outgoing and incoming
e-mails. Patients are surely making copies of the e-mails you
send to them, and you need to document their questions and
your responses in their clinical chart. It is a good idea to note
the patient’s name on all printed e-mails. Sometimes only the
e-mail address shows up on the e-mail, and you are not likely
to remember who “tennis.player75@yahoo.com” is. All copies
of printed e-mails should be filed in the patient’s chart.
Adherence to the HIPAA confidentiality and security
requirements will cover the usual computer-related sugges-
tions about e-mails, but they are worth repeating. Ensure that
encryption is used for all messages. Password-protected screen
savers should be used for all desktop computers in the physi-
cian’s office and at the physician’s home, if a computer is used
there to answer patient e-mails.
■ SUMMARY
Risk management in oral and maxillofacial surgery is not just
a bunch of forms. It is effective communication with patients
and co-treaters. It is proper documentation of patient care so
that any physician can look at the chart and determine what
has been done, why, and what needs to be done. It is having
appropriate office policies to ensure that the excellent care
being rendered is not compromised by process issues. All of
these things contribute to a good patient experience. Good
patient experiences build trust. When trust is there, complica-
tions that occur in the absence of negligence will be seen as
386 SECTION III ■ Practice Management

such. All of this leads to better care, better patient experi- 2. Health Insurance Portability and Accountability Act, 42 US
ences, and more satisfied physicians. This is a true win-win Code, section 1395 et Seq, 1996.
3. Title VI of the Civil Rights Act of 1964, 42, US Code, section
situation.
2000d et seq.
4. Emergency Medical Treatment and Active Labor Act, 42 US
REFERENCES
Code 1395dd et Seq.
1. Americans with Disabilities Act of 1990, 42 US Code, section 5. The Advisor, AAOMS Risk Manage J 2(3):7-9, 1987.
12101.

PHARMACOLOGY FOR IMPLANT DENTISTRY
James L. Rutkowski • Joseph M. Thomas • David A. Johnson
The primary goal of implant dentistry is to restore patients to
oral health and full dental function. Often the practitioner
has a patient that may have a suboptimal healing outcome.
Drugs that the practitioner may use during implant or grafting
surgeries can have an impact on the success of these proce-
dures. Likewise, medications that the patient may be taking
can also have a positive or negative effect on treatments.
Patients desire success, and the clinician can optimize treat-
ments by using pharmacologic adjuncts to increase the prob-
ability of attaining that goal. Pharmacologic treatments can
be systemic or localized and may be of benefit during the
perioperative phase or later. The guiding principles when
choosing a pharmacologic adjunct should always aspire to
meet the following criteria:
1. There should be a justifiable indication for each medica-
tion that is used.
2. Each medication should be used at the lowest effective
dose and for the shortest possible period of time.
3. Whenever possible, the selection of a medication
regimen should be based on evidence obtained from
controlled clinical trials.
4. The clinician must understand that dose (or concentra-
tion), route of administration, dosing frequency, and
duration are critical pharmacokinetic factors that deter-
mine if a treatment is beneficial or detrimental to the
success of an implant or bone grafting procedure.
All pharmacologic agents should have their use based upon
scientific principles and a proven record of increasing the rates
of short- and long-term success.
This chapter will review the following:
1. The rationale supporting the addition of antibiotics to
bone grafting materials
2. The proper prescribing of prophylactic antibiotics in
relation to implant placement and bone grafting
3. Pharmacologic management of periimplantitis (PI)
4. The effect of bisphosphonates (BPs) on dental implants,
with guiding science-based principles for managing the
dental implant patient receiving these drugs
S E C T I O N IV • Implant Surgery
CHAPTER 23
5. The effect of mineral, hormonal, and vitamin supple-
ments on dental implants
6. The effects that commonly used nonsteroidal
antiinflammatory drugs have on bone healing and
development
7. The effect bioactive fatty acids have on bone
development
Each of these issues has a varying impact on treatment
success and should be considered as warranted by the clinical
situation.
■ ANTIBIOTIC PROPHYLAXIS IN
IMPLANT DENTISTRY
Antibiotic (antimicrobial) surgical prophylaxis is often mis-
understood and used incorrectly. The true definition refers to
the prevention of infectious complications following surgical
procedures. The shortest possible duration of antibiotic admin-
istration should be used to minimize the risk of serious adverse
effects, the development of antibiotic resistance, or the pro-
liferation of nonsusceptible bacteria. The goal of surgical anti-
microbial prophylaxis is to achieve sufficient antibiotic tissue
concentration before possible contamination of the relevant
tissues of the oral cavity and to ensure adequate levels through-
out the operative procedure to prevent subsequent bacterial
growth. This involves high blood and tissue antibiotic con-
centrations at the time of surgery, when contamination is
possible, followed by a reduction to no antibiotic within 24
hours. Regrettably, antibiotic coverage is often begun 1 day
preoperatively and extended for several days postoperatively.
This practice has led to unnecessary antibiotic use. The prob-
ability of negative side effects and the development of resis-
tant bacteria increase with longer durations of antibiotic
administration.1
Controversy surrounds the need for presurgical antibiotic
prophylaxis with dental implant surgical procedures. It is
accepted that antibiotic prophylaxis is recommended for those
patients at high risk for endocarditis, as recommended by the
American Heart Association (AHA) guidelines, or patients
387
388 SECTION IV ■ Implant Surgery
with one or more of the following: immune deficiencies, meta-
bolic diseases, history of irradiation in the head and neck area,
and when an extensive or prolonged surgery is anticipated.
The overriding question is does surgical antibiotic prophylaxis
affect dental implant and/or bone grafting success? Osseous
integration and/or bone graft success can be jeopardized by the
presence of bacteria in the tissues and the concomitant inflam-
matory reactions.2
Laskin et al. (2000)3 examined 2973 implants at each stage
of implant placement and restoration and correlated the find-
ings with implant failure or loss of osseous integration, up to
36 months after placement. The results demonstrated a sig-
nificantly higher survival rate at each stage of treatment in
patients who had received preoperative prophylactic antibiot-
ics. A previous study examined implant success only to the
time of uncovering and found that significantly fewer failures
occurred when preoperative antibiotics were used.4 These
findings were contrary to those of Morris et al. (2004) who
examined the effect of prophylactic antibiotic coverage with
1500 implants for up to 5 years and found that the use of
antibiotics provided no beneficial effects. None of these studies
were randomized controlled clinical trials (RCTs), but rather
retrospective analyses. The Cochran Database System Review
of 2003 found that no RCTs had been reported and concluded
that there is no appropriate scientific evidence to recommend
or discourage the use of prophylactic systemic antibiotics to
prevent complications and failures of dental implants in
healthy patients.5
The question of single-dose preoperative antibiotic cover-
age versus long-term postoperative coverage has been
addressed. Kahani et al. (2005)6 conducted a retrospective
study comparing implant survival rates following a single-dose
preoperative antibiotic regimen with that of a 7-day postop-
erative antibiotic protocol. They found no significant differ-
ences in complication incidence and implant survival rates
between the two groups. Therefore, it was concluded that a
single-dose prophylactic antibiotic regimen with routine
implant procedures would be best.6 A prospective study was
performed by Binahmed et al.7 in 2005 comparing the efficacy
of a prophylactic single-dose antibiotic and a 7-day postopera-
tive antibiotic regimen. No advantage or benefit was found
with long-term antibiotic coverage over single-dose preopera-
tive antibiotic regimens.7
When considering antibiotic prophylaxis for bone grafting
procedures, a prospective placebo-controlled double-blind
clinical trial revealed that there was a statistically significant
increased risk of having an infectious complication without
antibiotic prophylaxis. Phenethicillin 2 g was administered 1
hour preoperatively to the treatment group.7 Another pro-
spective randomized study involving 124 patients compared
the effects of a single 600-mg dose of clindamycin versus
clindamycin 600 mg preoperatively and 300 mg every 6 hours
for 24 hours postoperatively. It was concluded that there was
no statistically significant difference between the single-dose
and the 24-hour regimen in connection with postoperative
infection in patients undergoing bone grafting procedures.9
BOX 23-1
Preoperative antibiotic prophylaxis:
For patients not allergic to clindamycin (Cleocin): Clindamycin 150 mg
Sig: Take four capsules 1 hour before dental implant surgery
Clindamycin 600 mg was compared with the beta-lactam
phenethicillin 2 g 1 hour preoperatively for bone grafting pro-
cedures. It was determined that there was no significant dif-
ference between groups regarding postoperative infection.10
A suggested treatment protocol for routine implant or bone
grafting surgeries in the healthy individual without medical
complications would be clindamycin 600 mg either intrave-
nously, intramuscularly, or orally 1 hour preoperatively. The
scientific evidence available at this time does not support the
use of long-term postoperative therapy. The literature is
divided on the impact that prophylactic antibiotic therapy has
on implant or grafting success, therefore accounting for the
varying opinions on possible benefits. Historically, there has
been reluctance by some practitioners to not use clindamycin
because of concern regarding potential adverse events, in par-
ticular the development of Clostridium difficile diarrhea or
pseudomembranous colitis.11 Reviews of the risk factors for
C. difficile infection associated with clindamycin reveal that
this concern is unwarranted.11,12 C. difficile-associated prob-
lems are rare when clindamycin is used in outpatient ambula-
tory care settings.13 This unwarranted misconception about
clindamycin should be acknowledged, and the true value of
clindamycin as a prophylactic antibiotic should be recognized.
Clindamycin’s broad-spectrum activity against aerobic, anaer-
obic, and β-lactamase–producing pathogens plus its high oral
absorption, significant soft and bone tissue penetration, and
stimulatory effects on the host immune systems make it an
excellent choice for antibiotic prophylaxis11(Box 23-1).
■ ANTIBIOTICS ADDED TO BONE
GRAFTING MATERIALS
It has become common practice to empirically add antibiotics
to autogenous, allograft, or xenograft bone grafting materials.
Unfortunately, a variety of anecdotal antibiotic bone grafting
cocktails has been advocated, with little scientific evidence
for their use. The blood supply to a recent bone graft is com-
promised, and therefore systemic use of antibiotics for either
prophylaxis or treatment of an infected bone graft site may be
insufficient to provide adequate antibacterial concentration
levels. There is great interest in both orthopedics and implant
dentistry for the local administration of antibiotics. Locally
administered antibiotics may achieve a twenty-fold higher
concentration in a contained area versus intravenous admin-
istration. This local administration is seen to offer promise in
both prevention and treatment of localized osseous infec-
tions.14,15 Sanders et al.17 in 1983 reported that bone grafts
containing antibiotics had greater predictability than those
not containing antibiotics.16,17 Mabry et al.18 reported that the
combination of gentamicin and tetracycline mixed with
 CHAPTER 23 •
Effect of Antibiotic Concentration on
TABLE 23-1
Primary Human Osteoblast (PHO)
Antibiotic Mean IC (Proliferation, Metabolic
Activity; mg/mL)
IC20 IC50
Cefazolin 380, >400 >400, >400
Lincomycin No effect No effect
Clindamycin 30, 340 150, >400
Erythromycin 30, 210 180, >400
Azithromycin 20, 80 25, 160
Roxithromycin 20, 110 70, 210
Ciprofloxacin 70, 260 170, >400
Moxifloxacin 80, 190 160 >400
Tetracycline 40, * 180, *
400 mg/mL was maximum concentration used in study.
*Could not be determined as a result of inference with assay.
Adapted from Duewelhenke N, Krut O, Eysel P: Influence on mitochondria and
cytotoxicity of different antibiotics administered in high concentrations on primary
human osteoblast and cell lines, Antimicrob Agents Chemother 51(1):54-63, 2007.
freeze-dried bone allografts increased osseous regeneration.18
Other studies have shown that the addition of antibiotics to
graft material had a depressive effect on bone formation.19,21
These conflicting reports may be due in part to potential toxic
effects of various antibiotics and their localized concentra-
tions. Studies have demonstrated that some antibiotics are
toxic to osteoblast-like cells, especially at higher concentra-
tions.19-23 During the initial healing process of the bone graft,
osteoblasts are present along with human mesenchymal stem
cells (hMSCs), which migrate into the bone graft, where they
proliferate and differentiate.14,24,25 If these progenitor cells
should fail to mobilize, proliferate, or differentiate, a failure in
bone development may occur.14,16 Knowing that high concen-
trations of antibiotics have influence on bone-forming cells
and that anaerobes would most likely be the bacteria of
concern, the clinician should consider these factors when
making a choice of which antibiotic to add to the bone graft.
Cavalier use of an inappropriate locally administered antibi-
otic may lead to toxic effects and result in the failure of the
bone graft.
Duewelhenke et al.26 investigated the effect of 20 antibiot-
ics from different classes and antibacterial mechanisms in cell
cultures of primary human osteoblasts (PHO).26 The mean
inhibitory concentrations (ICs) (IC20, IC50) for proliferation
and metabolic activity were compared (Table 23-1). Cytotox-
icity could not be observed 24 hours after treatment of PHO
with inhibitors of bacterial cell wall synthesis, aminoglyco-
sides, tetracycline, rifampin, and lincomycin at any concen-
tration. Aminoglycosides and antibiotics that inhibit bacterial
cell wall synthesis, with the exception of higher concentra-
tions of cefazolin, did not have an effect on proliferation or
metabolic activity. Cefazolin decreased the proliferation of
PHO at higher concentrations. Clindamycin and erythromy-
cin demonstrated cytotoxicity at higher concentrations, but
not at lower concentrations. At ultralow concentrations,
clindamycin and erythromycin did not affect proliferation or
Pharmacology for Implant Dentistry 389
metabolic activity, but did have an effect at moderate to high
concentrations. Azithromycin and roxithromycin demon-
strated cytotoxicity, inhibited proliferation, and decreased
metabolic activity even at lower doses.
The fluoroquinolones (ciprofloxacin and moxifloxacin)
inhibited PHO proliferation and interfered with metabolic
activity at all concentrations. Tetracycline and rifampin
inhibited proliferation of PHO. However, both of these agents
had a direct effect on the thiazolyl blue tetrazolium bromide
(MTT) assay used to assess metabolic activity. Therefore, no
conclusions could be drawn as to their effect on metabolic
activity.
The observed cytotoxic and cytostatic effects of clindamy-
cin, macrolides, fluoroquinolones, linezolid, chloramphenicol,
rifampin, and tetracycline on PHO can be explained by an
impairment of mitochondrial energetics. It is known that
macrolides and clindamycin accumulate intracellularly.27,28
These agents at high localized concentrations could be cyto-
toxic or cytostatic for bone cells in vivo after local administra-
tion. Some of these agents might impair bone metabolism,
even in accepted therapeutic serum concentrations.26 The
inhibitors of bacterial cell wall synthesis (with the exception
of cefazolin with an unknown eukaryotic target)19,26 and ami-
noglycosides had no effect on PHO cytotoxicity because they
are unable to enter the cells in the absence of a specific recep-
tor.26,29,30 Interestingly, lincomycin had no effect on cytotoxic-
ity, proliferation, or metabolic activity, even at higher
concentrations.
Aminoglycosides (gentamicin) are the most frequently
used antibiotics for local treatment of bone infections and are
known to affect mitochondrial protein synthesis.26 Despite
this effect on protein synthesis, Duewelhenke et al. did not
find any effect on PHO.26 This finding is in contrast to Isefuku
et al.,21 Pedersen et al.,31 and Yuhan et al.14 who found that
gentamicin at higher concentrations inhibits proliferation and
differentiation of hMSCs, which could compromise the bone
healing process.14,21,31 Gentamicin applied topically to local-
ized bone infections has been reported to be effective and to
circumvent the problems associated with systemic administra-
tion. However, gentamicin at 100 μg/mL (0.1 μg/μL) and
higher was shown to have a substantial inhibitory effect on
hMSCs in vitro and in vivo.14 Because hMSCs are instrumental
for bone formation following bone grafting procedures, the use
of gentamicin in concentrations higher than 100 μg/mL may
compromise or delay new bone formation.
Kim et al.16 evaluated the effect of high local concentra-
tions of gentamicin or tetracycline versus normal saline on
bone repair, induced by demineralized bone in rats.16 Genta-
micin was used at a concentration of 15 mg/0.5 mL (30 μg/μL)
of demineralized freeze-dried bone (DFDB), and tetracycline
was used at 30 mg/0.5 mL (60 μg/μL) of DFDB. In this study,
antibiotic-treated groups demonstrated cellular necrosis or
growth inhibition as opposed to the saline-treated group. This
result suggests that saline mixed with bone grafts is an effec-
tive material for the regeneration of osseous defects; however,
if an infection is present, then the use of gentamicin or tetra-
390 SECTION IV ■ Implant Surgery
TABLE 23-2 Protocol for Antibiotic Preparation From Stock
Antibiotic Dilution
Cefazolin, 500 mg powder Mix with 9.5 mL of 0.9% normal saline (final volume 10 mL)
Clindamycin, 150 mg/mL Dilute 1 : 20 (e.g., 0.5 mL stock with 9.5 mL 0.9% normal saline)
(final volume 10 mL)
*Use 0.3 cc of final diluted antibiotic for every 1 g of bone grafting material.
cycline would be of value. Locally applied gentamicin is used
in orthopedics for the treatment of osteomyelitis. It has also
been used as gentamicin-containing cement for implantation
and is one of the most recognized localized antibiotic treat-
ments for skeletal infections.31,32 However, prophylactic addi-
tion of gentamicin and tetracycline to bone graft mixtures
in an effort to facilitate the (re)generation of bone is
questionable.
Lincomycin did not inhibit proliferation or affect meta-
bolic activity at any concentration, and it displays good activ-
ity against anaerobes. Lincomycin, when used systemically, is
known for causing pseudomembranous colitis and, as a result,
has fallen into disuse. Local application at the time of graft
placement should circumvent this systemic toxic effect. This
is an area of implant therapy that warrants further
investigation.
Penicillin and amoxicillin did not affect PHO proliferation
or metabolic activity, even at high concentrations, but these
two agents have minimal activity against anaerobes. Kuriyama
et al.19 tested 800 bacterial isolates and found that 34% pro-
duced β-lactamase, therefore making penicillin or amoxicillin
an inferior choice as a prophylactic antibiotic when mixed
with bone grafting material. Cefazolin does have greater activ-
ity against anaerobes found in the mouth and is more resistant
to hydrolysis by β-lactamases.26,34
For cefazolin the mean IC that inhibited proliferation 20%
(IC20) is 380 μg/mL. The minimum bacterial inhibitory con-
centration (MIC90) for 155 isolates for cefazolin is 64 μg/mL.34
To prepare a solution that is cefazolin 250 μg/mL, dilute
500 mg of cefazolin with 9.5 mL of 0.9% normal saline (final
volume 10 mL), then take 250 μL (25 units) of this initial
dilution and add to 50 mL of 0.9% normal saline. This final
concentration would be approximately 4 times the MIC90 for
the various isolates.34 The 25 units can be measured by using
an insulin U-100 syringe of which 100 units represent 1 mL,
therefore 1 unit equals 10 μL. A reasonable final solution
volume to add to each gram of grafting material would be
0.3 mL (300 μL) of diluted antibiotic.
For clindamycin the mean IC that inhibited proliferation
20% (IC20) is 30 μg/mL. The minimum dental-related MIC90
for more than 750 isolates is 0.03 to 0.25 μg/mL.33 To prepare
a solution that is clindamycin 20 μg/mL, dilute 0.5 mL of a
150-mg/mL stock solution with 9.5 mL of 0.9% normal saline
(1 : 20 dilution), then using an insulin U-100 syringe, take
133 μL (13.3 units) of this initial dilution and add to 50 mL
of 0.9% normal saline. This final concentration would be
approximately 140 times the MIC90 for the various isolates.31
Add to 50 mL of 0.9% Normal Saline*
250 μL, 25 units
133 μL, 13.3 units
A reasonable final solution volume to add to each gram of
grafting material would be 0.3 mL (300 μL) of diluted antibi-
otic. Clindamycin would be a preferred agent because of its
activity against anaerobes, but it must be used at a subtoxic
concentration (Table 23-2).
In summary, lincomycin may be the agent of choice because
it does not interfere with proliferation or metabolic activity
at any concentration, but there are no clinical studies to
confirm in vivo efficacy. Tetracycline and gentamicin have
extensive anecdotal clinical data, but are known to inhibit
osteoblastic activity and therefore may not be suitable for the
prophylactic addition to grafting material. Cefazolin does
have documented efficacy and may be a suitable choice, but
it does not have an extended anaerobic spectrum. Clindamy-
cin does have a broader anaerobic spectrum of activity and
documented efficacy with a large therapeutic index. There-
fore, its use is evidence based and a rational choice.
It is obvious that more in vitro and in vivo studies are needed
to offer complete guidance in this area. From what is known,
it is obvious the final administered concentration of the com-
monly used anecdotal bone grafting antibiotics, including
tetracycline or clindamycin, is very important.
■ PERIIMPLANTITIS
Implant success is not defined simply by osseous integration
or a technically correct prosthesis, but rather by long-term
function. Implant dentistry has a remarkable long-term success
rate for both complete and partially edentulous patients.35-41
Schwartz-Arad et al.42 in 2005 reported that the 10-year
cumulative survival rate for maxillary and mandibular dental
implants when restored by overdentures was 95.4% (maxilla,
83.5%, mandible, 99.5%). Another study reported a 12-year
cumulative implant survival rate for nonsmokers of 97.7%.43
These long-term success rates support the concept that implant
dentistry is a predictable modality and thus an excellent
option for practitioners and their patients. Most failures occur
during the initial healing phase or during the first year after
prosthetic loading.40,41 Occasional complications do arise
during maintenance and retention of implants. The hard and
soft tissues supporting dental implants are susceptible to
microbial disease that may lead to the loss of what had been
a previously successful functioning implant.44,45 Chronic
inflammation and infection of the tissues surrounding the
dental implant can lead to the loss of supportive alveolar
bone. This condition is known as periimplantitis (PI).46-49 PI
has a confirmed infectious cause, with high levels of periodon-
tal pathogens, including Actinobacillus actinomycetemcomitans
 CHAPTER 23 •
(AA), Porphyromonas gingivalis, Porphyromonas intermedia,
Tannerella forsythia, and Treponema denticola, reported.41,50-52
Even with the confirmed infectious cause, it must be recog-
nized that PI is a multifaceted disease process, which may also
include host immune response and susceptibility, host modify-
ing factors, and local environment. The contribution of
factors, such as implant surface type, occlusal loading scheme,
smoking, and a history of chronic periodontitis, is still
unknown.53
PI is mainly a localized lesion, and therefore local treat-
ment seems logical. The known bacterial cause supports the
concept that PI is a site-specific inflammatory response to
bacteria, rather than simply a patient-associated specific host
response.41 Limited studies that have examined the outcome
of PI treatment suggest that systemic antibiotics in combina-
tion with mechanical débridement are partially successful in
controlling PI.54 There is a lack of studies reporting 1-year
microbial profiles when systemic antibiotics are used as the
primary form of treatment.
PI is not synonymous with “failing implant” or “ailing
implant,” as defined by the first European workshop on peri-
odontology in 1993.46 Dental implant loss as a result of PI is
not inevitable, and the severity of it may be kept to a minimum
if the lesion is detected at an early stage and the disease is
intercepted by appropriate means.55 Logical and evidence-
based criteria should be used in the development of an appro-
priate strategy.
The cumulative interceptive supportive therapy (CIST)
protocol, developed at the University of Bern School of Dental
Medicine (2000), has demonstrated that periimplant infec-
tions can be successfully controlled by a protocol that is cumu-
lative in nature and includes four sequential steps. These steps
begin with mechanical débridement and proceed sequentially
through antiseptic therapy, antibiotic therapy, and regenera-
tive or resective surgery.48,56 This section will focus on the
various pharmacologic agents used in PI treatment. Table 23-3
provides a treatment protocol for varying degrees of PI.
TABLE 23-3 Treatment Algorithm for Peri-implantitis
Clinical Parameters
Plaque Bleeding on Suppuration Periimplant Probing
Probing Depth (mm)
± − − <4
+ + − <4
+ + ± 4-5
+ + ± >5
+ + ± >5
Treatment.
A. Mechanical débridement only.
B. Antiseptic therapy. Rinse with 0.1% to 0.2% chlorhexidine digluconate for 30 sec using approximately 10 mL for 3 to 4 weeks supplemented by irrigating locally with
chlorhexidine (0.2% to 0.5%).
C. Antibiotic therapy: Systemic: metronidazole 250 mg t.i.d. for 10 days or combination metronidazole (250 mg b.i.d.) with amoxicillin (375 mg daily) for 10 days. Local: application
of antibiotics using controlled-release devices (25% tetracycline fibers).
D. Surgical. Regenerative surgery using saline, barrier membrane or resective surgery with apical repositioning following osteoplasty around defect.
From Lang NP, Wilson TG, Corbet EF: Biological complications with dental implants: their prevention, diagnosis and treatment, Clin Oral Implants Res 11(suppl 1):146-55, 2000.
Pharmacology for Implant Dentistry 391
Mechanical débridement (treatment A) with antiseptic
treatment (treatment B) is indicated in situations where there
is plaque present, bleeding on gentle probing, periimplant
probing depth 4 to 5 mm, possible incipient radiographic bone
loss, and suppuration. Antiseptic treatment includes the appli-
cation of a potent agent, such as chlorhexidine digluconate,
either in the form of a daily rinse (0.1%, 0.125%, or 0.2%),
or as a gel applied to the PI site. Three to four weeks of regular
application are necessary to achieve a positive result.56
Chlorhexidine is available with or without alcohol and with
0.055% sodium fluoride. All preparations have been shown to
exhibit equal clinical efficacy with respect to gingival index,
plaque index, discoloration index, and bleeding on probing.57
There are several oral antiseptic mouth rinses available, but
unfortunately most have not been subject to controlled studies
evaluating their efficacy in the treatment of PI; therefore, we
are unable to address their use.
Localized antiseptic (treatment B) and systemic antibiotic
therapy (treatment C) are indicated when periodontal probing
depth values of the periimplant sulcus or pocket increase to
greater than 5 mm or more, plaque deposits are present, bleed-
ing occurs on probing, and evidence of bone loss on radio-
graphs is present. Suppuration may or may not be present.
This periimplant lesion and pocket represents an ecologic
niche, which is conducive to colonization with Gram-
negative anaerobic, periodontopathic bacteria.58 The antibac-
terial treatment must include antibiotics to eliminate or at
least appreciably reduce the pathogens in the submucosal eco-
system. Mombelli and Lang57 in 1992 demonstrated that if the
previous treatment is used, soft tissue healing can be achieved.57
Before the administration of antibiotics, both mechanical
débridement and antiseptic treatments must be performed.
Systemic antibiotic therapy (treatment C) should be
directed toward the elimination of Gram-negative anaerobic
bacteria. Metronidazole (Flagyl) would be the preferred anti-
biotic. Systemic antibiotics are unlikely to penetrate the
established biofilm on the dental implant, and therefore thor-
Maintenance Treatment
Radiographic Classification
Bone Loss
− 0 (A)
− 1 A
+ 2 A+B
++ 3 A+B+C
+++ 4 A+B+C+D
392 SECTION IV ■ Implant Surgery
ough local débridement is necessary.59 The clinical experi-
mental study by Mombelli and Lang validated the use of
débridement and oral antibiotics. They found that periim-
plant infections treated with this protocol were resolved and
remained stable for a documented period of 1 year. Prophy-
lactic procedures should be instituted to prevent reinfection.57
The protocol suggested by Mombelli and Lang is that metro-
nidazole when used as a single agent should be prescribed as
250 mg t.i.d. for 10 days. They also suggest the use of metro-
nidazole 250 mg b.i.d. plus amoxicillin 375 mg/day for 10 days.
Metronidazole has also been used in combination with amoxi-
cillin and clavulanic acid (Augmentin) or ciprofloxacin in the
treatment of periodontitis involving AA and may therefore
be of value in treating PI.58 It is important that systemic anti-
biotic therapy should be continued for 10 days.60 For those
cases that are refractory in nature, it would be logical and
prudent to prescribe metronidazole 250 to 500 mg t.i.d. in
conjunction with amoxicillin 500 mg t.i.d.
Matrix metalloproteinases (MMPs) form a family of
enzymes that mediate multiple functions involved in tissue
destruction and immune responses related to periodontal
inflammation. The expression and activity of MMPs in healthy
periodontium surrounding teeth is low, but is drastically
enhanced to pathologically elevated levels in the presence of
dental plaque and infection-induced periodontal inflamma-
tion. Hard and soft tissue destruction during PI is thought to
be the result of a cascade involving bacterial virulence factors
and/or enzymes, proinflammatory cytokines, reactive oxygen
species, and MMPs. Ironically, recent studies suggest that
MMPs can also exert antiinflammatory effects in defense of
the host by processing antiinflammatory cytokines and che-
mokines and by regulating apoptotic and immune responses.61
In spite of this antiinflammatory host defense mechanism for
MMPs, they do induce the fragmentation of an epithelial-cell
derived adhesion protein (laminin-5), which can induce the
apical migration of epithelial cells during the development of
periodontal pockets. Low-dose doxycycline (LDD) (Periostat),
administered orally, is an MMP-inhibitor drug that reduces
laminin-5 levels.62 Thus, LDD therapy may also be used as an
adjunct to mechanical débridement in the treatment of peri-
odontal lesions. Clinical studies are needed to further explore
the possible efficacy of this treatment form.
The application of local antibiotics through the use of
controlled delivery devices has emerged recently as a suitable
treatment concept. It is important that only release devices
that ensure adequate release-kinetics be used to ensure suc-
cessful clinical results. The antibiotic must remain at the site
of action for at least 7 to 10 days in a concentration high
enough to penetrate the submucosal biofilm.57 Tetracycline
periodontal fibers (Actisite), minocycline hydrochloride
microspheres 1 mg (Arestin), and sustained-release doxycy-
cline (Atridox) are three commercially available delivery
systems.
Mombelli et al.64 found that tetracycline periodontal fibers
significantly lowered the anaerobic colony-forming units
(CFUs) from baseline at months 1, 3, and 6 (P < 0.001). There
was also a significant decrease in mean periimplant probing
depth from 6.0 to 4.1 mm (P < 0.001), which was sustained
for more than 12 months. The bleeding tendency was signifi-
cantly reduced after 1 month and thereafter (P < 0.001).
Minocycline microspheres 1 mg have also been used with
favorable results in treating PI, following mechanical débride-
ment and chlorhexidine treatment. Minocycline is a tetracy-
cline derivative that exhibits both antimicrobial activity on
periodontal pathogens and inhibitory properties on MMPs
associated with tissue destruction.64 Oringer et al.64 found that
these microspheres, placed subgingivally, induced reductions
in AA, P. gingivalis, T. forsythia, and T. denticola up to 180
days after treatment. This study contained only 25 subjects
and therefore may not be statistically significant.32 Minocy-
cline microspheres have demonstrated an effective short-term
reduction in the gingival cervical fluid biomarker interleukin
1-beta (IL-1β). IL-1β, when chronically present, is a bone-
resorptive cytokine that is associated with periodontal disease
activity.64
A clinical trial for the treatment of PI revealed that the
treatment group receiving mechanical débridement with
application of a locally applied biodegradable sustained-release
doxycycline experienced significant benefits over mechanical
débridement alone. There was a mean reduction in pocket
probing depth of 1.15 mm with an improvement in probing
attachment levels of 1.17 mm. The doxycycline-treated group
demonstrated a significant reduction in pocket probing depths
and mean probing attachment levels (0.6 mm), accompanied
by a significant reduction in mean bleeding on probing (P =
0.001).60 Sustained-release doxycycline in conjunction with
mechanical débridement appears to be beneficial in the treat-
ment of PI.
It is not fully known if bacteria and their by-products need
to be completely removed from an implant surface to obtain
a predictable and successful result. There have been numerous
attempts to gain a “decontaminated” implant surface. These
efforts include use of citric acid, chlorhexidine gluconate,
hydrogen peroxide, tetracycline HCl, polymyxin B, and stan-
nous fluoride. At this time, no one particular agent or combi-
nation has proven to be convincingly superior.52
Conclusion:
PI is a significant risk factor that is preventable and
treatable. Although it can, it does not have to lead to late
implant failure. Mechanical débridement and surface decon-
tamination are certainly key components for treatment of PI,
but the addition of the proper pharmacologic agent, either
locally or systemically, will improve the prognosis and success
rate.
■ NSAIDS AND BONE
DEVELOPMENT
The process of normal bone healing or formation can be
divided into four phases: immediate, early, regenerative, and
remodeling.66 The immediate phase consists of localized tissue
hypoxia and hematoma formation. Hypoxia is thought to ini-
tiate a signaling cascade that begins the healing process.66-69
 CHAPTER 23 •
Following the initiation of this signaling cascade, the early
phase begins and is characterized by an inflammation response
with the recruitment of cells to the surgical site through che-
moattraction and increased proliferation.66,69-71 The regenera-
tive phase involves the development of new woven bone
through intramembranous ossification and requires angiogen-
esis.66,72-76 Remodeling follows, with the maturation of the
newly formed woven bone into mature lamellar bone that will
have mechanical integrity.77
Even though all phases of the bone formation process are
important, the early phase is critical for the ultimate success
of bone formation. During the early phase, there are increased
levels or increased gene expression of proinflammatory cyto-
kines, mitogenic growth factors, and cell-differentiating
growth factors. Inflammation, which occurs at the onset of
early phase injury-induced bone formation, is hypothesized to
provide the initial signaling molecules for continuation of the
healing cascade.66,78 Mitogenic growth factors and cell-
differentiation growth factors act on osteoblast’s precursor
cells, which are provided primarily by the periosteum. Existing
bone marrow (when present), small blood vessels, and fibro-
blasts are secondary sources of precursor cells.
The enzyme cyclooxygenase-2 (COX-2) is important to
the course of normal inflammation.66,79-81 The rate-limiting
step in the synthesis of prostaglandins (PGs) from arachidonic
acid is catalyzed by COX-2. PGs are bioactive lipids and are
of significance because they possess proinflammatory effects
plus other varied physiologic effects.66,82 COX-2 is responsible
for PGE2 and PGF2 formation.82 PGE and PGF have been
detected at increased levels during the early phase of healing
in rabbit osteotomy callus and surrounding muscle.83 This
finding suggests that both PGE and PGF have a functional
role in healing.83
NSAIDs are often used at the time of dental implant place-
ment or bone grafting procedures for their analgesic and anti-
inflammatory efficacy. The inhibition of COXs is the
mechanism by which NSAIDs achieve their intended effects.
Traditional NSAIDs (tNSAIDs), which inhibit COX-1 and
COX-2, are drugs such as aspirin, indomethacin, ibuprofen,
ketoprofen, flurbiprofen, naproxen, and diclofenac. There are
also drugs that specifically inhibit COX-2, such as celecoxib
(Celebrex), valdecoxib (Bextra), and meloxicam (Mobic).
Following the hypothesis that inflammation is necessary for
normal bone healing and formation, postoperative NSAID
therapy may potentially delay bone healing. This phenome-
non has been demonstrated in several animal models.66,84-88
Also, there is clinical evidence that nonselective and COX-
2-specific NSAIDs exert inhibitory effects on new bone for-
mation.89-94 This evidence has been challenged by others who
found that the use of tNSAIDs did not significantly influence
fracture consolidation or ectopic bone formation induced by
demineralized bone matrix in rodent models.95,96 Three differ-
ent research groups found that in male rats the COX-2 inhibi-
tor celecoxib is metabolized so quickly by the liver that even
high doses given once daily will yield too low a serum con-
centration to be relevant.97-99
Pharmacology for Implant Dentistry 393
Simon in 200766 demonstrated that higher doses and longer
periods of celecoxib treatment in female rodents (8 mg/kg/day;
normal human dose is 2.67 to 5.34 mg/kg/day) were more
detrimental to fracture healing than lower doses (2 mg/kg/
day) and shorter periods of celecoxib treatment. Female
rodents that were treated with a modest dose of celecoxib
(4 mg/kg/day) for 5 days following a fracture had significantly
worse outcomes after 8 weeks of healing than control rats.
Therefore, one may suggest that NSAID therapy following a
fracture could adversely affect healing in humans. Two recent
human studies do offer support for this conclusion. The
Giannoudis study may have the greatest correlation to dental
implant surgery.100,101 They found a marked association
between nonunion of femoral diaphysis fractures that were
stabilized with implant fixation and the use of NSAIDs after
injury (p = 0.000001). The test population that received
NSAID therapy (mean therapy time 21.2 weeks) did not
develop union of the fracture. Those that received NSAIDs
for only 1 week did attain fracture union, but at a slower rate
(7.5 months) than those that did not receive any NSAIDs
(5.5 months). All NSAID therapy patients (both long term
and short term) had an odds ratio for nonunion of 10.74 (95%
confidence interval 3.55 to 33.23; p = 0.000001). The dosages
of the two main NSAIDs used, ibuprofen and diclofenac, were
not reported.100 Their conclusion was that, even though there
are many factors involved in bone healing, the main associa-
tion of nonunion or delayed union of implant-stabilized frac-
tures with the use of NSAIDs was noteworthy, and therefore
they recommend excluding these drugs from clinical use in
patients with diaphyseal fracture.100 The dental literature
offered an animal study that examined the effect of COX-2−/−
(lacking the COX-2 gene in both alleles) knockout mice on
osseointegration. The results suggested that COX-2 played an
essential role in osseointegration and that COX-2-selective
NSAIDs may interfere with osseointegration clinically.102
Another animal study examining indomethacin and aspirin
found that a decreased rate of, or lack of, bone healing may
be dose dependent.103 The same study further concluded that
low-dose aspirin therapy (100 to 200 mg/day) did not have a
statistically significant effect on healing.103 Gerstenfeld et al.
in 200792 concluded from an animal study (male rats) that
inhibition of COX-2 impairs fracture healing and that the
effects are dependent on both the dose and duration of treat-
ment. COX-2 inhibition is associated with an initial delay in
healing, and the delay is dependent on both the dose of COX-
2 inhibitor and the duration of treatment, but the healing
process is restored when inhibition is removed. The inhibitory
effects of a COX-2-specific inhibitor (valdecoxib) were greater
than those of a nonspecific COX-1, COX-2 inhibitor (ketoro-
lac) when used in doses equivalent to the ED50 and compara-
ble with those used in a clinical setting. When either was
administered for only the first 7 days after fracture, there was
no significant difference in the rate of nonunion when com-
pared with control animals at either 21 or 35 days after
fracture. The COX-2-specific inhibitor (valdecoxib) when
administered for 21 days did display inhibition of bone healing,
394 SECTION IV ■ Implant Surgery
but when discontinued, the effect was shown to be reversible,
as no effect on the nonunion rate was noted at 35 days. With
the 7-day administration, neither of the NSAID agents
affected the torque strength of the healing calluses. However,
at 35 days, there was a significant decrease in the biomechani-
cal strength in animals that had been administered the COX-
2-specific inhibitor valdecoxib for 21 days. It was noted that
initially reduced PGE2 levels in the treatment groups rebound
with drug withdrawal, and the impairment in the mechanical
integrity of the healing fracture is reversed after short-term
therapy.92
Flurbiprofen (Ansaid) has been reported to enhance bone
growth. Li et al.104 in 1989 reported that flurbiprofen when
administered to animals by subcutaneous injection induced
anabolic changes in rapidly growing long bones by reducing
osteoclast activity and recruitments, increased cortical bone
mass by stimulating periosteal bone growth, and increased
cancellous bone mass by depressing trabecular bone resorption
without affecting bone formation. These findings were con-
firmed by another animal study, but again the route of admin-
istration had been by subcutaneous injection. This anabolic
effect on bone was found to exist only for the subcutaneous
route of administration and not oral administration.105 Reddy
et al.106 examined the effects of flurbiprofen on alveolar bone
height around dental implants in a clinical study. Flurbiprofen
appeared to be associated with increased bone density sur-
rounding dental implants when using digital subtraction radi-
ography as the measurement tool.106 Jeffcoat et al.107 conducted
a study in which patients received either low-dose (50 mg
b.i.d.), high-dose (100 mg b.i.d.), or placebo for 3 months after
implant placement. Implants were uncovered and loaded at 3
months. Patients were followed for an additional 9 months,
but without flurbiprofen during this period. During the buried
implant healing phase (initial 3 months), there was no signifi-
cant change in bone height for any of the groups. Between
the third and sixth month, the high-dose group experienced
approximately half the bone loss of the low-dose or placebo
groups (P < 0.001). Bone loss for all groups stabilized thereaf-
ter, with no significant differences in bone height observed
between the sixth and twelfth months.107
Bergenstock et al.108 compared celecoxib with acetamino-
phen in an animal study using female rats. Comparable human
oral doses were used, and treatment was every 4 hours for a
10-day period. Celecoxib significantly impaired fracture
healing, but acetaminophen did not display significant nega-
tive effects. Histologic examination revealed that celecoxib
induced cartilage formation rather than new bone formation
at the fracture site. Acetaminophen’s mechanism of action is
inhibition of COX-3, which is a spliced variant of COX-1,
found in the CNS.108-113 Acetaminophen does not exhibit
peripheral effects and therefore helps confirm that it is inhibi-
tion of COX-2 and not analgesia that is the principle reason
that fracture healing is impaired.108
Reported effects of NSAIDs on soft tissue healing are
as varied as they are for bone formation and healing.114-120 It
has been documented that acetylsalicylic acid, indomethacin,
or phenylbutazone in rats increased collagen deposition
and the strength of skin.114,115 Tissue culture studies have
shown decreased collagen synthesis with naproxen and
indomethacin.114,115 The experimental COX-2 inhibitor DFU
(5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulphonyl)phenyl-
2(5H)-furanone) has been shown to have a negative effect on
ligament healing in the only study to date.114,121 NSAIDs
appear to be of benefit in soft tissue healing, but the results
are inconclusive.114
Unfortunately, there are too few direct double-blind con-
trolled clinical studies examining the effect of NSAIDs or
COX-2-specific inhibitors on dental implant integration or
bone grafting success at this time. Platelet-rich plasma (PRP)
has been used in patients who were also taking ibuprofen as
part of the study design. Ibuprofen was used in conjunction
with PRP in a human clinical study by Mattout (2000) that
examined guided bone regeneration (GBR) with dental
implants and/or autogenous or allogenic bone grafting.122
Patients took ibuprofen 600 mg t.i.d. for 5 days. In 19 cases of
membrane exposure, after 3 months the regenerated tissue was
soft and removed. All cases after 6 months or more of closure
showed tissue that was dense and resistant to probe pressure.
Another clinical study by Camargo et al.123 in 2002 examined
the effect of PRP and bovine porous bone mineral (BPBM)
combined with guided tissue regeneration in the treatment of
intrabony defects in humans. All subjects (control and test
populations) were exposed to ibuprofen 800 mg every 8 hours
as needed. This study confirmed that PRP in conjunction with
BPBM enhanced the results with clinical significance, even
though the patients were taking ibuprofen.
It is well confirmed that NSAIDs block PGE2 production.
Proper levels of PGE2 are important to bone formation. PGE2
at low concentration enhances bone growth and at high con-
centration induces bone resorption. PRP may be a suitable
agent to offset this lack of production of PGE2 when NSAIDs
are prescribed for a short postoperative course. PRP contains
platelets and monocytes, which contain the cytokine inter-
leukin-1a (IL-1a).124,125 IL-1β is involved in the local regula-
tion of bone homoeostasis.126 It is also known that IL-1β
stimulates PGE2 formation.127-131 This IL-1β-induced stimula-
tion of PGE2 formation would counter the PGE2 inhibition
induced by systemic postoperative NSAID administration.
Transient IL-1β has been shown to have a potent stimulatory
effect on bone formation.127,132 PRP administration is transient
in nature. The platelets in PRP also contain several growth
factors, which work in concert in bone development and
repair. Therefore, PRP use would most likely counter PGE2
inhibition induced by short-term NSAID use.
Clinically, the full effect of NSAID use on bone formation
is still not fully understood. There may be an individual
patient response variable that may alter the clinical implica-
tion of NSAID use. Scientific reasoning advocates that
NSAID use be kept to a short-term therapy because it is
obvious that the biology of early implant fixation is being
challenged.133 Numerous clinicians can argue that they have
never seen a problem with short-term NSAID use postopera-
 CHAPTER 23 •
tively in implant or grafting surgeries. But in all fairness, clini-
cians are not examining the bone formation histologically,
only macroscopically. They may take comfort in referring to
a simplified aspect of evidence-based medicine, claiming that
as long as there have been no sufficiently large, double-blind
randomized studies, there is no evidence worth considering
and therefore no reason for caution.133 It is obvious that further
clinical trials are needed to clarify this issue.
A logical protocol for use of NSAIDs at the time of implant
or graft surgery would be to use a nonspecific NSAID (unless
the patient’s medical history dictates otherwise) for a short
period and with the use of PRP to counter the PGE2 inhibitory
effects of the NSAID. A suggested protocol might be to use
ibuprofen 600 mg every 6 hours for 5 to 7 days and to supple-
ment it with acetaminophen 500 mg every 6 hours if the
ibuprofen does not offer adequate pain control. Acetaminophen-
narcotic combinations are often used, but then the patient
may experience many of the unwanted side effects of the nar-
cotic. NSAIDs have been shown to offer better patient accep-
tance and superior pain control than narcotics. Any negative
effects of the NSAIDS will be reversed quickly, and the use
of PRP may actually offset the possible detrimental effects.
For patients on chronic, nonspecific or COX-2-specific
NSAIDs, one may consider changing the NSAID to flurbipro-
fen (Ansaid) 100 mg b.i.d. because of the evidence that it may
actually preserve bone. This change should only be recom-
mended if the patient’s medical history permits.
As with many aspects of dental implantology, this is an
issue that does not have a definitive answer. Persson et al.134
emphasizes the biologic nature of implant fixation: “Cellular
events immediately after the procedure can be influenced by
drugs, leading to changes in orthopedic implant fixation
immediately or years later. Good bone carpentry is critical,
but the clinician must not forget biology.”
■ BISPHOSPHONATES
Osteoporosis is a condition that is becoming more prevalent
as people live to an older age. There are many options for
dealing with the bone loss that is associated with osteoporosis,
but the most effective is estrogen therapy followed by the use
of bisphosphonates (BPs). BP therapy is a major tool used to
combat bone loss in postmenopausal women, especially since
the Women’s Health Initiative (WHI) study of 2002 reported
deleterious effects of hormonal replacement therapy, which
have since been disputed.135
BPs are frequently prescribed drugs that inhibit the resorp-
tion of bone. All BPs share a similar structure, as shown
below.136 The P-C-P bond is extremely resistant to hydrolysis.
Pharmacology for Implant Dentistry 395
BPs possess a high affinity for hydroxyapatite, specifically
calcium through the negatively charged oxygen atoms found
in the BP structure.
BP drugs fall into two major classes, nonnitrogenous and
nitrogenous, and differ by their side chains (R1 and R2). The
nonnitrogenous bisphosphonates (NNBPs) are the first-
generation drugs. Their mechanism of action involves disrup-
tion of osteoclast cellular metabolism, resulting in apoptosis
of the osteoclast.137 The loss of osteoclast activity leads to a
decrease in bone resorption. The NNBPs are etidronate (Didr-
onel), clodronate (Bonefos), and tiludronate (Skelid) and are
used infrequently.
The nitrogenous bisphosphonates (NBPs) are the second-
and third-generation BPs. Their mechanism of action is dif-
ferent in that they inhibit the mevalonate pathway (HMG-CoA
reductase pathway), specifically at the site of the enzyme
farnesyl diphosphate synthase (FPPS).138 The inhibition of
FPPS leads to decreased levels of the intracellular proteins,
Ras, Rho, and Rac that are responsible for protein trafficking
and cytoskeleton attachment to the osteoclast’s “ruffled
border.”139 Therefore, NBPs interfere with the function of the
“ruffled border,” which is responsible for the breakdown of the
bone’s hydroxyapatite matrix. NBPs include pamidronate
(Aredia), alendronate (Fosamax), ibandronate (Boniva), rise-
dronate (Actonel), and zoledronate (Zometa, Reclast). Fol-
lowing is a table summarizing the commonly prescribed NBPs
and their relative potencies (Table 23-4).
NBPs can be administered orally or intravenously and are
used principally for the treatment of osteopenia, osteoporosis,
or skeletal metastasis. Other conditions that NBPs have been
approved for include Paget’s disease, multiple myeloma, and
osteogenesis imperfecta.
NBP therapy is more effective in preventing and treating
osteopenia or osteoporosis if calcium supplementation is taken
concurrently. Side effects of the oral preparations include
inflammation and irritation of the esophagus and stomach as
a result of their acidity. NBP irritation to the upper GI tract
can be severe; therefore, patients are instructed to remain
upright for 30 minutes after oral administration. Osteonecrosis
of the jaw (ONJ) is a manifestation that has been associated
with BP therapy. Patients receiving IV-administered BPs are
at the highest risk, although cases have been reported with
long-term use of the oral preparations.140-146
ONJ, first described by Marx143 and Wang et al.144 in 2003,
is characterized by pain, swelling, exposed bone, and purulent
exudate. The majority of cases of ONJ resulting from oral NBP
therapy have been reported with alendronate 70 mg/wk for
more than 3 years, or 35 mg/wk for more than 5 years.146 The
pathophysiology of this debilitating oral condition is unknown;
however, recent evidence suggests that patients with ONJ
have reduced circulating endothelial cells,145 supporting an
antiangiogenesis hypothesis. This hypothesis is supported by
evidence that the more potent BP zoledronate, commonly
prescribed for cancer treatment (and more recently for osteo-
porosis), inhibited the survival and migration of endothelial
cells through multiple intracellular signaling pathways.147
396 SECTION IV ■ Implant Surgery

TABLE 23-4 Commonly Prescribed Biphosphonates

Drug Name Trade Name Dose for Osteoporosis Treatment/Prevention Relative Potency*
Pamidronate Aredia 30 mg, 60 mg, 90 mg monthly (IV) 100
Alendronate Fosamax 70 mg/75 mL solution (PO) 500
5 mg, 10 mg daily; 35 mg, 40 mg, 70 mg weekly (PO)
Ibandronate Boniva 150 mg/mo (PO) 1000
Risedronate Actonel 5 mg daily; 35 mg, 75 mg weekly (PO) 2000
Zoledronate Reclast 5 mg/100 mL/yearly (IV) 10,000
*Relative to the first-generation BP etidronate’s potency of 1.

Adornato et al. in 2007 demonstrated that autologous plate-
let-derived growth factors were effective in soft tissue healing
in patients suffering from BP-associated ONJ.148 This provides
support for the use of PRP, which is characterized by its high
concentration of platelet-derived growth factors and cyto-
kines, which are responsible for angiogenesis and soft tissue
formation. Anecdotally, ONJ has been successfully treated
with PRP combined with an Alloderm barrier.
Other complications are currently under investigation, but
have been linked to acute tubular necrosis, atrial fibrillation,
and severely suppressed bone turnover (SSBT).148,150,151 There
is evidence to suggest that the BP-associated ONJ is due to
endothelial cell apoptosis, as a result of an accumulation of
the drug in bone. When taken orally, 3% of the drug is
absorbed from the gut, and 1% of this amount is deposited
into the bone hydroxyapatite matrix.152-154 Food greatly
decreases the absorption of NBPs.154 Initially the bone con-
centration of the NBP is very low and only inhibits osteoclast-
induced bone resorption, although there is evidence that a
10−14 molar concentration does stimulate osteoblast forma-
tion.155 The half-life of the various agents in the bone is vari-
able, but most NBPs have a known half-life in bone of up to
10 to 12 years.156 NPBs exhibit a high binding affinity for
hydroxyapatite, which prevents their release from bone other
than through osteoclast breakdown. With prolonged admin-
istration (years), the NBP accumulates in the bone leading to
higher concentrations that induce apoptosis of osteoclasts,
osteoblasts, and endothelial cells.139,157
Therefore, NBP therapy early on would be beneficial when
placing implants in the osteopenic or osteoporotic patient.
With extended therapy (e.g., alendronate 70 mg/wk longer
than 3 years or 35 mg/wk longer than 5 years), NBPs may be
detrimental to dental implant osseointegration or retention
because of a suppression of bone turnover.151
Further investigations into the benefits provided by
BP therapy have been addressed in both the fracture interven-
tion trial (FIT) and the FIT long-term extension. These
studies shed light on the concerns surrounding dental implants
and patients taking NBPs.158,159 There is evidence that NBP
therapy for a period of 5 years with discontinuation thereafter
protects an individual for an additional 5 years. This “holiday”
period could possibly prevent the negative side effects that
have been observed with long-term NBP therapy, such as
ONJ.
There is much confusion about concurrent NBP therapy
and placement of dental implants. Upon examining this
controversy from a scientific perspective and comprehensive
literature review, it would appear that a careful evaluation of
the patient’s bone vitality status is warranted. Bone strength
is evaluated by considering both bone mineral density (BMD)
and bone quality. BMD is expressed as grams of mineral per
area or volume and is defined by the individual peak bone
density and the resorption rate from the peak. Bone quality is
determined by characteristics of the bone matrix, such as
microarchitecture, bone turnover, microdamage accumula-
tion, the degree of calcification, and collagen.160-163 Therefore,
a true evaluation of bone quality cannot be determined by
BMD alone. BMD can be accessed by dual-X-ray absorptiom-
etry (DXA scan). To assess the bone quality, bone turnover
markers must be measured.
Bone turnover markers, developed in the 1990s, that
evaluate bone resorption include the following: deoxypyridi-
noline—urine (DPD), type I collagen cross-linked N-
telopeptide—serum or urine (NTX), and type I collagen
cross-linked C-telopeptide—serum or urine (CTX).160 Cur-
rently, the DPD, NTX, and CTX are the best tools for the
assessment of bone resorption.160 When urinary levels of NTX
or CTX are used, they need to be corrected by measuring
creatinine excretion to accurately assess bone resorption.
Evaluation of bone formation by bone turnover markers
examines direct or indirect products produced from osteo-
blasts. Alkaline phosphatase (AP) is an enzyme that plays an
important role in osteoid formation and calcification. The
total AP serum pool is made up of several isoenzymes derived
from various tissues, including the liver, bone, intestine,
spleen, and kidney. When liver function is normal, approxi-
mately, 50% of the total AP in serum is derived from the liver,
and 50% is derived from bone. Immunoassays for bone-specific
alkaline phosphatase (BAP) are available to assess metabolic
bone diseases.160 Note that a BAP assay is different from a total
AP assay with report of bone fraction. These two tests should
not be confused. The proper test to order for determining bone
development levels is a BAP.
These bone turnover markers are available for the diagnosis
of osteoporosis, assessment of NBP therapy effectiveness, and
bone quality. Measurements of bone turnover markers dem-
onstrate circadian variability for each parameter.160 Therefore,
NTX and BAP serum samples should be collected in the early

morning. These two assays are not affected by dietary intake;
thus, an overnight fast is not required. BAP urine tests and
CTX serum tests are affected by dietary intake and require an
8-hour fast. Urine samples for DPD, NTX, and CTX should
be first or second urine samples in the morning and must be
corrected by creatinine excretion measurement. Repeated
measurements must be obtained under the same test condi-
tions. Ideally, these bone turnover markers should be obtained
before the initiation of NBP therapy and then at periodic time
periods (6-month or yearly intervals) after therapy has been
initiated to properly assess the NBP’s effect on bone.160
When is it safe to place implants in a patient who is cur-
rently on NBP therapy? The absolute answer to the question
is not known, but in light of the preceding information, it
would be prudent to consider the following protocol in con-
sultation with the patient’s physician:
1. If the oral NBP therapy benchmark time period is less
than 2½ years, there may not be a conflict, and bone
marker turnover assays may not be necessary.
2. If the oral NBP therapy benchmark time period exceeds
2½ years at 70 mg/wk or 5 years at 35 mg/wk (e.g.,
alendronate or corresponding doses and times for other
NBPs) or longer, it may be prudent to acquire a BAP
and NTX serum level.
3. The therapy benchmark time period should be appro-
priately applied when considering more potent NBPs.
4. If the BAP or NTX serum level is out of the range noted
for a female reference population age 30 to 44 years
(example in Table 23-5), it may be reasonable to dis-
continue therapy. How long one should discontinue
therapy before implant surgery is not known. A reason-
able estimate would be to discontinue the NBP for 3 to
6 months, then to repeat the bone turnover marker tests
to see if the bone turnover is now within the reference
range.
5. If the bone turnover markers are within range either on
initial testing or after discontinuation of therapy, it would
most likely be safe to perform the implant procedure.
The protocol discussed earlier is meant to serve as a guide-
line based on what little is known at this time. There will be
much variability as to when and if a particular patient will
reach a toxic bone concentration of NBPs. It is known that
Bone Turnover Marker Levels Indicative of Bone Diseases (e.g., Metastatic One Tumor) and Abnormal
TABLE 23-6
Calcium Metabolism
Bone Marker Men
BONE RESORPTION MARKER
NTX (serum; nmol BCE/L) >17.7
BONE FORMATION MARKER
BAP (units/L)* (serum) >44.0
When high levels of bone turnover markers (exceeding the range of the mean ±1.96 SD) are exhibited, the presence of metastatic bone tumor, metabolic bone disease, or
abnormal calcium metabolism should be considered.
Note: There is interlaboratory variability for each cutoff level.
BCE, bone collagen equivalent.
*EIA method.
From Nishizawa Y et al: Guidelines for the use of biochemical markers of bone turnover in osteoporosis (2004), J Bone Miner Metab 23(2):97-104, 2005.
CHAPTER 23 • Pharmacology for Implant Dentistry 397
patient compliance with NBP administration is very poor, and
food intake with NBP administration greatly decreases absorp-
tion and would therefore delay or prevent eventual toxicity.163
It is also known that NBPs accumulate in areas of highest
osteoclast activity, and therefore there is not an even skeletal
distribution of the drug. The bone turnover markers are also
not site specific and only provide a total skeletal picture of
bone turnover.
Table 23-6 identifies the BAP and NTX serum values
that are indicative of bone disease and should not be confused
with the more restrictive reference ranges to assess bone
turnover.
The earlier suggestions apply not only to patients who will
be receiving dental implants and/or bone grafts, but should be
considered for patients who already have implants. Dental
practitioners whose patients are on prolonged NBP therapy
must be aware of the potential toxicity to bone vitality. There-
fore, when patients reach NBP benchmark time periods, bone
turnover assays and possible discontinuation of therapy should
be considered.
These guidelines are proposed for evaluating bone quality
before dental implant placement in patients who have a
history of NBP therapy. These markers are of value and are
used extensively in Japan to diagnose osteoporosis and monitor
Reference Ranges for Bone Turnover
TABLE 23-5
Markers
Bone Marker Range Reference
Population
BONE RESORPTION MARKER
NTX (serum) 7.5-16.5 nmol BCE/L Age, 40-44 yr;
female
BONE FORMATION MARKER
BAP* (serum) 7.9-29.0 units/L Age, 30-44 yr;
female
Reference ranges for markers of bone turnover are within the range of the mean ±
1.96 SD established for healthy premenopausal women.
Note: There is interlaboratory variability for each range.
BCE, bone collagen equivalent.
*Enzyme Immunoassay (EIA) method.
From Nishizawa Y et al: Guidelines for the use of biochemical markers of bone
turnover in osteoporosis (2004), J Bone Miner Metab 23 (2):97-104, 2005.
Women (Premenopausal) Women (Postmenopausal)
>16.5 >24.0
>29.0 >75.7
398 SECTION IV ■ Implant Surgery
NBP therapy. Because NBPs have been shown to inhibit bone
metabolism, it is prudent to aspire to maintain target bone
turnover marker values of bone metabolism within the refer-
ence ranges for premenopausal women.161
■ MINERAL, HORMONAL, AND
VITAMIN SUPPLEMENTS
Supplementation with calcium and magnesium has been
shown to be effective in preventing bone loss.165-167 A small
increase in bone density is noted with calcium supplementa-
tion. The data indicate a reduction in fractures, though further
studies would be required to test if calcium supplementation
reduces the incidence of such fractures or microarchitectural
damage. When calcium supplementation is paired with BP
therapy, a greater benefit is noted than with calcium alone.165,176
Sahota et al. identified three significant risk factors in the
osteoporotic population: decreased levels of magnesium,
decreased levels of vitamin D, and chronically elevated para-
thyroid hormone (PTH) levels.167
Vitamin D and calcium are regarded as the nutrients that
have the largest impact on bone health and vitality.168 The
current recommendations for vitamin D are 600 international
units daily, but patients 65 and older may require 800 to 1000
international units daily for optimal bone health.168 Many
patients need 5 to 6 times what they are currently receiving
from their diet. Vitamin D is obtained not only from dietary
sources, but also from activation of 7-dehydrocholesterol in
the skin by sunlight, containing ultraviolet B (UVB). Patients
living in the northern United States may not be getting
enough vitamin D because of the small amount of sunlight
that they receive between October and March. Dark-skinned
individuals and those who use copious amounts of sunscreen
generally have lower levels of vitamin D.
Deficiencies in circulating calcium or vitamin D will result
in reduced calcium absorption.168 A decrease in absorbed
calcium induces an increase in secreted PTH from the para-
thyroid gland. Chronic high levels of PTH induce the release
of Ca2+ from bone, which leads to osteoporosis. The combined
effect of chronically elevated PTH levels with deficiencies in
calcium or vitamin D can lead to bone loss and subsequent
fractures.168
Ironically, pulsed PTH itself has become an effective
therapy for combating bone loss. Recombinant PTH (teripa-
ratide, [rhPTH(1-34)], Forteo) has been shown to increase the
effectiveness of hormonal replacement therapy (HRT) on
bone mass density in a population of postmenopausal women.169
Greenspan et al.170 found that pulsed PTH therapy was effec-
tive in postmenopausal women for fracture prevention. In a
recently completed trial examining teriparatide, BMD
increased in the hip and spine, with no new documented
fractures throughout the course of the trial.170,171 It should be
remembered that chronic PTH release induces bone break-
down to increase plasma calcium concentration; however,
when given in pulse dosages, bone formation is stimulated.172,173
Teriparatide is pulsed as a subcutaneous injection, 20 μg
daily.
Other hormones that may impact bone development are
melatonin and human growth hormone. Recent in vitro work
suggests that melatonin supplementation may prevent osteo-
porosis because it increases the rate of osteoblastic differentia-
tion and influences the effects of other drugs and hormones
by yet unknown mechanisms.174 Melatonin in vivo is an endog-
enously circadian rhythm–released hormone from the pineal
gland. Supplemental melatonin 0.5 to 5.0 mg should be taken
daily, close to bedtime.175 Human growth hormone has been
shown to be integral in the developing skeleton, and supple-
mentation subsequently decreased bone turnover markers in
postmenopausal populations.176
Another supplement that more controlled trials will address
is vitamin K. Vitamin K mediates the synthesis of proteins
that are involved in bone metabolism, such as osteocalcin and
coagulation factors.177,178 Two forms of vitamin K exist: one
derived from leafy greens (K1), another produced by bacteria
in the gut (K2).178 It was found that Vitamin K2 supplementa-
tion 45 mg/day over a 3-year period improved both BMD and
bone geometry at sites deemed to be critical, with no differ-
ence in side effects from placebo, even at this high dose.179
Future studies are planned focusing on the prevention of
bone loss in women already diagnosed with osteoporosis.
Caution should be used when informing patients who are on
anticoagulant drugs, such as warfarin (Coumadin), because
vitamin K at any dose is an absolute contraindication for
concurrent use.
Vitamin B12 is thought to play a role in increasing
osteoblast proliferation.180 A deficiency in vitamin B12 (in
conjunction with folic acid deficiencies) may increase homo-
cysteine (Hcy) levels. Increased Hcy levels may interfere with
bone collagen cross-linking and therefore increase bone
fragility.181
The following table summarizes current supplements and
dosing regimens to prevent bone loss (Table 23-7).
Despite the growing body of evidence that low-dose estro-
gen may be the most effective pharmacologic agent in pre-
venting postmenopausal bone loss and menopause symptoms,
estrogen supplementation has lost support since the WHI
results of 2002.182-187 This report noted that an increase in
breast cancer was found among patients who received a com-
bination of estrogen and progesterone and that portion of the
study was aborted.187 A reevaluation of the data found that
there were limitations of the study, which brings its usefulness
into question, such as 50% of the participants were past or
present smokers,188 and the average time past menopause was
12 years.189 Nicotine consumption has been shown to dramati-
cally reduce or negate the effects of estrogens taken orally.188
It is suggested that those women who continue to consume
nicotine should receive estrogen replacement therapy through
a transdermal patch.188 Through the reanalysis of the WHI
data, it was found that there was a relationship between the
time of menopause onset and the initiation of a hormone
replacement regimen with regards to adverse effects.190
MacLennan also stated that many of the adverse effects noted
by the patients in the study could be reduced or eliminated by
 CHAPTER 23 •
Recommended Daily Values for Selected
TABLE 23-7
Nutrients
Nutrient/Hormone Suggested Daily Value
Calcium 700-800 international units; however,
800-1000 international units may be
required for optimal bone health in patients
>65 yr of age
Magnesium 400 mg
Vitamin D 400-800 international units
Vitamin K1, K2 80 μg
Vitamin B12 6 μg
Vitamin C 60 mg/day
Estrogen 0.1 mg transdermal patch
Parathyroid Hormone (PTH) 20-μg pulse dose
Adapted from Kitchin B, Morgan SL: Not just calcium and vitamin D: other nutritional
considerations in osteoporosis, Curr Rheumatol Rep 9(1):85-92, 2007.
reducing the dosages of the administered estrogens, eliminat-
ing or reducing supplemental progesterones, and using a
nonoral route for some patients, such as the transdermal
patch.190 Transdermal patch administration of estrogen allows
for continuous, low-dose absorption of the bone-essential
estrogen, 17-β estradiol, while bypassing the liver-induced
toxic metabolites.191
In summary, estrogen is the most effective way to combat
bone loss associated with menopause. However, other effec-
tive methods exist. Pulsed PTH is effective in fracture preven-
tion in postmenopausal women, and melatonin may be
beneficial when analyzed through future controlled clinical
trials. Supplementations with calcium, magnesium, vitamin
D, and vitamin K2 have all shown benefits in controlled
trials.167,168,181 It may be prudent to recommend that patients
add daily vitamin supplementation (vitamin D, K2, B12,
calcium, and magnesium) to their diet with the exception of
patients who are currently taking warfarin (Coumadin) or
other drugs where supplementation would be a contraindica-
tion.181 The therapeutic effects that megadoses of the various
supplements have on bone physiology are not extensively
documented in controlled trials. It should be noted that daily
supplementation alone may not prevent bone loss,181 and it is
important to appreciate the larger picture of good health and
exercise.
■ BIOACTIVE FATTY ACIDS AND
BONE DEVELOPMENT
It is well documented that bioactive fatty acids play an impor-
tant role in skeletal biology and bone health. For many people,
the American diet consists of a large proportion of these fatty
acids. Fat is regarded as an energy source, but it also facilitates
the absorption of fat-soluble vitamins (A, D, E, and K), all of
which are integral to bone physiology.192 Fat plays an impor-
tant role in the regulation of eicosanoids, including PGE2.192
The essential fatty acids (EFA) linoleic acid (18:2n-6, omega-
6 fatty acid,) and linolenic acid (18:3n-3, omega-3 fatty acid),
are the major food nutrients serving as precursors to the family
Pharmacology for Implant Dentistry 399
of eicosanoids.192 Eicosanoids include PGs, leukotrienes, and
various epoxides and are synthesized by the enzymes COX,
lipoxygenase, and epoxygenase, respectively. Each of these
eicosanoids has specific physiologic roles, including control of
inflammation and immunity. For optimal bone metabolism,
there must be a proper balance of the various eicosanoids,
which can be disrupted by increased levels of omega-6 in
conjunction with decreased levels of omega-3 fatty acids.
Excess omega-6 fatty acids can induce the overproduction of
eicosanoids that lead to a proinflammatory state,93 in contrast
with the omega-3 fatty acids that induce eicosanoids that
primarily affect bone metabolism. Arachidonic acid (AA),
derived from omega-6 fatty acids, is released from cell mem-
branes when disrupted by trauma or in the presence of growth
factors, cytokines, or other stimuli. The preferred substrate for
COX is the proinflammatory AA, rather than the omega-3-
derived eicosapentaenoic acid (EPA). EPA stimulates osteo-
calcin and AP activity, leading to bone formation.192
Conjugated linoleic acids (CLA) and EPA have negative
effects on the synthesis of PGE2 through a COX-2 mechanism,
therefore keeping the concentration of PGE2 low, stimulating
bone formation.192,194 The effects of CLA on bone physiology
in vitro and in animal models were found to be dependent on
omega-6 and omega-3 fatty acids.195 Watkins et al. in 2000194
reported that in rats’ diets high in omega-3 or with a low ratio
of omega-6 to omega-3 fatty acids were beneficial in bone
formation, as seen by an increase in the bone formation
marker, BAP. These results led to the speculation that dietary
fatty acids could have dramatic influence on bone growth and
remodeling.194 Eicosanoids derived from omega-6 fatty acids
have greater efficacy on eicosanoid receptors than those
derived from omega-3 fatty acids.196 Therefore, by decreasing
the dietary ratio of omega-6 to omega-3, it may be possible to
slow the development of disease states, such as bone loss, by
decreasing tissue AA reservoirs, leading to decreased PGE2
production. The point of convergence in this complex pathway
is COX-2, whose activity can be influenced by other cytokines
and hormones that are present in the bone microenviron-
ment, such as interleukin-1, PTH, and tumor necrosis
factor.192
The impact that PGE2 has on bone formation has been the
subject of many studies, with conflicting results. The effects
of PGE2 on bone formation may be dose related: stimulatory
at low physiologic concentrations and inhibitory at high con-
centrations, which are often associated with inflammation.197-
199
These dose-related effects are possibly due to multiple PGE2
receptor isoforms located on osteoblasts.200 High concentra-
tions of PGE2 increased the activation and differentiation of
osteoclasts and subsequently decreased activity of osteo-
blasts.191,202-204 The osteoporosis drug strontium ranelate (Pro-
telos) was found to increase bone formation through a PGE2
mechanism.195 This drug is not yet available in the United
States; however, it is popular in Europe and is in clinical
testing for FDA approval in the United States.
There are clinical reports that dietary omega-3, in appro-
priate amounts, can have a positive effect on bone physiology
400 SECTION IV ■ Implant Surgery
in humans, validating previous findings. A study completed
by Griel et al.205 found that over the course of 6 weeks, patients
receiving a diet containing omega-3 polyunsaturated fatty
acids had a decrease in the bone breakdown marker NTX, but
no significant increase in the bone formation marker BAP.205
This indicates an inhibition of bone breakdown, while bone
formation levels remained constant.
Soy isoflavones are another dietary source of fat that has
an impact on osteoblasts and osteoclasts. These compounds
are similar in structure to estrogen, have the ability to bind to
the estrogen receptor found in bone, and are beginning to be
studied as a supplement for the prevention of postmenopausal
bone loss.206
Similar to the PGs, leukotrienes may also play an impor-
tant role in bone metabolism. Ren et al.207 demonstrated that
leukotriene B4 (LTB4) inhibited osteoblast cell proliferation
in a dose-dependent manner. Several studies have demon-
strated that lipoxygenase products, including LTB4, increased
bone resorption and osteoclast numbers in vivo and in
vitro.208-212
For further information on the influence that COX-2-
specific inhibitors, other NSAIDs, and PGs have on bone
development, please refer to the NSAIDs and Bone Develop-
ment section in this chapter.
■ SUMMARY
Many techniques used in implant dentistry have developed
from a trial-and-error philosophy, which became mainstream
practices without proper evidenced-based scientific studies.
Implant dentistry owes much to the pioneers who blazed the
trail that patients and practitioners enjoy today. But with
newer research techniques and expanded information resources
at the hands of all clinicians, we must continue the evolution
process and use techniques and pharmacologic adjuncts that
offer true benefits. Clinicians must not use pharmacologic
agents in a cavalier way, but in a responsible manner that
demonstrates understanding of pharmacodynamic and phar-
macokinetic principles.
REFERENCES
1. Binahmed A, Stoykewych A, Peterson L: Single preoperative
dose versus long-term prophylactic antibiotic regimens in
dental implant surgery, Int J Oral Maxillofac Implants 20(1):115-
117, 2005.
2. Hultin M et al: Microbiological findings and host response in
patients with peri-implantitis, Clin Oral Implants Res 13:349-
358, 2002.
3. Laskin DM et al: The influence of preoperative antibiotics on
success of endosseous implants at 36 months, Ann Periodontol
5(1):166-174, 2000.
4. Dent CD et al: The influence of preoperative antibiotics
on success of endosseous implants up to and including stage
II surgery: a study of 2,641 implants, J Oral Maxillofac Surg
55(suppl 5):19-24, 1997.
5. Esposito M et al: Antibiotics to prevent complications follow-
ing dental implant treatment, Cochrane Database Syst Rev 3:
CD004152, 2003.
6. Kashani H, Dahlin C, Alse’n B: Influence of different
prophylactic antibiotic regimens on implant survival rate: a
retrospective clinical study, Clin Implant Dent Relat Res 7(1):32-
35, 2005.
7. Binahmed A, Stoykewych A, Peterson L: Single preoperative
dose versus long-term prophylactic antibiotic regimens in
dental implant surgery, Int J Oral Maxillofac Implants 20(1):115-
117, 2005.
8. Lindeboom JA, van den Akker HP: A prospective placebo-
controlled double-blind trial of antibiotic prophylaxis in intra-
oral bone grafting procedures: a pilot study, Oral Surg Oral Med
Oral Pathol Oral Radiol Endod 96(6):669-672, 2003.
9. Lindeboom JA et al: A randomized prospective controlled trial
of antibiotic prophylaxis in intraoral bone grafting procedures:
single-dose clindamycin versus 24-hour clindamycin prophy-
laxis, Mund Kiefer Gesichtschir 9(6):384-388, 2005.
10. Lindeboom JA et al: A randomized prospective controlled trial
of antibiotic prophylaxis in intraoral bone-grafting procedures:
preoperative single-dose penicillin versus preoperative single-
dose clindamycin, Int J Oral Maxillofac Surg 35(5):433-436,
2006. Epub Feb, 2006.
11. Brook I et al: Clindamycin in dentistry: more than just effective
prophylaxis for endocarditis? Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 100(5):550-558, 2005.
12. Bignardi GE: Risk factors for Clostridiujm difficile infection,
J Hosp Infect 40:1-15, 1998.
13. Levy DG et al: Antibiotics and Clostridium difficile diarrhea
in the ambulatory care setting, Clin Ther 22:91-102, 2000.
14. Chang Y, Goldberg VM, Caplan AI: Toxic effects of gentami-
cin on marrow derived human mesenchymal stem cells, Clin
Orthop Relat Res 452:242-249, 2006.
15. Gerhart TN et al: Antibiotic release from experimental biode-
gradable bone cement, J Orthop Res 6:585-592, 1988.
16. Kim SG et al: The Effect of high local concentrations of anti-
biotics on demineralized bone induction in rats, J Oral Maxil-
lofac Surg 62:708-713, 2004.
17. Sanders JJ et al: Clinical evaluation of freeze-dried bone
allografts in periodontal osseous defects. Part III. Composite
freeze dried bone allografts with and without autogenous bone
grafts, J Periodontol 54:1, 1983.
18. Mabry TW, Yukna RA, Sepe WW: Freeze dried bone allografts
combined with tetracycline in the treatment of juvenile peri-
odontitis, J Periodontol 56:74, 1985.
19. Edin ML et al: Effect of cefazolin and vancomycin on osteo-
blasts in vitro, Clin Orthop Relat Res 333:245-251, 1996.
20. Isefuku S, Joyner CJ, Simpson AH: Toxic effects of rifampicin
on human osteoblasts-like cells, J Orthop Res 19:950-954, 2001.
21. Isefuku S, Joyner CJ, Simpson AH: Gentamicin may have an
adverse effect on osteogenesis, J Orthop Trauma 17:212-216,
2003.
22. Miclau T et al: Bone toxicity of locally applied aminoglyco-
sides, J Orthop Trauma 401-406, 1995.
23. Miclau T et al: Effect of ciprofloxacin on the proliferation of
osteoblasts-like MG-63 human osteosarcoma cells in vitro,
J Orthop Res 16:509-512, 1998.
24. Rockwood CA Jr et al: Rockwood and Green’s fractures in adults,
ed 4, Philadelphia, 1996, Lippincott-Raven.
25. Yoo JU, Johnstone B: The role of osteochondral progenitor
cells in fracture repair, Clin Orthop Relat Res 355(suppl):S73-
S81, 1998.
26. Duewelhenke N, Krut O, Eysel P: Influence on mitochondria
and cytotoxicity of different antibiotics administered in high
concentrations on primary human osteoblast and cell lines,
Antimicrob Agents Chemother 51(1):54-63, 2007.
27. Hand WL, King-Thompson NL: Membrane transport of clinda-
mycin in alveolar macrophages, Antimicrob Agents Chemother
21:241-247, 1982.
28. Villa P et al: Toxicity, uptake, and subcellular distribution in
rat hepatocytes of roxithromycin, a new semisynthetic macro-
 CHAPTER 23 •
lide and erythromycin base, Antimicrob Agents Chemother
32:1541-1546, 1988.
29. Moestrup SK et al: Evidence that epithelial glycoprotein 330/
megalin mediates uptake of polybasic drugs, J Clin Invest
96:1404-1413, 1995.
30. Schmitz C et al: Megalin deficiency offers protection from renal
aminoglycoside accumulation, J Biol Chem 277:618-622, 2002.
31. Pedersen JG, Lund B: Effects of gentamicin and monomer on
bone. An in vitro study, J Arthroplasty 3(suppl 1):S63-68,
1988.
32. Hedstrom SA et al: Antibiotic containing bone cement beads
in the treatment of deep muscle and skeletal infections, Acta
Orthop Scand 51:863-869, 1980.
33. Burton LL, et al, eds. Goodman and Gilman’s the pharmacological
basis for therapeutics, ed 11, Graw-Hill, New York, 2006.
34. Tally FP et al: Susceptibility of anaerobes to cefoxitin and other
cephalosporins, Antimicrob Agents Chemother 7(2):128-132,
1975.
35. Adell R et al: A 15-year study of osseointegrated implants in
the treatment of the edentulous jaw, Int J Oral Surg 10(6):387-
416, 1981.
36. Albrektsson T: A multicenter report on osseointegrated oral
implants, J Prosthet Dent 60(1):75-84, 1988.
37. Jemt T, Lekholm U: Oral implant treatment in posterior par-
tially edentulous jaws: a 5-year follow-up report, Int J Oral
Maxillofac Implants 8(6):635-640, 1993.
38. Nevins M, Langer B: The successful application of osseointe-
grated implants to the posterior jaw: a long-term retrospective
study, Int J Oral Maxillofac Implants 8(4):428-432, 1993.
39. Buser DA, Tonetti M: Clinical trials on implants in regenerated
bone, Ann Periodontol 2(1):329-342, 1997.
40. Hultin M et al: Factors affecting late fixture loss and marginal
bone loss around teeth and dental implants, Clin Implant Dent
Relat Res 2(4):203-208, 2000.
41. Hultin M et al: Microbiological findings and host response in
patients with peri-implantitis, Clin Oral Implants Res 13(4):349-
358, 2002.
42. Schwartz-Arad D, Kidron N, Dolev E: A long-term study of
implants supporting overdentures as a model for implant
success, J Periodontol 76(9):1431-1435, 2005.
43. Aykent F et al: A 1- to 12-year clinical evaluation of 106 endos-
seous implants supporting fixed and removable prostheses, Int
J Periodontics Restorative Dent 27(4):358-367, 2007.
44. Malmstrom HS et al: Osseo-integrated implant treatment of a
patient with rapidly progressive periodontitis, A case report,
J Periodontol 61(5):300-304, 1990.
45. Fardal O, Johannessen AC, Olsen I: Severe, rapidly progressing
peri-implantitis, J Clin Periodontol 26(5):313-317, 1999.
46. Albrektsson TO, Johansson CB, Sennerby L: Biological aspects
of implant dentistry: osseointegration, Periodontol 2000 4:58-73,
1994.
47. Tonetti MS, Schmid J: Pathogenesis of implant failures, Peri-
odontol 2000 4:127-138, 1994.
48. Mombelli A, Lang NP: The diagnosis and treatment of peri-
implantitis, Periodontol 2000 17:63-76, 1998.
49. Esposito M et al: Histopathologic observations on early oral
implant failures, Int J Oral Maxillofac Implants 14(6):798-810,
1999.
50. Salcetti JM et al: The clinical, microbial, and host response
characteristics of the failing implant, Int J Oral Maxillofac
Implants 12(1):32-42, 1997.
51. Heydenrijk K et al: Microbiota around root-form endosseous
implants: a review of the literature, Int J Oral Maxillofac Implants
17(6):829-838, 2002.
52. Roos-Jansåker AM, Renvert S, Egelberg J: Treatment of peri-
implant infections: a literature review, J Clin Periodontol
30(6):467-485, 2003.
Pharmacology for Implant Dentistry 401
53. Quirynen et al: Impact of supportive periodontal therapy and
implant surface roughness on implant outcome in patients with
a history of periodontitis, J Clin Periodontol 34(9):805-815, 2007.
54. Leonhardt A, Dahlén G, Renvert S: Five-year clinical, micro-
biological, and radiological outcome following treatment of
peri-implantitis in man, J Periodontol 74(10):1415-1422, 2003.
55. Rutar A et al: Retrospective assessment of clinical and micro-
biological factors affecting periimplant tissue conditions, Clin
Oral Implants Res 12(3):189-195, 2001.
56. Lang NP, Wilson TG, Corbet EF: Biological complications
with dental implants: their prevention, diagnosis and treat-
ment, Clin Oral Implants Res 11(suppl 1):146-155, 2000.
57. Lorenz K et al: Effect of two new chlorhexidine mouth rinses
on the development of dental plaque, gingivitis, and discolou-
ration. A randomized, investigator-blind, placebo-controlled,
3-week experimental gingivitis study, J Clin Periodontol
33(8):561-567, 2006.
58. Mombelli A, Lang NP: Antimicrobial treatment of peri-implant
infections, Clin Oral Implants Res 3(4):162-168, 1992.
59. Moeintaghavi A et al: Adjunctive effects of systemic amoxicil-
lin and metronidazole with scaling and root planing: a random-
ized, placebo controlled clinical trial, J Contemp Dent Pract
8(5):51-59, 2007.
60. Mombelli A: Microbiology and antimicrobial therapy of peri-
implantitis, Periodontol 2000 28:177-189, 2002.
61. Büchter A et al: Sustained release of doxycycline for the treat-
ment of peri-implantitis: randomised controlled trial, Br J Oral
Maxillofac Surg 42(5):439-444, 2004.
62. Sorsa T et al: Matrix metalloproteinases: contribution to patho-
genesis, diagnosis and treatment of periodontal inflammation,
Ann Med 38(5):306-321, 2006.
63. Emingil G et al: Effectiveness of adjunctive low-dose doxycy-
cline therapy on clinical parameters and gingival crevicular
fluid laminin-5 gamma2 chain levels in chronic periodontitis,
J Periodontol 75(10):1387-1396, 2004.
64. Mombelli A et al: Treatment of peri-implantitis by local deliv-
ery of tetracycline. Clinical, microbiological and radiological
results, Clin Oral Implants Res 12(4):287-294, 2001.
65. Oringer RJ et al: Effect of locally delivered minocycline micro-
spheres on markers of bone resorption, J Periodontol 73(8):835-
842, 2002.
66. Rutger Persson GE et al: Antimicrobial therapy using a local
drug delivery system (Arestin®) in the treatment of peri-
implantitis. I: microbiological outcomes, Clin Oral Implants Res
17:386-393, 2006.
67. Simon AM, O’Connor JP: Dose and time-dependent effects of
cyclooxygenase-2 inhibition of fracture-healing, J Bone Joint
Surg 89A(3):500-511, 2007.
68. Bouletreau PJ et al: Hypoxia and VEGF up-regulate BMP-2
mRNA and protein expression in microvascular endothelial
cells: implications for fracture healing, Plast Reconstr Surg
109:2384-2397, 2002.
69. Lennon DP, Edmison JM, Caplan AI: Cultivation of rat
marrow-derived mesenchymal stem cells in reduced oxygen
tension: effects on in vitro and in vivo osteochondrogenesis,
J Cell Physiol 87:345-355, 2001.
70. Probst A, Spiegel HU: Cellular mechanisms of bone repair,
J Invest Surg 10:77-86, 1997.
71. Einhorn TA et al: The expression of cytokine activity by frac-
ture callus, J Bone Miner Res 10:1272-1281, 1995.
72. Wang H et al: Thrombin peptide (TP508) promotes fracture
repair by up-regulating inflammatory mediators, early growth
factors, and increasing angiogenesis, J Orthop Res 23:671-679,
2005.
73. Gerber HP et al: VEGF couples hypertrophic cartilage remodel-
ing, ossification, and angiogenesis during endochondral bone
formation, Nat Med 5:623-628, 1999.
402 SECTION IV ■ Implant Surgery
74. Zelzer E et al: Skeletal defects in VEGF (120/120) mice reveal
multiple roles for VEGF in skeletogenesis, Development
129:1893-1904, 2002.
75. Maes C et al: Impaired angiogenesis and endochondral bone
formation in mice lacking the vascular endothelial growth
factor isoforms VEGF164 and VEGF188, Mech Dev 111:61-73,
2002.
76. Hausman MR, Schaffler MB, Majeska RJ: Prevention of frac-
ture healing in rats by an inhibitor of angiogenesis, Bone
29:560-564, 2001.
77. Street J et al: Vascular endothelial growth factor stimulates
bone repair by promoting angiogenesis and bone turnover, Proc
Natl Acad Sci USA 99:9656-9661, 2002.
78. Carter DR et al: Mechanobiology of skeletal regeneration, Clin
Orthop Relat Res 355(suppl 1):S41-S55, 1998.
79. Champagne CM et al: Macrophage cell lines produce osteoin-
ductive signals that include bone morphogenetic protein-2,
Bone 30:26-31, 2002.
80. Smith WL, DeWitt DL, Garavito RM: Cyclooxygenases: struc-
tural, cellular, and molecular biology, Annu Rev Biochem
69:145-182, 2000.
81. Vane JR, Bakhle YS, Botting RM: Cyclooxygenases 1 and 2,
Annu Rev Pharmacol Toxicol 38:97-120, 1998.
82. Simon LS: Role and regulation of cylooxygenase-2 during
inflammation, Am J Med 106:37S-42S, 1999.
83. Funk CD: Prostaglandins and leukotrienes: advances in eico-
sanoid biology, Science 294:1871-1875, 2001.
84. Dekel S, Lenthall G, Francis MJ: Release of prostaglandins from
bone and muscle after tibial fracture. An experimental study in
rabbits, J Bone Joint Surg Br 63:185-189, 1981.
85. Bo J, Sudmann E, Marton PF: Effect of indomethacin on
fracture healing in rats, Acta Orthop Scand 47:588-599,
1976.
86. Sudmann E et al: Inhibition of fracture healing by indometha-
cin in rats, Eur J Clin Invest 9:333-339, 1979.
87. Allen HL, Wase A, Bear WT: Indomethacin and aspirin: effect
of nonsteroidal anti-inflammatory agents on the rate of fracture
repair in the rat, Acta Orthop Scand 51:595-600, 1980.
88. Huo MH et al: The influence of ibuprofen on fracture repair:
biomechanical, biochemical, histological, and histomorpho-
metric parameters in rats, J Orthop Res 9:383-390, 1991.
89. Altman RD et al: Effect of nonsteroidal antiinflammatory drugs
on fracture healing: a laboratory study in rats, J Orthop Trauma
9:392-400, 1995.
90. Harder AT, An YH: The mechanism of the inhibitory effects
of nonsteroidal anti-inflammatory drugs on bone healing: a
concise review, J Clin Pharmacol 43(8):807-815, 2003.
91. Endo K et al: Cyclooxygenase-2 inhibitor delays fracture healing
in rats, Acta Orthop 76(4):470-474, 2005.
92. Aspenberg P: Postoperative Cox inhibitors and late prosthetic
loosening–suspicion increases! Acta Orthop 76(6):733-734,
2005.
93. Gerstenfeld LC et al: Selective and nonselective cyclooxygen-
ase-2 inhibitors and experimental fracture-healing. Reversibil-
ity of effects after short-term treatment, J Bone Joint Surg Am
89(1):114-125, 2007.
94. Bergenstock M: A comparison between the effects of acet-
aminophen and celecoxib on bone fracture healing in rats.
J Orthop Trauma 19(10):717-723, 2005.
95. Gregory LS, Forwood MR: Cyclooxygenase-2 inhibition delays
the attainment of peak woven bone formation following
four-point bending in the rat, Calcif Tissue Int 80(3):176-183,
2007.
96. Tiseo BC: Experimental study of the action of COX-2 selective
nonsteroidal anti-inflammatory drugs and traditional anti-
inflammatory drugs in bone regeneration, Clinics 61(3):223-
320, 2006.
97. Yazdi M et al: Effects of non-steroidal anti-inflammatory drugs
on demineralized bone-induced bone formation, J Periodont Res
27(1):28-33, 1992.
98. Halpin RA et al: The absorption, distribution, metabolism and
excretion of rofecoxib, a potent and selective cyclooxygenase-2
inhibitor, in rats and dogs, Drug Metab Dispos 28(10):1244-
1254, 2000.
99. Paulson SK et al: Pharmacokinetics, tissue distribution, metab-
olism, and excretion of celecoxib in rats, Drug Metab Dispos
28(5):514-521, 2000.
100. Simon AM, Manigrasso MB, O’Connor JP: Cyclo-oxygenase 2
function is essential for bone fracture healing, J Bone Miner Res
17(6):963-976, 2002.
101. Giannoudis PV et al: Nonunion of the femoral diaphysis. The
influence of reaming and non-steroidal anti-inflammatory
drugs, J Bone Joint Surg Br 82(5):655-658, 2000.
102. Burd TA, Hughes MS, Anglen JO: Heterotopic ossification
prophylaxis with indomethacin increases the risk of long-bone
nonunion, J Bone Joint Surg Br 85(5):700-705, 2003.
103. Chikazu D et al: Cyclooxygenase-2 activity is essential for the
osseointegration of dental implants, Int J Oral Maxillofac Surg
36(5):441-446, 2007.
104. Allen HL, Wase A, Bear WT: Indomethacin and aspirin:
effect of nonsteroidal anti-inflammatory agents on the rate of
fracture repair in the rat, Acta Orthop Scand 51(4):595-600,
1980.
105. Li XJ, Jee WS, Li YL: Flurbiprofen enhances growth and cancel-
lous and cortical bone accumulation in rapidly growing long
bones, Bone 10(1):35-44, 1989.
106. Wechter WJ et al: Chiral pharmacokinetics of Rac-flurbiprofen
and pharmacodynamics of anabolic bone response in the normal
rat, Chirality 6(6):457-459, 1994.
107. Reddy MS, Jeffcoat MK, Richardson RC: Assessment of adjunc-
tive flurbiprofen therapy in root-form implant healing with
digital subtraction radiography, J Oral Implantol 16(4):272-276,
1990.
108. Jeffcoat MK et al: The effect of systemic flurbiprofen on bone
supporting dental implants, J Am Dent Assoc 126(3):305-311,
1995.
109. Bergenstock M et al: Comparison between the effects of acet-
aminophen and celecoxib on bone fracture healing in rats,
J Orthop Trauma 19(10):717-723, 2005.
110. Chandrasekharan NV et al: COX-3, a cyclooxygenase-1 variant
inhibited by acetaminophen and other analgesic/antipyretic
drugs: cloning, structure, and expression, Proc Natl Acad Sci
USA 99:13926-13931, 2002.
111. Ayoub SS et al: Acetaminophen-induced hypothermia in
mice is mediated by a prostaglandin endoperoxide synthase 1
gene-derived protein, Proc Natl Acad Sci USA 101:11165-
11169, 2004.
112. Kis B et al: Putative cyclooxygenase-3 expression in rat brain
cells, J Cereb Blood Flow Metab 23:1287-1292, 2003.
113. Shaftel SS et al: COX-3: a splice variant of cyclooxygenase-1
in mouse neural tissue and cells, Brain Res Mol Brain Res
119:213-215, 2003.
114. Kis B et al: Regional distribution of cyclooxygenase-3 mRNA
in the rat central nervous system, Brain Res Mol Brain Res
126:78-80, 2004.
115. Dahners LE, Mullis BH: Effects of nonsteroidal anti-inflamma-
tory drugs on bone formation and soft-tissue healing, J Am Acad
Orthop Surg 12(3):139-143, 2004.
116. Cox M et al: Matrix metabolism and cell proliferation in
tendon: the effects of NSAIDs on tendon repair, Trans Orthop
Res Soc 24:67, 1999.
117. Vogel HG: Mechanical and chemical properties of various con-
nective tissue organs in rats as influenced by nonsteroidal anti-
rheumatic drugs, Connect Tissue Res 5:91-95, 1977.
 CHAPTER 23 •
118. Moorman CT III et al: The early effect of ibuprofen on the
mechanical properties of healing medial collateral ligament,
Am J Sports Med 27:738-741, 1999.
119. Dahners LE et al: The effect of a nonsteroidal antiinflammatory
drug on the healing of ligaments, Am J Sports Med 16:641-646,
1988.
120. Almekinders LC, Gilbert JA: Healing of experimental muscle
strains and the effects of nonsteroidal antiinflammatory medi-
cation, Am J Sports Med 14:303-308, 1986.
121. Tayyar M, Basbug M: The effects of intraperitoneal piroxicam
and low molecular weight heparin in prevention of adhesion
reformation in rat uterine horn, Res Exp Med (Berl) 198:269-
275, 1999.
122. Li C, Wunder J, Alman BA: Cyclooxygenase-two regulates
proliferation in aggressive fibromatosis (desmoid tumor), Trans
Orthop Res Soc 24:419, 1999.
123. Mattout P, Mattout C: Conditions for success in guided bone
regeneration: retrospective study on 376 implant sites, J Peri-
odontol 71(12):1904-1909, 2000.
124. Camargo PM et al: Platelet-rich plasma and bovine porous
bone mineral combined with guided tissue regeneration in the
treatment of intrabony defects in humans, J Periodont Res
37(4):300-306, 2002.
125. Alderson MR: CD40 expression by human monocytes: regula-
tion by cytokines and activation of monocytes by the ligand for
CD40. J Exp Med 178(2):669-674, 1993.
126. Sedlmayr P: Platelets contain interleukin-1 alpha and beta
which are detectable on the cell surface after activation, Scand
J Immunol 42(2):209-214, 1995.
127. Evans DB, Bunning RA, Russell RG: The effects of recombi-
nant human interleukin-1 beta on cellular proliferation and the
production of prostaglandin E2, plasminogen activator, osteo-
calcin and alkaline phosphatase by osteoblast-like cells derived
from human bone, Biochem Biophys Res Commun 166(1):208-
216, 1990.
128. Linkhart TA, MacCharles DC: Interleukin-1 stimulates release
of insulin-like growth factor-I from neonatal mouse calvaria by
a prostaglandin synthesis-dependent mechanism, Endocrinology
131(5):2297-2305, 1992.
129. Dinarello CA: Biology of interleukin 1, Faseb J 2:108-115,
1988.
130. Sato K et al: Parathyroid hormone related protein and inter-
leukin-lcr synergistically stimulate bone resorption in vitro and
increase the serum calcium concentration in mice in vivo,
Endocrinology 124:2172-2178, 1989.
131. Evans DB, Bunning RAD, Russell RG: The effects of
recombinant interleukin-l beta on cellular proliferation and the
production of prostaglandin E2, plasminogen activator, osteo-
calcin, and alkaline phosphatase by osteoblast-like cells derived
from human bone, Biochem Biophys Res Commun 166:208-216,
1992.
132. Ikeda E et al: Effect of interleukin lp on osteoblastic clone
MC3T3- El cells, Calcif Tissue Int 43:162-166, 1988.
133. Boyce BF et al: Effects of interleukin-1 on bone turnover in
normal mice, Endocrinology 125:1142-1150, 1989.
134. Aspenberg P: Postoperative Cox inhibitors and late prosthetic
loosening–suspicion increases! Acta Orthop 76(6):733-734,
2005.
135. Persson PE, Nilsson OS, Berggren AM: Do non-steroidal anti-
inflammatory drugs cause endoprosthetic loosening? A 10-year
follow-up of a randomized trial on ibuprofen for prevention of
heterotopic ossification after hip arthroplasty, Acta Orthop
76(6):735-740, 2005.
136. MacLennan AH: HRT: a reappraisal of the risks and benefits,
Med J Aust 186(12):643-646, 2007.
137. Fleisch H: Development of bisphosphonates, Breast Cancer Res
4(1):30-34, 2002.
Pharmacology for Implant Dentistry 403
138. Frith J et al: Clodronate and liposome-encapsulated clodronate
are metabolized to a toxic ATP analog, adenosine 5’-
(beta, gamma-dichloromethylene) triphosphate, by mamma-
lian cells in vitro, J Bone Miner Res 12(9):1358-1367,
1997.
139. van Beek E et al: Differentiating the mechanisms of antiresorp-
tive action of nitrogen containing bisphosphonates, Bone
33(5):805-811, 2003.
140. van Beek E et al: The role of geranylgeranylation in bone
resorption and its suppression by bisphosphonates in fetal bone
explants in vitro: a clue to the mechanism of action of nitrogen-
containing bisphosphonates, J Bone Miner Res 14(5):722-729,
1999.
141. Woo S, Hellstein J, Kalmar J: Narrative [corrected] review:
bisphosphonates and osteonecrosis of the jaws, Ann Intern Med
144(10):753-761, 2006.
142. Dello Russo NM et al: Osteonecrosis in the jaws of patients
who are using oral bisphosphonates to treat osteoporosis, Int J
Oral Maxillofac Implants 22(1):146-153, 2007.
143. Dunstan CR et al: Therapy insight: the risks and benefits of
bisphosphonates for the treatment of tumor-induced bone
disease, Nat Clin Pract Oncol 4(1):42-55, 2007.
144. Marx RE: Pamidronate and zoledronate induced avascular
necrosis of the jaws: a growing epidemic, J Oral Maxillofac Surg
61:1115-1117, 2003.
145. Wang J, Goodger NM, Pogrel MA: Osteonecrosis of the jaws
associated with cancer chemotherapy, J Oral Maxillofac Surg
61:1104-1107, 2003.
146. Yarom N et al: Osteonecrosis of the jaw induced by orally
administered bisphosphonates: incidence, clinical features, pre-
disposing factors and treatment outcome, Osteoporos Int
18:1363-1370, 2007.
147. Hasmin M et al: Zolendronate inhibits endothelial cell adhe-
sion, migration and survival through the suppression of multi-
ple, prenylation-dependent signaling pathways, J Thromb
Haemost 5(1):166-173, 2007.
148. Hasmim M, Bieler G, Ruegg C: Zoledronate inhibits endothe-
lial cell adhesion, migration and survival through the suppres-
sion of multiple, prenylation-dependent signaling pathways,
J Thromb Haemost 5(1):166-173, 2007.
149. Adornato MC, Morcos I, Rozanski J: The treatment of bisphos-
phonate-associated osteonecrosis of the jaws with bone resec-
tion and autologous platelet-derived growth factors, J Am Dent
Assoc 138(7):971-977, 2007.
150. Szeto CC, Chow KM: Nephrotoxicity related to new therapeu-
tic compounds, Renal Failure 27(3):329-333, 2005.
151. Cummings SR, Schwartz AV, Black DM: Alendronate
and atrial fibrillation, N Engl J Med 356(18):1895-1896,
2007.
152. Odvina CV et al: Severely suppressed bone turnover: a poten-
tial complication of alendronate therapy, J Clin Endocrinol
Metab 90:1294, 2005.
153. Gertz BJ et al: Studies on the oral bioavailability of alendro-
nate, Clin Pharmacol Ther 58:288-298, 1995.
154. Mitchell DY et al: Risedronate gastrointestinal absorption is
independent of site and rate of administration, Pharm Res
15:228-232, 1998.
155. Lin JH: Bisphosphonates: a review of their pharmacokinetic
properties, Bone 18:75-85, 1996.
156. Im GI et al: Osteoblast proliferation and maturation by bisphos-
phonates, Biomaterials 25:4105, 2004.
157. Green J, Clezardin P: Mechanisms of bisphosphonate effects on
osteoclasts, tumor cell growth, and metastasis, Am J Clin Oncol
25(suppl 1):S3, 2002.
158. Black DM et al: Randomized trial of effect of alendronate on
risk of fracture in women existing vetebral fractures, Lancet
348:1535-1541, 1996.
404 SECTION IV ■ Implant Surgery
159. Cummings SR et al: Effect of alendronate on risk of fracture in
women with low bone density but without vertebral fractures,
JAMA 280:2077-2082, 1998.
160. Bonnick S et al: Treatment with alendronate plus calcium,
alendronate alone, or calcium alone for postmenopausal
low bone mineral density, Curr Med Res Opin 23(6):1341-1349,
2007.
161. Nishizawa Y et al: Guidelines for the use of biochemical markers
of bone turnover in osteoporosis (2004), J Bone Miner Metab
23(2):97-104, 2005.
162. Weinstein RS: True strength, J Bone Miner Res 15:621-625,
2000.
163. Chesnut CH III, Rosen CJ for the Bone Quality Discussion
Group: Reconsidering the effects of antiresorptive therapies in
reducing osteoporotic fracture, J Bone Miner Res 16:2163-2172,
2001.
164. Briesacher BA et al: Consequences of poor compliance with
bisphosphonates, Bone 41(5):882-887, 2007.
165. Shea B et al: Calcium supplementation on bone loss in post-
menopausal women, Cochrane Data Base Syst Rev 2004(1):
CD004526.
166. Mitchell DY et al: Risedronate gastrointestinal absorption is
independent of site and rate of administration, Pharm Res
15:228-232, 1998.
167. Nishizawa Y et al: Guidelines for the use of biochemical markers
of bone turnover in osteoporosis (2004), J Bone Miner Metab
23(2):97-104, 2005.
168. Sahota O et al: Vitamin D insufficiency and the blunted PTH
response in established osteoporosis: the role of magnesium
deficiency, Osteoporos Int 17(7):1013-1021, 2006.
169. Neives JW: Osteoporosis: the role of micronutrients, Am J Clin
Nutr 81(5):1232S-1239S, 2005.
170. Ste-Marie LG et al: Effect of teriparatide [rhPTH(1-34)] on
BMD when given to postmenopausal women receiving hor-
monal replacement therapy, J Bone Miner Res 21(2):283-291,
2006.
171. Greenspan Sl et al: Treatment of osteoporosis with parathyroid
hormone study group, Ann Intern Med 146(5):326-339, 2007.
172. Knapen MHJ, Schurgers LJ, Vermeer C: Vitamin K2 supple-
mentation improves hip bone geometry and bone strength
indices in postmenopausal women, Osteoporos Int 2007
18(7):963-972, 2007.
173. Stroup JS et al: Two-year changes in bone mineral density and
T scores in patients treated at a pharmacist-run teriparatide
clinic, Pharmacotherapy 27(6):779-788, 2007.
174. Kroll MH: Parathyroid hormone temporal effects on bone
formation and resorption, Bull Math Biol 62(1):163-188,
2000.
175. Witt-Enderby PA et al: Therapeutic treatments potentially
mediated by melatonin receptors: potential clinical uses in the
prevention of osteoporosis, cancer and as an adjuvant therapy,
J Pineal Res 41(4):297-305, 2006.
176. Herxheimer A, Petrie KJ: Melatonin for the prevention and
treatment of jet lag, Cochrane Database Syst Rev (2):CD001520,
2002.
177. Agnusdei D, Gentilella R: GH and IGF-I as therapeutic agents
for osteoporosis, J Endocrinol Invest 28(suppl 8):32-36, 2005.
178. Braam LA et al: Vitamin K1 supplementation retards bone loss
in postmenopausal women between 50 and 60 years of age,
Calcif Tissue Int 73(1):21-26, 2003.
179. Schurgers LJ, Vermeer C: Determination of phylloquinone and
menaquinones in food: effect of food matrix on circulating
vitamin K concentrations, Haemostas 30:298-307, 2000.
180. Knapen MH, Schurgers LJ, Vermeer C: Vitamin K2 supple-
mentation improves hip bone geometry and bone strength
indices in postmenopausal women, Osteoporos Int (7):963-972,
2007.
181. Dhonukshe-Rutten RA et al: Vitamin B-12 status is associated
with bone mineral content and bone mineral density in frail
elderly women but not in men, J Nutr 133(3):801-807, 2003.
182. Kitchin B, Morgan SL: Not just calcium and vitamin D: other
nutritional considerations in osteoporosis, Curr Rheumatol Rep
9(1):85-92, 2007.
183. Bachmann GA et al: Lowest effective transdermal 17β-
estradiol dose for relief of hot flushes in postmenopausal women:
a randomized controlled trial, Obstet Gynecol 110(4):771-779,
2007.
184. Huang AJ et al: Endogenous estrogen levels and the effects of
ultra low-dose transdermal estradiol therapy on bone turnover
and bone density in postmenopausal women, J Bone Miner Res
22(11):1791-1797, 2007.
185. Grady D et al: Effect of ultra-low-dose transdermal estradiol on
breast density in postmenopausal women, Menopause 14(3 pt
1):391-396, 2007.
186. Yaffe K et al: Effects of ultra-low-dose transdermal estradiol on
cognition and health-related quality of life, Arch Neurol
63(7):945-950, 2006.
187. Prestwood KM et al: Ultralow-dose micronized 17 beta-estra-
diol and bone density and bone metabolism in older women: a
randomized controlled trial, JAMA 290(8):1042-1048, 2003.
188. Rossouw JE et al: Risks and benefits of estrogen plus progestin
in healthy postmenopausal women: principal results from the
Women’s Health Initiative randomized controlled trial, JAMA
288(3):321-333, 2002.
189. Mueck AO, Seeger H: Smoking, estradiol metabolism and
hormone replacement therapy, Curr Med Chem Cardiovasc
Hematol Agents 3(1):45-54, 2005.
190. Harman SM, Brinton EA, Clarkson T: Is the WHI relevant to
HRT started in the premenopause? Endocrine 24:195-202,
2004.
191. MacLennan AH: HRT: a reappraisal of the risks and benefits,
Med J Aust 186(12):643-646, 2007.
192. Richman S et al: Low-dose estrogen therapy for prevention of
osteoporosis: working our way back to monotherapy, Menopause
13(1):148-155, 2006.
193. BA Watkins et al: Bioactive fatty acid: role in bone biology and
bone cell function, Prog Lipid Res 40:125-148, 2001.
194. Lands WE et al: Maintenance of lower proportions of (n-6)
eicosanoid precursors in phospholipids of human plasma in
response to added dietary (n-3) fatty acids, Biochem Biophys
Acta 1180(2):147-162, 1992.
195. Watkins BA et al: Dietary ratio of (n-6)/(n-3) polyunsaturated
fatty acids alters the fatty acid composition of bone compart-
ments and biomarkers of bone formation in rats, J Nutr
130(9):2274-2284, 2000.
196. Choudhary S et al: Strontium ranelate promotes osteoblastic
differentiation and mineralization of murine bone marrow
stromal cells: involvement of prostaglandins, J Bone Miner Res
22(7):1002-1010, 2007.
197. Lands WE: Biochemistry and physiology of n-3 fatty acids,
Faseb J 6(8):2530-2536, 1992.
198. Klein-Nulend J, Pilbeam CC, Raisz LG: Effect of 1,25-
dihydroxyvitamin D3 on prostaglandin E2 production in cul-
tured mouse parietal bones, J Bone Miner Res 6(12):1339-1344,
1991.
199. Watkins BA et al: Dietary (n-3) and (n-6) polyunsaturates and
acetylsalicylic acid alter ex vivo PGE2 biosynthesis, tissue IGF-
I levels, and bone morphometry in chicks, J Bone Miner Res
11(9):1321-1332, 1996.
200. Watkins BA et al: Dietary lipids modulate bone prostaglandin
E2 production, insulin-like growth factor-I concentration and
formation rate in chicks, J Nutr (6):1084-1091, 1997.
201. Suzawa T et al: The role of prostaglandin E receptor subtypes
(EP1, EP2, EP3, and EP4) in bone resorption: an analysis using
 CHAPTER 23 •
specific agonists for the respective EPs, Endocrinology
141(4):1554-1559, 2000.
202. Gunnes M, Lehmann EH et al: Dietary calcium, saturated fat,
fiber and vitamin C as predictors of forearm cortical and tra-
becular bone mineral density in healthy children and adoles-
cents, Acta Paediatr 84(4):388-392, 1995.
203. Raisz LG, Koolemans-Beyen AR: Inhibition of bone collagen
synthesis by prostaglandin E2 in organ culture, Prostaglandins
8(5):377-385, 1974.
204. Norrdin RW, Jee WS, High WB: The role of prostaglandins in
bone in vivo, Prostaglandins Leukot Essent Fatty Acids 41(3):139-
149, 1990.
205. Watkins BA, Seifert MF: Conjugated linoleic acid on bone
biology, J Am Coll Nutr 19(4):478S-486S, 2000.
206. Griel AE et al: An increase in dietary n-3 fatty acids
decreases a marker of bone resorption in humans, Nutr J 6:2,
2007.
Pharmacology for Implant Dentistry 405
207. Heaney RP, Carey R, Harkness L: Roles of vitamin D, n-3
polyunsaturated fatty acid, and soy isoflavones in bone health,
J Am Diet Assoc 105(11):1700-1702, 2005.
208. Ren W, Dziak R: Effects of leukotrienes on osteoblastic cell
proliferation, Calcif Tissue Int 49(3):197-201, 1991.
209. Gallwitz WE et al: 5-Lipoxygenase metabolites of arachidonic
acid stimulate isolated osteoclasts to resorb calcified matrices,
J Biol Chem 268(14):10087-10094, 1993.
210. Garcia C et al: Leukotriene B4 stimulates osteoclastic bone
resorption both in vitro and in vivo, J Bone Miner Res
11(11):1619-1627, 1996.
211. Garcia C et al: Effects of synthetic peptido-leukotrienes
on bone resorption in vitro, J Bone Miner Res 11(4):521-529,
1996.
212. Meghji S et al: Stimulation of bone resorption by lipoxygenase
metabolites of arachidonic acid, Prostaglandins 36(2):139-149,
1988.
CHAPTER 24
AUTOGENOUS BONE GRAFTING FOR
DENTAL IMPLANTS
Craig M. Misch
In many ways, autogenous bone grafts continue to remain the
gold standard for repair of jaw atrophy and bone defects.
Autogenous bone grafting is a well-documented procedure for
reconstruction of the atrophic maxilla and mandible for reha-
bilitation with implant prostheses. Advancements in biologic
engineering will produce alternatives to autogenous bone that
may very well exceed existing clinical outcomes and replace
traditional indications for its use.1 However, the increased
costs of technology can be an obstacle to routine use of new
products. Autogenous bone grafting offers a well-proven, pre-
dictable method for ridge augmentation and defect repair for
dental implant placement.
The use of autogenous bone with dental implants was origi-
nally discussed by Branemark et al.2 Early studies focused on
the use of iliac bone grafts in the treatment of the atrophic,
edentulous maxilla and mandible.3 Although the iliac crest is
most often used for major jaw reconstruction, it has the dis-
advantages of the need for hospitalization, general anesthesia,
and alteration of ambulation. Additional donor sites have
been evaluated, including the calvarium, proximal tibia, and
maxillofacial regions. Autogenous bone can be used in several
forms, including cancellous marrow, particulate bone chips,
or cortical and corticocancellous blocks. The timing of graft
placement and implant insertion has been well researched.
The preferred approach in most cases today is delayed implant
placement into the healed bone graft. Earlier studies of
machined screw type of implants often found lower survival
rates in grafted bone.3 The use of implants with enhanced
surface features has improved outcomes in regenerated bone,
with success rates comparable with those in native bone.
■ BONE BIOLOGY
Autogenous bone is the only graft material with osteogenic
properties that can directly form bone. Bone cells, in higher
concentration in the cancellous marrow, surviving the trans-
plantation produce new bone. In addition, bone morphoge-
netic proteins and growth factors are present within the
autograft that induce bone formation in the surrounding
tissues.4 Osteocompetent mesenchymal cells are transformed
into osteoblasts through osteoinduction. The cortical portion
of the autogenous bone graft acts as an osteoconductive scaffold
for bone formation.5 The graft is remodeled and replaced with
new bone over time (creeping substitution) (Figure 24-1). Free
autogenous bone grafts must become revascularized to incorpo-
rate into the recipient bed. The cancellous portion of the graft
406
revascularizes faster than the cortex.6 The denser cortical bone
revascularizes through its existing haversian system.6
The subject of embryologic origin of autologous bone grafts
has received much attention regarding graft incorporation and
resorption. Membranous bone grafts, from the mandible or
calvarium, have been found to reveal less resorption than
grafts from endochondral sites, such as the iliac crest.7,8,9,10
Most studies examining the influence of graft origin on resorp-
tion refer to onlay augmentation with block bone grafts. It is
important to make a distinction between the graft morphology
(particulate, block) and whether the graft is used for onlay or
interpositional placement. Interpositional bone grafts typi-
cally resorb less bone than is used for onlay augmentation.
Sinus floor augmentations are more comparable with interpo-
sitional rather than onlay bone grafts, and therefore less
resorption would be expected. More recent studies examining
graft loss have challenged the hypothesis of embryologic origin
and emphasize the microarchitecture of the bone used for
grafting.5,11 Ozaki and Buchman11 found that regardless of
their embryologic origin, cortical bone grafts reveal less
volume loss than cancellous bone grafts. Cortical bone grafts
from the mandible exhibit minimal resorption and maintain
their dense quality, making them ideal for onlay augmentation
before implant placement12 (Figures 24-2, 24-3).
Following harvest, the bone graft should immediately be
stored in sterile saline to maintain cellular vitality, and
minimal time should elapse between graft procurement and
placement.13 However, the number of viable cells contained
in mandibular cortical grafts is probably insignificant in new
bone formation. If block grafts or trephine cores are milled
into particulate bone, the particle size should not be too fine.
Some burs or mills pulverize the bone graft into a powder or
paste. Whereas bone powder is quickly resorbed, slightly larger
particles are more osteoconductive and act as a better scaffold
for bone formation.14,15,16 The other potential disadvantages of
bone powder collected by a suction trap include the negative
effects of heat generated in bone preparation and desiccation
of the particles. Bone scrapers produce ribbonlike shavings
that have a favorable three-dimensional morphology for revas-
cularization and graft incorporation17 (Figure 24-4).
The addition of supplemental autologous growth factors,
such as platelet-rich plasma, has been reported to enhance and
accelerate the incorporation of autologous cancellous bone
grafts.18 In addition, platelet-rich plasma may be useful as a
matrix for soft tissue repair, adhesive of bone graft particles,
 CHAPTER 24 • Autogenous Bone Grafting for Dental Implants 407

FIGURE 24-1. Histologic view of cortical bone graft after 4 months of

healing. The new bone (deeper red) is growing within the old haversian
system. FIGURE 24-4. Electron microscopic view of bone shaving harvested with
a bone-scraping device. (Courtesy of Maxilon Laboratories)

FIGURE 24-2. Cortical onlay bone graft used to reconstruct the atrophic FIGURE 24-5. Platelet-rich plasma added to autogenous cancellous
posterior mandible. bone graft.

and for improving surgical hemostasis (Figure 24-5). Adding

a prepared concentrate of the patient’s platelets to the bone
grafted site can also enhance and accelerate soft tissue wound
healing. The various cytokines and mediators found in the
alpha granules of the platelets promote angiogenesis and col-
lagen synthesis.19 This may diminish the risk of wound dehis-
cence and bone graft exposure to the oral cavity.

■ PREOPERATIVE EVALUATION
A comprehensive evaluation of the graft recipient site is nec-
essary for planning of the bone graft surgery. Panoramic and
periapical radiographs are used to evaluate the bone defect,
surrounding dentition, and regional anatomy. Computed
tomography (CT) is useful for three-dimensional views of the
FIGURE 24-3. Incorporation of the cortical graft after 4 months of
bone deficiency and can also be used to assess intraoral donor
healing. Minimal graft resorption is noted.
sites. Implant planning software can be used with the scan
to more precisely evaluate the reconstructive needs of the
patient20 (Figure 24-6). A stereolithographic model of the jaw
can be generated from the scan to further plan the case21
(Figure 24-7). Mounted study casts and diagnostic waxing
408 SECTION IV ■ Implant Surgery
FIGURE 24-6. Implant planning software used with a CT scan to deter-
mine graft requirements for ideal implant placement.
FIGURE 24-7. Stereolithographic model of the maxillary bone defect
fabricated from the CT scan.
allow the clinician to better appreciate the ridge morphology
in relationship to planned prosthetic outcome (Figure 24-8).
They also may be used for the fabrication of a radiographic
template worn during the CT scan.22 The template reveals the
radiopaque outline of the prosthetic tooth position in the
tomographic view of the residual ridge. This allows a determi-
nation of graft size requirements and donor site options. A
template of the planned prosthetic tooth position is also
helpful for use during graft surgery to confirm graft positioning
and fulfillment of the grafting requirements.
Treatment of the anterior maxilla requires an aesthetic
zone evaluation. This includes determination of the high lip
line and need for lip support. A diagnostic wax up will help
determine tooth length and need for vertical augmentation to
develop the correct tooth size. An emphasis must be placed
on creating adequate osseous volume for implant placement
and providing a proper soft tissue profile for the implant
restoration.
The soft tissue character should be assessed, including
quantity of keratinized tissue, thickness of the mucosa, muscle
FIGURE 24-8. Diagnostic waxing of the reconstructed alveolar defect
and prosthetic tooth replacement.
FIGURE 24-9. Lack of keratinized gingiva and high muscle attachment
in the atrophic posterior mandible.
attachments, and the presence of scar tissue. It is often better
to correct soft tissue problems before bone grafting. The lack
of keratinized tissue in a region is best treated with autogenous
free gingival grafting (Figures 24-9, 24-10, 24-11). Areas of
thin alveolar mucosa can be enhanced with the interposi-
tional placement of allogeneic dermis or connective tissue
grafts. The removal of scar tissue improves blood supply to the
area and helps improve the mobility of the soft tissue flap over
the bone graft. The removal of a frenum or high muscle
attachments in the recipient site will reduce tension on the
incision line. Soft tissue corrective surgery should be per-
formed at least 8 weeks before bone graft surgery to allow
incorporation of any grafts and reestablishment of vascularity
to the area.
The periodontal health and endodontic status of teeth
adjacent to the graft recipient site should be evaluated before
grafting. It may be prudent to extract hopeless teeth before
grafting, especially if infection is present. The marginal bone
height on the teeth bordering the bone defect determines the
level that may be achieved with vertical bone augmentation.
It may be necessary to extract stable teeth if they have bone
loss that limits the augmentation requirements.
 CHAPTER 24 •
FIGURE 24-10. Free gingival graft from the hard palate.
FIGURE 24-11. Incorporation of the gingival graft after 2 months of
healing.
■ PATIENT PREPARATION
Patients undergoing autogenous bone grafting require anti-
biotic prophylaxis. The antibiotic of choice for most cases is
amoxicillin. For patients allergic to amoxicillin, either a ceph-
alosporin or clindamycin may be considered. Antibiotics
should be administered before surgery to obtain proper blood
levels and continued for 1 week. The use of short-term gluco-
corticoids can diminish postoperative facial swelling, local flap
edema, and discomfort. Narcotic analgesics are prescribed for
use during the immediate postoperative course. Thereafter,
the patient may transition into the use of nonsteroidal anti-
inflammatory medications. Some studies have found bacterial
contamination of orally harvested bone grafts, especially when
suction traps are used to collect drilled bone debris.23 Chlorhex-
idine rinsing before surgery has been shown to significantly
reduce this problem. Preoperative antisialagogue agents, such
as glycopyrrolate, are also useful to decrease salivary flow,
which may carry bacteria into the graft site. Aseptic surgical
technique should be maintained because these reconstructive
procedures are more involved and may often require more
operative time. Most cases involving autogenous bone grafting
in the office are performed under intravenous anesthesia.
Autogenous Bone Grafting for Dental Implants 409
FIGURE 24-12. A chisel is used to harvest tuberosity bone.
Shorter, less involved graft procedures may be treated using
oral sedation techniques.
■ BONE GRAFT DONOR SITES
MAXILLARY TUBEROSITY
Although the maxillary tuberosity offers a smaller amount of
bone than other donor sites, the softer consistency of the graft
is often favorable for filling bone defects.24 The bone in the
tuberosity area is porous, and the outer cortical layer is thin.
Because the tuberosity is in the same surgical field when per-
forming a lateral approach to sinus grafting, it should be rou-
tinely considered for bone harvest.25 The amount of bone that
may be obtained can be deceiving because the mucosa over
the tuberosity is usually much thicker. A periapical or pan-
oramic radiograph can be used to better assess the underlying
bone. CT of the maxillary sinus region can allow three-
dimensional quantification of the area. The anatomic limita-
tions of tuberosity bone harvest include the maxillary sinus,
pterygoid plates, molar teeth, and the greater palatine canal.
To gain access to the area for bone harvest, an incision is made
along the ridge crest over the tuberosity. A vertical releasing
incision is made along the lateral aspect of the posterior
maxilla. Mucoperiosteal reflection exposes the tuberosity,
ridge crest, and lateral maxilla. The palatal tissue should also
be elevated to reveal the entire width of the tuberosity. The
graft may be harvested with a chisel or rongeurs (Figures 24-
12, 24-13). The chisel edge should be kept slightly superficial
to the maxilla to shave off pieces of tuberosity bone and
prevent inadvertent sinus communication.26 A chisel can also
be used along the posterior lateral maxilla to obtain a thin
piece of cortical bone, used to cover the window following
grafting of the sinus floor.
MANDIBULAR SYMPHYSIS
The symphysis of the mandible has been used extensively for
sinus and onlay bone grafting.* Techniques to harvest block
*References 12, 27, 28, 29, 30, 31
410 SECTION IV ■ Implant Surgery

FIGURE 24-13. The particulate tuberosity bone is used to graft the sinus FIGURE 24-14. An oscillating saw is used to perform the osteotomies in
floor. the symphysis for graft harvest.

or particulate bone grafts from the anterior mandible have

been reported. The symphysis donor site offers the greatest
volume of intraoral bone. The average interforaminal distance
is approximately 5.0 cm, and the depth of the anterior man-
dible usually exceeds 1.0 cm.32 A CT scan or panoramic radio-
graph is used to evaluate the available bone in this donor site.
A lateral cephalometric radiograph can be useful to determine
the anteroposterior dimension of the anterior mandible. Peri-
apical radiographs give a more accurate measurement of the
tooth root lengths.
The ease of surgical access is one of the main advantages
of the symphysis region. Bilateral mandibular blocks and local
infiltration in the anterior mandible are administered using
2% lidocaine, 1 : 100,000 epinephrine. Exposure of the sym-
physis may be obtained through a sulcular or vestibular inci-
FIGURE 24-15. The unicortical osteotomies form a rectangular outline
sion. The vestibular incision is made in the mucosa between in the symphysis.
the cuspid teeth, approximately 1 cm from the mucogingival
junction. Limiting the distal extent of the incision will reduce
the risk of mental nerve injury. A vestibular approach allows removed with a chisel. A unibeveled chisel is tapped along
easy access, but produces more soft tissue bleeding and possible the osteotomies, with the exception of the inferior border,
intraoral scar formation. The sulcular approach should not be to fracture the block from its base (Figure 24-16). The block
used when mucogingival defects are present and may result in bone graft may also be harvested in segments by sectioning
gingival recession. The sulcular incision should extend to the the rectangular piece in the midline. Two bone blocks are
premolar regions bilaterally. A mucoperiosteal flap is reflected often easier to harvest because the second block can be frac-
to expose the mental foramina and the inferior border of tured from its lingual base with the chisel. Some additional
the mandible (pogonion). Additional local anesthesia is cancellous bone may be procured with a curette, chisel,
often needed at the base of the mandible to block cervical rongeur, or trephine after the block is removed, but the volume
innervation. is meager.32 Following the removal of the block graft, hemo-
After the symphysis region is exposed, the osteotomies for static materials, such as collagen or gelatin, may be placed
graft harvest are planned. The dimensions of the graft are over the cancellous bone. When larger bone grafts are har-
determined by the bone volume necessary to reconstruct the vested, the donor site should be filled with a bone substitute,
recipient site. Osteotomies should be kept at least 5 mm from such as resorbable hydroxyapatite, to maintain facial contour.12
the root apices and the mental foramina.12,33,34 In most cases, Smaller or particulate bone grafts may be procured using tre-
the inferior and lingual cortices of the mandible are left intact. phine burs, bone collection traps, or bone-scraping instru-
The facial cortex is thick, and the underlying cancellous bone ments.17,35,36 Closure of the donor site is typically performed
is usually dense. The osteotomies may be made with a carbide after the graft is inserted into the recipient site. This mini-
fissure bur (#557 or 701) in a surgical hand piece or sagittal mizes the time between graft harvest and placement. The
saw (Figures 24-14, 24-15). Following an osteotomy through mucosa superior to the vestibular incision is reflected to reduce
the outer cortex and into the cancellous bone, the graft is tension on the flaps from edema and lip movement. The
 CHAPTER 24 • Autogenous Bone Grafting for Dental Implants 411

FIGURE 24-16. A unibevel chisel is used to fracture the block bone graft FIGURE 24-17. Preoperative view of a severe vertical maxillary defect.
from its cancellous base.

vestibular incision is closed in layers using resorbable sutures.

The deeper layers may be sutured with 4-0 Vicryl, and the
superficial mucosa can be closed primarily with 4-0 chromic
gut. Postoperative pressure dressings are used over the chin to
reduce edema, hematoma formation, and incision line
opening.
The mandibular symphysis is associated with a higher inci-
dence of postoperative complications than other maxillofacial
donor sites.30,37,38,39 Altered sensation of the lower anterior
teeth is a relatively common postoperative symptom when
bone blocks or trephine cores are removed.12,30,37,38,39 The con-
tents within the incisive canal of the symphysis that innervate
the teeth are disrupted during bone harvest. Patients describe FIGURE 24-18. Osseous distraction is used to manage the vertical
dullness in sensation of the incisors, which usually resolves component of the bone deficiency.
within 6 months. The need for endodontic treatment of ante-
rior teeth is very rare. Neurosensory disturbances in the chin
region also may be encountered, even when a sulcular incision
is used.37,38,39 The incidence of temporary mental nerve pares-
thesia for symphysis graft patients is usually low, but has been
found to be as high as 43%.37 Meteorotropism of the chin has
also been reported.37 Although the vast majority of these
nerve injuries recover, they are disconcerting to patients. It is
prudent to discuss the possibility of temporary altered sensa-
tion of the teeth and chin before surgery. Although no post-
operative alteration in soft tissue chin contour has been
reported, patients are often concerned with the possible aes-
thetic consequences of bone removal from this area.37 Radio-
graphic evidence of incomplete bony regeneration has been
reported in elderly patients.40 Filling the donor site with a
resorbable bone substitute, such as bank or bovine bone, can
FIGURE 24-19. The maxilla is allowed to heal for 2 months following
help alleviate the patient’s concerns.12 Ptosis of the chin has
removal of the distraction device. A significant horizontal bone deficiency
not occurred and can be prevented by avoiding complete remains.
degloving of the mandible.41 As there is greater morbidity
associated with harvesting chin bone, this donor site is usually
reserved for cases requiring greater graft thickness than the
ramus can offer (greater than 4.0 mm) (Figures 24-17 through
24-21).
412 SECTION IV ■ Implant Surgery
FIGURE 24-20. The symphysis graft is fixated to the maxillary ridge with
screws for horizontal augmentation.
FIGURE 24-21. The symphysis graft has healed for 4 months before
implant placement is performed.
MANDIBULAR RAMUS
The posterior mandible is an excellent donor site for bone
harvest, and this region offers several advantages over the
symphysis.30,39,42,43,44 A CT scan or panoramic radiograph is
used to evaluate the bony anatomy, including the ramus,
external oblique ridge, and mandibular canal. A mandibular
block and buccal infiltration in the posterior mandible is
administered using 2% lidocaine, 1 : 100,000 epinephrine. The
incision design for access to this region differs for block and
particulate bone harvest. When taking a block graft, the inci-
sion is made similar to one used in third molar removal. A
sulcular incision is made along the posterior teeth. The inci-
sion is continued posteriorly and lateral at a 45-degree angle
from the distobuccal aspect of the second molar or the base
of the retromolar pad if no molar is present. The incision
extends superiorly along the ascending ramus. Following the
incision, a mucoperiosteal flap is reflected to expose the lateral
ramus and body of the mandible. The masseter muscle is
reflected laterally with a large retractor to form a large open
pocket. Additional local anesthesia is often required in this
area to block cervical innervation. The limits of the ramus
FIGURE 24-22. Osteotomies performed with a #701 carbide bur for
harvest of a ramus graft.
area are dictated by clinical access in addition to the coronoid
process, molar teeth, and inferior alveolar canal. The average
anteroposterior dimension of the mandibular ramus is 30.0 mm,
and the lingula is typically in the posterior third.45
Four osteotomies are made to harvest a block bone graft—
external oblique, superior ramus, anterior body, and inferior44
(Figure 24-22). The length of the osteotomies is determined
by the bone volume necessary to reconstruct the site. The
cortical cuts are made with a carbide fissure bur (#557 or 701)
in a straight hand piece under sterile saline irrigation. The
external oblique cut is made along the anterior border of the
ramus, approximately 4.0 to 6.0 mm medial to the external
oblique ridge. This osteotomy can extend as high as the base
of the coronoid process and anteriorly up to the first molar
area. This can produce a graft that may approach up to
40.0 mm in length. The superior ramus cut is made through
the lateral cortex of the ramus and perpendicular to the exter-
nal oblique cut. It may extend as far posteriorly on the ramus
as the opposing lingula on the medial ramus. However, the
length of this cut is typically about 10.0 mm. The anterior
body cut may often extend over the path of the mandibular
canal. Although the buccolingual position of the mandibular
canal is variable, the distance from the canal to the medial
aspect of the buccal cortical plate (medullary bone thickness)
was found to be greatest at the distal half of the first molar
(mean: 4.05 mm).46 Therefore, the anterior body cut should
be made in this area and not in the third molar region, where
the canal is closer to the buccal surface. This anterior body
cut is progressively deepened until bleeding from the underly-
ing cancellous bone is visible. The inferior osteotomy is only
 CHAPTER 24 •
FIGURE 24-23. The cortical graft is harvested with an extraction
elevator.
a partial-thickness cut made with a round carbide bur (#8). It
connects the inferior aspects of the superior ramus and ante-
rior body cuts. This osteotomy on the lateral aspect of the
ramus parallels the external oblique cut and creates the base
of the rectangular bone block. It extends only partially through
the cortex and creates a line of fracture. The block graft is
then removed with a chisel wedged within the external oblique
osteotomy. Care should be taken to parallel the chisel with
the lateral surface of the mandible and limit the depth of
penetration. An alternative technique is to insert an extrac-
tion elevator and pry the graft free (Figure 24-23). This donor
site is not augmented with bone substitutes because the infe-
rior alveolar nerve may be exposed and irritated by the graft
particles. The incision is closed primarily with resorbable
sutures (4-0 chromic gut). A rectangular piece of bone approx-
imately 4.0 mm in thickness may be harvested from the ramus
(Figure 24-24). This morphology is well suited for veneer
grafting to gain additional ridge width or the block may be
particulated in a bone mill.
The mandibular ramus is a convenient donor site for bone
harvest in conjunction with third molar removal.47 This is
often planned for the repair of alveolar deficiencies from con-
genitally absent teeth in young adults. If the third molar is
partially erupted, the tooth is removed before bone harvest. If
the molar is bony impacted, then the block graft is harvested,
and the tooth can be removed laterally through the donor site.
The cortical block graft can be used to reconstruct the ridge
deficiency.
The posterior mandible is the preferred area for harvesting
large amounts of particulate bone with a scraper device.17 The
Autogenous Bone Grafting for Dental Implants 413
FIGURE 24-24. A cortical bone graft harvested from the mandibular
ramus.
FIGURE 24-25. A vestibular incision is used for harvesting particulate
bone with a scraper from the body and ramus of the mandible.
initial incision for this approach is made in the buccal vesti-
bule, similar to one used in sagittal split osteotomies. It is
made just lateral to the external oblique ridge and extends the
length of the molar regions. This incision design requires
minimal time to reflect and gain access to the mandible and
is equally easy to close. A larger area of mandibular exposure
allows longer strokes with the scraper blade and expedites
graft harvest. The dense cortical bone should be repeatedly
lubricated with sterile saline during the scraping. Routinely,
4 cc of particulate autograft may be harvested from this area
(Figures 24-25, 24-26). There is minimal morbidity in harvest-
ing bone from the cortical surface with a scraper blade.
Compared with the symphysis region, the ramus donor site
is associated with a much lower incidence of complications.30,39
Patients have shown less concern with bone removal from the
ramus area. The masseter muscle provides soft tissue bulk, and
augmentation of this donor site has been unnecessary. Neuro-
sensory disturbances from bone harvest have not been encoun-
tered. However, the potential for damage to the inferior
alveolar nerve, as opposed to its peripheral mental branches,
414 SECTION IV ■ Implant Surgery

FIGURE 24-26. The particulate bone scrapings harvested from the pos-
terior mandible.

is of greater concern with the ramus graft technique. It is

important to plan osteotomies in the posterior mandible
around the position of the mandibular canal. In contrast to
the common complaint of altered sensation of the incisors
with chin bone harvest, no ramus graft patients have noted
numbness of their molar teeth.30,39 Although the posterior FIGURE 24-27. The planned incision over Gerdy’s tubercle on the lateral
incision along the external oblique ridge could possibly damage aspect of the proximal tibia.
the buccal nerve, reports of sensory loss in the buccal mucosa
are rare and will most likely go unnoticed.48 Ramus graft
patients appear to have fewer difficulties with managing post-
operative edema and pain compared with chin graft surgery.30,39
Patients may experience trismus following surgery and should
be placed on postoperative glucocorticoids and nonsteroidal
antiinflammatory medications to help reduce dysfunction.
The mandibular ramus has significantly less morbidity than
the symphysis and has become the preferred donor site of
many clinicians.17,30,38,39

TIBIA
The proximal tibial metaphysis provides an excellent source
of cancellous bone for grafting.49,50,51 This donor site offers up
to 40 mL of cancellous bone, with low reported morbidity.49,50
The surgery may be performed in an office environment, and
most patients prefer intravenous sedation. The most common
approach to the donor site is laterally at Gerdy’s tubercle, a
bony protuberance located 1.5 cm below the articulating
surface of the tibia49 (Figure 24-27). However, a medial
approach to the tibia has also been proposed.52 The leg is
elevated with a rolled towel or firm pillow, and the knee is
slightly bent. The leg is shaved, and the skin is prepped with
an antimicrobial solution (povidone-iodine or chlorhexidine).
Sterile drapes are positioned to isolate the surgical field, and
the surgical team should follow strict aseptic technique,
including sterile gowns and gloves. A sterile surgical marking
pen is used to plan the incision, and local anesthetic with a
vasoconstrictor is infiltrated along the site. The local anes-
thetic needle is then directed to the bone for additional infil-
tration over the area. A 2.0- to 3.0-cm oblique incision is
made through the skin on the anterolateral aspect of the leg
FIGURE 24-28. A trephine bur is used through the outer cortex to gain
access to the cancellous bone for graft harvest.
directly over Gerdy’s tubercle.50 No major nerves or arteries
are located in this site. Therefore, placement of a tourniquet
is usually unnecessary, and bleeding is controlled with elec-
trocautery. After incising through the subcutaneous and fascial
layers of the iliotibial tract, the periosteum is visualized. An
oblique incision is made over the bone with short inferior
releasing incisions. The periosteum is reflected to expose the
cortex of the tibia. Rake retractors are helpful in reflecting the
dense tissue flaps. The 1.5-cm opening through the cortical
bone is made with a carbide fissure bur (#702). Alternatively
a large trephine bur (10.0 mm) may be used (Figures 24-28
through 24-31). The surgeon should direct the bur medial and
inferiorly to avoid the knee joint. The cortex is fairly thin, so
the block piece of cortical bone may be pried from the donor
 CHAPTER 24 •
FIGURE 24-29. The cortical plug is removed and may be used as a block
graft for ridge reconstruction.
FIGURE 24-30. The cancellous bone and cortical plug harvested from
the proximal tibia.
FIGURE 24-31. The cancellous bone is mixed with bovine hydroxyapatite
and used for sinus bone grafting in this pneumatized sinus.
site and placed aside for reconstruction of the ridge defect.
The cancellous bone is harvested using orthopedic bone
curettes or a 2-4 Molt curette. If needed, hemostatic agents,
such as microfibrillar collagen (Avitene), may be placed into
the bony void. The wound is closed in layers with resorbable
Autogenous Bone Grafting for Dental Implants 415
FIGURE 24-32. A significant maxillary defect from an industrial accident.
The maxillary anterior teeth and alveolar bone were avulsed.
sutures (3-0 Vicryl). The skin is closed with sutures (5-0
Prolene) or staples. Antibiotic ointment is applied, and the
knee is wrapped with an elastic pressure dressing. Patients are
encouraged to keep the leg elevated and apply ice. They may
begin ambulation on the donor leg following the surgery, but
should avoid full weight bearing for a few days. Although
normal activities can be resumed, the patient should avoid
strenuous exercise for 4 to 6 weeks.
Postoperative pain from tibia bone harvest is well managed
with moderate narcotic analgesics. Ecchymosis of the leg distal
to the donor site is quite common. There has been a low
reported incidence of significant complications with this pro-
cedure.49,50,51,53 Complications may include hematoma forma-
tion, wound dehiscence, infection, and fracture. Although
quite rare, most cases of tibia fracture are due to a bony access
too low on the leg.54
ILIUM
The grafting of larger areas of bone deficiency often requires
bone harvest from the ilium. Severe bone loss from trauma,
infection, or advanced atrophy usually demands the iliac crest
as a donor site to provide the volume of bone necessary to
reconstruct the defect (Figures 24-32 through 24-46). Because
the tibia offers a convenient site for harvesting cancellous
bone, the ilium is most often reserved for cases requiring cor-
ticocancellous block grafting. In most cases, adequate bone
may be harvested using an anterior approach to the hip. A
posterior approach to the ilium is less often required and is
usually reserved for major reconstructive surgeries requiring
large amounts of cancellous bone. In addition, the need to
rotate the patient after posterior bone harvest is an inherent
disadvantage. Although posterior bone harvest is reported to
result in lower postoperative pain,55 the use of an anesthetic
pain pump can minimize the problem with anterior harvest.
There are varying shapes to the blocks that may be har-
vested from the hip. A reciprocating saw and chisels are used
to perform the osteotomies for bone harvest. Square or rect-
angular corticocancellous blocks used for width augmentation
416 SECTION IV ■ Implant Surgery

FIGURE 24-33. A corticocancellous block bone graft harvested from the FIGURE 24-34. The corticocancellous block bone grafts are fixated to
medial aspect of the ilium. the maxillary defect with screws.

FIGURE 24-35. Cancellous bone harvested from the ilium is packed FIGURE 24-36. Following a 4-month healing period, the bone graft is
around the block bone grafts. well incorporated for implant placement.

FIGURE 24-37. The placement of five endosteal implants in the recon- FIGURE 24-38. Delivery of a fixed implant supported prosthesis.
structed maxilla.
 CHAPTER 24 • Autogenous Bone Grafting for Dental Implants 417

FIGURE 24-39. A panoramic view of the reconstructed maxilla. FIGURE 24-40. Severe maxillary atrophy associated with long-term
denture use.

FIGURE 24-41. Exposure of the atrophic maxillary residual ridge. FIGURE 24-42. The use of corticocancellous block bone grafts from the
ilium to reconstruct the anterior maxilla.

FIGURE 24-43. The bone grafts are well incorporated after 4 months of FIGURE 24-44. Implant placement in the reconstructed maxilla.
healing for implant placement.
418 SECTION IV ■ Implant Surgery

FIGURE 24-45. An implant connecting bar is used to support the over- FIGURE 24-47. A medial approach to the anterior iliac crest for harvest
denture prosthesis. of the corticocancellous bone graft. The osteotomies are performed with a
reciprocating saw and chisels.

FIGURE 24-46. The final maxillary overdenture. FIGURE 24-48. Harvest of the block corticocancellous block graft from
the ilium.

are harvested from the medial cortex or lateral cortex56 (Figures

24-47, 24-48). The crestal osteotomy should begin at least
1.0 cm from the anterior iliac spine. Otherwise the remaining
anterior segment of bone may be weakened and fracture.56 The
iliac crest is cut along its length for unicortical bone harvest,
leaving the opposing cortex intact. When thicker pieces of
bone are needed for vertical bone augmentation, a bicortical
bone graft may be harvested from the entire width of the crest.
The gluteal muscle attachments are reflected from the lateral
cortex along the crest of the ilium. This graft geometry is
typically used for reconstructing the severely atrophic premax-
illa (Figure 24-49). Following the harvest of the corticocan-
cellous block(s), additional cancellous bone may be harvested
with bone curettes. Edges of the iliac cortex should be FIGURE 24-49. A bicortical block is harvested from the iliac crest for
smoothed with a rasp or file. Following the removal of the reconstruction of the severely atrophic anterior maxilla.
bone graft, hemostatic materials, such as a sheet of microfibril-
lar collagen (Avitene) or gelatin, can be placed over the layer. The infusion device delivers controlled amounts of local
cancellous bone. The use of a pain pump with long-acting anesthetic to the area for improved postoperative pain man-
local anesthetic has dramatically reduced the level of postop- agement. The muscle layers and subcutaneous tissues are
erative pain from the hip area57 (Figure 24-50). A catheter is closed with Vicryl mattress and interrupted sutures. The skin
placed into the wound following closure of the periosteal may be closed with Prolene interrupted sutures or surgical
 CHAPTER 24 • Autogenous Bone Grafting for Dental Implants 419

FIGURE 24-50. A catheter attached to a pain pump is used for continu- FIGURE 24-51. Perforation of the cortex over the graft recipient site.
ous infusion of long-acting local anesthetic.

staples. The pain pump is removed a few days after surgery

when the local anesthetic has been pumped out. The patient
is instructed to avoid full leg weight bearing on the side of
graft harvest for 1 week. Crutches or a walker may be used for
ambulatory assistance. Using the left hip for harvest allows
patients to return to driving earlier. The patient should avoid
exercise and heavy lifting for 6 weeks following surgery.58

■ GRAFT RECIPIENT SITE

The bone defect and graft recipient site are usually exposed
and prepared before bone graft harvest. This allows a better
determination of the needs for bone repair and minimizes the
length of time from bone harvest to graft placement. Incisions
to expose the recipient site are typically made along the ridge
crest through attached gingiva. Crestal incisions maintain
vascular supply to the flaps because vessels facial to the ridge
do not cross over to the palatal or lingual regions.59 Divergent
releasing incisions remote to the defect facilitate closure and
also maintain blood supply to the flap. For larger grafts in the
anterior edentulous maxilla or mandible, a vestibular incision
through the mucosa may be considered, especially if vertical
augmentation is planned. The mucoperiosteal reflection is
made over a broad area, well beyond the defect margins. All FIGURE 24-52. A cortical bone graft is harvested form the ramus.
soft tissue remnants are removed from the defect site.
The osseous recipient bed is prepared to improve the fit
and contact of the bone block to the ridge. Perforation of the
cortex with a small round bur releases growth factors, expe-
dites revascularization of the graft, and improves the graft-to-
host union60 (Figures 24-51 through 24-54). The bone graft
should have intimate contact with the underlying host bone.
The clinician should preferably decorticate the host bone to
mortise the cortical bone block to the ridge rather than sig-
nificantly adjusting the graft.60 Corticocancellous block grafts
require less adjustment because the softer cancellous bone will
often mold to the ridge.
Following harvest, the bone graft may be stored in sterile
saline. Block bone grafts should be oriented with the cancel-
lous side against the host bone. Block bone grafts do not toler- FIGURE 24-53. The block cortical bone graft is fixated to the lateral
ate micromovement and will fail to incorporate unless rigidly aspect of the narrow posterior mandible.
420 SECTION IV ■ Implant Surgery
FIGURE 24-54. The cortical graft is well incorporated after 4 months of
healing.
FIGURE 24-55. The lag fixation screws should easily pass through the
holes in the cortical graft.
fixated. The graft is mortised into position and fixated to the
ridge with screws. Fixation screws typically range from 1.0 to
2.0 mm in diameter. A screw length that maximizes retention
within the host bone should be selected. A lag screw tech-
nique is used for fixation of cortical onlay bone grafts (Figure
24-55). The screw engages and threads the host bone, but fits
passively through the cortical bone graft to compress and
rigidly fixate the block. Although one screw may be consid-
ered for small block grafts, repairing single tooth sites, two or
more screws should be used for larger grafts. The fixation
screws may also have a positive effect on graft retention
because they tent the periosteum during remodeling.
The periphery of the block graft and small discrepancies
between the graft and host bone may be filled with a variety
of graft materials. If available, autogenous cancellous bone is
preferred. An alternative is to harvest cortical shavings from
local intraoral sites using a bone-scraping device. Particulate
mineralized bone allograft or resorbable hydroxyapatite xeno-
graft may also be considered for this purpose. The particulate
bone may be mixed with platelet-rich plasma to improve the
handling and placement. The routine necessity for barrier
FIGURE 24-56. Small cortical bone grafts are fixated to the anterior
maxilla. Particulate bone scrapings are packed around the periphery of the
block grafts.
FIGURE 24-57. The grafted site is covered with a collagen barrier
membrane.
membranes over block bone grafts has been a debated topic.
Cortical bone grafts exhibit minimal resorption and do not
typically require membrane protection.11,12,61,62 Grafts with a
larger cancellous component and particulate grafts are more
susceptible to volume loss. When using corticocancellous
block grafts, compaction of the cancellous bone with an
instrument can help minimize overall resorption during
healing. The use of a barrier membrane may improve the
incorporation of the peripheral particulate graft around the
block (Figures 24-56 through 24-59). They should always be
used with particulate grafts for ridge augmentation. Collagen
membranes are preferred because they are associated with
fewer complications than polytetrafluoroethylene (PTFE)
membranes, such as exposure and infection.63 Another
approach for particulate cancellous bone is to use titanium
mesh to support and protect the graft during healing64 (Figures
24-60 through 24-62).
Complete flap coverage and tension-free closure are essen-
tial to the successful incorporation of the bone graft. Incision
of the periosteum along the base of the facial flap allows
 CHAPTER 24 • Autogenous Bone Grafting for Dental Implants 421

FIGURE 24-58. The cortical block grafts are well incorporated after 4 FIGURE 24-61. The titanium mesh and particulate bone are fixated over
months of healing. The peripheral areas around the blocks are filled with the atrophic mandible with screws.
bone.

FIGURE 24-62. Vertical bone gain for implant placement following a

6-month healing period.
FIGURE 24-59. Four endosteal implants are inserted into the recon-
structed anterior maxilla.
advancement of the flap over the grafted site. After the peri-
osteal releasing incision is made, the flap is gently stretched
to assess closure without tension (Figures 24-63, 24-64). If
resistance to the adaptation of the wound margins is noted,
further flap release can be obtained with blunt dissection
through the periosteal release and beyond the vestibular
depth. Blunt scissors or a hemostat can be advanced through
a plane parallel to the facial bone. This will prevent compro-
mising the blood supply to the flap. Procedures to enhance
graft coverage will usually result in a loss of vestibular depth.
This is rarely a problem with implant retained restorations
because the prosthesis does not require a soft tissue seal for
retention. The advancement of the facial flap over the graft
may often reposition the keratinized gingiva more palatal or
lingual. In some cases, soft tissue grafting may be necessary,
but the keratinized tissue can usually be moved facially during
FIGURE 24-60. Cancellous bone from the tibia is packed into the tita- second stage uncovery of the implants. Although it is impor-
nium mesh. tant that the flap margins are well approximated, the sutures
should not be pulled too tightly or ischemia will occur. The
flaps should be closed over the bone graft with suture materials
that maintain their tensile strength until the wound has
422 SECTION IV ■ Implant Surgery
FIGURE 24-63. The periosteum along the base of the flap is gently
incised to allow advancement over the bone graft.
FIGURE 24-64. The soft tissue flap easily advances over the graft for
tension-free wound closure.
completely healed. Vicryl and PTFE sutures are preferred over
materials such as chromic gut or silk. Multiple interrupted or
mattress sutures are used to close the flaps over the grafted
site.
It is imperative that the graft is immobilized during healing.
A fixed provisional prosthesis, such as a temporary bridge or
bonded prosthesis, is preferred for tooth replacement over the
grafted site. The use of a soft tissue borne removable prosthesis
is discouraged for the first few weeks until the incision has
healed. Removable prostheses should then be adjusted to
minimize any contact with the grafted site. The facial flange
is completely removed, and the ridge area is relieved. The
prosthesis may be relined with tissue conditioner, and denture
adhesive is often necessary for added retention. The patient
is instructed to use the removable prosthesis for cosmetic
appearance and minimize function. Unfavorable concentra-
tion of forces from the opposing dentition should be avoided,
and a broad distribution of occlusal contacts is preferred.65
Patients wearing removable prostheses over larger bone grafts
should maintain a softer diet for at least 2 months after surgery.
After this time period, the onlay graft has formed a union to
the host bone and relies less on the fixation screws for immo-
bility. Transitional implants have been used successfully to
support fixed interim prostheses for patients less tolerant of
complete or partial dentures.
Postoperatively the patient should continue antibiotic
therapy for at least 1 week. The short-term use of glucocorti-
coids can diminish swelling and edema of the soft tissues.
Narcotic analgesics are prescribed for initial use after surgery.
Thereafter, nonsteroidal antiinflammatory drugs may be con-
sidered for pain control. Chlorhexidine rinsing is used for oral
hygiene until the sutures are removed. Smoking has been
associated with a high rate of wound dehiscence and graft
failure.66 A smoking cessation protocol is followed, including
the use of prescription medications, such as bupropion, and
the nicotine patch. Patients are instructed to quit 1 week
before surgery and told not to smoke at least until the incision
is completely closed.
■ SINUS BONE GRAFTING
Over the years, numerous bone graft materials, including auto-
graft, allografts, alloplasts, xenografts, and combinations, have
been successfully used for sinus grafting. The 1996 sinus graft
consensus evaluated retrospective data on various graft mate-
rials and concluded that they all seemed to perform well.67
However, the data analysis did not factor the amount of resid-
ual bone below the sinus. Bone substitutes have been sug-
gested for the posterior maxilla with less resorption or sinus
pneumatization. When the maxilla is severely atrophic, auto-
logous bone has been shown to provide very predictable results
for reconstruction.
There are many advantages in using autologous bone in
sinus grafts, especially when minimal bone remains below the
sinus floor.68,69 Several studies have found an increase in bone
formation when autologous bone is used alone or added to
other grafting materials in sinus grafts.68,70,71,72 Froum et al70
found a statistically significant increase in vital bone forma-
tion when as little as 20% autologous bone was added to
bovine-derived grafts. The use of a barrier membrane over the
sinus window has also been advocated to increase bone forma-
tion when bone substitutes are used.73 A membrane may not
be necessary when a significant portion of the graft is autolo-
gous bone.
The healing time requirements of autologous bone grafts
are shorter, compared with bone substitutes, especially in
larger pneumatized sinuses. The healing period for sinuses
grafted with autologous bone can be as short as 3 to 4 months
compared with the 8 to 10 months often recommended for
bone substitutes.70 The addition of autologous bone to com-
posite bone grafts can also shorten healing times.39,70 This
offers a significant advantage because patients often object to
extended treatment lengths. Froum et al70 found a mean vital
bone formation of 27.1% at 6 to 9 months after sinus grafting
with mostly bovine hydroxyapatite and a small amount of
autogenous bone (20%). Misch and Krauser74 found an average
of 36.5% vital bone at 4 to 6 months when autograft was used
in equal proportions with bovine hydroxyapatite.
 CHAPTER 24 • Autogenous Bone Grafting for Dental Implants 423

FIGURE 24-65. Preoperative view of an atrophic maxilla. There is inad- FIGURE 24-67. A collagen membrane is placed over the grafted sites.
equate bone below the sinus for implant placement and a lateral ridge
deficiency.

FIGURE 24-68. The bone grafts are well incorporated after 4 months of
healing.
FIGURE 24-66. The sinus is grafted with particulate autogenous bone
mixed with mineralized bone allograft. A cortical block graft is used to recon-
struct the ridge.

It is also beneficial to use autologous bone for sinus grafting

when additional simultaneous onlay augmentation is desired
(Figures 24-65 through 24-69). The posterior maxilla resorbs
medially following tooth loss, and this pattern of bone loss
often results in an unfavorable ridge relationship with the
opposing lower dentition. It is not unusual to require sinus
bone grafting to increase the vertical bone dimension and
onlay bone grafting to augment the ridge width and/or correct
bone deficiencies in the posterior maxilla. Autologous bone
may be harvested for sinus bone grafting and simultaneous
residual ridge reconstruction using autologous block grafts.
The healing period of the onlay block and sinus bone grafts FIGURE 24-69. Implant placement into the reconstructed posterior
will be similar, allowing for earlier implant placement. This maxilla.
approach may be preferred to a staged reconstruction, where
sinus grafting is performed first using bone substitutes, and
autologous block bone grafts are placed at a later date. Not
only do autologous bone grafts heal faster than bone substi-
tutes, the quality of the regenerated bone is often better.
424 SECTION IV ■ Implant Surgery

Histologic studies have shown greater bone formation and An appropriate drilling sequence for dense bone and even
higher bone-implant contact when autologous bone grafts are tapping may be necessary for implant insertion in cortical
used compared with allografts.72 This improved bone forma- bone grafts.
tion at an earlier time can allow for shorter implant healing The healing period of implants placed into incorporated
periods compared with the use of bone substitutes. bone grafts is similar to native bone. Microtextured implant
surfaces have diminished healing implant periods to as little
■ IMPLANT PLACEMENT IN ONLAY as 6 weeks.79 Immediate implant loading in grafted bone may
BONE GRAFTS even be considered if primary implant stability is adequate
Reconstruction of the atrophic jaws for implant placement is (Figures 24-71 through 24-77). Additional graft resorption
usually staged with implant placement after graft healing. following implant placement and delayed loading has not
Previous studies on simultaneous bone graft and implant been noted radiographically.80
placement reveal lower success rates, unpredictable bone
remodeling, and diminished bone-to-implant contact.3,28,75,76
Onlay bone grafts should be allowed to incorporate before
dental implant placement. Enough time should elapse for graft
incorporation, but implants should be inserted early enough
to stimulate and maintain the regenerated bone.77 Autogenous
block grafts should heal for approximately 4 months before
implant placement.12,78 Particulate cancellous bone grafts with
barrier membranes or titanium mesh used for ridge augmenta-
tion often require longer healing periods of at least 6
months.
The placement of implants into healed bone grafts is similar
to their use in sites that have not been grafted. However, the
implant site is often at the junction between the block and
host bone. The surgeon should be careful not to displace the
block from the ridge during the implant osteotomy and
placement.
Fixation screws are usually removed before implant inser-
tion. Elevation of large flaps simply for screw removal is dis- FIGURE 24-71. Preoperative view of edentulous atrophic maxilla.
couraged because this disrupts the vascular supply to the
healed graft. Small mucosal incisions over the screw heads
allow for easy retrieval. If a fixation screw is not in the path
of implant insertion, it may be left intact, especially if it will
provide added stability to the graft (Figure 24-70). Upon
healing, the quality of block mandibular bone grafts is often
dense, regardless of the original quality of the recipient bone.

FIGURE 24-70. The fixation screw is left intact during implant

placement. FIGURE 24-72. Narrow residual ridge in the anterior maxilla.
 CHAPTER 24 • Autogenous Bone Grafting for Dental Implants 425

FIGURE 24-76. Implant placement in the reconstructed maxilla. Favor-

able primary implant stability allows the consideration of immediate loading.

FIGURE 24-73. A cortical bone graft is harvested from the mandibular

ramus.

FIGURE 24-77. The immediate load fixed conversion prosthesis.

REFERENCES
FIGURE 24-74. The cortical bone graft is fixated to the narrow residual
ridge.
FIGURE 24-75. The bone grafts are well incorporated after 4 months of
healing.
1. Boyne PJ et al: De novo bone induction by recombinant human
bone morphogenic protein-2 (rhBMP-2) in maxillary sinus floor
augmentation, J Oral Maxillofac Surg 63:1693-1707, 2005.
2. Branemark PI, Lindstrom J, Hallen O: Reconstruction of the
defective mandible, Scand J Plast Reconstr Surg 9:116-128,
1975.
3. Breine U, Branemark PI: Reconstruction of alveolar jaw bone.
An experimental and clinical study of immediate and preformed
autologous bone grafts in combination with osseointegrated
implants, Scand J Plast Reconstr Surg 14(1):23-48, 1980.
4. Goldberg VM, Stevenson S: The biology of bone grafts, Semin
Arthroplasty 4:58-63, 1993.
5. Manson PN: Facial bone healing and bone grafts. A review of
clinical physiology, Clin Plast Surg 21:331-348, 1994.
6. Burchardt H: The biology of bone graft repair, Clin Orthop Relat
Res 174:28-42, 1983.
7. Smith JD, Abramson M: Membranous vs. endochondral auto-
grafts, Arch Otolaryngol 99:203-209, 1974.
8. Zins JE, Whitaker LA: Membranous vs endochondral autografts:
implications for craniofacial reconstruction, Plast Reconstruct
Surg 72:778-785, 1983.
9. Lin KY, Barlett SP, Yaremchuk MJ: The effect of rigid fixation
on the survival of onlay bone grafts: an experimental study, Plast
Reconstruct Surg 86:449-456, 1990.
426 SECTION IV ■ Implant Surgery
10. Hardesty RA, Marsh JL: Craniofacial onlay bone grafting: a
prospective evaluation of graft morphology, orientation and
embryonic origin, Plast Reconstruct Surg 85:5-14, 1990.
11. Ozaki W, Buchman SR: Volume maintenance of onlay bone
grafts in the craniofacial skeleton: micro-architecture versus
embryologic origin, Plast Reconstr Surg 102(2):291-299, 1998.
12. Misch CM et al: Reconstruction of maxillary alveolar defects
with mandibular symphysis grafts for dental implants: a prelimi-
nary procedural report, Int J Oral Maxillofac Implants 7(3):360-
366, 1992.
13. Steiner M, Ramp WK: Short-term storage of freshly harvested
bone, J Oral Maxillofac Surg 46:868-871, 1988.
14. Fonseca RJ, Clark PJ, Burkes EJ: Revascularization and healing
of onlay particulate autologous bone grafts in primates, J Oral
Surg 38:572-577, 1980.
15. Dado DV, Izquiedo R: Absorption of onlay bone grafts in imma-
ture rabbits: membranous versus endochondral bone and bone
struts versus paste, Ann Plast Surg 23:39-48, 1989.
16. Pallesen l, Schou S, Aaboe M et al: Influence of particle size of
autogenous bone grafts on the early stages of bone regeneration.
A histologic and serologic study in rabbit calvarium, Int J Oral
Maxillofac Implants 17:498-503, 2000.
17. Peleg M et al: Maxillary sinus and ridge augmentations using a
surface-derived autogenous bone graft, J Oral Maxillofac Surg
62(12):1535-1544, 2004.
18. Marx RE, Carlson ER, Eichstaedt RM: Platelet-rich plasma:
growth factor enhancement for bone grafts, Oral Surg Oral Med
Oral Pathol 85:638-646, 1998.
19. Cromack DT, Porras-Reyes B, Mustoe TA: Current concepts in
wound healing: growth factor and macrophage interaction,
J Trauma 30S(12):129-133, 1990.
20. Mecall RA, Rosenfeld AL: Influence of residual ridge resorption
patterns on fixture placement and tooth position, part III: Pre-
surgical assessment of ridge augmentation requirements, Int
J Periodontics Restorative Dent 16(4):322-337, 1996.
21. Misch CM: Use of a surgical template for autologous bone graft-
ing of alveolar defects, J Prosthodont 8(1):47-52, 1999.
22. Rosenfeld AL, Mecall RA: The use of interactive computed
tomography to predict the esthetic and functional demands
of implant-supported prostheses, Compend Contin Educ Dent
17:1125-1128, 1996.
23. Young MP et al: The effects of an immediately pre-surgical
chlorhexidine oral rinse on the bacterial contaminants of bone
debris collected during dental implant surgery, Clin Oral Implants
Res 13(1):20-29, 2002.
24. ten Bruggenkate CM, Kraaijenhagen HA, van der Kwast WAM:
Autogenous maxillary bone grafts in conjunction with place-
ment of ITI endosseous implants: a preliminary report, Int J Oral
Maxillofac Surg 21:81-84, 1992.
25. Misch CE: Maxillary sinus augmentation for endosteal implants:
organized alternative treatment plans, Int J Oral Implantol 4:49-
58, 1987.
26. Silva FM et al: Complications of intraoral donor site for bone
grafting prior to implant placement, Implant Dent 15(4):420-426,
2006.
27. Sindet-Pedersen S, Enemark H: Reconstruction of alveolar clefts
with mandibular or iliac crest bone grafts: a comparative study,
J Oral Maxillofac Surg 48:554-558, 1990.
28. Jensen J, Sindet-Petersen S, Oliver AJ: Varying treatment strate-
gies for reconstruction of maxillary atrophy with implants: results
in 98 patients, J Oral Maxillofac Surg 52:210-216, 1994.
29. Lundgren S et al: Augmentation of the maxillary sinus floor with
particulated mandible: a histologic and histomorphometric
study, Int J Oral Maxillofac Implants 11:760-766, 1996.
30. Misch CM: Comparison of intraoral donor sites for onlay graft-
ing prior to implant placement, Int J Oral Maxillofac Implants
12:767-776, 1997.
31. Khoury F: Augmentation of the sinus floor with mandibular
bone block and simultaneous implantation: a 6-year clinical
investigation, Int J Oral Maxillofac Implants 14:557-601, 1999.
32. Buhr W, Coulon JP: Limits of the mandibular symphysis as a
donor site for bone grafts in early secondary cleft palate osteo-
plasty, Int J Oral Maxillofac Surg 25:389-393, 1996.
33. Borstlap WA et al: Early secondary bone grafting of alveolar cleft
defects: a comparison between chin and rib grafts, J Craniomaxil-
lofac Surg 18:201-205, 1990.
34. Hoppenreijs TJM, Nijdam ES, Freihofer HPM: The chin as a
donor site in early secondary osteoplasty: a retrospective clinical
and radiographic evaluation, J Craniomaxillofac Surg 20:199-224,
1992.
35. Hunt DR, Jovanovic SA: Autogenous bone harvesting: a chin
graft technique for particulate and monocortical bone blocks, Int
J Periodontics Restorative Dent 19:165-173, 1999.
36. Zide MF: Autogenous bone harvest and bone compacting for
dental implants, Compend Contin Educ Dent 21:585-590, 2000.
37. Raghoebar GM, Louwerse C, Kalk WWI: Morbidity of chin
bone harvesting, Clin Oral Implant Res 12:503-507, 2001.
38. Nkenke E, Schulze-Mosgau S, Radespiel M: Morbidity of har-
vesting of chin grafts: a prospective study, Clin Oral Implant Res
12:495-502, 2001.
39. Hallman M, Hedin M, Sennerby L: A prospective 1 year clinical
and radiographic study of implants placed after maxillary sinus
floor augmentation with bovine hydroxylapatite and autogenous
bone, J Oral Maxillofac Surg 60:277-284, 2002.
40. Jensen J, Sindet-Pedersen S: Autogenous mandibular bone grafts
and osseointegrated implants for reconstruction of severely
atrophied maxilla: a preliminary report, J Oral Maxillofac Surg
49:1277-1287, 1991.
41. Rubens BC, West RA: Ptosis of the chin and lip incompetence:
consequences of lost mentalis support, J Oral Maxillofac Surg
4:359-366, 1989.
42. Wood RM, Moore DL: Grafting of the maxillary sinus with
intraorally harvested autogenous bone prior to implant place-
ment, Int J Oral Maxillofac Implants 3:209-214, 1988.
43. Misch CM: Ridge augmentation using mandibular ramus bone
grafts for the placement of dental implants: presentation of a
technique, Pract Periodont Aesthetic Dent 8:127-135, 1996.
44. Misch CM: Use of the mandibular ramus as a donor site for onlay
bone grafting, J Oral Implantol 26:42-49, 2000.
45. Smith BR et al: Mandibular anatomy as it relates to rigid fixation
of the sagittal ramus split osteotomy, J Oral Maxillofac Surg
49:222-226, 1991.
46. Rachel J, Ellis E, Fonseca RJ: The anatomic location of the
mandibular canal; its relationship to the sagittal ramus osteot-
omy, Int J Adult Orthod Orthognathic Surg 1:37-42, 1986.
47. Misch CM: The harvest of ramus bone in conjunction with third
molar removal for onlay grafting prior to placement of dental
implants, J Oral Maxillofac Surg 57:1376-1379, 1999.
48. Hendy CW, Smith KG, Robinson PP: Surgical anatomy of the
buccal nerve, Br J Oral Maxillofac Surg 34:457-460, 1996.
49. O’Keefe RM, Reimer BL, Butterfield LS: Harvesting of autoge-
nous cancellous bone graft from the proximal tibial metaphysis:
a review of 230 cases, J Orthop Trauma 5:469-474, 1991.
50. Catone GA, Reimer LB, McNeir D: Tibial autogenous cancel-
lous bone as an alternative donor site in maxillofacial surgery: a
preliminary report, J Oral Maxillofac Surg 50:1258-1263, 1992.
51. Mazock JB, Schow SR, Triplett RG: Proximal tibia bone harvest:
review of technique, complications, and use in maxillofacial
surgery, Int J Oral Maxillofac Implants 19(4):586-593, 2004.
52. Herford AS et al: Medial approach for tibial bone graft: anatomic
study and clinical technique, J Oral Maxillofac Surg 61(3):358-
363, 2003.
53. Chen YC et al: Donor site morbidity after harvesting of proximal
tibia bone, Head Neck 28(6):496-500, 2006.
 CHAPTER 24 •
54. Thor A, Farzad P, Larsson S: Fracture of the tibia: complication
of bone grafting to the anterior maxilla, Br J Oral Maxillofac Surg
44(1):46-48, 2006.
55. Nkenke E et al: Morbidity of harvesting of bone grafts for the
iliac crest for preprosthetic augmentation procedures: a prospec-
tive study, Int J Oral Maxillofac Surg 33:157-163, 2004.
56. Cricchio G, Lundgren S: Donor site morbidity in two different
approaches to anterior iliac crest bone harvesting, Clin Implant
Dent Relat Res 5:161-169, 2003.
57. Hahn M et al: Local bupivacaine infusion following bone graft
harvest from the iliac crest, Int J Oral Maxillofac Surg 25(5):400-
401, 1996.
58. Kalk WW et al: Morbidity from iliac crest bone harvesting,
J Oral Maxillofac Surg 54(12):1424-1429, 1996.
59. Whetzel TP, Sanders CJ: Arterial anatomy of the oral cavity: an
analysis of vascular territories, Plast Reconstr Surg 100:582-587,
1997.
60. Carvalho P, Vasconcellos L, Pi J: Influence of bed preparation
on the incorporation of autogenous bone grafts: a study in dogs,
Int J Oral Maxillofac Implants 15:565-570, 2000.
61. Dongieux JW et al: The effect of different membranes on onlay
bone graft success in the dog mandible, Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 86:145-151, 1998.
62. Proussaefs P, Lozada J, Kleinman A: The use of ramus autogenous
block grafts for vertical alveolar ridge augmentation and implant
placement: a pilot study, Int J Oral Maxillofac Implants 17:238-
248, 2002.
63. von Arx T, Buser D: Horizontal ridge augmentation using autog-
enous block grafts and the guided bone regeneration technique
with collagen membranes: a clinical study with 42 patients, Clin
Oral Implants Res 17:359-366, 2006.
64. Boyne P, Peetz M: Osseous reconstruction of the maxilla and man-
dible: surgical techniques using titanium mesh and bone mineral,
Carol Stream, IL, 1997, Quintessence Publishing.
65. Becktor JP et al: The influence of mandibular dentition on
implant failures in bone grafted edentulous maxillae, Int J Oral
Maxillofac Implants 17:69-77, 2002.
66. Levin L, Schwartz-Arad D: The effect of cigarette smoking on
dental implants and related surgery, Implant Dent 14:357-361,
2005.
67. Jensen OT et al: Report of the sinus consensus conference
of 1996, Int J Oral Maxillofac Implants 13(suppl):11-45,
1998.
68. Block MS, Kent JN: Sinus augmentation for dental implants: the
use of autogenous bone, J Oral Maxillofac Surg 55:1281-1286,
1997.
Autogenous Bone Grafting for Dental Implants 427
69. Misch CM: Discussion. A prospective 1 year clinical and radio-
graphic study of implants placed after maxillary sinus floor aug-
mentation with bovine hydroxylapatite and autogenous bone,
J Oral Maxillofac Surg 60:285, 2002.
70. Froum SJ et al: Sinus floor elevation using anorganic bovine
bone matrix (OsteoGraf/N) with and without autogenous bone:
a clinical, histologic, radiographic and histomorphometric anal-
ysis-part 2 of an ongoing study, Int J Periodont Rest Dent 18:529-
543, 1998.
71. Lorenzetti M et al: Bone augmentation of the inferior floor of
the maxillary sinus with autogenous bone or composite bone
grafts: a histologic-histomorphometric preliminary report, Int J
Oral Maxillofac Implants 13:69-76, 1998.
72. Jensen OT, Sennerby L: Histological analysis of clinically
retrieved titanium microimplants placed in conjunction with
maxillary sinus floor augmentation, Int J Oral Maxillofac Implants
13:513-521, 1998.
73. Tarnow DP et al: Histologic and clinical comparison of bilateral
sinus floor elevations with and without barrier membrane place-
ment in 12 patients: part 3 of an ongoing prospective study, Int
J Periodont Rest Dent 20:116-125, 2000.
74. Misch CM: Maxillofacial donor sites for sinus floor and alveolar
reconstruction. In Jensen OT, editor: The Sinus bone graft,
Chicago, 2006, Quintessence Publishing.
75. Adell R et al: Reconstruction of severely resorbed edentulous
maxillae using osseointegrated fixtures in immediate autogenous
bone grafts, Int J Oral Maxillofac Implants 5:233-246, 1990.
76. Friberg B: Bone augmentation at single-tooth implants using
mandibular grafts: a one-stage surgical procedure, Int J Periodon-
tics Restorative Dent 15:436-445, 1995.
77. Nystrom E et al: Autogenous onlay bone grafts fixed with screw
implants for the treatment of severely resorbed maxillae. Radio-
graphic evaluation of preoperative bone dimensions, postopera-
tive bone loss, and changes in soft-tissue profile, Int J Oral
Maxillofac Surg 25:351-359, 1996.
78. Matsumoto MA, Filho HN, Francishone CE: Microscopic analy-
sis of reconstructed maxillary alveolar ridges using autogenous
bone grafts from the chin and iliac crest, Int J Oral Maxillofac
Implants 17:507-516, 2002.
79. Attard NJ, Zarb GA: Immediate and early implant loading pro-
tocols: a literature review of clinical studies, J Prosthet Dent
94:242-258, 2005.
80. Buser D, Ingimarsson S, Dula K: Long term stability of osseoin-
tegrated implants in augmented bone: a 5-year prospective study
in partially edentulous patients, Int J Periodontics Restorative Dent
22:108-117, 2002.
CHAPTER 25
GUIDED TISSUE REGENERATION IN IMPLANT
DENTISTRY: TECHNIQUES FOR MANAGEMENT OF
LOCALIZED BONE DEFECTS
The science of bone regeneration has evolved into a highly
complex and specialized area of study. The understanding of
the molecular and cellular cascade of events involved in bone
repair and regeneration continues to evolve at a rapid pace.
Promising technologies, such as tissue engineering, recombi-
nant growth factors, and gene therapy, offer tremendous hope
for the future. Notwithstanding these recent advances, the
principle of guided tissue regeneration (GTR) continues to
play a major role in contemporary clinical practice and is
particularly important in the management of localized bone
defects associated with dental implants.
The development of GTR has a long and interesting
history. As early as 1944, the principle of compartmentaliza-
tion to achieve regeneration of specific tissues was under
investigation. Researchers in the field of neural regeneration,
using allogeneic aorta as a protective conduit over the cut
ends of a peripheral nerve, reported regeneration of nerve
fibers, even in the absence of a distal segment. It had previ-
ously been observed that nerve regeneration was prevented by
fibrous tissue ingrowth and scarring.1
In 1957, Murray found that if a section of cortical bone
was removed from the dog ilium and subsequently protected
with a plastic cage, the interior of the cage would fill with
new bone. Murray also found that if the three-dimensional
design of the cage permitted, new bone would form on the
cortical surface surrounding the defect and also proliferate
vertically within the cage.2 Hurley et al., seeking to improve
bone regeneration in spinal fusion, found that insertion of a
cellulose acetate filter over the grafted site effectively excluded
the overlying, fully differentiated tissues from the bony
defects.3 Subsequently, Linghorne reported on tube-guided
osteogenesis in fracture repair. In this study, discontinuity
defects 15 mm in length were produced in the fibulae of dogs
by removal of a section of bone and periosteum. A hollow
polyethylene tube was then placed across the gap, connecting
the cut ends of the bone. It was demonstrated that in the
presence of the tube, osseous healing occurred instead of a
fibrous union.4
The work of Murray and Linghorne was expanded on by
Melcher using dome-shaped cellulose acetate barriers over
surgically created defects in the rat. Melcher theorized that
428
Barry Kyle Bartee • John L. Lignelli II
the barrier served two purposes: to provide protection of the
hematoma from invasion by nonosteogenic extraskeletal soft
tissue and to prevent physical distortion of the hematoma by
pressure from the overlying tissues.5
The use of GTR in the realm of oral surgery was first
reported by Boyne, who used a cellulose acetate filter to regen-
erate bone in surgically created mandibular defects.6 Later he
would use the same material to line the interior of metallic
mesh cribs in combination with autogenous bone to treat
major mandibular defects.7 Using a slightly different material,
Kahnberg later described the successful use of perforated
Teflon mantle leaf on regeneration of mandibular bone defects
in rabbits.8
The potential for the regeneration of specific, differentiated
periodontal structures was described by Linghorne and
O’Connell in 1950.9-11 In surgically created bone defects adja-
cent to teeth and grafted with autogenous bone chips, they
observed a new connective tissue attachment and regenera-
tion of bone, cementum, and the periodontal ligament. An
occlusive membrane was not used in this study; however, they
observed that in cases where a new connective tissue attach-
ment formed coronal to the bone defect, effectively excluding
the more aggressive gingival epithelial cells, regeneration of
alveolar bone and cementum occurred. Conversely, if connec-
tive tissue attachment failed to occur coronally, allowing the
down growth of oral epithelium, there was subsequent failure
of osteogenesis and cementogenesis.
In 1976, Melcher published a frequently quoted paper on
the repair of periodontal tissues. Taking the concept well
beyond the epithelial exclusion theory, his work delineating
the specific role and kinetics of progenitor cells would herald
the development of regenerative therapy in periodontics.11
The use of GTR membranes in implantology, more specifi-
cally the concept of guided bone regeneration (GBR) or
osteopromotion, was recognized as a method of alveolar ridge
augmentation and for managing localized defects associated
with the placement of dental implants.13,14 These concepts
would fundamentally change the practice of implantology,
increasing the ability of clinicians to provide more predictable
restoration of form, function, and aesthetics through more
ideal implant placement.15-17
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry
■ FUNCTIONAL AND DESIGN
REQUIREMENTS OF GTR
MEMBRANES
The requirements for achieving successful bone regeneration
include the attraction of appropriate precursor cells to the
target site, an abundant nutrient supply, appropriate molecu-
lar signals, and a stable, protected environment conducive to
the development of the target tissue.18 A primary function
of the GTR membrane is to provide isolation and protection
of the initial blood clot, which is crucial for the proper elabo-
ration, distribution, and function of growth factors, cytokines,
and inflammatory mediators involved in wound healing. In
addition, the membrane should provide sufficient protection
from bacterial invasion. The membrane should have adequate
density to prevent infiltration of cells from nonosteogenic
tissues, and the membrane must remain intact for as long as
necessary for the defect to be populated by cells derived from
adjacent bone.19
STABILITY
During the first few hours and days, inflammatory cells and
fibroblasts are predominant within the blood clot. Fibroblasts
then lay down the collagenous framework, which is ultimately
mineralized by osteoblasts to form new bone. Stability of the
wound, as in the case with fracture healing and osseous implant
integration, is required for conversion of mesenchymal cells
into the osteoblastic phenotype. Continuous motion results
in the production of prostaglandins and prolongation of the
inflammatory response. Thus, the overlying membrane must
provide a stable environment with minimal micromotion;
otherwise, formation of fibrous tissue rather than bone will
result.20
SPACE MAINTENANCE
The earliest investigations of GBR revealed that successful
GBR was dependent on the creation and maintenance of
adequate space under the membrane to allow migration of
cells and ingrowth of blood vessels from adjacent osteogenic
tissues to occur. In the oral cavity, pressure from overlying soft
tissues, muscles, or prostheses may result in membrane col-
lapse and failure. In large defects, this requires the presence of
particulate bone grafting materials or some other method of
providing mechanical support to the membrane, such as the
use of titanium tenting screws. Alternatively, membranes
reinforced with titanium struts may be used, or titanium mesh
may be used in conjunction with an occlusive membrane.
Smaller, vertically oriented defects tend to be less critical in
this regard as long as the membrane is being adequately sup-
ported by the adjacent bone.21
BIOCOMPATIBILITY
Upon implantation, the membrane material should evoke
minimal inflammatory response and remain biologically
inert for the duration of the regeneration procedure. Biocom-
patibility is related to the chemical, structural, and physical
429
characteristics of the material. Bioresorbable materials may
present additional concerns with regard to inflammatory or
cytotoxic by-products released during their degradation. Other
consequences of degradation, such as proteolytic activity,
free radical formation, or local change in pH, all of which
have the potential to interfere with bone formation, are of
concern.22,23 Materials that have been found to be suitable for
GBR include cellulose acetate, Teflon mantle leaf, expanded
polytetrafluoroethylene (ePTFE),24 high-density polytetrafluo-
roethylene (dPTFE),25 type I bovine collagen,26 porcine
collagen,27 laminar freeze-dried bone,28 polylactide and polyg-
lycolide copolymer,29 silicone sheet,31 lyophilized dura mater,32
autologous periosteum,32 and latex rubber dam.33
EASE OF USE
Because alveolar bone defects often have complex three-
dimensional morphology, GTR membranes should be manu-
factured from materials that are easy to trim, adapt, and place
with a high degree of precision. Once placed, the membrane
should lie passively within the wound and adapt well to the
surrounding bone and soft tissues, yet should have enough
stiffness to withstand collapse into the defect.
■ SURGICAL PRINCIPLES
Although a wide variety of membrane materials are available,
both resorbable and nonresorbable, the fundamental surgical
principles involved in their use are remarkably similar. Achiev-
ing predictable success in GBR requires careful planning,
meticulous technique, and attention to detail. Clinicians
becoming familiar with this technique should also realize that
certain defects are more challenging than others, and some
defects are better managed with alternative techniques. A
number of factors have been identified over the years that,
taken in their entirety, will help ensure success, regardless of
the material used.
PATIENT SELECTION AND PREPARATION
Because infection is the most significant risk factor associated
with augmentation procedures, candidates for GTR should
exhibit excellent oral hygiene. Chronic periodontal disease
should be controlled, and the dentition should be in an
optimal state of health. Sites with inadequate soft tissue thick-
ness or poor tissue quality will benefit from soft tissue grafting
before regenerative therapy. The use of tobacco in any
form in the perioperative period should be strongly discour-
aged. Cigarette smoking, heavy alcohol use, uncontrolled sys-
temic diseases such as diabetes mellitus, or any other condition
typically associated with poor wound healing will increase
the incidence of complications. The presence of active infec-
tion at the graft site, characterized by pain, erythema, swell-
ing, or purulent drainage, is a contraindication to regenerative
therapy.
In the preoperative phase, consideration should be given
to the type of prosthesis, if any, to be used during the healing
period following GTR procedures. The use of soft tissue borne
430 SECTION IV ■ Implant Surgery
prostheses should be avoided in favor of tooth-supported pros-
thetics, if possible. This will help to prevent compressive
forces that can result in a reduction of graft volume, dehis-
cence, or other wound healing complications. If the use of a
tissue-borne prosthesis is unavoidable, it should remain out of
functional occlusion and be removed from the mouth as much
as possible for the first 3 weeks.
Systemic antibiotic prophylaxis should be used for regen-
erative procedures involving the placement of membranes
and/or graft materials, but is generally not necessary beyond
the first 7 days postoperatively. Chlorhexidine rinse should be
prescribed to begin 12 hours preoperatively and then locally
applied to the surgical site until suture removal. Where mem-
brane exposure occurs, local application of chlorhexidine
should be done until the time of membrane removal. Patients
should be instructed specifically to keep these areas clean and
free of bacterial plaque and debris.
INCISION DESIGN
Conservation of blood supply to the flap overlying a GTR
membrane is of paramount importance in maintaining viable,
healthy soft tissues and minimizing complications.34-36 Mid-
crestal incisions are typically used in edentulous sites, and
vertical incisions are made at least one tooth width (5 to
10 mm) from the site of the anticipated membrane margin. A
tension-relieving cut-back incision, as described by Sclar,37
can be employed at the apical extent of vertical incisions as
an alternative.
DÉBRIDEMENT
Following flap reflection, meticulous débridement of all soft
tissues within and adjacent to the defect should be done with
sharp curettage or piezo surgery. In extraction sockets, sharp
curettage should be used to remove all remnants of the peri-
odontal ligament. The apex of the socket should be carefully
explored, and any residual periapical soft tissue should be
thoroughly removed. The surrounding bone should be smooth,
level, and free of projections, which would interfere with
adaptation of the membrane.
DECORTICATION
Decortication is a principle used in the placement of autoge-
nous grafts in a variety of orthopedic and maxillofacial proce-
dures and may be done in all GBR procedures. Successful bone
regeneration cannot occur without the availability of osteo-
progenitor cells and an adequate blood supply. The adjacent
marrow space is a source of both, and more rapid access to the
endosteal compartment is believed to have the potential to
enhance bone regeneration. This can be accomplished by the
use of a slow-speed round bur and copious irrigation (see Case
Report 25-4, Figure 25-35).
MEMBRANE TRIMMING AND PLACEMENT
When handling and trimming membranes, talc-free gloves
should be used to prevent contamination of the surface. To
minimize contamination of the membrane during trimming,
a template made from sterile foil or surgical wrap may be used
to determine the final outline. This information is then trans-
ferred to the actual membrane. Sharp corners or frayed edges
on the membrane should be eliminated because this can
lead to irritation or perforation of the overlying soft tissue.
With titanium-reinforced membranes, avoid trimming within
2.0 mm of the titanium struts to prevent inadvertent delami-
nation of the membrane. Properly trimmed, the membrane
should completely cover and extend 3 mm to 4 mm beyond
the margins of the defect. This distance is usually sufficient to
provide an adequate seal between the margin of the mem-
brane and the defect.
A notable exception, however, is when placing a
membrane adjacent to natural teeth or between natural
tooth roots. In this case, to prevent sloughing of the flap
and loss of the interdental papilla, the membrane should
be trimmed so that it is no closer than 1.0 mm to the
adjacent tooth roots. In addition, avoiding contact of the
membrane with the tooth root prevents percolation of oral
fluids beneath the membrane, an occurrence that can lead to
infection. Similarly, if placement of two membranes is required,
they should not overlap in an area that may subsequently
become exposed to the oral cavity, such as near the crest of
the ridge.
Once the membrane has been trimmed and is in place, the
surgeon should reposition the soft tissue flaps to ensure that
the membrane is stable and that no wrinkles or folds occur
during closure. Membranes that are soft and compliant with
the overlying soft tissues may be stabilized adequately by
tucking the membrane subperiosteally under the flaps,38
achieving stability via cell ingrowth or attachment. More rigid
materials, which are sometimes required in certain cases,
require stabilization with tacks or microscrews to prevent
micromotion.
SPACE MAKING
Consideration must be given to creating and maintaining
sufficient space under the membrane for bone regeneration
to occur. The tendency for membrane collapse is related to
both the morphology of the bone defect and the inherent
stiffness of the membrane. Narrow, intrabony defects with
three or four adjacent walls present less risk of membrane
collapse than broad defects with only two or three walls. The
most common method of providing additional membrane
support and stability is the addition of resorbable particulate
bone grafting materials under the membrane. Autogenous
bone, allogenic bone, xenografts, or alloplasts may be used
individually or in combination. Other methods include
the use of tenting screws or perforated mesh in addition to a
GTR membrane. Titanium-reinforced membranes are also
available, which provide additional stability and added pro-
tection against collapse (Figures 25-1 and 25-2). When using
large titanium-reinforced membranes, strong consideration
should be given to stabilizing these devices with bone tacks
or screws.
 CHAPTER 25 •
A
B the membrane will be exposed, special precautions and slight
C channel for migration of oral fluids and bacteria under the flap
FIGURE 25-1. A, B, The addition of a titanium strut to PTFE barriers
allows shaping of the device to facilitate ease of placement. C, The increased
stiffness prevents membrane collapse in wide defects.
■ CLOSURE
PROCEDURES REQUIRING PRIMARY CLOSURE
Generally, ePTFE membranes require primary closure as a
result of the open surface microstructure and the risk of infec-
tion and graft failure when exposed.39,40 Collagen membranes,
although more forgiving of exposure, perform more predict-
ably when primary closure is maintained.41 Vertical incisions
can be used to assist in achieving primary closure provided
they are made remote from the position of the membrane.
Horizontal periosteal releasing incisions made at the flap base,
followed by tissue release via blunt dissection, can be used to
ensure a tension-free primary closure. However, it should be
appreciated that this technique can result in damage to blood
vessels and therefore compromise the blood supply to the flap
margin. A bilayered suturing technique can be employed using
a combination of horizontal mattress and interrupted sutures.
For closure of crestal incisions, a monofilament suture mate-
Guided Tissue Regeneration in Implant Dentistry 431
rial, such as PTFE, is ideal because it will not encourage
wicking of bacteria into the wound. Crestal sutures should be
left in place for 10 to 14 days. Vertical incisions can be closed
with fine chromic gut suture.
PROCEDURES NOT REQUIRING
PRIMARY CLOSURE
dPTFE42-46 and certain high-density collagen membranes47
have been used successfully without intentional primary
closure in a so-called open technique. The membrane in this
technique can be viewed as a “second flap” to cover extraction
sites, either for immediate implant placement or ridge preser-
vation procedures.38 This approach can be advantageous,
particularly in applications, such as anterior extraction
sites, where minimal disruption of the soft tissue architecture
is desirable. Because primary closure is not required, vertical
incisions can be avoided, and the mucogingival junction is
left in its native position. Furthermore when a flapless tech-
nique is employed, the gingival margin can be left in its native
position, maximizing the width of keratinized gingiva. Because
variations in standard GBR technique are required.
When preparing for final closure in the open technique,
care should be taken to ensure precise soft tissue adaptation
and the development of an adequate seal at the membrane
margins. There should be no exposed membrane edges, and
the membrane should be carefully positioned so that it is not
wrinkled or folded. If the use of two or more membranes is
required, they should be arranged so that they do not overlap
in an exposed region. It is imperative that no stray graft par-
ticles are left between the flap and membrane; otherwise, a
can occur. This is best accomplished by using copious irriga-
tion and suction, followed by inspection under magnification.
Stability of the membrane will be dependent on the soft tissue
flaps, so it is imperative that the membrane should extend a
minimum of 3 to 5 mm beyond the margins of the bone defect
and at least this far beyond the flap margins. Sutures are rec-
ommended to eliminate dead space and further stabilize the
flap and membrane, using an interrupted, horizontal mattress,
or crisscross technique. A monofilament suture is recom-
mended and should be left in place for 14 days.48
■ POSTOPERATIVE
CONSIDERATIONS
The use of removable dental prostheses is commonly associ-
ated with wound healing complications in GBR procedures.
Whenever possible a tooth-supported provisional restoration
should be used, either fixed or removable. If a conventional,
tissue-supported, removable prosthesis is used, it should be
removed from the mouth except for brief periods of use for the
first 4 to 5 days of healing. It is prudent for the surgeon to
generously relieve the tissue surface of the acrylic prosthesis
at the time of surgery to ensure that there is no contact with
the incision line or soft tissue overlying the GBR membrane.
Adequate space should be provided to accommodate postop-
432 SECTION IV ■ Implant Surgery

A B

C D

FIGURE 25-2. A-D, Titanium-reinforced membranes are indicated where increased space making capability is
required. Nonexpanded, reinforced dense PTFE (Cytoplast Ti250) provides additional stability and may be left exposed in
this application for either immediate implant placement or ridge preservation procedures.

erative swelling. Patients should be instructed to use the pros-
thesis only for cosmetic reasons for the first 2 to 3 weeks. A
soft diet should be prescribed, and patients should be advised
to avoid functional loading of the surgical site until soft tissue
healing has occurred. Oral hygiene should be meticulous, and
local application of chlorhexidine rinse should be done until
sutures are removed. If an open technique is used as described
earlier, local application of chlorhexidine should be continued
until the time of membrane removal.
In contrast to the relatively predictable outcomes with
exposure of dPTFE, premature exposure of microporous PTFE
(ePTFE) barriers can lead to complications or even failure of
the procedure. Macheti, in a meta-analysis of regenerative
procedures, found that exposure of microporous membranes
resulted in a sixfold decrease in bone formation compared with
sites where the membranes remained covered by soft tissue.49
Exposure of ePTFE leads to rapid surface contamination,
migration of bacteria within the interstices of the material, and
finally entry of bacteria into the surgical site.40 Small exposures
do not necessarily indicate impending failure, but if infection
occurs under the barrier, failure of the augmentation procedure
will occur. Exposures of ePTFE should be managed expectantly
with local cleansing and treatment with chlorhexidine. Weekly
observation is suggested, and removal of the barrier should be
done at the first sign of infection. If exposure of the edge of the
barrier occurs or if there is instability or mobility of the barrier
observed, the barrier should be removed at that time. Exposure
of collagen membranes and subsequent colonization by oral
bacteria can lead to premature degradation by bacterial prote-
ases.50 However, highly cross-linked membranes and those
with sufficient thickness and density are claimed to better
withstand clinical exposure without graft failure.47
■ MEMBRANE SELECTION
RATIONALE
Since it is often stated that bioresorbable membranes were
developed to avoid a second surgical procedure for membrane
removal, one might question the rationale for the continued
use of nonresorbable barriers. There are at least three major
indications for their use. First, nonresorbable barriers are indi-
cated in large, non–space-making types of defects. In this
instance, the use of titanium-reinforced membranes is highly
desirable. Second, there may be cases where achieving primary
closure is difficult and there is a high risk of incision line
opening. In this case, the use of a dPTFE membrane may be
advisable, allowing the clinician to “buy time” in the event of
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry 433

A B

D
C

FIGURE 25-3. Scanning electron microscopy comparing expanded and dense PTFE surfaces. A, The typical node
and fibril structure of ePTFE is seen (10,000×). The pore size is determined by the degree of stretching during the manu-
facturing process. B, dPTFE is shown at 22,000×. Surface features, such as parallel grooves, in this case 1.0 to 3.0 μm
in width, encourage cell attachment. C, The flattened cell morphology and development of lamellipodia are indications
of a biologically compatible surface (6,000×). D, The submicrometer pore structure of dPTFE can be appreciated. These
small voids allow the passage of small organic molecules and oxygen through the membrane (22,000×).

an exposure. Third, with the emphasis on noninvasive surgical
techniques, sometimes the maneuvers necessary to achieve
primary closure may be undesirable. In this case, one may elect
to use an open technique with a high-density membrane,
leaving the soft tissues in their native position.44,48
In the nonresorbable category, there are two products
available in the U.S. market: ePTFE (Gore-Tex W.L. Gore &
Associates, Inc. Flagstaff, AZ) and dPTFE (Cytoplast, Osteo-
genics Biomedical, Inc. Lubbock, TX). Although chemically
identical, the two products differ primarily in density and pore
size. ePTFE is a sintered material, having pores in the size
range of 8 to 30 μm. dPTFE is a nonsintered material, having
a nominal pore size less than 0.2 μm (Figures 25-3 and
25-4).
In the resorbable category, there are a wide variety of prod-
ucts available, differing substantially in terms of resorption
time and material density. Collagen may be derived from
human, bovine, and porcine sources. Bovine collagen prod-
ucts are manufactured from reconstituted dermis or Achilles
tendon. The raw material is ground, hydrolyzed in weak
organic acid, and then dispersed in an aqueous solution. The
solution is further purified to remove noncollagenous protein,
lyophilized, and then formed into the final product (Figure
25-5). Various techniques are used to cross-link the collagen
to achieve biologic stability and a clinically useful resorption
profile. Chemical cross-linking methods include glycosylation
and exposure to formaldehyde, glutaraldehyde, hexameth-
ylene diisocyanate (HMDC) cyanamide, 1-ethyl-3-(3-
434 SECTION IV ■ Implant Surgery

A B

FIGURE 25-4. Dense PTFE is available in a microtextured surface, which increases the surface area available for
cell attachment. A, The “hex”-shaped dimples are seen in the low power SEM view of the surface of B. An increase in
surface area of more than 400% is achieved without creating a porous microstructure.

A B

FIGURE 25-5. A, B, Processed type I collagen is available from both bovine and porcine sources. Cytoplast RTM
is a cross-linked bovine type I collagen with a 4- to 6-month resorption profile. C, Scanning electron microscopy reveals
a highly organized, layered structure, which is cell occlusive and biocompatible (300×).

dimethylaminopropyl) carbodiimide (EDC), hydrazine, or
diphenylphosphoryl azide (DPPA). Nonchemical methods
include the use of ultraviolet radiation and dehydrothermal
cross-linking.
GTR membranes manufactured from native collagen are
also available. One such product is manufactured from porcine
dermis (Bio-Gide, Osteohealth Co. Shirley, N.Y.), resulting
in a bilayered material with both a cell occlusive and porous
layer. A similar approach using acellular processed human
dermis results in a dense collagen membrane, relying on native
cross-links for stability (Alloderm, LifeCell Inc. Branchburg,
NJ). A related example is a product manufactured from thin
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry
sheets of demineralized human cortical bone (Lambone Pacific
Coast Tissue Bank, Los Angeles), which relies on the native
collagen matrix for strength and stability.
As a result of a desire to have alternatives to the use of
animal- and human-derived products, synthetic bioresorb-
able membranes have been introduced. Currently the
poly(hydroxyortho esters), such as polylactic acid (PLA),
polyglycolic acid (PGA), and their copolymers, are most com-
monly used. These biomaterials have a long history of use,
primarily as suture materials and surgical mesh.
Specific biomechanical and resorption characteristics can
be engineered into these products by varying the ratio of
PLA : PGA in the final product. PGA is the weaker of the two
biomechanically, more hydrophilic, more flexible, and exhib-
its a more rapid degradation rate. PLA is strong biomechani-
cally, more hydrophobic, more brittle, and has a very long
degradation rate. The inherent stiffness of these materials is
overcome either by using a mesh-type structure, by the addi-
tion of a plasticizing agent, or by the addition of a third
polymer.
In vivo degradation of these materials occurs through hydro-
lysis of the polymer backbone into organic acids and esters,
which ultimately are metabolically eliminated as CO2 and
water. Although the degradation products are endogenous and
nontoxic at physiologic concentrations, biochemical changes
in the local environment and their potential effects on bone
formation have been of concern to researchers.
Aliyev et al. evaluated the levels of reactive oxygen species
involved in the degradation of PLA barrier membranes. The
free radical scavenging enzymes catalase and superoxide dis-
mutase, considered to be markers for compounds deleterious
to wound healing, were found to be significantly higher in sites
treated with PLA membranes than in controls.23 There has
also been concern over the effect that degradation products,
such as glycolic and lactic acid, could have on local pH. In an
in vitro study of the local pH effects of degrading PLA and
PGA implants, Agrawal and Athanasiou found that the local
pH dropped to as low as 3.0 in 9 weeks, and the addition of
calcium carbonate maintained the pH between 7.4 and 6.3.51
It is unknown if the addition of a calcium source, such as
mineralized bone allograft or tricalcium phosphate, would
have similar effects in vitro.
The selection of the appropriate membrane for a given
problem is ultimately a clinical decision because there are no
well-designed, randomized controlled human clinical trials
indicating a clearly superior membrane material. There is good
data regarding the use of ePTFE in implant-associated defects,
before or concomitant with implant placement, provided that
primary closure is achieved and maintained over the barrier.
Similarly, titanium-reinforced ePTFE has been shown to be
an effective adjunct when additional stiffness and space
making ability of the membrane is desired. Bioresorbable
membranes, such as bovine collagen and PLA-PGA compos-
ites, have been shown to be functional as GBR membranes,
(provided the resorption profile of the device matches the
clinical situation) and compare favorably with nonresorbable
membranes. In cases where primary closure is not desired, or
435
short-term coverage of graft material is all that is required, the
use of dPTFE has been suggested as a viable alternative, with
its claimed ability to remain exposed in the oral cavity without
complications. In the next section, we will consider specific
clinical indications for the use of membranes in conjunction
with implant placement.
■ CLINICAL APPLICATION OF
GUIDED BONE REGENERATION
IN ASSOCIATION WITH DENTAL
IMPLANT PLACEMENT
DEHISCENCE DEFECTS
A common clinical problem encountered during placement of
dental implants in the anterior maxilla is dehiscence or thin-
ning of the buccal cortical plate, particularly in maxillary
lateral sites. Not only may this type of defect lead to progres-
sive loss of implant stability, but contour deficiency can also
compromise aesthetics. This most commonly manifests as a
gingival darkness or shadow in the affected area. The use of a
particulate graft material and membrane is a predictable and
well-documented method of bone regeneration and contour
enhancement in this scenario.41,54
Dehiscence defects may be treated at the time of implant
placement or in a staged approach. If the defect is small and
narrow—less than 5.0 mm in length and less than 2.0 mm in
width—and the implant is stable, a healing abutment can be
placed in a single-stage approach. A resorbable membrane and
particulate bone graft can be used; in this case, the membrane
will not extend over the crest of the ridge, but will only cover
the facial dehiscence.
In the case of larger defects—greater than 5.0 mm in depth
and 4.0 mm in width or extending beyond the line angles of
the implant in width—a two-stage approach with particulate
grafting, a membrane, and primary closure will yield the most
predictable results. In this setting, the membrane should com-
pletely cover the defect, extending from the most apical extent
of the defect on the facial dehiscence, over the crest of the
ridge, and then tucked under the palatal flap.
Dehiscence defects may also be encountered while placing
implants into extraction sites, particularly in cases exhibiting
a thin, scalloped gingival biotype. In these cases, immediate
implant placement may still be accomplished provided there
is primary stability of the implant. Simultaneous with implant
placement, socket reconstruction and GTR may be done.
Following extraction of the tooth using minimally invasive
technique, all soft tissue remnants are removed from the
socket using sharp curettage. The implant osteotomy is typi-
cally positioned slightly toward the lingual or palatal cortical
plate, taking care to plan for an acceptable restorative emer-
gence profile. Once the implant is stable, a particulate bone
graft, consisting of autogenous bone recovered from the
implant osteotomy combined with an allograft, is placed into
the gap between the implant and socket wall. The dehiscent
area is slightly overcontoured to account for the expected
contraction in graft volume. A GTR membrane is then
placed over the socket, extending 3.0 to 4.0 mm under the
436 SECTION IV ■ Implant Surgery
palatal flap and as far apically as required to cover the facial
dehiscence. If primary stability of the implant is not achieved,
the implant surgeon simply uses the same procedure with
particulate grafting and GBR. This will conserve both hard
tissue and the soft tissue regenerative envelope, allowing for
predictable implant placement in 4 to 6 months. Ridge pres-
ervation techniques will be discussed in detail in a later
section.
FENESTRATION DEFECTS
Occasionally, as a result of anatomic factors or bone loss,
exposure of the midbody of the implant will occur, while
maintaining intact bone at both the apex and coronal aspect
of the implant. The anterior maxilla, and in particular the
canine fossa, is a common location for this type of defect.
Without advanced imaging techniques, the presence of a
concave ridge may not be clinically evident until the time of
implant placement. If primary implant stability is achievable,
fenestration defects are best managed with a particulate graft
material covered with a GTR membrane. Small defects are
appropriately managed with allografts, alloplasts, or combina-
tions thereof, covered with a resorbable membrane. This may
be done with a separate incision to prevent disruption of the
coronal soft tissue.55 Larger defects may require additional
stabilization for space making purposes. This is most easily
achieved by the use of a titanium-reinforced PTFE membrane
stabilized with tacks or microscrews. In larger fenestration or
dehiscence type of defects, the implant surgeon should give
strong consideration to the use of autogenous bone shavings
or chips to increase the biologic capacity of the graft.56
CORONAL DEFECTS
The immediate placement of implants into extraction sites is
a predictable and clinically advantageous approach, but can
be perilous from an aesthetic standpoint as a result of continu-
ous remodeling of the socket wall and associated soft tissue.57,58
The management of the gap between the implant and the
socket wall has been controversial, with some groups advocat-
ing routine grafting of the gap and others suggesting that it
makes no difference in clinical outcome. Indeed, a critical
review of the available evidence on this subject fails to provide
the implant surgeon with reliable data on which to base clini-
cal decisions. First, the initial studies on the “jumping dis-
tance” were done on experimentally created defects, which
have been shown to heal more readily than extraction defects.59
Second, achieving osseointegration or vital bone formation at
the implant interface has been used as the criteria for success,
rather than maintenance of bone and soft tissue volume. Aes-
thetic outcomes or long-term stability of the restorative soft
tissue envelope has not been evaluated. Third, there are no
controlled, randomized prospective human studies comparing
grafted sites and ungrafted sites with immediate implant
placement.
The evidence does show the outcome when the gap is not
grafted. Covani et al.60 reported that histologically, gaps
greater than 1.5 mm heal with connective tissue apposition to
the implant surface rather than direct bone contact, a condi-
tion claimed to be clinically “successful.” The same group, in
a prospective study, evaluated the buccolingual changes in
bone width in sockets with immediately placed implants.
They found that all implants integrated successfully; however,
there was a decrease in buccolingual width of the socket from
a mean of 10.5 mm to a mean of 6.8 mm, a 56% decrease in
ridge width.61 Araujo et al. confirmed in a recent dog study
that implant placement into extraction sites does not prevent
bone loss, but they found “marked attenuation” of both buccal
and lingual walls, and resolution of the gap between the
implants and socket walls occurred via simultaneous of apposi-
tion and resorption.62
Clearly, additional studies are warranted to determine the
most effective materials and techniques for managing the
gap around implants placed into extraction sites. It is widely
agreed, however, that bone-implant contact occurs via appo-
sitional growth from lateral walls and the apex of the socket.
It is also evident that isolation of the socket from advancing
soft tissues is warranted, following the principles of GTR. In
this regard, the coronal margins of a fresh extraction site are
no different than any other bone defect.
■ THE USE OF GUIDED TISSUE
REGENERATION MEMBRANES IN
SUBANTRAL AUGMENTATION
The posterior maxilla can be a particularly difficult area to
restore when periodontal disease or pneumatization of the
maxillary sinus causes a loss in the height of alveolar bone.
Subantral bone augmentation is a well-documented technique
for increasing bone height in this area before or in conjunc-
tion with the placement of endosseous implants (Figure 25-6).
Because the traditional surgical approach requires entry into
the subantral space via a lateral antral window, upon closure
the bone graft is directly opposed to soft tissue. Although
clinically successful, residual bone defects and ingrowth of
connective tissue into sinus grafts at the lateral wall opening
have been reported by McAllister et al.6
In order to achieve the maximum percentage of vital bone
in the grafted sinus, the placement of a GTR membrane over
the window was suggested and has been shown to be beneficial
in several studies. A retrospective analysis by Froum et al.,
reporting on 113 grafted sinuses grafted with a variety of mate-
rials, indicated a substantial increase in bone formation when
an ePTFE membrane was used over the window.64 A trial by
Tarnow et al. using a bilateral sinus model on 12 patients, using
histologic and histomorphometric data, showed that vital bone
formation in the membrane-covered sinus averaged twice that
of sinuses not covered by a membrane and an increased implant
survival rate compared with controls.65 Tawil and Mawla,
using anorganic bovine bone and a bilayered collagen mem-
brane, found a higher overall implant survival rate with
machined surface implants when a membrane was used com-
pared with sinuses grafted with no membrane.66
Both bioresorbable and nonresorbable membranes have
been evaluated for this application. In a study comparing
 CHAPTER 25 •
A B
FIGURE 25-6. A, Increases in vital bone density and implant survival have been found when an occlusive membrane
is used to cover sinus-lift access windows. Without a membrane, soft tissues derived from the overlying flap may invade
the particulate graft. B, The use of type I bovine collagen is a reasonable choice because a second surgery to remove
the barrier is not desirable.
ePTFE and PGA membranes in nine sinus grafting proce-
dures, Avera et al. found similar clinical and histologic
results.67 A recent prospective trial was conducted by Wallace
et al. comparing ePTFE membranes with resorbable collagen
membranes and controls. Data was collected from 64 sinus
grafts in 51 patients followed by the placement of 135 implants.
At 6 and 10 months, histologic analysis revealed a vital bone
percentage of 17.6%, 16.9%, and 12.1% respectively, indicat-
ing no significant difference among the membrane groups.
Implant survival rates were similar.68
In summary, the available clinical data indicates that the
use of an occlusive membrane over the sinus window is clini-
cally effective, resulting in an increase in vital bone formation
compared with conventional treatment. These benefits likely
occur through exclusion of nonosteogenic connective tissue
from the grafted sinus and increased isolation of the bone
defect.
Statistically an increased implant survival rate has been
found, although the numbers of failures in these studies are
very limited. Both resorbable and nonresorbable membranes
have been shown to be effective for this application. Because
space making is usually not an issue in this setting and second
surgical procedures to expose the lateral antral wall are typi-
cally not associated with subsequent implant placement, use
of a resorbable membrane is preferable.
■ MEMBRANES OVER
BLOCK GRAFTS
The use of autogenous corticocancellous bone blocks for local-
ized ridge augmentation has been shown to be a predictable
method of augmentation. A logical question is whether or not
the simultaneous use of a barrier membrane results in improve-
ment in success rates, improved retention of graft volume, or
a decrease in complication rates.
The use of barrier membranes to cover autogenous bone
grafts for lateral ridge augmentation was evaluated by Buser.69
Guided Tissue Regeneration in Implant Dentistry 437
Forty partially edentulous patients were treated with autoge-
nous grafts in block form and in particulate form, which were
then covered by an ePTFE membrane. Evaluation 7 to 10
months later revealed a mean increase in width of 3.53 mm,
and it was concluded that the use of the membrane resulted
in no clinically evident resorption of the block grafts. In a
pilot study using seven consecutive patients, Proussaefs and
Lozada evaluated the results of resorbable collagen membrane
in conjunction with autogenous bone graft and anorganic
bovine bone for buccal ridge augmentation. Clinical and
radiographic assessment at 6 months revealed a net gain of
4.61 mm in width and 13.79% resorption between months 1
and 6.70
These results stand in stark contrast to previous reports of
cortical graft resorption. Ten Bruggenkate et al., in a series of
22 patients, reported a mean increase in ridge width from 2.9
to 6.5 mm immediately after augmentation. The mean crestal
width 6 months later was only 4.5 mm, indicating a resorption
of approximately 50%.71
Animal studies provide insight into the biologic effects of
the membrane barrier in this particular clinical setting. With
a block onlay graft, there are two potential sources of blood
supply to the grafted bone: the host bone adjacent to the block
and the overlying periosteum. Histologic evaluation reveals
that if an occlusive membrane is used, revascularization of the
graft occurs only from the osseous recipient bed.72 Therefore,
with a membrane, revascularization is a somewhat slower
process, resulting in greater apparent bone volume when com-
pared with grafts without membranes. However, significant
data from controlled clinical trials is scant.
A recent case series, published by von Arx and Buser,73
evaluated the use of autogenous block grafts, anorganic bovine
bone “filler,” and a resorbable collagen membrane for horizon-
tal ridge augmentation of 58 sites in 42 patients. Over a mean
healing time of 5.8 months before reentry, they reported a
mean increase in ridge width of 4.6 mm with a mean resorp-
438 SECTION IV ■ Implant Surgery
tion of only 0.36 mm. They concluded that the technique was
a predictable means of achieving an increase in bone volume,
with minimal complications. In the rare instance of mem-
brane exposure after primary closure, infection was not
observed.73
Based on the available evidence, the use of a membrane
barrier over autogenous block grafts appears advisable at this
time. Either nonresorbable or resorbable membranes can be
used. Clinicians should recognize that the apparent beneficial
effect of reduced apparent graft resorption is due to reduced
revascularization of the graft,74 and therefore longer healing
times may be required before remodeling of the graft into vital
bone takes place.
■ ALVEOLAR RIDGE PRESERVATION
AND IMPLANT SITE
DEVELOPMENT: THE USE OF
GUIDED TISSUE REGENERATION
TO REDUCE POSTEXTRACTION
BONE LOSS
A similar controversy exists regarding the routine grafting
of extraction sites, whether in preparation for placement of
implants or for preservation of the alveolar ridge. In the next
section, we will examine the clinical impact of postextraction
bone loss and then develop a rationale for the application of
GBR to extraction-site healing and ridge preservation.
Following tooth extraction, healing of alveolar bone and
the associated soft tissues progresses quickly, predictably, and
usually without complications. However, the close proximity
of aggressive gingival soft tissues results in only partial osseous
repair of the socket. Classical descriptions of extraction-site
healing indicate that two-thirds of the extraction socket typi-
cally fills with bone with the most coronal aspect of the socket
filling with fibrous tissue.75,76 In the anterior maxilla, this
pattern of healing and subsequent physiologic modeling of the
alveolus may result in a loss of as much as 40% in height and
60% in alveolar width during the first 6 months,77 with the
majority of the horizontal width loss occurring at the expense
of the buccal plate.78 The impact of bone loss in terms of
optimal implant placement is significant. Malposed implants
are subject to biomechanical overload and are technically dif-
ficult to restore, increasing the difficulty in achieving a natural
emergence profile and pleasing soft tissue framework surround-
ing the restoration. The number of procedures developed in
recent years to augment deficient ridges, including GTR, autog-
enous block grafting, and distraction osteogenesis, is a testa-
ment to the scope of the problem. Less dramatic, but equally
relevant, is the impact of bone loss on soft tissue aesthetics.
The consequences of postextraction bone loss have been
assessed in several studies using measurements taken at the
time of extraction, at the time of implant placement, and at
the time of second-stage surgery. Covani et al., evaluating
bone healing in extraction sites with immediately placed
implants, concluded that the gap between the implant and
the buccal wall would spontaneously fill with bone with no
graft material or membrane if it was less than 2.0 mm in width.
However, they reported a mean net reduction in ridge width
of 3.7 mm.61 In a related study, the same group compared
healing in immediately placed implants with delayed place-
ment. The mean ridge width at the time of extraction was
10.0 mm, whereas the mean ridge width found in the delayed
group (as measured 6 to 8 weeks postextraction) was 8.86 mm.
At the time of second-stage surgery, the mean ridge width in
the immediately placed group was 8.1 mm and in the delayed
group was 5.8 mm, indicating a net loss of 1.9 mm and 4.2 mm,
respectively. They concluded that ridge resorption began
immediately after tooth extraction and continued nonuni-
formly, even after delayed implant placement.60
Further evidence of clinically significant postextraction
bone loss has been documented by Schropp et al. In a 12-
month prospective study of single-tooth extraction sites, they
reported a mean reduction in alveolar width of 6.1 mm, with
two thirds occurring in the first 3 months.79 Botticelli, report-
ing on the healing of extraction sites with immediately placed
implants, reported a reduction in buccal ridge width of 56%
and a reduction in lingual ridge width of 30% in 4 months.80
RIDGE PRESERVATION STUDIES
Nemkovsky et al.81 performed a ridge preservation study using
dense hydroxyapatite granules in fresh extraction sites. The
granules were covered with a split-thickness connective tissue
flap rotated from the palate. The missing teeth were replaced
with a fixed prosthesis. Ridge dimensions were observed and
recorded over 12 to 24 months using the base of the pontics
as a fixed reference point. A mean horizontal tissue loss of
0.6 mm was observed, whereas a mean vertical loss of 1.4 mm
was reported, indicating the potential efficacy of the procedure
as long as primary closure was maintained to prevent particle
loss.
In a more recent study, Nevins et al. evaluated the effect
of augmenting sockets with anorganic bovine bone compared
with untreated controls.82 CT scans were taken immediately
postoperatively and from 60 to 90 days postoperatively. Using
the nasal floor as a fixed point of reference, they compared the
preoperative and postoperative change in ridge height at a
width of 6.0 mm, considered sufficient for placement of stan-
dard diameter dental implants. There was significantly less
bone resorption seen in the sites grafted with anorganic bovine
bone, with a mean loss of 2.42 mm in height compared with
5.24 mm in controls. In the control sites, this represented a
net loss of nearly 30% in ridge height. No membrane was used
in this study; a split-thickness flap and primary closure was
achieved to contain the graft material.
There is clinical evidence showing that the principles of
GTR can be applied to extraction sites, resulting in more
complete bone healing and a reduction in early bone loss. In
a clinical study designed to evaluate the effect of GTR mem-
branes on healing extraction sites, Lekovic et al. reported
significantly less bone resorption in sockets covered with
membranes.83 In this controlled, prospective pilot study, two
teeth were extracted from the same patient in the same dental
arch. Immediately following extraction, one socket was
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry
covered with an ePTFE membrane and primary closure,
whereas the other was treated with flap advancement and
primary closure. The sites were evaluated 6 months later using
measurements taken from study models and direct bone mea-
surements made during reentry surgery. The experimental
sites averaged 0.50 mm in vertical bone loss compared with
1.20 mm in controls, as determined by direct bone measure-
ment. In the horizontal dimension, experimental sockets aver-
aged 1.8 mm in bone loss compared with 4.40 mm in controls.
Measurements were made to evaluate internal bone fill. The
experimental sockets averaged a reduction in depth of 4.90 mm
versus 3.00 mm in controls, indicating more vigorous osseous
regeneration under the membrane. The authors concluded
that the larger dimensional changes observed in the control
group were statistically significant and that the technique
offered a predictable method of ridge preservation. However,
a relatively high (30%) incidence of premature exposure of
the ePTFE membranes occurred in this study. In these sites,
even in the absence of infection, clinical bone measurements
were similar to controls. With regard to future use of the pro-
cedure, the authors suggest the development of membranes
with specific properties designed for use in extraction sites.
In a second clinical study, Lekovic et al. evaluated the effect
of resorbable membranes (polylactide-co-glycolide) on healing
extraction sites.84 In this blinded, prospective, randomized,
controlled clinical trial, two teeth were extracted in the same
dental arch. The sockets were either treated with a resorbable
membrane and primary closure or primary closure alone. Tita-
nium pins were placed at the time of extraction to serve as
fixed reference points, and measurements were taken immedi-
ately postextraction. Six months after the initial surgery,
reentry surgical procedures were performed. Internal socket fill
and external horizontal and external vertical bone measure-
ments were all repeated and compared with the immediate
postextraction values. Experimental sites averaged 0.38 mm of
vertical bone loss compared with 1.5 mm in controls. In the
horizontal dimension, experimental sites averaged 1.31 mm of
bone loss compared with 4.56 mm in controls. With regard to
internal bone fill, the experimental sites averaged a reduction
in depth of 5.81 mm versus 3.94 mm in controls. The authors
noted that the mean postoperative ridge width of 6.06 mm for
experimental sites compared with 2.94 mm for controls was
especially significant when considering future implant place-
ment. The authors suggest that the reduction in bone loss is
likely a result of the ability of the membrane to stabilize the
blood clot and prevent migration of epithelial and gingival
connective tissue cells into the defect area.
As an alternative to using a GTR membrane, a technique
for augmenting extraction sites using calcium sulfate as a
“barrier” has been proposed. Camargo and Lekovic et al. per-
formed a prospective clinical trial using bioactive glass particles
placed into extraction sites and covered with a layer of calcium
sulfate.85 No attempt was made to achieve primary closure.
Titanium pins were placed to serve as fixed reference points,
and surgical reentry was done at 6 months. Clinical measure-
ments indicated less, although not statistically significant,
439
resorption of alveolar bone height, indicating 0.38 ± 3.18 mm
for experimental sites compared with 1.00 ± 2.25 mm for con-
trols. In the horizontal plane, experimental sites averaged a
similar degree of resorption to controls averaging 3.48 ±
2.68 mm compared with 3.06 ± 2.41 mm for controls. There
was a statistical improvement in internal socket fill, with an
average decrease in defect depth of 6.43 mm versus 4.00 mm
in controls. The authors conclude by stating that the combina-
tion of bioactive glass and calcium sulfate is of “some benefit”
in preserving alveolar ridge dimensions after tooth extraction.
The results of this study are particularly interesting in that they
can be compared with the previously mentioned studies by
Carmago et al. and Lekovic et al. because of the similarity of
the study design and participation of common investigators.
In a clinical study of extraction sites grafted with mineral-
ized bone allograft and covered with collagen membranes,
Iasella et al. compared grafted versus nongrafted sites at 4 and
6 months.86 Parameters evaluated were dimensional changes;
implant success rates; bone quality, as determined by histo-
logic examination; and gingival thickness. Clinical measure-
ments were taken at the time of extraction and then at implant
placement. In the experimental sites, an increase in vertical
height, as opposed to bone loss, was achieved. The average
vertical gain was 1.3 ± 2.0 mm versus an average loss of 0.9 ±
1.6 mm in controls. In the horizontal dimension, the experi-
mental sites had an average loss of 1.2 mm compared with
2.7 mm in control sites. Histologic analysis of bone cores
revealed a slightly higher bone density in experimental sites
compared with controls (65% versus 54%), although this
included both vital and nonvital allograft bone in the grafted
sites. The authors concluded that the most predictable main-
tenance of ridge width, height, and position was achieved
when a ridge preservation procedure was employed. The pres-
ence of residual, nonvital allograft demonstrates the impor-
tance of using a rapidly resorbable graft material for implant
site development. As a result, clinicians should be aware of
the potential for dense, slowly degrading materials to interfere
with or delay vital bone formation.
■ A RATIONALE AND TECHNIQUE
FOR RIDGE PRESERVATION
USING DPTFE MEMBRANE
A technique developed by the author using dPTFE as a mem-
brane for extraction site grafting can be used for either
immediate implant placement into extraction sites or ridge
preservation following tooth extraction (Figure 25-7). The
procedure is designed to afford the implant surgeon the pre-
dictability of a nonresorbable membrane with the simplicity
and ease of use typical of a resorbable device. The submicrom-
eter porosity of dPTFE allows the clinician flexibility with
regard to achieving primary closure. Historically, achieving
and maintaining primary closure over GTR membranes has
been a major problem associated with immediate grafting of
extraction sites. Even when primary closure is achieved, sub-
sequent membrane exposure occurs approximately one third
of the time.81,85 Depending on the timing and extent of the
440 SECTION IV ■ Implant Surgery

1A 1B 1C

2A 2B

3A 4A 4B
FIGURE 25-7. 1A and 1B, Minimally invasive, atraumatic extraction technique should be used. The use of periotomes or surgical sectioning is encouraged
to minimize mechanical trauma to the thin cortical bone. 1C, All soft tissue remnants should be removed with sharp curettage. Special care should be taken to
remove residual soft tissues at the apical extent of the socket of endodontically treated teeth. Bleeding from the socket walls should be noted and if necessary,
decortication of the socket wall can be done with a #2 round burr to increase early vascularization and access to osteoprogenitor cells. 2A and 2B, The subperi-
osteal pocket is created with a small periosteal elevator or curette, extending 3-4 mm beyond the socket margins (or defect margins) on the palatal and the facial
aspect of the socket. In the esthetic zone, rather than incising and elevating the interdental papilla, it is left intact and undermined in a similar fashion. The d-PTFE
membrane will be tucked into this subperiosteal pocket. 3A, Particulate augmentation material is placed into the socket with a syringe or curette. Ensure that the
material is evenly distributed throughout the socket, but not condensed or packed too tightly. This will only reduce the available space between particles, which
is critical for vascular ingrowth and subsequent bone formation. 4A and 4B, The d-PTFE membrane is trimmed to extend 3-4 mm beyond the socket walls and
then tucked subperiosteally under the palatal flap, the facial flap and underneath the interdental papilla with a curette. The membrane should rest on bone 360-
degrees around the socket margins, if possible. Note that minimal flap reflection is necessary to stabilize the membrane. 5A, Prior to suturing, ensure that there
are no folds or wrinkles in the membrane and that it lies passively over the socket. Remove any stray bone graft particles which may be present between the
membrane and the flap. To prevent bacterial leakage under the membrane, take care to avoid puncturing the membrane, and do not overlap two adjacent mem-
branes. 5B, The membrane is further stabilized with a criss-cross d-PTFE suture. Alternatively, interrupted sutures may be placed. The PTFE sutures, which cause
minimal inflammatory response, are left in place for 10 to 14 days. 6A-C, The membrane is removed, nonsurgically, in 21-42 days. With intact sockets, the
membrane may be removed as early as 3 weeks. Studies have shown that by 21-28 days there is a dense, vascular connective tissue matrix in the socket and
early osteogenesis is observed in the apical 2/3 of the socket. Sockets with missing walls may benefit from a longer time frame. Topical anesthetic is applied,
the membrane is grasped with tissue forceps and simply removed with a gentle tug. 7A, Immediately following membrane removal, a dense, highly vascular,
osteoid matrix is observed filling the socket. Adjacent gingival epithelium migrates across the osteoid matrix upon removal of the membrane. 7B, The socket at
6 weeks. Thick, keratinized gingiva is beginning to form over the grafted socket. The natural soft tissue architecture is preserved, including the interdental papillae.
New bone is beginning to form in the socket.
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry 441

5A 5B

6C
6A 6B

7A1 7A2

7B1 7B2

FIGURE 25-7, cont’d.

442 SECTION IV ■ Implant Surgery
exposure, the outcome may or may not be affected; however,
complications, such as infection, particle loss, and even overt
graft failure, are frequently reported. To prevent the perceived
complications associated with the use of an occlusive mem-
brane, alternative techniques have been suggested in which—
instead of using an occlusive membrane—a rapidly resorbing
material, such as Gelfoam, a collagen sponge, or calcium
sulfate, is used as a temporary “barrier” over the graft mate-
rial.88,89 Although clinical success may be achieved using these
techniques in single, relatively intact sockets, the use of a
membrane is required for more demanding cases, such as
where there is a buccal plate defect.90
In contrast, the use of an occlusive membrane, over even
an intact socket, ensures predictable exclusion of soft tissue
from the healing extraction site. If an associated bone defect
is encountered, the margins of the membrane may be easily
extended beyond the margins of the defect while simultane-
ously providing coverage for the socket. Finally, as a result of
the sub-micron level porosity, tissue ingrowth into the mem-
brane does not occur. This feature facilitates simple, nonsurgi-
cal removal of the barrier at a time determined by the
surgeon.
TECHNIQUE
The procedure is indicated following the extraction of single
or multiple adjacent teeth and is equally effective in the aes-
thetic zone or the posterior quadrants. The procedure is con-
traindicated in the presence of symptomatic, active infection,
characterized by purulence or pain.
Extraction of the involved teeth should be carried out using
minimally invasive and atraumatic techniques. The use of
periotomes and careful surgical sectioning of teeth is suggested,
along with gentle application of luxation and extraction force.
Following tooth removal, all adherent soft tissue, remnants of
the periodontal apparatus, and associated soft tissue should be
removed with sharp curettage. The apex of the socket should
be carefully explored to eliminate the possibility of residual soft
tissue, which may harbor pathogenic bacteria. There should
be brisk bleeding noted from the socket walls. If not, decortica-
tion with a surgical bur is suggested. Graft material is then
placed into the socket with a small curette, taking care to
evenly distribute the material throughout the socket and any
associated defects. However, care should be taken to avoid
overpacking the graft particles because this can impede the
early ingrowth of blood vessels, which are critical to bone for-
mation. The socket may be slightly overfilled with material;
however, with the use of a membrane, the implant surgeon
should keep in mind that 100% of the blood supply to the graft
will originate from the osseous compartment rather than the
overlying flap or periosteum.
The membrane is then carefully trimmed to fit over the
site, extending 3.0 to 4.0 mm beyond the margins of the socket
and any associated bone defects. The corners of the membrane
should be gently rounded and smooth. The membrane should
also be trimmed to provide a minimum of 1.0 mm of space
between the membrane and any adjacent tooth roots. This
will allow for rapid reattachment of the interdental papilla
and result in the most predictable and aesthetic soft tissue
healing.
The membrane should lie passively across the socket and
under the adjacent flaps. If necessary, the membrane may be
stretched slightly over the fingertips or curved over an instru-
ment handle to help achieve a passive fit. All fold and wrin-
kles should be eliminated because they can be irritating or
provide easy access for bacteria to migrate under the soft tissue
flaps. If two pieces of membrane are being used, care should
be taken to avoid overlapping segments, particularly in an area
where they might become exposed to the oral cavity. Such an
overlap will provide ready access to bacterial migration under-
neath the membrane. In this case, either a larger membrane
should be used or two membranes should be placed inde-
pendently with complete soft tissue coverage between their
exposed edges. Immediately before final membrane placement,
the surgical site should be carefully irrigated with sterile saline.
Special attention should be paid to removal of stray graft par-
ticles, which if left between the flap and membrane, may result
in infection or provide a conduit for oral bacteria to infiltrate
the graft.
Monofilament PTFE suture is recommended for closure.
Tension-free adaptation of the flap to the membrane and
elimination of dead space are required. Care should be taken
to avoid puncturing the membrane during suturing maneuvers
in any area that is exposed to the oral cavity. A criss-cross
suture technique may be used in single sockets, or alterna-
tively, two interdental interrupted sutures combined with a
horizontal mattress suture across the midportion of the socket
can be used. Following closure, the surgical site should be
carefully examined to ensure adequate blood supply to the flap
margins. The temporary prosthesis, if present, should be care-
fully trimmed to avoid placing any pressure on the surgical
site.
Postoperatively the patient can be seen in 1 week for obser-
vation and removal of loosened sutures. Local application of
chlorhexidine rinse to the exposed membrane and gentle
cleaning with a Q-tip is advised. Suture removal is done at 2
weeks, and the membrane is again inspected to ensure
complication-free healing. Gentle pressure applied to the
exposed membrane with an instrument should reveal a solid,
noncompressible and nontender graft site.
On the third postoperative week (21 to 28 days) in intact
sockets, the membrane is removed. Larger defects or those
missing adjacent walls may require additional time before
membrane removal, but in no case longer than 6 to 8 weeks.
Topical anesthetic may be applied, and the membrane is
simply removed by grasping the exposed membrane with a
cotton forceps and gently removing it from the tissue bed. A
glistening, well-vascularized, well-consolidated graft should
be observed at that time. If loose graft particles are observed,
they are simply removed with sterile irrigation. The patient is
instructed to keep the surgical site clean and free of debris,
and initial reepithelialization of the underlying tissue will
occur in 7 to 10 days.
Text continued on p. 455
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry 443

CASE REPORT 25-1 Flapless Buccal Wall Reconstruction Using Titanium-Reinforced dPTFE Membrane

TI REINFORCED FLAPLESS PROCEDURE
A flapless approach to socket reconstruction, developed by the author
(BKB), is facilitated by the use of a titanium-reinforced membrane. A
severe buccal wall defect is present secondary to a vertical root fracture
(Figures 25-8 and 25-9), and a chronic fistula was present. The tooth is
removed using an intrasulcular incision (Figure 25-10). The entire buccal
wall was missing, and granulation tissue, which was adherent to the
facial flap, was removed with sharp dissection (Figure 25-11). Next, a
subperiosteal pocket is developed on the facial and palatal aspect of the
socket, extending 3 mm beyond the defect margins (Figure 25-12). A
composite graft of mineralized and demineralized allograft is placed into
the socket (Figure 25-13). A titanium-reinforced dPTFE membrane
in single-tooth configuration is trimmed to completely cover the facial
defect and coronal aspect of the socket. The membrane is introduced
into the facial pocket first (Figure 25-14) and then tucked under the
palatal flap (Figure 25-15).The single titanium strut facilitates precise
placement and stabilization of the device. Primary closure is not achieved
in this case to preserve the soft tissue architecture (Figure 25-16). The
membrane was nonsurgically removed at 4 weeks, and at 6 months
there was adequate ridge width for placement of a dental implant and
maintenance of the soft tissue architecture (Figure 25-17). Complete
regeneration of the socket and facial bone was evident at 6 months at
the time of implant placement (Figure 25-18). A biopsy taken at the time
of implant placement revealed 80% vital bone (Figure 25-19). (Histology
courtesy of Michael Rohrer, D.D.S., M.S.)

FIGURE 25-8 FIGURE 25-9

FIGURE 25-10 FIGURE 25-11

FIGURE 25-12 FIGURE 25-13

Continued
444 SECTION IV ■ Implant Surgery

CASE REPORT 25-1 Flapless Buccal Wall Reconstruction Using Titanium-Reinforced dPTFE Membrane—cont’d

FIGURE 25-14 FIGURE 25-15

FIGURE 25-16 FIGURE 25-17

FIGURE 25-18
FIGURE 25-19. To view a color version of this illustration, refer to
the color insert section at the back of this book.
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry 445

CASE REPORT 25-2 A Dual-Layer Guided Tissue Regeneration Technique for Immediate Implant Placement

DUAL-LAYER GUIDED SOCKET REGENERATION TECHNIQUE
This is a 65-year-old female with a crown-root fracture of the maxillary
right central incisor. The crown was retained with denture adhesive.
There is a thin biotype and multiple, adjacent porcelain fused to metal
restorations (Figure 25-20), increasing the aesthetic risk. The tooth root
was extracted using only an intrasulcular incision, an implant was
placed, and the facial gap (2.5 mm) was grafted with demineralized
allograft bone and beta tricalcium phosphate (Figure 25-21). To thicken
the soft tissue, a subperiosteal pocket was developed on the facial and
palatal aspect of the socket, and a type I bovine, cross-linked collagen
membrane was placed to extend approximately 5 mm beyond the
socket margins (Figure 25-22). To protect the collagen membrane and
further stabilize the site, a textured dPTFE membrane was placed over
the collagen (Figure 25-23), and closure was achieved with a criss-
cross dPTFE suture (Figure 25-24). The suture was removed at 2
weeks, and at 4 weeks the dPTFE membrane was nonsurgically
removed with topical anesthesia (Figure 25-25).

FIGURE 25-20A FIGURE 25-20B

FIGURE 25-21 FIGURE 25-22

FIGURE 25-23 FIGURE 25-24

FIGURE 25-25A FIGURE 25-25B

Continued
446 SECTION IV ■ Implant Surgery

CASE REPORT 25-2 A Dual-Layer Guided Tissue Regeneration Technique for Immediate Implant Placement—cont’d

After 4 months of healing, the soft tissue architecture is stable, with interdental crest (Figure 25-26 B). A Procera Zirconia abutment was
full interproximal papillae (Figure 25-26 A). A removable temporary fabricated on an implant level model and provisionally restored (Figures
partial denture was used with an ovate pontic. Radiographically, there 25-27 and 25-28).
is good bone density adjacent to the implant and maintenance of the

FIGURE 25-26A

FIGURE 25-26B

FIGURE 25-27 FIGURE 25-28

 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry 447

CASE REPORT 25-3 Repair of Localized Dehiscence Defects Associated with Implant Placement

This dehiscence defect was encountered after removal of residual soft I bovine collagen membrane. At 4 months, the implant was restored in
tissue from a recent, nongrafted extraction site. The implant was stable, a conventional two-stage technique (Figure 25-29 through 25-33).
and the defect was managed with a combination of allograft and a type

FIGURE 25-29 FIGURE 25-30

FIGURE 25-31

FIGURE 25-32 FIGURE 25-33

448 SECTION IV ■ Implant Surgery
CASE REPORT 25-4 Alveolar Ridge Augmentation Using Allograft Bone Putty and Resorbable Collagen Membrane
The preoperative view (Figure 25-34) demonstrates inadequate ridge
width requiring augmentation before placement of endosseous implants.
A midcrestal, full-thickness incision and reflection reveals the atrophic
ridge, which is perforated with a #2 round surgical bur in preparation
for augmentation (Figure 25-35). A composite graft consisting of auto-
genous bone shavings (Figure 25-36) combined with mineralized and
demineralized allograft putty (Exactech, Inc. Gainesville, Fla.) is placed
(Figure 25-37). A type I bovine, cross-linked bovine collagen membrane
(Osteogenics Biomedical, Inc. Lubbock, TX) is positioned to completely
FIGURE 25-34
FIGURE 25-36
FIGURE 25-38
cover the graft (Figure 25-38). Tension-free primary closure is achieved
with dPTFE suture (Figure 25-39). After 6 months, the augmented site
was well healed (Figure 25-40). On exposure, the graft was found to
be well consolidated and endosseous implants were placed (Figure
25-41). Histologic analysis of the grafted ridge revealed 43% bone by
volume, 97% of which was vital bone, and 3% residual, nonvital allograft
(Figure 25-42). The implants were allowed to integrate for 3 months
and then progressively loaded with an acrylic provisional restoration
(Figure 25-43).
FIGURE 25-35
FIGURE 25-37
FIGURE 25-39
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry 449

Alveolar Ridge Augmentation Using Allograft Bone Putty and Resorbable Collagen
CASE REPORT 25-4 Membrane—cont’d

FIGURE 25-40 FIGURE 25-41

FIGURE 25-43

FIGURE 25-42. To view a color version of this illustration, refer

to the color insert section at the back of this book.
450 SECTION IV ■ Implant Surgery
Alveolar Ridge Augmentation Using Allograft and Xenograft Bone with Titanium-Reinforced
CASE REPORT 25-5 dPTFE Membrane
This case demonstrates the use of titanium-reinforced, dPTFE mem-
brane (Osteogenics Biomedical, Lubbock, TX) for lateral ridge augmen-
tation of the posterior mandible. A combination of allograft bone and
anorganic bovine bone mineral was used, and primary closure was
achieved and maintained over the membrane for 4 months (Figure
25-44). At the time of implant placement, the membrane was removed
using a midcrestal incision (Figure 25-45). An increase in ridge width
FIGURE 25-44
FIGURE 25-46
was evident (Figure 25-46), and implants of adequate width were
placed (Figure 25-47). The implants (Tapered Screw-Vent, Zimmer
Dental, Carlsbad, CA) were restored with a fixed prosthesis (Figure
25-48). The postoperative panoramic radiograph demonstrates good
bone density after 12 months of use (Figure 25-49). (Case photos
courtesy of Dr. Joel Rosenlicht, Manchester, CT)
FIGURE 25-45. To view a color version of this illustration, refer
to the color insert section at the back of this book.
FIGURE 25-47
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry 451

Alveolar Ridge Augmentation Using Allograft and Xenograft Bone with Titanium-Reinforced
CASE REPORT 25-5 dPTFE Membrane—cont’d

FIGURE 25-48

FIGURE 25-49
452 SECTION IV ■ Implant Surgery

The Use of dPTFE Membrane in Combination with Corticocancellous Block Augmentation of

CASE REPORT 25-6 the Posterior Mandible

This case illustrates the use of GTR in conjunction with a corticocancel-
lous block graft. The preoperative evaluation revealed inadequate
height and width for the placement of endosseous implants (Figures
25-50, 25-51, and 25-52). The ridge was exposed with a midcrestal
incision and elevation of a full-thickness mucoperiosteal flap (Figure
25-53). A corticocancellous block was harvested from the left ramus
(Figure 25-54) and secured to the deficient alveolar ridge with rigid fixa-
tion. The gap between the block graft and the ridge was augmented
with an allograft bone (Figure 25-55) and covered with a dPTFE mem-
brane (Figures 25-56 and 25-57). Tension-free primary closure was
achieved with 5-0 dPTFE suture (Figure 25-58) (Osteogenics Biomedi-
cal, Inc. Lubbock, TX). Eight months later, the membrane was
exposed with a midcrestal incision simultaneous with implant place-
ment. An increase in ridge width was clinically evident (Figures 25-59
through 25-62). (Case photos courtesy of Dr. Joel Rosenlicht, Man-
chester, CT)

FIGURE 25-51

FIGURE 25-50

FIGURE 25-53

FIGURE 25-52

FIGURE 25-55

FIGURE 25-54
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry 453

The Use of dPTFE Membrane in Combination with Corticocancellous Block Augmentation of

CASE REPORT 25-6 the Posterior Mandible—cont’d

FIGURE 25-56 FIGURE 25-57

FIGURE 25-58 FIGURE 25-59

FIGURE 25-60 FIGURE 25-61

FIGURE 25-62
454 SECTION IV ■ Implant Surgery
CASE REPORT 25-7 Guided Bone Regeneration in Extraction Sites Using an Open Technique
This patient sustained a traumatic injury to his maxillary anterior teeth
requiring extraction and replacement with dental implants (Figure
25-63). Following extraction of teeth 6, 7, 8, 9, and 10 and minor alveo-
loplasty to remove sharp bony projections (Figure 25-64), dPTFE mem-
branes are trimmed to extend 3 to 5 mm beyond the socket margins
(Figure 25-65) and then tucked under the buccal flap. The sockets were
then augmented with autogenous bone, freeze-dried bone allograft,
anorganic bovine bone, and platelet-rich plasma to preserve ridge
contour (Figure 25-66). The flaps were closed with no attempt to
achieve primary closure over the membrane (Figure 25-67). The
FIGURE 25-63
FIGURE 25-65
FIGURE 25-67
membrane was left exposed for 4 weeks and then removed. Epithelial
migration over the osteoid bed results in increased thickness and width
of keratinized tissue compared with flap advancement and primary
closure (Figures 25-68 and 25-69). Exposure of the augmented eden-
tulous ridge at the time of implant placement 4 months later reveals
adequate ridge width for implant placement without the need for
adjunctive procedures (Figure 25-70). The patient is restored with a
provisional fixed prosthesis 4 months after implant placement (Figure
25-71).
FIGURE 25-64
FIGURE 25-66
FIGURE 25-68
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry
CASE REPORT 25-7 Guided Bone Regeneration in Extraction Sites Using an Open Technique—cont’d
FIGURE 25-69
FIGURE 25-71
■ SUMMARY
Implantology has rapidly evolved from a surgically oriented
discipline, focused on osseointegration, into a complex inter-
disciplinary field encompassing virtually every specialty area
in dentistry. With the current emphasis on aesthetics and
ever-increasing demands on the part of patients and the pro-
fession, the ability to predictably create, enhance, and pre-
serve alveolar bone has never been more important. The
availability of an array of membrane devices, both nonresorb-
able and resorbable, affords the surgeon a high degree of clini-
cal flexibility. The technology is mature, with more than 2
decades of clinical application, resulting in technical refine-
ments and refinements from a treatment planning perspective.
Even as we enter the era of clinical genomics and proteomics,
armed with new molecular tools and techniques, the concepts
of GBR will likely remain vital in the armamentarium of the
implant surgeon.
REFERENCES
1. Weiss PA, Taylor AC: The technology of nerve regeneration. A
review. Sutureless tubulation and related methods of nerve
repair, J Neurosurg 1:400-450, 1944.
455
FIGURE 25-70
2. Murray G, Holden R, Roachlau W: Experimental and clinical
study of new growth of bone in a cavity, Am J Surg 93:385-387,
1957.
3. Hurley L et al: The role of soft tissues in osteogenesis. An experi-
mental study of canine spinal fusions, J Bone Joint Surg 41A:1243-
1254, 1959.
4. Linghorne WJ: The sequence of events in osteogenesis as studied
in polyethylene tubes, Ann NY Acad of Sci 85:445-455, 1960.
5. Melcher AH, Dreyer CJ: Protection of the blood clot in healing
circumscribed bone defects, J Bone Joint Surg 44B(2):424-430,
1962.
6. Boyne PJ: Regeneration of alveolar bone beneath cellulose
acetate filter implants, J Dent Res 43:827, 1964.
7. Boyne PJ: Osseous grafts and implants in the restoration of large
oral defects, J Periodontol 45(5):378-384, 1974.
8. Kahnberg KE: Restoration of mandibular jaw defects in the
rabbit by subperiosteally implanted Teflon mantle leaf, Int J Oral
Surg 8:449-456.
9. Linghorne WJ, O’Connell DC: Studies in the regeneration and
reattachment of supporting structures of the teeth. I. Soft tissue
attachment, J Dent Res 29(4):419-428, 1950.
10. Linghorne WJ, O’Connell DC: Studies in the regeneration and
reattachment of supporting structures of the teeth. II. Regenera-
tion of alveolar process, J Dent Res 30(5):604-614, 1951.
11. Melcher AH: On the repair potential of periodontal tissues,
J Periodontol 47:256-260, 1976.
456 SECTION IV ■ Implant Surgery
12. Dahlin C et al: Generation of new bone around titanium
implants using a membrane technique: an experimental study in
rabbits, J Oral Maxillofac Implants 4:19-25, 1989.
13. Becker W et al: Bone formation at dehisced dental implant sites
treated with implant augmentation material: a pilot study in
dogs, Int J Periodontics Restorative Dent 10:93-101, 1990.
14. Seibert J, Nyman S: Localized ridge augmentation in dogs: a pilot
study using membranes and hydroxyapatite, J Periodontol 61:157-
165, 1990.
15. Rominger JW, Triplett RG: The use of guided tissue regenera-
tion to improve implant osseointegration, J Oral Maxillofac Surg
52(2):106-112, 1994.
16. Hammerle CH, Jung RE, Feloutzis A: A systematic review of the
survival of implants in bone sites augmented with barrier mem-
branes (guided bone regeneration) in partially edentulous
patients, J Clin Periodontol 29(suppl 3):226-231, 2002.
17. Simion M et al: Long-term evaluation of osseointegrated implants
inserted at the time or after vertical ridge augmentation. A ret-
rospective study on 123 implants with 1-5 year follow-up, Clin
Oral Implants Res 12(1):35-45, 2001.
18. Franceschi RT: Biological approaches to bone regeneration by
gene therapy, J Dent Res 12:1093-1103, 2005.
19. Hardwick R, Hayes BK, Flynn C: Devices for dentoalveolar
regeneration: an up-to-date literature review, J Periodontol
66(6):495-505, 1995.
20. Kalfas IH: Principles of bone healing, Neurosurg Focus 10(4):1-
4, 2001.
21. Tinti C, Parma-Benfenati S, Polizzi G: Vertical ridge augmenta-
tion: What is the limit? Int J Periodontics Restorative Dent
16(3):220-229, 1996.
22. Ratner BD: Replacing and renewing: synthetic materials, biomi-
metics and tissue engineering in implant dentistry, J Dental Edu-
cation 65(12):1340-1347, 2005.
23. Aliyev E et al: The effect of polylactide membranes on the levels
of reactive oxygen species in periodontal flaps during wound
healing, 25(19):4633-4637, 2004.
24. Gottlow J et al: New attachment formation as the result of con-
trolled guided tissue regeneration, J Clin Periodontol 11:494-503,
1984.
25. Bartee BK, Carr JA: Evaluation of a high-density polytetrafluo-
roethylene membrane as a barrier to facilitate guided bone regen-
eration in the rat mandible, J Oral Implantol 21:88-95, 1995.
26. Pitaru S et al: Partial regeneration of periodontal tissues using
collagen barriers. Initial observations in the canine, J Periodontol
59:380-386, 1988.
27. Becker J, Jeukam FW, Schliephake H: Restoration of the lateral
sinus wall using a collagen type I membrane for guided tissue
regeneration, Int J Oral Maxillofac Surg 21(4):243-246, 1992.
28. Fugazzotto PA: The use of demineralized laminar bone sheets in
guided bone regeneration procedures: report of three cases, Int J
Oral Maxillofac Implants 11(2):239-344, 1996.
29. Kon S et al: Regeneration of periodontal ligament using resorb-
able and non-resorbable membranes: clinical, histological and
histometric study in dogs, Int J Periodontics Restorative Dent
11:58-71, 1991.
30. Aukhil I, Pettersson E, Suggs C: Guided tissue regeneration-an
experimental procedure in beagle dogs, J Periodontol 57:727-734,
1986.
31. Zaner DJ, Yukna RA, Malinin TI: Human freeze-dried dura
mater allografts as a periodontal biological bandage, J Periodontol
60:617-623, 1989.
32. Lekovic V et al: The use of autogenous periosteal grafts as barri-
ers for the treatment of class II furcation involvements in lower
molars, J Periodontol 62:775-780, 1991.
33. Salama H et al: The utilization of rubber dam as a barrier mem-
brane for the simultaneous treatment of multiple periodontal
defects by the biologic principle of guided tissue regeneration:
case reports, Int J Periodontics Restorative Dent 14(1):16-33,
1994.
34. Kleinheinz J et al: Incision design in implant dentistry based on
vascularization of the mucosa, Clin Oral Implants Res 16(5):518-
523, 2005.
35. Park SH, Wang HL: Clinical significance of incision location on
guided bone regeneration: human study, J Periodontol 78(1):47-
51, 2007.
36. Fugazzatto PA: Maintaining primary closure after guided bone
regeneration procedures: introduction of a new flap design and
preliminary results, J Periodontol 77(8):1452-1457, 2006.
37. Sclar AG: Soft tissue and esthetic considerations in implant dentistry,
Hanover Park, IL, 2003, Quintessence Publishing.
38. Triplett RG: Guided tissue regeneration. In Assael LA, Misiek
DJ, editors: Atlas of the oral and maxillofacial surgery clinics of North
America. Anatomic problems in implant surgery, Philadelphia,
1994, WB Saunders.
39. Mattout P, Mattout C: Conditions for success in guided bone
regeneration, J Periodontol 71(12):1904-1909, 2000.
40. Simion M et al: Bacterial penetration in vitro through GTAM
membrane with or without topical chlorhexidine application: a
light and scanning electron microscopic study, J Clin Periodontol
22:321, 1995.
41. Moses O et al: Healing of dehiscence-type defects in implants
placed together with different barrier membranes: a comparative
clinical study, Clin Oral Implants Res 16(2):210-219, 2005.
42. Lamb JWIII et al: A comparison of porous and non-porous
Teflon membranes plus demineralized freeze-dried bone allograft
in the treatment of class II buccal/lingual furcation defects: a
clinical re-entry study, J Periodontol 72(11):1580-1587, 2001.
43. Walters SP et al: Comparison of porous and non-porous Teflon
membranes plus a xenograft in the treatment of vertical osseous
defects: a clinical re-entry study, J Periodontol 74(8):1161-1168,
2003.
44. Barber HD et al: Using a dense PTFE membrane without primary
closure to achieve bone and tissue regeneration, J Oral Maxillofac
Surg 2007. Accepted for publication.
45. Bartee BK: The use of high density polytetrafluoroethylene to
treat osseous defects: clinical reports, Implant Dent 4:21-26, 1995.
46. Bartee BK: Evaluation of a new polytetrafluoroethylene guided
tissue regeneration membrane in healing extraction sites, Comp
Continuing Education Dent 19:1256-1264, 1998.
47. Park SH, Wang HL: Management of localized buccal dehiscence
defects with allografts and acellular dermal matrix, Int J Periodon-
tics Restorative Dent 26(6):589-595, 2006.
48. Bartee BK: Extraction site reconstruction for alveolar ridge pres-
ervation. Part 2: membrane-assisted surgical technique, J Oral
Implantol 27(4):194-197, 2001.
49. Machtei EE: The effect of membrane exposure on the outcome
of regenerative procedures in humans: a meta-analysis, J Peri-
odontol 72(4):512-516, 2001.
50. Sela MN et al: Enzymatic degradation of collagen guided tissue
regeneration membranes by periodontal bacteria, Clin Oral
Implants Res 14(3):263-268, 2003.
51. Agrawal CM, Athanasiou KA: Technique to control pH in
vicinity of biodegrading PLA-PGA implants, J Biomed Materials
Res 38(2):105-114, 1997.
52. Pretorius JA et al: A histomorphometric evaluation of factors
influencing the healing of bony defects surrounding implants, Int
J Oral Maxillofac Implants 20(3):387-398, 2005.
53. Simion M et al: Guided bone regeneration using resorbable and
nonresorbable membranes: a comparative histologic study in
humans, Int J Oral Maxillofac Implants 11(6):735-742, 1996.
54. Blanco J, Alonso A, Sanz M: Long-term results and survival rate
of implants treated with guided bone regeneration: a 5-year case
series prospective study, Clin Oral Implants Res 16(3):294-301,
2005.
 CHAPTER 25 • Guided Tissue Regeneration in Implant Dentistry
55. Evian CI et al: Therapeutic management for immediate implant
placement in sites with periapical deficiencies where coronal
bone is present, Int J Oral Maxillofac Implants 21(3):476-480,
2006.
56. Widmark G, Ivanoff CJ: Augmentation of exposed implant
threads with autogenous bone chips: a prospective clinical study,
Clin Implant Dent Relat Res 2(4):178-183, 2000.
57. Esposito MA et al: Interventions for replacing missing teeth:
dental implants in fresh extraction sockets (immediate, immedi-
ate-delayed and delayed implants), Cochrane Database Syst Rev
18(4):CD005968, 2006.
58. Fugazzotto PA: Treatment options following single-rooted tooth
removal: a literature review and proposed hierarchy of treatment
selection, J Periodontol 76(5):821-831, 2005.
59. Botticelli D et al: Bone tissue formation adjacent to implants
placed in fresh extraction sockets: an experimental study in dogs,
Clin Oral Implants Res 17(4):351-358, 2006.
60. Covani U et al: Bucco-lingual crestal bone changes after imme-
diate and delayed implant placement, J Periodontol 75(12):1605-
1612, 2004.
61. Covani U, Cornelini R, Barone A: Bucco-lingual bone remodel-
ing around implants placed into immediate extraction sockets:
a case series, J Periodontol 74(2):268-273, 2003.
62. Araujo MG, Wennstrom JL, Lindhe J: Modeling of the buccal
and lingual walls of fresh extraction sites following implant
placement, Clin Oral Implants Res 17(6):606-614, 2006.
63. McAllister B et al: Residual lateral wall defects following sinus
grafting with recombinant human osteogenic protein-1 or Bio-
Oss in the chimpanzee, Int J Periodontics Restorative Dent 18:227-
239, 1998.
64. Froum et al: Sinus floor elevation using anorganic bovine bone
matrix (OsteoGraf/N) with and without autogenous bone: a
clinical, histologic, radiographic, and histomorphometric analy-
sis: part 2 of an ongoing prospective study, Int J Periodontics
Restorative Dent 18:529-543, 1998.
65. Tarnow D, Wallace S, Froum S: Histologic and clinical compari-
son of bilateral sinus floor elevation with and without barrier
membrane placement in 12 patients: part 3 of an ongoing pro-
spective study, Int J Periodontics Restorative Dent 20:116-125,
2000.
66. Tawil G, Mawla M: Sinus floor elevation using bovine bone
mineral (Bio-Oss) with or without the concomitant use of a
bilayered collagen barrier (Bio-Guide): a clinical report of imme-
diate and delayed implant placement, Int J Oral Maxillofac
Implants 16:713-721, 2001.
67. Avera SP, Stampley WA, McAllister BS: Histologic and clinical
observations of resorbable and non resorbable membranes used
in maxillary sinus graft containment, Int J Oral Maxillofac
Implants 12(1):88-94, 1997.
68. Wallace N et al: Sinus augmentation utilizing anorganic bovine
bone (Bio-Oss) with absorbable and nonabsorbable membranes
placed over the lateral window: histomorphometric and clinical
analyses, Int J Periodontics Restorative Dent 25(6):551-559,
2005.
69. Buser D et al: Evaluation of filling materials in membrane-
protected bone defects. A comparative histomorphometric
study in the mandible of miniature pigs, Clin Oral Implants Res
9:137-150, 1998.
70. Proussaefs P, Lozada J: The use of resorbable collagen membrane
in conjunction with autogenous bone graft and inorganic bovine
bone mineral for buccal/labial alveolar ridge augmentation: a
pilot study, J Prosthet Dent 90(6):530-538, 2003.
71. ten Bruggenkate CM et al: Autogenous maxillary bone grafts
in conjunction with placement of I.T.I endosseous implants. A
457
preliminary report, Int J Oral Maxillofac Surg 21(2):81-84,
1992.
72. DeMarco AC, Jardini MA, Lima LP: Revascularization of autog-
enous block grafts with or without an e-PTFE membrane, Int J
Oral Maxillofac Implants 20(6):867-874, 2005.
73. von Arx T, Buser D: Horizontal ridge augmentation using autog-
enous block grafts and the guided bone regeneration technique
with collagen membranes: a clinical study with 42 patients, Clin
Oral Implants Res 17(4):359-366, 2006.
74. Salata LZ, Rasmusson L, Kahnberg KE: Effects of a mechanical
barrier on the integration of cortical onlay bone grafts placed
simultaneously with endosseous implants, Clin Implant Dent Relat
Res 4(2):60-68, 2002.
75. Amler MH: The sequence of tissue regeneration in human
extraction wounds, Oral Surg Oral Med Oral Path 27:309-318,
1969.
76. Amler MH: Age factor in human alveolar bone repair, J Oral
Implantol 19:138-142, 1993.
77. Lekovic V et al: Preservation of alveolar bone in extraction
sockets using bioresorbable membranes, J Periodontol 69:1044-
1049, 1998.
78. Pietrokovski J, Massler M: Alveolar ridge resorption following
tooth extraction, J Prosthet Dent 17:21-27, 1967.
79. Schropp L et al: Bone healing and soft tissue changes following
single-tooth extraction: a clinical and radiographic 12-month
prospective study, Int J Periodontics Restorative Dent 23(4):313-
323, 2003.
80. Botticelli D, Berglundh T, Lindhe J: Hard tissue alterations fol-
lowing immediate implant placement in extraction sites, J Clin
Periodontol 31(10):820-828, 2004.
81. Nemcovsky CE, Serfaty V: Alveolar ridge preservation following
tooth extraction of maxillary anterior teeth. Report on 23 con-
secutive cases, J Periodontol 67:390-395, 1996.
82. Nevins M et al: A study of the fate of the buccal wall of extrac-
tion sockets of teeth with prominent roots, Int J Periodontics
Restorative Dent 26(1):19-29, 2006.
83. Lekovic V et al: A bone regenerative approach to alveolar ridge
maintenance following tooth extraction. Report of 10 cases,
J Periodontol 68:563-570, 1997.
84. Lekovic V et al: Preservation of alveolar bone in extraction
sockets using bioabsorbable membranes, J Periodontol 69:1044-
1049, 1998.
85. Camargo PM et al: Influence of bioactive glass on changes in
alveolar process dimensions after exodontia, Oral Surg Oral Med
Oral Pathol Oral Radiol Endod 90(5):581-586, 2000.
86. Iasella JM et al: Ridge preservation with freeze-dried bone
allograft and a collagen membrane compared to extraction alone
for implant site development: a clinical and histologic study in
humans. J Periodontol 74(7):990-999, 2003.
87. Dies F et al: Bone regeneration in extraction sites after immedi-
ate placement of an ePTFE membrane with or without a bioma-
terial. A report on 12 consecutive cases, Clin Oral Implants Res
7(3):277-285, 1996.
88. Sottosanti JS: Aesthetic extractions with calcium sulfate and
the principles of guided tissue regeneration, Pract Periodontics
Aesthetic Dent 5(5):61-69, 1993.
89. Sclar AG: Preserving alveolar ridge anatomy following tooth
removal in conjunction with immediate implant placement. The
Bio-Col technique, Atlas Oral Maxillofac Surg Clin North Am
7(2):39-59, 1999.
90. Sclar AG: Strategies for management of single tooth extraction
sites in aesthetic implant therapy, J Oral Maxillofac Surg 62(Suppl
2):90-105, 2004.
CHAPTER 26
CONTEMPORARY SINUS-LIFT SUBANTRAL
SURGERY AND GRAFT
Dennis G. Smiler • Muna Soltan • Michelle Soltan Ghostine
The atrophic edentulous posterior maxilla often poses prob-
lems for implant placement. Following loss of teeth, there is
a gradual loss of alveolar bone, and in many patients the sinus
floor dips close to the alveolar ridge, leaving less than optimal
bone height or width for placing implants. In some patients,
the loss of alveolar bone coupled with increased antral pneu-
matization may result in only 2 to 3 mm thickness of alveolar
bone height. The result is insufficient bone to place implants.1
It is for these patients that the sinus-lift procedures represent
a treatment of choice.
Sinus-lift subantral augmentation has produced excellent
results with few complications.2,3 Autogenous bone alone or
in combination with particulate allografts, xenografts, or allo-
plasts have provided excellent results.4 More recently, to
reduce donor site morbidity, increased blood loss, operative
time, and postoperative complications allografts, xenografts,
and/or alloplasts alone, or in combinations, are used as the
graft of choice and without the addition of autogenous bone.5
The grafts are combined with the patient’s blood, platelet-
rich plasma, bone marrow aspirate, aqueous antibiotics, or
sterile saline.6 In some cases, depending on the volume of
alveolar bone, simultaneous sinus-lift subantral augmentation
and implant placement can be accomplished for the
patient.7,8
■ HISTORICAL PERSPECTIVE
As far back as the eighteenth century, successful sinus surger-
ies were performed using calcium sulfate as the graft material.9
In 1893, an American physician George Caldwell and French
laryngologist Henry Luc accessed the maxillary sinus by creat-
ing a lateral window, providing access to lift the sinus mem-
brane. Hilt Tatum in 1975 introduced a technique to increase
alveolar bone height that placed graft material under the
maxillary sinus membrane before placing implants.10 In 1980,
Boyne and James, using the Caldwell-Luc procedure, grafted
autogenous bone between the sinus membrane and antral
floor.11 Smiler and Holmes reported a series of five successful
subantral grafts performed via a lateral window approach
using porous hydroxyapatite alone as the graft material in
1987.12
458
■ BIOLOGIC AND ANATOMIC
CONSIDERATIONS
MORPHOLOGY
The adult maxillary sinus, antrum of Highmore, lies within
the body of the maxilla. It is the largest paranasal sinus, mea-
suring on average 34 mm × 33 mm × 23 mm with a 15 mL
volume. It can occupy the body of the maxilla from the tuber-
osity to the canine fossa. The root apices of molar teeth can
extend into the sinus, with only a thin sheet of bone or con-
nective tissue separating the antrum from the oral cavity.13
With age and loss of maxillary posterior teeth, there is progres-
sive alveolar atrophy, increased pneumatization of the sinus,
and thinning of the buccal wall.
The maxillary sinus is shaped as a quadrangular pyramid.
The sides are directed superiorly, inferiorly, posteriorly, and
anteriorly. The apex of the pyramid is pointed laterally into the
zygomatic process. The base is directed medially toward the
lateral wall of the nose. The medial wall of the sinus is the most
complex. It contains the nasolacrimal duct, which lies on
average 4 to 9 mm anterior to the maxillary ostium. This duct
drains tears and runs from the lacrimal fossa in the orbit, down
the posterior aspect of the maxillary vertical buttress, and
empties into the anterior aspect of the inferior meatus.
The ostium of the maxillary antrum is located in the supe-
rior aspect of the medial wall of the sinus and empties mucus
into the posterior aspect of the hiatus semilunaris. The ante-
rior wall contains the infraorbital foramen with the infraor-
bital nerve running over the roof of the sinus and exiting
through the foramen. The thinnest portion of the anterior
wall is just above the canine fossa. The posterior wall is located
behind the pterygomaxillary fossa and is pierced by the pos-
terior superior alveolar nerves and lies in close proximity to
the internal maxillary artery, the sphenopalatine ganglion, the
foramen rotundum, and the greater palatine nerve.
The superior wall of the maxillary sinus is the floor of the
orbit, through which runs the infraorbital canal and nerve.
The floor of the sinus is approximately 1.00 to 1.25 cm below
the level of the nasal cavity.
 CHAPTER 26 • Contemporary Sinus-Lift Subantral Surgery and Graft
The mucosal lining of the sinus has a rich vascular network
of complex vascular loops that help warm and filter inspired
air. Pseudostratified columnar ciliated epithelium and connec-
tive tissue line the maxillary sinus. The rapid, rhythmic sweep-
ing movements of the cilia remove the mucus that goblet cells
secrete, with the debris and bacterial contaminants, toward
the ostium to the middle meatus of the nose.14-17
■ VASCULAR SUPPLY—LYMPHATIC
DRAINAGE AND INNERVATIONS
ARTERIAL SUPPLY
Branches of the maxillary artery, via the external carotid
artery, supply the maxillary sinus. These include: the infraor-
bital artery as it runs with the infraorbital nerve, the terminal
branches of the sphenopalatine artery, and the posterior lateral
nasal artery that supplies the medial wall of the maxillary sinus
and the mucous membrane lining of the lateral nasal wall.
Branches of the facial artery18 and from the pterygopalatine
artery, the greater palatine artery, the alveolar artery, and the
posterior superior alveolar artery supply the lateral wall of the
sinus.19-21
VENOUS RETURN AND LYMPHATIC DRAINAGE
Venous return of the anterior region of the maxillary sinus
drains from the cavernous plexus into the facial vein. The
posterior return is into the pterygoid plexus of veins via the
sphenopalatine vein and the retromandibular and facial veins.
These empty into the internal jugular vein.22 The lymphatic
drainage from the maxillary sinus is via the infraorbital
foramen through the ostium and into the submandibular lym-
phatic system.
NERVE INNERVATION
The maxillary branch of the trigeminal nerve and its subdivi-
sions innervate the maxillary sinus. The infraorbital subdivi-
sion divides into three branches before exiting the infraorbital
foramen. The posterior superior alveolar, middle superior
alveolar, and the anterior superior alveolar nerve subdivisions
innervate the maxillary sinus, the maxillary teeth, and the
buccal surfaces of the gingiva. The anterior superior alveolar
nerve, off the infraorbital nerve, lies within the infraorbital
canal, situated in the anterior wall of the maxillary sinus. The
middle superior alveolar nerve travels first in the roof of the
maxillary sinus and then converges with the posterior superior
alveolar nerve. Both the anterior superior alveolar nerve and
middle superior alveolar nerve also innervate the mucosa of
the inferior meatus and floor of the nasal cavity.
■ PREOPERATIVE PREPARATION
To ensure antibiotic coverage before the incision, surgical
antibiotic prophylaxis of either penicillin (amoxicillin
2000 mg, or Augmentin 2000 mg) or clindamycin 600 mg is
taken orally 2 hours before the procedure. Before the patient
is seated for surgery, the teeth are brushed and the mouth
rinsed with chlorhexidine solution. The oral and perioral
459
FIGURE 26-1. Incision and mucoperiosteal flap reflection. To
view a color version of this illustration, refer to the color insert
section at the back of this book.
regions are then prepared and draped for a sterile surgery
procedure.
■ ANESTHESIA
The sinus-lift subantral augmentation surgery and all of its
variations can be performed with local anesthesia with
1 : 200,000 epinephrine. The posterior superior alveolar nerve
block combined with the anterior superior alveolar nerve
block and palatal infiltration with local anesthesia is usually
sufficient to obtain complete anesthesia. Another option is
injection of the greater palatine foramen. Local anesthesia can
be combined with oral sedation, intravenous sedation, or
general anesthesia.
■ INCISION
A crestal incision is made along the alveolar crest from the
tuberosity to the anterior border of the sinus. A vertical relax-
ing incision, anterior to the planned osteotomy, is made to
the depth of the vestibule to facilitate tissue release. Dissec-
tion is initiated at the apex of the crestal and vertical relaxing
incisions. The mucoperiosteal flap is reflected with a periosteal
elevator or molt curette to expose the canine fossa, malar
buttress, and the infratemporal fossa (Figure 26-1). Care is
taken not to tear the periosteum.
■ QUADRILATERAL BUCCAL
OSTEOTOMY
Although the hinge osteotomy was one of the first approaches
for sinus-lift grafting, this procedure only worked well when
there was sufficient vertical maxillary bone height.12 The
quadrilateral buccal osteotomy is indicated for either normal
or minimal vertical maxillary bone height. An advantage of
quadrilateral osteotomy is that it permits the sinus membrane
to be elevated higher than the superior horizontal osteotomy.
The surgery proceeds after reflection of the mucoperiosteal
flap and exposure of the lateral wall of the maxilla, the canine
fossa, the malar buttress, and infratemporal fossa. An inferior
horizontal osteotomy begins 2 to 3 mm above the floor of the
460 SECTION IV ■ Implant Surgery
FIGURE 26-2. Inferior horizontal osteotomy. To view a color
version of this illustration, refer to the color insert section at
the back of this book.
FIGURE 26-3. Complete quadrilateral osteotomy. To view a
color version of this illustration, refer to the color insert section
at the back of this book.
antrum in the area of the first molar, using a #6 or #8 round
bur and copious irrigation23 (Figure 26-2). A small round bur
or a fissure bur must not be used because this will most likely
cause tearing of the schneiderian membrane.
The osteotomy is done with a light touch, stripping away
bone until the membrane is exposed. The anterior limit of the
osteotomy is the anterior limit of the sinus. If bicuspid teeth
are present, the anterior limit is 3 to 4 mm distal to the tooth.
The osteotomy extends to the region of the second molar as
the posterior limit of the bone cut.
The anterior vertical bone cut is begun from the inferior
horizontal osteotomy and extended as high as access permits.
The superior horizontal osteotomy extends from the superior
limit of the anterior vertical bone cut posterior to approximate
the length of the inferior horizontal osteotomy. A posterior
vertical osteotomy connects the inferior and superior horizon-
tal bone cuts to complete the quadrilateral osteotomy (Figure
26-3).
FIGURE 26-4. Superior membrane elevation. To view a color
version of this illustration, refer to the color insert section at
the back of this book.
FIGURE 26-5. Elevate membrane higher than superior bone
cut. To view a color version of this illustration, refer to the color
insert section at the back of this book.
■ ELEVATION OF THE
SCHNEIDERIAN MEMBRANE
The quadrilateral osteotomy exposes the schneiderian mem-
brane circumferentially around the bone cuts. The membrane
is first lifted along the superior horizontal osteotomy using
broad-based freer elevators or curettes (Figure 26-4). The
membrane can be elevated higher than the superior bone cut
(Figure 26-5). This is especially important when the anatomy
and resorption patterns restrict visibility and exposure.
With the sharp border of the dissection elevators placed on
bone and its broad base supporting the membrane, the mem-
brane is lifted from its anterior and posterior walls (Figure
26-6). Further dissection exposes the medial wall of the sinus
(Figure 26-7). The buccal osseous window stays attached to
the schneiderian membrane as elevation continues. The bony
wall turns inward and is positioned horizontally in the superior
aspect of the dissection.
 CHAPTER 26 • Contemporary Sinus-Lift Subantral Surgery and Graft
FIGURE 26-6. Sharp border of elevator on bone. To view a
color version of this illustration, refer to the color insert section
at the back of this book.
FIGURE 26-7. Expose the medial wall of the sinus. To view a
color version of this illustration, refer to the color insert section
at the back of this book.
Piezosurgery with the diamond-coated insert or saw insert
will cut a precision osteotomy (Figure 26-8). The quadrilateral
osteotomy (Figure 26-9) can be removed, exposing the sinus
membrane (Figure 26-10). Using the noncutting, smooth
insert, the membrane is elevated (Figure 26-11). The elevated
membrane exposes the medial, inferior, and posterior bone
walls of the sinus (Figure 26-12).
■ GRAFTING THE OSSEOUS CAVITY
Graft material is placed under the membrane within the
osseous cavity in an anterior inferior direction and with a
loose compaction. It is important that the graft is in contact
with the medial osseous wall (Figure 26-13). Graft is added
until the cavity is loosely filled, reconstituting the buccal wall
(Figure 26-14). Overpacking the site and/or pressure in a
superior direction is avoided because this might tear the mem-
brane. Also, overcompressing the graft restricts blood flow
into the material, inhibits angiogenesis, and decreases oxygen
tension and compromises success. The mucoperiosteal flap is
then repositioned and sutured. If the periosteum is torn, a
461
FIGURE 26-8. Piezosurgery with diamond insert. To view a
color version of this illustration, refer to the color insert section
at the back of this book.
FIGURE 26-9. Complete quadrilateral osteotomy with piezo-
surgery. To view a color version of this illustration, refer to the
color insert section at the back of this book.
hemostatic collagen wound dressing or a guided bone regen-
eration (GBR) membrane can be placed over the buccal
window to inhibit fibrovascular into the graft (Figure
26-15).
■ POSTOPERATIVE INSTRUCTIONS
In most cases, normal activities are permitted, and the patient
can wear a removable partial or full-denture appliance. The
patient is instructed not to blow his or her nose for a minimum
of 10 days because this might dislodge the graft, tear the
membrane, and produce infraorbital subcutaneous air. Smoking
is to be avoided.
Analgesics, antihistamines, antibiotics, and antiinflamma-
tory medications can be prescribed. Postoperative analgesics
include Tylenol with codeine, Vicodin, or 600 mg ibuprofen
every 4 to 6 hours. Antibiotics of amoxicillin or Augmentin
500 mg every 6 hours or clindamycin 300 mg every 6 hours
are taken for 5 to 7 days. Instructions to maintain oral hygiene
and oral rinses of Peridex or Peroxyl are prescribed.
462 SECTION IV ■ Implant Surgery

FIGURE 26-10. Piezosurgery and removing buccal window FIGURE 26-11. Smooth foot insert for piezosurgery to lift
exposing membrane. To view a color version of this illustration, membrane. To view a color version of this illustration, refer to
refer to the color insert section at the back of this book. the color insert section at the back of this book.

FIGURE 26-12. Elevated sinus membrane to expose medial FIGURE 26-13. Graft placed under sinus membrane. To view
wall of sinus. To view a color version of this illustration, refer a color version of this illustration, refer to the color insert
to the color insert section at the back of this book. section at the back of this book.

FIGURE 26-14. Graft is loosely compacted filling cavity. To FIGURE 26-15. Guided bone regenerative membrane over
view a color version of this illustration, refer to the color insert buccal window. To view a color version of this illustration, refer
section at the back of this book. to the color insert section at the back of this book.
 CHAPTER 26 •
FIGURE 26-16. Small tear of the sinus membrane. To view
a color version of this illustration, refer to the color insert
section at the back of this book.
FIGURE 26-17. Collagen membrane with platelet-rich plasma.
■ COMPLICATIONS
DEHISCENCE OF THE INCISION
A vestibular horizontal buccolabial incision should be avoided.
The blood supply in the vestibule is diminished when com-
pared with alveolar crest–attached keratinized tissue. Suturing
in this area is also more difficult.24 In addition, flanges of an
appliance must be reduced because they impinge on the ves-
tibule and push the incision apart.25
DELAYED HEALING—SMOKING
Smokers are at greater risk for postoperative infection and
wound breakdown.26-30
SWELLING AND ECCHYMOSIS
Tearing of the periosteum will increase postoperative swelling
and ecchymosis. Further, rents in the periosteum permit fibro-
vascular invasion into the graft.
SMALL MEMBRANE TEARS
Small membrane tears can be repaired with coverage of a
resorbable collagen wound dressing (Figure 26-16). The mem-
Contemporary Sinus-Lift Subantral Surgery and Graft 463
FIGURE 26-18. Collagen membrane placed under sinus membrane.
To view a color version of this illustration, refer to the color insert
section at the back of this book.
FIGURE 26-19. Bone tacks stabilize membrane on
buccal bone. To view a color version of this illustration,
refer to the color insert section at the back of this book.
brane can be soaked with an aqueous antibiotic solution or
platelet-rich plasma (Figure 26-17). Excess fluid is squeezed
out of the membrane, and it is shaped to fit under the tear. It
is important to elevate the schneiderian membrane to expose
the bony medial wall of the antrum before placing the colla-
gen membrane (Figure 26-18).
LARGER MEMBRANE TEARS
At times the membrane is very fragile and easily torn, expos-
ing the entire antral cavity. The surgery proceeds with elevat-
ing the membrane and exposing the medial wall of the sinus.
A GBR collagen membrane of sufficient size to cover the
defect is soaked with an aqueous antibiotic and/or platelet-
rich plasma. It is then secured to the facial aspect of the buccal
wall with transosseous sutures or bone tacks (Figure 26-19).
The membrane is pressed inward with its margin against the
medial wall. A collagen wound dressing is prepared and placed
under the GBR membrane. Caution is observed when placing
the graft material to neither overpack the cavity nor overly
compress the graft material in a superior direction.
464 SECTION IV ■ Implant Surgery
FIGURE 26-20. Vertical osteotomy over septum divides sinus
into two cavities. To view a color version of this illustration, refer
to the color insert section at the back of this book.
FIGURE 26-21. Two sinus compartments elevated. To view
a color version of this illustration, refer to the color insert
section at the back of this book.
ANTRAL SEPTUM
Bony septum may be part of normal sinus anatomy.31 One
option is to view the sinus as two compartments. A vertical
bone cut is made through buccal bone over the septum (Figure
26-20). The membrane is elevated as described, but with two
compartments (Figure 26-21). Another alternative is to cut
the septum at its base, tearing the membrane. Continued ele-
vation of the membrane exposes the medial wall. The tear is
patched with either a collagen wound dressing or GBR
membrane.
INFECTIONS
A subperiosteal infection at the incision or under the muco-
periosteum is first treated with antibiotics, and incision and
drainage. Persistent infection requires elevation of the muco-
periosteal flap, débridement, curettage, and copious irrigation.
If the graft material is not infected, a 7- to 10-day course of
antibiotics is prescribed. When the graft material shows signs
and symptoms of infection, purulent exudate, a high tempera-
ture, and/or fetid oris, the graft material must be removed. The
FIGURE 26-22. Incision on palatal aspect. To view a
color version of this illustration, refer to the color insert
section at the back of this book.
FIGURE 26-23. Reflection of mucoperiosteal flap over
crestal bone. To view a color version of this illustration,
refer to the color insert section at the back of this book.
exudate is sent for culture and sensitivity. Following complete
removal of the graft, the cavity is copiously irrigated. Antibi-
otics are prescribed for 2 to 3 weeks, and the patient is kept
under observation.
■ TREPHINE CORE MEMBRANE
ELEVATION
The trephine bone core sinus elevation technique can be done
at multiple sites to add 4 to 8 mm of bone height in prepara-
tion for placing implants. It is especially indicated when teeth
are adjacent to the edentulous site.32 A minimum of 6 mm of
alveolar bone is necessary for this technique. When less than
6 mm of bone remains between the alveolar crest and the floor
of the sinus, the patient is best treated with the buccal quad-
rilateral osteotomy approach or the balloon sinus membrane
elevation technique.
The incision is made on the palatal aspect between adja-
cent teeth (Figure 26-22). The mucoperiosteal flap is reflected
over crestal bone (Figure 26-23). Rarely a buccal vertical
relaxing incision is needed for exposure.
A trephine drill of appropriate diameter (Ace Surgical
Supply, G. Hartzell & Son, and Salvin Instrument Supply) is
positioned on the alveolar crest. A minimum of 2 mm of bone
 CHAPTER 26 •
FIGURE 26-24. Trephine drill in crestal position with
2 mm of bone around trephine. To view a color version of
this illustration, refer to the color insert section at the
back of this book.
FIGURE 26-25. Trephined bone core partially intruded
into sinus cavity. To view a color version of this illustration,
refer to the color insert section at the back of this book.
must remain circumferentially between the trephine and
buccal-palatal bone and between adjacent teeth. The trephine
is drilled with copious irrigation through the alveolar crest to
the floor of the sinus (Figure 26-24). This separates the bone
core from the alveolus.
The trephine is removed, and the bone core is intruded
into the sinus, lifting the membrane (Figure 26-25). A
minimum of one-half to one-third of the bone core must
remain in contact with alveolar bone. This distance can be
measured with a periodontal probe. When the bone core
remains within the trephine, it is removed and placed into the
osteotomy site. The surgically produced crestal five-wall defect
is grafted with only enough allogeneic, xenograft, or alloplast
material to loosely fill the defect (Figure 26-26). The intact
mucoperiosteal flap covers the graft site and is sutured (Figure
26-27).
Overpacking the defect pushes the bone core into the
sinus. When this occurs, it cannot be retrieved and remains
until it is resorbed. The resultant oral-antral defect is treated
by placing a collagen hemostatic wound dressing into the
defect and grafting the oral-antral osseous defect before repo-
sitioning the mucoperiosteal flap and suturing. After 4 to 6
Contemporary Sinus-Lift Subantral Surgery and Graft 465
FIGURE 26-26. Loose compaction of five-wall crestal
defect. To view a color version of this illustration, refer
to the color insert section at the back of this book.
FIGURE 26-27. Sutured palatal incision. To view a
color version of this illustration, refer to the color insert
section at the back of this book.
months of healing, the site can be treated with a conventional
sinus-lift elevation technique.
Postoperative healing is uneventful, and only mild analge-
sics are needed for relief of discomfort. After 4 to 6 months of
healing, the site can be prepared for implant placement.
BALLOON ELEVATION
The antral membrane balloon elevation (AMBE) technique,
introduced by Soltan and Smiler,33 is especially useful when
teeth are adjacent to the edentulous region. There is limited
reflection of the mucoperiosteal flap, and this procedure ele-
vates the membrane to the medial wall of the antrum. The
AMBE technique is indicated when there is moderate to
severe resorption of the posterior maxilla and deficient bone
height for implant placement.
Local anesthesia is obtained with infiltration of the buccal
and palatal tissues. The incision can be midcrestal or more
palatal (Figure 26-28). The mucoperiosteal flap is reflected to
expose the buccal wall of the edentulous region. A vertical
relaxing incision extending into the vestibule may be neces-
sary for sufficient exposure.
466 SECTION IV ■ Implant Surgery

FIGURE 26-28. Palatal incision for antral membrane balloon FIGURE 26-30. Sinus membrane is slightly elevated from
elevation. To view a color version of this illustration, refer to the sinus floor. To view a color version of this illustration, refer to
color insert section at the back of this book. the color insert section at the back of this book.

FIGURE 26-31. Saline expands balloon to check for

leaks.
FIGURE 26-29. Small buccal window made with round bur.
To view a color version of this illustration, refer to the color
insert section at the back of this book.

A limited buccal osteotomy begins slightly above the sinus

floor (Figure 26-29). The osteotomy is performed with copious
irrigation with a large round bur, trephine drill, or piezosurgery
saws. The integrity of the sinus membrane is preserved, and
dissection begins at the bottom of the osteotomy. Freer eleva-
tors or large spoon elevators lift the membrane slightly from
the sinus floor, and dissection progresses toward the medial
wall of the sinus (Figure 26-30).
The balloon is checked for leaks by inflation with 3 to 4 cc
of sterile saline (Figure 26-31). The empty balloon is placed
against the sinus floor midway between the lateral and medial FIGURE 26-32. Balloon is positioned and slowly inflated. To
walls. The balloon is slowly expanded with 1.5 to 2.0 cc of view a color version of this illustration, refer to the color insert
sterile saline, and the membrane is elevated (Figure 26-32). section at the back of this book.
The balloon is emptied and withdrawn, leaving a cavity bor-
dered by the reflected membrane and attached buccal bone, An alternative approach is developing the buccal osteot-
the medial wall of the sinus, and the nonreflected membrane omy to the step of slight elevation of the membrane from the
(Figure 26-33). With loose compaction, the bone graft mate- sinus floor. Sequential drilling prepares the final implant
rial is placed under the membrane (Figure 26-34). The muco- diameter and perforates through the bony sinus floor, but does
periosteal flap is repositioned and sutured (Figure 26-35). not perforate the sinus membrane. The balloon is inserted
 CHAPTER 26 • Contemporary Sinus-Lift Subantral Surgery and Graft 467

FIGURE 26-33. Balloon is removed, exposing elevated

membrane and sinus cavity. To view a color version of this
illustration, refer to the color insert section at the back FIGURE 26-35. Suturing repositioned mucoperiosteal flap. To
of this book. view a color version of this illustration, refer to the color insert
section at the back of this book.

FIGURE 26-34. Loose compaction of graft material. To view

a color version of this illustration, refer to the color insert
section at the back of this book. FIGURE 26-36. Balloon placed through implant osteotomy to
elevate membrane. To view a color version of this illustration,
through the implant receptor site and inflated (Figure 26-36). refer to the color insert section at the back of this book.
Graft material is placed through the implant receptor site and
is observed from the buccal window (Figure 26-37). The
implant is placed (Figure 26-38), and the mucoperiosteal flap
is repositioned and sutured (Figure 26-39).
Alternatively, before placing the balloon, the implant
receptor site diameter is prepared to the floor of the sinus via
the flapless surgical approach (Figure 26-40). If there is concern
about a perforation of the sinus membrane, a resorbable
collagen dressing or collagen capsule is positioned through the
crestal implant receptor site under the membrane before
depositing the graft and placing the implant. The balloon is
inserted through the implant receptor site and inflated (Figure
26-41). The graft material is placed through the implant
receptor site (Figure 26-42), and the implant is placed (Figure
26-43).

■ GRAFT MATERIALS
Graft materials to reconstitute the antral floor before placing FIGURE 26-37. Graft placed from crestal region into sinus
implants may or may not include autogenous bone.34,35,36 cavity. To view a color version of this illustration, refer to the
However, the graft scaffold should mimic the extracellular color insert section at the back of this book.
468 SECTION IV ■ Implant Surgery
FIGURE 26-38. Implant placed into grafted sinus. To view a
color version of this illustration, refer to the color insert section
at the back of this book.
FIGURE 26-39. Mucoperiosteal flap repositioned and sutured. To
view a color version of this illustration, refer to the color insert section
at the back of this book.
FIGURE 26-40. Flapless preparation of implant site and only to
floor of sinus. To view a color version of this illustration, refer to
the color insert section at the back of this book.
FIGURE 26-41. Balloon placed through implant receptor site to
elevate membrane. To view a color version of this illustration, refer to
the color insert section at the back of this book.
FIGURE 26-42. Graft placed through implant receptor site into
sinus cavity. To view a color version of this illustration, refer to
the color insert section at the back of this book.
matrix of autogenous bone.37 It must be nontoxic, biocompat-
ible, and biodegradable at a rate that is compatible with bone
remodeling without lowering the pH of surrounding tissues;
have a microporous structure of a geometry that promotes
angiogenesis and capillary ingrowth; and be easily integrated
into new bone.38,39 The ultimate success of the bone graft
depends on the presence of cells and in particular osteoblasts.40
Osteoblasts and other precursor stem cells found within bone
marrow promote osteogenesis.41-44 Bone graft success can be
increased when marrow is incorporated into the graft
scaffold.45,46
■ BONE MARROW ASPIRATE
Bone marrow aspiration from the anterior iliac crest is virtually
free of complications. Smiler and Soltan describe the rationale
and technique of combining extracted bone marrow with the
graft matrix.47,48 The technique is an outpatient procedure with
local anesthesia, with or without intravenous sedation or
general anesthesia. The procedure continues with the inser-
 CHAPTER 26 • Contemporary Sinus-Lift Subantral Surgery and Graft 469

FIGURE 26-43. Implant positioned into osteotomy site. To

view a color version of this illustration, refer to the color insert
section at the back of this book. FIGURE 26-44. Bone aspiration needle with stylet and handle.

FIGURE 26-45. Insertion of bone aspiration needle through skin and FIGURE 26-46. Remove the stylet.
subcutaneous tissue to cortical bone and into the bone marrow.

FIGURE 26-47. Aspirate 2 to 4 cc of bone marrow. FIGURE 26-48. Place pressure over aspiration site for 5 minutes.
470 SECTION IV ■ Implant Surgery
tion of the aspirating needle (Figure 26-44). With a twisting
motion, the needle is through the skin, subcutaneous tissue,
and down to and through the cortical bone into the marrow
cavity (Figure 26-45). After removing the obturator and/or
stylet (Figure 26-46), 2 to 4 cc of bone marrow is aspirated
(Figure 26-47). After pressure over the site continues for about
5 minutes (Figure 26-48), an adhesive bandage is placed.
REFERENCES
1. Chanavaz M: Maxillary sinus: anatomy, physiology, surgery, and
bone grafting related to implantology-eleven years of surgical
experience, J Oral Implantol 16:199-209, 1990.
2. Adell R, Eriksson B, Lekholm U: A long-term follow-up study
of osseointegrated implants in the treatment of totally edentu-
lous jaws, Int J Oral Maxillofac Implants 5:347-359, 1990.
3. Tatum H: Maxillary and sinus implant reconstruction, Dent Clin
North Am 30:207-229, 1986.
4. Hall HD: Bone graft of the maxillary sinus floor for Branemark
implants, Oral Maxillofac Surg Clin North Am 3:869-875,
1991.
5. Smiler DF et al: Sinus lift grafts and endosseous implant treat-
ment of the atrophic posterior maxilla, Dent Clin North Am
36:151-186, 1992.
6. Tatum H: Lectures presented at the Alabama Implant Study
Group, 1977. In Smiler DF et al: Sinus lift grafts and endosseous
implant treatment of the atrophic posterior maxilla, Dent Clin
North Am 36:151-186, 1992.
7. Su-Gwan Kim, Masaharu Mitsuge, Byung-Ock Kim: Simultane-
ous sinus lifting and alveolar distraction of the atrophic maxillary
alveolus for implant placement: a preliminary report, Implant
Dent 14:344-348, 2005.
8. Misch CE: Maxillary sinus augmentation for endosteal implants:
organized alternative treatment plans, Int J Oral Implantol 4:49-
58, 1987.
9. Johansson B et al: Volumetry of simulated bone grafts in the
edentulous maxilla by computed tomography: and experimental
study, Dentomaxillofac Radiol 30(3):153-156, 2001.
10. Tatum H Jr: Maxillary and sinus implant reconstruction, Dent
Clin North Am 30:207-229, 1986.
11. Boyne P, James R: Grafting of the maxillary floor with autoge-
nous marrow and bone, J Oral Surg 38:613-616, 1980.
12. Smiler DG, Holmes RE: Sinus lift procedure using porous
hydroxylapatite: a preliminary clinical report, J Oral Implantol
13:239-253, 1987.
13. Gray H: Upper respiratory tract. In Goss CM, editor: Anatomy
of the human body, Philadelphia, 1967, Lea & Fibiger.
14. Killey HC, Kay LW: The maxillary sinus and its dental implica-
tions. In The Anatomy, physiology, function, growth and applied
surgical anatomy of the maxillary sinus, Bristol, 1975, John Wright
& Sons.
15. Sicher H: Oral anatomy. In The nerves of the head and neck, ed
3, St Louis, 1960, CV Mosby.
16. Donal PJ: The sinuses. In Donald PJ, Gluckman JL, Rice DH,
editors: Anatomy and histology, New York, 1994, Raven Press.
17. Provenza DV, Seibel W: Oral histology. In Nasal passage and
paranasal sinuses, ed 2, Philadelphia, 1986, Lea & Febiger.
18. Hollinshead WH: Anatomy for surgeons. In The head and neck,
ed. 2, vol 1, NY, 1968, Harper & Row.
19. Elian N et al: Distribution of the maxillary artery as it relates to
sinus floor augmentation, Int J Oral Maxillofac Implants 20:784-
787, 2005.
20. Flanagan D: Arterial supply of the maxillary sinus and potential
for bleeding complication during lateral approach sinus eleva-
tion, Implant Dent 14:336-338, 2005.
21. Standring S: Nose, nasal cavity, paranasal sinuses, and pterygo-
palatine fossa. In Ellis H, editor: Gray’s anatomy: the anatomical
basis of clinical practice, ed 39, Edinburgh, NY, 2005, Elsevier
Churchill Livingstone.
22. Sicher H: Oral anatomy. The blood vessels of the head and neck,
ed 3, St Louis, 1960, CV Mosby.
23. Smiler DG: The sinus lift graft: basic technique and variations,
Pract Periodontics Aesthetic Dent 9(8):885-893, 1997.
24. Farmand M: Horse-shoe sandwich osteotomy of the edentulous
maxilla as a preprosthetic procedure, J Maxillofac Surg 14:238-
244, 1986.
25. Miller PD Jr: Regenerative and reconstructive periodontal plastic
surgery: mucogingival surgery, Dent Clin North Am 32:287-306,
1988.
26. Ague C: Urinary catecholamines, flow rate and tobacco smoking,
Bio Psychol 1:229-236, 1974.
27. Armitage AK, Turner DM: Absorption of nicotine in cigarette
and cigar smoking throughout the oral mucosa, Nature 226:1231-
1232, 1970.
28. Kenney EB et al: The effect of cigarette smoke on human
polymorphonuclear leukocytes, J Periodont Res 12:227-234,
1977.
29. Mosely LH, Finseth F, Goody M: Nicotine and its effects on
wound healing, Plast Reconstr Surg 61:570-575, 1978.
30. Rees TD, Liverett DM, Guy CL: The effect of cigarette smoking
on skin-flap survival in the face lift patient, Plast Reconstr Surg
73:911-915, 1984.
31. Underwood AS: An inquiry into the anatomy and pathology of
the maxillary sinus, J Anat Physiol 44:354-369, 1990.
32. Soltan M, Smiler D: Trephine bone core sinus elevation graft,
Implant Dent 13:148-151, 2004.
33. Soltan M, Smiler D: Antral membrane balloon elevation, Implant
Dent 21:85-90, 2005.
34. Branemark PI: Bone marrow microvascular structure and func-
tion, Adv Microcirc 1:1-65, 1968.
35. Glowacki J et al: Application of the biological principle of
induced osteogenesis for craniofacial defects, Lancet 14:23-48,
1981.
36. Jensen J, Simonsen EK, Sindet-Pedersen S: Reconstruction of
the severely resorbed maxilla with bone grafting and osseointe-
grated implants: a preliminary report, J Oral Maxillofac Surg
48:27-32, 1990.
37. Smiler D: Bone grafting: materials and modes of action, Pract
Periodontics Aesthetic Dent 8:413-416, 1996.
38. Wiesmann H, Joos U, Meyer U: Biological and biophysical prin-
ciples in extracorporal bone tissue engineering part II, Int J Oral
Maxillofac Surg 33:523-530, 2004.
39. Jones D, Leivseth G, Tenbosch J: Mechano-reception in osteo-
blast-like cells, Biochem Cell Biol 73:525-534, 1995.
40. Smiler D, Soltan M: The bone-grafting decision tree: a system-
atic methodology for achieving new bone, Implant Dent 15:122-
128, 2006.
41. Kassem M et al: Formation of osteoclasts and osteoblast-like cells
in long-term human bone marrow cultures, APMIS 99:262-268,
1991.
42. Bereford JN: Osteogenic stem cells and the stromal system of
bone and marrow, Clin Orthop 240:270-280, 1989.
43. Burwell RG: The function of bone marrow in the incorporation
of a bone graft, Clin Orthop 200:125-141, 1985.
44. Chase SW, Herndon CH: The fate of autogenous band homog-
enous bone grafts, J Bone Joint Surg 37:809, 1955.
45. Connolly JF, Guse R, Lippiello L: Development of an osteogenic
bone marrow preparation, J Bone Joint Surg 71A:681-691,
1989.
46. Nade S: Clinical implications of cell function in osteogenesis,
Ann R Cool Surg Engl 61:189-194, 1976.
47. Soltan M, Smiler D: A new platinum standard for bone grafting:
autogenous stem cells, Implant Dent 14:322-327, 2006.
48. Smiler D, Soltan M: Bone marrow aspiration rationale and tech-
nique, Implant Dent 15:229-234, 2006.

DENTOALVEOLAR MODIFICATION
OSTEOPERIOSTEAL FLAPS
Ole T. Jensen
Alveolar bone mass deficiency can be corrected by multiple
techniques, which frequently use onlay bone grafting or guided
bone regeneration. These two techniques have been the
mainstay of oral and maxillofacial surgery reconstruction for
dental implants over the past 2 decades.1,2
A newer approach that has the advantage of less distur-
bance to osteogenic periosteum, improved continuity of crestal
gingivoalveolar form, and greater resistance of the augmenta-
tion to resorption remodeling is the use of the osteoperiosteal
flap.
The osteoperiosteal flap or “bone flap,” commonly used in
segmental orthognathic surgery, is a bone fragment moved in
space without detachment of the investing periosteum. The
best example of this concept in reconstructive alveolar surgery
as it relates to implant osseointegration is the interpositional
bone graft or “sandwich graft.” Other uses of the bone flap in
dentoalveolar augmentation are the alveolar split graft (book
flap), edentulous alveolar repositioning osteotomy, and various
alveolar distraction osteogenesis procedures that add width or
height to an alveolar segment.3-7
■ INTERPOSITIONAL BONE GRAFT
The interpositional bone graft can be done anywhere in the
mouth, but is most indicated in the aesthetic zone and the
posterior mandible. A depth-of-vestibule, horizontal incision
is made to bone with complete reflection away from the alveo-
lar crest and minimal reflection crestally. Vital structures, such
as nerve, tooth roots, and the respiratory space, are identified
to be avoided. The osteotomy design in the posterior mandible
is a “smile line,” tapering anterior and posterior with at least
4 mm of height in the middle of the segment—though less is
possible. A through and through osteotomy is done from
buccal plate to lingual plate, and an osteotome is used to
gently free the segment. The segment can be elevated up to
10 mm vertically (Figures 27-1 through 27-6). A bone plate
and interpositional graft material is placed, usually autograft,
though bone morphogenetic protein (BMP-2), platelet-
derived growth factor (PDGF-bb), and/or alloplast with
PDGF-bb have been used successfully. (However, the use of
alloplast next to nerve tissue should be avoided.) Four months
following bone healing, the plate is removed, and dental
implants are placed. Often the alveolar ridge will need to be
split or grafted laterally at the time of implant placement
CHAPTER 27
BY
in these settings, but vertical augmentation should be
adequate.5
The major advantage of an interpositional graft is an end-
osteal, marrow-accessed graft site—a highly vascular area con-
ducive to graft incorporation. Very few seams, scar encleftations,
bone graft exposure, bone graft resorption, or infections occur
with this approach. Other advantages for using the interposi-
tional graft technique are undisturbed alveolar crestal bone,
improved gingival aesthetic form in anterior locations, and a
stable postgrafting architecture.
■ ALVEOLAR SPLIT GRAFT
(BOOK FLAP)
The common alveolar finding from a late-healed extraction
socket is a loss of alveolar width as a result of resorption of
the buccal plate. The alveolus can be widened using a crestal
incision that does not reflect beyond the crest buccally and
lingually, but serves to identify the set point for osteotome or
piezoknife osteotomy. Vertical cuts of the buccal plate are
made blindly without flap reflection 1 or 2 mm from adjacent
tooth roots and then connected sagittally to a depth of about
10 mm. Then the buccal plate is split sagittally; the buccally
directed out-fracture is done without detachment of the
mucoperiosteum from the mobilized osseous segment (Figures
27-7 through 27-10).7
The intraosseous defect created is then grafted, or an
implant is placed with adjacent bone grafting. Primary closure
or near primary closure is obtainable if the initial crestal inci-
sion is placed a few millimeters palatally.
This technique requires about a 4-mm wide alveolar
minimum, but if a piezoknife is used, a 3-mm width is easily
managed.
The alveolar split bone flap easily augments the majority
of healed maxillary dental extraction sites. It can be used in
the mandible, though hard bone is less flexible to greenstick
fracture, and therefore flap detachment is a greater risk.
INTRAALVEOLAR SPLIT GRAFT
Another alveolar split graft approach is done with the sand-
wich osteotomy, which when elevated, can be split from below
using a piezoknife. This procedure, currently in development,
gains width and height at the same time.8 An alveolar split
can also be used to narrow an excessively wide ridge.9
471
472 SECTION IV ■ Implant Surgery

FIGURE 27-2. Alveolar elevation to the alveolar plane made with a

“smile”-shaped osteotomy before graft insertion. To view a color version of
this illustration, refer to the color insert section at the back of this
FIGURE 27-1. Preoperative view showing bilateral atrophic posterior
book.
mandibular ridges. To view a color version of this illustration, refer to the
color insert section at the back of this book.

FIGURE 27-3. Particulate graft is inserted after bending the plate to FIGURE 27-4. Particulate graft and PDGF-bb placed. To view a color
orient the ridge into proper alignment. To view a color version of this illus- version of this illustration, refer to the color insert section at the back
tration, refer to the color insert section at the back of this book. of this book.

FIGURE 27-5. Right side “smile” osteotomy elevated 6 mm to the alveo- FIGURE 27-6. Wound closure (left side) of the vestibular incision is done
lar plane. To view a color version of this illustration, refer to the color in layers with resorbable suture. To view a color version of this illustration,
insert section at the back of this book. refer to the color insert section at the back of this book.
 CHAPTER 27 • Dentoalveolar Modification by Osteoperiosteal Flaps
FIGURE 27-7. A moderately difficult single-tooth site, commonly the
result of loss of the buccal plate. To view a color version of this illustration,
refer to the color insert section at the back of this book.
FIGURE 27-8. Exposure of the site is done using a crestal incision made
about 2 to 3 mm toward the palatal side. To view a color version of this
illustration, refer to the color insert section at the back of this book.
FIGURE 27-9. An alveolar split to widen the ridge is first limited by verti-
cal cuts made about 2 mm from the adjacent tooth. This protects the subpapil-
lary bone from fracturing off during the crest-splitting procedure. To view a
color version of this illustration, refer to the color insert section at the
back of this book.
473
FIGURE 27-10. The alveolus is split crestally by inserting a straight
osteotome about 10 mm, stopping at about vestibular depth. The wedged
osteotome is then brought forward, spreading apart the alveolus until it green-
stick out-fractures at the vestibular level. This is done without detachment of
the mucoperiosteum. Bone graft is then placed in the gap and left to heal for
4 months before implant installation. To view a color version of this illustra-
tion, refer to the color insert section at the back of this book.
FIGURE 27-11. An anterior alveolar crossbite is present despite adequate
alveolar width for implants. To view a color version of this illustration, refer
to the color insert section at the back of this book.
■ ALVEOLAR REPOSITIONING
OSTEOTOMIES
Sometimes the alveolus has enough bone mass, but the alveo-
lar crest is in an off-axis position, such as in an anterior or
lateral crossbite. An alveolar segment can be freed and repo-
sitioned and fixated without grafting, as shown in Figures
27-11 through 27-14. And, of course, an entire jaw can be
changed in position to optimize alveolar relation.
IMPLANT REPOSITIONING OSTEOTOMY
Integrated dental implants that cannot be easily removed
without leaving a substantial osseous defect can be moved
with a segmental osteotomy. This is usually done to improve
aesthetic emergence of the implant (Figures 27-15 through
27-17).
474 SECTION IV ■ Implant Surgery
FIGURE 27-12. Following segmental osteotomy to move the alveolus
forward 4 mm, the guide stent shows the improved alveolar projection. To
view a color version of this illustration, refer to the color insert section
at the back of this book.
FIGURE 27-13. Transgingival implant placement is done using the guide
stent. To view a color version of this illustration, refer to the color insert
section at the back of this book.
FIGURE 27-14. Implants are placed 3 mm below tissue level. To view
a color version of this illustration, refer to the color insert section at the
back of this book.
FIGURE 27-15. A poorly aligned dental implant can be moved bodily
using a single-tooth osteotomy from a vestibular incision. To view a color
version of this illustration, refer to the color insert section at the back
of this book.
FIGURE 27-16. An implant transposition osteotomy is a risky one
because tooth roots are likely nearby and it is difficult to keep enough bone
on the implant to maintain osseointegration following mobilization of the
implant segment. To view a color version of this illustration, refer to the
color insert section at the back of this book.
■ ALVEOLAR WIDTH DISTRACTION
OSTEOGENESIS
One area in which alveolar width can be achieved by distrac-
tion is the posterior mandible, a sometimes difficult area to
bone graft. It can be alveolar split in a relatively brief opera-
tion in which no bone graft is required. A bone spreader is
tapped into place and activated 1 week later. Adequate width
is achieved in 7 to 10 days because activation is 0.4 mm per
day. The site is left to heal for a month; implants are then
placed through the distraction zone into apical bone. Treat-
ment time and morbidity are less for this approach when
compared with onlay or veneer bone grafting. The procedure
can be done in either the maxilla or the mandible, as shown
in Figures 28-18 through 27-27.11
 CHAPTER 27 • Dentoalveolar Modification by Osteoperiosteal Flaps 475

FIGURE 27-17. Once the implant cervical margin is placed at a more FIGURE 27-18. A narrow maxillary posterior alveolus can be widened by
optimal position, typically a 4-mm coronal movement, grafting and stabilization a split made through a crestal incision without periosteal reflection. To view
of the implant can be done. The crown of the tooth is trimmed back to the a color version of this illustration, refer to the color insert section at the
occlused plane to be remade at a later date. A healing time of 4 to 6 months back of this book.
is advisable before finalization in a setting like this for what is primarily done
to improve the aesthetic profile. To view a color version of this illustration,
refer to the color insert section at the back of this book.

FIGURE 27-19. Following alveolar splitting, a bone spreader is placed. FIGURE 27-20. Immediate postoperative x-ray with a Laster crest dis-
To view a color version of this illustration, refer to the color insert section tractor in place.
at the back of this book.
476 SECTION IV ■ Implant Surgery

FIGURE 27-23. The alveolar width distraction flap should be carefully

reflected. In the mandible, vertical cuts are made, but not reflected or con-
nected to the crestal soft tissue wound. Bone cuts are made through these
sites with very minimal reflection. To view a color version of this illustration,
refer to the color insert section at the back of this book.

FIGURE 27-21. The distractor is removed 6 to 8 weeks later and implants

are placed. To view a color version of this illustration, refer to the color
insert section at the back of this book.

FIGURE 27-24. The distractor is placed. To view a color version of this

illustration, refer to the color insert section at the back of this book.

FIGURE 27-22. X-ray finding at the time of placement of two implants.

FIGURE 27-25. Implants are placed 2 months later. To view a color

version of this illustration, refer to the color insert section at the back
of this book.
 CHAPTER 27 • Dentoalveolar Modification by Osteoperiosteal Flaps 477

FIGURE 27-28. A maxillary defect as a result of traumatic loss of #7, 8,

9, and 10 in a patient with apertognathia and a high smile line. X-ray findings
show about 5 to 6 mm of vertical bone loss.
FIGURE 27-26. X-ray finding 4 months later.

FIGURE 27-27. Final restoration shows an increase in alveolar width. To FIGURE 27-29. Preoperative views. To view a color version of this
view a color version of this illustration, refer to the color insert section illustration, refer to the color insert section at the back of this book.
at the back of this book.

ALVEOLAR VERTICAL DISTRACTION

OSTEOGENESIS
Alveolar vertical distraction osteogenesis is now well founded
as a technique, but still is not broadly used. Vertical distrac-
tion most always requires supplemental bone grafting before
or after distraction. Vertical distraction osteogenesis is techni-
cally difficult, and therefore this factor must be a consideration
for selecting this treatment alternative.
The most common indication for vertical distraction osteo-
genesis is in the anterior maxilla, where for aesthetic reasons,
the alveolus needs to be brought down and usually forward.
Figures 27-28 through 27-33 show an anterior maxillary
defect treated with a bone flap translated by distraction. After
the segment is cut and fixated with the distractor, the segment
is moved down and forward at a rate of 0.8 mm per day until FIGURE 27-30. Placement of a vestibular bone distractor (Mommaerts-
the segment engages the provisional or prosthetic guide. After Laster) following osteotomy mobilization of the anterior segment. To view a
a 4-month consolidation period, the implants follow with color version of this illustration, refer to the color insert section at the
eventual prosthetic rehabilitation.12 back of this book.
478 SECTION IV ■ Implant Surgery
FIGURE 27-31. The wound is closed primarily with a small access hole
for distraction. To view a color version of this illustration, refer to the color
insert section at the back of this book.
FIGURE 27-32. Following distraction and a 4-month healing time period,
the distractor is removed, and implants are placed transgingivally. To view a
color version of this illustration, refer to the color insert section at the
back of this book.
■ SUMMARY
In summary, the use of an osteoperiosteal flap allows the
surgeon to handle most dentoalveolar defects with a relatively
simple surgical technique that requires no major bone grafting.
It also allows for bone healing that is more stable, less likely
to resorb, and more likely to consolidate or integrate into the
graft site. The use of interpositional bone access engages the
FIGURE 27-33. Implants 4 months later before final single-tooth restora-
tions. To view a color version of this illustration, refer to the color insert
section at the back of this book.
marrow vascular space—a place where graft material is less
likely to sequester, become infected, or resorb away. The use
of bone flap distraction also generates osteogenic bone of high
quality, conducive to implant osseointegration.
Bone flap procedures in general present a more certain
way of accomplishing greater alveolar width and height
augmentation, with less complication than commonly used
approaches.
REFERENCES
1. Collins T: Onlay bone grafting in combination with Branemark
implants, Oral Maxillofac Surg Clin North Am 3:893-902, 1991.
2. Buser D, Bragger U, Lang S: Regeneration and evaluation of jaw
bone using guided tissue regeneration, Clin Oral Implants Res
1:22-32, 1990.
3. Jensen OT: Alveolar segmental “sandwich” osteotomies for pos-
terior edentulous mandibular sites for dental implants, Int J Oral
Maxillofac Surg 64:471-475, 2006.
4. Jensen OT et al: Alveolar segmental sandwich osteotomy for
anterior maxillary vertical augmentation prior to implant place-
ment, J Oral Maxillofac Surg 64:290-296, 2006.
5. Jensen OT: PDGF-bb and dento-alveolar modification by osteo-
periosteal flaps. In Lynch S, Nevins M, Marx R, editors: Tissue
engineering, vol II, Chicago, 2008, Pub Quintessence (In Press).
6. Jensen OT: Segmental alveolar osteotomies for relocation of
osseointegrated dental implants, (In Process).
7. Jensen OT, Ellis E: The book flap: a technical note, J Oral Maxil-
lofac Surg 2008 (In Press).
8. Jensen OT: Intra alveolar split graft: a technical note, (In
Process).
9. Jensen OT: Narrowing an edentulous prognathic maxillary alve-
olus using a bone flap prior to implant placement, (In Process).
10. Jensen OT, Leopardi A, Gallegos L: The case for bone graft
reconstruction including sinus grafting and distraction osteogen-
esis for the atrophic edentulous maxilla, J Oral Maxillofac Surg
62:1423-1428, 2004.
11. Laster Z, Rachmiel A, Jensen OT: Alveolar width distraction
osteogenesis for early implant placement, J Oral Maxillofac Surg
(63)12:1724-1730, 2005.
12. Jensen OT et al: Alveolar distraction osteogenesis, Selected Read-
ings Oral Maxillofac Surg 10(4):1, 2002.

SOFT TISSUE PROCEDURES AROUND IMPLANTS
Glenn Jividen Jr.
The increasing acceptance of dental implant therapy has
largely been the result of the ability to predictably obtain a
rigid bone-implant interface. The overlying soft tissue archi-
tecture and consistency are now being scrutinized in an
attempt to achieve improved implant longevity and/or aes-
thetics. This chapter will review the indications for soft tissue
procedures around implants and describe techniques to
improve these soft tissue parameters.
■ SOFT TISSUE HEALTH
CONSIDERATIONS AROUND
IMPLANTS
The composition of the epithelial and connective soft tissues
surrounding dental implants has been established to be similar
to that of natural teeth.1-6 A junctional epithelium forms a
hemidesmosomal attachment to the implants and natural
teeth, approximating 2 mm in length (Figure 28-1). The con-
nective tissue interface, however, is different based on the
attachment orientation geometry and type of attachment.
The connective tissue zone is approximately 1 mm around
teeth and 2 mm around implants. Collectively, the junctional
and connective tissue attachment is referred to as the soft
tissue “seal.”
Differences in the soft tissue connections involve the fact
that connective tissue directly attaches to the acellular root
cementum of a tooth, whereas the connective tissue around
implants runs parallel to the implant surface and inserts into
the bone.7,8 In addition, the periimplant connective tissue
has significantly higher collagen content and less fibroblasts.7,9
The significantly reduced vascularity of the periimplant con-
nective tissue10 is thought to place this attachment mecha-
nism at higher risk for bacteria-induced inflammatory
breakdown.11,12 It is therefore preferable to provide dimensions
and quality of soft tissue that are more resistant to bacterial-
induced bone loss and thus reduce the chance of subsequent
implant failure or aesthetically compromising recession.
Historically, adequate dimensions of bound keratinized
tissue have been the gold standard for mucogingival health
around teeth and implants. Wennstrom13 challenged this
belief, suggesting that a movable mucosa around an implant
permucosal extension or abutment can be a stable end point
if adequately maintained. Most authors,9,14,15,16 however, agree
that long-term stability is more probable with bound tissue,
keratinized or not. Unbound tissue of either keratinized or
CHAPTER 28
mucosal origin would be least desirable because of the poten-
tial for either increased pocket depth or recession.
■ SOFT TISSUE AESTHETIC
CONSIDERATIONS FOR IMPLANTS
Lack of aesthetics around implants can be a deficiency of
several soft tissue factors, including color, contour, and con-
sistency. Specific problems within these categories include loss
or reduction of the interdental papilla, increased crown height,
and exposure of implant margin. It is the author’s observation
that many of these common problems arise during the restor-
ative phase of treatment when surgical solutions are not pos-
sible, feasible, or well accepted by the patient. It therefore
behooves the surgeon to understand and communicate to the
patient any potential or preexisting aesthetic compromises
that are present or may occur as a result of anatomic consid-
erations. The patient’s expectations should be elucidated,
recorded, and harmonious with those of the treating
clinician.
Methods of communicating expectations of this sort use a
nomenclature system, such as established by Palacci and Erics-
son9 or Misch.17 The Palacci and Ericsson defect classification
scheme is based on four classifications of vertical dimension
and four classifications of horizontal dimension. The three-
category classification system of Misch is of particular utility
when discussing the anticipated appearance of the final resto-
ration with patients. The system for fixed implant restorations
classification divides the desired prosthesis into one of three
categories: FP-1, FP-2, and FP-3. These options depend on the
amount of hard and soft tissue replaced and serve to convey
the appearance of the final prosthesis to all implant team
members17 (Table 28-1). Ridge deficiencies described by these
systems are most frequently the result of a hard tissue defi-
ciency, which should be addressed early in the treatment
plan.
Advanced diagnostic techniques, such as CT imaging, are
useful to assess and quantify the need for hard and soft tissue
support. Preliminary replacement of deficient hard tissues
should be addressed before considering soft tissue augmenta-
tion. A ridge deficiency at the implant site should be corrected
to within 3 mm of its optimal contour.18,19 Techniques for
diagnosing and treating hard tissue defects are addressed in
another chapter.
479
480 SECTION IV ■ Implant Surgery
CT insertion
into root
cementum
A B
FIGURE 28-1. A, Soft tissue attachment around natural tooth. B, Soft tissue attachment around dental implant.
TABLE 28-1 Prosthodontic Classification
Type Definition
FP-1 Fixed prosthesis; replaces only the crown; looks like a natural
tooth.
FP-2 Fixed prosthesis; replaces only the crown and a portion of the
root; crown contour appears normal in the occlusal half, but is
elongated or hypercontoured in the gingival half.
FP-3 Fixed prosthesis; replaces missing crowns and gingival color and
portion of the edentulous site; prosthesis most often uses
denture teeth and acrylic gingival, but may be porcelain to metal.
RP-4 Removable prosthesis; overdenture supported completely by
implant.
RP-5 Removable prosthesis; overdenture supported by both soft tissue
and implant.
The likelihood of developing aesthetic complications is
additionally based on tissue biotype. Tissue types have been
categorized into two forms: thin and scalloped, or thick and
flat.20 The stability of the osseous crest and position of the
free-gingival margin are directly proportional to the thickness
of the bone and gingival tissue. Kan et al.21 found that with
implants, the level of the interproximal papilla of the implant
is independent of the proximal bone level next to the implant,
but is related to the interproximal bone level next to the
adjacent teeth. He also found that even with ideal execution,
facial and/or interproximal gingival recession may occur, espe-
cially with a thin, scalloped periodontium.22 The most predict-
able and expedient method of addressing an interproximal
papilla deficit is to increase the gingival emergence of the
adjacent restorations and/or moving the cervical contact
point apically.22
Another common problem with implant aesthetics, espe-
cially when replacing a single anterior tooth with an implant,
is a discrepancy in crown heights, especially in the presence
CT
parallel to
abutment
and
implant
of a high lip line (Figure 28-2). A useful resource to determine
the appropriate aesthetic surgical procedure, if any, is the
algorithm described by Kokich in a series of three articles23-25
on aesthetics and anterior tooth position. He notes that the
most common crown length discrepancy with natural teeth
occurs when one maxillary central incisor is shorter than the
other, but the incisal edges are even. The problem can and
should be anticipated before implant placement with proper
diagnostic planning and establishment of patient expecta-
tions. If faced with the problem during the restorative phase
the following options exist: (1) gingival surgery to correct soft
tissue form or (2) intrusion and restoration of the shorter
(natural) tooth.
Determination of the appropriate surgical technique is
determined by periodontal probing of the labial sulci and
measurement of the existing band of attached and keratinized
tissue. If the incisal edges are even and cementoenamel junc-
tions (CEJs) are level, a gingivectomy would be performed to
remove the excess tissue. If a narrow band of attached tissue
is present or there are differing bone heights, a flap procedure
would be needed to allow for osseous recontouring (Figure
28-2).
Kokich also describes preoperative planning and tech-
niques to address problems with anterior tooth vertical posi-
tioning and mediolateral relationships.24,25 It should be noted
that corrections usually involve orthodontics and restorative
dentistry, not soft tissue surgical techniques.
■ SURGICAL TECHNIQUES FOR
SOFT TISSUE HEALTH AND
AESTHETICS AROUND IMPLANTS
The techniques described following may be used to achieve
objectives in improving tissue health, aesthetics, or both in
varying degrees and may involve either augmentation and/or
resection.
 CHAPTER 28 • Soft Tissue Procedures Around Implants 481

A B

C D

E F

FIGURE 28-2. A, Pretreatment photo, right central incisor has advanced periodontal disease. B, Lip line. C, Implant
crown/natural tooth crown height discrepancy. D, Crown lengthening of hard and soft tissues performed on adjacent
teeth. E, and F, Final crowns and adjacent veneers in place. (Restorations courtesy of Dr. William Gioello.) To view a
color version of this illustration, refer to the color insert section at the back of this book.

(Figure 28-3). This creeping attachment phenomenon has

GINGIVAL AUGMENTATION PROCEDURES TO
IMPROVE SOFT TISSUE HEALTH
Techniques to provide more attached gingiva are best per-
formed before abutment connection and are commonly free
gingival, connective tissue, or variants thereof. These muco-
gingival procedures are also used to correct soft tissue prob-
lems that can arise during the preimplant bone augmentation,
stage I integration, and postrestoration time periods. For bone
augmentation procedures, incision line opening is a common
complication. Soft tissue grafting will not be able to address
the primary problem (bone exposure), and this compounded
failure or complication will cause the patient to lose confi-
dence in the treating surgeon. This combination of soft and
hard tissue complication is best addressed by serial removal or
recontouring of the exposed bone and deepithelialization of
the wound edges (for non–bisphosphonate-induced cases)
also been observed following first-stage implant surgery (Figure
28-4).
It is thought that platelet-rich plasma may be useful in
accelerating soft tissue healing and thereby reduce the inci-
dence of incision line opening, but this has not been estab-
lished by controlled clinical trials.
Gingivectomy
Removal or recontouring of gingival tissue may be necessary
to improve implant health during the integration phase, for
treatment of an ailing implant, and for restorative access.
During the integration phase, Tal et al.26 established that
partially exposed implants have inflamed tissue over the cover
screw that is inflamed and may contain bone debris that
potentially could affect the healing implant (Figure 28-5). For
an ailing implant, gingival recontouring may be needed as part
482 SECTION IV ■ Implant Surgery

A B

C D

E F

FIGURE 28-3. A, Pretreatment photo, note horizontal ridge defect. B, Autogenous block bone graft from symphysis.
C, Incision line opening 2.5 weeks after surgery. D, Serial recontouring of graft every 2 weeks. E, Almost complete soft
tissue coverage 12 weeks after bone graft surgery. F, Osteotomy preparation at 16 weeks.

of a treatment protocol, with the objective to minimize GINGIVAL GRAFTING

implant pocket depths. For staged procedures, gingivectomy
may be performed with a tissue punch assuming adequate sur-
rounding tissue quality (Figure 28-6). In the context of aes-
thetic implant treatment, gingivectomies may be necessary
around the implant abutment or the adjacent natural teeth
to allow for the most harmonious gingival contours (Figure
28-2D).
Several techniques may be used to improve tissue thickness
and attachment. Augmentation techniques include epithelial
free-gingival and connective tissue grafting.
Epithelialized Free-Gingival Grafting
This technique has a long history dating to the 1960s. The
Sullivan and Akins27 description and overview of the proce-
 CHAPTER 28 • Soft Tissue Procedures Around Implants 483

G H

I J
FIGURE 28-3, cont’d. G, Four months after implant placement, note minimal amount of attached and keratinized
tissue surrounding implant. H, Seven weeks following epithelialized graft placement. I, Abutment in place. J, Provisional
crown with improved surrounding tissue quality. To view a color version of this illustration, refer to the color insert
section at the back of this book.

dure prompted adoption of free, autogenous gingival grafting
into common clinical practice. Its predictable and versatile
nature has allowed for clinicians to provide increased zones of
attached gingiva around teeth and implants with minimal
difficulty.
The recipient site is prepared first to allow minimal time
to elapse between harvesting and graft placement. The auto-
graft can be placed directly on bone (perforated or not), but
is most commonly placed on periosteum. The recipient “bed”
should be overextended to allow for some degree of tissue
shrinkage of up to 25% to 45%, depending on tissue thickness.
It is important to remove any residual alveolar mucosa, muscle
fibers, and connective tissue fibers from the periosteal bed.
These fibers may either cause inadvertent movement of the
graft or directly block revascularization.
Donor site selection and graft tissue thickness will depend
on the defect being treated. Thick grafts of 1.5 to 2 mm have
been generally recommended for ridge augmentation, root
coverage, and around implant abutments. In contrast to
thinner grafts of 0.75 mm or less, the thick grafts are more
dimensionally stable and therefore are better able to withstand
functional stresses, such as from mastication and plaque
control procedures. These grafts, however, tend to have an
unaesthetic, patchlike appearance. Non–rugae-containing
palatal tissue is the most common donor site, with alternative
sites including the tuberosity area and edentulous ridge(s).
The graft should be free of fat or glandular tissue to allow for
plasmatic circulation (see Figures 28-3 H-J).
Connective Tissue Grafting
Subepithelial connective tissue grafting may be described as a
combination of a partial-thickness flap and a nonepithelialized
free connective tissue graft technique, first used to correct
ridge defects. Introduced by Langer,28 its success is based on
use of a bilaminar flap with the graft having a double blood
supply from both the gingival flap and the recipient bed. It is
frequently used in conjunction with a coronally positioned
pedicle graft to achieve coverage of crown and abutment
margins and tooth roots. In addition, the connective tissue
graft is useful for edentulous ridge augmentation or repair, soft
tissue root eminence formation, and masking gingival discol-
orations or abutment “show through.” Improved periimplant
soft tissue health can be accomplished by providing bound
tissue around implant abutments. These indications, com-
bined with the technique’s high predictability for root cover-
age, color matching, and minimal donor site invasiveness,
484 SECTION IV ■ Implant Surgery

A B

C D

E F

FIGURE 28-4. A, Pretreatment photo of mandibular left lateral incisor with advanced periodontal disease.
B, Exposure of crest module and implant body during integration period. C, Creeping attachment of soft tissue over
implant. D, Complete coverage of implant up to cover screw at 4 months. E, Abutment in place. F, Provisional crown.
To view a color version of this illustration, refer to the color insert section at the back of this book.

support the contention that connective tissue grafting is the

single most versatile soft tissue procedure for both natural
teeth and implants (Figure 28-7 and Figure 28-8).14,20 Its major
limitation is the inability to harvest adequate thickness of
donor material.

FIGURE 28-5. Partial exposure of healing abutment necessitating gingi-
vectomy to establish hygienic gingival contour. To view a color version of
this illustration, refer to the color insert section at the back of this
book.
AlloDerm
The major limitation of the subepithelial connective tissue
graft may be mitigated by use of AlloDerm, an allograft. It can
therefore be used to bulk out ridge defects that may have pre-
viously required hard tissue grafting beyond that necessary for
ideal implant positioning and support (Figure 28-9). This
tissue is composed of an acellular dermal matrix derived from
donated human skin tissue supplied by accredited tissue banks.
As AlloDerm is regarded as minimally processed and not sig-
 CHAPTER 28 • Soft Tissue Procedures Around Implants 485

A B

FIGURE 28-6. A, Use of tissue punch. B, Implant uncovered with remaining adequate dimensions of attached
tissue. To view a color version of this illustration, refer to the color insert section at the back of this book.

A B

FIGURE 28-7. A, Soft tissue ridge defect around implant. B, Connective tissue repair after 2 years. To view a
color version of this illustration, refer to the color insert section at the back of this book.

nificantly changed in structure from the natural material, it
has been classified as banked human tissue. Its first applica-
tions in 1995 were in the medical field, where it continues be
used in varied disciplines, such as urology and orthopedic
surgery. It has been used in soft tissue dental applications since
1997. Commercially available dermis is processed by conven-
tional freeze-drying. The uniqueness of AlloDerm tissue
centers on the proprietary processing, including a cryogenic
aspect that involves removal of the antigenic cellular compo-
nents, leading to increased preservation of the tissue’s essen-
tial biochemical and structural composition.
Pediculated Connective Tissue Graft (PCTG)
The pediculated connective tissue graft is a vascularized sub-
epithelial connective tissue graft that involves the rotation of
a periosteal-connective tissue flap from the palatal soft tissues
onto the recipient edentulous site. Because of the mainte-
nance of a vascular supply, this graft has the potential to gain
large volumes of soft tissue for vertical and buccal ridge aug-
mentation. Postoperative aesthetic results are excellent, with
minimal shrinkage. It is limited by the size and shape of the
donor palate, and care must be taken not to overthin the
donor tissue, which can result in sloughing.14,20
The PCTG has been found to be particularly useful in the
treatment of aesthetic dilemmas around implants that have
been caused by improper implant placement and inadequate
soft tissue management.29
Modified Roll Tissue Graft
As described by Abrams,30 this technique involves rotating a
deepithelialized connective tissue pedicle from the palate to
a labial pouch. Originally designed for buccal and vertical
augmentation around fixed prosthetics, it has been adapted for
use around implants. It is not in common use because of the
utility of alternative procedures and the potential for donor
site morbidity despite technique modification by Scharf and
Tarnow to prevent total bone denudation14,30,31 (Figure
28-10).
FLAP DESIGNS TO IMPROVE AESTHETICS
It is always desirable to have a zone of attached tissue around
an implant. Appropriate incision design either at the time of
486 SECTION IV ■ Implant Surgery

A B

C D

FIGURE 28-8. A, Pretreatment. B, Facial ridge defect. C, Connective tissue graft used to fill out defect. D, Provi-
sional with soft tissue contour reestablished. To view a color version of this illustration, refer to the color insert
section at the back of this book.

implant placement or (for a staged procedure) at uncovery can
allow for this desirable result without the need for subsequent
mucogingival surgery. For first-stage procedures, the use of a
limited, papilla-sparing, flap design (Figure 28-11) is recom-
mended to minimize interproximal crestal bone loss and pos-
sible loss of the papillae. A study by Gomez-Roman32 attributed
decreased interproximal crestal bone levels to periosteal denu-
dation and therefore recommended leaving a minimum papilla
width of 1 mm.
Incisions can be designed to bisect minimal areas of
attached tissue to conserve and/or reposition attached and
keratinized tissue for improved aesthetics and health. One
specific technique is described following.
Papilla Regeneration Technique
Palacci9 described a technique to address the common aes-
thetic problem of missing or reduced-height papillae adjacent
to dental implants. He proposed making implant uncovery
incisions more palatal, thus creating a wider flap from which
one or more pedicles could be disengaged. These pedicles
could be rotated, creating one or more papillae. Variations of
this procedure have been published by Kinsel and Lamb33 and
Nembcovsky,34 with varying success in augmenting papillary
form. A technique variation by Misch et al. uses a split-finger
approach to create both a cervical and elevated interdental
and/or interimplant soft tissue. This approach is based on the
manipulation of both palatal and facial soft tissues to provide
sufficient additional tissue volume to increase the interim-
plant papillae height (Figure 28-12).
■ SUMMARY
The established acceptance and use of dental implants for
tooth replacement has led to an associated interest in the
surrounding soft tissue. Practitioners need to be able to manage
the parameters of health and aesthetics with regard to the soft
tissue. It cannot be emphasized enough that soft tissue proce-
dures to improve health and especially aesthetics are best
accepted by the patient as part of an initial plan of treatment
that has taken into account patient expectations. Practitio-
ners and patients should also be aware of the importance of
hard tissue relationships in the overall treatment plan and
the less-than-ideal outcomes that can result if neglected. Even
under the best of circumstances, aesthetic dilemmas can arise.
Soft tissue procedures can help address these problems, but
the multifaceted nature of implant aesthetics demands con-
sideration of all options, including prosthetic. This chapter
 CHAPTER 28 • Soft Tissue Procedures Around Implants 487

A B

C D

FIGURE 28-9. A, Pretreatment photo. B, Horizontal ridge width deficiency. C, Permucosal extensions in place before
coverage with dermal matrix graft. D, Reestablishment of buccal ridge contour. E, Ridge after 4 months of healing.
F, Provisionals in place. To view a color version of this illustration, refer to the color insert section at the back of this book.
488 SECTION IV ■ Implant Surgery

A B

C D

E F

FIGURE 28-10. A, Laser deepithelialization before rollback of tissue for improved facial tissue contour on the left
central incisor. B, Tissue roll back. C, Rollback of tissue showing intact buccal plate. D, Tissue sutured in position. E,
Widened facial contour. F, Thirteen-year follow-up. To view a color version of this illustration, refer to the color
insert section at the back of this book.
 CHAPTER 28 • Soft Tissue Procedures Around Implants 489

FIGURE 28-11. A limited, papilla-sparing, flap design is recommended to minimize

interproximal crestal bone loss and possible loss of the papillae. (From Gomez-Roman G:
Influence of flap design on periimplant interproximal crestal bone loss around single-tooth
implants, Int J Oral Maxillofac Implants 16:61–67, 2001.)

A B

C D

E F

FIGURE 28-12. Split-finger technique: A, Pretreatment. B, Initial incisions. C, Secondary incisions. D, Vertical
mattress suturing of papillae. E, Postsurgical tissue contours. F, Final restoration. To view a color version of this
illustration, refer to the color insert section at the back of this book.
490 SECTION IV ■ Implant Surgery
has given an overview of such concepts. The reader is encour-
aged to review more detailed references on specific topics that
are beyond the scope of this writing.
REFERENCES
1. Gould TR, Brunette DM, Westbury L: The attachment mecha-
nism of epithelial cells to titanium in vitro, J Periodont Res
16:611-616, 1981.
2. Schroeder A, Vander Zypen E, Stich H: The reactions of bone,
connective tissue and epithelium to endosteal implants with
titanium-sprayed surfaces, J Oral Maxillofac Surg 9:15, 1981.
3. Jansen JA: Ultrastructural study of epithelial cell attachment to
implant materials, J Dent Res 65:5, 1985.
4. McKinney RV, Steflik DE, Koth DL: Evidence for junctional
epithelial attachment to ceramic dental implants: a transmission
electron microscope study, J Periodontol 6:425-436, 1985.
5. Hashimoto M et al: Single crystal sapphire endosseous dental
implant loaded with functional stress: clinical and histological
evaluation of the peri-implant tissues, J Oral Rehabil 15:65-66,
1988.
6. Van Drie HJY, Beertson W, Greers A: Healing of the gingiva
following installment of Biotes implants in beagle dogs, Adv
Biomater 8:465-490, 1988.
7. Berglundh T et al: The soft tissue barrier at implants and teeth,
Clin Oral Implants Res 2:81-90, 1991.
8. Listgarden MA et al: Light and transmission electron microscopy
of the intact interfaces between nonsubmerged titanium-coated
epoxy resin implants and bone or gingiva, J Dent Res 71:364-371,
1992.
9. Palacci P, Ericsson I: Esthetic implant dentistry: soft and hard tissue
management, Chicago, 2001, Quintessence.
10. Berglundh T et al: The topography of the vascular systems in the
periodontal and peri-implant tissues in the dog, J Clin Periodontol
21:189-193, 1994.
11. Buser D et al: Soft tissue reactions to nonsubmerged unloaded
titanium implants in beagle dogs, J Periodontol 63:226-236,
1992.
12. Ericsson I et al: Long-standing plaque and gingivitis at implants
and teeth in the dog, Clin Oral Implants Res 3:99-103, 1992.
13. Wennstrom JL, Bengazi F, Lekholm U: The influence of the
masticatory mucosa on the peri-implant soft tissue condition,
Clin Oral Implants Res 5:1-8, 1994.
14. Sclar AG: Soft tissue and esthetic considerations in implant therapy,
Chicago, 2003, Quintessence.
15. Silverstein LH, Lefkove MD, Garnick JJ: The use of free gingival
soft tissue to improve the implant/soft-tissue interface, J Oral
Implantol 20(1):36-40, 1994.
16. Alpert A: A rationale for attached gingiva at the soft-tissue/
implant interface: esthetic and functional dictates, Compendium
(3):356, 358, 360-362, 1994.
17. Misch CE: Dental implant prosthetics, St Louis, 2005, Mosby.
18. Leblebicioglu B, Rawal S, Mariotti A: A review of the functional
and esthetic requirements for dental implants, J Am Dent Assoc
138(3):321-329, 2007.
19. Evian CL, Al-Maseeh J, Symeonides E: Soft tissue augmentation
for implant dentistry, Compend Continuing Education Dent
24(3):195-206, 2003.
20. Cohen E: Atlas of cosmetic and reconstructive periodontal surgery,
ed 3, Hamilton, Ontario, BC, 2007, Decker.
21. Kan JYK et al: Dimensions of peri-implant mucosa: an evalua-
tion of maxillary anterior single implants in humans, J Periodon-
tol 74:557-562, 2003.
22. Kan JYK, Rungcharassaeng K: Interimplant papilla preservation
in the esthetic zone: a report of six consecutive cases, Int J Peri-
odontics Restorative Dent 23:249-259, 2003.
23. Kokich VG: Anterior dental esthetics: an orthodontic perspec-
tive. I. Crown length, J Esthetic Dent 5:19-23, 1993.
24. Kokich VG: Anterior dental esthetics: an orthodontic perspec-
tive. II. Vertical relationships, J Esthetic Dent 5:174-178, 1993.
25. Kokich VG: Anterior dental esthetics: an orthodontic perspec-
tive. III. Mediolateral relationships, J Esthetic Dent 5:200-207,
1993.
26. Tal H, Dayan D: Spontaneous early exposure of submerged
implants. II. Histopathology and histomorphometry of non-
perforated mucosa covering submerged implants, J Periodontol
71:1224-1230, 2000.
27. Sullivan HC, Atkins JH: Free autogenous gingival grafts. 3.
Utilization of grafts in the treatment of gingival recession, Peri-
odontics 6(4):152-160, 1968.
28. Langer B, Calagna LJ: The subepithelial connective tissue graft.
A new approach to the enhancement of anterior cosmetics, Int
J Periodontics Restorative Dent 2:22-33, 1982.
29. Mathews DP: The pediculated connective tissue graft: a tech-
nique for improving unaesthetic implant restorations, Prac Peri-
odontics Aesthetic Dent 14(9):719-724, 2002.
30. Abrams L: Augmentation of the deformed residual edentulous
ridge for fixed prosthesis, Compend Educ Gen Dent 1:205-213,
1980.
31. Scharf DR, Tarnow DP: Modified roll technique for localized
alveolar ridge augmentation, Int J Periodontics Restorative Dent
12:415-425, 1992.
32. Gomez-Roman G: Influence of flap design on peri-implant inter-
proximal crestal bone loss around single-tooth implants, Int J
Oral Maxillofac Implants 16:61-67, 2001.
33. Kinsel RD, Lamb RE: Development of gingival esthetics in the
terminal dentition patient prior to dental implant placement
using full arch transitional prosthesis: a case report, Int J Oral
Maxillofac Implants 16:583-589, 2001.
34. Nemcovsky CE, Moses O, Artize Z: Interproximal papillae
reconstruction in maxillary implants, J Periodontol 71:308-314,
2000.

ZYGOMATIC IMPLANT: A GRAFTLESS APPROACH
TREATMENT OF THE EDENTULOUS MAXILLA
Edmond Bedrossian • Per-Ingvar Brånemark
The edentulous maxillae have a unique anatomic presenta-
tion, which limits the number and the distribution of implants
within the alveolar ridge. The maxillary sinuses bilaterally and
the position of the nasal floor in the premaxillary region may
limit the vertical volume of alveolar bone available for place-
ment of implants in the maxilla for a fixed, implant-supported
prosthesis. The palatal and posterior resorption pattern of the
edentulous maxillae may also limit the horizontal bony volume
necessary to house endosseous implants. Therefore, in review
of the literature,1 the recommended treatment for the eden-
tulous maxilla has been the tissue-supported, overdenture
appliance. To establish support for a fixed prosthesis, recon-
struction of the maxilla with various bone grafting techniques
has been designed to recreate the alveolar volume and topog-
raphy needed for stabilization of dental implants.2-5 If the
sinuses are pneumatized, sinus grafting6 or tilted implants7-9
have also been recommended.
For patients with significant anterior extension of their
maxillary sinuses, extending forward into the bicuspid region,
the zygomatic implant is recommended. The zygomatic
implant allows for establishing posterior maxillary support by
using the limited crestal alveolar bone in the bicuspid region
and the os zygomaticum for establishing initial stability of the
implant. The use of the zygomatic implant and its success rate
have been studied internationally, with a success rate between
94% and 100% as reported by the authors.10-15
The 94% survival, as reported by Branemark et al., repre-
sents three failures out of 52 zygoma fixtures placed in their
initial study. The first failure was due to enveloping of muscle
tissue around the zygoma fixture. The second involved the
inadequate centering of the implant within the zygomatic
bone. The third failure occurred in a patient with Paget’s
disease who had loosely textured and low density bone.14
Overall, this highly predictable implant allows establishing
posterior maxillary support for reconstruction with a fixed
prosthesis without the need for bone grafting.
■ HISTORICAL PERSPECTIVE
The treatment of the moderately to severely resorbed maxillae
presents a challenge for the implant surgical-restorative team.
The typically large pneumatized sinuses in this group of
patients require extensive bone grafting if conventional
implant placement is envisioned. Various procedures have
been available for treatment of the resorbed maxillae. Adell,16
Breine, and Branemark17 used composite grafts to provide a
CHAPTER 29
FOR
tooth anchorage system. Le Fort I osteotomy18 and iliac block
graft19,20 have also been used to reestablish bony volume for
placement of implants. To create bone mass in the posterior
maxillae, sinus-lift grafting procedures19,20 have been per-
formed. Survival of implants in sinus-lift procedures was
studied in the sinus consensus conference.6 The conclusion
reached was similar to Tolman’s report in 1995: The material
was so “multivariate and multifactorial that it was difficult to
draw definitive conclusions; these must await controlled pro-
spective studies.”23 Grafting of the maxillae with delayed
implant placement has been described in the literature.24
Rasmusson presented success with autogenous grafting to
establish favorable topography of the resorbed maxillae for
implant placement using inlay, onlay, and/or Le Fort I proce-
dures.25 A success rate of 80% was reported for grafting with
delayed implant placement and 77% for grafting with simul-
taneous implant placement. The success rate of implants
placed in nongrafted bone was only 89% in the group studied.
Keller and Tolman, who used inlay grafts in their report on
the reconstruction of the compromised maxillae,24 reported an
87% implant survival rate and a prosthetic survival of 95%.
The somewhat limited success with these adjunctive proce-
dures has deterred patients from seeking reconstruction of
their resorbed maxillae. An alternative for the treatment of
this group of patients is the zygomatic implant, which was
introduced by Professor Branemark in 1988.
■ PATIENT SELECTION
A systematic preoperative evaluation of the patient is required
before the surgical treatment.45 Both surgical and prosthetic
needs must be considered before initiation of the surgical
treatment to allow for a predictable outcome. The preopera-
tive evaluation protocol takes into consideration the available
alveolar bone in the different zones of the maxilla (Figure
29-1). It also determines whether the final prosthesis is a
ceramometal bridge or profile prosthesis.26 The determination
is based on the lack or the presence of composite defect.12
Evaluation of the aesthetics of the final prosthesis is made by
recognizing the transition line between the prosthesis and the
residual edentulous crestal soft tissues (Figure 29-2). The zygo-
matic implant is considered in the group of patients who
demonstrate bone in zone 1 only. In patients who also have
limited horizontal alveolar width in zone 1, veneer grafting27
before placement of the conventional implants for the ante-
rior support is considered. A separate group of patients with
491
492 SECTION IV ■ Implant Surgery

Zone 3: Molars
Zone 2: Bicuspids

Zone 1: Premaxilla

FIGURE 29-1. Zones of the maxilla.

Transition line

Smile line

FIGURE 29-2. Smile line as it relates to the transition line.

FIGURE 29-4. Frontal CT demonstrating the os zygomaticum.

evaluation of the patient.12,13,15 The presence of alveolar bone

FIGURE 29-3. Quad zygoma.
advanced maxillary alveolar atrophy present with complete
lack of the alveolus. This group may be candidates for the quad
zygoma treatment concept (Figure 29-3).14 The surgical pro-
cedure may be performed in the hospital setting using general
anesthesia or in the office under IV sedation and local anes-
thesia.12 The surgical candidate should be free of any sinus
disease before consideration for this treatment concept.
■ RADIOGRAPHIC EVALUATION
Although computerized and conventional tomography can
be used, the Panorex radiograph is critical in the initial
in the premaxilla (zone 1) and the lack of bone in the bicuspid
and the molar regions, zones 2 and 3 respectively, are the
indications for considering the zygomatic concept. Axial CT
scans can be obtained to further evaluate the maxillary sinus.
The width of the residual alveolar bone and the width and
height of the zygomatic body can be visualized in frontal
reformatted sections of the axial CT scans.
Further evaluation of the zygomatic bone has also been
described.27 Although not absolutely necessary, the refor-
matted frontal images in 2 to 3 mm cuts afford the less expe-
rienced operator more information for planning the surgery
(Figure 29-4). The presence of sinus pathologic conditions,
including, but not limited to, thickening of the schneiderian
membrane and air fluid levels, may be ruled out in both the
Panorex and tomographic studies.
■ OS-ZYGOMATICUM: REGIONAL
ANATOMY
The quantity and the quality of the zygomatic bone have been
studied and reported by Nkenke et al.27 The morphology and
the microstructure of the os zygomaticum were assessed by
quantitative computer tomography and histomorphometry.
 CHAPTER 29 • Zygomatic Implant 493

Bone mineral density of 30 human zygomatic bone specimens

was studied. The trabecular bone mineral density, the trabecu-
lar bone volume, and the trabecular bone pattern factor were
correlated with each other. The conclusion reached suggested
that the trabecular bone of the os zygomaticum was not a
favorable site for implant placement. However, Nkenke
further suggests that the success seen with the zygomatic
implant is due to the engagement of four cortices during the
placement of the implant. The lingual cortex of the maxillary
alveolus along with the cortical floor of the maxillary sinus
provide for bicortical stabilization at the crestal portion of the
implant. The superior-lateral portion of the roof of the maxil-
lary sinus is formed by the inferior portion of the zygomatic
bone. This portion of the zygoma along with its lateral supe-
rior cortical covering form the bicortical stabilization at the
apical portion of the zygomatic implant.
To quantify the dimensions of cortical and trabecular bone FIGURE 29-5. Axis of zygoma implant.
of the os zygomaticum, morphometric analysis of the zygo-
matic bone was consistent with the following results: medio-
lateral dimension of 7.6 mm in males and 8.0 mm in females.
The anterior-posterior dimension of the zygoma body was
25.4 mm in males and 24.9 mm in females. The lateral cortical
thickness was 1.75 mm in males and 1.71 mm in females. The
length of the zygomatic implant within the zygomatic bone
was 16.5 mm in males and 14 mm in females. Zygomatic
implants placed following ablative surgery have been reported
by Weingart et al.28 The implant survival rate was 65% to
75%. However, with the increased popularity of the zygomatic
implant used in the atrophic maxilla, implant survival has
increased to 97% to 100%.10-15

■ PREOPERATIVE CONSIDERATIONS
The surgical procedure is usually performed in the office
setting under IV sedation.12 All patients are premedicated 1
hour before the surgical procedure. The proper administration
of sufficient local anesthesia is critical in the management of
these patients under IV sedation. The various infiltrations and
nerve blocks include circumvestibular infiltration of the
maxilla, greater palatine blocks, and bilateral transcutaneous
infiltration of the temporal areas over the zygomatic body.
Bilateral inferior alveolar nerve blocks are considered to allow
retraction of the lower jaw during the surgery without undo
stimulation of the sedated patient. It is recommended that
direct visualization of the path of the implant from the pre-
molar area to the base of the zygoma be visualized whenever
possible.12,30 Direct visualization of the base of the zygomatic
body has also been advocated in clinicians who have used
computer-assisted treatment planning and surgical templates
for placement of the zygomatic implant.30 Having a clear view
of the path of the instruments needed in establishing the
osteotomy and visualizing the path of the implant during its
insertion prevent disorientation and potential complications
associated with placement of the zygomatic implant. Gener-
ally, three potential axes of insertion are possible. The proper
axis is a path extending from the bicuspid region through the
maxillary sinus, entering the midportion of the zygomatic
FIGURE 29-6. Implant and available drill sizes.
body. If the entry point in the zygomatic body is more anterior
to this line axis, potential for penetration into the orbit exists.
However, if the line axis is posterior to this line, the potential
for entering the pterygomaxillary space, leading to soft tissue
enveloping and the subsequent lack of osseointegration of the
implant among the potential for unexpected hemorrhage,
exists (Figure 29-5). The zygomatic implant has a unique
design. The diameter of the apical two thirds of the implant
is 4.0 mm, yet the alveolar one third widens to a diameter of
5.0 mm. The zygomatic implants are available in lengths
ranging from 30 to 52.5 mm. A specialized series of long
zygoma drills are used to prepare the osteotomy (Figure
29-6).
■ SURGICAL OPTIONS
In reconstruction of the edentulous maxilla with the
zygomatic implant, the traditional two-stage protocol10,12,29
or the immediate-load protocol12,30 may be considered. The
494 SECTION IV ■ Implant Surgery
FIGURE 29-7. Cal bar stabilizing implants at stage II surgery. To view a
color version of this illustration, refer to the color insert section at the
back of this book.
FIGURE 29-8. Access into the right maxillary sinus. To view a color
version of this illustration, refer to the color insert section at the back
of this book.
two-stage protocol requires the immediate cross arch splinting
of the zygoma implants at the time of the uncovering proce-
dure. This can be accomplished efficiently by using the Cal
technique (Figure 29-7) for the fabrication of a passive bar
before the uncovering procedure.32 However, the alternative
immediate-load technique cross arch splints the zygomatic
implant with each other by conversion of the patient’s exist-
ing denture into a fixed provisional bridge. The immediate
loading of the zygomatic implants has been reported in the
literature with favorable results.26,30
■ SURGICAL PROTOCOL
The surgical procedure begins by making a crestal incision
across the edentulous maxillary arch. Bilateral releasing inci-
sions are made over the maxillary tuberosity, similar to the
hockey stick incisions for removal of maxillary wisdom teeth.
A vertical window is made on the lateral wall of the maxilla
paralleling the junction of the posterior aspect of the lateral
maxillary wall and the lateral aspect of the posterior maxillary
wall accessing the sinus (Figure 29-8). The schneiderian mem-
brane may be removed or reflected away from the inside of the
lateral wall of the maxillary sinus (Figure 29-9). It is critical
FIGURE 29-9. Reflecting the schneiderian membrane after accessing
the sinus.
FIGURE 29-10. Round drill.
to be aware of the position of the schneiderian membrane and
to ensure that it does not attach to the zygomatic implant
during its insertion into the body of the zygoma. Introduction
of the soft tissue schneiderian membrane into the body of the
zygoma will lead to nonosseointegration of the zygomatic
implant.
The osteotomy is initiated by the use of a round bur (Figure
29-10) followed by a 2.9-mm twist drill (Figure 29-11). A
2.9- to 3.5-mm pilot drill stabilizes the 3.5-mm drill, which
completes the osteotomy both at the maxillary crest and the
body of the zygoma (Figure 29-12). If greater than 3 mm of
crestal bone is identified, the alveolar portion of the osteot-
omy is completed by introduction of the 4.0-mm twist drill.
In cases where there is a limited crestal bone width and
or height, the 4.0-mm drill is not used. Before implant place-
ment and at all times during preparation of the osteotomy
(Figure 29-13), the entire surgical paths of the drills are
visualized.12,30
The 45° angulations of the zygomaticus implant (Figure
29-14) allow for the platform of the implant to be in the same
plane as the vertically placed implants in the premaxilla. To
facilitate implant placement, the premounted implant carrier
allows for easy handling of the implant with the straight zygo-

FIGURE 29-11. 2.9-mm drill.
FIGURE 29-12. 3.5-mm drill.
FIGURE 29-13. Direct visualization of the osteotomy. To view a color
version of this illustration, refer to the color insert section at the back
of this book.
matic hand piece (Figure 29-15). To ensure proper orientation
of the angulated implant head, the premounted fixture carrier
screw head is used as a guide. Once the zygoma implant is
placed to the proper depth a “stargrip” screwdriver is inserted
into the head of the fixture screw, which secures the implant
CHAPTER 29 • Zygomatic Implant 495
FIGURE 29-14. 45° platform.
FIGURE 29-15. Premounted fixture carrier, straightening the implant.
carrier to the 45° zygoma implant platform, is made (Figure
29-16).The shaft of this screwdriver must be at right angles to
the edentulous ridge to ensure proper orientation of the
implant platform.
A minimum of two premaxillary implants are required
(Figure 29-17).33 If four implants can be distributed evenly
within the premaxilla (zone 1), it may be considered. In the
two-stage protocol where both the premaxillary and the zygo-
matic implants are submerged, single-thread NobelSpeedy
Groovy (Nobel Biocare, Goteborg, Sweden) implants have
been used. However, in cases where immediate loading is
considered, the double-thread NobelSpeedy implants (Nobel
Biocare, Goteborg, Sweden) have been used. The zygomatic
implant is an external hex implant. The use of the external
hex premaxillary implants is recommended to maintain uni-
formity and ease during the restorative treatment. All immedi-
ate premaxillary implants were placed with an initial insertion
torque setting of 20 Ncm. Upon “stalling” of the hand piece,
the insertion torque setting is increased to 40 Ncm, allowing
complete insertion and seating of the implants. The “onion”
hand insertion instrument (Figure 29-18) is used in cases
where the hand piece stalls at the 40 Ncm setting. The zygo-
496 SECTION IV ■ Implant Surgery

A B

FIGURE 29-16. A, Confirming orientation of the zygoma implant platform. B, Platform of the zygoma implants in
same plane as premaxillary implants. To view a color version of this illustration, refer to the color insert section
at the back of this book.

J
G

Zygomatic fixtures L
K
F
Branemark fixtures
A
X3 I
x1 x H
3
x2 X2 E

X1
B D
C
A Bridge

B
FIGURE 29-17. A, Zhao-Skalak-Brånemark’s biomechanical analysis. B, Zygoma implant with minimum of two
premaxillary implants.

matic implant is hand driven to its final insertion depth,
where the implant platform is intimately in contact with the
lateral wall of the maxillary alveolus. The criteria for the
immediate loading of the premaxillary implants and the
zygoma implants include a minimum of 40 Ncm of insertion
torque.26
The surgical wound is closed using 4-0 Vicryl sutures in
cases where the implant surgery was performed in the two-
stage manner. The denture base over the gingiva covering the
platform of the zygomatic implants is relieved to prevent
loading and wound breakdown. In patients who received
immediate provisional fixed prostheses, 3-0 gut is used to close
the soft tissue wound, and their existing full denture is con-
verted to the immediate provisional fixed prostheses by the
use of multiunit abutments and titanium temporary cylinders
(Figure 29-19).
■ PROSTHETIC CONVERSION
TECHNIQUE
To provide the surgical patient with a fixed provisional pros-
thesis immediately following the surgical procedure, conver-
sion of the patient’s existing full denture or the conversion of
the newly fabricated immediate denture is undertaken.26,37
The preoperative denture should be at the proper vertical

FIGURE 29-18. The onion driver.
FIGURE 29-19. Temporary titanium cylinders. To view a color version
of this illustration, refer to the color insert section at the back of this
book.
dimension of occlusion (VDO) and proper tooth position.34-36
Once the implants have been placed with 40 Ncm insertion
torque, healing abutments are connected. The heights of
the healing abutments are chosen so that after suturing of the
crestal incision, 1 mm of the healing abutment is above the
soft tissue line. The patient’s denture is adjusted to allow
passive seating without interference from the healing abut-
ments and distortion of the soft tissues. Blue mouse bite reg-
istration is flowed into the denture as it is seated in the mouth,
ensuring proper occlusion with the apposing dentition and
proper midline orientation. The positions of the healing abut-
ments are imprinted into the blue mouse as it sets (Figure 29-
20). An acrylic bur is used to perforate the denture base,
marking and relating the positions of the implants with the
denture acrylic. Care must be taken not to make excessive
holes or to fracture the denture base. The denture with the
CHAPTER 29 • Zygomatic Implant 497
FIGURE 29-20. Imprint of implant positions.
FIGURE 29-21. Multiunit abutments seated. To view a color version
of this illustration, refer to the color insert section at the back of this
book.
prepared holes is once again seated in the mouth in the proper
position. Relating the position of the temporary healing abut-
ments to the holes in the denture base allows one to determine
whether straight, 17°, or 30° abutments will be used for the
fabrication of the screw-retained provisional profile prosthesis.
Once the abutments are chosen and seated onto the implants,
reconfirmation of the screw access holes are made by proper
seating of the denture in the patient’s mouth. The abutments
are torqued to 35 Ncm (Figure 29-21). To fabricate this fixed
prosthesis, temporary multiunit titanium cylinders are used
(Figure 29-22). The temporary titanium cylinders are cold
cured to the denture base using quick-setting denture repair
acrylic (Figure 29-23). Upon hardening of the acrylic, the
denture is removed from the patient’s mouth by unscrewing
the retaining screws. The voids on the tissue surface of the
denture base, around the temporary titanium cylinders, are
further reinforced with the quick-setting acrylic, ensuring not
to introduce any acrylic into the seating surfaces of the cylin-
ders (Figure 29-24). The palate and the denture flanges are
removed. Recontouring of the acrylic on the undersurface of
the prosthesis is completed in an attempt to remove all con-
cavities, which may trap food. The patient’s occlusion is
498 SECTION IV ■ Implant Surgery
FIGURE 29-22. Temporary cylinders placed. To view a color version of
this illustration, refer to the color insert section at the back of this book.
FIGURE 29-23. Luting of the temporary cylinders to the denture. To
view a color version of this illustration, refer to the color insert section
at the back of this book.
FIGURE 29-24. Keeping the inner surface of the temporary cylinder
clean. To view a color version of this illustration, refer to the color insert
section at the back of this book.
checked, ensuring group function and uniform loading across
the entire prosthesis in centric occlusion.38,39 To avoid bending
moments, as close to 0° teeth are used in the fabrication of
this provisional prosthesis. A temporary material of choice is
used to cover the retaining screw holes (Figure 29-25).
■ POSTOPERATIVE CARE
Patients are asked to maintain a soft diet. Incising of food is
discouraged for the first three months. Postoperative medica-
tions include oral antibiotics for 1 week and an analgesic of
choice, as needed. All patients are asked to use 2% chlorhexi-
dine rinse 20 minutes before sleeping every night. A 1-week
follow-up appointment is made to ensure proper occlusion,
wound healing, and stability of the prosthesis. If screw loosen-
ing is encountered, occlusion is checked, eliminating hyperoc-
clusion on selected areas and interference in lateral excursions.
Patients are seen as needed over the next 6 months. Bruxism
on occasion will result in the fracture of the provisional pros-
thesis. The prosthesis may be repaired intraorally or indexed
and removed for a laboratory repair at the fracture site. The
use of night guards made for the provisional prosthesis and the
continual use of a new night guard made after the fabrication
of the final definitive prosthesis may aid in management of
the excessive forces generated by this group of patients.
■ SURGICAL COMPLICATIONS
Potential complications include penetration of the orbit and
the pterygomaxillary space. Inability to place the zygomatic
implant in patients with abnormal anatomy secondary to con-
genital deformities, trauma, and postcancer resection cases has
been reported.40 Several authors have reported on complica-
tions with the zygomatic implant and its management.15,40,41
Potential complications include soft tissue irritations around
the abutment connection with the zygomatic implant,15,41
which were corrected by minor soft tissue procedures. Delayed
acute sinusitis was reported by Aparicio15 14, 23, and 27
months after surgical procedures. These infections were
resolved following oral antibiotic regimens without further
complications. Bjorn Peterson reported on foreign bodies in
FIGURE 29-25. Completed immediate load prosthesis.

FIGURE 29-26. Sinoscopy of maxillary sinus.
the nose and the maxillary sinus (Figure 29-26). One-year
follow-ups of 14 patients, using an endoscope for rhinoscopy
and sinoscopy, determined no signs of infection or inflamma-
tion in the mucosa around the fixtures.29 Neurosensory distur-
bance of the zygomaticofacial nerve has been reported as a
result of commonly encountering this nerve during the soft
tissue reflecting over the lateral aspect of the zygomatic body.42
Failure of one immediate-load zygomatic implant has been
experienced by this author. The failed zygomatic implant was
noted at initiation of the fabrication process for the final
prosthesis. The zygomatic implant rotated during a reverse
torque test. This was corrected by the simultaneous removal
of the one failed zygomatic implant and placement of a new
zygomatic implant immediately below the existing failed oste-
otomy site. The new zygoma implant was immediately loaded
by connecting it to the existing provisional prosthesis. After
an additional 6-month osseointegration period, all implants
were stable, and the final profile prosthesis was completed.
■ FINAL PROSTHESIS FABRICATION
After 6 months of osseointegration time, the prosthesis is
removed, and the stability of the implants is checked. Osseo-
integration is confirmed by observation of the lack of mobility
of the implants and the lack of sensitivity during percussion.
Fazad et al.43 measured implant stability using Osstell (Integra-
tion Diagnostics, Savedalen, Sweden). Resonance frequency
analysis showed mean ISQ values for the premaxillary implants
and zygomatic implants to be 61.6 (range 48 to 71) and 65.9
(range 42 to 100), respectively. Aparicio et al. used the
Periotest (Siemens AG, Bensheim, Germany) measurement
values, which compared favorably with previously reported
measurements of osseointegrated implants. Zwahlen et al.40
used the reverse torque technique (10 Ncm) at the second-
stage surgery, 6 months after placement of the implants, to
determine osseointegration. Upon determination of osseoin-
tegration, the patient is ready for either the fabrication of an
all-acrylic profile prosthesis44 or a metal-based and acrylic
profile prosthesis using resin teeth.
CHAPTER 29 • Zygomatic Implant 499
■ SUMMARY
The zygomatic implant is a predictable fixture to establish
posterior maxillary support for a fixed, implant-supported
maxillary prosthesis without the need for bone grafting. In the
hands of experienced surgical and prosthetic teams, the zygo-
matic implant is a viable addition to existing treatment
modalities. The implant may be used in either the two-stage
protocol or the immediate-load protocol with favorable long-
term stability.
REFERENCES
1. Wood M, Vermilyea SG: A review of selected dental literature
on evidence-based treatment planning for dental implants:
report of the committee on research in fixed prosthodontics of
the Academy of Fixed Prosthodontics, J Prosthet Dent 92:447-
462, 2004.
2. Breine U, Branemark PI: Reconstruction of alveolar jaw
bone. An experimental and clinical study of immediate
and performed autologous bone grafts in combination with
osseointegrated implants, Scand J Plast Reconstr Surg 14:23-48,
1980.
3. Issaksson S et al.: Early results from reconstruction of severely
atrophic (class VI) maxillas by immediate endosseous implants
in conjunction with bone grafting and Lefort I osteotomy, J Oral
Maxillofac Surg 22:144-148, 1993.
4. Adell R et al.: Reconstruction of severely resorbed edentulous
maxillae using osseointegrated fixtures in immediate autogenous
grafts, Int J Oral Maxillofac Implants 5:233-246, 1990.
5. Isaksson S, Alberius P: Maxillary alveolar ridge augmentation
with onlay bone grafts and immediate endosseous implants,
J Craniomaxillofac Surg 20:2-7, 1992.
6. Jensen OT et al.: Report of the sinus consensus conference
of 1996, Int J Oral Maxillofac Implants 13(suppl 1):11-32,
1998.
7. Fortin Y, Sullivan RM, Rangert BR: The Marius implant bridge:
surgical and prosthetic rehabilitation for the completely edentu-
lous upper jaw with moderate to severe resorption: a 5-year ret-
rospective clinical study, Clin Implant Dent Relat Res 4:69-77,
2002.
8. Krekmanov L et al.: Tilting of posterior mandibular and maxil-
lary implants for improved prosthesis support, Int J Oral Maxil-
lofac Implants 15:405-414, 2000.
9. Aparicio C, Perales P, Rangert B: Tilted implants as an alterna-
tive to maxillary sinus grafting: a clinical, radiologic, and
Periotest study, Clin Implant Dent Relat Res 1:39-49, 2001.
10. Stevenson ARL, Austin BW: Zygomatic fixtures-the Sydney
experience, Ann R Australas Coll Dent Surg 15:337, 2000.
11. Higuchi KW: The zygomatic fixture: an alternative approach for
implant anchorage in the posterior maxilla, Ann R Australas Coll
Dent Surg 15:28-33, 2000.
12. Bedrossian E, Stumpel LJ: The zygomatic implant: preliminary
data on treatment of severely resorbed maxillae. A clinical
report, Int J Oral Maxillofac Implants 17:861-865, 2002.
13. Malevez C et al.: Clinical outcome of 103 consecutive zygomatic
implants: a 6-48 month follow-up study, Clin Oral Implant Res
115:18-22, 2004.
14. Branemark PI et al.: Zygoma fixture in the management of
advanced atrophy of the maxilla: technique and long-term
results, Scand J Reconstr Surg Hand Surg 38:70-85, 2004.
15. Aparicio C et al.: A prospective clinical study on titanium
implants in the zygomatic arch for prosthetic rehabilitation of
the atrophic maxilla: a follow-up of 6 months to 5 years, Clin
Implant Dent Res 8:114-122, 2006.
500 SECTION IV ■ Implant Surgery
16. Adell R et al.: A 15-year study of osseointegrated implants in
the treatment of the edentulous jaw, Int J Oral Surg 10:387-416,
198, 1981.
17. Breine U, Branemark PI: Reconstruction of alveolar jaw bone.
An experimental and clinical study of immediate and performed
autologous bone grafts in combination with osseointegrated
implants, Scand J Plast Reconstr Surg 14:23-48, 1980.
18. Issaksson S et al.: Early results from reconstruction of severely
atrophic (class VI) maxillas by immediate endosseous implants
in conjunction with bone grafting and Lefort I osteotomy, J Oral
Maxillofac Surg 22:144-148, 1993.
19. Adell R et al.: Reconstruction of severely resorbed edentulous
maxillae using osseointegrated fixtures in immediate autogenous
grafts, Int J Oral Maxillofac Implants 5:233-246, 1990.
20. Isaksson S, Alberius P: Maxillary alveolar ridge augmentation
with onlay bone grafts and immediate endosseous implants,
J Craniomaxillofac Surg 20:2-7, 1992.
21. Boyne PJ, James RA: Grafting of the maxillary sinus floor
with autogenous marrow and bone, J Oral Surg 38:613-616,
1980.
22. Wood RM, Moore DI: Grafting of the maxillary sinus with
intraorally harvested autogenous bone prior to implant place-
ment, Int J Oral Maxillofac Implants 3:209-214, 1988.
23. Tolman DE: Reconstructive procedures with endosseous implants
in grafted bone: a review of the literature, Int J Oral Maxillofac
Implants 10:275-294, 1995.
24. Keller E, Tolman DE, Eckert SE: Maxillary antral-nasal inlay
autogenous bone graft reconstruction of compromised maxillae:
a 12-year retrospective study, Int J Oral Maxillofac Implants
14:707-721, 1999.
25. Rasmusson L et al.: The influence of simultaneous versus delayed
placement on stability of titanium implants in onlay bone grafts.
A histologic and biomechanic study in rabbit, Int J Oral Maxil-
lofac Surg 28:224-231, 1999.
26. Bedrossian E et al.: Immediate function with the zygomatic
implant-a graftless solution for the patient with mild to advanced
atrophy of the maxilla, Int J Oral Maxillofac Surg 21:1-6,
2006.
27. Nkenke E et al.: Anatomic site evaluation of the zygomatic bone
for dental implant placement, Clin Oral Implants Res 14:72-79,
2003.
28. Weingart D, Schilli W, Strub JR: Preprosthetic surgery and
implantology, Schweizer Monatsschrift Zahnmedizin 102:1075-
1082, 1992.
29. Bedrossian E, Tawfilis A, Alijanian A: Veneer grafting: a tech-
nique for augmentation of the resorbed alveolus prior to implant
placement: a clinical report, Int J Oral Maxillofac Implants 15:853-
858, 2000.
30. Chow J et al.: Zygomatic implants-protocol for immediate
loading: a preliminary report, J Oral Maxillofac Surg 64:804-811,
2006.
31. Branemark PI: Surgery and fixture installation. Zygomaticus
fixture clinical procedure, Goteborg, Sweden, 1995, Nobel
Biocare.
32. Bedrossian E, Stumpel L: Immediate stabilization at phase II of
zygomaticus fixtures: a simplified technique, J Prosthet Dent
86(1):10-14, 2001.
33. Zhao Y, Skalak R, Branemark PI: Analysis of a dental prosthesis
supported by zygomatic fixtures, The Institute for Applied Bio-
technology, Gothenberg, Sweden.
34. Swerdlow H: Vertical dimension literature review, J Prosthet
Dent 15:241-247,1965.
35. Frush J, Fisher R: Introduction to dentogenic restorations,
J Prosthet Dent 11:586-595, 1955.
36. Rothman R: Phonetic considerations in denture prosthesis,
J Prosthet Dent 11:214-223, 1961.
37. Balshi TJ: The Biotes conversion prosthesis: a provisional fixed
prosthesis supported by osseointegrated titanium fixtures for res-
toration of the edentulous jaws, Quintessence Int 16:667-677,
1985.
38. Gapski R et al.: Critical review of immediate implant loading,
Clin Oral Implants Res 14:515-527, 2003.
39. van Steenberghe D et al.: A custom template and definitive
prosthesis allowing immediate implant loading in the maxilla: a
clinical report, Int J Oral Maxillofac Implants 17:663-670, 2002.
40. Zwahlen R et al.: Survival rate of zygomatic implants in atrophic
or partially resected maxillae prior to functional loading: a ret-
rospective clinical report, Int J Oral Maxillofac Implants 21:413-
420, 2006.
41. Farzad P et al.: Rehabilitation of severely resorbed maxillae with
zygomatic implants: an evaluation of implant stability, tissue
conditions, and patient’s opinion before and after treatment, Int
J Oral Maxillofac Implants 21:399-404, 2006.
42. Reichert TE et al.: The zygomatic implant indications and first
clinical experiences, Zeitschrift fur Zahnarztliche Implantologie
15:65-70, 1999.
43. Olive J, Aparicio C: The Periotest method as a measure of
osseointegrated oral implant stability, Int J Oral Maxillofac
Implants 5:390-400, 1990.
44. Malo P, Rangert B: All-on-4 immediate function concept with
Branemark system implants for completely edentulous maxillae:
1 year retrospective clinical study, Clin Implant Dent Rel Res 1:
S88-S94, 2005.
45. Bedrossian E et al.: Fixed prosthetic implant restoration of
the edentulous maxilla: a systematic pretreatment evaluation
method, J Oral Maxillofac Surg 66:112-122, 2008.

PLATELET-RICH PLASMA AND
IMPLANT SURGERY
H. Dexter Barber • Roger L. Myers • Brandon Iverson • Brian M. Smith
■ WHAT IS PLATELET-RICH AND
PLATELET-POOR PLASMA?
The concept of platelet-rich plasma (PRP) or platelet gel
represents an autologous centrifuged blood sample composed
of intrinsic growth factors intended for regeneration of soft
and hard tissue (Figure 30-1). It consists of a concentration of
platelets and the seven fundamental protein growth factors
evidenced to be actively secreted by platelets to initiate all
wound healing processes. Collectively, these growth factors
include the three isomers of platelet-derived growth factors
(PDGFs) (PDGF-αα, PDGF-ββ, and PDGF-αβ), two of the
numerous transforming growth factors (TGFs) (TGF-β1 and
TGF-β2), vascular endothelial growth factor, and epithelial
growth factor. It has been scientifically determined that all of
the growth factors have been documented to derive from
platelets.1 Specific growth factors associated with PRP initiate
soft tissue healing and bone regeneration. The premise of PRP
is based on methods to concentrate autologous platelets for
the addition to surgical wounds or grafts, which require the
influence of growth factors to support and accelerate healing.2
The PRP provides approximately a 2.16 increase in the matu-
ration rate and considerably greater density of the final bone-
graft product. In addition, soft tissue healing is also substantially
improved through the employment of PRP via increasing col-
lagen content, promotion of angiogenesis, and increasing early
wound strength. Finally, growth factors found in PRP regulate
key cellular processes, such as mitogenesis, chemotaxis, and
cell differentiation.3 PRP simulates the last step of the coagu-
lation cascade, which leads to the formation of a fibrin clot.
As a result, the fibrin clot consolidates and adheres to the site
of application. The healing characteristics and hemostatic
properties of PRP enable it to support tissues and structures in
desired configurations. In addition, many other inherent ben-
efits derived from PRP are: (1) biocompatible and biodegrad-
able components prevent the PRP from initiating foreign body
reactions, tissue necrosis, or extensive fibrosis; (2) the fibrin
clot is absorbed within a few weeks of the wound healing
process; (3) PRP has been used in innumerable transplant
procedures to include the field of dentistry; and (4) PRP can
be attributed to the increased healing of wounds and surgical
sites, which is correlated with less postsurgical pain.4 More
importantly, PRP has a measure of safety that relates to its
autologous derivation and appears to decrease the risk of
CHAPTER 30
BONE GRAFTING IN
transmissible diseases (HIV, Hepatitis B, C, and D, etc.).
Finally, some of the other benefits of PRP include its degree
of safety, nontoxicity to tissue, ease of preparedness, cost-
effectiveness, and promotion of local tissue growth and
repair.
Autologous platelet gel is created from the processing and
treatment of PRP and possesses two to four times the concen-
tration of platelets. As a comparison, an individual’s normal
platelet range is between 150,000 to 350,000 mm3. However,
PRP or platelet gel concentrate consists of 1,000,000 platelets
per cubic millimeter. Therefore, one would conjecture that
the capacity for initiating growth and repair in the form of a
platelet gel far exceeds the normal platelet capacity. In addi-
tion, a natural blood clot contains 95% red blood cells (RBCs),
5% platelets, less than 1% white blood cells, and numerous
amounts of fibrin strands. A PRP blood clot contains 4%
RBCs, 95% platelets, and 1% white blood cells.2
Since 1990 medical science has identified several compo-
nents in blood that facilitate the natural healing process. The
relative use of PRP-like components was initially proposed in
1970 and was identified as fibrin glue. Fibrin glue was formed
by active polymerization of fibrinogen with thrombin and
calcium. It was originally prepared by using donor plasma;
however, because of the low concentration in plasma, the
stability and quality of the fibrin glue were low. The use of
cryoprecipitate-based fibrin glue yielded far better results.6
However, in more recent times, the development of fibrin glue
has evolved to a more complex biologic material, essential to
tissue and bone regeneration. The autologous concentration
of PRP requires a centrifugation process for differentiation of
cellular components, which is mainly designed to allow the
delineation of PRP and platelet-poor plasma (PPP) (Figure
30-2). When PRP is combined with thrombin and calcium
chloride, platelet gel is created (Figure 30-3). This product is
a rich source of growth factors and has been found to be effec-
tive in accelerating significant tissue repair and regeneration.6
Once again the process is aimed at eliciting the beneficial
effects related to the growth factors obtained from PRP. Also
as a result of the platelets releasing specific growth factors, the
processes of osteogenesis, angiogenesis, and wound healing are
activated.
Autologous PPP was first described in 1972.7 PPP is pro-
duced by separating plasma from RBCs using a high spin to
pellet platelets with the RBCs (Figure 30-4). Coincidentally,
501
502 SECTION IV ■ Implant Surgery

FIGURE 30-4. Plasma has been centrifuged, separating into a bottom

layer called the red blood cell button (concentrated platelets), a middle layer
FIGURE 30-1. PRP or platelet gel. of platelet white blood cells, and a superior layer of PPP.

this represents the starting point for production of most blood

FIGURE 30-2. Salvin PRP centrifuge machine for separation of autolo-
gous blood into PRP and PPP.
components. The rationale for the separation of platelets is
desirable because they provide an additional source of foreign
antigens and microaggregation, which can cause fusion reac-
tions.2 PPP is acellular in composition and contains fibrino-
gen, which can be used for soft tissue hemostatic management
and wound healing.3 The intrinsic growth factors are minimal,
and PPP’s capacity to initiate regenerative influence is less-
ened. Upon the completion of the centrifugation process of
whole blood to produce PRP, PPP is the least dense layer and
comprises 45% of the sample obtained.
It is important to note that platelet counts and growth
factor content are usually dependent upon the method or
technique used to obtain the PRP. In addition, the donor’s
biologic condition may be the determining factor in the com-
position of PRP and its observed biologic effects. Acknowl-
edging the fact that there are many methods employed to
obtain PRP, the ending results seem to conclude with three
resultants: PRP, PPP, and RBCs.

■ WHAT ARE THE BENEFITS

OF PRP?
1. “Jump-starts” osteogenesis: By releasing growth factors
at a local site, osteoblasts can be enticed to move across
a greater distance by creating a scaffold system (fibrin)
that will assist in their movement. Because the growth
factors are added to the graft at the time of graft replace-
ment (in the platelet gel) instead of being released by
the coupled process of resorption and the obligatory
replacement, there is approximately a 2-month accel-
eration in the maturation of the bone graft.8
2. Early consolidation of the graft: The increased amount
of PDGF in the graft initiates osteocompetent cell activ-
ity at an enhanced molecular rate. Many other growth
factors assist in graft success and bone regeneration,
FIGURE 30-3. Topical thrombin and calcium chloride is combined with such as bone morphogenic protein (BMP). The primary
PRP to create the platelet gel. response of osteoblasts is activated by BMP. The BMP
 CHAPTER 30 • Platelet-Rich Plasma and Bone Grafting in Implant Surgery
provided by PRP with the addition of that provided by
the initial resorption of bone occurring during the oste-
ophyllic phase (lasts approximately a month) results in
earlier maturation of the grafted bone.8
3. Speeds of mineralization: Because mineralization of a
graft site is a coupled phenomenon, osteogenesis must
proceed in such a way that activation and bone forma-
tion is greater than resorption. Mineralization of the
collagen matrix occurs more rapidly because PDGF is
added right from the start in the mineralized bone
segment of the graft, instead of released from collagen.
As a result, the use of PRP has shown to improve the
rate of bone formation by 1.62 to 2.18 times the normal
bone healing time.8
4. Improves trabecular bone density: It has been reported
in the literature that there has been a 15% to 30%
improvement in trabecular bone density when PRP
factors are added to the graft site.8
5. Eliminates the risk of infection or disease: PRP is an
autologous process and obviates the concern for disease
transmission and allergenicity. More patients are eligi-
ble for the procedures because the strict criteria for
blood bank donations do not have to be met.8
■ WHAT IS THE ROLE OF PRP IN
BONE REGENERATION?
Weibrich et al. revealed that platelet counts and growth factor
contents are highly dependent on the technique of processing
PRP. Also, the biologic condition of the donor may influence
the efficacy of PRP and its biologic effects.11 To understand
how PRP affects bone regeneration, the sequence of regenera-
tion should be made clear.
Platelets are composed of cytoplasmic fragments of mega-
karyocytes that circulate in the blood. As a result, platelets
are responsible for hemostasis and the initiation of regenera-
tion of tissue from trauma episodes.3 The most integral bio-
logic unit of PRP is the presence of platelets and the platelet’s
composition to produce growth factors. Sanchez et al. indi-
cated that the properties of PRP were highly dependent upon
the production and release of growth and differentiation
factors during platelet activation. The factors assume an inte-
gral role in the regulation and stimulation of the wound
healing process and the cellular processes of mitogenesis, che-
motaxis, and metabolism.12
Tsay et al. conveyed that chemotaxis of osteoblast precur-
sors to the site of bone regeneration is directed by specific
structural proteins, such as collagen and/or osteocalcin, and
growth factors, such as PDGF and TGF-β. This process is then
followed by osteoblast proliferation and aggregation. PDGF,
TGF-β, fibroblastic growth factor (FGF), insulin-like growth
factor (IGF)-I, and IGF-II have all been proven to illustrate
stimulation in osteoblastic growth. Osteoblast differentiation
is controlled by growth factors, and this interaction allows the
formation of mature bone cells from the primitive osteoblastic
stage. The growth factors most responsible for facilitating the
maturation stage are IGF-I and BMPs.9
503
The previously mentioned growth factors assume an impor-
tant role in mediating normal bone healing and regeneration.
The growth factors inherent to platelets help facilitate regen-
erative changes in many biologic circumstances. Platelets are
responsible for initiation of regeneration of tissue that has
been traumatized. During the reparative process, platelets
become entrapped in a fibrin clot and degranulate, releasing
two primary growth factors: PDGF and TGF-β. PDGF binds
to endothelial cells to produce capillary ingrowth, and TGF-β
attaches to osteoblasts and stem cells to initiate mitosis and
stimulate osteoid production.13 As a result, growth factors
contained and released from PRP should enhance and acceler-
ate soft tissue healing and the process of regenerating bone,12
thereby emphasizing the importance of the common platelet
function in PRP to generate growth factors to mediate healing
at a specified site.
According to Tsay et al., growth factors are activated at
the appropriate temporal sequence and spatial distribution. As
a result, the aforementioned concepts profoundly affect the
influence of growth factors related to tissue regeneration.9
The function and action of the growth factors are very
complex. Each individual growth factor may have a different
effect on the same tissues and different responses that are
dependent on the specific tissues targeted. Growth factors also
interact with one another, consequently forming a cascade of
different signal proteins with multiple pathways, which inevi-
tably progress to gene activation and protein production. This
enables PRP to differentiate its own actions from recombinant
growth factors that are directed toward a single regenerative
pathway.12
Many bone-grafting procedures concomitantly combine
the graft with PRP to attempt to ensure proliferation, vascu-
larization, and incorporation (Figure 30-5). It is important to
FIGURE 30-5. PRP mixed with alloplastic graft material, to be placed at
recipient site.
504 SECTION IV ■ Implant Surgery
note that bone regeneration requires growth factors, nutrient
supplies, and an osteogenic cell source. PRP alone does not
have osteoconductive or osteoinductive effects on bone
regeneration and is usually used in conjunction with bone
grafts or bone-substitute materials. The correlation between
PRP and bone grafts has many inherent advantages, such as
acting to “jump start” the cascade of osteogenesis in a bone
graft, promoting early consolidation of the graft, speeding up
mineralization of the graft, improving trabecular bone density,
providing early availability of growth factor and BMP, and
finally, enhancing osteoconduction. The BMP acts as a
“trigger” that couples bone formation and resorption to mod-
ulate bone activity. BMP is released by osteoclastic resorption
when normal bone remodels and acts on stem cells to differ-
entiate into osteoblasts. The resorptive element of bone is
controlled by osteoclasts, which derive from the native vas-
culature within the fibrin clot of the graft. However, the
presence of stem cells in the original graft and surrounding
vessels and/or tissue react to growth factors and transform
into osteoblasts. This, in effect, leads to initiating the cascad-
ing phenomenon to promote osteogenesis. The osteoblasts
are normally nonmotile cells and do not move greater than
a distance of 0.4 mm (400 μm). But in the graft “scaffold”
system of osteoconduction, the osteoblasts can be assisted to
migrate greater distances. When the osteoblasts engage in
“endocytosis” there is a methodical and incremental
movement of the cell along the “scaffold.” This, in essence,
allows the formation of the osteoid component of bone
regeneration.
Initially, macrophages are attracted into the graft site
through an oxygen gradient of 30 to 40 mm Hg. These mac-
rophages then take over the role platelets started and drive
the remaining bone regeneration and healing process. The life
span of platelets in a wound and their influence on growth
factors is less than 5 days; therefore, bone regeneration is
extended by two mechanisms. The first mechanism is the stem
cell increase into osteoblasts, which can then produce TGF-β.
The second mechanism for bone regeneration extension is
from macrophage replacement of platelets. In the range of 14
days, complete revascularization of the graft is seen. In the
range of 4 to 6 weeks, random cellular bone, called woven
bone, is formed, which is immature and disorganized.13 Finally,
lamellar bone is formed in phase two and seems to be repre-
sentative of more organized bone formation.
■ HOW DOES PRP ENHANCE BONE
REGENERATION IN
AUTOGENOUS, ALLOGRAFT, AND
ALLOPLASTIC MATERIALS?
Boyan et al. indicated that bone-grafting materials are used
for a plethora of reasons and applications in oral and cranio-
facial surgery. In situations requiring diminutive amounts of
bone and where vascular supply is sufficient, autologous bone
can be harvested from the specific site itself.14 However, there
are also other alternatives to bone-grafting materials that are
FIGURE 30-6. 3I (Implant Innovations) PRP machine.
not autogenous in nature. Materials of this kind include
allografts, anorganic bone, and alloplastic materials that are
frequently used for grafting necessary sites (Figure 30-6).
Despite whether the bone-grafting material is autogenous in
nature or not, the procedure has certain goals to establish the
optimal result. The objectives of bone-graft procedures are to
restore function, provide relief from pain, and provide ade-
quate cosmesis. Although the latter two goals are important,
the mechanical function of the reconstructed bone is the
overriding goal. A bone graft can fail as a result of purely bio-
logic factors, but most often a mechanical failure can be the
main etiologic factor.15 In general, two physical factors deter-
mine the incidence and speed of union between bone grafts
and the adjacent host bone more than the characteristics of
the grafts themselves. These determinants of host-graft union
are stability of the construct and contact between host bone
and the graft.
It has been proven that graft stability of placement plays
an important role in the overall success of bone-graft consoli-
dation. The stability of the graft allows the biologic elements
to establish a foundation to activate and promote an environ-
ment conducive to graft survival. The advent of PRP has
allowed the biologic aspect of bone grafting to become an
almost routine practice. PRP has been tested in autogenous
and allogenic (allograft) bone-grafting procedures and has
revealed tremendous value. Most of these reports also suggest
that PRP improves the handling properties of the graft mate-
rial with which it is combined, facilitating graft placement and
stability. PRP provides a highly concentrated dose of autolo-
gous platelets containing a variety of biologic mediators that
can be applied directly to the healing site, thereby promoting
the formation of bone via application of osteoinductive and
osteoconductive processes. Recent reports have suggested that
more rapid epithelialization, more dense and mature bone
with better organized trabeculae, and greater bone regenera-
tion take place when PRP is added to bone autografts and
 CHAPTER 30 • Platelet-Rich Plasma and Bone Grafting in Implant Surgery
allografts. Most of these reports also suggest that PRP improves
the handling properties of the graft material with which it is
combined, facilitating graft placement and stability.12
A graft moved from one site to another within the same
individual is an autograft.16 In recent years, there have been
efforts to illustrate the important role that PRP can assume
in autogenous bone-grafting procedures. For example, in
1994 Tayapongsak et al. introduced the novel idea of adding
autologous fibrin adhesive (AFA) to cancellous bone during
mandibular continuity reconstructions. They identified early
radiographic bone consolidation in 33 cases; they attributed
this to enhanced osteoconduction afforded to the osteocom-
petent cells in the graft by virtue of the fibrin network devel-
oped by AFA. They also reported the remarkable adhesive
advantage of binding cancellous marrow particles during graft
placement.17 However, in 1998 Marx et al. reported that
adding PRP to an autogenous cancellous bone graft caused a
more rapid maturation rate and greater amount of new bone
formation in an alveolar defect.18 The use of PRP with auto-
genous bone was first introduced by Marx et al. In his study,
mandibular continuity defects were randomized and recon-
structed with autogenous bone grafts in 88 patients. The
autogenous bone grafts were to be placed with and without
the incorporation of PRP. Radiographs were used to evaluate
the maturation rate of the bone to which PRP was added. The
analysis revealed that the autogenous bone graft treated with
PRP matured at a rate of 1.6 to 2.2 times faster. Histomorpho-
metric evaluation of core samples taken at 6 months revealed
a significantly greater percentage of trabecular bone with the
addition of PRP (74% with PRP compared with 55% without
PRP). This study alone provides innuendos that the use of
PRP in autogenous bone-grafting procedures highly influences
the quality and quantity of grafting. However, another study
often quoted or referenced as showing little benefit from PRP
is the study by Ahgaloo et al. Their study used non–critical-
sized defects in the New Zealand white rabbit model. Their
results showed no benefit of PRP alone in the defect, but actu-
ally showed significant enhancement when PRP was com-
bined with autogenous bone compared with autogenous bone
alone.1 Oyama et al. indicated that PRP extracted from autol-
ogous whole blood is known to have a number of varying
growth factors in high concentration.19 These growth factors
play an important role leading to the incorporation and con-
solidation of the autogenous graft material. The ultimate
potency of the PRP to improve the adhesion of an autologous
bone graft by forming a fibrin gel and to release factors leading
to an enhancement of bone regeneration is replete in the lit-
erature.18 PRP enhances osteoprogenitor cells in host bone
and bone grafts. According to Marx et al., PRP has a similar
clinical application related to autogenous bone grafts and
composites of autogenous bone grafts, with a combination of
bone substitutes of 20% or less autogenous bone. As a result,
PRP has demonstrated improvement in repairing continuity
defects, sinus-lift augmentation, and ridge preservation
grafting.1
505
Fennis et al. conducted a study in which 28 goats incurred
mandibular resection in the angle region. The marrow was
extracted from the resected segment, and cortical perforations
were performed with the intent to establish vascular ingrowth
channels. The cortical graft segment was packed with auto-
genous iliac crest bone graft, which may or may not have
included PRP. Through the process of rigid fixation, the corti-
cal graft “crib” and autogenous cancellous bone material
(with or without PRP) was affixed in its original position at
the angle of the mandible. Radiographs taken at three time
intervals (3, 6, and 12 weeks) were blindly evaluated and
scored for five different variables, for a total of 15 possible
comparisons. In 4 of the 15 comparisons, the group with
PRP showed statistically superior healing. For example,
healing at the osteotomy sites appeared significantly improved
at 6 and 12 weeks, but not at 3 weeks. Healing of the cortical
perforations was not significantly improved at any time period
by the addition of PRP.20 Similarly, Jakse et al. performed a
study evaluating the effect of PRP in sinus-lift procedures
using autogenous bone. The procedure involved 12 sheep in
which bilateral sinus lifts were conducted and provided with
iliac crest bone grafts. The iliac crest bone grafts either did
or did not have the additive of PRP. In addition, one sinus
with graft placement did have PRP, and the other did not.
At 4 weeks, there was an average 26.1% new bone formation
in the sinus grafts with autogenous bone used individually,
compared with 29.2% when PRP was incorporated. At 12
weeks, the percentage of new bone increased to 46.9% with
bone alone, compared with 51.1% with the application of
PRP. This 3% to 4% increase with PRP showed minimal
benefit, and the authors concluded that their results “show a
regenerative capacity of PRP of quite low potency or
potential.”20
An allograft (adjective, allogeneic) is tissue transferred
between two genetically different individuals of the same
species. The variability of osteoinductivity associated with
commercially available allografts currently used in clinical
practice has been at least partially responsible for ongoing
investigation into techniques by which to enhance osteogen-
esis.21 Therefore, PRP has emerged on the scene to propagate
the dynamic relationship between allograft bone procedures
and the biologic properties of PRP.
The allografts most commonly used are demineralized
freeze-dried allograft (DFDBA) and freeze-dried bone allograft
(FDBA), and the controversy exists with respect to the osteo-
inductive potential of these materials.12 To increase an
allograft’s capacity to regenerate bone, PRP can presumably
be added and produce results very similar to autogenous bone
grafts. Kassolis et al. presented case reports of 15 patients
undergoing ridge and sinus floor augmentation treated with
PRP and FDBA. Seventeen areas, including 14 sinuses and
3 maxillary ridges, were treated and 36 endosseous implants
were placed. Twenty-nine implants were placed at the time
of the guided bone regeneration (GBR) procedure. Thirty-two
of the 36 implants (89%) were successful, and four implants
506 SECTION IV ■ Implant Surgery
were determined to have failed at the time of uncovering.
Histologic study of bone retrieved from two patients con-
firmed the presence of vital bone formation in apposition to
residual FDBA particles.12 Kim et al. placed dental implants
into the iliac crest of dogs and created bone defects around
the most superficial implant threads. These defects were
grafted with freeze-dried demineralized bone powder, with or
without the addition of PRP. More direct bone-to-implant
contact was seen in the group with PRP.20
■ PRP PROCESSING
PRP is a relatively recent development in the surgical com-
munity. In the early 1990s, PRP was only available in an
operating room setting and required expensive equipment and
staff trained in perfusion technology. This hospital-based
practice required large amounts of blood collection and was
only used in large critical surgeries. These problems are the
primary reasons that early PRP technology was not suited for
outpatient or surgery center practice. The science of PRP and
the benefit in wound healing was well established. The need
for more appropriate office-based armamentarium led to tech-
nologic advancement in PRP procurement and processing
techniques. As many as eight different PRP processing devices
are currently on the market with FDA approval (Figure 30-6).
The different manufacturers claim different characteristics
that make their specific products more appealing than the
competition. The clinical importance of machine performance
mainly lies in the ease and ability to concentrate platelet
product. Marx et al. outline the following criteria important
for comparison between various manufacturers.21
Technologically sound: Increasing computer technology
has made possible the processing of PRP with relatively little
human control. Surgery staff time can remain dedicated to the
surgery and not to the production of PRP.
High platelet yield: The ability to concentrate the platelets
is the key factor in PRP processing. Research has clearly dem-
onstrated that wound healing and mesenchymal cell rates
increase in direct proportion as platelet concentration levels
increase. Every available machine has variance in the actual
platelet separation and concentration process. Machines with
a single spin cycle are incapable of concentrating platelets to
the levels of double-cycle machines. Much of this has to do
with the concave shape of the erythrocyte and the entrapment
of platelets during single phase concentration. Research has
shown that the use of gravitational force applied in the correct
manner is the true test of the machine. The gravitational force
is usually measured as force over time, usually in minutes. This
is recorded as g-minutes. It is not the total centrifuge force
applied that matters, but rather the judicious and timely use
of certain amounts of gravitational force during the produc-
tion phase. Effective machines use two separate spin cycles in
the production process. The first separation spin separates the
erythrocytes from the leukocytes, platelets, and plasma. The
concentration spins then compacts the platelets. The most
effective machines use a separation cycle that uses forces in
the range of 1000 g forces during a 4-minute spin. The platelet
concentration phase then follows at 800 g forces for 8 to 9
minutes.
Platelet viability and activity after processing: Platelets
must be alive and able to secrete their various growth factors
and proteins after processing. Platelets are very resilient to the
g forces applied during centrifugation. Platelet cell membranes
can withstand up to 30,000 g-minutes. All of the currently
FDA-approved machines for platelet processing stay under
this limit. Each machine, however, can vary on the number
of steps in the process. Blood handling, membrane sterility,
and temperature are just a few of the different variables that
can affect the viability of the collected platelets.
Autologous blood volume required: Collection of autolo-
gous blood in the outpatient setting should be restricted to
120 cc or less. The technologic advancements that have been
made in producing more compact platelet harvest using less
blood is the reason PRP methods are possible in the outpatient
setting.
The focus of this chapter is to review the current technol-
ogy of PRP, its importance in bone grafting, and the surgical
implications. This is not a scientific review or rating of the
currently available PRP machines. The reader interested in
specific manufacturer comparisons is referred to scientific
reviews conducted by Dr. Kevy and Dr. Jacobson at Harvard
Medical School and Dr. Marx and colleagues.22,23 Current
research has shown no saturation limits with the efficacy of
platelet concentrate. The more concentrated the PRP, the
more growth factors and higher the healing rate. Current
technology will undoubtedly be improved upon, and accept-
able PRP concentration will likewise increase.
■ PRP PROCESSING PROCEDURES
The collection of autologous blood follows the same proce-
dural steps independent of what PRP system is to be used. The
following outline is based on the SmartPReP system, manu-
factured by Harvest Technologies.24 The outline and volumes
given are appropriate for 20 cc of blood harvest. All proce-
dures should be completed using aseptic package and speci-
men handling (Figure 30-7).
Phlebotomy: Aseptic blood harvest is completed with a
large peripheral vein at the patient’s wrist or antecubital fossa
(Figure 30-8). Before IV access, draw 2 cc of acid citrate
dextrose A (ACD-A) into a sterile 20 cc syringe. The citrate
acts as a specimen anticoagulant. The white concentration
chamber of the centrifuge module also requires the deposit of
1 cc of citrate to keep the concentrating platelets from coagu-
lating. We consolidate our phlebotomy efforts and IV access
with the use of an 18-gauge peripheral IV catheter. The IV
access can easily and quickly be connected to the IV line for
use in IV sedation. The IV placement should follow the stan-
dard aseptic and universal precaution protocol. The blood
harvest and IV transfer is most readily completed with the aid
of an additional office staff member. Once access is estab-
lished, attach the sterile 20 cc syringe preloaded with 2 cc of
citrate. Slowly draw from the vein until you have a total
syringe volume of 22 cc. Transfer the collected specimen to
 CHAPTER 30 • Platelet-Rich Plasma and Bone Grafting in Implant Surgery 507

another staff member while attaching and securing the IV

line. We then slowly titrate our sedation medications for anx-
iolysis to aid in patient comfort during our PRP initiation
time.
PRP processing: The collected anticoagulated specimen is
then transferred to the sterile red-topped container on the
SmartPReP centrifuge unit (Figure 30-9). The white-topped
chamber should have 1 cc of calcium chloride deposited before
phlebotomy. It is important to note that care should be taken
to keep the container membranes and all needles used in
transfer sterile throughout the process. The centrifuge module
is then placed into the SmartPReP machine along with the
appropriate-sized counterbalance. The counterbalance weights
are clearly marked 20 cc or 60 cc, depending on the blood
volume harvested. The lid is closed. The automated start
button initializes the separation phase. The timing and cen-
FIGURE 30-7. SmartPReP phlebotomy and processing tray setup.
trifuge speed will automatically change to the concentration
spin setting without further manual input. The surgeon and
staff are free to start the surgical procedure as the blood prod-
ucts are centrifuged. The SmartPReP will automatically shut
down after its 15- to 17-minute complete cycle, and the
surgery team can remove it when ready. When the centrifuge
module is removed, you will note that both sides of the module
have liquid contents. The red chamber in which the harvest
is placed will still be red, but the adjacent white-capped
chamber will have two separate distinct colored layers. You
will see an upper, yellowish plasma layer representing the PPP
with a distinct red button at the bottom of the white chamber.
This small red button represents the platelet concentrate.
PRP storage and use: Clinical studies have shown that PRP
can be stored at room temperature up to 8 hours without
complication. If the surgery goes longer than 8 hours, it is
recommended that the PRP be discarded and fresh blood
be drawn from the patient. The centrifuge module can be
retrieved when the surgeon is ready for PRP application. The
FIGURE 30-8. Standard sterile phlebotomy technique. SmartPReP module is packaged with a series of sterile syringes

A B

FIGURE 30-9. Placement of whole blood into SmartPReP centrifuge unit.

508 SECTION IV ■ Implant Surgery

and blunt aspiration needles. The needles are assembled with • The PRP can be placed into a sterile mixing bowl with
specific length stoppers that allow for sequenced removal of autogenic or allogenic bone-graft material (Figure
first the majority of the PPP and then a small amount of PPP 30-11). The two drops of calcium chloride-thrombin can
(7 cc) and the concentrated platelet plug. The remaining 7 cc then be mixed with the PRP and bone material. The
of PPP is aspirated and gently expressed three times to recon- mixture of too much calcium thrombin will act to slow
stitute the platelet plug. This reconstituted 7 cc of PPP coagulation.
combined with the platelet plug is the PRP that will be used
in the surgical application.
Citrate inhibits coagulation by binding calcium. In reverse,
PRP is activated by adding calcium. This is accomplished by
mixing 5 mL of 10% calcium chloride solution to 5000 units
of topical bovine thrombin. A tuberculin syringe is then used
to aspirate 1 cc of the calcium chloride–thrombin mixture.
The anticoagulated PRP should still be in the 10 cc syringe
that was used to remove it from the centrifuge module. The
PRP can then be activated in many ways.
• The 10 cc syringe with anticoagulated PRP can be
attached to an ejection assembly that concomitantly
attaches a 1 cc tuberculin syringe to a nozzle (Figure
30-10). The mixture nozzle acts to mix the PRP and
calcium chloride-thrombin in a 10 : 1 ratio.
• PRP can be activated by aspirating the equivalent of two
drops of the calcium chloride–thrombin mixture into
the syringe. The PRP will begin to coagulate within 6
to 10 seconds. At this point, the gel PRP can be expressed FIGURE 30-10. PRP ejection syringe loaded with PRP and calcium chlo-
onto the surgical site. ride. Beta tricalcium phosphate (chronOS) block also pictured.

A B

FIGURE 30-11. A, PRP is added to chronOS brand beta tricalcium phosphate. B, Activated PRP and bone graft at
recipient site. To view a color version of this illustration, refer to the color insert section at the back of this
book.
 CHAPTER 30 • Platelet-Rich Plasma and Bone Grafting in Implant Surgery 509

CASE REPORT 30-1

A twenty-three-year-old male was involved in a motor vehicle accident, screws (Figure 30-12 C). The patient’s blood was secured for PRP
which resulted in the loss of tooth #22 and the associated alveolar bone processing, and the PRP was placed at the graft site (Figure 30-12 D).
(Figure 30-12 A). A block graft from the patient’s symphysis was Four months later, a significant amount of bone was regenerated at the
secured (Figure 30-12 B) and fixated to the recipient site with fixation recipient graft site (Figure 30-12 E).

A B

C D

FIGURE 30-12. A, Tooth #22 avulsed and loss of associated

alveolar bone. B, Block graft from symphysis. C, Block graft secured with
fixation screw. D, PRP added to block graft site. E, Graft site 4 months
after block graft and PRP placed. Significant bone regeneration present.
E To view a color version of this illustration, refer to the color insert
section at the back of this book.
510 SECTION IV ■ Implant Surgery
REFERENCES
1. Marx RE: Platelet-rich plasma: evidence to support its use, J Oral
Maxillofac Surg 62:489-496, 2004.
2. Ovaginian J: Platelet rich plasma. ELE 382 biomedical engineer-
ing seminar II, Biomedical Engineering, Department of Electri-
cal and Computer Engineering, University of Rhode Island.
3. Tischler M: Platelet-rich plasma-utilizing autologous growth
factors for dental surgery to enhance bone and soft tissue grafts,
NY Dent J 68(3):22-24.
4. Gimeno FL et al.: Preparation of platelet-rich plasma as a tissue
adhesive for experimental transplantation in rabbits, Thromb J
4:18, 2006.
5. Man D et al.: The use of autologous platelet-rich plasma (platelet
gel) and autologous platelet poor plasma(fibrin glue) in cosmetic
surgery, Plast Reconstr Surg 107(1):229, 2001.
6. Floryan KM, Berghoff WJ: Home study program: intraoperative
use of autologous platelet-rich and platelet-poor plasma for
orthopedic surgery patients, AORN J 80(4):668-674, 2004.
7. Platelet-rich plasma factor, Implant Dentistry of Washington.
8. Tsay RC et al.: Differential growth factor retention by platelet-
rich plasma composites, J Oral Maxillofac Surg 63:521-528,
2005.
9. Tozum TF, Demiralp B: Platelet-rich plasma: a promising inno-
vation in dentistry, J Can Dent Assoc 69(10):664, 2003.
10. Weibrich G et al.: Growth factor levels in platelet-rich plasma
and correlations with donor age, sex and platelet count,
J Craniomaxillofac Surg 30:97-102, 2002.
11. Sanchez AR, Sheridan PJ: Is platelet-rich plasma the perfect
enhancement factor? A current review, Int J Oral Maxillofac
Implants 18(1):93-103, 2003.
12. Nandukumar AS, Nandukumar K: Applications of platelet rich
plasma for regenerative therapy in periodontics, Trends Biomater
Artif Organs 20(1):78-83, 2006.
13. Boyan BD et al.: Use of growth factors to modify osteoconductiv-
ity of demineralized bone allografts: lessons for tissue engineering
of bone, Dent CLin North Am 50:217-228, 2006.
14. Davy DT: Biomechanical issues in bone transplantation, Orthop
Clin North Am 30(4):553-563, 1999.
15. Stevenson S: Biology of bone grafts, Orthop Clin North Am
30(4):543-552, 1999.
16. Marx RE et al.: Platelet-rich plasma: growth factor enhancement
of bone grafts, Oral Surg Oral Med Oral Pathol 85(6):638-646,
1998.
17. Arpornmaeklong P et al.: Influence of platelet-rich plasma
(PRP) on osteogenic differentiation of rat bone marrow stromal
cells. An in vitro study, Int J Oral Maxillofac Surg 33:60-70,
2004.
18. Oyama T et al.: Efficacy of platelet-rich plasma in alveolar bone
grafting, J Oral Maxillofac Surg 62:555-558, 2004.
19. Freymiller EG, Aghaloo TL: Platelet-rich plasma: ready or not?
J Oral Maxillofac Surg 62:484-488, 2004.
20. Shanaman R et al.: Localized ridge augmentation using GBR and
platelet-rich plasma: case reports, Int J Periodontics Restorative
Dent 21(4):345-355, 2001.
21. Marx R, Garg A: Development of platelet rich plasma and
its clinical importance. In Marx R, Garg A, editors: Dental
and craniofacial applications of platelet-rich plasma, 2005,
Quintessence.
22. Kevy S, Jacobson M: Preparation of growth factor enriched
autologous platelet gel, Presented at the SVG Biomaterials 27th
Annual Meeting, Minneapolis, MN, April 2001.
23. Marx R: Platelet-rich plasma (PRP): What is PRP and what is
not PRP? Implant Dent 10(4):225-228, 2001.
25. Harvest Technologies Corporation: Automated autologous
platelet concentrate system. Product insert. (A SmartPReP
system) Norwell, MA.

IMMEDIATE IMPLANT LOADING
Louis F. Clarizio
Since the 1980s, bone-anchored dental implants have become
a well-established and predictable treatment for restoring
missing teeth. Today many researchers and clinicians are
focusing on ways to achieve these successful results while
simplifying and shortening the treatment process.
One of these approaches involves immediate implant
loading. Immediate implant loading generally involves inserting
one or more dental implants and attaching the fixed prosthesis
on the same day or within just a few days.
The obvious advantage to this increasingly popular tech-
nique is that it allows patients to regain function and natural-
looking “teeth” more quickly. In cases where there is immediate
implant placement and loading, this technique also helps to
maintain the soft and hard tissue architecture.
Immediate implant loading was first successfully used for
overdentures.1,2 During the past several years, however, a
plethora of studies and reports published in the dental litera-
ture have reported excellent success rates with immediate
implant loading for partial edentulism and single crowns in
either the maxilla or mandible and for complete edentulism
of the mandible. In select cases, immediate implant loading
can provide equally good results as delayed loading.3-5
It is important to put these papers into proper context,
however. Most of the published studies on immediate implant
loading through 2006 are essentially anecdotal reports. Very
few include a “gold standard” randomized clinical trial design
comparing the outcomes of immediate loading with delayed
loading. There is also considerable variability among pub-
lished studies and case reports in terms of the data quality, the
techniques employed, the cases treated, the implant and pro-
visional types used, clinician experience, and so forth.5 As
such, it is difficult to establish standard clinical guidelines for
immediate implant loading. In fact, based on published scien-
tific data, there is limited evidence to support or guide most
clinical applications of immediate implant loading.5
Most published reports concur, however, with regard to the
following requirements for a successful immediate implant
loading case:
• The implant(s) must be primarily stable in the native
bone.
• Occlusal loading of the implant should be minimized as
much as possible to ensure optimal osseointegration.
• The patient should be fully informed of the risks and
benefits of immediate implant loading and understand
that results can vary.
CHAPTER 31
• Patient candidates must be carefully selected (e.g.,
smoking patients tend to have a much higher failure
rate).
• Immediate implant loading is best undertaken by a well-
experienced surgical and restorative team with advanced
knowledge of implant dentistry.
• Immediate implant loading is contraindicated in patients
with compromised immune systems, uncontrolled diabe-
tes mellitus, or psychiatric illnesses.6
Based on this author’s extensive experience with immediate
implant loading, the use of tapered, surface-treated implants
helps to ensure the best results in these cases. The tapered
design offers good compression of bone and stability. Surface
treatment encourages quicker integration. Using an implant
that is as long as possible is also recommended to engage more
and better quality bone based on the anatomic boundaries.
This chapter provides a clinical outline for immediate
implant loading for single-tooth replacements, other partially
edentulous cases, and the completely edentulous mandible
and maxilla. The techniques are based on the author’s nearly
10 years of experience with immediate implant loading and
placement of several thousand implants.
■ IMMEDIATE IMPLANT LOADING
FOR SINGLE-TOOTH OR OTHER
PARTIALLY EDENTULOUS
RESTORATION CASES
Compared with conventional crown and bridge restorations,
the main disadvantage to restoring teeth with implant-
supported restorations is that the patient must typically wear
a removable provisional restoration for up to 6 months. This
well-established healing period allows dental implants to opti-
mally osseointegrate and to build the supportive foundation
for a long-lasting restoration.
In many partially edentulous cases, however, this waiting
period can be avoided with immediate nonfunctional loading
of the implants.7 To be done successfully, two important prin-
ciples must be met. First, the implant must be stable in the
native bone. An important first step is to do a thorough radio-
graphic study to assess bone quality and quantity. Although it
is important to look for adequate bone apical to the tooth,
sufficient bone on the sides of the tooth sockets can also be
engaged to promote stability. Second, occlusal load on the
implant must be prevented to deter macromovement that can
lead to fibrous encapsulation of the implant. If this occurs,
511
512 SECTION IV ■ Implant Surgery

osseointegration can be lost, or worse, the implant may become

ailing yet still integrated.
The success rate may be lower when implants are immedi-
ately loaded after being placed in fresh extraction sites. This
may be related to the surgical dentist’s skill and comfort level.
Whereas a fresh extraction site certainly offers the advantage
of preserving hard and soft tissue architecture,8 it can be easier
to get initial stability when placing implants into a solid,
healed ridge.

HEALED EXTRACTION SITE WITH ADEQUATE

HEIGHT AND WIDTH OF ALVEOLAR BONE
In most cases, a midcrestal or slightly lingual incision is made
to reveal the underlying bone in the healed extraction site.
Subsequently, standard surgical preparations are made for
implant placement. A round bur followed by pilot drills and
a series of increasing-diameter drills are used until the osteot-
omy is properly completed. Depending on the bone density,
narrower drills may be used as the final drills to achieve good
primary stability.
It is common to place the implant with a torque wrench
and to achieve at least 30 Ncm of required torque for final FIGURE 31-1. Preoperative nonrestorable tooth #9.
seating of the implant.

IMMEDIATE PLACEMENT AND LOADING OF

IMPLANTS IN FRESH EXTRACTION SITES
In many cases, a tooth extraction is required for endodontic
or periodontal reasons or because of root fracture, resorption,
or carious lesions. These extracted teeth can often be restored
with immediately placed implants followed by immediate
nonfunctional loading. As mentioned, the advantage of
immediate placement and loading in a fresh extraction site is
that the maximum amount of bone and soft tissue are
preserved.
Whenever an implant will be placed into a fresh extraction
site, patients should be placed on an antibiotic 2 to 3 days
before the appointment to deter infection.
To be most successful, the extraction must be performed as
atraumatically as possible to prevent damaging the surround- FIGURE 31-2. Immediate implant placed into a lingual position. To view
ing bone. This can be the most difficult aspect of immediate a color version of this illustration, refer to the color insert section at the
implant placement. back of this book.
The socket should be carefully curetted with small, long
curets to ensure that the apex of the socket is thoroughly Because the palatal cortical plate is stronger, it is common
débrided to the bone. during the next series of drill preparations for the osteotomy
Once the extraction is complete, care must be taken to to slide or drift toward the empty socket and labial plate.
place the implant into the ideal axial direction. In most cases, Starting with a palatal approach helps to seat the implant in
this is not the same as the direction of the tooth socket itself. the center of the ridge at the end of the placement procedure.
The clinician should be careful to avoid slipping down the Care should be taken to end up slightly palatal to the planned
palatal wall of the socket and starting the osteotomy at the incisal edge (Figures 31-1 through 31-6).
socket’s apex. If that occurs, the clinician will often create a Bone grafting is almost always required when doing any
more labial location for the implant than planned. Thus, the immediate implant placement. This is generally because the
palatal wall of the socket should be prepared or perforated shape of the socket is not the same as the shape of the implant,
slightly with a round bur on the apical third of the socket. It and there are often voids of more than 1 or 2 mm around the
is very important to start with a round bur and be very defini- implant. Autologous, bovine, or Puros cancellous particulate
tive in starting the osteotomy. The socket should never dictate allograft material is often used. Care must be taken not to
placement of the implant; ideal location should. overprepare the site. In fact, undersizing it can help to ensure
 CHAPTER 31 • Immediate Implant Loading 513

that the implant is fully seated with a torque of at least

30 Ncm.
If sutures are needed, and often they are not, 5-0 sutures
should be placed. Care should be taken to place the knots on
the palatal aspect. This avoids creating a nuisance for the restor-
ative clinician when preparing the provisional restoration.

RESTORATIVE CONSIDERATIONS FOR PARTIALLY

EDENTULOUS CASES
For any partially edentulous case, the restorative protocol is
the same.
Immediately after implant placement, either: (1) the abut-
ment is placed with 10 to 15 Ncm of torque after preparing the
abutment out of the mouth (Figures 31-7 through 31-9); (2) a
temporary abutment is placed and torqued, which usually
requires no preparation (Figures 31-10 and 31-11); or (3) a
FIGURE 31-3. Nonrestorable tooth #5.
healing cap is placed (see Figure 31-6); or (4) a single stage

A B

FIGURE 31-4. A, B, Implant placed slightly palatal. To view a color version of this illustration, refer to the
color insert section at the back of this book.

A B

FIGURE 31-5. A, B, Nonrestorable tooth #9. Ten-year-old implant #8. To view a color version of this illustra-
tion, refer to the color insert section at the back of this book.
514 SECTION IV ■ Implant Surgery

A B

FIGURE 31-6. A, B, Immediate implant placed with healing cap. To view a color version of this illustration,
refer to the color insert section at the back of this book.

A B

FIGURE 31-7. A, B, Abutment placed after bone grafting. To view a color version of this illustration, refer to
the color insert section at the back of this book.

A B

FIGURE 31-8. A, B, Nonrestorable teeth #8 and #9.


B temporary crown is then fabricated and cemented in place
FIGURE 31-9. A, B, Implants placed. Abutments prepared and torqued.
To view a color version of this illustration, refer to the color insert section
at the back of this book.
FIGURE 31-10. Immediate temporary abutment torqued into position. To
view a color version of this illustration, refer to the color insert section
at the back of this book.
CHAPTER 31 • Immediate Implant Loading 515
FIGURE 31-11. Postoperative immediate implant with immediate tempo-
rary abutment.
one-piece implant with abutment as part of the implant is
placed.
If an abutment or temporary abutment was torqued into
position or a single-stage, one-piece implant was placed, a
(Figures 31-12 and 31-13). Very small amounts of cement
should be applied with care taken to remove any excess
because it is toxic to bone. Another useful precaution is to
take a periapical radiograph after cementation and analyze
this for excess material (Figures 31-14 and 31-15).
Screw-retained provisional restorations obviously elimi-
nate cement entrapment problems. These also allow the
restorative physician to precisely manipulate the soft tissue
profile around the implant without worrying about cement
(Figures 31-16 through 31-18). For that reason, this author
prefers screw-retained provisionals whenever possible.
However, many restorative clinicians work only with cemented
crowns because they require less specialized skill and chair
time.
NONFUNCTIONAL LOADING
For any partially edentulous case involving immediately
loaded implants, the temporary restoration(s) should be out
of occlusion by at least 1 mm to achieve nonfunctional loading
(Figures 31-19, 31-13, and 31-18). Nonfunctional immediate
loading means that although the lips, tongue, or food may put
some force on the restoration, there is no occlusal loading
from the opposing teeth. The dentist must adjust the occlu-
sion as needed and explain to the patient the importance of
keeping pressure out of the treated area. As mentioned,
nonfunctional loading is critical to deter any implant macro-
516 SECTION IV ■ Implant Surgery

movement that could cause fibrous encapsulation or lost

osseointegration.
For implant restorations placed in the posterior maxilla,
the author suggests significantly reducing or removing the
lingual cusp.
According to Choquet et al.,9 the distance from the contact
area to the bone should be no more than 5 mm to reliably
maintain the papilla. In their study, the customized provi-

FIGURE 31-13. Temporary placed out of occlusion.

FIGURE 31-12. A, B, Immediate temporary fabricated using crown of FIGURE 31-14. Periapical radiograph check for excess cement.
natural tooth. To view a color version of this illustration, refer to the color
insert section at the back of this book.

A B

FIGURE 31-15. A, B, Temporaries cemented. Radiograph to check for excess cement.


FIGURE 31-16. Screw-in temporary fabricated using rubber dam to
protect site. To view a color version of this illustration, refer to the color
insert section at the back of this book.
FIGURE 31-17. Screw-in temporary.
FIGURE 31-18. Screw-in type provisional inserted 1 hour after surgery.
Note blanching. To view a color version of this illustration, refer to the
color insert section at the back of this book.
sional crown restorations were fabricated and contoured for
optimal marginal fit emergence profile and interproximal con-
tacts. Occlusal centric and eccentric contacts were not per-
mitted on the provisional restoration. When evaluating and
modifying the occlusion, the clinician should place the patient
CHAPTER 31 • Immediate Implant Loading 517
A
FIGURE 31-19. A, B, Temporary out of occlusion.
in both the upright and reclined positions. Patients should
always be asked if they can “hit” the provisional when biting
down. If they can, it must be modified to prevent this contact
and protect against implant macromovement.
POSTOPERATIVE INSTRUCTIONS FOR
IMMEDIATELY LOADED IMPLANTS IN PARTIALLY
EDENTULOUS PATIENTS
After implant placement and loading, patients should be
instructed to eat a soft diet for 6 weeks and to avoid placing
food near the implant and provisional crown. The provisional
crowns serve both aesthetic and transitional purposes during
implant osseointegration, in place of transitional partial den-
tures or invisible retainers. If the patient wears a mouth guard
or retainer, it must be adjusted after the provisional crown is
placed. If it is worn without adjustment, it will place untoward
forces on the implant. Patients should also be instructed to
lightly brush around the implants with a soft-bristle tooth-
brush during the first 3 weeks and to rinse daily with over-the-
counter alcohol-free mouth rinse containing cetylpyridinium
chloride or with 0.12% chlorhexidine. Thereafter, conven-
tional brushing and flossing can be resumed (Figures 31-20
through 31-22).
518 SECTION IV ■ Implant Surgery

FIGURE 31-22. Final restoration.

FIGURE 31-20. Soft tissue healing at 6 weeks. To view a color version
of this illustration, refer to the color insert section at the back of this book.
edentulous jaw also has no periodontal ligament for proprio-
ception, and this can cause difficulties.
Obviously, implants placed into edentulous jaws and
immediately provisionalized will undergo occlusal loading, but
certain steps can be taken to minimize the impact.

IMMEDIATE IMPLANT LOADING TO RESTORE THE

EDENTULOUS MANDIBLE
Because bone quantity and quality in the edentulous mandible
are often excellent, immediate implant loading has demon-
strated predictably good results in many studies.10-14 In most
cases, implant stability can be predictably achieved in
this area.
A
If the implants and the abutment or healing caps are placed
in a single-stage fashion, an impression can be taken at the
time of initial surgery or soon thereafter. The final prosthesis
or provisional can be fabricated and placed as soon as
possible.
Implants placed in an edentulous mandible must endure
functional loading, even when the patient eats a soft diet.
Nonetheless, these implants are generally able to withstand
the functional loads and to osseointegrate if they are properly
placed and splinted to distribute the load forces. With proper
splinting, implant macromovement or critical micromove-
ments of 50 to 150 μm that can hinder osseointegration15 are
prevented.
Although the current dental literature does support imme-
diate implant loading of the edentulous mandible, this author
B typically recommends waiting 6 weeks between implant place-
ment and loading to better ensure osseointegration. Subse-
FIGURE 31-21. A, B, Porcelain-fused-to-metal abutment. quently the case can be finished as quickly as possible from
that point. If patients are unable or unwilling to tolerate a
complete lower denture provisional, a fixed provisional can be
■ IMMEDIATE IMPLANT LOADING IN created and immediately loaded without a great deal of risk.
THE EDENTULOUS JAWS
Immediate implant loading in the fully edentulous jaws IMMEDIATE IMPLANT LOADING TO RESTORE THE
requires a different approach than in the partially edentulous EDENTULOUS MAXILLA
jaws. This is because there are no natural teeth to rely on to Immediate implant loading in the completely edentulous
support the load during the first 6 weeks of healing. The maxilla poses a higher failure risk than the edentulous man-
 CHAPTER 31 • Immediate Implant Loading 519

dible. This is because the bone quantity and quality is often

poor. Achieving bicortical primary stability of the implant in
the maxilla is often more difficult.
The dental literature includes far fewer published studies
of immediate implant loading in the edentulous maxilla
on which to guide any evidence-based treatment with this
approach.16-20
When clinicians plan for immediate implant loading in the
edentulous maxilla, it should be undertaken with extreme
caution and only after fully discussing the risks versus the
benefits with the patient.
To help ensure the best possible outcome, this author rec-
ommends placing one implant per missing tooth with the
possible exception of the lateral incisors. This author also
FIGURE 31-23. Hopeless maxillary teeth.
cautions against the well-advertised “all-on-four” technique,
in which four implants placed in the arch are used to support
the restoration.21-23 Adequate long-term evidence to support
this approach is still lacking.
As with the edentulous mandible, implants should be
splinted together using the provisional restoration to deter
macromovements that can compromise osseointegration.
Using thinner drills and a tapered implant design may improve
implant stability.16
As with any case where immediate implant loading
is planned, patients should always be informed that such
plans may change, depending on what is encountered during
surgery. Minimum insertion torque or implant stability may
be unachievable. As a result, immediate implant loading may
not be a good option, and the patient may need a removable
provisional. FIGURE 31-24. Fourteen implants placed and four implants torqued.
Immediate loading in the edentulous maxilla is more
technically difficult than in the mandible. Because of the
number of implants, it is difficult to create a provisional that
splints all implants together in a passive fashion. This can
create a difficult case for the restorative dentist to do
chairside.
Many restorative clinicians are not convinced that imme-
diate implant loading “works” without a high degree of failure.
They often request that more implants be placed than actually
needed as an insurance policy. Some of the implants are
loaded, whereas others are left to osseointegrate unloaded.
Should any loaded implants fail, the other integrated implants
would be available to support the maxillary restoration (Figures
31-23 through 31-30).
Good results can often be achieved by loading just four
to six of the implants and allowing the remainder to FIGURE 31-25. Metal-reinforced fixed provisional cemented. To view a
osseointegrate for 6 weeks unloaded. In many cases, selected color version of this illustration, refer to the color insert section at the
natural teeth can be used to anchor the provisional, or if back of this book.
the patient has healthy second molars in place, good
results can also sometimes be achieved by immediately
loading the first bicuspid implants and connecting these to RESTORATIVE CONSIDERATIONS FOR COM-
the second molars for the provisional (Figures 31-31 PLETELY EDENTULOUS CASES
through 31-34). There are typically two options for restoring the edentulous
With all these caveats in mind, immediate implant loading arches.
for the edentulous maxilla should be approached with caution Often a duplicate of the complete denture wax up is made
at this time. and used as a template that is luted to copings on the day of
520 SECTION IV ■ Implant Surgery

surgery. Once the luting is completed, the flanges are removed

(palate in the maxilla), and the fixed hybrid or screw-retained
provisional is polished and delivered, often with bicuspid
occlusion only (Figures 31-35 through 31-41). There should
be no molar occlusion at this point. The occlusion must be
carefully adjusted and evaluated. The contact points should
be minimized and brought over the long axis of the implants
as much as possible. No posterior contact should exist, and
canine guidance should be employed. The passive fit should
be demonstrated with a panoramic radiograph employing the
one-screw technique. This option is quite time intensive for
both restorative dentists, who may encounter a steep learning
curve, and for the patient, who has just undergone immediate
implant placement at the surgeon’s office.
The second option is to place abutments, and this is usually
done by the surgeon (Figures 31-42 through 31-44). A stan-
dard cemented fixed provisional is fabricated, with or without
metal reinforcement. The occlusal considerations here are FIGURE 31-28. Transfer copings. To view a color version of this
the same with no molar contact and other contact points illustration, refer to the color insert section at the back of this book.

FIGURE 31-26. Six weeks postoperative. To view a color version of this

illustration, refer to the color insert section at the back of this book. FIGURE 31-29. Fourteen single units.

A B

FIGURE 31-27. A, B, Six-week radiograph.

 CHAPTER 31 • Immediate Implant Loading 521

minimized. Cement entrapment is also a concern with this
approach. Applying small amounts of cement, taking care to
remove excess, and taking periapical radiographs for added
observation are necessary to ensure excess cement is totally
removed. Using a metal-reinforced provisional is sensible here
to limit the amount of micromovement and hopefully to
improve the odds of a better success rate.
It is important to inform edentulous maxillary patients that
they may need a hybrid or a full removable prosthesis, depend-
ing on their phonetics and aesthetics when we attempt to
place them in a fixed provisional. In some cases, air-escape
problems can affect phonetics, or lack of lip support may
require a flange for aesthetics.

A FIGURE 31-31. Failed periosteal prosthetic case. To view a color

version of this illustration, refer to the color insert section at the back
of this book.

FIGURE 31-30. A, B, Five-year follow-up. FIGURE 31-33. Canine implant abutments placed. To view a color
version of this illustration, refer to the color insert section at the back
of this book.

A B

FIGURE 31-32. A, B, Immediately placed maxillary implants with second molars saved to aid in loading. To view
a color version of this illustration, refer to the color insert section at the back of this book.
522 SECTION IV ■ Implant Surgery

FIGURE 31-34. Immediate provisional cemented using second molars FIGURE 31-37. Implants placed immediately.
and implants.

FIGURE 31-38. Healing caps placed. To view a color version of this

illustration, refer to the color insert section at the back of this book.
FIGURE 31-35. Lower teeth hopeless. To view a color version of this
illustration, refer to the color insert section at the back of this book.

FIGURE 31-39. Temporary denture luted to copings. To view a color

FIGURE 31-36. Abundant bone quantity. version of this illustration, refer to the color insert section at the back
of this book.

■ FINAL POINTS ON IMMEDIATE
IMPLANT LOADING
Immediate implant loading certainly offers certain benefits
over delayed loading as described in this chapter; however,
this approach should be undertaken only by a well-
experienced team of surgery and restorative clinicians. Primary
implant stability is also a key factor in the success of this
approach.
There is evidence, although largely anecdotal at this point,
to indicate that immediate implant loading can be a good
 CHAPTER 31 • Immediate Implant Loading 523

FIGURE 31-40. Screw-retained provisional in place. FIGURE 31-41. Final restoration.

A B
FIGURE 31-42. A, B, Nonrestorable lower teeth. To view a color version of this illustration, refer to the color insert section at the back of this
book.

A B

FIGURE 31-43. A, B, Immediate implants placed and abutments torqued. To view a color version of this illustration, refer to the color insert section
at the back of this book.
524 SECTION IV ■ Implant Surgery
A B
FIGURE 31-44. A, B, Prefabricated temporary placed.
option, particularly for single-crown or other partially eden-
tulous mandible or maxilla cases. The benefits versus risks of
immediate implant loading in the fully edentulous maxilla are
still questionable. This may change as new research and tech-
nologic advances come our way.
REFERENCES
1. Spiekermann H, Jansen VK, Richter EJ: A 10-year-follow-up
study of IMZ and TPS implants in the edentulous mandible using
bar-retained overdentures, Int J Oral Maxillofac Implants 10:231-
243, 1995.
2. Chiapasco M et al.: Implant-retained mandibular overdentures
with immediate loading. A retrospective multicenter study on
226 consecutive cases, Clin Oral Implants Res 8:48-57, 1997.
3. Naito T: Immediate loading of dental implants in selected cases
may provide similar success rates as compared with delayed
loading, J Evidence Based Dent Pract 5:213-214, 2005.
4. Ghanavati F et al.: The effects of loading time on osseointegra-
tion and new bone formation around dental implants: a histo-
logic and histomorphometric study in dogs, J Periodontol
77:1701-1707, 2006.
5. Jokstad A, Carr AB: What is the effect on outcomes of time-to-
loading of a fixed or removable prosthesis placed on implant(s)?
Int J Oral Maxillofac Implants 22(suppl):19-48, 2007.
6. Jiminez-Lopez V: Introduction and general consideration for
immediate implant loading. In Jiminez-Lopez V, editor: Immedi-
ate loading in implant dentistry: surgical, prosthetic, occlusal, and
laboratory aspects, Barcelona, Spain, 2005, Quintessence.
7. Wang HL et al.: Consensus conference on immediate loading:
the single tooth and partially edentulous areas, Implant Dent
15:324-333, 2006.
8. DeKok IJ et al.: A retrospective analysis of peri-implant tissue
responses at immediate load/provisionalized microthreaded
implants, Int J Oral Maxillofac Implants 21:405-412, 2006.
9. Choquet V et al.: J Periodontol 72:1364-1371, 2001.
10. Chiapasco M, Gatti C, Gatti F: Immediate loading of dental
implants placed in severely resorbed edentulous mandibles
reconstructed with autogenous calvarial grafts, Clin Oral Implants
Res 18:13-20, 2007.
11. Tukyilmaz I et al.: A 2-year clinical report of patients treated
with two loading protocols for mandibular overdentures: early
versus conventional loading, J Periodontol 77:1998-2007, 2006.
12. Drago CJ, Lazzara RJ: Immediate occlusal of Osseotite implants
in mandibular edentulous patients: a prospective observational
report with 18-month data, J Prosthodont 15:187-194, 2006.
13. Attard NJ, David LA, Zarb GA: Immediate loading of implants
with mandibular overdentures: one-year clinical results of a pro-
spective study, Int J Prosthodont 18:463-470, 2005.
14. Chiapasco M, Gatti C: Implant-retained mandibular overden-
tures with immediate loading: a 3- to 8-year prospective study
on 328 implants, Clin Implant Dent Rel Res 5:29-38, 2003.
15. Szmukler-Moncler S et al.: Time of loading and effect of micro-
motion on bone dental implant interface: review of experimental
literature, J Biomed Matererials Res 43:192-203, 1998.
16. Ostman PO, Hellman M, Sennerby L: Direct implant loading in
the edentulous maxilla using a bone density-adapted surgical
protocol and primary implant stability criteria for inclusion, Clin
Implant Dent Rel Res 7(suppl):S60-S69, 2005.
17. Gallucci GO et al.: Immediate loading with fixed screw-retained
provisional restorations in edentulous jaws: the pickup tech-
nique, Int J Oral Maxillofac Implants 19:524-533, 2004.
18. Fischer K, Stenberg T: Early loading of ITI implants supporting
a maxillary full-arch prosthesis: 1-year data of a prospective,
randomized study, Int J Oral Maxillofac Implants 19:374-381,
2004.
19. Jaffin RA, Kumar A, Berman CL: Immediate loading of dental
implants in the completely edentulous maxilla: a clinical report,
Int J Oral Maxillofac Implants 19:721-730, 2004.
20. Portmann M, Glauser R: Report of a case receiving full-arch
rehabilitation in both jaws using immediate implant loading
protocols: a 1-year resonance frequency analysis follow-up, Clin
Implant Dent Rel Res 8:25-31, 2006.
21. Klee de Vasconcellos D et al.: A new device in immediately
loaded implant treatment in the edentulous mandible, Int J Oral
Maxillofac Implants 21:615-622, 2006.
22. Malo P, Rangert B, Nobre M: “All-on-Four” immediate-function
concept with Branemark system implants for completely eden-
tulous mandibles: a retrospective clinical study, Clin Implant
Dent Rel Res 5:2-9, 2003.
23. Malo P, Rangert B, Nobre M: All-on-4 immediate-function
concept with Branemark system implants for completely eden-
tulous maxillae: a 1-year retrospective clinical study, Clin Implant
Dent Rel Res 7:S88-S94, 2005.

IMPRESSIONS AT SURGICAL PLACEMENT
PROVISIONALIZATION OF IMPLANTS
Joel Rosenlicht • James Ward • Jack T. Krauser
From the earliest attempts to successfully design and place
dental implants, immediate loading and function have been
hallmarks of treatment.1 Abundant failures in the early devel-
opmental stages of implants were commonplace and often
occurred immediately or after a short period of functional
loading. In many cases, patients were left with clinical prob-
lems more severe than their original edentulism.2 Although
those early failure rates were unacceptable by today’s stan-
dards, many cases did survive and provide long-term support
for functioning prostheses.1-3
Retrospective analysis of those early, immediately, or pro-
visionally loaded implants allows us to now understand why
so many of those cases were successful and why others were
not.4 For example, the successful biologic use of metals was
highly limited until the development of clean surgical tech-
niques and antibiotics in the nineteenth century.4 Early exper-
imentation with various implant materials showed that the
necessary characteristics of tissue compatibility, corrosion
resistance, and strength could not be entirely met in all
metals.5 Gold, silver, and platinum were tissue compatible and
corrosion resistant, but lacked strength under high stress.4-6
Metals that provided better strength, such as brass, copper,
and steel, had poor tissue compatibility and corrosion
resistance.4
During the 1930s, the first surgical implants were stainless
steel alloyed with 18% chromium and 8% nickel, which had
good corrosion resistance and strength and were well tolerated
by the body.4 Molybdenum, added later, improved corrosion
resistance and formed the basis of an alloy (i.e., Type 316L)
commonly used today for orthopedic implants.4 During the
same decade, an alloy used for casting dental appliances,
cobalt chromium-molybdenum, was also used for surgical
implants.4
Corrosion or mechanical failure, such as wear, fretting, and
fatigue of coatings, can release particulate debris capable of
eliciting both local and systemic biologic responses.7 Metals
are usually not tolerated in large amounts by the body.7 The
ideal implant material would have to be passive to prevent an
immunologic response and inert to resist corrosion that could
harm local tissues and organs and compromise the long-term
functioning of an implant in the biologic environment. Fur-
thermore, the ideal implant material should not yield during
insertion, fracture, or fatigue or otherwise fail during in vivo
use.4 Therefore, an implant material’s intrinsic properties of
elasticity, yield point, ultimate tensile strength, compressive
CHAPTER 32
AND
strength, fatigue strength, hardness, and corrosion behavior
must be appropriate for the function it is called to perform.4
In 1940, Bothe et al.8 experimented with the surgical use
of titanium and first reported its extreme biocompatibility. It
was not until the 1950s, however, that research by Gottlieb
and Leventhal9 and Clarke and Hickman10 documented tita-
nium’s superior ability to withstand corrosion and remain rela-
tively inert in the body.11-13 In the mid-1960s, Branemark et
al.14 reported that ordered, living bone forms a direct structural
and functional connection with a load-carrying titanium
implant in the process that we now call “osseointegration.”
The modern understanding of biomaterials, implant surface
textures, bone physiology, biomechanical loading and/or func-
tion, and the systemic health of patients thus enables clini-
cians to achieve high survival rates and long-term predictability
in implant placement. Armed with this knowledge, selecting
patients appropriate for immediate functional implants offers
advantages, including shorter total treatment time, improved
stabilization of hard and soft tissue anatomy, fewer patient
visits, and an overall increase in patient comfort and function
over a traditional two-stage approach.15-20
Today, with the use of exceptional diagnostic information
and sophisticated radiographs, such as CT scanning and com-
puterized analysis programs, the unknowns of the anatomy
and bone quality are no longer left to assumptions. Reformed
three-dimensional views, anatomic models, surgical guides,
and presurgical prosthetics can help ensure that implants
placed into immediate functional loading are able to achieve
aesthetic results and long-term survival rates that equal or
surpass implants placed according to the standard, two-stage
surgical approach.
■ HISTORY OF IMMEDIATE
LOADING
As we look back into the history of dental implantology, we
see a natural progression from immediate functional loading
to predictable two-stage procedures and the concept of how
to achieve and maintain osseointegration. Now we see a
return to immediate functional and provisional restoration
when patient criteria are well suited to achieve osseointegra-
tion, predictability, and healthy, stable, and maintainable
aesthetic results (Box 32-1).
In 1937, Dr. Alvin Strock,21 a Boston oral and maxillofa-
cial surgeon, placed an orthopedic bone screw into an immedi-
ate extraction site of a periodontally involved mandibular
525
526 SECTION IV ■ Implant Surgery

BOX 32-1 History of Endosteal Implants

Egypt—slaves selling teeth (Kibrick et al 1975)
Sixteenth century—reimplantation of avulsed teeth
1886—Bugnot—implant tooth buds
1880-1900—gold, porcelain, gutta percha, platinum, etc.
1937—First endosseous implant (Dr. Alvin Strock)
1940—Screw type (Formiggini)
1962—Screw type (Cherceve) chrome cobalt
1966—Blade implant (Linkow, Weiss)
1967—Acrylic (Hodosh)
1968—TPS screw (Ledermann)
1975—Vitreous carbon
1980—Two stages systems (Branemark, Niznick)
1985—Implant placement by guided tooth position
1986—Immediate loading of traditional two-stage implants (Rosenlicht)
1988—Primary impressions for two-stage implants/indexing (Rosenlicht)
1992—CT scanning and presurgical diagnostic (Simplant)
1994—Computerized milled abutment (Atlantis abutment)

B
FIGURE 32-2. A, Immediate extraction of tooth #7 with orthopedic bone
screw placed with the screw head prepared as an abutment (placed 1938).
B, Periapical x-ray taken at 8 and 9 years (notice bone fill and integration
around implant).

Implants placed in subsequent years had a variety of shapes,

FIGURE 32-1. Orthopedic bone screw placed into an immediate extrac-
tion site of tooth #25, first endosseous implant placed.
central incisor (Figure 32-1). This implant, although never
restored, met several criteria for success of a one-stage immedi-
ate implant. During the subsequent year, Dr. Strock placed
another implant into an immediate extraction of an upper
lateral incisor with a bone screw with a prepared head to
receive a prosthetic crown.21 This implant and restoration
survived until 1955 (Figure 32-2 A, B).
designs, materials, and techniques for placement. One common
procedure, however, was that many of these implants were
placed and restored according to a one-stage procedure that
included direct impressioning and rigid splinting of the
implants with provisional restorations at the time of surgical
placement (Figure 32-3).22-26
Early, well-documented studies of the titanium plasma
sprayed screw (TPS), developed by Dr. P. Ledermann27-28
in the 1960s, showed that by following basic biologic and
biomechanical principles immediate provisional function of
implants could be achieved (Figure 32-4). It was recognized
that the selected biomaterial, a roughened TPS implant,
placed in a dense bone osteotomy that had been prepared
slightly undersized resulted in gentle compression of the bone
and excellent initial implant stability. The protocol required
that four implants be placed in the anterior mandible between
the mental foramina to allow adequate support for an immedi-
 CHAPTER 32 • Impressions at Surgical Placement and Provisionalization of Implants
FIGURE 32-3. Subperiosteal implant, one-stage implant designed for
immediate restoration (1935).
FIGURE 32-4. First implant system with long-term validated study
showing efficacy of one-stage immediate-load endosseous implants. (Kent
Babbish, 1984.)
ate (within 24 hours) overdenture supported by a passive-
fitting bar that rigidly splinted the implants together.
According to the protocol, a complete, tissue-supported, max-
illary denture was to provide the opposing dentition. This
technique was designed to increase the strength, stability, and
support of the implants to withstand the functional forces of
the maxillary denture within physiologic limits that allowed
bone healing and osseointegration of the implants.
In a 1986 study (unpublished), the author used traditional,
two-stage implants for immediate bar overdenture and fixed
partial denture cases and achieved clinical results that were
comparable with those reported by Ledermann27-28 and
Babbush et al.29 who reported an unprecedented success rate
of 94.04% at 5 years. Numerous case reports and studies have
verified these same statistics, clearly showing that implant
restorations subjected to one-stage placement and immediate
functional loading can achieve comparable or higher rates
when compared with the traditional, two-stage implant
approach.18-20,30-36
■ PRIMARY BONE-LEVEL
IMPRESSIONS
In the late 1980s, the techniques of making a primary bone-
level impression for both one- and two-stage implant systems
became more frequent. Having the information available to
527
start the prosthetic reconstruction of the case while the patient
continued to undergo osseointegration enhances the second-
stage procedure by having the final abutment and anatomic
restoration ready to be placed. For the first time, certified labo-
ratory technicians were given information from these primary
impressions that had not been available from traditional,
second-stage impressions. We know from a number of
studies37-39 how important knowing the level of the osseous
crest is to the contact points of teeth for interdental papilla
support, formation, and maintenance. With an immediate
impression, this information is now visible and available on
the master cast.
There are several materials available when choosing an
impression material for use in immediate impression taking.
The use of polyethers, silicones, and polysulfides is preferable
as a result of their durability and rigidity. These materials aid
in avoiding flexion upon removal and help prevent positional
distortion. Other factors contributing to selection are material
accuracy, working time, ease of handling, and physician
experience.
Polysulfide rubber base impression materials exist in three
phases: light, regular, and heavy bodied, based upon their
viscosity and ability to flow under loading. The base material
consists of 80% low-molecular-weight organic polymer, con-
taining reactive mercaptan groups and 20% reinforcing agents,
including titanium dioxide, zinc sulfate, copper carbonate, or
silica. The catalyst is usually lead dioxide, which functions as
an accelerator.40
Silicone impression materials exist as two types: condensa-
tion and addition. The condensation type is composed of a
base and a catalyst. The base consists of dimethylsiloxane
paste, a relatively low-molecular-weight silicone liquid. The
catalyst is made up of a tin organic ester suspension and an
alkyl silicate in liquid form. The addition type is usually a
two-paste or two-putty combination. Included in the reac-
tion are a low-molecular-weight silicone with terminal vinyl
groups, filler for reinforcement, and a chloroplatinic acid cata-
lyst together with low-molecular-weight silicone with saline
hydrogens and reinforcing filler.40
Polyether rubber base impression materials also exist
as base and catalyst reactions. The base is usually a low-
molecular-weight polyether with ethylene imine terminal
groups. An aromatic sulfonic acid ester catalyst causes a
reaction among the terminal groups forming cross-linked
high-molecular-weight rubber.40
The choice of impression material is usually made by exam-
ining their properties. All of the previously mentioned impres-
sion materials provide excellent reproduction of detail.
Condensation silicone and polyether materials have shorter
working times, whereas addition silicone is slightly longer and
polysulfide longer still. Polyether materials have the shortest
setting time, whereas addition and condensation silicones are
moderate, and polysulfide has the longest setting time. Flexi-
bility on removal from lowest to greatest is: polyether, addi-
tion silicone, condensation silicone, and polysulfide. Polysulfide
materials have the highest tear strength followed by addition
528 SECTION IV ■ Implant Surgery
silicones, condensation silicones, and polyether.40 All of these
impression materials possess adequate properties to be used as
impressions for dental implants. The choice is usually made
based on ease of use, cost, and physician comfort with the
material.
Day-of-surgery impressions and indexing can allow for
placement of the final restoration earlier in the healing period
after implant integration. These immediate impressions are
also useful in CAD/CAM technology for creating custom
abutments. There are several implant impression techniques.
The more common techniques are direct, indirect, and direct-
splinted. The majority of the current literature suggests that
a direct technique is the most accurate, whereas indirect is the
least accurate.41-43 Whether or not to use a custom tray or stock
design for implant impressions is usually based on the material
used and the discretion of the practitioner. A similar decision-
making process determines the use of an open-tray or closed-
tray technique. Open-tray technique is advocated for multiple
splinted restorations because of its increased accuracy in these
cases.
Once the implant has been placed, impression material
chosen, and the transfer post applied, the impression may be
taken. Closure of open gingival flaps is not required, although
it is imperative that all impression material be removed before
closure to prevent foreign body reaction. An adhesive is
applied to the impression tray and allowed to dry for the speci-
fied time. Care is then taken to insert the impression tray,
which is held with gentle pressure until the impression mate-
rial is primarily set. The tray and impression material are
removed ideally in one motion to prevent excessive distortion
of the material. Casts are then made using dense stone, and
the implant analogs are used for creation of either a temporary
or permanent restoration.
Whichever technique is chosen, impressions at the time of
implant placement provide the laboratory technician with the
information to create appropriate emergence, gingival contour,
and aesthetic form. Recognizing the importance of having this
information and the demonstrated effect of immediate func-
tion, the placement of an impression post allows the implant
surgeon to make an impression of the implant immediately
after placement for the fabrication of provisional or definitive
abutments and provisional prostheses (Figure 32-5 A-G).
Zimmer Dental, Inc. has incorporated a premounted fixture
mount transfer pin in its product line. This feature allows for
implant placement and impression taking to occur without
changing any parts on the implant (Figure 32-6 A-E).
■ IMMEDIATE PROVISIONALIZATION
Provisionalization of implants on the day of surgery has been
reported with high success rates.44-46 Prior technique recom-
mended a healing time of 4 to 6 months before functional
loading.47-51 Immediate provisionalization allows the patient
to return to proper form and satisfies the patient’s desire to
maintain aesthetics. The goals of immediate provisionaliza-
tion of implants include: maintaining interdental space,
development of the gingival sulcus contour, minimizing delay
in final restoration, elimination of second-stage surgery, and
avoidance of a temporary removable appliance.52
Provisionalization encompasses the majority of the implant
process. The physician must choose the use of a temporary or
permanent abutment, what type of abutment to use, and the
mechanism by which to provisionalize. The use of a perma-
nent abutment at the time of immediate provisionalization
obviously requires either predesigned and meticulously
planned implant placement guiding systems or an in-house or
nearby laboratory with which the restorative dentist would
work closely. The lab may also fabricate a provisional restora-
tion for placement, or the provisional restoration may be
created by the practitioner using either a prefabricated shell,
custom mold, or block carve techniques. Regardless of the
technique chosen, the importance of proper occlusal adjust-
ment with immediately loaded implants is paramount.
Several abutment systems exist for provisionalization of
dental implants. The restorative dentist must choose between
custom, stock, and computer-designed and computer-generated
abutments. Computer-aided design and computer-aided man-
ufacturing (CAD/CAM) is gaining in popularity as a result of
the elimination of laboratory fabrication. The CAD/CAM
technology was expanded to include abutment fabrication for
dental implants in the 1990s. Stock or cast custom abutments
have been incorporated in implantology since its inception.
They are available in titanium, noble metal alloys, and ceram-
ics. The primary difference between stock and cast custom
abutments is the need to prepare stock abutments.
Advantages of stock abutments include lower cost, prepara-
tion is intraoral or extraoral, and potentially minimal prepara-
tion time. Intraoral preparation adds additional disadvantages
to stock abutments, including the need for patient anesthesia,
gingival retraction, and risk to adjacent structures. The major
disadvantage of stock abutments is their cylindric shape. This
requires the addition of antirotational grooves that may com-
promise strength. The cylindric shape also prevents the emer-
gence profile from beginning at the implant platform and must
begin at the prepared edge of the abutment. Abutments with
fixed angulations often do not match the exact angulations
needed, and additional preparation is required.53
Cast custom abutments solve some of the problems of stock
abutments in that they are produced specifically to replace the
lost structure.54 The transition of the abutment begins at the
implant surface, thereby improving the emergence profile and
overall aesthetic results. The disadvantages to cast custom
abutment include the high cost of fabrication, the dependence
on the technician for design and contour, and the potential
for voids inherent in the investment, casting, and finishing
process.
The technologic advancements in CAD/CAM design
avoid the assembly line nature of both stock and cast abut-
ments. They provide an abutment design specific to the indi-
vidual (Figure 32-7 A, B). The technician learning curve is
assisted by software design allowing virtual creation of the
abutment before computer-assisted milling. This allows for the
elimination of most of the dimensional inaccuracies inherent
 CHAPTER 32 • Impressions at Surgical Placement and Provisionalization of Implants 529

A B

C D

E F

G H

FIGURE 32-5. A, Implant and transfer pin. B, Abutment fabricated with placement stent. C, Lab-processed crown. D, Papilla-sparing incision. E, Placement
of abutment with positioning jig. F, Immediate placement of crown. G, Final Panorex. H, Final porcelain-fused-to-metal restoration on implant at 1 year.
530 SECTION IV ■ Implant Surgery

A B

C D

FIGURE 32-6. A, Implant fixture mount transfer abutment. B, Transfer impression with analog in place. C, Immedi-
ate temporary provisional restoration. D, Immediate provisional restoration in place. To view a color version of this
illustration, refer to the color insert section at the back of this book.

A B

C D
FIGURE 32-7. A, Prefabricated CAD/CAM zirconia abutment. B, Temporary crown. C, Prefabricated coping.
D, Positioning guide for implant placement.
 CHAPTER 32 • Impressions at Surgical Placement and Provisionalization of Implants 531

E F

G H

FIGURE 32-7, cont’d. E, Implant placement and immediate final zirconia abutment. F, Provisional crown. G, Final
porcelain-fused-to-metal restoration at 1 year. H, Postoperative x-ray at 1 year.

in the casting process. The CAD/CAM process is especially
beneficial in using titanium abutments producing a more
homogenous result with optimal material properties. Even
when laboratory steps are followed, the heat-induced changes
occurring during casting reduce the contact between abut-
ments and their retaining screws.55 Because CAD/CAM abut-
ments do not require manipulation after production, they
provide the potential for superior fit, allowing for increased
precision. The overall cost of CAD/CAM abutment systems
remains high; however, the initial monetary commitment may
be distributed over the number of abutments used.
Provisionalization at the time of surgery provides several
benefits. First, the periimplant tissue is contoured to the
expected profile of the final restoration (Figure 32-7 C-F).
This allows for maturation of the attached tissue to occur with
the minimal need for manipulation upon delivery of the final
restoration. Overdentures and temporary fixed appliances may
be created on the day of surgery by in-house or nearby labo-
ratories, when available, and attached to these implants before
the fabrication of the final restoration. The principles of
occlusion must be followed in the creation of these temporary
restorations. Abnormal distribution of the occlusal forces may
lead to implant and case failure. Lateral excursive forces and
excessive contact in centric occlusion produce forces off the
implant axis. Ideally, occlusal forces should be directed along
the long axis of the implant.56
The concepts of bone level impressions, immediate provi-
sionalization, and immediate loading of implants may be com-
bined to allow for maximum patient benefit. The surgeon,
restorative dentist, and laboratory technician work in unison
to provide restoration of form and function in a timely manner.
Several versions of this philosophy have been advocated. One
such combination and treatment pathway will be described.
■ SMARTSTEPS: THE CONCEPT
Primary impression taking, immediate restoration, and imme-
diate functional loading are a treatment philosophy that offers
tremendous benefits to the surgeon, restorative dentist, labora-
tory technician, and ultimately the patient. It is a set of
bundled surgical and prosthetic techniques that also takes the
complexity out of implant restorations.
Why do SmartSteps?
Benefits to the surgeon
Increase patient referrals
Benefits to the restoring physician
Reduced chair time
Simple implant cases
Increased patient acceptance
Benefits to the patient
Fewer visits
Earlier function
Earlier aesthetics
532 SECTION IV ■ Implant Surgery

CASE REPORT 32-1 Immediate Impression with Restoration Placed at Second-Stage Surgery

This 47-year-old woman had an endodontically failing mandibular right Laboratory work (Figure 32-11 A, B).
first bicuspid (#28) that served as the anterior abutment connecting a • Abutments
four-unit fixed partial denture to a distal abutment and a severely • Provisional prosthesis
decayed mandibular right second molar (#31) (Figure 32-8). • Final cast framework for the restoration (no picture available)
The hopeless abutment teeth (#28, #31) were atraumatically extracted • Placement jig for abutments
to preserve the bony architecture around the socket. Two 3.7-mm
diameter and two 4.7-mm diameter Tapered Screw-Vent implants were
placed into the two prepared sockets (Figure 32-9). Impression material
was injected around implants with the soft tissue flap open to allow for
accurate impressioning of implant impression posts and surrounding
osseous crest, soft tissue, and teeth (Figure 32-10).
The laboratory technician was sent the primary impression by the
restorative dentist with the appropriate information for the work to be
done. The technician was instructed to not be concerned with the lack
of soft tissue on the working cast and to fabricate an appropriate defini-
tive abutment. The instructions also included fabrication of the provi-
sional prosthesis and a framework for the definitive crown that directed
that the contact point not be more than 5 mm from the osseous crest.
A coping could also have been made for the final impression after all
functional and aesthetic concerns have been resolved with the
patient.

FIGURE 32-10. Polyvinyl impression material injected over impression

pins to obtain a bone level impression. To view a color version of this
illustration, refer to the color insert section at the back of this book.

FIGURE 32-8. Panoramic x-ray of patient with failing four-unit

bridge.

B
FIGURE 32-9. Placement of four Zimmer Tapered Screw Vent implants
with immediate impression components premounted on the implant. To view
FIGURE 32-11. A, B, Laboratory-prepared abutments with placement
a color version of this illustration, refer to the color insert section at
jig and temporary crowns. To view a color version of this illustration,
the back of this book.
refer to the color insert section at the back of this book.
 CHAPTER 32 • Impressions at Surgical Placement and Provisionalization of Implants 533

CASE REPORT 32-1 Immediate Impression with Restoration Placed at Second-Stage Surgery—cont’d

At the second-stage surgery, soft tissue–sparing incisions were

made to maximize the attached gingival tissue and drape around the
aesthetic, anatomic restorations (Figure 32-12).
Final restoration (Figure 32-13) and final Panorex (Figure 32-14).

FIGURE 32-12. Minimal incision exposure for placement of abutments
and temporary restorations. To view a color version of this illustration,
refer to the color insert section at the back of this book.
FIGURE 32-13. Final crowns after soft tissue healing. To view a color
version of this illustration, refer to the color insert section at the back
of this book.

FIGURE 32-14. Postoperative panoramic x-ray.

534 SECTION IV ■ Implant Surgery

CASE REPORT 32-2 Immediate Extraction, Implant Placement, and Provisional Restoration

A 41-year-old woman had tooth #11 with significant internal resorption
and a poor prognosis. Aesthetic and function were an important factor
because of a very high smile line and her need to speak clearly without
any removable appliances (Figure 32-15 A, B). The tooth was extracted
atraumatically using Periotomes, and the site was grafted before
implant-site preparation and insertion (Figure 32-16 A, B). A plastic
temporary abutment, which can be very easily prepared, was placed,
and an acrylic provisional crown was fabricated (Figure 32-17 A, B).
This was very functional and aesthetic, and the final restoration was
placed at 3 months (Figure 32-18 A, B, C). Figure 32-18 C shows the
provisional restoration at 1 week. The final restoration was fabricated
at 3 months.

A B

FIGURE 32-15. A, Frontal. B, Lateral preoperative presentation of internal and external resorption of tooth #11.

A B

FIGURE 32-16. A, Atraumatic extraction with Periotomes and preparation of site with socket grafting. B, Implant
placement with fixture mount transfer.
 CHAPTER 32 • Impressions at Surgical Placement and Provisionalization of Implants 535

CASE REPORT 32-2 Immediate Extraction, Implant Placement, and Provisional Restoration—cont’d

A B C

FIGURE 32-17. A, Zimmer plastic temporary abutment on the analog. B, Preparation of the plastic temporary
abutment on the implant. C, Temporary acrylic restoration anatomically contoured to the temporary plastic abutment.

A B

C D

FIGURE 32-18. A, Immediate placement of temporary crown on the implant. B, One week later. C, D, Lateral and
frontal view of final porcelain-fused-to-metal restorations.
536 SECTION IV ■ Implant Surgery

Placement of Implants in the Areas of Teeth #4 and #6 with Placement of Prefabricated

CASE REPORT 32-3 Ceramic Abutments and Temporary Crowns Done as a One-Stage Procedure

This 38-year-old woman was wearing a partial denture and requested

a fixed bridge to extend from tooth #4 to #6. The residual bone as seen
on Panorex was adequate in both height, width, and density for an
immediate restoration (Figure 32-19). The model taken was sent to the
laboratory for placement of the implant analogs so that surgical guides,
final abutments, and a temporary bridge could be fabricated (Figure
32-20 A, B, C). Using the surgical guide, the implants were placed, final
zirconia custom abutments secured, and the immediate provisional
bridge placed (Figure 32-21 A, B, C). After 3 months of function and
soft tissue healing, the final restoration was placed (Figure 32-22). Final
Panorex (Figure 32-23).

FIGURE 32-19. Preoperative panoramic x-ray showing adequate bone

height in areas in the right maxillary.
B

FIGURE 32-20. A, Presurgical model preplanned with implants and

Procera ceramic abutments. B, Immediate temporary restorations on pre-
planned model. C, Surgical guide for implant placement. To view a color
version of this illustration, refer to the color insert section at the back
of this book.
 CHAPTER 32 • Impressions at Surgical Placement and Provisionalization of Implants 537

Placement of Implants in the Areas of Teeth #4 and #6 with Placement of Prefabricated

CASE REPORT 32-3 Ceramic Abutments and Temporary Crowns Done as a One-Stage Procedure—cont’d

FIGURE 32-22. Three-month postoperative view with final crown res-

torations. To view a color version of this illustration, refer to the color
insert section at the back of this book.

FIGURE 32-23. Final 6-month postoperative panoramic x-ray.

FIGURE 32-21. A, Immediate placement position of 4.3 Nobel Biocare

Replace Select implant. B, Ceramic abutments secured and torqued in place.
C, Temporary provisional crown ridge spanning teeth #5 through #6. To view
a color version of this illustration, refer to the color insert section at
the back of this book.
538 SECTION IV ■ Implant Surgery
■ SUMMARY
When primary stability of the implant is apparent, making an
immediate impression has been shown to significantly improve
all aspects of the restorative process and enhance soft tissue
aesthetics. There is no evidence that making an impression at
stage-one surgery in any way impairs the ability of the implant
to heal and integrate. Certainly, extreme care is taken to see
that all impression material is removed and that proper tech-
niques are executed. The implant must also not be altered in
position by rotating it after the impression has been made,
when tightening the healing screw, or attaching the abut-
ment. When there is appropriate support of the implant in
bone and the restoration can be protected from excessive
trauma, the placement of an immediate provisional restora-
tion should be considered. This protection may come from a
guarded occlusion provided by adjacent teeth to prevent
trauma and/or carefully adjusting the restoration to be in a
very light or nonoccluding relationship to the opposing
teeth.
REFERENCES
1. Ring ME: A thousand years of dental implants: a definitive
history-part 1. Compend Continuing Education Dent 16(10):1060-
1069, 1995, [Passim].
2. Diskell TD: History of implants, Can Dent Assoc J 15(10):16-25,
1987.
3. Ring ME: A thousand years of dental implants: a definitive
history-part 2, Compend Continuing Education Dent 16(11):1132-
1142, 1995, [Passim].
4. Luckey HA, Kubli Jr F: Summary. In Luckey HA, Kubli Jr F,
editors: Titanium alloys in surgical implants, Philadelphia, 1983,
American Society for Testing and Materials.
5. Branemark PI: Introduction to osseointegration. In Branemark
PI, Zarb GA, Albrektsson T, editors: Tissue-Integrated prostheses.
Osseointegration in clinical dentistry, Chicago, 1985,
Quintessence.
6. Bannon BP, Mild EE: Titanium alloys for biomaterial applica-
tion: an overview. In Luckey HA, Kubli Jr F, editors: Titanium
alloys in surgical implants, Philadelphia, 1983, American Society
for Testing and Materials.
7. Kohn DH: Overview of factors important in implant design,
J Oral Implantol 18(3):204-219, 1992.
8. Bothe RT, Beaton LE, Davenport HA: Reaction of bone to
multiple metallic implants, Surg Gynecol Obstet 71:598-602,
1940.
9. Gottlieb S, Leventhal GS: Titanium, a metal for surgery, J Bone
Joint Surg 33(A):473-474, 1951.
10. Clarke EGC, Hickman J: An investigation into the correlation
between the electric and potential of metals and their behavior
in biological fluids, J Bone Joint Surg 35(B):467-473, 1953.
11. Brunski JB: Biomaterials and biomechanics in dental implant
design, Int J Oral Maxillofac Implants 3(2):85-97, 1988.
12. Williams DF: Titanium as a metal for implantation.
Part 1: physical properties, J Med Eng Technol 7:196-198, 202,
1977.
13. Clarke AE: Principles of tissue implant material interactions. In
Caswell CW, Clark Jr AE, editors: Dental implant prosthodontics,
Philadelphia, 1991, JB Lippincott 317-322, 1991.
14. Brånemark PI et al.: Osseointegrated implants in the treatment
of the edentulous jaw. Experience from a 10-year period, Scand
J Plast Reconstr Surg 111(suppl 16):1-132, 1977.
15. Rosenlicht JL: Immediate implant placement and immediate
provisionalization: steps for integration. In Implantology 2003,
Mahwah, NJ, 2003, Montage Media.
16. Rosenlicht JL: Update on primary impression taking: improved
aesthetic results, enhanced accuracy of castings, and shortened
treatment time, Int J Dent Symp 4(1):20-25, 1997.
17. Rosenlicht JL: SmartStepsSM to immediate implant impressions,
Australasian Dent Pract 13(2):70-74, 2002.
18. Cannizzaro G, Leone M: Restoration of partially edentulous
patients using dental implants with microtextured surface: a pro-
spective comparison of delayed and immediate full occlusal
loading, Int J Oral Maxillofac Implants 18(4):512-522, 2003.
19. Siddiqui AA, Ismail JYH, Kukunas S: Immediate loading of
dental implants in the edentulous mandible: a preliminary case
report from an international prospective multicenter study,
Compend Continuing Education Dent 22(10):867-882, 2001.
20. Schiroli G: Immediate tooth extraction, placement of a Tapered
Screw-Vent® implant, and provisionalization in the esthetic
zone: a case report, Implant Dent 12(2):123-131, 2003.
21. Strock AE: Experimental work on a method for the replacement
of missing teeth by direct implantation of a metal support
into the alveolus. Preliminary report, Am J Orthod Oral Surg
25(5):467-472, 1939.
22. Linkow LI: The Blade Vent-a new dimension in endosseous
implantology, Dent Concepts 11:3-18, 1968.
23. Roberts RA: Types, uses, and evaluation of the Plate-form
implant, J Oral Implantol 22(2):111-118, 1996.
24. Turner HF: The Ramus frame implant, J Oral Implantol 1(1):14-
16, 1981.
25. Schou S et al.: A 41-year history of a mandibular subperiosteal
implant, Clin Oral Implant Res 11:171-178, 2000.
26. Bailey JH, Yanase RT, Bodine RL: The mandibular subperiosteal
implant denture: a fourteen-year study, J Prosthet Dent 60(3):358-
364, 1988.
27. Ledermann PD: Stegprothetische Versorgung des zahnlosen
Unterkiefers mit Hilfe von Plasma-beschichteten Titan-
schrauben-implantaten, Dtsch Zahnartl Z 34:907-918, 1979.
28. Ledermann PD: Die plasmabeschichtete Titanschraube als enos-
sales Implantat. Methodic der Implantaten und der postopera-
tiven Versorgung, Dtsch Zahnarzrt Z 35:577-579, 1980.
29. Babbusch CA: Titanium plasma spray screw implant system for
reconstruction of edentulous mandible, Dent Clin North Am
30:117-131, 1986.
30. Garber DA, Salama MA, Salama H: Immediate total tooth
replacement, Compend Continuing Education Dent 22:210-218,
2001.
31. Wöhrle PS: Single-tooth replacement in the aesthetic zone with
immediate provisionalization: fourteen consecutive case reports,
Pract Periodont Aesthet Dent 10:1107-1114, 1998.
32. Cooper L et al.: A multicenter 12-month evaluation of single-
tooth implants restored 3 weeks after 1-stage surgery, Int J Oral
Maxillofac Implants 16:182-192, 2001.
33. Kupeyan HK, May KB: Implant and provisional crown place-
ment: a one-stage protocol, Implant Dent 7:213-219, 1998.
34. Gomes A et al.: Immediate loading of a single hydroxyapatite-
coated threaded root form implant: a clinical report, J Oral
Implantol 24(3):159-166, 1998.
35. Maló P, Rangert B, Dvarsater L: Immediate function of
Branemark implants in esthetic zone: a retrospective clinical
study with 6 months to 4 years of follow-up, Clin Oral Implant
Res 2:137-145, 2000.
36. Misch CE: Nonfunctional immediate teeth in partially edentu-
lous patients: a pilot study of 10 consecutive cases using the
Maestro Dental Implant System, Compendium 19:25-36, 1998.
37. Tarnow D et al.: Vertical distance from the crest of bone to the
height of the interproximal papilla between adjacent implants,
J Periodontol 74(12):1785-1788, 2003.
 CHAPTER 32 • Impressions at Surgical Placement and Provisionalization of Implants
38. Salama H et al.: The interproximal height of bone: a guidepost
to predictable aesthetic strategies and soft tissue contours in
anterior tooth replacement, Pract Periodont Aesthet Dent
10(9):1131-1141, 1998.
39. Gomez-Roman G: Influence of flap design on peri-implant inter-
proximal crestal bone loss around single tooth implants, J Oral
Maxillofac Implants 16(1):61-67, 2001.
40. Craig R, O’Brien W, Powers J: Dental materials, properties and
manipulation, ed 6, St Louis, 1996, Mosby.
41. Hsu CC, Millstein PL, Stein RS: A comparative analysis of the
accuracy of implant transfer techniques, J Prosthet Dent 69:588,
1993.
42. Spector M, Donovan TE, Nicholls JI: An evaluation of impres-
sion techniques for osseointegrated implants, J Prosthet Dent
63:444, 1990.
43. Carr AB: Comparison of impression techniques for a five-
implant mandibular model, Int J Oral Maxillofac Implants 6:488,
1991.
44. Tarnow DP, Emtiaz S, Classi A: Immediate loading of threaded
implants at stage 1 surgery in edentulous arches: ten consecutive
case reports with 1 to 5 year data, Int J Oral Maxillofac Implants
12:319, 1997.
45. Ibanez JC, Jalbot ZN: Immediate loading of Osseotite implants:
two-year results, Implant Dent 11:128, 2002.
46. Kan J, Rungcharassaeng K, Lozada J: Immediate placement and
provisionalization of maxillary anterior single implants: 1-year
prospective study, Int J Oral Maxillofac Implants 18:31, 2003.
539
47. Branemark PI: Osseointegration and its experimental back-
ground, J Prosthet Dent 50:399, 1983.
48. Andreassen B et al.: Single-tooth restorations supported by
osseointegrated implants: results and experiences from a prospec-
tive study after 2 to 3 years, Int J Oral Maxillofac Implants 10:702,
1995.
49. Friberg B, Jemt T, Lekholm U: Early failures in 4,641 consecu-
tively placed Branemark dental implants: a study from stage 1
surgery to the connection of completed prostheses, Int J Oral
Maxillofac Implants 6:142, 1991.
50. Henry P, Laney WR, Jemt T: Osseointegrated implants for
single-tooth replacement: a prospective 5-year multicenter study,
Int J Oral Maxillofac Implants 11:450, 1996.
51. Lazzara RJ et al.: A prospective multicenter study evaluating
loading of Osseotite implants two-months after placement: one
year results, J Esthetic Dent 10:280, 1998.
52. Castellon P, Casadaban M, Block M: Techniques to facilitate
provisionalization of implant restorations, J Oral Maxillofac Surg
63:72-79, 2005.
53. Priest G: Virtual-designed and computer-milled implant abut-
ments, J Oral Maxillofac Surg 63:22-32, 2005.
54. Lewis SG, Llamas D, Avera S: The UCLA abutment: a four-year
review, J Prosthet Dent 67:509, 1992.
55. Byrne D et al.: The fit of cast and premachined implant abut-
ments, J Prosthet Dent 80:184, 1998.
56. Engleman MJ: Clinical decision making and treatment planning in
osseointegration, Chicago, 1997, Quintessence.
CHAPTER 33
IMPLANT PLACEMENT IMMEDIATELY FOLLOWING
TOOTH EXTRACTION
For more than 3 decades, the criteria for successful replace-
ment of teeth with restored dental implants followed a narrow
construct of scientific and clinical protocols.1-3 Whether the
goals of tooth replacement focused on a single site, a partially
edentulous quadrant, or an edentulous arch, it was assumed
that dental implants had to be located at sites where the
alveolar bone was of sufficient quality, quantity, and morphol-
ogy.1 Furthermore, the protective role of periimplant gingiva
or detrimental effects of microorganisms in the gingival crevice
surrounding the restored implant was seldom considered.
These findings were among the original ideology proposed by
Brånemark that assumed multiple root form dental implants
should only be placed in healed edentulous sites, covered with
alveolar mucosa for 3 to 6 months before second-stage abut-
ment connection and restoration, and located mostly in the
anterior region of the edentulous mandible. Single-tooth and
partially edentulous treatment comprised less than 5% of their
restorative cases, and dental implant placement distal to the
mandibular foramen was considered experimental.2
These principles were mandated to achieve a 1-year implant
survival outcome of 88% in the anterior maxilla and 94% for
the anterior mandible. For a series of dental implants penetrat-
ing the maxillary sinus, the result showed a 5- to 10-year
functioning percentage between 70% and 72%.3 The scientific
documentation of the Brånemark group and their protocol for
osseointegration strongly influenced clinical applications of
dental implant therapy until about the early 1990s.
To achieve osseointegration, which was considered to be
intimate contact of bone to dental implant as assessed at the
light microscopic level, this initial protocol required that the
implant must be one inserted with a low trauma surgical tech-
nique, be placed with initial stability, and should not be func-
tionally loaded until sufficient bone has been deposited in
mineralized form.4
This traditional clinical protocol for placing dental implants
demanded a uniform intimate contact between the dental
implant and surrounding walls of bone from the most coronal
aspect of the implant to its most apical extent. This was
achieved by employing a set of drills or burs that would suc-
cessively increase in diameter. Bone to implant contact was
further clinically enhanced by the use of an osteotomy that
was narrower than the intended dental implant. Finally, the
fixture was slowly turned or tapped into the osteotomy with
540
H. Dexter Barber • James Spivey
copious and cool saline irrigation until the most apical extent
engaged in osteotomy.
Subsequent to this initial protocol, it has been determined
that it is not always possible to prepare an osteotomy without
clinical voids or gaps surrounding the fixture. Subsequently,
clinical guidelines were developed that led to employing prin-
ciples of guided tissue regeneration to create mineralized tissue
that supported frustrations or dehiscence at the time of implant
placement.4 Seeing that the initial protocol for dental implant
placement required a completely healed extraction site,
the next logical phase of implant therapy focused on placing
dental implants in extraction sockets immediately upon tooth
removal and delivering a comfortable, aesthetic, semifunc-
tional provisional restoration.
Many of the available studies concerning the placement of
dental implants in extraction sites describe their use in the
anterior and premolar regions,7 but careful applications of
surgical principles resulted in predictable success of dental
implants placed in extraction sites immediately following the
removal of molars. This chapter will review principles associ-
ated with root form dental implants immediately placed in
extraction sockets.
■ HEALING OF EXTRACTION
SOCKETS: THE RESPONSE OF
ALVEOLAR BONE FOLLOWING
ROUTINE TOOTH EXTRACTION
(WITHOUT SOCKET GRAFTING,
RIDGE PRESERVATION OR
IMMEDIATE IMPLANT
PLACEMENT)
Once a tooth is extracted, the remodeling of the alveolar bone
and the adaptation of the gingiva and mucosal tissue could
compromise an idealized dental implant location. Depending
on the quality, quantity, and morphology of the alveolar bone,
extensive presurgical protocols aimed at preparing the area for
dental implant placement might be needed if the alveolar
bone is allowed to remodel after extraction. One significant
factor driving clinicians toward placing dental implants in
extraction sockets is based, in part, on the desire to avoid
these hard and soft tissue site development techniques. Under-
standing the process of alveolar bone remodeling after tooth
 CHAPTER 33 • Implant Placement Immediately Following Tooth Extraction
extraction is crucial in planning the location of dental implant
placement at the time of tooth removal.
■ ADAPTIVE MORPHOLOGY OF THE
MAXILLARY ALVEOLAR PROCESS:
RESPONSE IN THE AESTHETIC
ZONE (THIN LABIAL BONE)
After tooth extraction, the alveolar bone is affected by a
complex and progressive process. These changes can have a
significant influence on the planned dental implant site.
According to Atwood,5 the alveolar ridge atrophy is a chronic,
progressive, irreversible disease. This process results in pro-
found loss in the height and width as a result of the mas-
sive loss of bone volume a few months after a tooth is
extracted.8-10
■ FACTORS THAT AFFECT THE
AMOUNT OF BONE LOSS
FOLLOWING AN EXTRACTION
There are several factors that may influence the amount of
bone loss that occurs following an extraction.7-11 The labial
bone in the anterior maxilla is thin. Even a simple, atraumatic
extraction may lead to extensive bone loss in this area as a
result of the natural thin labial bone in this area.12 Atraumatic
extraction techniques, including the use of Periotomes, mini-
mizes trauma to the bone and soft tissue, thus minimizing the
amount of bone loss resulting from the extraction.13 Extrac-
tion of endodontically treated teeth, teeth with curved roots,
and retained roots of endodontically treated teeth all increase
the possibility of a surgical flap and bone removal to extract
the tooth (Figure 33-1 A, B).
■ ATRAUMATIC EXTRACTION
TECHNIQUES: THE USE
OF PERIOTOMES
To minimize the amount of bone loss associated with a tooth
extraction and to enhance the opportunity for immediate
implant placement, atraumatic extraction techniques are
A B
FIGURE 33-1. A, Extraction of tooth, previously treated with a root canal procedure. B, Extraction of this root canal
tooth resulted in facial bone loss. To view a color version of this illustration, refer to the color insert section at
the back of this book.
541
extremely important. The use of Periotomes has greatly sup-
ported the opportunity to achieve an atraumatic extraction of
a tooth13 (Figure 33-2 A, B). A Periotome is an instrument
that is used to separate the periodontal attachments and fibers
from the tooth root. Once the fibers or attachments are
released from the roots, the tooth can be easily and atraumati-
cally removed from the socket (Figure 33-2 C).
■ CLASSIFICATION OF EXTRACTION
SOCKET DEFECTS
The classification of extraction socket defects are based upon
the presence or lack of the walls that make up the extraction
socket.12,14
1. Five-wall defect
A five-wall defect has the buccal or facial wall, palatal or
lingual wall, mesial and distal walls, and the apical walls
of the extraction socket intact. This type of defect lends
itself ideally for immediate implant placement if the
root trajectory is appropriate (Figure 33-3 A).
2. Four-wall defect
A four-wall defect is missing one of the previously men-
tioned socket walls (Figure 33-3 B, C). This type of
defect usually requires either grafting in conjunction
with implant placement or grafting and placing the
implant at a later time.
3. Three-wall defect
A three-wall defect generally requires bone grafting before
implant placement because of the lack of bony support
for primary fixation of the implant. The use of bone
grafting and regenerative barrier membrane techniques
prepare the site for future implant placement (Figure
33-3 D).
4. Two-wall and one-wall defects
An extraction socket that is missing three or four of the
extraction socket walls generally requires significant
bone grafting and/or alveolar distraction, with probably
soft tissue grafting (Figure 33-3 E, F).
542 SECTION IV ■ Implant Surgery
A B
FIGURE 33-2. A, Various Periotomes that are used to sever periodontal ligament attachments. B, Periotome used
to sever periodontal attachments of tooth #8. C, Tooth easily removed after use of Periotome. To view a color version
of this illustration, refer to the color insert section at the back of this book.
■ CLINICAL SITUATIONS AND
INDICATIONS FOR IMMEDIATE
IMPLANT PLACEMENT
A simple clinical indication for the immediate dental implant
placement is the avulsed tooth. If a patient undergoes a trau-
matic incident (i.e., sports injury) and the tooth is unable to
be reimplanted within a sufficient interval to ensure surviv-
ability, a dental implant placed immediately within the socket
is highly indicated. This would depend on the timing of treat-
ment and the extent of the injury to the alveolar bone
and adjacent teeth. Strong consideration must be given to
adjacent vital structures, such as roots, nerves, and sinus
cavities.
Another indication for immediate dental implant place-
ment occurs subsequent to intentional tooth removal. There
are a number of reasons for intentional tooth removal. These
include carries, aberrant tooth position, failed endodontically
restored teeth, chronic localized periodontitis, and external or
internal root resorption. As a result of such situations, espe-
cially in the aesthetic zone, a strong argument can be made
in favor of extracting a tooth and immediately placing a dental
implant within the socket. A key benefit associated with all
of these cases is to shorten the treatment sequence and allow
the patient to obtain a biologic replacement that mimics their
natural tooth. Such a protocol for immediate placement
within the extraction stock is preferred over the traditional
sequence for dental implant placement and restoration. The
C
typical protocol would require a 4- to 6-month waiting period
after tooth removal. This would allow sufficient healing and
maturation of alveolar bone in preparation for dental implant
placement. However, some patients and clinicians may desire
to accelerate this traditional approach to achieve this seem-
ingly natural result.
Primary stability is obviously required for immediate
implant placement. As previously mentioned, the five-
wall defect lends itself optimally for immediate implant
placement.
CONTRAINDICATIONS FOR IMMEDIATE
IMPLANT PLACEMENT
Contraindications for immediate implant placement include
inadequate root trajectory, three-, two-, and one-wall defects,
quality of bone inadequate for primary fixation, acute infec-
tion or periodontitis, and situations in which aesthetics would
be compromised if grafting or soft tissue procedures are not
completed before implant placement.12
ADVANTAGES OF IMMEDIATE
IMPLANT PLACEMENT
Advantages of immediate implant placement include short-
ened treatment time, marginal bone preservation, enhance-
ment of soft tissue support, and immediate provisional
restorations.12,15-17
 CHAPTER 33 • Implant Placement Immediately Following Tooth Extraction 543

A B

C D

E F

FIGURE 33-3. A, Five-wall defect with all walls of the extraction socket intact. B, Four-wall defect with the labial
wall missing. C, Four-wall defect grafted with autogenous block graft. D, Three-wall defect. Socket with two missing
walls. E, One-wall defect. Thin plate of maxillary bone. No labial-palatal dimension, with mesial and distal wall defects.
F, Block graft to reconstruct the labial, mesial, distal, and apical wall defects. To view a color version of this illustra-
tion, refer to the color insert section at the back of this book.

PREOPERATIVE EVALUATION OF THE POTENTIAL
IMMEDIATE IMPLANT SITE
The preoperative evaluation of the potential immediate
implant site should include several clinical and radiographic
assessments. Probing of the tooth before extraction allows the
clinician to assess the pocket depth or bone levels and to assess
papilla level.12 Probing also assists the clinician in assessing
the number of intact socket walls.
The significance of the gingival and/or tissue biotype asso-
ciated with the soon-to-be extracted tooth is an important
clinical assessment. The thicker the tissue biotype, the less the
chances of facial bone resorption and extraction gingival
margin recession (Figure 33-4 A, B).12,18-21 Significant gingival
margin recession can lead to display of the implant collar and
discrepancy of the gingival margin relative to the gingival
margin of the adjacent teeth.
544 SECTION IV ■ Implant Surgery

A B

FIGURE 33-4. A, Thick periodontal biotype facial view. B, Occlusal view of periodontal biotype.

A B C

FIGURE 33-5. A, Preextraction radiograph tooth #8. B, Atrau-

matic extraction of tooth #8 following use of Periotome. C, Sizing
implant bur within extraction socket. Verifying bur adjacent to palatal
wall. D, Implant placed with healing abutment inserted. Notice
implant position at expense of palatal wall. E, IAJ 1 to 2 mm below
socket crest. To view a color version of this illustration, refer to
D E
the color insert section at the back of this book.

The use of CT scans allows preoperative evaluation of the 5. May require graft between the labial bone and the
palatal and lingual bone levels. This provides information implant
relative to the potential socket wall defects.

PROCEDURE FOR IMMEDIATE IMPLANT SUCCESS RATE FOR IMMEDIATE IMPLANT

PLACEMENT (Figure 33-5 A-E)
1. The use of a Periotome to sever the periodontal fiber
attachments of the tooth root
2. Curettage or use of a small round bur may be required
to remove periodontal debris
3. Preparation for implant placement at the expense of the
palatal bone, not the thin labial bone
4. Implant-abutment-junction (IAJ) placed 1 to 2 mm
below socket crest
PLACEMENT CASES VERSUS DELAYED
IMPLANT PLACEMENT
The placement of implants in extraction sites has proven to
be a successful and predictable procedure.22-25 When compared
with delayed implant placement, studies have shown that
there is no difference in the success rates. Failures when
placing implants in immediate extraction sites seem to be
related to the presence of periodontitis as the reason for the
extraction procedure.25
 CHAPTER 33 • Implant Placement Immediately Following Tooth Extraction 545

CASE REPORT 33-1

A B C

D E

FIGURE 33-6. A, Preextraction view of tooth #7. B, Atraumatic extraction of tooth #7. C, View of extraction socket
with all walls intact. D, Implant in place. E, Implant crown.

CASE REPORT 33-2

A B C

D E

FIGURE 33-7. A, Fractured crown of tooth #9. B, Atraumatic extraction of tooth #9. C, Extraction socket. D, Implant
in place in preparation for provisional restoration. E, Provisional restoration on #9.
546 SECTION IV ■ Implant Surgery
REFERENCES
1. Albrektsson T, Jansson T, Lekholm U: Osseointegrated dental
implants, Dent Clin North Am 30(1):151-174, 1986.
2. Albrektsson T et al.: Osseointegrated titanium implants. Require-
ments for ensuring a long-lasting direct bone-to-implant anchor-
age in man, Acta Orthop Scand 52:155-170, 1981.
3. Brånemark et al.: Osseointegrated implants in the treatment of
edentulous jaw. Experience from a 10-year period, Scand J Plast
Reconstr Surg 16(suppl)16:1-132, 1977.
4. Wilson TG Jr: Guided tissue regeneration around dental implants
in immediate and recent extraction sites: initial observations, Int
J Periodontics Restorative Dent 12(3):185-193, 1992.
5. Atwood DA: Reduction of residual ridges in the partially eden-
tulous patient, Dent Clin North Am 17(4):747-754, 1973.
7. Chen ST, Wilson TG, Hammerle CH: Immediate or early place-
ment of implants following tooth extraction: review of biologic
basis, clinical procedures, and outcomes, Int J Oral Maxillofac
Implants 19:12-25, 2004.
8. Camargo PM, Lekovic V, Weinlaender M: Influence of bioactive
glass on changes I alveolar process dimensions after exodontias,
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 90(5):581-586,
2000.
9. Lekovic V, Camargo PM, Klokkevold PR: Preservation of alveo-
lar bone in extraction sockets using bioabsorbable membranes,
J Periodontol 69(9):1044-1049, 1998.
10. Schropp L, Wenzel A, Kostopoulos L: Bone healing and soft-
tissue contour changes following single-tooth extraction: a clini-
cal and radiographic 12-month prospective study, Int J Periodontics
Restorative Dent 23(4):313-323, 2003.
11. Araujo MG, Lindhe J: Dimensional ridge alterations following
tooth extraction. An experimental study in the dog, J Clin Peri-
odontol 32(2):212-218, 2005.
12. Block MS: Color atlas of dental implant surgery, ed 2, Philadelphia,
2007, Saunders Elsevier.
13. Caplanis N, Lozada JL, Kan JYK: Extraction defect assessment,
classification and management, J Calif Dent Assoc 3(11):853-
856, 2005.
14. Goldman HM, Cohen DW: The infrabony pocket. Classifica-
tion and treatment, J Periodontol 29:272, 1958.
15. Garber DA, Salama MA, Salama H: Immediate total tooth
replacement. Compend Continuing Education Dent ee 22(3):210-
216, 218, 2001.
16. Paolantonia M, Dolci M, Scarano A: Immediate implantation
in fresh extraction sockets. A controlled clinical and histological
study in man, J Periodontol 72:1560-1571, 2001.
17. Wagenberf G, Froum SJ: A retrospective study of 1925 consecu-
tively placed immediate implants from 1988 to 2004, Int J Oral
Maxillofac Implants 21:71-80, 2006.
18. Ingber JS, Rose LF, Coslet JG: The “biologic width”-a concept
in periodontics and restorative dentistry, Alpha Omegan 70:62-
65, 1977.
19. Saadoun AP, Le Gall MG: Periodontal implications in implant
treatment for anesthetic results, Pract Periodontics Aesthet Dent
10:655-664, 1998.
20. Tarnow D et al.: Vertical distance from the crest of bone to the
height of the interproximal papilla between adjacent implants,
J Periodontol 74:1785-1788, 2003.
21. Tarnow DP, Cho SC, Wallace SS: The effect of interimplant
distance on the height of the interimplant bone crest, J Periodon-
tol 71:546-549, 2000.
22. Lazzara RJ: Immediate implant placement into extraction sites:
surgical and restorative advantages, Int J Periodontics Restorative
Dent 9:332-343, 1989.
23. Block MS, Kent JN: Placement of endosseous implants into
tooth extraction sites, J Oral Maxillofac Surg 49:1269-1276,
1991.
24. Rosenquist B, Grenthe B: Immediate placement of implants into
extraction sockets: implant survival, Int J Oral Maxillofac Implants
11:205-209, 1996.
25. Polizzi G et al.: Immediate and delayed implant placement into
extraction sockets: a 5-year report. Clin Implant Dent Relat Res
2:93-99, 2000.

RADIOGRAPHY FOR DENTAL IMPLANTOLOGY
Jerry L. Soderstrom • Joseph P. Mulligan • James Ward
Ever since the first dental radiographic image was introduced
in the early 1900s, the technology of dental radiology has
expanded rapidly. Radiation dosage to patients has been mini-
mized, and the various types of radiographic imaging used by
dentists have expanded. Since the advent of dental implantol-
ogy, radiographic evaluation of potential implant sites has
changed as radiographic technology advances.
Radiographic evaluation, as in all aspects in radiology, is
an important adjunct to a thorough physical exam. It is impor-
tant to remember that even with the current use of three-
dimensional reconstructions for implant treatment planning,
the practitioner should not dismiss the importance of the
physical examination. Visual inspection and palpation of the
potential implant site should provide initial clues to ridge
characteristics and bone width. The overlying gingival and
dental health of the patient should be ascertained during the
history and physical exam.
With success rates of dental implants exceeding 90%, the
use of dental implants is becoming the treatment of choice for
restoration of edentulous areas.1-6 Endosteal implants have
been shown to be effective in restoring single teeth and eden-
tulous areas in addition to restoration of the maxillary and
mandibular edentulous arches.7,8 All therapeutic restoration
options should be explored and discussed with the patient.
Once the decision is made to restore with dental implants, the
selection of an appropriate radiographic modality should be
determined based on the relevant anatomy of the area to be
restored.9-14 The various modalities for radiographic evalua-
tion including their advantages and disadvantages will be
discussed.
■ RADIOGRAPHIC PRINCIPLES FOR
IMPLANTOLOGY
Patients evaluated for dental implants usually require one
or a combination of all available radiography used in the
field of dentistry. Previously, patients were evaluated using
panoramic, intraoral, and cephalometric techniques or tomog-
raphy. These techniques possess an inherent distortion based
on either magnification or patient positioning. A recent
increase has been noted in the use of conventional and com-
puted tomography for implant evaluation. Software systems
have been designed for these methods specific to implant
placement.15-18
In the selection of radiographs for implant evaluation, the
practitioner should abide by the basic principles of radiogra-
CHAPTER 34
phy. First, an adequate number of images should be taken to
provide all necessary anatomic information. In implantology,
this includes the amount and type of bone, which requires
multiple images at perpendicular angles. Second, the imaging
technique chosen should be precise and dimensionally accu-
rate. Patient positioning should be standardized to allow com-
parison of preoperative and postoperative images. Third, the
location of the images should be reproducible in the patient’s
anatomy. This is usually accomplished via radiopaque markers
or stents in edentulous regions or via the existing dentition
(Figure 34-1). Fourth, the chosen techniques should minimize
distortion, whether positional or related to artifacts on the
imaging surface. Lastly, the radiation dosage and cost to the
patient should be minimized. If more than one assessment
system can be used with minimal disparity in diagnostic infor-
mation, the ALARA (as low as reasonably achievable) prin-
ciple should preside. This refers to minimizing the patient’s
exposure to the radiation necessary to obtain an adequate
radiographic assessment.
The use of radiography for dental implants is primarily
focused on obtaining pertinent diagnostic information related
to their placement. Several criteria for placement of implants
are based on information obtained during various radiographic
techniques. Ideally, the radiographic technique used should
be able to identify several critical factors about the implant
site. The presence of disease, such as cysts, periapical lesions,
and intraosseous pathologic conditions, should be easily iden-
tified (Figure 34-2). The location of critical anatomic struc-
tures and their relationship to the alveolus should also be
easily identified and their distances accurately measured
(Figures 34-3 through 34-7). Osseous morphology, such as
knife-edge ridges, location of the submandibular fossa, ana-
tomic variations, abnormal marrow spaces, and cortical thick-
ness, should be easily visualized. The type, orientation, and
amount of available bone and its orientation are crucial in
treatment planning for implant location.
The bone quality has been assessed in using several systems.
One of the most widely recognized is the system proposed by
Lekholm and Zarb.19 In this system, bone is classified into four
classifications based on the relative amounts of cortical and
trabecular bone. In the first classification, almost the entirety
of bone is composed of compact cortical bone. In the second
classification, compact trabecular bone is surrounded by a
thick layer of cortical bone. The third classification is described
as a thin layer of cortical bone encompassing high density
547
548 SECTION IV ■ Implant Surgery

FIGURE 34-1. Radiopaque marker used for determining implant size.

FIGURE 34-2. Periapical radiolucency seen on orthopantomogram. FIGURE 34-4. Inferior alveolar nerve position.

FIGURE 34-5. Inferior alveolar nerve position.

FIGURE 34-3. Nasal floor.

trabecular bone with favorable strength properties. Finally, in
the fourth and least desirable bone type, a thin layer of compact
bone surrounds loosely arranged trabecular bone.
To identify the bone type, cross-sectional imaging is neces-
sary. In 1996, Lindh et al.20 proposed a system of identifying
bone quality based on periapical radiographs. This system
describes the bone quality by identifying and categorizing the
trabeculation of the bone on periapical radiographs and is
reserved for medullary bone only. The bone is described as
having dense, sparse, or alternating dense and sparse orbicular
regions. Although this technique does not require cross-
sectional imaging, it is less specific in its categorization.
 CHAPTER 34 •
FIGURE 34-6. Maxillary sinus.
FIGURE 34-7. Maxillary sinus.
■ PLAIN FILMS (PERIAPICAL,
OCCLUSAL, AND
CEPHALOMETRIC EVALUATION)
Intraoral radiographs, such as periapical and occlusal radio-
graphs, reproduce detailed anatomy of the proposed implant
site (Figures 34-8 and 34-9). Trabecular patterns and relation-
ships to anatomic structures, such as adjacent roots, can be
accurately reproduced. Low cost, ease of availability, high
resolution, and patient acceptance make periapical and occlu-
sal radiographs a good choice for initial evaluation. However,
image reproducibility is rarely precise, and these images lack
any cross-sectional data, often vital in implant treatment
planning (Figure 34-10). Despite these drawbacks, periapical
radiographs continue to be used postoperatively to monitor
crestal bone height changes.
Cephalometric evaluation, either lateral or anterior-
posterior evaluations, can be useful in treatment planning for
implants.21-23 These images can provide angulations, bone
height and thickness, and soft tissue profiles (Figures 34-11
and 34-12). They also offer skeletal jaw relationships and the
relation of the maxilla and mandible. A lateral cephalogram
in particular is often crucial in determining whether or not an
Radiography for Dental Implantology 549
FIGURE 34-8. Preoperative periapical films showing adequate reproduc-
tion of trabecular pattern and relevant anatomy.
FIGURE 34-9. Postoperative periapical films showing adequate repro-
duction of trabecular pattern and relevant anatomy.
edentulous patient can be reconstructed with dental implants.
Orthognathic surgery may be recommended before implant
reconstruction to relieve the increased occlusal forces often
present when restoring patients without a Class I jaw relation-
ship.24 Several disadvantages dominate cephalometric films.
First, only the anterior mandible is visible in cross-sectioning
(Figures 34-13 and 34-14). In both the anterior and lateral
views, a majority of the maxilla and mandibular dentition and
osseous structures overlap, producing distortion and inaccu-
racy of measurement (Figure 34-15). Patient positioning is
also difficult to reproduce for purposes of comparison.
■ DIGITAL RADIOGRAPHY
With the advent of digital radiography, it is now possible to
assess implant sites preoperatively and postoperatively with
550 SECTION IV ■ Implant Surgery
FIGURE 34-10. Occlusal radiograph shows maxillary bony defect.
FIGURE 34-11. Lateral cephalogram of a dentate and edentulous
patient.
digital imaging. Studies have shown that digital imaging is as
accurate as plain film radiography in its assessment for bone
levels and distances from anatomic structures.25,26 The transfer
of these digital images to paper or analog film does not affect
the accuracy of the assessment (Figure 34-16).25 Software pro-
grams for periapical and occlusal digital images allow for the
manipulation of the images to show greater anatomic detail
in some cases (Figure 34-17). The technique for digital imaging
of implant sites does not differ significantly from that of plain
film intraoral radiographs, although the radiation dosage
FIGURE 34-12. Lateral cephalogram of a dentate and edentulous
patient.
FIGURE 34-13. Anterior mandible in cross-section on lateral
cephalogram.
is reduced by 75% to 90% with digital radiographic
techniques.27-29
Proposed advantages of digital radiography when compared
with traditional plain film techniques are based on the
increased speed and elimination of developing x-rays.30 Soft-
ware systems for digital radiographic images allow for pseudo–
three-dimensional evaluation, alteration in color, contrast,
and image rotation. Linear measurements may also be made
on the computerized image. These features, although useful,
do not eliminate the inherent variance in patient positioning
and lack of cross-sectional data. The disadvantages of tradi-
tional film radiographs, which would require supplemental
imaging, are still present with digital imaging.
 CHAPTER 34 •
FIGURE 34-14. Anterior mandible in cross-section on lateral
cephalogram.
FIGURE 34-15. Anterior-posterior cephalogram. Although useful in
determining transverse jaw relationships, inherent distortion of the implant
placement sites is evident.
■ SUBTRACTION RADIOGRAPHY
Subtraction evaluation of implant placement uses two radio-
graphic images and a digital computerized assessment of
changes between them. It allows for definitive evaluation of
postoperative bone loss or gain over time. Radiographic
density changes in the periimplant bone matrix may also be
visualized. The immediate postoperative radiograph is used to
compare bone heights over follow-up visits. The subtraction
technique may also be useful in visualizing early vertical and
periimplant bone loss. Currently, this technique is not widely
used because of high implant success rates, operator prefer-
Radiography for Dental Implantology 551
FIGURE 34-16. Digital periapical radiograph of the anterior mandible.
FIGURE 34-17. Image manipulation of digital periapical film.
ence, and cost-effectiveness. Mechanical techniques to assess
osseointegration combined with standard postoperative radio-
graphic examination continue to be the standard of care.
■ ORTHOPANTOMOGRAM
Panoramic evaluation is part of the current standard of care
for implant site evaluation and follow-up assessment.21,31
Advantages of panoramic films include visualization of all
anatomic structures of the maxilla and mandible, low cost to
the patient, and availability to the practitioner (Figures 34-18
through 34-22). Disadvantages include variance in magnifica-
tion in the horizontal plane, positioning artifacts, and lack
of cross-sectional imaging. Projection geometry also causes
lingual structures to be oriented superior to structures of facial
position distorting their relationship in the vertical plane.32
Vertical magnification on panoramic images is usually uniform
552 SECTION IV ■ Implant Surgery

FIGURE 34-18. Pre-operative panoramic images of a patient with mul- FIGURE 34-22. Postoperative panoramic evaluation including final
tiple implant placement. restoration.

and is able to be assessed and accommodated via markers of

FIGURE 34-19. Post-operative panoramic images of a patient with mul-
tiple implant placement.
known length placed at the time of radiographic imaging (see
Figure 34-1).23 Horizontal plane magnification, however,
varies widely based on the location in the dental arch, dis-
tance and position related to the focal trough, and patient
positioning. Some panoramic machines are able to produce
cross-sectional imaging via curved layer tomography. This
mechanism usually produces thicker image layering, lower
detail, and increased distortion when compared with linear or
conventional tomography. Despite these disadvantages, the
information obtained in this manner is adequate in many
cases,33 but may not be useful in areas of decreased bone quan-
tity (Figure 34-23). In these instances, the cross-sectional
imaging is more critical for assessment of the implant site.34

FIGURE 34-20. Pre-operative panoramic evaluation.
FIGURE 34-21. Postoperative panoramic evaluation.
■ LINEAR TOMOGRAPHY
Linear tomography may be used when evaluating implant sites
for the assessment of the area in cross-section. In regions of
the mandible and maxilla where proximity to anatomic struc-
tures may dictate implant size and placement, such as the
regions of the inferior alveolar nerve, maxillary sinus, and
nasal fossa concavity, this cross-sectional information is
important in appropriate treatment planning. Linear tomog-
raphy uses coordinated film and x-ray beam movement to
create thin slices of the desired area to be viewed. Advantages
of conventional tomography include moderate expense,
uniform magnification, cross-sectional imagery, and reproduc-
ibility when used with a positioning device. Several devices
are available for reproducible patient positioning, such as the
cephalostat, laser positioning system, and plastic positioning
devices. Disadvantages of these systems include limited avail-
ability, increased time for image production when compared
with panoramic imaging, and difficulty in image interpreta-
tion when not combined with a software program. Some form
of radiopaque marker is necessary for relating the cross-
sectional image to patient anatomy.35,36 Tomographic abilities
are currently being added to commercially available pan-
oramic machines.

■ COMPUTED TOMOGRAPHY
The start of three-dimensional imaging was in 1917 when
the Austrian J. H. Radon proved that the image of a three-
 CHAPTER 34 • Radiography for Dental Implantology 553

FIGURE 34-23. Inadequate mandibular ridge height seen

on panorex image.

dimensional object could be calculated from an infinite

number of two-dimensional projections called back projec-
tion. Sir Godfrey Hounsfield conceived the first primitive
computed tomography (CT) scanner in 1948, but the concept
failed as a result of mathematic calculations that were too
taxing for the technology of that time frame. The attenuation
coefficient of a slice of an object from a series of projections
was first computed by Allen M. Cormack in the Journal of
Applied Physics in 1964. Hounsfield first described the original
CT scanner manufactured by the British engineering and
recording firm EMI in 1972. Hounsfield and Cormack shared
the Nobel Prize for medicine for these developments.37
The original EMI CT scanner was designed to make cross-
sectional images of the brain. There were two detectors and a
tube that moved parallel from side to side across a specialized
hollow round mounting bracket called a gantry. The tube and
detectors rotated 1° and traversed again for 180°. Maximum FIGURE 34-24. Axial view of reformatted CT scan demonstrating exces-
sive streak artifacts due to acquiring data in coronal plane rather than axial
resolution of the initial scans was 1 cm.37 Calculations created
plane.
an image of 80 rows of 80 picture elements called pixels. The
original CT scanners were named computerized axial tomog-
raphy (CAT) scanners because they were designed to acquire
images in the axial plane with the patient in a dorsal position CT scans, especially in areas of arch curvatures, such as the
on the table. The host computer calculated algorithms that canines.39
could produce image data in the coronal and sagittal planes. Major improvements in axially acquired CT scans have
Coronal CT scans were first described in 1978. These scans expanded the capabilities beyond evaluation of cross-sectional
were used to view the sinuses and orbits. They can be acquired images of the brain at a resolution of 1 cm. CT scanners
on a CT scanner by tilting the gantry maximally to a negative evolved to a 360° rotation of the detector and tube and a
30° and having the patient lay prone with the neck hyperex- decrease in the maximum resolution to 2 mm by 1984.
tended. Coronal CT scans have a disadvantage for dentistry, Dynamic scanning was introduced and allowed for acquisition
especially when metallic restorations are present. Scatter is of a set of data and mathematic calculations to be completed
produced that creates extreme streak artifacts throughout the at the end of the scan, cutting down significantly on the time
scan38 (Figure 34-24). Three-dimensional calculations that the patient spent on the scanner table. Helical or spiral scan-
will be further described later in the chapter are meaningless ning was the next development that allowed for the mathe-
with gantry positions other than 0°. This is due to the fact matic calculations to be completed as the scan was aquired.40
that voxels are rectangular in CT scanners. Cone beam tech- The Elsinct Twin Flash was the first axial CT scanner that
nology, which also will be described later in the chapter, is had multiple tubes and multiple detectors. It was introduced
based on perfectly cubic voxels and does not have this disad- in 1990. Other manufacturers followed, and presently, full
vantage in three-dimensional calculations. Height measure- body CT scanners are in use at most major hospitals and scan
ments of the dental alveolar ridge are exaggerated in coronal centers that allow for acquisition of 64 axial images on each
554 SECTION IV ■ Implant Surgery
subsecond spin of the gantry. Maximum resolution for high-
contrast tissues such as bone is 0.25 mm or less. Scan time has
been dramatically reduced, and issues in the 1980s, such as
control of patient motion for three-dimensional modeling,
have become much less significant.
Accuracy in determination of the position of anatomic
structures, such as the position of the inferior alveolar neuro-
vascular bundle, is much improved in axial CT scans com-
pared with dental periapical radiographs. This is a major
improvement in treatment planning for dental implants, par-
ticularly in posterior areas. The inferior alveolar nerve cannot
be identified 25% of the time in periapical radiographs. Mea-
surements on periapical dental films are within 1 mm of the
actual distance to the inferior alveolar canal only 53% of the
time. Measurements from CT scans of distances to the inferior
alveolar canal are within 1 mm 94% of the time.41
The result of developments that have greatly increased
sophistication of CT scanners in the hospital setting have
made available used axial CT scanners with helical or spiral
technology, single second rotations, and dynamic scanning
that allow for 1-minute scans of the mandible and maxilla.
Expensive service contracts necessary in the hospital environ-
ment are not necessary in a dental office because the number
of scans and the elective nature of dental applications are less
critical than the emergency applications of the CT scanner in
the hospital. Mobile services are widely available for CT scan-
ning. The present situation makes medical-grade full body CT
scanners a luxury that is within the grasp of the dental clini-
cian. This author has a 6-year experience with mobile or in-
house full body CT scanners that has opened up an entirely
new level of diagnostic service for the dental patient.
Cone beam technology has been used to produce three-
dimensional scanners that have been adapted to dental appli-
cations. The first commercially available cone beam scanner
in the United States was the New Tom 9000, marketed by
Aperio. Other manufacturers have marketed cone beam scan-
ners over the past several years, including Hitachi, iCAT, and
others. The footprint or clinical area needed for these scanners
is much less than for a CAT scanner. Electrical requirements
are also much less. Cone beam scanners are becoming more
common in dental clinics and dental school settings.
Images are acquired in cone beam scanners as the tube and
detectors rotate around the patient. An image is taken every
degree for 360° in some such as the New Tom 3G or one image
every 2° in the iCAT. Scatter from metallic restorations and
tissue is present throughout each image. Scatter from metallic
restorations in axial CT scans is limited to slices in the area
of the occlusal plane when the central beam is positioned
parallel to the occlusal plane. Scatter from dental restorations
is managed by proprietary filters and software in cone beam
scanners. Contrast resolution tends to be less in cone beam
scans compared with axial CT scans depending somewhat on
the number and size of metallic restorations of the patient.
Parameters of the scans are preset in cone beam scanners. Kv
and Ma settings are lower than in medical CT scanners, and
radiation exposure levels to the patient are generally less
depending on the specific cone beam scanner and parameter
selected. Three-dimensional calculations are based upon cubic
voxels, making control of the direction of the beam not criti-
cal as with axial CT scanning.
Three-dimensional modeling becomes more challenging
from cone beam scans, especially on patients with multiple
metallic restorations as a result of scatter from restorations and
tissue, low Kv and Ma settings, the plane of acquisition of the
data, and with certain cone beam scanners the lack of a rela-
tionship between the gray scale and bone density or Houns-
field units. A Hounsfield unit is a measure of the attenuation
of a biologic object to a given dose of radiation. Bone is +1000,
air is −1000, and water is 0. The Hounsfield unit is named
after Sir Godfrey Hounsfield. Another name for a Hounsfield
unit is CT number.37
The first applications of CT scans to dental implants were
in 1984 with CNC technology applied to subperiosteal
implants. Truitt and James at Loma Linda University devel-
oped the first plaster models from CT scans.38,42 Golec of
Escondido, California, first promoted widespread application
of CNC using epoxy models of wax carvings using five plane
CNC.43 There was no direct connection of the electronic data
to the final model, causing some inherent inaccuracies. Under-
cut areas were difficult to develop in early models using these
techniques. The resolution of the CT scanners of the time,
the lack of dynamic scanning and slip ring technology, and
the limitation of mathematic ability of computers were factors
that affected accuracy of the technique. Patient motion could
be difficult to control because of time. Limitation of patient
motion by application of thermoplastic masks used in oncol-
ogy to direct radiation to reproducible areas and to take
sequential CT scans was proposed by Soderstrom (Figure
34-25).
Electronic data from axial CT scans were imported into a
rapid prototyping program, such as Mimics. Virtual three-
dimensional images were created by selection of the desired
range of bone densities using Hounsfield units in a process
called thresholding, and scatter was erased from each axial
FIGURE 34-25. Thermoplastic mask in place on extraoral jig with patient
on therapy board to acquire axial CT scan.
 CHAPTER 34 • Radiography for Dental Implantology 555

FIGURE 34-26. Right lateral view of virtual mandible with motion analyz-
ing rods from Mimics demonstrating lack of motion.
FIGURE 34-28. Right lateral virtual mandible with motion analyzing rods
from Mimics demonstrating unacceptable motion.

FIGURE 34-27. Anterior-posterior view of virtual mandible with motion

analyzing rods from Mimics demonstrating lack of motion.
FIGURE 34-29. Anterior-posterior view of virtual mandible with motion
analyzing rods from Mimics demonstrating unacceptable motion.
image by segmentation. These changes were automatically
included in the sagittal and coronal views, and a virtual three-
dimensional model was calculated. Glass motion analyzing
rods were taped to the outside of the thermoplastic mask to
help in identification of patient motion during acquisition of
the axial CT scan. A right lateral virtual three-dimensional
image is shown in Figure 34-26, and an anterior-posterior
virtual image is shown in Figure 34-27. These images are
examples of an axial CT scan acquired with a lack of patient
motion. Patient motion can be a primary reason to reject an
axial CT scan for use in rapid prototyping for construction of
subperiosteal implants. An example of unacceptable motion
diagnosed from a virtual three-dimensional model can be seen
in the right lateral view (Figure 34-28) and in the anterior-
posterior view in Figure 34-29. Implants constructed from
rapid prototype models with motion will not fit and require
modification of the patient’s bone, grafting, or a remake using FIGURE 34-30. Left lateral posterior of custom cast hydroxyapitite
a direct bone impression.38,44 coated Grade 5 titanium alloy implant seated on mandible.
Improvements in CT technology, such as dynamic scan-
ning, slip ring technology, and multirow, multislice scanning,
have helped to greatly decrease scan time from 20 to 30 effects of the CNC techniques, resulting in extremely predict-
minutes in the mid-1980s to less than 10 seconds with modern able fits of complex three-dimensional structures to bone. A
axial CT scanners. Techniques in rapid prototyping have like- typical adaptation of a subperiosteal implant framework is
wise improved with the use of stereolithography and three- shown in Figure 34-30. Note that the bone screw site has not
dimensional printing. A direct connection of the electronic been used because of the excellent fit of the implant into
data to the rapid prototype model is used with both stereo- undercut areas between the area inferior to the external
lithography and three-dimensional printing. This improves oblique ridges bilaterally, bone lateral to the genial tubercles
accuracy, development of undercut areas, and stair-stepping bilaterally, and the mandibular symphysis, resulting in a snap
556 SECTION IV ■ Implant Surgery

FIGURE 34-32. Reformatted CT scan cross sectional paraxial oblique

view demonstrating atrophic bone loss area number 7.
FIGURE 34-31. Three-dimensional printed model from CT scan of maxilla
demonstrating atrophic bone loss in area number 7.

fit to the hydroxyapatite plasma spray–coated cast ASTM F-

136 Eli Titanium/Aluminum/Vanadium implant. Soderstrom
has demonstrated a series of 74 consecutively placed mandibu-
lar bilateral subperiosteal implants made of both hydroxyapa-
tite (HA)-coated ASTM F-136 Eli and ASTM F-75 Cobalt
Chrome Molybdenum made from both axial CT scan and
cone beam scan data over the past 18 years with an implant
survival of 100%. Martin has a similar series of HA-coated
ASTM F-75 bilateral mandibular subperiosteal implants from
axial CT scans over the past 20 years with a 100% survival.
Other long-term evaluations on mandibular subperiosteal
implants have been done with both direct bone impression
techniques and rapid prototype models using CNC.43,45,46,47 FIGURE 34-33. Alloplastic irradiated block secured with two bone
Additional applications of three-dimensional modeling screws area number 7. To view a color version of this illustration, refer to
the color insert section at the back of this book.
related to dental implants using Dicom data from either axial
CT scanners or cone beam scanners include treatment plan-
ning and shaping of bone grafts, treatment planning of root
form implants, construction of bone and tooth or soft tissue–
supported surgical drill guides, and treatment planning of
sinus augmentations.
Treatment planning, shaping, and construction of bone
grafts may be done with three-dimensional models. A rapid
prototype model from an axial CT scan produced with three-
dimensional printing is shown in Figure 34-31. This model
was covered with sterile foil and used to shape a block of
irradiated bone. The sculpted bone block was used to restore
width and height in the atrophic recipient site, shown in the
cross-sectional paraxial oblique view in Figure 34-32. The
irradiated block shaped from the three-dimensional printed
model is shown secured to the recipient site with two bone
screws in Figure 34-33. The implant placed with the restor-
ative abutment is shown in Figure 34-34.
A second example of the use of rapid prototyping to treat-
A B
ment plan for and construct bone augmentation is shown with
the Porex eposteal implant positioned on the stereolitho- FIGURE 34-34. A, B, Digital periapical radiographic image of Quantum
graphic model (Figure 34-35). A second copy of the Porex implant placement number 7 and four month post operative digital periapical
implant was successfully used to replace a left zygomatic arch radiograph with Quantum Morse taper abutment for cement retained fixed
and infraorbital rim on a 35-year-old male patient subsequent prosthetics in place.
 CHAPTER 34 •
FIGURE 34-35. Porex eposteal implant copy replacing infraorbital rim
and zygomatic arch in place on stereolithography model.
FIGURE 34-36. Porex eposteal implant copy on three-dimensional
printed model same case as in Figure 34-27.
to a motor vehicle accident and a failed vascularized scapula
graft. Mirroring of the right intact zygomatic arch and infra-
orbital rim facilitated construction of this implant. The Porex
implant is shown again in Figure 34-36 in place on a three-
dimensional printed model made from the original Dicom
data 5 years later.
The first electronic reformatting software program that
extensively used virtual three-dimensional models was Surgi-
Case. This software program imported stl files created in
another software program, Mimics. SurgiCase has now been
combined with the first software program, SimPlant, to use
Virtual Implant Placement (VIP) in electronically reformat-
ted CT scan data. The newer versions of SimPlant support
creation of virtual three-dimensional models and implant
placement into the reformatted images. Construction of
virtual three-dimensional models is the final step in electronic
reformatting of axial CT scan and cone beam scan Dicom
data.
SimPlant and other electronic reformatting programs of
this nature, such as VIP and the Procera system, are all of great
value in treatment planning, placement, and restoration of
endosteal implants. SimPlant Master will be described because
it is the program for which the authors have the greatest
Radiography for Dental Implantology 557
FIGURE 34-37. CT scan dicom data seen as initially imported into
SimPlant Master.
FIGURE 34-38. Profile line drawn for thresholding of CT scan images
seen in Figure 34-29.
experience. Dicom data archived on compact discs or optical
discs from axial CT scanners or cone beam scanners are first
imported into the electronic reformatting program. The data
will first appear as images in the axial, sagittal, and coronal
planes as in Figure 34-37, which were imported from a compact
disc of Dicom data obtained on an iCAT cone beam scan. A
profile line is drawn across an axial view, and a value of bone
density desired in the virtual three-dimensional model is
selected in Hounsfield units (Figure 34-38). Because the exter-
nal dimensions of cortical bone are necessary for construction
of the virtual three-dimensional model, values from 450 to
3000 Hounsfield units could be selected. This would eliminate
those Hounsfield values or numbers for bone of poor density
and for soft tissues. Dicom data imported from an axial CT
scan would be manipulated in a similar manner. This process
is called thresholding.
Streak artifacts from metallic restorations would be elimi-
nated from the remaining data saved by the thresholding
process by erasing, which is part of the segmentation process.
558 SECTION IV ■ Implant Surgery
FIGURE 34-39. Segmentation to erase streak artifacts from fillings in
CT scan images. To view a color version of this illustration, refer to the
color insert section at the back of this book.
FIGURE 34-40. Purple mask of maxilla used to region grow selected
bone threshold levels in each of the CT scan data slices in Mimics. To view
a color version of this illustration, refer to the color insert section at the
back of this book.
Erasing of streak artifacts is completed each axial slice. Erasing
is shown in (Figure 34-39). The color of the data has been
changed to green from the gray scale in the thresholding
process to create a mask. The mask contains only the data with
Hounsfield units or CT numbers selected from 450 to 3000.
When Dicom data from an axial CT or iCAT cone beam are
subject to segmentation, it is only necessary to complete the
process in each axial slice, and the sagittal and coronal planes
are automatically altered by the software. Dicom data acquired
on a cone beam scanner that is not based on Hounsfield units,
such as the New Tom 9000, require that segmentation be
completed in each axial, sagittal, and coronal slice for each of
360° or a total of 1080 adjustments for streak artifacts from
metallic restorations in the three-dimensional modeling
process. A second mask is constructed after segmentation, a
combination of erasing, drawing, or thresholding back the
original 450 to 3000 Hounsfield units in each axial slice. This
mask is created by region growing the thresholded data of 450
to 3000 Hounsfield units of the segmented axial slices. The
new mask is shown in Figure 34-40 and is colored purple. The
FIGURE 34-41. Virtual three dimensional model of maxilla in SimPlant
Master made from CT scan data. To view a color version of this illustration,
refer to the color insert section at the back of this book.
FIGURE 34-42. Virtual three-dimensional models of maxilla, mandible,
and teeth in SimPlant Master from CT scan data. To view a color version of
this illustration, refer to the color insert section at the back of this book.
virtual three-dimensional model shown in Figure 34-41 was
calculated based upon the purple mask and is colored blue.
Similar masks were made of the mandible in yellow and the
maxillary teeth in red in Figure 34-42. The shape and dimen-
sions of the available mandibular and maxillary bone and the
relationship of the arches and the prosthetic tooth position are
easily seen in the virtual three-dimensional models.
Segmentation can be used to draw supports between the
maxilla mask and mandible mask and the maxilla mask and
denture tooth mask. Region growing is then used to make
another mask from which a virtual three-dimensional model
can be calculated. If this process is done in a modeling program
that saves an stl file, such as Mimics, the stl file may be rapidly
prototyped by CNC, fused-material deposition, stereolithog-
raphy, or three-dimensional printing. This model may be
articulated and used in treatment planning, drill guide con-
struction, or restoration of implants. A three-dimensional
print of a segmented maxilla, mandible, and maxillary denture
teeth is shown in Figure 34-43. This model may be articulated
and the struts created by segmentation cutout. This process
 CHAPTER 34 • Radiography for Dental Implantology 559

FIGURE 34-43. Three-dimensional model of atrophic mandible, maxil-

lary denture teeth, and maxilla segmented and printed to capture vertical
dimension and centric relation.

FIGURE 34-45. Different curve and panoramic slice which shows inferior
alveolar nerve as an oval in same case as Figure 34-36 in SimPlant Master
from CT scan data. To view a color version of this illustration, refer to the
color insert section at the back of this book.

FIGURE 34-44. Nerve draw mandibular right in panoramic slice in

SimPlant Master from CT scan data.

allows for the capture of occlusal relationships and vertical

dimension in the axial CT scan or cone beam scan. Bite reg-
istrations and impressions are eliminated from the diagnostic
process. Soft tissue masks may also be created, if desired, for
complex treatment planning or construction of the final res-
toration, as with the Nobel Biocare system.
After creation of the desired virtual three-dimensional
models in SimPlant, the electronic data are reformatted by
drawing a curve in the selected axial slice as shown in Figure
34-44. For mandibular models, the inferior alveolar nerve may
be drawn using the selected panoramic slice. It may be neces-
sary to toggle between individual panoramic slices and the
drawing in a series of ovals to obtain the entire inferior alveo-
lar neurovascular bundle. SimPlant allows for the panoramic
curve to be altered accommodating this process. The same FIGURE 34-46. Width and height of bone in cross sectional paraxial
oblique view in reformatted CT scan with nerve draw in SimPlant Master. To
reformatted data used to draw the nerve in Figure 34-44 is
view a color version of this illustration, refer to the color insert section at
shown in Figure 34-45 with alteration of the panoramic curve
the back of this book.
to produce an oval-shaped radiolucency, which is the anterior
segment of the inferior alveolar neurovascular bundle. The Once the nerve draw is complete, the next step in the
anatomic course of the inferior alveolar nerve from labial in virtual treatment planning process for endosteal root form
the area of the mental foramen to lingual at the lingula related implants is to measure width and height of available bone and
to the position of the panoramic curve established in the axial evaluate the trajectory of bone as in Figure 34-46. The bone
slice is responsible for the change. A similar electronic refor- density in Hounsfield units and a standard deviation is shown
matting program, VIP, supports nerve draws, but the pan- for medullary bone in Figures 34-47 and 34-48. The position
oramic curve is set and may not be altered during the nerve of the bone density determination has been moved to the
draw process as with SimPlant. In the VIP program, a change lingual cortical plate at the area just superior to the undercut
in the panoramic curve necessitates a restart on the nerve in Figure 34-49. Note that the Hounsfield or CT number has
draw. increased by more than three times, and the standard devia-
560 SECTION IV ■ Implant Surgery
FIGURE 34-47. Bone density of same case in Figure 34-46 in medullary
area in Hounsfield units. To view a color version of this illustration, refer
to the color insert section at the back of this book.
FIGURE 34-48. Bone density of same case in Figure 34-46 in lingual
cortical plate area in Hounsfield units. To view a color version of this illustra-
tion, refer to the color insert section at the back of this book.
tion has increased in cortical bone on the lingual plate in this
particular area.
Next, a virtual root form implant of the operator’s choice
is selected from the library, which contains most major implant
manufacturers. If the implant desired is not there, the operator
may add it to the library. The implant is placed into the
selected cross-sectional paraxial oblique view (Figure 34-50).
The position of the implant may be manipulated as desired.
The abutment may also be selected. Cross-sectional clipping
of the virtual three-dimensional model allows precise visual-
ization of the relationship of the planned implant in position
#19 to the inferior alveolar neurovascular bundle (Figure
34-51). When all implants have been placed and the final
positions defined, the treatment plan is saved, and the opera-
FIGURE 34-49. Virtual implant in position in same case as Figure 34-46
in cross sectional oblique reformatted view. To view a color version of this
illustration, refer to the color insert section at the back of this book.
FIGURE 34-50. Cross sectional clipping of virtual implant number 19
with nerve draw.
tor has the option to create a SurgiGuide that may be used to
transfer the virtual treatment plan to the patient with precise
control of the emergence point and trajectory of the implant.
The same SurgiGuide may be used to place implant body
analogs into actual three-dimensional models. Abutment
work may be completed and temporary restorations with
control of the occlusal relationships fashioned (Figure 34-52).
The SurgiGuides may then be sterilized and used to place the
implants into the same position in the patient.
The maxillary sinuses are of special interest with three-
dimensional treatment planning. Periapical radiographs may
 CHAPTER 34 •
FIGURE 34-51. Implant analogs placed with SurgiGuide, abutments pre-
pared, and acrylic temporaries in place out of occlusion on stereolithography
models.
FIGURE 34-52. Pre-operative digital periapical image of maxillary right
posterior area.
underestimate available bone in these areas. Figure 34-53 is a
digital periapical image taken preoperatively of the right pos-
terior maxillary. Quantum QVS root form implants have been
placed in the postoperative digital periapical image in Figure
34-54. The implants appear to violate the maxillary sinus and
the root of natural tooth #4, which has been treated with
endodontics. A reformatted axial CT scan used in treatment
planning these implants is shown in Figures 34-55 through
34-57. These three cross-sectional paraxial oblique views from
axial CT scan Dicom data reformatted in SimPlant Master
indicate bone available palatal to the right maxillary sinus
inferior wall. The position of the root of the natural maxillary
right second bicuspid is also positioned labial to the planned
implant placement. The implant passes palatal to the apex of
the second bicuspid. Precise control of the emergence point
Radiography for Dental Implantology 561
FIGURE 34-53. Post-operative digital periapical image of Quantum Bio-
engineering root form implants placed areas number 3 and number 4.
FIGURE 34-54. Reformatted CT scan cross sectional paraxial oblique
view of natural tooth number 4.
of the implant and the trajectory of placement can be obtained
for cases such as this with tooth and bone-supported Surgi-
Guide drill guides. Sinus augmentation, which is indicated
with only periapical radiographs, was eliminated from the
treatment plan in this case.
Reformatted CT scans and three-dimensional models are
also useful when maxillary sinus augmentation is indicated.
The reformatted Dicom data from an iCAT cone beam pre-
operative scan of the maxillary left sinus at the center of a
562 SECTION IV ■ Implant Surgery
FIGURE 34-55. Cross sectional paraxial oblique view of virtual implant
placement number 3. To view a color version of this illustration, refer to
the color insert section at the back of this book.
FIGURE 34-56. Cross sectional paraxial oblique view of planned implant
site number 2.
FIGURE 34-57. Reformatted cone beam scan from iCAT used for treat-
ment planning lateral wall maxillary sinus augmentation.
FIGURE 34-58. Photograph of window in lateral wall of maxillary sinus
number 14 area. To view a color version of this illustration, refer to the
color insert section at the back of this book.
FIGURE 34-59. Lateral wall maxillary sinus augmentation area number
14 with graft placed. To view a color version of this illustration, refer to the
color insert section at the back of this book.
missing maxillary left first molar are shown in Figure 34-57.
The outline of the lateral wall approach and instrumentation
used in reflection of the membrane and placement of the graft
was completed in this case using a solid three-dimensional
printed model. Often evaluation of the virtual three-
dimensional model will suffice for this purpose. Photographs
of the lateral wall outline before membrane reflection (Figure
34-58) and placement of the lateral wall sinus augmentation
(Figure 34-59) are demonstrated for this case. A postoperative
iCAT cone beam scan is shown after reformatting in SimPlant
Master (Figure 34-60). Axial clipping is useful in the evalua-
tion of the postoperative fill in three dimensions as shown in
Figure 34-61. A solid fill extending to the palatal wall is dem-
 CHAPTER 34 •
FIGURE 34-60. Reformatted cone beam scan from iCAT demonstrating
adequate fill of lateral wall maxillary sinus augmentation area number 14.
FIGURE 34-61. Axial clipping in reformatted CT scan demonstrating
adequate fill of lateral wall maxillary sinus augmentation area number 3 (a
different but similar case than illustrated in Figures 34-50 through 34-53). To
view a color version of this illustration, refer to the color insert section at
the back of this book.
onstrated in the postoperative cone beam scan. This case is
courtesy of Chad Lewison, D.D.S. of Canton, South Dakota.
Cone beam scans are more practical for postoperative eval-
uation of maxillary sinus augmentations during the procedure
than axial CT scans. A lateral wall maxillary sinus augmenta-
tion that has an incomplete fill on the palatal and mesial walls
is shown in SimPlant Master using axial clipping (Figure
34-62) and cross-sectional clipping (Figure 34-63). Had a
cone beam scan been taken postoperatively at the time of the
augmentation there would be an opportunity to increase the
fill of the augmentation. Compromise in implant position,
trajectory, and length is necessary after healing is complete.
Cone beam scans may also be used to evaluate implant
position at the time of placement. A Quantum QVS 4 mm
diameter by 14 mm length root form implant was treatment
planned for placement in position #29 with an external hex
restoration. Low bone density allowed the implant to inadver-
tently be extended into bone to the full length of placement
for a Morse taper restorative application. Because the preop-
erative iCAT cone beam reformatted image had indicated
Radiography for Dental Implantology 563
FIGURE 34-62. Axial clipping in a reformatted CT scan demonstrating
unfilled palatal area of a lateral wall maxillary sinus augmentation in the maxil-
lary right posterior. To view a color version of this illustration, refer to the
color insert section at the back of this book.
FIGURE 34-63. Cross sectional clipping in reformatted CT scan demon-
strating unfilled palatal area of the same lateral wall maxillary sinus augmenta-
tion illustrated in Figure 34-54. To view a color version of this illustration,
refer to the color insert section at the back of this book.
that the mental nerve may be impinged at the insertion length
of 16 mm, the plan was to use a 12-mm or 13-mm placement
and an external hex abutment. A reformatted iCAT cone
beam scan taken during the implant placement surgery before
closure indicated the apex of the implant to be lingual to the
inferior alveolar neurovascular bundle (Figure 34-64). The
implant was left and the restorative plan changed to the Morse
taper application of the versatile length of the Quantum QVS
implant. Postoperative altered sensation was not noted.
Healing of bone around root form implants and periodic
evaluation of root form implants is generally best done using
periapical radiography rather than cone beam scanning. One
reason for this is the phenomena of “ghosting” of cone beam
scans. This has to do with the large difference in density
between the implant body and the surrounding bone. An
iCAT cone beam scan of implants placed several years previ-
ously into a maxillary lateral wall sinus augmentation indi-
cates dark areas surrounding the implants (Figure 34-65).
564 SECTION IV ■ Implant Surgery
FIGURE 34-64. Cone beam scan from iCAT view of Quantum QVS root
form implant placed lingual to inferior alveolar neurovascular bundle.
FIGURE 34-65. Cone beam scan from iCAT demonstration ghosting of
root form implants in low density bone.
Digital periapical radiographs indicate normal bone height.
Clinically the implants lack mobility, and periodontal probing
is within normal limits with no exudates. Implant failure is
most often seen radiographically by cuffing defects on periapi-
cal radiographs. Defects as a result of “ghosting” surround the
entire implant and do not match findings on conventional
radiographs or clinical findings.
Cone beam and axial CT scans may be useful in determina-
tion of endodontic involvement of natural teeth.50,51 Examples
of periapical radiolucency found coincidentally on a reformat-
ted axial GE Prospeed SX CT scan is shown in Figure 34-66
and on an iCAT cone beam scan in Figure 34-67. The involved
teeth were asymptomatic, and recent periapical radiographs
did not indicate a pathologic condition. Another sign of end-
odontic involvement seen on cone beam and axial CT scans
is illustrated in the appearance of the right maxillary sinus in
the iCAT cone beam scan (Figure 34-68).
Three-dimensional scans open new opportunities for diag-
nosis and treatment planning for implants. With the advent
FIGURE 34-66. Reformatted CT scan cross sectional paraxial oblique
view of natural tooth number 6 with periapical radiolucency not adequately
visible in periapical radiograph.
FIGURE 34-67. View in iCAT software of cone beam scan demonstrating
periapical radiolucencies of endodontic origin on natural teeth numbers 4
and 20.
of cone beam technology and larger and faster microprocess-
ing, three-dimensional scans will become practical for use in
not only the oral and maxillofacial surgery setting, but also
the general dental office.
■ SUMMARY
Several authors have attempted to create an algorithm for
selection of radiographic evaluation of implant sites. Often
these determinations are based on the number of implants
to be placed and their location in the maxillary or mandi-
bular arch. Rather than create a formula for selection of
 CHAPTER 34 •
FIGURE 34-68. Panoramic slice in iCAT software of cone beam scan
demonstrating pathology in the right maxillary sinus associated with natural
tooth number 2.
radiographic technique, an emphasis should be placed on the
practitioner to have adequate knowledge of the anatomic
structures in the areas for implant placement. Initial evalua-
tion of the planned implant site with periapical or panoramic
imaging is appropriate in most cases. Patients with abnormal
dental-skeletal relationships should be evaluated with lateral
cephalometric films. Patients exhibiting physical examination
findings consistent with potential anatomic hazards, such as
knife-edge ridges, lingual mandibular concavity, or short ridge
height, should be evaluated with CT.
With the decreasing cost and increasing availability of CT
technology to the dental practitioner, CT evaluation may be
increasingly used in the placement of multiple implants.
Several companies currently exist that seek to provide practi-
tioners with in-office CT scan capabilities. Although CT scan
technology aids in treatment planning and software programs
have made planning for implant placement nearly foolproof,
the practitioner must keep the patient’s best interest in mind.
Cost-effectiveness and minimal radiation exposure may
warrant the use of CT scan technology for only those patients
at risk for complications during implant placement. All
aspects of implant placement must be incorporated into the
decision.
REFERENCES
1. Adell R et al.: A 15-year study of osseointegrated implants in
the treatment of the edentulous jaw, Int J Oral Surg 10:387-416,
1981.
2. James RA et al.: Subperiosteal implants, Can Dent Assoc J 16:10-
14, 1988.
3. Schnitman PA, Shulman LB, editors: NIH-Harvard consensus
development conference. Dental implants: benefit and risk.
HHS summaries, DHHS (NIH) 81-1531, 1980.
4. Smithloff M, Fritz ME: The use of blade implants in a selected
population of partially edentulous patients: a ten year report, J
Periodontol 53:413-418, 1982.
Radiography for Dental Implantology 565
5. Albrektsson T et al.: The long term efficacy of currently used
dental implants: a review and proposed criteria of success, Int J
Oral Maxillofac Implants 1:11-25, 1986.
6. Branemark PI et al.: Osseointegrated implants in the treatment
of the edentulous jaw. Experience from a 10-year period, Scan J
Plast Reconstr Surg 16(suppl):1-132, 1977.
7. Block MS, Kent JN: Endosseous implants for maxillofacial recon-
struction, Philadelphia, 1995, WB Saunders.
8. Tan KBC: The use of multiplanar reformatted computerized
tomography in the surgical-prosthodontic planning of implant
placement, Ann Acad Med Singapore 24:68, 1995.
9. Kraut RA: Utilization of 3D/dental software for precise implant
site selection: clinical reports, J Implant Dentistry 1(2):134, 1992.
10. Kraut RA: Effective uses of radiographs for implant placements-
panographs, cephalograms, CT scans [Interview], Dent Implantol
Update 4(4):29, 1993.
11. Lima-Verde MAR, Morgano M: A dual-purpose stent for the
implant supported prosthesis, J Prosthet Dent 69:276, 1993.
12. Kraut RA: Interactive radiographic diagnosis and case planning
for implants, Dent Implantol Update 5(7):49, 1994.
13. Basten CHJ: The use of radiopaque templates for predictable
implant placement, Quintessence Int 26:609, 1995.
14. Borrow JW, Smith JP: Stent marker materials for computer
tomograph-assisted implant planning, Int J Periodont Restorative
Dent 16:61, 1996.
15. McGivney GP et al.: A comparison of computer-assisted tomog-
raphy and data-gathering modalities in prosthodontics, Int J Oral
Maxillofac Implants 1:55-68, 1986.
16. Rothman SLG et al.: CT in the preoperative assessment of the
mandible and maxilla for endosseous implant surgery. Work in
progress, Radiology 168:171-175, 1988.
17. Quirynen M et al.: CT scan standard reconstruction technique
for reliable jaw bone volume determination, Int J Oral Maxillofac
Implants 5:384-389, 1990.
18. Abrahams JJ: CT assessment of dental implant planning, Oral
Maxillofac Clin North Am 4:1-18, 1992.
19. Lekholm U, Zarb GA: Patient selection and preparation. In
Branemark PI, Zarb GA, Albrektsson T, editors: Tissue-integrated
prosthesis: osseointegration in clinical dentistry, Chicago, 1985,
Quintessence.
20. Lindh C, Petersson A, Rohlin M: Assessment of the trabecular
pattern before endosseous implant treatment. Diagnostic
outcome of periapical radiography in the mandible, Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 82:335-343, 1996.
21. Strid KG: Radiographic procedures. In Branemark PI, Zarb GA,
Albrektsson T, editors: Tissue-integrated prostheses. Osseointegra-
tion in clinical dentistry, Chicago, 1985, Quintessence.
22. Watson RM et al.: Considerations in design and fabrication of
maxillary implant-supported prostheses, Int J Prosthodont 4:232-
239, 1991.
23. Babbush CA: Evaluation and selection of the endosteal implant
patient. In McKinney RV, editor: Endosteal dental implants,
St Louis, 1991, Mosby Year Book.
24. Babbush CA: Dental implants: the art and science, Philadelphia,
2001, WB Saunders.
25. De Smet E et al.: The accuracy and reliability of radiographic
methods for the assessment of marginal bone level around oral
implants, Dentomaxillofac Radiol 31(3):176-181, 2002.
26. Borg E et al.: Marginal bone level around implants assessed in
digital and film radiographs: in vivo study in the dog, Clin Implant
Dent Relat Res 2(1):10-17, 2000.
27. Wakoh M et al.: Radiation exposures with the RadioVisioGra-
phy-S and conventional intraoral radiographic films, Oral Radiol
(Japan) 10:33, 1994.
28. Scarfe WC et al.: Tissue radiation dosages using the
RadioVisioGraphy-S with and without niobium filtration, Aust
Dent J 42:335, 1997.
566 SECTION IV ■ Implant Surgery
29. Farman AG, Farman TT: RadioVisioGraphy-UI: a sensor to
rival direct exposure intra-oral x-ray film, Int J Comput Dent
2:183, 1999.
30. I.D.T. Seminar, Atlanta, Dec 3-5, 1992.
31. ten Bruggenkate CM, van der Linden LW, Oosterbeek HS: Par-
allelism of implants visualized on the orthopantomogram, Int J
Oral Maxillofac Surg 18:213-215, 1989.
32. Welander U, Tronje G, McDavid WD: Theory of rotational
panoramic radiography. In Langland OE et al, editors: Panoramic
radiology, ed 2, Philadelphia, 1989, Lea & Febiger.
33. Potter BJ et al.: Implant site assessment using panoramic cross-
sectional tomographic imaging, Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 84:436-442, 1997.
34. Tyndall DA, Brooks SA: Selection criteria for dental implant
site imaging: a position paper of the American Academy of Oral
and Maxillofacial Radiology, Oral Surg Oral Med Oral Pathol
89:630-637, 2000.
35. Stella JP, Tharanon W: A precise radiographic method to deter-
mine the location of the inferior alveolar canal in the posterior
edentulous mandible: implications for dental implants. Part 1:
technique, Int J Oral Maxillofac Implants 5:15-22, 1990.
36. Kassebaum DK et al.: Cross-sectional radiography for implant
site assessment, Oral Surg Oral Med Oral Pathol 70:674-678,
1990.
37. Rothman, Steven LG: Computerized tomography, Chicago, 1988,
Quintessence.
38. Boyne PJ, James RA: Advances in subperiosteal implant recon-
struction, Dent Clin North Am 30:259, 1986.
39. Schwarz MS et al.: Computed tomography in dental implanta-
tion surgery, Dent Clin North Am 33:577, 1989.
40. Stoler A: Helical CT scanning for CAD/CAM subperiosteal
implant construction, J Oral Implantol 22:247, 1996.
41. Klinge B, Petersson A, Maly P: Localization of the mandibular
canal: comparison of macroscopic findings, conventional radiog-
raphy, and computed tomography, Int J Oral Maxillofac Implants
4:327-332, 1989.
42. Truitt HP et al.: Use of computer tomography in subperiosteal
implant therapy, J Prosthet Dent 59:474, 1988.
43. Golec TS et al.: CAD-CAM multiplanar diagnostic imaging for
subperiosteal implants, Dent Clin North Am 30:85, 1986.
44. Golec TS, Krauser JT: Long-term retrospective studies on
hydroxyapatite-coated endosteal and subperiosteal implants,
Dent Clin North Am 36:39, 1992.
45. Lozada JL: Long term clinical experience and statistical analysis
of cat scan subperiosteal implants at Loma Linda University, J
Oral Implantol 22:34, 1996.
46. Yanase RT et al.: The mandibular subperiosteal implant denture:
a prospective survival study, J Prosthet Dent 71:369, 1994.
47. Young L, Michel JD, Moore DJ: A twenty-year evaluation of
subperiosteal implants, J Prosthet Dent 49:690, 1983.
48. Bradley JC: Age changes in the vascular supply of the mandible,
Br Dent J 132:142, 1972.
49. Castelli VA, Nasjleti CE, Diaz-Perez R: Interruption of the arte-
rial inferior alveolar flow and its effects on mandibular collateral
circulation and dental tissues, J Dent Res 54:708, 1975.
50. Lofthag-Hansen S et al.: Limited cone beam CT and intraoral
radiography for the diagnosis of periapical pathology, Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 103(1):114-119, 2007,
Epub, 2006.
51. Nakata K et al.: Effectiveness of dental computed tomography
in diagnostic imaging of periradicular lesion of each root
of a multirooted tooth: a case report, J Endod 32(6):583-587,
2006.

MINIIMPLANTS AND TRANSITIONAL IMPLANTS
Talib A. Najjar • Kasey E. Call • Russel S. Bleiler III
A mini dental implant (MDI) has a diameter ranging from 1.8
to 2.4 mm, whereas an implant with a diameter of 2.75 to
3.25 mm is referred to as a small diameter implant (SDI). The
smallest conventional implant measures 3.25 mm.1,2 For the
purposes of this chapter, all implants with a diameter of less
than or equal to 3.25 mm will be referred to as miniimplants.
For comparison, Figure 35-1 shows three Entegra implants of
decreasing diameter and an INTRA-LOCK miniimplant of
2 mm in diameter (Figure 35-1).
Miniimplants were initially used as transitional implants to
support overdentures during phase 1 of conventional implant
placement. The miniimplants were temporarily placed
between conventional implants, allowing them to osseointe-
grate while the miniimplants bore the load of the dentures
(Figure 35-2 A, B); however, when the time arrived to remove
the temporary miniimplant, the practitioner often found it
had integrated with the bone and was difficult to remove.
Balkin reports two cases where miniimplants were used as
transitional implants and later explanted and found to be
osseointegrated when studied under light microscopy.3
Although miniimplants are still used for transitional purposes,
many manufacturers are now approved by the Food and Drug
Administration to market their product for long-term use.
Various modifications and implant head morphologies have
been developed to increase the versatility of the miniimplant.
Current uses now include:
• Prosthodontic applications
• Stabilization of complete dentures
• Stabilization of removable partial dentures (RPDs)
• Pontic support of a fixed partial denture (FPD)
• Retention of obturators
• Single-tooth implant restorations in narrow spaces
• Orthodontic anchorage
■ STABILIZATION OF COMPLETE
DENTURES
Achieving stability of dentures has been a major challenge for
prosthodontists and general dentists when making dental
prostheses for patients with atrophic alveolar ridges. These
patients complain of difficulty talking and eating as a result of
poor retention of their dentures. Miniimplants with an o-ring
attachment may be placed transmucosally beneath an existing
full denture, and the denture may be retrofitted, or a new
denture can be fabricated with o-ring receptors to engage the
implants, affording patients added stability and retention of
CHAPTER 35
their denture (Figure 35-3 A-D). Griffitts conducted a study
in which 100% of subjects who returned a questionnaire 5
months after receiving miniimplants under their existing
denture reported dramatic improvements in comfort, reten-
tion, chewing ability, and speaking ability.4
Miniimplants also contribute to patient satisfaction as a
result of their relatively simple placement and ability to be
immediately loaded after placement. A gingivoperiosteal flap
is not necessary to place a miniimplant. The Imtec website
recommends that the site of placement simply be marked
with ink or with a bleeding point created by the tip of the
pilot bur before making the pilot hole transgingivally.5 Ahn
recommends that the pilot hole only be drilled one-half
the length of the miniimplant, thus allowing the implant to
provide primary mechanical retention immediately after
placement.6 If primary stability is achieved, the miniimplants
may be immediately loaded, allowing the patient to avoid
an awkward edentulous phase, which is sometimes required
while conventional implants osseointegrate.1,7,8 The Imtec
Web page describes the surgical protocol for placing MDI
miniimplants and states that the primary reason for not
achieving adequate primary stability and nonintegration is
overinstrumentation of the bone. If no significant resistance
is encountered while advancing the miniimplant, overinstru-
mentation may have occurred or the bone may lack the
required density, and the prognosis for the miniimplant
reaching its full potential is doubtful.5 If adequate primary
stability is encountered while placing the miniimplant, the
long-term prognosis of the implant after immediate loading
is improved.
Bone density is a major determining factor of the primary
stability and success of miniimplants. The highest success rate
is found in the dense bone of the anterior mandible with lower
rates in the maxilla.6 When placing a miniimplant in very
dense bone, it has been suggested that upon encountering
resistance the implant be unscrewed one-half to one full turn
and then advanced again. This process may need to be repeated
multiple times, but will decrease the risk of implant fracture
during placement. The use of titanium alloy implants rather
than pure titanium may also decrease the risk of implant
fracture during placement.6,9
If you are placing miniimplants for transitional purposes, it
has been suggested that the implant be placed at least 2 mm
from the intended long-term implant to prevent bone
resorption.6,9,10
567
568 SECTION IV ■ Implant Surgery
Miniimplants are an excellent solution to provide stability
to dentures for transitional purposes and for long-term use.
When placed using proper technique, they provide immediate
stability and contribute to patient satisfaction aesthetically,
functionally, and financially.
■ STABILIZATION OF REMOVABLE
PARTIAL DENTURES
Christensen suggests that miniimplants are an excellent way
to improve patient satisfaction for those who wear a remov-
able partial denture. In situations where there are bilateral
distal extensions (Kennedy class I), unilateral distal exten-
sions (Kennedy class II), or an anterior edentulous extension
(Kennedy class IV), a miniimplant may be recommended to
a patient to improve retention and decrease rocking of the
RPD toward the edentulous span.11 Placement of the miniim-
plant in this situation is similar to placement under a full
denture and will require that the denture be retrofitted to
engage the miniimplant.
FIGURE 35-1. Three Entegra implants of varying decreasing diameters
of 4.75 mm, 4 mm, and 3.25 mm and one INTRA-LOCK miniimplant with a
2 mm diameter.
A B
FIGURE 35-2. A, A Panorex of Dentatus miniimplant placed between conventional implants to bear the load of an
overdenture allowing the conventional implants to osseointegrate. B, Overdentures retrofitted with attachments to engage
the miniimplants.
■ PONTIC SUPPORT OF A FIXED
PARTIAL DENTURE
If a bridge has become dislodged from one of its abutments
and may be removed from the other abutment without damage,
it is possible to salvage the bridge by recementing the bridge
to its abutments after placing a miniimplant under the pontic
for supplemental retention.11 This manner of salvaging an
FPD will be agreeable to a financially concerned patient
because a miniimplant is much less expensive than remaking
a bridge. Patient satisfaction is improved because the bridge
may be cemented the same day the implant is placed.
■ RETENTION OF OBTURATORS
In patients with a history of trauma or a pathologic condition,
which has left them with large orofacial defects, such as a
hemimaxillectomy, treatment with a miniimplant-retained
obturator is an ideal treatment plan. In such cases, existing
bone may be insufficient to maintain a conventional implant,
but could adequately accommodate a miniimplant. In these
circumstances if a miniimplant-retained obturator is not used,
alternative treatments include a temporalis rotational flap or
radial forearm free flap followed by a bone graft harvested
from the iliac crest or a microosseous flap from the fibula or
scapula.12,13,14 If sufficient bone is retained from the grafts,
conventional implants may be placed to support a dental
prosthesis. These procedures are laborious and carry associated
risks, including aesthetic morbidity. These risks can be pre-
vented with an implant-retained obturator.
Not only do miniimplants allow surgeons to minimize sur-
gical risks, but the ease of placement will be more tolerable
for an already traumatized patient. One major miniimplant
manufacturer claims that their implant can be placed using a
five-step technique compared with the customary 30-step
technique required for conventional implant placement.5
Dilek reports the case where a partial maxillectomy was
performed for tumor removal, and miniimplants were chosen
 CHAPTER 35 • Miniimplants and Transitional Implants 569

A B

C D

FIGURE 35-3. A, Panorex of an edentulous mandible. B, Dentatus implant kit including wrench, winged thumb-
wrench, pilot drill, and five implants. C, Postprocedure Panorex after placement of four Dentatus miniimplants. D, Post-
procedure photograph of miniimplants after placement. (Courtesy H. Dexter Barber, Temple University Hospital Oral and
Maxillofacial Surgery.) To view a color version of this illustration, refer to the color insert section at the back of
this book.

for retention of the obturator because of lack of adequate bone
and the simplicity of the surgical procedure. He reported res-
toration of function and patient satisfaction and concludes
that in many cases a miniimplant retained obturator is a suit-
able alternative to more complicated and invasive surgical
procedures.15
■ SINGLE-TOOTH IMPLANT
RESTORATIONS IN
NARROW SPACES
One drawback of conventional implants is the amount of
space required between adjacent teeth and the bone required
for their placement. Bone in a buccolingual dimension must
be at least 4.25 to 5.25 mm to accommodate the smallest
conventional implant, leaving 0.5 to 1 mm of sound bone to
the buccal and lingual sides of the implant.7,11 A margin of
1.25 mm is required on either side of the implant in a mesio-
distal dimension if teeth are present in these areas. This guide-
line allows for 0.25 mm for periodontal space and 1 mm of
sound bone between tooth and implant requiring a minimum
of 5.75 mm of space if the smallest conventional implant is to
be used for the restoration. In areas where a 4.25 × 5.75 block
of bone is not present, costly bone grafting or time-consuming
orthodontic treatment is indicated to provide ideal conditions
to place a conventional implant. With their reduced diameter,
miniimplants can be placed in areas where there is insufficient
bone for conventional implants without the need for ortho-
dontics or bone grafting (Figure 35-4 A-D). In some cases
even despite orthodontic efforts to provide adequate space for
an implant, the actual space available remains insufficient
(Figure 35-5 A-F). In a 5-year retrospective study, Vigolo
reported a similar success rate with miniimplants as with con-
ventional implants in restoring function and aesthetics to
single-tooth edentulous spaces.16 Dilek provided a case report
where the edentulous space of a maxillary first premolar was
insufficient for a conventional implant as a result of drifting
of the adjacent tooth. The patient refused orthodontic treat-
ment, and a miniimplant was placed and loaded 4 days later.
Twelve months after placement of the miniimplant, it was
found by a Periotest device to be osseointegrated.7
570 SECTION IV ■ Implant Surgery

A B

C D

FIGURE 35-4. A, Edentulous area of tooth #25. B, Although placement of a miniimplant does not require direct
visualization of the bone, a gingivoperiosteal flap was employed in this instance because of the fine alveolar ridge and
need for placement precisely on the thin crest of bone. C, Miniimplant in place. D, Final restoration. (Photo courtesy H.
Dexter Barber, Temple University Hospital Oral and Maxillofacial Surgery.) To view a color version of this illustration,
refer to the color insert section at the back of this book.

■ ORTHODONTIC ANCHORAGE
Miniimplants can also be used as an anchor in orthodontics.
In the past, orthodontic anchorage has depended upon seg-
ments of teeth or entire arches. When intraoral anchorage was
insufficient, the orthodontist used extraoral anchorage devices,
such as headgear and face masks. These appliances, however,
were cumbersome and resulted in poor patient compliance.17
Miniimplants can be used to aid in a full range of orthodontic
movements.18 Miniimplants employed for orthodontic pur-
poses have been placed in a variety of sites intraorally,
including:
• Buccal or labial surfaces of alveolar bone
• Palate—midline or paramedian
• Anterior nasal spine
• Zygomatic buttress
Placement of miniimplants in alveolar bone and on the
palate are the most common sites of orthodontic miniimplant
anchorage and will be discussed later.
The alveolar bone between the maxillary second molar and
first molar is a common site of miniimplant placement. A
study involving micro-CT analysis of five skulls with no evi-
dence of periodontal disease revealed that the most promising
level for miniimplant placement is 6 to 8 mm apical to the
crest of the alveolar bone. In this area 6 to 8 mm from
the crest of the alveolar margin, the bone was found to be the
thickest for miniimplant placement while not encountering
the maxillary sinus.19 Taking into account that the first molar
has only one palatal root and two buccal roots, it was logical
that the CT analysis revealed there would be more space for
miniimplant placement on the palatal side of the maxillary
ridge with less risk of root damage than when placed on the
buccal19 (Figure 35-6 A-C).
Another common location for placement of orthodontic
miniimplants is on the retromolar ridge or on the buccal shelf
of the mandible. Anchorage here allows for distalization of
the mandibular teeth without the need for headgear or may
provide substitute anchorage for a missing first molar (Figure
35-7 A-H).
The palate is another site for implant placement to aid in
orthodontic anchorage. The palatal implant application has
 CHAPTER 35 • Miniimplants and Transitional Implants 571

A B

C D

E F

FIGURE 35-5. A, Congenitally missing teeth #7 and #10. B-E, Miniimplant placed transmucosally in space of #7
and #10. F, Final restorations. (Photo Courtesy of H. Dexter Barber, Temple University Hospital Oral and Maxillofacial
Surgery.) To view a color version of this illustration, refer to the color insert section at the back of this book.
572 SECTION IV ■ Implant Surgery

two limitations. There must be sufficient palatal bone height,

A indicated that their parameters of lateral cephalogram assess-
B he advises that the angle of implant placement should not be
C dicularly to the axis of the implant. If this perpendicular force
FIGURE 35-6. Axial views in bony windows of a CT maxillofacial. A, At
the level of the pulp chamber. B, At the midroot level. C, At the level of the
apices of the teeth. Notice the space on the palatal than the buccal between
the roots of the first molar and the second premolar at the midroot level 6 to
8 mm apical to the alveolar crest.
and the surgery must avoid the nasal cavity and the incisive
foramen.20 Kang demonstrated that the thickness of palatal
bone varies greatly, but in general the bone is thickest in the
anterior midline of the palate. He suggests that if the miniim-
plant must be placed paramedian or on the posterior palate, a
shorter implant should be considered.21 Each patient must be
evaluated radiographically and clinically before placement of
a palatal miniimplant. The palate is a difficult site to use when
increased concavity and reduced transverse diameter is noted.20
The thickness of the palatal mucosa at the placement site may
render it less susceptible to inflammation.22 Wehrbein et al.
ment for placing the palatal implant are as follows: (1) posi-
tion of the implant with regard to the section of the palate:
anterior, middle, and posterior; (2) the angle between the
implant axis and a line formed by ANS-PNS; (3) the distance
between the most cranial border of the implant and the most
cranial border of the palatal complex (Figure 35-8). These
parameters were evaluated preoperatively and verified after
implant placement. Warhbein’s findings confirmed those of
Wangs in that there was more bone available in the anterior
palate than the posterior palate, enabling placement of longer,
more stable implants. He also found an inverse relationship
with the angle of the implant relative to the ANS-PNS line
and the amount of remaining vertical bone between the most
coronal portion of the implant and the nasal floor. However,
arbitrary to the ANS-PNS line, but it should be placed
orthogonal to the buccal surface of the palate.22 Wehrbein
states that there is actually 2 mm more vertical bone of the
palate than is routinely displayed on the lateral cephalogram.
He found that the most coronal point of midline palatal
implants that appeared to perforate into the nasal cavity by
2 mm or less actually had no communication with the nasal
cavity.22
The palate is a good site for orthodontic anchorage when
clinical and radiographic parameters are within range. The
implant placement and removal are generally simple and
without serious risk.
Forces on miniimplants used for orthodontic anchorage
may be less than occlusal forces, but they are directed perpen-
does not allow osseointegration of the miniimplant and a
fibrous layer of tissue separates the implant from the bone, the
miniimplant’s function as an anchor may still be served
because the fibrous layer may provide enough mechanical
retention to resist orthodontic forces.18 One literature review
observed that a period of 0 to 2 weeks was allowed to pass

FIGURE 35-7. A, Panorex of orthodontic patient with missing tooth #19. B, Intended miniimplant site visualized. C, KLS Martin orthodontic anchorage mini-
implant kit. D, KLS Martin orthodontic implant. E, Pilot holes being drilled. F, Placement of miniimplant. G, Miniimplants in place. H, Panorex of miniimplants in
place. (Photos courtesy H. Dexter Barber and John Lignelli Jr, Temple University Hospital Oral and Maxillofacial Surgery.) To view a color version of this illus-
tration, refer to the color insert section at the back of this book.
 CHAPTER 35 • Miniimplants and Transitional Implants 573

A B

C D

E F

G H
574 SECTION IV ■ Implant Surgery
ANS
PNS
FIGURE 35-8. The implant should be placed orthogonal to the buccal
surface of the palate, and a proper length of implant should leave adequate
bone between the implant and the nasal floor. (Design of image courtesy
Wehrbein et al.) To view a color version of this illustration, refer to the
color insert section at the back of this book.
before loading the miniimplant with orthodontic forces, and
treatment expectations of the implants were fulfilled.18
An important factor to consider when placing a miniim-
plant for orthodontic anchorage is drifting of the implant
through the bone. The anchor screw has been reported to drift
up to 1.5 mm in the direction of the orthodontic force and
should therefore be placed at least 2 mm from any vital
structures.18
■ SUMMARY
Miniimplants are versatile and effective tools for both tempo-
rary and long-term uses. They are able to retain prostheses in
cases where a conventional implant is not suitable and are
more affordable than conventional implants. They are becom-
ing the standard of care in orthodontics by providing anchor-
age without reliance on bulky extraoral devices. A full
understanding of the potential of miniimplants has not yet
been reached, but past results have been promising. Miniim-
plants should be given consideration in cases where conven-
tional implant use is limited and in orthodontics.
REFERENCES
1. Bulard RA, Vance JB: Multi-clinic evaluation using mini-dental
implants for long-term denture stabilization: a preliminary bio-
metric evaluation, Compend Continuing Education Dent (12):892-
897, 2005.
2. Shatkin TE et al.: Mini dental implants for long-term fixed and
removable prosthetics: a retrospective analysis of 2514 implants
placed over a five-year period, Compend Continuing Education
Dent 28(2):92-99, 2007.
3. Balkin BE, Steflik DE, Naval: Mini-dental implant insertion
with the auto-advance technique for ongoing applications, J Oral
Implantol 27(1):32-37, 2001.
4. Griffitts TM, Collins CP, Collins PC: Mini dental implants: an
adjunct for retention, stability and comfort for the edentulous
patient, Oral Surg Oral Med Oral Pathol Oral Radiol Endod 100:
E81-84, 2005.
5. www.imtec.com (accessed Sep 4, 2007).
6. Ahn MR et al.: Immediate loading with mini dental implants in
the fully edentulous mandible, Implant Dent 13(4):367-372,
2004.
7. Dilek OC, Tezulas E: Treatment of a narrow, single tooth eden-
tulous area with mini-dental implants: a clinical report, Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 103:e22-e25, 2007.
8. Misch CE: Density of bone. Effect on treatment plans, surgical
approach, healing and progressive bone loading, Int J Oral
Implantol 6:23-31, 1990.
9. Sohn DS: Color atlas, immediate loading with temporary implants,
2002, Jiseong Publication.
10. Froum S et al.: The use of transitional implants for immediate
fixed temporary prostheses in cases of implant restorations, Pract
Periodont Aesthetic Dent 10:737-746, 1998.
11. Christensen GJ: The “mini”-implant has arrived. J Am Dent
Assoc 137:387-390, 2006.
12. Mathes plastic surgery, vol 3, ed 2, Philadelphia, Saunders,
Elsevier.
13. Futran ND, Haller JR: Considerations for free-flap reconstruc-
tion of the hard palate, Arch Otolaryngol Head Neck Surg 125:665,
1999.
14. Foster RD et al.: Vascularized bone flaps versus nonvascularized
bone grafts for mandibular reconstruction: an outcome analysis
of primary bony union and endosseous implant success, Head
Neck 21:66, 1999.
15. Dilek OC, Tezulas E, Dincel M: A mini dental implant-
supported obturator application in a patient with partial maxil-
lectomy due to tumor: case report, Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 103(3):e6-10, 2007.
16. Vigolo P, Givani A: Clinical evaluation of single-tooth mini-
implant restorations: a five-year retrospective study, J Prosthet
Dent 84(1):50-54, 2000.
17. Cho HJ: Clinical applications of mini-implants as orthodontic
anchorage and the peri-implant tissue reaction upon loading, J
Calif Dent Assoc 34(10):813-820, 2006.
18. Ohashi E et al.: Implant vs screw loading protocols in orthodon-
tics, Angle Orthod 76(4):721-727.
19. Ishii T et al.: Evaluation of the implantation position of mini-
screws for orthodontic treatment in the maxillary molar area by
a micro CT, Bull Tokyo Dent Coll 45(3):165-172, 2004.
20. Giancotta et al.: Straumann orthosystem method for orthodon-
tic anchorage step by step procedure, World J Orthod 3:140-146,
2002.
21. Kang S et al.: Bone thickness of the palate for orthodontic
mini-implant anchorage in adults, Am J Orthod Dentofac Orthop
131(4) (supp 1): S74-S81.
22. Wehrbein H et al.: The Orthosystem: a new implant system for
orthodontic anchorage in the palate, J Orofac Orthop 57:142-
153, 1996.
INDEX
This index contains all entries from Volumes I, II, and III. Each entry is called out first by page number, followed by volume number (V1, V2, or V3).
Page numbers followed by f, t, or b indicate figures, tables, or boxes, respectively.
A Medical Education, 308 (V1)
A beta fiber, 962 (V2)
A beta pain, 998 (V2)
A delta fiber, 78-79 (V1), 962 (V2)
A delta fiber nociceptor, 137-138 (V1)
AAAHC; See Accreditation
Association for Ambulatory Health
Care
Abbe flap, 329, 330f (V2)
for lip defect, 343 (V2)
for midface defect, 350f (V2)
ABCDE and P method of skin
evaluation, 750 (V2)
Abdomen
assessment of
in cranio-maxillofacial trauma, 11
(V2)
in multi-system trauma, 65-67, 66f,
67f (V2)
secondary survey and, 40 (V2)
penetrating injury of, 42 (V2)
Abdominal compartment syndrome, 45-
46, 46f (V2)
Abdominal fat for sinus obliteration in
frontal sinus fracture, 264, 267,
268f (V2)
Abducens nerve
chronic orofacial pain and, 117 (V1)
evaluation in head injury, 51-52
(V2)
eyelid and, 584f (V3)
Aberrant bone healing, 22-23 (V2)
Ablative procedures
for posttraumatic trigeminal
neuralgia, 157 (V1)
in skin cancer, 734-735 (V2)
ABN; See Advanced beneficiary notice
Abnormal bleeding, preoperative
evaluation of, 16 (V1)
Abnormal wound healing, 22 (V2)
Abrasion
corneal, 78-79, 79f, 213, 306f, 306
(V2)
during exodontia, 214 (V1)
in facial trauma, 289 (V2)
gingival, 115t, 130 (V2)
mucosal, 115t (V2)
Abscess
brain, 267 (V2)
parotid gland, 541, 542f (V2)
Absorption of laser wave, 514, 514f
(V3)
Academic marketing, 319 (V1)
Acalculous cholecystitis, 45 (V2)
Acanthomatous ameloblastoma, 477,
480f (V2)
Accessory ligaments of
temporomandibular joint, 804-805,
805f (V2)
Accessory meningeal artery, 163f (V2)
Accessory nerve examination, 118 (V1)
Accommodation failure in midface
fracture, 254 (V2)
Accountant, practice management and,
286 (V1)
Accounting, financial management and,
293 (V1)
Accounts receivable turnover, 298 (V1)
Accreditation, 308-309 (V1)
ambulatory orthognathic surgery and,
491-492 (V3)
of surgicenter, 304-306, 305t (V1)
Accreditation Association for
Ambulatory Health Care, 304,
305t (V1), 516 (V3)
Accreditation Committee for Graduate
Accutane; See Isotretinoin
Acetaminophen, 84t, 86t, 86 (V1)
bone healing and, 394 (V1)
for chronic facial pain, 972, 973t
(V2)
for pain in complicated exodontia,
207t (V1)
for temporomandibular disorders, 886
(V2)
Acetic acids, 887t (V2)
Acetylsalicylic acid, 84t, 85-86, 86t
(V1)
bone healing and, 393 (V1)
preoperative management of, 2t (V1)
for temporomandibular disorders,
887t (V2)
for venous malformation, 587 (V2)
Achondroplasia, 851 (V3)
Acid-etch resin splint, 129f, 129-130
(V2)
Acinic cell carcinoma of parotid gland,
549 (V2)
Acitretin, 740 (V2)
Acne
formation after chemical peel, 662,
662f (V3)
laser skin resurfacing and
formation after, 539-540, 540f
(V3)
history of, 517 (V3)
improvement of scars in, 529 (V3)
Acoustic nerve examination, 118 (V1)
Acoustic neuroma, 120f (V1)
Acquired immunodeficiency syndrome,
salivary gland disease in, 543 (V2)
Acral lentiginous melanoma, 751t, 752f
(V2)
Actinic cheilitis, 518 (V3)
Actinic keratosis, 726, 734 (V2)
laser skin resurfacing and
preoperative evaluation in, 518
(V3)
treatment of, 529 (V3)
ultraviolet exposure and, 513 (V3)
Actinobacillus actinomycetemcomitans
diode laser treatment of, 255 (V1)
in periimplantitis, 390-391 (V1)
Active FX, 532, 536f (V3)
Active jaw exercises, 406, 407f (V3)
Active range of motion, 825 (V2)
Activity, postoperative, 411-412 (V3)
Activity sponsorship, marketing and,
345 (V1)
Actonel; See Risedronate
Acupuncture in temporomandibular
disorders, 986 (V2)
Acute adrenal insufficiency, 46-47 (V2)
Acute breakthrough pain, 971 (V2)
Acute herpes zoster, 151-152 (V1), 994
(V2)
Acute lung injury, 44, 44t (V2)
Acute monocytic leukemia, gingival
enlargement in, 179 (V1)
Acute osteomyelitis, 636t (V2)
Acute pain, 136 (V1)
postoperative, 78-92 (V1)
assessment of, 87, 87b, 88f, 89f
(V1)
local anesthetics for, 82-83 (V1)
neuroanatomy and pathophysiology
of, 78-80, 79f, 80f (V1)
nonsteroidal antiinflammatory
drugs for, 83-86, 84t, 85b, 86t
(V1)
Acute pain (Continued)
opioid analgesics for, 80-82, 81b,
81t, 82t (V1)
patient-controlled analgesia for, 88
(V1)
perioperative considerations in, 87,
87b (V1)
physical methods for, 88-89 (V1)
preemptive analgesia therapy for,
87-88 (V1)
reassessment of, 89-90 (V1)
Acute renal failure, 46 (V2)
Acute respiratory distress syndrome, 43-
44, 44t (V2)
Acute respiratory tract infection, 5
(V1)
Acute sinusitis, zygomatic implant-
related, 498 (V1)
Acute subarachnoid hemorrhage, 82,
82f (V2)
Acute subdural hematoma, 60, 61t (V2)
Acute suppurative infection of
submandibular gland, 541-542,
542f (V2)
Acute suppurative parotitis, 540-541,
541f, 542f (V2)
Acute traumatic arthritis of
temporomandibular joint, 855
(V2)
Acute trigeminal nerve injury, 265-266,
266f, 267f (V1)
Acute tubular necrosis, 46 (V2)
Acyclovir
for herpes simplex virus infection,
249 (V1), 614-615, 616, 617
(V2)
for herpetic lesions, 520 (V3)
Addiction
barrier to chronic pain management,
970-971 (V2)
to opioid analgesics, 81 (V1)
treatment of, 408-410 (V2)
Adductor pollicis muscle monitoring,
30 (V1)
Adenocarcinoma
of minor salivary gland, 553-555,
555f (V2)
parotid gland, 119f (V1)
of salivary gland, 549-550,
552f (V2)
Adenoid cystic carcinoma, 549, 555,
555f, 784 (V2)
Adenomatoid odontogenic tumor, 181
(V1), 469-472, 470-472f (V2),
968, 968f (V3)
Adhesion
arthroscopic removal of, 924 (V2)
formation after arthrotomy, 940 (V2)
Adjunctive diagnostic testing in
temporomandibular disorders,
824 (V2)
Adjuvant chemotherapy, 780 (V2)
Adjuvant preoperative radiation
therapy, 771-772 (V2)
Adolescent internal condylar
resorption, 299-305, 303-304f,
306f (V3)
after mandibular surgery, 453-454
(V3)
Adrenocortical insufficiency
perioperative management of, 386
(V3)
preoperative evaluation of, 13-14, 14t
(V1)
Adult stem cells, 23, 23f (V2)
Advanced beneficiary notice, 370 (V1)
Advanced trauma life support, 1-16, 35-
42 (V2)
abdominal assessment in, 11, 40 (V2)
airway assessment in, 2-4, 3f, 4f, 35-
36 (V2)
breathing assessment in, 4-6, 36, 36f,
37f (V2)
chest imaging studies in, 11 (V2)
circulation assessment in, 6-7, 7t, 37-
38, 38f, 38t (V2)
disability status in, 7-8, 8t, 38-39, 39t
(V2)
ear examination in, 9 (V2)
exposure and environmental control
in, 8, 39, 39f (V2)
eye examination in, 9 (V2)
head injury and, 8-9 (V2)
historic perspective of, 1, 2f (V2)
history in, 8 (V2)
intraoperative management and, 12-
14, 12-14f (V2)
musculoskeletal assessment in, 11-12,
40 (V2)
nasal and neurologic evaluation in, 9
(V2)
neck examination in, 10f, 10-11, 40
(V2)
neurologic examination in, 11, 38-39,
39t (V2)
in penetrating injuries, 41-42 (V2)
perineal, rectal, and vaginal
assessment in, 11, 40 (V2)
postoperative management and, 9,
10f (V2)
primary survey in, 1 (V2)
secondary survey in, 8, 40 (V2)
throat examination in, 9, 10f (V2)
Advancement flap for unilateral cleft
lip, 722, 737-741 (V3)
Asensio technique and, 740f, 740-
741, 741f (V3)
comparison of cleft surgery
techniques, 736 (V3)
nasal reshaping in, 741 (V3)
postoperative care in, 741 (V3)
preoperative management in, 738
(V3)
surgical technique in, 738-739, 739f,
740f (V3)
wide cleft defect and, 742f, 743f (V3)
Adverse action in privileging, 315-316
(V1)
Advil; See Ibuprofen
Adynamic ileus, 45 (V2)
Aesthetic surgery; See Esthetic surgery
Aesthetic zone
adaptive morphology of maxillary
alveolar process and, 541 (V1)
evaluation in anterior maxilla
implant surgery, 408 (V1)
Afferent nerve fiber, 78-79, 80f (V1)
Afferent pupillary defect, 50 (V2)
Affidavit, 376 (V1)
Age
cranio-maxillofacial trauma and, 6
(V2)
dentoalveolar injury and, 104, 105f
(V2)
preoperative evaluation and, 6 (V1)
surgery for facial asymmetry and, 277
(V3)
Aging
of face and neck, 377 (V2)
facial bone changes in, 15-17, 17f
(V3)
facial skin changes in, 8-10, 10f (V3)
I-1
I-2 INDEX
Aging (Continued)
occlusion changes in, 18 (V3)
skin changes in, 513 (V3)
Agonist-antagonists, 59, 80 (V1)
Air bag blast injury, 313, 314f, 315f
(V2)
Airway
angioedema in mandibular surgery
and, 442 (V3)
combined maxillary and mandibular
osteotomies and, 239 (V3)
craniofacial dysostosis syndromes and,
881 (V3)
obstruction of
laryngeal trauma and, 2 (V2)
postsurgical, 404 (V3)
in trauma patient, 25, 36 (V2)
oculoauriculovertebral spectrum and,
926 (V3)
pediatric craniomaxillofacial tumors
and, 961 (V3)
Treacher Collins syndrome and, 939,
943f (V3)
Airway adjuncts, 26 (V2)
Airway evaluation
in ambulatory orthognathic surgery,
492-493 (V3)
multi-detector computed tomography
in, 95, 96f (V2)
pediatric, 97, 98f (V1)
preanesthetic, 69t, 69-70 (V1)
in trauma patient, 25, 26b, 35-36
(V2)
Airway management
in maxillectomy, 694, 694f, 695f
(V2)
in pediatric anesthesia and sedation,
100t, 100-102 (V1)
in trauma patient, 25-34 (V2)
airway assessment and, 25, 26b
(V2)
airway maneuvers and adjuncts in,
26, 26b (V2)
in avulsive facial injury, 327 (V2)
complications in, 33 (V2)
comprehensive patient care and,
396 (V2)
in cranio-maxillofacial trauma, 2-4,
3f, 4f (V2)
cricothyroidotomy in, 32f, 32-33
(V2)
endotracheal intubation in, 28-31,
31f (V2)
in nasal soft tissue injury, 301 (V2)
supraglottic airway devices for, 26-
28, 27f, 28f (V2)
systematic approach to, 25 (V2)
tracheostomy in, 33 (V2)
Airway maneuvers, 26 (V2)
Ala, unilateral versus bilateral oronasal
cleft deformity and, 784t (V3)
Alar base modification, 571-572 (V3)
Alar base resection, 564, 565f (V3)
Alar nasalis muscle, 554f (V3)
Alar sidewall, 554b (V3)
Alar-columellar relationship, 558-559,
559f (V3)
Alar-facial junction, 554b (V3)
Albinism, basal cell carcinoma and, 725
(V2)
Alcohol
cluster headache and, 148 (V1)
oral cavity cancer and, 706 (V2)
Aldara; See Imiquimod
Alendronate, 395, 396t (V1), 558t (V2)
Aleve; See Naproxen
Alkaline phosphate in bone formation
evaluation, 396-397, 397t (V1)
Allele, 648 (V2)
Allergic contact dermatitis, laser skin
resurfacing-related, 539 (V3)
Allergy, drug
local anesthetics and, 48 (V1)
preoperative evaluation of, 1-2, 2t
(V1)
AlloDerm, 486, 487f (V1)
Allodynia, 140 (V1), 966t (V2)
in posttraumatic trigeminal neuralgia,
154 (V1)
Allodynia (Continued)
in trigeminal nerve injury, 262f, 263
(V1)
Allogenic bone grafting
guided tissue regeneration procedures
and, 430-431, 431f, 432f (V1)
in alveolar ridge augmentation,
450f, 450-451, 451f (V1)
in localized dehiscence defect, 447,
447f (V1)
in subantral augmentation, 437
(V1)
platelet-rich plasma and, 504f, 504-
506 (V1)
Allograft
intraoral implant of, 685t (V3)
platelet-rich plasma and, 504f, 504-
506 (V1)
in sinus-lift subantral surgery, 458
(V1)
Allograft bone putty, 448f, 448-449,
449f (V1)
Alloplast
guided tissue regeneration procedures
and, 430-431, 431f, 432f (V1)
platelet-rich plasma and, 504f, 504-
506 (V1)
in sinus-lift subantral surgery, 458
(V1)
in trigeminal nerve repair, 269 (V1)
Alloplastic chin implant, 684f, 684-685,
685b, 685f (V3)
Alloplastic collagen tubule conduit,
267f, 268, 272 (V1)
Alloplastic temporomandibular joint
reconstruction, 947-950, 947-950f
(V2)
Alopecia
after forehead and brow lift
endoscopic, 607 (V3)
trichophytic, 615-616 (V3)
along rhytidectomy incision, 509,
509f (V3)
hair transplantation for, 651-657
(V3)
complications of, 655-656 (V3)
current medical treatment for
alopecia and, 651 (V3)
micrograft and minigraft technique
in, 651-653, 652-655f (V3)
pathophysiology of alopecia and,
651 (V3)
rotational flaps in, 655, 655f, 656f
(V3)
scalp reduction in, 655, 656f (V3)
radiation therapy-related, 774 (V2)
Alpha-hydroxy acids
for chemical peel, 663 (V3)
for skin preparation in laser skin
resurfacing, 520 (V3)
Alprazolam
half-life and protein binding of, 58t
(V1)
for myofascial pain, 144 (V1)
for temporomandibular disorders,
889t (V2)
ALT flap; See Anterolateral thigh free
flap
Altemir intubation in maxillectomy,
694, 694f, 695f (V2)
Alteration of occlusal plane, 248-271
(V3)
clockwise rotation in, 252-256 (V3)
center of rotation at anterior nasal
spine, 252, 252f, 252t (V3)
center of rotation at maxillary
incisor tip, 252, 252f, 253t
(V3)
center of rotation at pogonion,
255, 255t, 256f (V3)
center of rotation at zygomatic
buttress, 255-256, 256f, 256t
(V3)
mandibular excess and, 253f, 253-
255, 254f (V3)
counterclockwise rotation in, 256-
260 (V3)
center of rotation at anterior nasal
spine, 256, 259f, 259t (V3)
Alteration of occlusal plane (Continued)
center of rotation at posterior nasal
spine, 256-260, 260f, 260t
(V3)
center of rotation at zygomatic
buttress, 256, 259f, 259t (V3)
in Treacher Collins syndrome, 954
(V3)
in unilateral adolescent internal
condylar resorption, 303-304f,
305, 306f (V3)
in vertical maxillary deficiency and
mandibular anteroposterior
deficiency, 257f, 257-258,
258f (V3)
in vertical maxillary excess and
mandibular anteroposterior
deficiency, 261-263, 261-263f
(V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-249,
249f, 250f (V3)
geometry of treatment design using
constructed maxillomandibular
triangle in, 261f, 261-262 (V3)
linear dimensions between maxillary
length and vertical facial height
in, 250, 250f (V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-268
(V3)
Alteration of record, 381 (V1)
Altered radiation fractionation schemes,
772 (V2)
Alternative autograft in trigeminal
nerve repair, 269 (V1)
Alternative pain management therapies
in chronic orofacial pain, 122 (V1)
Alveolar bone
immediate implant loading and, 512
(V1)
response following tooth extraction,
540-541 (V1)
Alveolar bone grafting technique, 808-
810, 808-811f (V3)
Alveolar bone removal
in complicated exodontia, 193-194,
194f (V1)
in impacted third molar tooth, 205-
206, 207-210f (V1)
Alveolar cleft, 806-812 (V3)
bone grafting technique for, 808-810,
808-811f (V3)
grafting materials for, 806-807 (V3)
history and timing of repair in, 806
(V3)
missing teeth and crowded arches in,
810-811, 811f (V3)
orthodontics for, 807f, 807-808 (V3)
postoperative care in, 810 (V3)
Alveolar distraction, 349-354, 349-354f
(V3)
Alveolar nerve block, hematoma and,
219 (V1)
Alveolar osteitis, 209b, 216 (V1)
Alveolar process fracture, 114t, 126-
128, 127f, 128f, 142, 142f (V2)
Alveolar ridge, 705 (V2)
squamous cell carcinoma of, 716-719
(V2)
Alveolar ridge augmentation
guided tissue regeneration for
functional and design requirements
for membranes in, 429-431,
431f, 432f (V1)
to reduce postextraction bone loss,
438-440 (V1)
Alveolar ridge augmentation (Continued)
subantral augmentation and, 436-
438, 437f (V1)
using allograft and xenograft bone
with titanium-reinforced
membrane, 450f, 450-451,
451f (V1)
using allograft bone putty and
resorbable collagen
membrane, 448f, 448-449,
449f (V1)
using high-density
polytetrafluoroethylene
membrane, 440f, 440-442,
441f (V1)
osteoperiosteal flap and, 471-478
(V1)
alveolar repositioning osteotomies
and, 473, 473f, 474f (V1)
alveolar split graft and, 471, 473f
(V1)
alveolar width distraction
osteogenesis and, 474-477,
475-478f (V1)
interpositional bone graft and, 471,
472f (V1)
sinus-lift subantral augmentation and,
458-470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic
considerations in, 458-459
(V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f,
464f (V1)
elevation of schneiderian
membrane in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
trephine core membrane elevation
in, 464-468, 464-468f (V1)
vascular supply, lymphatic
drainage, and innervation in,
459 (V1)
Alveolar socket wall fracture, 115t, 126
(V2)
Alveolar split graft, 471, 473f (V1)
Alveolar vertical distraction
osteogenesis, 477, 477f, 478f (V1)
Alveolar width distraction osteogenesis,
474-477, 475-478f (V1)
Alveolus
of child, 95-96 (V1)
immediate implant loading and, 512
(V1)
AMBE; See Antral membrane balloon
elevation
Ambien; See Zolpidem
Ambulatory anesthesia, 67-77 (V1)
airway assessment and, 69t, 69-70
(V1)
concept of rescue in, 68-69 (V1)
fluid administration and, 72 (V1)
goals of sedation in, 67-68 (V1)
laryngeal mask airway and, 70 (V1)
levels of sedation in, 67 (V1)
patient positioning and, 75 (V1)
pharmacology of drugs in, 56-66 (V1)
benzodiazepines and, 56-59, 58t,
59f (V1)
inhalation anesthetics and, 63-65,
64t (V1)
intravenous sedative-hypnotics
and, 60-62, 62t (V1)
ketamine and, 62-63 (V1)
opiates and opioids and, 59-60
(V1)
postoperative recovery and discharge
and, 75-76 (V1)

Ambulatory anesthesia (Continued)
preoperative fasting and, 71-72 (V1)
smoking and, 70-71 (V1)
Ambulatory center, 490-492, 491t, 492f
(V3)
Ambulatory orthognathic surgery, 490-
496 (V3)
absolute contraindications for, 494
(V3)
airway evaluation and, 492-493 (V3)
comorbidities and, 493 (V3)
complexity of surgical procedure and,
494-495 (V3)
facility for, 490-492, 491f, 492f (V3)
patient selection and, 492 (V3)
postoperative care and, 495-496, 496t
(V3)
surgeon skill and comfort level and,
494 (V3)
Ameloblastic fibrodentinoma, 524-527,
527f (V2)
Ameloblastic fibroma, 522-524, 523f
(V2), 968-970, 970f (V3)
Ameloblastic fibro-odontoma, 524,
525f, 526f (V2), 970, 970f (V3)
Ameloblastic fibrosarcoma, 532-533
(V2)
Ameloblastic sarcoma, 532-533 (V2)
Ameloblastoma, 476-502 (V2), 964f
(V3)
clinical forms and mechanisms of
growth, 478 (V2)
clinicopathologic considerations in,
477-478, 478-481f (V2)
management of, 500-502 (V2)
marked aggressive behavior and
metastases in, 492-500, 499f
(V2)
pediatric, 967f, 967-968 (V3)
peripheral, 485-492, 496-499f (V2)
solid and multicystic, 479-485, 486-
495f (V2)
unicystic, 478-479, 482-484f, 486f
(V2)
American Association of Oral and
Maxillofacial Surgeons
on credentialing and privileging, 307
(V1)
resources concerning hospital staff
issues, 312 (V1)
American Board of Medical Specialties,
308 (V1)
American Board of Oral and
Maxillofacial Surgery, 308 (V1)
American College of Cardiology cardiac
risk assessment, 3, 4f (V1)
American College of Surgeons, 309
(V1)
American Dental Association
on credentialing, 308 (V1)
Current Dental Terminology codes
of, 367-368 (V1)
American Dental Society of
Anesthesiology guidelines for
intraoperative monitoring, 23b, 23-
24 (V1)
American Dentistry Association,
Council on Dental Education and
Licensure, 309 (V1)
American Heart Association
cardiac risk assessment and, 3, 4f
(V1)
maximum recommended dosages of
vasoconstrictors and, 45t (V1)
American Joint Committee on Cancer
Staging
of melanoma, 754 (V2)
of skin cancer, 733-734 (V2)
American Osteopathic Association, 308
(V1)
American Society of Anesthesiologists
on documentation of anesthesia care,
31-32, 32t (V1)
fasting guidelines of, 71 (V1)
NPO recommendations of, 387f (V3)
Physical Status Classification System
of, 2 (V1)
preoperative risk stratification of,
389t (V3)
American Society of Cosmetic
Surgeons, 309 (V1)
American Spinal Injury Association,
52, 53f (V2)
Americans with Disabilities Act, 383-
384 (V1)
Amide local anesthetics, 36t, 36-37,
37f, 83 (V1)
Amifostine, 641, 774, 785 (V2)
Aminoglycosides
effects on osteoblast, 389 (V1)
preoperative management of, 2t (V1)
5-Aminolevulinic acid, 741 (V2)
Amitriptyline
for chronic facial pain, 973t (V2)
for complex regional pain syndrome,
158 (V1)
for migraine, 148 (V1)
for myofascial pain, 144 (V1)
for neuropathic orofacial pain, 999,
999t (V2)
for posttraumatic headache,
153 (V1)
for temporomandibular disorders,
888, 889t, 986 (V2)
for temporomandibular osteoarthritis,
146 (V1)
Amoxicillin
effect on osteoblast, 390 (V1)
prophylactic, 383t (V3)
for endocarditis, 5t (V1)
in sinus-lift subantral
augmentation, 459, 462 (V1)
Amoxicillin and clavulanic acid
for periimplantitis, 392 (V1)
in sinus-lift subantral augmentation,
459, 462 (V1)
Ampicillin, 5t (V1), 383t (V3)
Amyloidosis in multiple myeloma, 686,
686f (V2)
Analgesia, 966t (V2)
for acute postoperative pain, 78-92
(V1)
assessment in, 87, 87b, 88f, 89f
(V1)
in exodontia, 207t, 207-208 (V1)
local anesthetics in, 82-83 (V1)
neuroanatomy and pathophysiology
of pain and, 78-80, 79f, 80f
(V1)
nonsteroidal antiinflammatory
drugs in, 83-86, 84t, 85b, 86t
(V1)
opioid analgesics in, 59, 80-82,
81b, 81t, 82t (V1)
patient-controlled analgesia in, 88
(V1)
perioperative considerations and,
87, 87b (V1)
physical methods in, 88-89 (V1)
preemptive analgesia therapy in,
87-88 (V1)
reassessment of, 89-90 (V1)
anaphylaxis in pediatric anesthesia
and sedation and, 107t (V1)
for bone graft harvest, 415 (V1)
for bone graft in implant surgery, 422
(V1)
for chronic facial pain, 971-972, 972t
(V2)
for chronic orofacial pain, 120-121
(V1)
ketamine for, 62-63 (V1)
for myofascial pain, 144-145 (V1)
for neuropathic orofacial pain, 999
(V2)
nonopioid mediated, 83, 84t (V1)
pharmacology of, 59-60 (V1)
for sinus-lift subantral augmentation,
462 (V1)
for temporomandibular disorders, 131
(V1), 886-887, 888t (V2)
for temporomandibular osteoarthritis,
146 (V1)
Anaphylaxis, pediatric anesthesia and
sedation and, 107, 107t (V1)
Anaplastic ameloblastoma, 481f, 499f
(V2)
Anaprox; See Naproxen sodium
Anchorage, orthodontic, 223-236 (V1)
basic orthodontic mechanics and,
224-225 (V1)
bone plates in, 232-233, 233f, 234f
(V1)
for closure of anterior open bite, 232
(V1)
devices for, 225f, 225-226, 226f (V1)
historical perspective of, 223-224
(V1)
mesial or distal movement of teeth
and, 226-231f (V1)
miniimplants in, 570-574, 572-574f
(V1)
miniscrews in, 233-235 (V1)
orthopedic growth modification and,
232 (V1)
outcomes and complications in, 235-
236 (V1)
postoperative regimen in, 234-235
(V1)
for uprighting and intruding molar
teeth, 232 (V1)
Andreasen classification of
dentoalveolar injury, 111-112 (V2)
Anemia
accuracy of pulse oximetry
measurements and, 27 (V1)
postoperative, 390 (V3)
preoperative evaluation of, 14t, 14-
15, 15f, 15t (V1)
Anesthesia, 1-77 (V1)
airway assessment and, 69t, 69-70
(V1)
ambulatory, 56-66 (V1)
benzodiazepines in, 56-59, 58t, 59f
(V1)
inhalation anesthetics in, 63-65,
64t (V1)
intravenous sedative-hypnotics in,
60-62, 62t (V1)
ketamine in, 62-63 (V1)
opiates and opioids in, 59-60 (V1)
techniques in, 72-75, 73t (V1)
in cervicofacial liposuction, 621-622
(V3)
in chemical peel, 663 (V3)
in closed reduction of nasal fracture,
276 (V2)
in combined maxillary and
mandibular osteotomies, 241
(V3)
concept of rescue in, 68-69 (V1)
in endoscopic forehead and brow lift,
603 (V3)
in facial soft tissue injury, 284 (V2)
fluid administration and, 72 (V1)
general, 22, 67 (V1)
for child, 103-106, 105t (V1)
for geriatric patient, 385, 385b
(V2)
laryngeal mask airway and, 70
(V1)
in open rhinoplasty, 567 (V3)
in trigeminal nerve repair, 268
(V1)
goals of sedation in, 67-68 (V1)
in laser skin resurfacing, 521, 522f
(V3)
levels of sedation in, 67 (V1)
in lip filler injection, 633-634, 634f
(V3)
local, 35-55 (V1)
for acute postoperative pain, 82-83
(V1)
for acute trigeminal nerve injury,
266 (V1)
for arthrocentesis of
temporomandibular joint, 913
(V2)
for bone graft harvest, 410, 412,
414 (V1)
in cervicofacial liposuction, 621-
622 (V3)
in chemical peel, 663 (V3)
chemistry of, 36t, 36-37, 37f (V1)
chronic facial pain after, 969 (V2)
for chronic orofacial pain, 114-
115, 115-117f (V1), 974 (V2)
INDEX I-3
Anesthesia (Continued)
efficacy and duration of action of,
39t, 39 (V1)
in endoscopic forehead and brow
lift, 603 (V3)
for facial soft tissue injury, 284
(V2)
historical perspective of, 35-36
(V1)
injection-related trigeminal nerve
injury and, 267f, 273-274
(V1)
in laser skin resurfacing, 521, 522f
(V3)
latest development and future
direction of, 50-51 (V1)
for Le Fort I osteotomy, 176 (V3)
localized complications of, 45-47,
46f, 46t (V1)
mechanism of action of, 38 (V1)
in Moh’s micrographic surgery, 735
(V2)
in Mustard[ac]e method of
otoplasty, 673 (V3)
in open rhinoplasty, 567 (V3)
pH effects on, 37t, 37-38,
38f (V1)
for placement of skeletal anchorage
miniscrews, 234 (V1)
potency of, 38t, 38-39 (V1)
in rhytidectomy, 500 (V3)
in sinus-lift subantral
augmentation, 459 (V1)
in skeletal anchorage plate
placement, 233 (V1)
systemic complications of, 47-48
(V1)
topical, 48-50 (V1)
use of vasoconstrictors with, 39-45,
40t, 43-45t, 44b (V1)
in zygomatic implant, 493 (V1)
monitoring during, 22-34 (V1)
anesthesia record and, 31-32, 32t
(V1)
body temperature and, 29 (V1)
child and, 99-100 (V1)
circulatory system and, 24-25 (V1)
definitions in, 22 (V1)
depth of sedation and, 30b, 30-31,
31f (V1)
history and evolution of guidelines
for, 22-24, 23b (V1)
neuromuscular blockade and, 29-
30 (V1)
during recovery, 32-33, 33t (V1)
respiratory system and, 25-29, 26f,
28f (V1)
in open rhinoplasty, 567 (V3)
in otoplasty, 668, 670f (V3)
patient positioning and, 75 (V1)
pediatric, 67-68, 93-111 (V1)
airway equipment preparation for,
100t, 100-102 (V1)
anaphylaxis and, 107t, 107 (V1)
bronchospasm and, 107 (V1)
carbon dioxide monitoring during,
28 (V1)
cardiovascular system and, 93-94,
94t (V1)
developmental pharmacology and,
96-97 (V1)
fentanyl for, 104 (V1)
gastric contents aspiration and,
107 (V1)
inhalation anesthesia for, 104-105
(V1)
intraoperative fluids and, 102-103
(V1)
intravenous access and, 102, 102f
(V1)
ketamine for, 104 (V1)
laryngospasm and, 106-107 (V1)
liver function and, 96 (V1)
malignant hyperthermia and,
107-108 (V1)
midazolam for, 103-104 (V1)
monitoring during, 99-100 (V1)
Pediatric Anesthesia Worksheet
for, 101b (V1)
I-4 INDEX
Anesthesia (Continued)
preanesthetic assessment and, 97-
99, 98f (V1)
premedication for fear and anxiety
in, 103 (V1)
propofol for, 104, 105t (V1)
renal system and, 96 (V1)
respiratory system and, 94-96, 95f,
96t (V1)
techniques for, 105-106 (V1)
thermoregulation and, 96 (V1)
postoperative recovery and discharge
and, 75-76 (V1)
preoperative evaluation and, 1-21
(V1)
cardiovascular system and, 2-3, 3t,
4f, 5t (V1)
consent and preoperative
preparation and, 20 (V1)
endocrine system and, 11-14, 12-
14t (V1)
gastrointestinal system and, 7-11,
9-11t, 10f (V1)
hematologic system and, 14-17,
14-17t, 15f (V1)
history and physical examination
in, 1-2, 2t (V1)
immune system and, 18-19 (V1)
neurologic system and, 17-18, 18t
(V1)
preoperative testing and, 19t, 19-
20 (V1)
pulmonary system and, 3-6, 5-7t
(V1)
renal system and, 7-9t (V1)
preoperative fasting and, 71-72 (V1)
for sinus-lift subantral augmentation,
459 (V1)
smoking and, 70-71 (V1)
for soft tissue injuries, 284 (V2)
in total maxillary segmental
osteotomy, 193 (V3)
Anesthesia codes, 367 (V1)
Anesthesia dolorosa, 264 (V1)
Anesthesia machine, 360 (V1)
Anesthesia record, 31-32, 32t (V1)
Anesthetics
inhalation, 63-65, 64t (V1)
local, 35-55 (V1)
for acute postoperative pain, 82-83
(V1)
chemistry of, 36t, 36-37, 37f (V1)
efficacy and duration of action,
39t, 39 (V1)
historical perspective of, 35-36
(V1)
latest development and future
direction of, 50-51 (V1)
localized complications of, 45-47,
46f, 46t (V1)
mechanism of action, 38 (V1)
pH effects on, 37t, 37-38, 38f (V1)
potency of, 38t, 38-39 (V1)
systemic complications of, 47-48
(V1)
topical, 48-50 (V1)
use of vasoconstrictors with, 39-45,
40t, 43-45t, 44b (V1)
proconvulsant and anticonvulsant
effects of, 18t (V1)
Aneurysmal bone cyst, 596-597, 597-
598f, 868 (V2), 972, 974-975 (V3)
Angiocentric lymphoma, 761-762 (V2)
Angioedema, 442 (V3)
Angiogenesis
tumor-stroma interactions in, 665f
(V2)
in wound healing, 61 (V3)
Angiography in pediatric
craniomaxillofacial tumor, 961-962
(V3)
Angiotensin-converting enzyme
inhibitors, 381 (V2)
Angle of mandible fracture, 141, 142f
(V2)
diagnostic imaging of, 101, 101f (V2)
pediatric, 364 (V2)
Angle’s classification, 890 (V2)
Angular artery, 555f (V3)
Angulation classification of impacted
teeth, 204f (V1)
Aniline derivatives, 86t (V1)
Animal bite wound, 290-292, 292f,
313-316, 314-317f (V2)
Animal studies in orofacial
embryogenesis, 705, 706-708f (V3)
Ankyloglossia, 174, 175f, 176f (V1)
Ankylosing spondylitis
facial asymmetry in, 309 (V3)
temporomandibular joint and, 860-
861 (V2)
temporomandibular joint ankylosis
and, 901-902 (V2)
Ankylosis of temporomandibular joint,
901-905, 952-953, 953f, 953t (V2)
Ann Arbor Staging System for
lymphoma, 758-759, 764b (V2)
Annandale, Thomas, 789, 790, 790f
(V2)
Anorganic bone, platelet-rich plasma
and, 504f, 504-506 (V1)
Ansaid; See Flurbiprofen
Anterior alveolar height
mandibular growth value, 48 (V3)
maxillary-midface growth value, 31
(V3)
Anterior auricular muscle, 668f (V3)
Anterior capsular release, 924, 925f
(V2)
Anterior chamber, nonperforating eye
injuries and, 79f, 79-80 (V2)
Anterior compartment lymph nodes,
neck dissection and, 711t (V2)
Anterior crus of external ear, 667f (V3)
Anterior disc displacement, 818-821,
819-821f (V2)
advanced imaging modalities in, 839
(V2)
chronic orofacial pain in, 127 (V1)
mandibular gait in, 825, 827f (V2)
splint therapy for, 885 (V2)
Anterior ethmoid artery, 553 (V3)
Anterior ethmoid foramen, 203t, 204
(V2)
Anterior ethmoidal nerve, 556, 557f
(V3)
Anterior facial height, 250, 250f (V3)
Anterior fontanel, 865f (V3)
Anterior lamella, 582f, 582-583 (V3)
Anterior line of craniofacial balance,
139, 139f (V3)
Anterior nasal spine
maxilla and, 172, 173f (V3)
maxillomandibular complex rotation
and
clockwise, 252, 252f, 252t (V3)
counterclockwise, 255, 255f, 255t
(V3)
maxillomandibular triangle and, 249,
250f (V3)
Anterior nasal spine to menton
distance, 137, 138, 138f, 140f (V3)
Anterior open-bite
mandibular lengthening by
distraction osteogenesis and, 345
(V3)
occlusal management of, 889-890
(V2)
postoperative, 414 (V3)
in rheumatoid arthritis of
temporomandibular joint, 858
(V2)
skeletal anchorage devices for, 232
(V1)
transoral vertical ramus osteotomy
and, 123, 124f (V3)
Anterior plagiocephaly, 868-871, 871f,
872f (V3)
Anterior repositioning splint, 984 (V2)
Anterior segment trauma, 76 (V2)
Anterior skull base ameloblastoma, 964f
(V3)
Anterior superior alveolar nerve, 459
(V1)
Anterior table fracture, 259, 261f, 262-
264, 263-265f (V2)
Anterior temporal nerve, 809 (V2)
Anterior tibial artery, 335f (V2)
Anterolateral approach in
temporomandibular joint
arthroscopy, 923f (V2)
Anterolateral neck dissection, 720f
(V2)
Anterolateral thigh free flap, 335, 335f
(V2)
for cheek reconstruction, 344 (V2)
for lip defect, 343-344f (V2)
for midface avulsive defect, 341f
(V2)
Anteroposterior globe displacement, 78,
78f (V2)
Anthropometrics, 2-9, 9b (V3)
cervicofacial area, 6-8, 9b, 9f (V3)
cheek, 4-5, 6f (V3)
in craniofacial growth evaluation,
856 (V3)
ear, 6, 8f (V3)
frontal face, 1-2, 2f (V3)
nose, 6, 7f (V3)
perioral area, 6-7, 8f (V3)
periorbital area, 4, 5f (V3)
profile, 3f, 3-4 (V3)
Antibiotics
added to bone grafting materials,
388-390, 389t, 390t (V1)
anaphylaxis in pediatric anesthesia
and sedation and, 107t (V1)
exodontia and, 217 (V1)
for frontal sinus fracture, 266 (V2)
in implant surgery, 387-388, 388b
(V1)
autogenous bone graft and, 409,
422 (V1)
guided tissue regeneration and, 430
(V1)
sinus-lift subantral augmentation
and, 459 (V1)
for osteomyelitis, 636-638 (V2)
for periimplantitis, 391-392 (V1)
prophylactic, 392-393, 410 (V3)
in animal bite, 315 (V2)
in laser skin resurfacing, 249 (V1),
520 (V3)
in mandibular surgery, 443 (V3)
in modified Le Fort III osteotomy,
212 (V3)
skeletal anchorage and, 235 (V1)
for surgical geriatric patient with
diabetes mellitus, 383-384
(V2)
for trauma patient, 73 (V2)
for recurrent cellulitis in lymphatic
malformation, 582 (V2)
Anticlenching medications, 409-410
(V3)
Anticoagulant therapy
geriatric patient and, 381 (V2)
preoperative evaluation of, 17, 17t
(V1)
Anticonvulsants
for acute trigeminal nerve injury, 266
(V1)
for complex regional pain syndrome,
158 (V1)
for myofascial pain, 144 (V1)
for postherpetic neuralgia, 152 (V1)
for trigeminal neuralgia, 150, 156
(V1)
Antidepressants
for chronic facial pain, 973, 973t
(V2)
for complex regional pain syndrome,
158 (V1)
interaction with local anesthetics
with vasoconstrictors, 42t, 42-43
(V1)
for migraine, 148 (V1)
for myofascial pain, 144 (V1)
for neuropathic orofacial pain, 999,
999t (V2)
for postherpetic neuralgia, 152 (V1)
for posttraumatic headache,
153 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)
for temporomandibular disorders,
888, 889t, 986 (V2)
Antiemetics for postoperative nausea
and vomiting, 410, 443 (V3)
Antiepileptic agents for trigeminal
neuralgia, 992, 992t (V2)
Antifungal agents for oral mucositis,
785 (V2)
Antigonial width, 51 (V3)
Antihelical fold, 665, 666f (V3)
deformity of, 669 (V3)
Farrior technique and, 673, 675f
(V3)
Mustard[ac]e method of otoplasty
and, 673, 674f (V3)
Antihelix, 666, 667f (V3)
Antihistamines
for laser skin resurfacing-related
pruritus, 538 (V3)
postoperative, 410 (V3)
for temporomandibular disorders,
889, 889t (V2)
Antihypertensives
geriatric patient and, 381 (V2)
interaction with local anesthetics
with vasoconstrictors, 42t, 42-43
(V1)
Antinuclear antibody in rheumatoid
arthritis, 858 (V2)
Antitragus, 667f (V3)
Antiviral agents
for herpes simplex virus infection,
614-615 (V2)
for herpetic lesions, 520 (V3)
for laser skin resurfacing-related viral
infection, 541 (V3)
Antiyeast medications, 410 (V3)
Antral fistula, maxillary surgery-related,
480 (V3)
Antral membrane balloon elevation,
465-468, 465-468f (V1)
Antral septum, complications in sinus-
lift subantral augmentation, 463,
464f (V1)
Anxiety, trauma patient and, 47 (V2)
Anxiolytics
benzodiazepines in, 57 (V1)
for temporomandibular disorders,
888-889, 889t (V2)
Apertognathia, 219 (V3)
Apert syndrome, 902-909 (V3)
assessment of treatment results in,
902-909 (V3)
cranial vault expansion and, 902
(V3)
cranio-orbital reshaping in infancy
and, 902, 903-905f (V3)
craniosynostosis in, 850, 874 (V3)
dentition and occlusion anomalies in,
881-882 (V3)
functional considerations in, 880-881
(V3)
genetic aspects of, 880 (V3)
Le Fort III osteotomy for midface
deformity in, 205-206 (V3)
maxillary distraction osteogenesis in,
1002, 1003f, 1004f (V3)
maxillary hypoplasia in, 861 (V3)
orbito-naso-zygomatic deformity in,
882 (V3)
orthognathic procedures in, 902 (V3)
total midface deformity and, 902,
906-907f (V3)
Aphthous stomatitis, 245 (V1), 619f,
619-620 (V2)
Apical vessels in maxillary central
incisor, 67f (V3)
Apically positioned flap for impacted
maxillary canine, 169-170, 170f
(V1)
Apoptosis, cancer cell and, 660-662,
661f (V2)
Appointment cancellation, 346 (V1)
Appointment to medical staff, 314-315,
315t (V1)
Apron-style incision in pediatric
craniomaxillofacial tumor, 963
(V3)
APTOS thread, 695, 696t (V3)
Arachidonic acid, omega-6 fatty acids
and, 399 (V1)

Arch bars, 147, 147f (V2)
Arch wires, 400 (V3)
Architectural and structural craniofacial
analysis for genioplasty, 138-139,
139f, 144f (V3)
Arcus marginalis, 205 (V2), 583 (V3)
forehead and brow lift and, 596 (V3)
ARDS; See Acute respiratory distress
syndrome
Aredia; See Pamidronate
Argon ion laser, 240, 241 (V1)
ArteFill, 630 (V3)
Arterial applanation tonometry, 25
(V1)
Arterial lines, 47-48 (V2)
Arterial supply
to ear, 667-668 (V3)
to eyelid, 585 (V3)
to hand, 334f (V2)
to leg, 335f (V2)
maxillary osteotomy healing and, 63,
63f (V3)
to maxillary sinus, 459 (V1)
nasal, 272-273, 273f (V2), 553-554,
555f (V3)
to nasal tip, 555 (V3)
to temporomandibular joint, 163,
163f, 809, 809f (V2)
Arteriovenous fistula, arthroscopic-
related, 926 (V2)
Arteriovenous malformation, 588-590,
589f, 870 (V2)
Artery of pterygoid canal, 66f, 175f
(V3)
Arthralgia, 966t (V2)
Arthritis
classification of, 854 (V2)
continuous passive motion and, 851-
852, 853f, 854f (V2)
cyclic tensile strain in, 851, 851f,
852f (V2)
temporomandibular, 145-146 (V1)
ankylosing spondylitis in, 860-861
(V2)
degenerative osteoarthritis in, 855-
857 (V2)
gout and pseudogout in, 865 (V2)
infectious, 861-864, 862-863f (V2)
juvenile rheumatoid, 859 (V2)
Lyme disease-associated, 864 (V2)
mixed connective tissue disease
and, 868 (V2)
psoriatic, 859-860 (V2)
Reiter syndrome and, 861 (V2)
rheumatoid, 857b, 857-858 (V2)
scleroderma and, 865-866 (V2)
Sj[um]ogren’s syndrome and, 866
(V2)
systemic lupus erythematosus and,
865 (V2)
traumatic, 854-855 (V2)
Arthrocentesis
history of, 798 (V2)
temporomandibular joint, 132 (V1),
912-917 (V2)
outcome assessment in, 915 (V2)
pathophysiology of
temporomandibular disorder
and, 912-913 (V2)
prognostic and predictive factors
in, 916 (V2)
surgical outcomes in, 133 (V1)
technique in, 913-915, 914f (V2)
Arthroscopic arthroplasty, 924 (V2)
Arthroscopy
history of, 798, 918 (V2)
laser-assisted, 246 (V1)
temporomandibular joint, 132 (V1),
918-928 (V2)
anatomic considerations in, 918-
920, 919f (V2)
arthroplasty and, 924 (V2)
capsular release in, 924, 925f (V2)
complications in, 926-927 (V2)
diagnostic uses of, 920 (V2)
disk repositioning in, 924-926,
925f, 926f (V2)
equipment for, 921-923, 922f (V2)
fluid analysis and, 921 (V2)
Arthroscopy (Continued)
inferolateral technique in, 923,
923f (V2)
in internal derangement, 920-921,
921f (V2)
lysis and lavage in, 924, 924f (V2)
postoperative care in, 927 (V2)
removal of adhesions in, 924 (V2)
surgical outcomes in, 133 (V1)
Arthrotomy
in internal derangement of
temporomandibular joint, 929-
944, 930b (V2)
capsular incisions in, 934, 934f
(V2)
condylotomy in, 939-940 (V2)
diagnostic imaging in, 931, 932f
(V2)
disk repair in, 936, 936f (V2)
disk repositioning in, 935f, 935-
936 (V2)
diskectomy in, 936 (V2)
diskectomy with replacement in,
936-939, 937-939f (V2)
endaural incision in, 933f, 933-
934, 934f (V2)
goals and criteria for surgery in,
931 (V2)
history and physical examination
in, 929-930 (V2)
pathogenesis of, 930-931 (V2)
postoperative care in, 940-941
(V2)
preauricular incision in, 932-933,
933f (V2)
preoperative therapies for, 931
(V2)
surgical complications in, 940 (V2)
wound closure in, 934, 935f (V2)
in temporomandibular joint disorders,
132 (V1)
Articaine
chemical structure of, 37f (V1)
duration of action of, 39t (V1)
lipid solubility of, 38t (V1)
pH effects on, 37t (V1)
prolonged sensory alteration with, 46t
(V1)
Articles of incorporation, 299 (V1)
Articular cartilage
extracellular matrix and, 849-850,
850f (V2)
osteoarthritis and, 855-856 (V2)
temporomandibular joint disorders
and, 127-128, 128f (V1)
Articular disc of temporomandibular
joint, 802-803, 803f (V2)
Articular eminence of
temporomandibular joint, 802,
802f (V2)
Articular tubercle, 802 (V2)
Articulation after cleft surgery, 794-
795, 797 (V3)
Articulator in model surgery, 364-365,
365f (V3)
Ascending palatine artery, 63f, 173f (V3)
Ascending pharyngeal artery, 63f, 69f,
173f, 174-175, 175f (V3)
Asch forceps for nasal fracture
reduction, 277-278, 279f (V2)
Asensio technique for rotation and
advancement flap in unilateral
cleft lip repair, 740f, 740-741, 741f
(V3)
Aseptic necrosis, Le Fort 1 osteotomy-
related, 64, 475 (V3)
Ashhurst,A.P.C., 790, 791 (V2)
Aspiration
of gastric contents, 107 (V1)
of tooth, crown, or restoration during
exodontia, 215 (V1)
Aspiration biopsy techniques, 414f,
414-415, 415f (V2)
Aspirin, 84t, 85-86, 86t (V1)
bone healing and, 393 (V1)
preoperative management of, 2t (V1)
for temporomandibular disorders,
887t (V2)
for venous malformation, 587 (V2)
Asplenia, 387-388 (V3)
Associate position, 290 (V1)
Asthma
geriatric patient and, 382 (V2)
pediatric preanesthetic assessment
and, 98-99 (V1)
perioperative management of, 383-
384, 384t (V3)
preoperative evaluation of, 6 (V1)
use of vasoconstrictors with local
anesthetics and, 44, 44b (V1)
Asymmetric face, 272-315 (V3)
categories of, 278 (V3)
clinical evaluation in, 272-274, 273f
(V3)
dentoalveolar and occlusal assessment
in, 274 (V3)
dentoalveolar asymmetry and, 282,
283-284f (V3)
developmental, 282 (V3)
diagnostic and treatment
considerations in, 275-277, 276f
(V3)
imaging in, 274-275 (V3)
in oculoauriculovertebral spectrum,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
maxilla and, 922-935 (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
overdevelopment and, 282-293 (V3)
in mandibular condylar
osteochondroma or osteoma,
285-291, 289-291f (V3)
in muscle hypertrophy, 291-292
(V3)
in neuromuscular disorders, 292,
292f (V3)
in tumor, 293, 293f (V3)
in unilateral condylar hyperplasia,
284-285, 286-288f (V3)
postoperative, 414-415 (V3)
presurgical patient preparation and,
277-278 (V3)
pseudoasymmetry and, 278-282 (V3)
condylar dislocation and, 281, 281f
(V3)
infection and, 281-282 (V3)
malocclusion and, 278-280, 279-
280f (V3)
muscle dysfunction and, 280-281
(V3)
unilateral facial underdevelopment
or degeneration and, 294-313
(V3)
in adolescent internal condylar
resorption, 299-305, 303-304f,
306f (V3)
in autoimmune and connective
tissue diseases, 309-313, 310-
313f (V3)
in hemifacial microsomia, 298-299,
300-302f (V3)
iatrogenic, 294 (V3)
in reactive arthritis, 305-309, 307-
309f (V3)
in temporomandibular joint
ankylosis, 294-298, 297f, 298f
(V3)
trauma-related, 294, 295f, 296f
(V3)
INDEX I-5
Asymmetric mandible
bilateral sagittal split osteotomy for,
99t, 99-102, 102-105f (V3)
transoral vertical ramus osteotomy
for, 130f, 130-131, 131f (V3)
Ativan; See Lorazepam
Atlanto-occipital joint extension, 97-98
(V1)
ATLS; See Advanced trauma life
support
ATN; See Acute tubular necrosis
Atraumatic extraction techniques, 541,
542f (V1)
Atrial fibrillation, 44-45 (V2)
Atrial septal defect, 382-383 (V3)
Atrophic mandibular fracture, 142, 156-
158 (V2)
Atrophic rhinitis, maxillary surgery-
related, 480 (V3)
Atropine
for laryngospasm in anesthetized
child, 106 (V1)
in rapid-sequence intubation, 29
(V2)
Attention deficit hyperactivity disorder,
388 (V3)
Attorney
for plaintiff, 376-378 (V1)
practice management and, 286-287
(V1)
Atypical facial pain, 158 (V1), 967-968
(V2)
Audit of participation contract, 369
(V1)
Augmentation procedures
guided tissue regeneration in, 428-
457 (V1)
for coronal defects, 436 (V1)
for dehiscence defects, 435-436,
447, 447f (V1)
dual-layered technique in, 445f,
445-446, 446f (V1)
for fenestration defects, 436 (V1)
flapless buccal wall reconstruction
in, 443f, 443-444, 444f (V1)
functional and design requirements
of membranes for, 429-431,
431f, 432f (V1)
posterior mandible, 452-453, 452-
453f (V1)
to reduce postextraction bone loss,
438-440, 454f, 454-455, 455f
(V1)
ridge preservation using high-
density PTFE membrane in,
440-441f, 440-442 (V1)
subantral, 436-438, 437f (V1)
using allograft and xenograft bone
with titanium-reinforced
membrane, 450-451, 450-451f
(V1)
using allograft bone putty and
resorbable collagen
membrane, 448f, 448-449,
449f (V1)
wound closure in, 431-435, 433f,
434f (V1)
osteoperiosteal flap and, 471-478 (V1)
alveolar repositioning osteotomies
and, 473, 473f, 474f (V1)
alveolar split graft and, 471, 473f
(V1)
alveolar width distraction
osteogenesis and, 474-477,
475-478f (V1)
interpositional bone graft and, 471,
472f (V1)
sinus-lift subantral augmentation in,
458-470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic
considerations in, 458-459
(V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f,
464f (V1)
computed tomography in, 561-563,
562f, 563f (V1)
I-6 INDEX
Augmentation procedures (Continued)
elevation of schneiderian
membrane in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
trephine core membrane elevation
in, 464-468, 464-468f (V1)
vascular supply, lymphatic
drainage, and innervation in,
459 (V1)
Augmentin; See Amoxicillin and
clavulanic acid
Auricle, 665, 666f (V3)
Auricular cartilage, 665-666 (V3)
Davis method for conchal
hypertrophy and, 670-673, 672f
(V3)
excessive, 669 (V3)
temporomandibular joint
reconstruction and, 946-947
(V2)
Auricular cartilage graft, 937-938, 938f
(V2)
Auricular deformity, otoplasty for, 665-
677 (V3)
blood supply to ear and, 667-668
(V3)
complications in, 675-676 (V3)
for congenital deformities, 668-669
(V3)
for correction of protruding earlobe,
675, 675f (V3)
Davis method in, 670-673, 672f (V3)
embryology of auricle and, 665, 666f
(V3)
Farrior technique in, 673, 675f (V3)
indications and timing of, 669 (V3)
Mustard[ac]e method in, 673, 674f
(V3)
nerve supply to ear and, 668-670f
(V3)
surgical anatomy in, 665-666, 666f,
667f (V3)
techniques in, 669-670, 671f (V3)
Auricular hematoma, 9 (V2)
Auricular temporal nerve, 165 (V2)
Auriculocephalic angle, 665, 666f (V3)
Auriculotemporal block, 914 (V2)
Auriculotemporal nerve, 600 (V3)
injury in arthrotomy, 940 (V2)
Auriculotemporalis nerve, 668f (V3)
Auscultation of temporomandibular
joint, 826-828 (V2)
Autism, 388 (V3)
Autodonation, 390 (V3)
Autogenous bone graft
in cleft maxilla, 806-812 (V3)
alveolar bone grafting technique
for, 808-810, 808-811f (V3)
grafting materials for, 806-807
(V3)
history and timing of repair in, 806
(V3)
missing teeth and crowded arches
in, 810-811, 811f (V3)
orthodontics for, 807f, 807-808
(V3)
postoperative care in, 810 (V3)
in cleft orthognathic surgery, 819,
820-825f (V3)
for dental implant, 406-427 (V1)
bone biology and, 406-407, 407f
(V1)
graft recipient site and, 419-422,
419-422f (V1)
ilium for, 415-419, 415-419f (V1)
mandibular ramus for, 412-414,
412-414f (V1)
mandibular symphysis for, 409-411,
410-412f (V1)
Autogenous bone graft (Continued)
maxillary tuberosity for, 409, 409f,
410f (V1)
onlay bone graft and, 424, 424f,
425f (V1)
patient preparation for, 409 (V1)
preoperative evaluation in, 407-
408, 408f, 409f (V1)
sinus bone grafting and, 422-424,
423f (V1)
tibia for, 414f, 414-415, 415f (V1)
guided tissue regeneration procedures
and, 430-431, 431f, 432f (V1)
in immediate implant placement,
512-513 (V1)
in internal derangement of
temporomandibular joint, 936,
937 (V2)
interpositional, 471, 472f (V1)
in Le Fort I osteotomy, 184 (V3)
in Le Fort III osteotomy, 211 (V3)
in sinus-lift subantral augmentation,
458-470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic
considerations in, 458-459
(V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f,
464f (V1)
elevation of schneiderian
membrane in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
trephine core membrane elevation
in, 464-468, 464-468f (V1)
vascular supply, lymphatic
drainage, and innervation in,
459 (V1)
in trigeminal nerve repair, 266f, 269
(V1)
Autogenous gingival graft, 483f, 484-
485 (V1)
Autogenous temporomandibular joint
reconstruction, 945-947, 946f, 947f
(V2)
Autograft, platelet-rich plasma and,
504f, 504-506 (V1)
Autoimmune disease, facial asymmetry
and, 309-313, 310-313f (V3)
Autologous fibrin adhesive, 505 (V1)
Autologous periosteum for guided bone
regeneration, 429 (V1)
Autologous platelet gel, 501-510 (V1)
allograft and alloplastic materials
and, 504f, 504-506 (V1)
benefits of, 502-503 (V1)
case report of, 509, 509f (V1)
concept of, 501-502, 502f (V1)
processing of, 506-508, 507f, 508f
(V1)
Autonomic block testing, 141 (V1)
Autotransplantation versus extraction of
impacted tooth, 171-172 (V1)
Avascular necrosis, 187-189, 475 (V3)
Aventyl; See Nortriptyline
AVM; See Arteriovenous malformation
AVPU mnemonic, 7-8 (V2)
Avulsed tooth, 114t, 120-122, 121f,
122b (V2)
immediate implant loading following
extraction of, 540-546 (V1)
adaptive morphology of maxillary
alveolar process and, 541
(V1)
atraumatic extraction techniques
and, 541, 542f (V1)
bone loss following extraction and,
541, 541f (V1)
Avulsed tooth (Continued)
classification of extraction socket
defects and, 541, 543f (V1)
clinical situations for, 542-544,
544f, 545f (V1)
healing of extraction socket and,
540-541 (V1)
Avulsion, 289-290, 290f, 291f, 327-351
(V2)
airway management in, 327 (V2)
of alveolus, 128 (V2)
of cheek, 293f, 320, 320f (V2)
clinical examination in, 327-328
(V2)
debridement in, 328 (V2)
of ear, 294, 297f (V2)
of eyelid, 88, 308-309, 310f (V2)
gingival, 130 (V2)
imaging in, 328 (V2)
nasal, 301, 302-303f, 305f (V2)
optic disc, 83, 84f (V2)
reconstruction in avulsive facial
trauma, 328-350 (V2)
Abbe flap in, 329, 330f (V2)
aesthetic and prosthetic
rehabilitation and, 346-350f
(V2)
anterolateral thigh free flap in,
335, 335f (V2)
cervicofacial flap in, 329-330, 333f
(V2)
of cheek defects, 344, 345-348f
(V2)
facial artery musculomucosal flap
in, 329 (V2)
fibular free flap in, 333-335, 335f
(V2)
of lip defects, 343f, 343-344 (V2)
of lower face and mandible, 335-
340f, 336-337 (V2)
of nasal defects, 337, 343 (V2)
paramedian forehead flap in, 329,
331-332f (V2)
pectoralis major myocutaneous flap
in, 330-331 (V2)
radial forearm flap in, 332-333,
334f (V2)
rectus abdominis free flap in, 335
(V2)
of scalp defects, 346 (V2)
submental island flap in, 331-332,
334f (V2)
temporoparietal fascia flap in, 330
(V2)
of scalp, 59, 293f, 324, 324f (V2)
wound assessment in, 327, 328f (V2)
Axial view
in facial asymmetry, 273f, 274 (V3)
of mandible, 145f (V2)
Axonotmesis, 998t (V2)
in bilateral sagittal split osteotomy,
112 (V3)
classification of, 260, 260t (V1)
during exodontia, 216 (V1)
Azathioprine, 624 (V2)
Azithromycin
effect on osteoblast, 389, 389t (V1)
prophylactic, 5t (V1), 383t (V3)
B Basion to nasion, 27 (V3)
Babinski reflex, 51 (V2)
Backward-Upward-Rightward-Pressure
maneuver, 30 (V2)
Baclofen
for temporomandibular disorders,
887-888 (V2)
for trigeminal neuralgia, 150 (V1),
992, 992t (V2)
Bacteremia, exodontia-related, 217
(V1)
Bacterial infection
animal bite-related, 313-314 (V2)
facial asymmetry after, 281-282 (V3)
in laser skin resurfacing, 540, 540
(V3), 541f (V3)
in otoplasty, 676 (V3)
in rhinoplasty, 573 (V3)
Bag-valve mask ventilation, 26 (V2)
Bair Hugger, 39f (V2)
Balance sheet, 295, 295t (V1)
Balancing side condyle, 811 (V2)
Baldness
hair transplantation for, 651-657
(V3)
complications of, 655-656 (V3)
current medical treatment for
alopecia and, 651 (V3)
micrograft and minigraft technique
in, 651-653, 652-655f (V3)
pathophysiology of alopecia and,
651 (V3)
rotational flaps in, 655, 655f, 656f
(V3)
scalp reduction in, 655, 656f (V3)
Norwood classification of, 654f (V3)
rhytidectomy and, 501-502, 502f
(V3)
Balloon elevation in trephine bone core
sinus elevation, 465-468, 465-468f
(V1)
Banker, practice management and, 287
(V1)
Barbiturates, 60-62, 62t (V1)
Bardach two-flap palatoplasty, 726,
729f, 763-771 (V3)
controversies in, 762 (V3)
fistula rates in, 765-766, 766t (V3)
growth outcomes in, 769-770 (V3)
history of, 764 (V3)
muscular reconstruction in, 768 (V3)
outcomes based on cleft type or
severity and, 768-769 (V3)
principle techniques in, 764, 764f,
765f (V3)
for residual palatal fistula closure,
830, 830f (V3)
speech outcomes in, 766-767, 767b
(V3)
surgical procedure in, 770f, 770-771,
771f (V3)
syndromic associations and outcomes
in, 769 (V3)
technique comparisons in, 768 (V3)
timing of, 767-768 (V3)
Barton bandage, 140f (V2)
Basal cell ameloblastoma, 480f (V2)
Basal cell nevus syndrome, 433f, 441b,
441-442, 442t, 444f, 725, 739 (V2)
Basal energy expenditure, 15, 45 (V2)
Base deficit, 70 (V2)
Base plus bonus model of compensation,
298-299, 299t (V1)
Basic exodontia, 185-192 (V1)
complications in, 191-192 (V1)
diagnosis and treatment planning in,
187 (V1)
indications for, 186-187 (V1)
pain management in, 192 (V1)
principles of, 187-190, 188-190f (V1)
socket preservation and wound
closure in, 190-191 (V1)
Basicranium, 961 (V3)
Basilar skull fracture, 59-60 (V2)
initial assessment of, 50 (V2)
management of, 59-60 (V2)
orbital fracture and, 212 (V2)
Basion to A-point, 37 (V3)
Basion to B-point, 54 (V3)
Basosquamous basal cell carcinoma, 725
(V2)
Bathing after surgery, 411 (V3)
Battle’s sign
in head injury, 50, 59 (V2)
in sixth cranial nerve palsy, 85 (V2)
Bauer retractor, 125f (V3)
B-cell lymphoma, 760-761, 761f (V2)
Beck’s Depression Inventory, 142 (V1)
BEE; See Basal energy expenditure
Behavioral management
for chronic head and neck pain, 144
(V1)
for chronic orofacial pain, 123-124
(V1)
for posttraumatic headache,
153 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)

Behavioral speech therapy after cleft
surgery, 802-803 (V3)
Beh[ced]cet’s syndrome, 620-622 (V2)
Belfast-Hamburg approach in
cleidocranial dysplasia, 177 (V1)
Bell’s palsy, 292 (V3)
Bell’s phenomenon, 589, 589f (V3)
Benefit plan, 291 (V1)
Benign melanocytic proliferation, 749-
750 (V2)
Benign nevus, 518 (V3)
Benign skin lesions, laser skin
resurfacing of, 529 (V3)
Benign tumors, 592-610 (V2)
aneurysmal bone cyst in, 596-597,
597-598f, 868 (V2)
central giant cell granuloma in, 592-
594, 593f, 593t, 869 (V2)
cherubism in, 595-596, 596f (V2)
chondroma in, 605-606 (V2)
desmoplastic fibroma in, 606-608,
607-608f (V2)
fibrous dysplasia in, 600-601, 870
(V2)
florid cemento-osseous dysplasia in,
601, 601f (V2)
focal cemento-osseous dysplasia in,
601 (V2)
giant cell tumor in, 594 (V2)
hyperparathyroidism lesion in, 594f,
594-595 (V2)
juvenile ossifying fibroma in, 599-
600, 600f (V2)
neurofibroma in, 602, 604f (V2)
ossifying fibroma in, 598, 599f (V2)
osteoblastoma in, 602-604, 605f, 871
(V2)
osteochondroma in, 606, 871 (V2)
osteoid osteoma in, 602, 871 (V2)
osteoma in, 604-605, 606f, 871 (V2)
of parotid gland, 547-549,
549-551f (V2)
periapical cemental dysplasia in,
601 (V2)
schwannoma in, 601-602,
603f (V2)
of temporomandibular joint, 868-872
(V2)
Bennett movement, 811 (V2)
Benzocaine
chemical structure of, 37f (V1)
topical, 49 (V1)
Benzodiazepines
pharmacology of, 56-59, 58t, 59f
(V1)
for temporomandibular disorders, 131
(V1), 889, 889t (V2)
for temporomandibular osteoarthritis,
146 (V1)
Berlin edema, 82, 82f (V2)
Beta-adrenergic blockers
geriatric patient and, 381 (V2)
interaction with local anesthetics
with vasoconstrictors, 43, 43t
(V1)
for migraine, 148 (V1)
Betamethasone
for chronic facial pain, 974 (V2)
for temporomandibular disorders,
887t (V2)
Bi-cole technique, 191 (V1)
Bicoronal craniosynostosis, 852f
(V3)
Bifocal distraction in bone transport by
distraction osteogenesis, 355-356,
356-359f (V3)
Bilaminar hypertrophy, 413 (V3)
Bilateral coronal suture
craniosynostosis, 874-876 (V3)
Bilateral oronasal cleft deformity,
783-790 (V3)
complications of, 786 (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t (V3)
presurgical nasoalveolar molding and,
783 (V3)
surgical goals in, 784-786, 788f, 789f
(V3)
Bilateral parotidectomy, 539 (V2)
Bilateral sagittal split osteotomy, 71,
87-118 (V3)
characteristics and advantages of, 89,
89b (V3)
hemorrhage in, 115, 115b (V3)
historical background of, 68, 68f, 87-
89, 88f (V3)
loss of gonial projection after, 454,
455-456f (V3)
for mandibular asymmetry, 99t, 99-
102, 102-105f (V3)
for mandibular deficiency, 89b, 89-97
(V3)
with long face, 95f, 95-96, 96f, 97,
97b (V3)
with normal face height, 90-92,
90-92f, 97, 97b (V3)
with short face, 93f, 93-94, 94f, 97,
97b (V3)
for mandibular prognathism, 97-99,
98f (V3)
with long face, 99, 99b, 101f (V3)
with short face, 98-99, 99b, 100f
(V3)
nerve injury in, 112-113, 113b (V3)
neurosensory disorder after, 275 (V1)
for obstructive sleep apnea syndrome,
323-330, 327-332f (V3)
in oculoauriculovertebral spectrum,
931 (V3)
osteosynthesis in, 109-111, 110f,
111b (V3)
osteotomy in, 106-109, 107f, 107t,
108f, 109b (V3)
postoperative sequelae in, 111-112
(V3)
postoperative wound infection in,
115, 116b (V3)
rare complications in, 116, 116b (V3)
relapse in, 115-116, 116b (V3)
soft tissue dissection in, 102-106,
106f (V3)
temporomandibular joint dysfunction
in, 113-114 (V3)
transoral vertical ramus osteotomy
versus, 119, 120f (V3)
in two-jaw surgery, 240 (V3)
unfavorable bony split in, 114b, 114-
115 (V3)
Bimaxillary surgery, 238-247 (V3)
cephalometric analysis and, 375 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
model surgery and, 364-371 (V3)
construction of intermediate splint
in, 368-369, 369f, 370f (V3)
marking cast in, 366-367 (V3)
measurements in, 367f, 367-368
(V3)
mounting case in, 364-366, 365f,
366f (V3)
positioning of maxilla in, 368, 368f
(V3)
for segmental surgery, 369-370,
370f (V3)
for special situations, 370-371
(V3)
occlusal plane rotation in, 248-271
(V3)
clockwise rotation in, 252-256,
252-256f (V3)
counterclockwise rotation in, 256-
260, 257-263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-
249, 249f, 250f (V3)
geometry of treatment design using
constructed
maxillomandibular triangle in,
261f, 261-262 (V3)
linear dimensions between
maxillary length and vertical
facial height in, 250, 250f
(V3)
Bimaxillary surgery (Continued)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-
268 (V3)
postsurgical complications in, 396
(V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
in unilateral adolescent internal
condylar resorption, 305 (V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
videocephalometric prediction and,
376 (V3)
Bioactive fatty acids, 399-400 (V1)
Biobrane in laser skin resurfacing, 528
(V3)
Biocompatibility in guided tissue
regeneration, 429 (V1)
Biologically based cancer treatments,
669-671, 670f (V2)
Biomechanics
of mandibular fracture, 142-143,
143f, 144f (V2)
of temporomandibular joint, 816-818
(V2)
abnormal, 817-818, 818f, 819f
(V2)
normal, 816-817, 817f (V2)
Bioocclusive dressing in laser skin
resurfacing, 526-528 (V3)
Biopsy, 414 (V2)
excisional, 467-468, 731f (V2)
in lymphoma, 758 (V2)
in malignant melanoma, 753 (V2)
incisional, 467, 731t (V2)
in skin cancer, 731f, 731-732, 732f
(V2)
Birbeck granule, 568, 569f (V2)
Bird face deformity, 859 (V2)
Bispectral Index monitor, 30-31, 31f,
73, 73t, 99 (V1)
Bisphosphonate(s)
for craniofacial fibrous dysplasia, 980
(V3)
implant dentistry pharmacology and,
395-398, 396t, 397t (V1)
Bisphosphonate-related osteonecrosis of
jaw, 217, 218t (V1), 557-566 (V2)
chronic facial pain and, 970 (V2)
clinical presentation of, 559-560,
560f, 561f (V2)
clinical use of bisphosphonates and,
558-559 (V2)
future research in, 564 (V2)
mechanism of action of
bisphosphonates and, 557-558,
558f, 558t (V2)
pathophysiology and risk factors for,
559 (V2)
staging of, 560-561, 561t (V2)
treatment outlines for, 561-564, 563f,
563t, 564f (V2)
Bite
mandibular asymmetry and, 99t (V3)
orthognathic surgery-related changes
in, 72 (V3)
Bite plane splint, 883-884, 884f (V2)
Bite wound, 290-292, 292f, 313-316,
314-317f (V2)
Bizygomatic width, 36 (V3)
Blair preauricular incision, 932-933,
933f (V2)
Blake, John, 790 (V2)
Blast injuries, 313, 314f, 315f (V2)
Bleaching of teeth, laser-assisted, 256
(V1)
INDEX I-7
Bleeding
arteriovenous malformation and, 589
(V2)
in bilateral sagittal split osteotomy,
115, 115b (V3)
in exodontia, 219 (V1)
in genioplasty, 439 (V3)
intra-abdominal, 65-67, 66f, 67f (V2)
in intraoral vertical ramus osteotomy,
435, 435f (V3)
intraorbital, 474 (V3)
in Le Fort I osteotomy, 467-469f,
467-470 (V3)
in lymphatic malformation of tongue,
582-583 (V2)
nasal, 404 (V3)
in nasal fracture, 275 (V2)
perioperative management of, 387
(V3)
in sagittal split ramus osteotomy,
429-431, 433f (V3)
simple extraction and, 191 (V1)
Bleomycin, 779, 779t, 781t (V2)
Blepharochalasia, 579, 580f (V3)
Blepharoplasty, 579-594 (V3)
complications in, 593 (V3)
eyelid anatomy in, 580-587, 581f
(V3)
anterior lamella and, 582f, 582-583
(V3)
innervation and blood supply in,
585 (V3)
lacrimal system and, 587 (V3)
middle lamella and, 583f, 583-585,
584f (V3)
posterior lamella and, 585, 586f,
587f (V3)
laser skin resurfacing with, 544-545,
545-547f (V3)
laser-assisted, 250-251 (V1)
nomenclature in, 579f, 579-580 (V3)
patient evaluation in, 587-589, 588f,
589f (V3)
postoperative care in, 591-593, 593f
(V3)
surgical procedure in, 589-591, 590-
592f (V3)
Blepharoptosis, 579, 580f, 588 (V3)
Blindness
after maxillary osteotomy, 473-475
(V3)
in craniofacial dysostosis syndromes,
881 (V3)
following blepharoplasty, 593 (V3)
Blister
in pemphigoid, 622-624, 623f (V2)
in pemphigus, 624-625, 625f (V2)
Block graft for condylar subluxation,
906-908f, 909 (V2)
Block testing in chronic head and neck
pain, 140-141 (V1)
Blood flow, revascularization and
healing and, 70 (V3)
Blood glucose monitoring, 383 (V2)
Blood loss
ambulatory surgery and, 494-495
(V3)
in bilateral sagittal split osteotomy,
115, 115b (V3)
in combined maxillary and mandibular
osteotomies, 241 (V3)
in genioplasty, 439 (V3)
hemorrhagic shock and, 6-7, 7t (V2)
in intraoral vertical ramus osteotomy,
435, 435f (V3)
in Le Fort I osteotomy, 467-469f,
467-470 (V3)
perioperative management of, 392
(V3)
in sagittal split ramus osteotomy,
429-431, 433f (V3)
in scalp laceration, 50 (V2)
in trauma, 37-38, 38t, 46 (V2)
Blood pressure
age-related values, 94t (V1)
of child, 93-94, 94t, 99 (V1)
hypertension and
in geriatric patient, 381-382 (V2)
trigeminal neuralgia and, 991 (V2)
I-8 INDEX
Blood pressure (Continued)
hypotension, 6, 37-38, 38t, 49 (V2)
monitoring during anesthesia, 24-25
(V1)
Blood supply
to ear, 667-668 (V3)
to eyelid, 585 (V3)
to hand, 334f (V2)
to leg, 335f (V2)
maxillary osteotomy healing and, 63,
63f (V3)
to maxillary sinus, 459 (V1)
nasal, 272-273, 273f (V2), 553-554,
555f (V3)
to nasal tip, 555 (V3)
to temporomandibular joint, 163,
163f, 809, 809f (V2)
Blood transfusion, 15t (V1)
Blood urea nitrogen, 19t (V1), 387
(V3)
Blood vessels
facial, 9, 513 (V3)
of forehead and brow, 599 (V3)
of hand, 334f (V2)
of leg, 335f (V2)
nasal, 272-273, 273f (V2)
of temporomandibular joint, 163,
163f (V2)
Blow-out fracture of orbital floor, 86f,
86-87, 87f, 207, 207f (V2)
primary reconstruction in, 229-231,
230f (V2)
Blunt trauma
to eye, 78-82, 78-82f (V2)
myocardial, 44 (V2)
BMI; See Body mass index
Body composition, developmental
pharmacology and, 97 (V1)
Body dysmorphic disorder, 678 (V3)
Body mass index, 386, 419 (V3)
Body temperature
monitoring during anesthesia, 29
(V1)
thermoregulation in child and, 96
(V1)
Bone(s)
biology of, 406-407, 407f (V1)
bisphosphonates and, 557-558, 558f,
558t (V2)
changes after genioplasty, 145, 146-
149f, 150 (V3)
development of
bioactive fatty acids and, 399-400
(V1)
nonsteroidal antiinflammatory
drugs and, 392-395 (V1)
platelet-rich plasma and, 504f,
504-506 (V1)
facial, 15-17, 17f (V3)
maxillary, 172-174, 173f (V3)
nasal, 270-272 (V2), 555-556
(V3)
skeletal anchorage for orthodontics
and, 223-236 (V1)
basic orthodontic mechanics and,
224-225 (V1)
bone plates in, 232-233, 233f, 234f
(V1)
for closure of anterior open bite,
232 (V1)
devices for, 225f, 225-226, 226f
(V1)
historical perspective of, 223-224
(V1)
mesial or distal movement of teeth
and, 226-231f (V1)
miniscrews in, 233-235 (V1)
orthopedic growth modification
and, 232 (V1)
outcomes and complications in,
235-236 (V1)
postoperative regimen in, 234-235
(V1)
for uprighting and intruding molar
teeth, 232 (V1)
Bone cyst
aneurysmal, 596-597, 597-598f, 868
(V2), 972, 974-975f (V3)
traumatic, 869 (V2)
Bone defects
classification of extraction socket
defects, 541, 543f (V1)
guided tissue regeneration for, 428-
457 (V1)
in augmentation using allograft
and xenograft bone with
titanium-reinforced
membrane, 450-451, 450-451f
(V1)
in augmentation using allograft
bone putty and resorbable
collagen membrane, 448f,
448-449, 449f (V1)
in coronal defects, 436 (V1)
in corticocancellous block
augmentation of posterior
mandible, 452-453, 452-453f
(V1)
in dehiscence defects, 435-436,
447, 447f (V1)
dual-layered technique in, 445f,
445-446, 446f (V1)
in fenestration defects, 436 (V1)
flapless buccal wall reconstruction
in, 443f, 443-444, 444f (V1)
functional and design requirements
of membranes for, 429-431,
431f, 432f (V1)
to reduce postextraction bone loss,
438-440, 454f, 454-455, 455f
(V1)
ridge preservation using high-
density PTFE membrane in,
440-441f, 440-442 (V1)
in subantral augmentation, 436-
438, 437f (V1)
wound closure in, 431-435,
433f, 434f (V1)
osteoperiosteal flaps for,
471-478 (V1)
alveolar repositioning osteotomies
and, 473, 473f, 474f (V1)
alveolar split graft and, 471, 473f
(V1)
alveolar width distraction
osteogenesis and, 474-477,
475-478f (V1)
interpositional bone graft and, 471,
472f (V1)
Bone density
bisphosphonate therapy and, 396
(V1)
miniimplant success and, 567 (V1)
radiographic evaluation of, 547-548
(V1)
Bone flap, 471-478 (V1)
alveolar repositioning osteotomies
and, 473, 473f, 474f (V1)
alveolar split graft and, 471, 473f
(V1)
alveolar width distraction
osteogenesis and, 474-477, 475-
478f (V1)
interpositional bone graft and, 471,
472f (V1)
Bone graft
antibiotic prophylaxis and,
388 (V1)
antibiotics added to, 388-390, 389t,
390t (V1)
in cleft maxilla, 806-812, 840 (V3)
alveolar bone grafting technique
for, 808-810, 808-811f (V3)
grafting materials for, 806-807
(V3)
history and timing of repair in, 806
(V3)
missing teeth and crowded arches
and, 810-811, 811f (V3)
orthodontics for, 807f, 807-808
(V3)
postoperative care in, 810 (V3)
in cleft orthognathic surgery, 819,
820-825f (V3)
in complete mandibular subapical
osteotomy, 158, 160f, 162f (V3)
for condylar subluxation, 906-908f,
909 (V2)
Bone graft (Continued)
guided tissue regeneration procedures
and, 430-431, 431f, 432f (V1)
flapless buccal wall reconstruction
and, 443f, 443-444, 444f (V1)
in localized dehiscence defect, 447,
447f (V1)
in subantral augmentation, 437
(V1)
in immediate implant placement,
512-513 (V1)
in implant surgery, 406-427 (V1)
bone biology and, 406-407, 407f
(V1)
graft recipient site and, 419-422,
419-422f (V1)
ilium for, 415-419, 415-419f (V1)
mandibular ramus for, 412-414,
412-414f (V1)
mandibular symphysis for, 409-411,
410-412f (V1)
maxillary tuberosity for, 409, 409f,
410f (V1)
onlay bone graft and, 424, 424f,
425f (V1)
patient preparation for, 409 (V1)
preoperative evaluation in, 407-
408, 408f, 409f (V1)
sinus bone grafting and, 422-424,
423f (V1)
tibia for, 414f, 414-415, 415f (V1)
in internal derangement of
temporomandibular joint, 936,
937 (V2)
in Le Fort I osteotomy, 184 (V3)
in Le Fort III osteotomy, 211 (V3)
in nasal fracture, 280 (V2)
osteoperiosteal flap and, 471-478
(V1)
alveolar repositioning osteotomies
and, 473, 473f, 474f (V1)
alveolar split graft and, 471, 473f
(V1)
alveolar width distraction
osteogenesis and, 474-477,
475-478f (V1)
interpositional bone graft and, 471,
472f (V1)
in pediatric tumor-related defect,
992-993 (V3)
platelet-rich plasma and, 501-510
(V1)
in allograft and alloplastic
materials, 504f, 504-506 (V1)
benefits of, 502-503 (V1)
bone healing and, 394, 503f, 503-
504 (V1)
case report of, 509, 509f (V1)
concept of, 501-502, 502f (V1)
processing of, 506-508, 507f, 508f
(V1)
in sinus-lift subantral augmentation,
458-470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic
considerations in, 458-459
(V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f,
464f (V1)
elevation of schneiderian
membrane in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
trephine core membrane elevation
in, 464-468, 464-468f (V1)
vascular supply, lymphatic
drainage, and innervation in,
459 (V1)
Bone graft (Continued)
temporomandibular joint
reconstruction in
oculoauriculovertebral spectrum,
927-928, 928f (V3)
Bone graft donor sites, 409-419 (V1)
ilium, 415-419, 415-419f (V1)
mandibular ramus, 412-414, 412-414f
(V1)
mandibular symphysis, 409-411, 410-
412f (V1)
maxillary tuberosity, 409, 409f, 410f
(V1)
Bone healing, 62 (V3)
aberrant, 22-23 (V2)
in genioplasty, 151 (V3)
of graft in implant surgery, 424, 425f
(V1)
laser therapy and, 253-254 (V1)
mandibular fracture and, 144-146,
146f, 147f (V2)
nonsteroidal antiinflammatory drugs
and, 392-395 (V1)
platelet-rich plasma and, 501-510
(V1)
allograft and alloplastic materials
and, 504f, 504-506 (V1)
benefits of, 502-503 (V1)
case report of, 509, 509f (V1)
concept of, 501-502, 502f (V1)
processing of, 506-508, 507f, 508f
(V1)
regeneration in, 22 (V2)
Bone loss
after tooth extraction, 188-189, 541,
541f (V1)
bisphosphonates for, 395-398, 396t,
397t (V1)
mineral, hormonal, and vitamin
supplements for, 398-399, 399t
(V1)
postextraction
guided tissue regeneration for, 438-
440, 454f, 454-455, 455f (V1)
sinus-life subantral surgery and
graft for, 458 (V1)
Bone marrow suppression, radiation
therapy-related, 774 (V2)
Bone morphogenic proteins, 22 (V2)
platelet-rich plasma and, 502-503
(V1)
Bone pain in multiple myeloma, 686
(V2)
Bone plate fixation
in cleft orthognathic surgery, 819 (V3)
in Le Fort I osteotomy, 180, 182f
(V3)
in Le Fort III osteotomy, 211 (V3)
in modified Le Fort III osteotomy,
211-212 (V3)
Bone powder, bone graft harvest and,
406 (V1)
Bone removal
in complicated exodontia, 193-194,
194f (V1)
in impacted third molar tooth, 205-
206, 207-210f (V1)
Bone scan
in osteomyelitis, 634-635, 635f (V2)
in tumor-related facial asymmetry,
293 (V3)
Bone scraper, bone graft harvest and,
406, 407f (V1)
Bone screw for orthodontic mechanics,
225 (V1)
Bone transport by distraction
osteogenesis, 354-360 (V3)
bifocal distraction in, 355-356, 356-
359f (V3)
distraction protocol in, 359 (V3)
docking site surgery in, 359-360,
360f, 361f (V3)
indications for, 354-355 (V3)
maxillary, 360-362, 362f (V3)
multifocal distraction in, 356-359
(V3)
physiotherapy and, 360 (V3)
presurgical preparation in, 355 (V3)
principles of, 355, 355f (V3)

Bone tumors
benign, 592-610 (V2)
aneurysmal bone cyst in, 596-597,
597-598f (V2)
central giant cell granuloma in,
592-594, 593f, 593t (V2)
cherubism in, 595-596, 596f (V2)
chondroma in, 605-606 (V2)
desmoplastic fibroma in, 606-608,
607-608f (V2)
fibrous dysplasia in, 600-601 (V2)
florid cemento-osseous dysplasia in,
601, 601f (V2)
focal cemento-osseous dysplasia in,
601 (V2)
giant cell tumor in, 594 (V2)
hyperparathyroidism lesion in,
594f, 594-595 (V2)
juvenile ossifying fibroma in, 599-
600, 600f (V2)
neurofibroma in, 602, 604f (V2)
ossifying fibroma in, 598, 599f
(V2)
osteoblastoma in, 602-604, 605f
(V2)
osteochondroma in, 606 (V2)
osteoid osteoma in, 602 (V2)
osteoma in, 604-605, 606f (V2)
periapical cemental dysplasia in,
601 (V2)
schwannoma in, 601-602, 603f
(V2)
sarcomas of jaw in, 680-704 (V2)
chondrosarcoma in, 684f, 684-685
(V2)
Ewing’s sarcoma in, 687, 688f, 689f
(V2)
mandibular approaches in, 699-
702, 701f, 702f (V2)
maxillectomy in, 692-699, 694f,
695f, 697-699f (V2)
metastatic tumors to jaw and, 687-
689 (V2)
multiple myeloma and, 685-687,
686f, 687f (V2)
osteosarcoma in, 680-684, 681f,
682f (V2)
patient evaluation in, 689-692,
690t, 691f (V2)
radiation-induced, 685 (V2)
Bone turnover markers, 396-397, 397t
(V1)
Bone-borne appliance
in alveolar distraction, 350 (V3)
in mandibular widening, 338 (V3)
Bone-specific alkaline phosphate, 396-
397, 397f (V1)
Boniva; See Ibandronate
Bony interorbital distance, 24 (V3)
Book flap, 471, 473f (V1)
Borrelia burgdorferi, 864 (V2)
Botox; See Botulinum toxin
Botryoid odontogenic cyst, 442-444 (V2)
Botulinum toxin, 658-661 (V3)
for chronic facial pain, 974-975 (V2)
contraindications and adverse effects
of, 661, 662f (V3)
before filler injection in lip, 636, 636f
(V3)
history and pharmacology of, 658
(V3)
for persistent rhytidectomy-related
parotid sialocele, 509 (V3)
preoperative use in laser skin
resurfacing, 521 (V3)
preparations of, 658-659, 659t (V3)
for temporomandibular disorders,
888, 888t (V2)
treatment technique for, 660-661,
661f (V3)
uses in facial cosmetics, 659f, 659-
660, 660f (V3)
Botulism, 658 (V3)
Bovine collagen membrane, 429 (V1)
in alveolar ridge augmentation, 448f,
448-449, 449f (V1)
bone healing and, 394 (V1)
for facial augmentation, 629 (V3)
selection rationale for, 433-435 (V1)
Bowen’s disease, 726 (V2)
Bowman, Karl, 794 (V2)
Brachial plexus injury, 95 (V2)
Brachycephaly, 874-876 (V3)
Brachytherapy, 773 (V2)
Bradycardia
in anesthetized child, 94, 94t (V1)
glossopharyngeal neuralgia and, 994
(V2)
during Le Fort I osteotomy, 470 (V3)
Bradykinin
chronic facial pain and, 962, 963f
(V2)
wound repair and, 17 (V2)
Brain
abscess after frontal sinus fracture
repair, 267 (V2)
pain sensation and, 79f, 79-80, 137f,
137-138, 138f (V1)
restricted growth in craniofacial
dysostosis syndromes, 880-881
(V3)
Brain stimulation procedures
for chronic head and neck pain, 157
(V1)
for posttraumatic trigeminal
neuralgia, 157 (V1)
for trigeminal neuralgia, 151 (V1)
Brain-derived growth factor, 976 (V2)
Branchial arch syndrome, 298-299, 300-
302f (V3)
Branchial cleft cyst, 458-460, 458-460f
(V2)
Breached standard of care, 374 (V1)
Break-even point, 299 (V1)
Breast cancer
bisphosphonates for, 558 (V2)
metastasis to jaw, 689 (V2)
Breastfeeding child with cleft lip and
palate, 718 (V3)
Breathing assessment, 4-6, 25, 26b, 35-
36 (V2)
Breslow’s millimetric depth system for
melanoma, 753, 753t (V2)
Bridge, miniimplant support of, 568
(V1)
Bronchospasm in pediatric anesthesia
and sedation, 107 (V1)
BRONJ; See Bisphosphonate-related
osteonecrosis of jaw
Broselow Emergency Pediatric Tape,
100 (V1)
Brow
Botox injection in, 659, 659f, 661f
(V3)
endoscopic forehead and brow lift
and, 595-609, 596f (V3)
bone anatomy and, 595-597 (V3)
complications in, 606-607 (V3)
endoscopic anatomy and, 600-602,
601f (V3)
muscle and fascial anatomy and,
597-598, 598f (V3)
postoperative care in, 606 (V3)
preoperative evaluation in, 602t,
602-603 (V3)
technique in, 603f, 603-606, 605f
(V3)
vessel and nerve anatomy and,
598-600, 598-600f (V3)
evaluation before blepharoplasty, 587
(V3)
trichophytic forehead and brow lift
and, 610-617 (V3)
comparison of lift techniques and,
611t (V3)
complications in, 614-616, 616f,
617f (V3)
fixation techniques in, 610-611
(V3)
patient selection for, 613-614,
615f, 616f (V3)
surgical technique in, 611-614f,
612-613 (V3)
Brow fat pad, 581f (V3)
Brow height, 4, 5f (V3)
Bruising
Botox injection and, 661 (V3)
injectable facial filler and, 643 (V3)
Bruising (Continued)
periorbital
in basilar skull fracture, 50 (V2)
in frontal sinus fracture, 256, 259f
(V2)
in orbital fracture, 208 (V2)
postoperative, 403-404 (V3)
in bilateral sagittal split osteotomy,
111-112 (V3)
in sinus-lift subantral
augmentation, 463 (V1)
in zygomatic fracture, 184f (V2)
Brush biopsy, 415, 709 (V2)
Bruxism
anticlenching medications for, 409-
410 (V3)
fracture of provisional prosthesis in
zygomatic implant and, 498
(V1)
postoperative, 406-407 (V3)
splint therapy for, 884 (V2)
temporomandibular joint disorders
and, 128, 128f (V1)
BSSO; See Bilateral sagittal split
osteotomy
Buccal artery, 66f, 68, 175f (V3)
Buccal bifurcation cyst, 421-424 (V2)
Buccal cortex osteotomy, 157, 157f
(V3)
Buccal flap
in impacted maxillary canine, 197,
198f (V1)
in mandibular resection, 700-701,
701f (V2)
Buccal mucosa, 705 (V2)
squamous cell carcinoma of, 714-715,
715f, 716f (V2)
Buccal mucosal flap in cleft maxilla
repair, 811f (V3)
Buccal osteotomy
in antral membrane balloon
elevation, 465-466, 466f (V1)
in inferior alveolar nerve repair, 270
(V1)
in sinus-lift subantral augmentation,
459-460, 460f (V1)
Buccal plate fracture, 424-426, 425-428f
(V3)
Buccal wall reconstruction, 443f, 443-
444, 444f (V1)
Budget variance report, 294t (V1)
Budgeting, financial management and,
291-293, 294t (V1)
Bullous pemphigoid, 623 (V2)
Bupivacaine
for acute postoperative pain, 83 (V1)
chemical structure of, 37f (V1)
for chronic orofacial pain, 115 (V1)
duration of action of, 39t (V1)
lipid solubility of, 38t (V1)
pH effects on, 37t (V1)
for trigeminal neuralgia, 150 (V1)
Burkitt’s lymphoma, 760-761,
763 (V2)
Burn
during exodontia, 214 (V1)
facial soft tissue injury in, 321-323,
321-323f, 322t (V2)
in laser skin resurfacing, 521-522
(V3)
Burning mouth syndrome, 967-968,
995-996 (V2)
Burning mucosa, 149, 158 (V1)
Burning tongue, 149, 158 (V1)
BURP maneuver, 30 (V2)
Business lunch, marketing and, 337
(V1)
Business management, 285-303 (V1)
financial management and, 291-299
(V1)
accounting in, 293 (V1)
budgeting in, 291-293, 294t (V1)
compensation plans in, 298t, 298-
299, 299t (V1)
financial policy in, 295 (V1)
financial reporting in, 297-298
(V1)
financial statement trend analysis
in, 295 (V1)
INDEX I-9
Business management (Continued)
financial statements in, 295, 295t,
296t (V1)
revenue cycle and, 293-295 (V1)
human resources and, 290b, 290-291,
291-294t (V1)
information technology and, 303
(V1)
joining or starting practice and, 285
(V1)
legal documents and, 299-301, 300t,
301t (V1)
legal entities and, 285-286, 286t (V1)
organizational styles and, 288-290
(V1)
practice advisors and, 286-287 (V1)
practice evaluation and, 287-288,
288t, 289t (V1)
risk management and, 301-303 (V1)
Business office area, 355f, 355-356, 356f
(V1)
Business office equipment, 361 (V1)
Buspirone, 889, 889t (V2)
Buttresses of midfacial skeleton, 91, 92f,
239, 240f (V2)
Buyout insurance, 303 (V1)
Buy-sell agreement, 299-301, 300t (V1)
Buy-sell agreement checklist, 301 (V1)
C
C corporation, 285-286, 286t (V1)
CAD/CAM technology in implant
provisionalization, 528-531, 530f
(V1)
Cafeteria plan benefit package, 291,
324-325 (V1)
Cal technique in zygomatic implant,
494, 494f (V1)
Calcifying epithelial odontogenic
tumor, 473-476, 474f, 475f (V2)
Calcifying odontogenic cyst, 445-447,
447f (V2)
Calcitonin, 593, 593f (V2)
Calcitonin gene-related peptide, 962,
963f (V2)
Calcium channel blockers, 381 (V2)
Calcium chloride, platelet-rich plasma
and, 501, 502f, 508, 508f (V1)
Calcium hydroxide, 274 (V1)
Calcium hydroxide root canal fill, 119,
119f (V2)
Calcium pyrophosphate dihydrate
arthropathy, 865 (V2)
Calcium sulfite, 439 (V1)
Calcium supplementation for
preventing bone loss, 398, 399t
(V1)
Calhoun and Gibson lower facial
triangle, 682t (V3)
Call-on-hold device, 345 (V1)
Callus, 62 (V3)
Calvarial graft in nasal fracture, 280
(V2)
Calvin Long injury factor, 45 (V2)
Canaliculus, 206 (V2)
Cancellation of appointment, 346 (V1)
Cancellous autogenous bone graft for
dental implant, 406-427 (V1)
bone biology and, 406-407, 407f (V1)
graft recipient site and, 419-422, 419-
422f (V1)
ilium for, 415-419, 415-419f (V1)
mandibular ramus for, 412-414,
412-414f (V1)
mandibular symphysis for, 409-411,
410-412f (V1)
maxillary tuberosity for, 409, 409f,
410f (V1)
onlay bone graft and, 424, 424f, 425f
(V1)
patient preparation for, 409 (V1)
preoperative evaluation in, 407-408,
408f, 409f (V1)
sinus bone grafting and, 422-424,
423f (V1)
tibia for, 414f, 414-415, 415f (V1)
Cancer, 645-788 (V2)
benign nonodontogenic tumors and,
592-610 (V2)
I-10 INDEX
Cancer (Continued)
aneurysmal bone cyst in, 596-597,
597-598f (V2)
central giant cell granuloma in,
592-594, 593f, 593t (V2)
cherubism in, 595-596, 596f (V2)
chondroma in, 605-606 (V2)
desmoplastic fibroma in, 606-608,
607-608f (V2)
fibrous dysplasia in, 600-601 (V2)
florid cemento-osseous dysplasia in,
601, 601f (V2)
focal cemento-osseous dysplasia in,
601 (V2)
giant cell tumor in, 594 (V2)
hyperparathyroidism lesion in,
594f, 594-595 (V2)
juvenile ossifying fibroma in, 599-
600, 600f (V2)
neurofibroma in, 602, 604f (V2)
ossifying fibroma in, 598, 599f
(V2)
osteoblastoma in, 602-604, 605f
(V2)
osteochondroma in, 606 (V2)
osteoid osteoma in, 602 (V2)
osteoma in, 604-605, 606f (V2)
periapical cemental dysplasia in,
601 (V2)
schwannoma in, 601-602, 603f
(V2)
infantile hemangioma and, 577-579,
578f (V2)
lymphoma, 758-766, 759b (V2)
angiocentric, 761-762 (V2)
diagnosis of, 758-759, 759f, 760f
(V2)
Hodgkin’s, 759-760, 760f (V2)
non-Hodgkin’s, 760-761, 761f (V2)
of parotid gland, 551, 556 (V2)
prognosis of, 763-764, 764b (V2)
radiographic evaluation of, 762f,
762-763 (V2)
treatment of, 763 (V2)
medical oncology in, 777-788 (V2)
background of, 777, 778f (V2)
chemotherapy for metastatic
carcinoma and, 778-781, 779t,
781t, 782t (V2)
epidemiology and, 777 (V2)
epidermal growth factor receptors
and, 782-783, 783t (V2)
induction chemotherapy and, 777-
778 (V2)
salivary gland cancers and, 783-
785, 785f (V2)
taxanes in, 781-782 (V2)
melanoma, 749-757 (V2)
diagnosis of, 752t, 752-754, 753f,
753t (V2)
epidemiology of, 749, 750b (V2)
incidence and etiology of, 749-750,
750b, 750t, 750-752f, 751t
(V2)
management of regional disease in,
754 (V2)
staging of, 754-755, 755t (V2)
treatment of, 755-756 (V2)
molecular biology of, 645-679 (V2)
cancer cell evasion of apoptosis
and, 660-662, 661f (V2)
cancer cell insensitivity to growth
inhibitory signals and, 658-
660, 659f (V2)
cancer cell release from growth
signal requirement and, 655-
658, 657f (V2)
cancer cell versus normal cell and,
646-647, 647f (V2)
chromosomal abnormalities in
cancer cells and, 652-653,
653-655f (V2)
epigenetic alteration of gene
expression in cancer cells and,
655 (V2)
gene regulation of cell function
and, 648-652, 649-651f (V2)
immortalization of cancer cell and,
662-664, 663f (V2)
Cancer (Continued)
molecular diagnostics in oncology
and, 666-669, 667f (V2)
neovascularization and, 664, 665f
(V2)
nucleotide sequence abnormalities
in cancer cells and, 653-655,
656f (V2)
strategies of cancer-related
molecular therapeutics and,
669-671, 670f (V2)
stromal changes in cells and, 645,
646f (V2)
targeted therapy based on tumor
behavior and, 671-673 (V2)
tissue invasion and metastases and,
664-666, 666f (V2)
non-melanoma skin cancer, 724-748
(V2)
aggressive behavior of, 728-730,
729f (V2)
basal cell carcinoma in, 725, 725f
(V2)
cryotherapy for, 734 (V2)
curettage/electrodesiccation in,
734, 735f (V2)
dermatofibrosarcoma protuberans
in, 727-728, 728f (V2)
epidemiology and etiology of, 724-
725 (V2)
laser ablation and resurfacing in,
734-735 (V2)
of lip, 742-744, 743f (V2)
lymph node involvement in, 737-
739 (V2)
Merkel cell carcinoma in, 727
(V2)
microcystic adnexal carcinoma in,
726-727, 727f (V2)
Mohs’ micrographic surgery in,
735-736, 736b, 736f (V2)
photodynamic therapy for, 741
(V2)
physical examination in, 730t,
730-733, 731b, 731-733t (V2)
radiation therapy in, 741-742 (V2)
sebaceous gland carcinoma in, 727,
727f (V2)
squamous cell carcinoma in, 725-
726, 726f (V2)
staging of, 733-734 (V2)
systemic and topical medications
for, 739-741 (V2)
traditional surgical excision in,
736-737 (V2)
odontogenic tumors, 466-538 (V2)
adenomatoid, 469-472, 470-472f
(V2)
ameloblastic fibrodentinoma in,
524-527, 527f (V2)
ameloblastic fibroma in, 522-524,
523f (V2)
ameloblastic fibro-odontoma in,
524, 525f, 526f (V2)
ameloblastoma in, 476-502 (V2);
See also Ameloblastoma
biopsy of, 467-468 (V2)
calcifying, 445-447, 447f, 473-476,
474f, 475f (V2)
cementoblastoma in, 510-512 (V2)
classification of, 466-467 (V2)
clear cell, 502-508, 503-507f (V2)
clinical considerations in, 467 (V2)
fibroma in, 508-510, 509f, 511f
(V2)
imaging of, 467 (V2)
intraosseous odontogenic
carcinoma in, 527-532, 528-
530f (V2)
management objectives in, 468-
469 (V2)
myxoma in, 512-517f, 512-518
(V2)
odontoameloblastoma in, 519-522
(V2)
odontoma in, 518-519, 519-521f
(V2)
sarcoma in, 532-533 (V2)
squamous, 472f, 472-473 (V2)
Cancer (Continued)
oral cavity, 705-723 (V2)
anatomy in, 705-706 (V2)
buccal mucosa, 714-715, 715f, 716f
(V2)
diagnostic adjuncts in, 708-709,
709f (V2)
floor of mouth, 714, 714f, 715f
(V2)
follow-up in, 719-720 (V2)
genetic abnormalities in, 707-708
(V2)
non-surgical management of, 710-
713 (V2)
pretreatment evaluation in, 710
(V2)
primary tumor and, 713-714 (V2)
retromolar trigone, alveolar ridge,
and palate, 716-719 (V2)
risk factors for, 706-707 (V2)
screening for, 708 (V2)
staging of, 710, 711t (V2)
tongue, 716-717, 716-718f (V2)
types of neck dissection in, 719,
719t, 720f (V2)
radiation therapy in, 767-776 (V2)
altered radiation fractionation
schemes and, 772 (V2)
complications of, 773-774 (V2)
definitive radiotherapy and, 771
(V2)
histologies and, 767-768 (V2)
preoperative and postoperative,
771-772 (V2)
sites of disease and, 768t, 768-771,
769f, 770f, 770t, 771t (V2)
systemic therapy with, 772, 772t
(V2)
techniques in, 772-773,
773f (V2)
salivary gland tumors, 546-555 (V2)
benign, 547-549, 549-551f (V2)
high-grade malignant, 549-550,
552f (V2)
low-grade malignant, 549 (V2)
nonsalivary, 550-555, 553-556f
(V2)
parotid gland, 546-547, 548f (V2)
sarcomas of jaws, 680-704 (V2)
chondrosarcoma in, 684f, 684-685
(V2)
Ewing’s sarcoma in, 687, 688f, 689f
(V2)
mandibular approaches in, 699-
702, 701f, 702f (V2)
maxillectomy in, 692-699, 694f,
695f, 697-699f (V2)
metastatic tumors to jaw and, 687-
689 (V2)
multiple myeloma and, 685-687,
686f, 687f (V2)
osteosarcoma in, 680-684, 681f,
682f (V2)
patient evaluation in, 689-692,
690t, 691f (V2)
radiation-induced, 685 (V2)
temporomandibular joint tumors,
866-875, 867b (V2)
aneurysmal bone cyst in, 868 (V2)
arteriovenous malformation in,
870 (V2)
benign osteoblastoma in, 871 (V2)
central giant cell granuloma in,
869 (V2)
chondroblastoma in, 868 (V2)
chondrosarcoma in, 872 (V2)
condylar hyperplasia in, 868 (V2)
fibrous dysplasia in, 870 (V2)
ganglion and synovial cysts in, 869
(V2)
Garr[ac]e’s osteomyelitis and, 874
(V2)
hemangioma in, 869-870 (V2)
heterotopic bone formation in,
874-875 (V2)
idiopathic bone cavity cyst in, 869
(V2)
Langerhans cell histiocytosis and,
874 (V2)
Cancer (Continued)
metastatic carcinoma and, 874
(V2)
multiple myeloma in, 873-874
(V2)
nonossifying fibroma in, 870 (V2)
osteochondroma in, 871 (V2)
osteoid osteoma in, 871 (V2)
osteoma in, 871 (V2)
osteosarcoma in, 873 (V2)
phantom bone disease and, 875
(V2)
pigmented villonodular synovitis
and, 871-872 (V2)
pseudocyst in, 868-869 (V2)
synovial chondromatosis and, 872
(V2)
synovial chondrosarcoma in, 872-
873 (V2)
synovial sarcoma in, 873 (V2)
Cancer-related molecular therapeutics,
669-671, 670f (V2)
Canine extraction
complicated, 196-197, 197-199f (V1)
simple, 188, 189f (V1)
Canker sore, 619f, 619-620 (V2)
Cannulation of Wharton’s duct, 539,
540f (V2)
Canthal tendon, 582f (V3)
laceration of, 308-309f (V2)
Capecitabine, 781t (V2)
Capillary malformation, 581, 581f (V2)
Capnography, 27-28, 28f, 99 (V1)
Capsaicin
for chronic facial pain, 973t, 975
(V2)
for cluster headache, 149 (V1)
for postherpetic neuralgia, 152 (V1)
Capsular incision in internal
derangement of
temporomandibular joint, 934,
934f (V2)
Capsular ligament of
temporomandibular joint, 162
(V2)
Capsular release, temporomandibular
joint arthroscopy in, 924, 925f
(V2)
Capsule of temporomandibular joint,
803-804, 804f (V2)
Capsulitis, 831t (V2)
Capsulopalpebral fascia, 581-583f, 586f,
587f (V3)
Captique, 630 (V3)
Carbamazepine, 150 (V1), 992, 992t
(V2)
Carbon dioxide laser, 240, 240f, 241f
(V1)
in incisional and excisional soft tissue
procedures, 244-245 (V1)
for preimplantation surgery, 245 (V1)
in skin resurfacing, 521-532 (V3)
anesthesia and, 521, 522f (V3)
fractional photothermolysis in,
532, 536f (V3)
laser properties in, 514f, 514-516,
515f (V3)
laser settings for, 521-522, 522f
(V3)
postoperative care in, 524-529,
526-528f, 530-531f (V3)
resurfacing acne scars in, 529 (V3)
single-pass resurfacing in, 529-532,
533-534f (V3)
traditional technique in, 522-524,
523f, 525-526f (V3)
traumatic and surgical scars
improvement in, 529 (V3)
treatment of benign skin lesions
in, 529 (V3)
Carbon dioxide monitoring during
anesthesia, 27-28, 28f (V1)
Carboplatin, 779, 779t, 781t, 782t (V2)
Carboxyhemoglobin level, effects of
smoking on, 70 (V1)
Cardiac arrhythmia, glossopharyngeal
neuralgia and, 994 (V2)
Cardiac assessment before surgery, 2-3,
3t, 4f, 5t (V1)

Cardiac ischemia, chronic orofacial
pain in, 118 (V1), 969 (V2)
Cardiac medications, 381 (V2)
Cardiac output of child, 93-94, 94t
(V1)
Cardiac risk assessment, 382, 383b, 383t
(V3)
Cardiac tamponade, 38, 38f (V2)
Cardinal gazes, 77, 77f (V2)
Cardiovascular disease
ambulatory orthognathic surgery and,
493 (V3)
geriatric patient and, 380-381 (V2)
perioperative management of, 382,
383b (V3)
use of vasoconstrictors with local
anesthetics and, 41 (V1)
Cardiovascular system
effects of thyroid disorders on, 13t
(V1)
intensive care of trauma patient and,
44-45 (V2)
liver disease-related alteration in, 10
(V1)
pediatric anesthesia and sedation
and, 93-94, 94t (V1)
postoperative monitoring of, 75 (V1)
preoperative evaluation of, 2-3, 3t, 4f,
5t (V1)
Carisoprodol, 887, 888t (V2)
Carnoy’s solution, 274 (V1)
Carotid artery
condylar head and, 163f (V2)
detection of blunt trauma to, 69-70
(V2)
initial examination in head injury, 50
(V2)
Carotid cavernous fistula, 89 (V2), 187
(V3)
Carpenter’s syndrome, 909 (V3)
functional considerations in, 880-881
(V3)
midface deformity in, 205-206 (V3)
Carroll-Girard screw, 186, 186f (V2)
Cartilage
articular
extracellular matrix and, 849-850,
850f (V2)
osteoarthritis and, 855-856 (V2)
temporomandibular joint disorders
and, 127-128, 128f (V1)
auricular, 665-666 (V3)
Davis method for conchal
hypertrophy and, 670-673,
672f (V3)
excessive, 669 (V3)
temporomandibular joint
reconstruction and, 946-947
(V2)
nasal, 173f (V3), 272 (V2), 556, 556f
(V3)
cephalic strip technique and, 566
(V3)
closed rhinoplasty and, 572-573
(V3)
dorsal reduction and, 568f, 568-
569 (V3)
septoplasty and, 570 (V3)
tip plasty and, 562-563, 563f (V3)
unilateral versus bilateral oronasal
cleft deformity and, 784t (V3)
Cartilage tip graft, 566 (V3)
Caruncle, 206f (V2)
Case mounting in model surgery, 364-
366, 365f, 366f (V3)
Cast custom abutment, 528 (V1)
Cat bite, 292, 313-316, 314-316f (V2)
Cataflam; See Diclofenac
Catapres; See Clonidine
Catecholamines in local anesthetics,
39-45, 40t, 43-45t, 44b (V1)
Catheter approach in sialolithiasis, 544
(V2)
Cationic form of local anesthetic, 37-
38, 38f (V1)
Cauda of external ear, 667f (V3)
Causalgia, 966t, 967, 997 (V2)
Cavum concha, 666, 667f (V3)
CDT; See Current Dental Terminology
Cefazolin
effect on osteoblast, 389, 389t (V1)
prophylactic, 5t (V1), 383t (V3),
392-393 (V3)
subtoxic concentration of, 390, 390t
(V1)
Ceftriaxone, 5t (V1), 383t (V3)
Celebrex; See Celecoxib
Celecoxib, 84t, 86 (V1)
bone healing and, 393 (V1)
for temporomandibular disorders,
887t (V2)
Celestone; See Betamethasone
Cell cycle clock, 658-660, 659f (V2)
Cell margination in wound healing, 61
(V3)
Cellulitis, 582 (V2)
Cellulose acetate for guided bone
regeneration, 429 (V1)
Cementoblastoma, 510-512 (V2)
Cemento-osseous dysplasias, 601, 601f
(V2)
Cemento-ossifying fibroma, 598, 599f
(V2)
Centers of Medicare and Medicaid
Services
on coding, 364 (V1)
on credentialing, 308 (V1)
Central biasing mechanism of
myogenous pain, 980 (V2)
Central cord syndrome, 63-64 (V2)
Central deafferentation syndrome, 264
(V1)
Central giant cell granuloma, 592-594,
593f, 593t, 869 (V2)
Central giant cell lesions, 970-972, 973f
(V3)
Central hypothesis of myogenous pain,
980 (V2)
Central mechanisms of chronic facial
pain, 963 (V2)
Central mediated pain in chronic
orofacial pain, 120-121 (V1)
Central nasoethmoidal buttress, 91, 92f
(V2)
Central nervous system
Beh[ced]cet’s syndrome and, 621
(V2)
pain sensation and, 79f, 79-80 (V1)
Central odontogenic fibroma, 509f,
509-510 (V2)
Central orbital fat pad, 584f, 585 (V3)
Central pain, 966t (V2)
Central poststroke pain, 994-995 (V2)
Central sensitization, 138 (V1), 963,
998 (V2)
Central sleep apnea, 317 (V3)
in craniofacial dysostosis syndromes,
881 (V3)
Central unicystic ameloblastoma, 482-
484f (V2)
Central visual field assessment, 75-76
(V2)
Centrax; See Prazepam
Centric relation, 365-366 (V3)
Cephalexin
in laser skin resurfacing, 521 (V3)
prophylactic, 5t (V1), 383t (V3)
Cephalic strip, 564, 565f, 566 (V3)
Cephalocaudal growth vector, 849f,
849-850 (V3)
Cephalometric evaluation, 10-17 (V3)
in adolescent internal condylar
resorption, 306f (V3)
changes with age, 15-17, 17f (V3)
in complete mandibular subapical
osteotomy, 155, 156f (V3)
in condylar hyperplasia, 288f (V3)
of craniofacial growth, 856 (V3)
dental relations in, 14-15, 16f (V3)
evaluation form for, 15b (V3)
in facial asymmetry, 312f (V3)
in hemifacial microsomia, 302f (V3)
in obstructive sleep apnea syndrome,
321-323, 325-327f (V3)
posteroanterior, 18-19 (V3)
postoperative, 416f (V3)
prediction of soft-tissue changes in,
372-375, 373f (V3)
Cephalometric evaluation (Continued)
radiography in, 549-551f (V1)
in rotation of maxillomandibular
complex, 248-249, 249f, 250f,
261, 262f, 264-266f (V3)
skeletal relations in, 12-14, 13-15f
(V3)
soft tissue relations in, 11-12, 12f
(V3)
in transverse maxillary deficiency,
221f, 221-222 (V3)
in trauma-related facial asymmetry,
296f (V3)
in Treacher Collins syndrome, 938
(V3)
in unilateral reactive arthritis, 309f
(V3)
Cephalosporins, 5t (V1)
Cerebellar function evaluation in head
injury, 52 (V2)
Cerebellopontine angle tumor, 992
(V2)
Cerebral contusion, 61-62 (V2)
Cerebral vasospasm, post-traumatic, 62
(V2)
Cerebrospinal fluid leak
after nasal fracture repair, 282 (V2)
in basilar skull fracture, 59 (V2)
in cranio-maxillofacial trauma, 9
(V2)
in frontal sinus fracture, 256, 267
(V2)
in midface fracture, 253-254 (V2)
Cerebrovascular accident, central
poststroke pain and, 994-995 (V2)
Cerebrovascular disease, 382 (V2)
Certificate of merit, 376 (V1)
Certification, 308-309 (V1)
Cervical incision in pediatric
craniomaxillofacial tumor, 962-963
(V3)
Cervical musculoskeletal macrotrauma,
143 (V1)
Cervical spine
initial examination in head injury
and, 11, 50 (V2)
injury of, 63-64, 64f (V2)
Cervicofacial area, detailed aesthetic
evaluation of, 6-8, 9f (V3)
Cervicofacial flap, 329-330, 333f (V2)
Cervicofacial liposuction, 618-625 (V3)
complications of, 623-624 (V3)
history of, 618 (V3)
patient selection in, 618-620, 619f
(V3)
preoperative preparation in,
620 (V3)
surgical technique in, 620-623, 620-
625f (V3)
Cervicofacial lymphatic malformation,
583, 584f, 585f (V2)
Cervicofacial venous malformation,
586f, 586-587 (V2)
Cervicogenic headache, 143 (V1)
Cervicomental angle, 619f (V3)
Cervicomental area, profile evaluation
and, 3f, 4 (V3)
Cetuximab, 772, 778, 779, 779t, 781t,
782t, 783 (V2)
C-fiber, 78-79 (V1), 962, 963 (V2)
C-fiber nociceptor, 137-138 (V1)
Chalazion, 206 (V2)
Change arch wires, 400 (V3)
Chart documentation, 358 (V1)
Charting, 358 (V1)
Cheek
detailed aesthetic evaluation of, 4-5,
6f (V3)
malar augmentation with injectable
fillers and, 639, 639f (V3)
trauma to, 320f, 320-321, 321f (V2)
reconstruction of, 344, 345-348f
(V2)
reconstructive flap options for,
336b (V2)
Cheek flap
in mandibular resection, 700-701,
701f (V2)
in rhytidectomy, 502, 503f (V3)
INDEX I-11
Cheek implant, 689f, 689-690, 690f,
690t (V3)
Cheerleader syndrome, 299-305, 303-
304f, 306f (V3)
Chemabrasion, 661-664, 662f, 664f
(V3)
Chemexfoliation, 661-664, 662f, 664f
(V3)
Chemical peel, 661-664, 662f, 664f
(V3)
Chemoprevention
in oral cavity cancer, 710-712 (V2)
in skin cancer, 739 (V2)
Chemosurgery, 661-664, 662f, 664f
(V3)
Chemotherapy, 777-788 (V2)
background of, 777, 778f (V2)
basic exodontia and, 186-187 (V1)
in desmoplastic fibroma, 608 (V2)
epidemiology and, 777 (V2)
epidermal growth factor receptors
and, 782-783, 783t (V2)
induction, 777-778 (V2)
in lymphoma, 763 (V2)
in malignant melanoma, 756 (V2)
in metastatic carcinomas, 778-781,
779t, 781t, 782t (V2)
in multiple myeloma, 687 (V2)
in osteosarcoma, 683 (V2)
in salivary gland cancers, 783-785,
785f (V2)
taxanes in, 781-782 (V2)
Cherubism, 595-596, 596f (V2)
Chest
penetrating injury of, 42 (V2)
secondary survey of, 40 (V2)
Chest radiography
in cranio-maxillofacial trauma, 11
(V2)
preoperative, 19t (V1)
Chest wall of child, 95, 95f (V1)
Chewing sequence, 811-812 (V2)
Chewing tobacco, oral cavity cancer
and, 706 (V2)
Child
anesthesia and sedation of, 67-68, 93-
111 (V1)
airway equipment preparation for,
100t, 100-102 (V1)
anaphylaxis and, 107, 107t (V1)
bronchospasm and, 107 (V1)
carbon dioxide monitoring during,
28 (V1)
cardiovascular system and, 93-94,
94t (V1)
developmental pharmacology and,
96-97 (V1)
fentanyl for, 104 (V1)
gastric contents aspiration and,
107 (V1)
inhalation anesthesia for, 104-105
(V1)
intraoperative fluids and, 102-103
(V1)
intravenous access and, 102, 102f
(V1)
ketamine for, 104 (V1)
laryngospasm and, 106-107 (V1)
liver function and, 96 (V1)
malignant hyperthermia and, 107-
108 (V1)
midazolam for, 103-104 (V1)
monitoring during, 99-100 (V1)
Pediatric Anesthesia Worksheet
for, 101b (V1)
preanesthetic assessment and, 97-
99, 98f (V1)
premedication for fear and anxiety
in, 103 (V1)
propofol for, 104, 105t (V1)
renal system and, 96 (V1)
respiratory system and, 94-96, 95f,
96t (V1)
techniques for, 105-106 (V1)
thermoregulation and, 96 (V1)
cleft lip and palate in, 713-734 (V3)
classification of, 715-716, 716f,
717f (V3)
embryology of, 714-715 (V3)
I-12 INDEX
Child (Continued)
feeding child with, 717-718 (V3)
genetics and etiology of, 715 (V3)
prenatal counseling and, 716-717
(V3)
cleft lip and palate repair in, 719-730
(V3)
cleft palate repair and, 723-727,
729f, 730f (V3)
complex facial clefting and, 727-
728, 731f (V3)
history of, 713-714 (V3)
lip adhesion and, 720 (V3)
outcome assessment in, 728-730
(V3)
presurgical taping and orthopedics
in, 719-720, 720f (V3)
primary bilateral lip repair and,
723, 724-728f (V3)
primary unilateral cleft lip repair
and, 720-723, 721-723f (V3)
treatment planning and timing in,
718t, 718-719 (V3)
cleft orthognathic surgery in, 813-827
(V3)
bone grafting in, 819, 820-825f
(V3)
obstructed nasal breathing and,
819 (V3)
preoperative evaluation in, 813-
814 (V3)
stabilization of mobilized cleft
maxilla and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-
819, 818f (V3)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
cleft palate repair in, 723-727, 729f,
730f, 759-782 (V3)
double-opposing Z-plasty in, 772-
775, 773-775f (V3)
fistulas and, 763 (V3)
history of, 759-760 (V3)
intravelar veloplasty in, 762-763
(V3)
outcomes in, 760-761 (V3)
palatoplasty technique in, 762 (V3)
speech evaluation in, 761 (V3)
timing of, 761 (V3)
two-flap palatoplasty for, 763-771,
764-765f, 766t, 767b, 770f,
771f (V3)
two-stage palate repair in, 776-778
(V3)
congenital heart disease in, 382-383,
383t (V3)
congenital hemangioma in, 579f,
579-581, 580f (V2)
craniofacial dysostosis syndromes in,
880-921 (V3)
Apert syndrome in, 902-909, 903-
907f (V3)
Carpenter syndrome in, 909 (V3)
cloverleaf skull anomaly in, 909-
914, 910-914f (V3)
Crouzon syndrome in, 886-902,
887-900f (V3)
dentition and occlusion anomalies
in, 881-882 (V3)
functional considerations in, 880-
881 (V3)
genetic aspects of, 880 (V3)
morphologic considerations in,
882-883 (V3)
Pfeiffer syndrome in, 909 (V3)
Saethre-Chotzen syndrome in, 909
(V3)
surgical management of, 883-886
(V3)
cranio-maxillofacial trauma in, 352-
373 (V2)
child abuse and, 372 (V2)
craniofacial growth and
development and, 352-353,
353f (V2)
Child (Continued)
dentoalveolar fractures in, 363-364
(V2)
epidemiology of, 353-354 (V2)
frontal bone and superior orbital
fractures in, 355 (V2)
frontal sinus and frontobasilar
injuries in, 355, 356-357f
(V2)
mandibular body and angle
fractures in, 364 (V2)
mandibular condyle fractures in,
364-369, 369f (V2)
midface fractures in, 253, 363 (V2)
nasal fractures in, 281, 362-363
(V2)
naso-orbito-ethmoid fractures in,
355-360, 358-359f (V2)
orbital fractures in, 360-361, 360-
361f (V2)
perioperative management of, 354-
355 (V2)
prevention of, 354 (V2)
rigid internal fixation and, 369-370
(V2)
Risdon cable and, 370f, 370-372
(V2)
soft tissue injuries in, 292, 293f,
371f, 372 (V2)
surgical anatomy in, 353 (V2)
symphyseal and parasymphyseal
mandibular fractures in, 364,
365-367f (V2)
zygomaticomaxillary complex
fractures in, 361-362, 362-
363f (V2)
craniosynostosis in, 864-879 (V3)
anterior plagiocephaly in, 868-871,
871f, 872f (V3)
brachycephaly in, 874-876 (V3)
delayed diagnosis of, 867-868
(V3)
diagnosis of, 865-866 (V3)
functional consequences of, 864-
865, 865f (V3)
posterior plagiocephaly in, 874,
877f, 878f (V3)
scaphocephaly in, 868, 869-870f
(V3)
surgical considerations in, 856-858,
866-867 (V3)
syndromes associated with, 850
(V3)
timing of surgery for, 867 (V3)
trigonocephaly in, 871-874,
874-876f (V3)
dentoalveolar surgery in, 165-184
(V1)
for cleidocranial dysplasia,
175-177, 176f, 177f (V1)
eruption pattern for deciduous and
permanent dentition, 165,
166t (V1)
for Gardner’s syndrome, 178f, 178
(V1)
for generalized gingival hyperplasia,
178-179, 179f (V1)
for hereditary ectodermal dysplasia,
177f, 177-178 (V1)
for impacted teeth, 165-173 (V1);
See also Impacted teeth
implants in, 181-183, 182f, 183f
(V1)
for localized gingival lesions, 179-
181, 180f, 181f (V1)
soft tissue procedures in, 173-174,
173-176f (V1)
desmoplastic fibroma in, 606-608,
607-698f (V2)
growth and development
considerations in
craniomaxillary surgery,
848-863 (V3)
clinical evaluation of craniofacial
growth and, 856 (V3)
concepts of craniofacial skeletal
growth and development and,
849f, 849t, 849-850, 850t
(V3)
Child (Continued)
cranio-orbital dysmorphology and,
856-858 (V3)
cranium and, 850-851, 852f (V3)
mandible and, 855-856, 856f, 857f
(V3)
mandibular hyperplasia and, 859-
860, 860f (V3)
mandibular hypoplasia and, 858-
859, 859f (V3)
maxilla and, 851, 854f, 855f (V3)
maxillary hypoplasia and, 860-861
(V3)
orbits and, 851, 853f (V3)
vertical maxillary excess and, 861f,
861-862 (V3)
zygoma and, 851, 853f (V3)
herpes simplex infection in, 615-617
(V2)
infantile hemangioma in, 577-579,
578f (V2)
juvenile ossifying fibroma in, 599-
600, 600f (V2)
juvenile rheumatoid arthritis in, 859
(V2)
facial asymmetry in, 309 (V3)
temporomandibular joint ankylosis
and, 902 (V2)
temporomandibular joint
reconstruction in, 961-962
(V2)
linear IgA disease in, 625-626 (V2)
otoplastic surgery for protruding ear,
665-677 (V3)
blood supply to ear and, 667-668
(V3)
complications in, 675-676 (V3)
for congenital deformities, 668-669
(V3)
for correction of protruding
earlobe, 675, 675f (V3)
Davis method in, 670-673, 672f
(V3)
embryology of auricle and, 665,
666f (V3)
Farrior technique in, 673, 675f
(V3)
indications and timing of, 669
(V3)
Mustard[ac]e method in, 673, 674f
(V3)
nerve supply to ear and, 668-670f
(V3)
surgical anatomy in, 665-666, 666f,
667f (V3)
techniques in, 669-670, 671f (V3)
presurgical dentofacial orthopedics
for, 783-790 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t
(V3)
presurgical nasoalveolar molding
and, 783 (V3)
prophylactic antibiotic regimen for,
383t (V3)
tumors in, 961-995 (V3)
adenomatoid odontogenic tumor
in, 968, 968f (V3)
ameloblastic fibroma in, 968-970,
970f (V3)
ameloblastic fibro-odontoma in,
970, 970f (V3)
ameloblastoma in, 967f, 967-968
(V3)
anatomic classification in, 962
(V3)
aneurysmal bone cyst in, 972, 974-
975 (V3)
central giant cell lesions in, 970-
972, 973f (V3)
craniofacial fibrous dysplasia in,
977-980, 980-985f (V3)
craniomaxillofacial access and,
962-967, 963-965f (V3)
endoscopic approaches in, 967
(V3)
imaging of, 961-962 (V3)
Child (Continued)
juvenile aggressive fibromatosis in,
970, 972f (V3)
juvenile nasopharyngeal
angiofibroma in, 972-974,
976-977f (V3)
juvenile ossifying fibroma in, 974-
977, 978-979f (V3)
neurofibromatosis in, 980-984, 986f
(V3)
odontogenic myxoma in, 968, 969f
(V3)
odontoma in, 970, 971f (V3)
reconstruction in, 988-993, 991f,
992f (V3)
rhabdomyosarcoma in, 984-986,
987f (V3)
salivary gland tumor in, 987-988
(V3)
sarcomas in, 986-987, 988-990f
(V3)
visual acuity in, 75 (V2)
Child abuse, 372 (V2)
Child-Pugh Scoring System, 10t (V1)
Chin
analysis for determining chin
position, 681-683t (V3)
Botox injection in, 660, 660f (V3)
cephalometric analysis of, 12-13, 13f
(V3)
cervicofacial liposuction and, 618-
625 (V3)
complications of, 623-624 (V3)
history of, 618 (V3)
patient selection in, 618-620, 619f
(V3)
preoperative preparation in, 620
(V3)
surgical technique in, 620-623,
620-625f (V3)
genioplasty and, 137-154 (V3)
cephalometric analysis and, 373
(V3)
before complete mandibular
subapical osteotomy, 162f,
163f (V3)
fixation devices in, 142-145, 144-
148f (V3)
functional, 137, 138f (V3)
indications for, 137-138 (V3)
Le Fort I segmental osteotomy
with, 199-203f (V3)
mandibular relapse in, 446-451,
449-452f (V3)
mandibular widening with, 339-
341, 340f, 341f (V3)
for obstructive sleep apnea
syndrome, 325-327, 329f (V3)
outpatient, 493 (V3)
relapse in, 446-451, 449-452f (V3)
results in, 148-151, 150-153f (V3)
surgical procedure in, 140-142,
141f, 142f (V3)
treatment planning in, 138-140,
139f, 140f (V3)
implants for large nose and small
chin, 679f, 679-684, 680f, 684f,
685b, 685f (V3)
mandibular asymmetry and, 99t (V3)
Chin implant
alloplastic, 684f, 684-685, 685b, 685f
(V3)
in facial skin laxity with weight loss,
686-688, 686-688f (V3)
Chin projection, 4, 7-8 (V3)
Chin-neck angle and length, 7, 9f (V3)
Chlordiazepoxide, 889t (V2)
Chlorhexidine rinsing
for aphthous stomatitis, 620 (V2)
in autogenous bone graft for implant,
422 (V1)
in guided tissue regeneration, 430
(V1)
postoperative, 410 (V3)
in splint care, 399 (V3)
in zygomatic implant, 498 (V1)
Chlorzoxazone, 888t (V2)
Cholinergic anti-inflammatory pathway,
21 (V2)

Chondroblastoma of
temporomandibular joint, 868
(V2)
Chondrocalcinosis articularis, 865 (V2)
Chondrocyte, 849 (V2)
Chondroitin sulfate, 849 (V2)
Chondroma, 605-606, 685 (V2)
Chondromalacia, 856 (V2)
Chondrosarcoma, 684f, 684-685 (V2)
of temporomandibular joint, 872
(V2)
CHOP regimen in lymphoma, 763 (V2)
Choroidal rupture, 82, 83f (V2)
Christensen, R.W., 795-796, 796f (V2)
Christensen implant system, 797 (V2)
Christensen TMJ Arthro-Chrome
Condylar Prosthesis, 904 (V2)
Christ-Stemens-Touraine syndrome,
177 (V1)
Chromatin, 648 (V2)
Chromophore, 239 (V1)
Chromosomal abnormalities in cancer,
652-653, 653-655f, 707 (V2)
Chromosomal deletion, 652-653, 655f
(V2)
Chronic anterior disc displacement,
818-821, 819-821f (V2)
mandibular gait in, 825, 827f (V2)
Chronic bronchitis, 382-384, 384b (V3)
Chronic bullous dermatosis of
childhood, 625-626 (V2)
Chronic obstructive pulmonary disease
geriatric patient and, 382 (V2)
perioperative management of, 383-
384, 384b (V3)
preoperative evaluation of, 6 (V1)
Chronic obstructive sialoadenitis, 545-
546, 547f (V2)
Chronic osteomyelitis, 636t (V2)
Chronic pain, 137-138, 138t (V1)
facial, 961-978 (V2)
antidepressants for, 973 (V2)
atypical facial pain and, 967-968
(V2)
barriers to management of, 970-
971 (V2)
botulinum toxin injection for, 974-
975 (V2)
of cardiac origin, 969 (V2)
central mechanisms of, 963 (V2)
clinically based comprehensive
pain management program
for, 975 (V2)
complex regional pain syndrome
and, 966-967 (V2)
Eagle’s syndrome and, 969-970,
970f (V2)
evaluation of, 963-966, 965f, 966t
(V2)
future directions in management
of, 975-976 (V2)
muscle relaxants for, 974 (V2)
nerve injury from dental
procedures and, 968f, 968-969
(V2)
neuralgia-inducing cavitational
osteonecrosis and, 967 (V2)
neuropathic agents for, 973-974
(V2)
nonsteroidal antiinflammatory
drugs for, 972-973, 973t (V2)
opioid therapy for, 971-972, 972t
(V2)
osteonecrosis-related, 970 (V2)
peripheral mechanisms of, 962,
963f (V2)
physical therapy for, 971 (V2)
surgical intervention for, 975
(V2)
therapeutic injections for, 974
(V2)
topical capsaicin for, 975 (V2)
trigeminal anatomy and, 961-962,
962f (V2)
head and neck, 136-163 (V1)
brain stimulation procedures for,
157 (V1)
characterization and measurement
of, 139 (V1)
Chronic pain (Continued)
clinical and laboratory
examination in, 139-140 (V1)
cluster headache and
trigeminoautonomic variants
and, 148-149 (V1)
complex regional pain syndrome
and, 157-158 (V1)
diagnosis of, 139, 139t (V1)
fibromyalgia and, 142 (V1)
idiopathic and atypical orofacial
pain syndromes and, 158 (V1)
incidence and demographics of,
137 (V1)
migraine and, 146-148, 147f (V1)
myofascial pain syndromes and,
143-145 (V1)
orofacial migraine variants and,
149 (V1)
pain definitions and, 137-138, 138t
(V1)
pathophysiology of pain and, 137f,
137-139, 138f (V1)
pharmacologic screening in,
140-141 (V1)
postherpetic neuralgia and,
151-152 (V1)
posttraumatic headache and,
152-153 (V1)
posttraumatic trigeminal neuralgia
and, 154-156 (V1)
psychiatric disorders and,
141-142 (V1)
sleep dysfunction and, 141 (V1)
surgical treatments for, 156-157
(V1)
systemic disease and, 141 (V1)
temporomandibular arthritis and,
145-146 (V1)
trigeminal neuralgia and, 149-151
(V1)
orofacial, 112-135 (V1)
changing treatment of, 121-122
(V1)
cranial nerve examination in, 116-
118, 119f, 120f (V1)
flexible diagnoses-management
concept in, 113-114 (V1)
follow-up visits for, 121 (V1)
individualized pain management
in, 122-124, 123f, 124f (V1)
initial visit for, 112-113 (V1)
local anesthetic injections for,
114-115, 115-117f (V1)
localized pathologic conditions
and, 115-116 (V1)
peripheral and central mediated
pain in, 120-121 (V1)
prevention of progression to, 124-
126 (V1)
reevaluation of diagnoses in, 121
(V1)
systemic pathologic conditions
and, 118 (V1)
in temporomandibular joint
disorders, 126-134, 128f, 129f
(V1)
temporomandibular joint
protection during surgical
procedures and, 125 (V1)
third molar pathologic conditions
and, 125-126 (V1)
third molar surgery and,
125 (V1)
Chronic paranasal sinus pain, 149 (V1)
Chronic refractory osteomyelitis, 638
(V2)
Chronic subdural hematoma, 61, 62f
(V2)
Ciprofloxacin
effect on osteoblast, 389, 389t (V1)
for laser skin resurfacing-related
bacterial infection, 540 (V3)
for periimplantitis, 392 (V1)
Circulation
cranio-maxillofacial trauma and, 6-7,
7t (V2)
monitoring during anesthesia, 24-25
(V1)
Circulation (Continued)
primary survey and, 37-38, 38f, 38t
(V2)
Circumvestibular approach in Le Fort I
osteotomy, 464 (V3)
Cirrhosis, 11t (V1)
Cisplatin, 781t (V2)
5-fluorouracil and taxanes with, 778,
782t (V2)
for metastatic tumors, 779, 779t (V2)
radiation therapy with, 771, 772
(V2)
13-cis-retinoic acid, 712 (V2)
CIST; See Cumulative interceptive
supportive therapy
Citric acid for chemical peel, 663 (V3)
Civil action, 374 (V1)
Claims adjudication, 370 (V1)
Claims made policy, 377 (V1)
Claims submission
fraudulent, 371 (V1)
to insurance company, 368-369 (V1)
to third-party payer, 369-370 (V1)
Clarithromycin, 5t (V1), 383t (V3)
Clark’s classification of melanoma, 753,
753t (V2)
Clark’s rule, 167, 168f, 196 (V1)
Class II malocclusion
complete mandibular subapical
osteotomy for, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
in hemifacial microsomia, 299, 302f
(V3)
in juvenile rheumatoid arthritis, 859
(V2)
postoperative, 414 (V3)
in rheumatoid arthritis of
temporomandibular joint, 858
(V2)
in transverse mandibular deficiency,
338 (V3)
in unilateral adolescent internal
condylar resorption, 305 (V3)
in unilateral reactive arthritis, 305
(V3)
Class III malocclusion
in cleft patient, 813 (V3)
complete mandibular subapical
osteotomy for, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
in craniosynostosis, 850 (V3)
occlusal plane rotation for, 248-271
(V3)
clockwise rotation in, 252-256,
252-256f (V3)
counterclockwise rotation in, 256-
260, 257-263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-
249, 249f, 250f (V3)
geometry of treatment design using
constructed
maxillomandibular triangle in,
261f, 261-262 (V3)
linear dimensions between
maxillary length and vertical
facial height in, 250, 250f
(V3)
muscle orientation and, 268-271,
270f (V3)
INDEX I-13
Class III malocclusion (Continued)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-
268 (V3)
in unilateral condylar hyperplasia,
284 (V3)
Classic migraine, 146-148, 147f (V1)
Classic trigeminal neuralgia, 990, 990t
(V2)
Clay shoveler’s fracture, 63, 64f (V2)
Clear cell carcinoma
of minor salivary gland, 553-555,
555f (V2)
odontogenic, 502-508, 503-507f (V2)
Cleft Audit Protocol for Speech, 767
(V3)
Cleft lip
presurgical dentofacial orthopedics
for, 783-790 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t
(V3)
presurgical nasoalveolar molding
and, 783 (V3)
secondary surgery for scar revision in,
841, 843f (V3)
unilateral cleft lip repair in, 735-758
(V3)
comparison of surgical techniques
for, 735-737 (V3)
functional approach in, 752-757,
752-757f (V3)
Millard rotation and advancement
flap technique in, 737-741,
739-743f (V3)
Tennison triangular flap technique
in, 743-751, 744-751f (V3)
timing of, 735 (V3)
Cleft lip and palate, 713-734 (V3)
classification of, 715-716, 716f, 717f
(V3)
cleft maxilla and, 806-812 (V3)
alveolar bone grafting technique
for, 808-810, 808-811f (V3)
grafting materials for, 806-807
(V3)
history and timing of repair in, 806
(V3)
missing teeth and crowded arches
in, 810-811, 811f (V3)
orthodontics for, 807f, 807-808
(V3)
postoperative care in, 810 (V3)
cleft orthognathic surgery in, 813-827
(V3)
bone grafting in, 819, 820-825f
(V3)
obstructed nasal breathing and,
819 (V3)
preoperative evaluation in, 813-
814 (V3)
stabilization of mobilized cleft
maxilla and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-
819, 818f (V3)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
embryology of, 714-715 (V3)
feeding child with, 717-718 (V3)
genetics and etiology of, 715 (V3)
history of cleft lip and palate repair
and, 713-714 (V3)
maxillary hypoplasia and, 860 (V3)
midface hypoplasia and, 855f (V3)
in oculoauriculovertebral spectrum,
927 (V3)
I-14 INDEX
Cleft lip and palate (Continued)
prenatal counseling and, 716-717 (V3)
presurgical dentofacial orthopedics
for, 783-790 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t
(V3)
presurgical nasoalveolar molding
and, 783 (V3)
revision surgery for, 828-847 (V3)
bone graft reconstruction of cleft
maxilla and palate in, 840
(V3)
complications of, 839 (V3)
comprehensive dental and
prosthetic rehabilitation in,
841-843, 844-845f (V3)
fistula closure in, 828-831, 830f,
832-834f (V3)
for management of submucous cleft
palate, 839-840 (V3)
for management of velopharyngeal
dysfunction, 831t, 831-835,
835f (V3)
operative techniques in, 836-839,
837f, 838f (V3)
orthognathic surgery for correction
of midfacial deficiency in, 840
(V3)
reconstruction of cleft nasal
deformity in, 840-841, 842f
(V3)
secondary surgery for cleft lip scar
revision in, 841, 843f (V3)
timing and indications for, 835-
836 (V3)
treatment planning and timing, 718t,
718-719 (V3)
Cleft lip and palate repair, 719-730
(V3)
cleft palate repair and, 723-727, 729f,
730f (V3)
complex facial clefting and, 727-728,
731f (V3)
history of, 713-714 (V3)
lip adhesion and, 720 (V3)
outcome assessment in, 728-730 (V3)
presurgical taping and orthopedics in,
719-720, 720f (V3)
primary bilateral lip repair and, 723,
724-728f (V3)
primary unilateral cleft lip repair and,
720-723, 721-723f (V3)
speech evaluation and management
after
articulation and intelligibility and,
794-795 (V3)
articulation testing in, 797 (V3)
dental and alveolar anomalies and,
791-792, 792t (V3)
intelligibility assessment and, 797
(V3)
lateral still cephalometry and, 797-
798 (V3)
multiview videofluoroscopy and,
798, 799f (V3)
nasal air emission and, 793-794
(V3)
nasal emission testing and, 796,
796f, 797b (V3)
nasometry and, 800-801, 801f (V3)
nostril pinch test and, 795-796
(V3)
perceptual rating scales and, 796-
797 (V3)
pressure-flow method of speech
assessment and, 798-800, 800f
(V3)
reduced intraoral air pressure and,
794 (V3)
resonance imbalance and, 793,
793f (V3)
velopharyngeal dysfunction and,
791, 792t, 801-803 (V3)
video nasoendoscopy and, 798
(V3)
vocal dysfunction and, 795 (V3)
Cleft lip and palate repair (Continued)
stages from infancy through
adolescence, 829t (V3)
treatment planning and timing in,
718t, 718-719 (V3)
Cleft maxilla, 806-812, 840 (V3)
alveolar bone grafting technique for,
808-810, 808-811f (V3)
cleft orthognathic surgery and, 819
(V3)
grafting materials for, 806-807 (V3)
history and timing of repair in, 806
(V3)
missing teeth and crowded arches in,
810-811, 811f (V3)
orthodontics for, 807f, 807-808 (V3)
postoperative care in, 810 (V3)
Cleft orthognathic surgery, 813-827
(V3)
bone grafting in, 819, 820-825f (V3)
for comprehensive dental and
prosthetic rehabilitation, 841-
843, 844-845f (V3)
obstructed nasal breathing and, 819
(V3)
preoperative evaluation in, 813-814
(V3)
stabilization of mobilized cleft maxilla
and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-819,
818f (V3)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
Cleft palate
cleft orthognathic surgery in, 813-827
(V3)
bone grafting in, 819, 820-825f
(V3)
obstructed nasal breathing and,
819 (V3)
preoperative evaluation in, 813-
814 (V3)
stabilization of mobilized cleft
maxilla and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-
819, 818f (V3)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
feeding child with, 717-718 (V3)
maxillary advancement-related
hypernasality and, 73 (V3)
submucous, 839-840 (V3)
in Treacher Collins syndrome, 939,
943f (V3)
Cleft palate repair, 723-727, 729f, 730f,
759-782 (V3)
double-opposing Z-plasty in, 772-775,
773-775f (V3)
fistulas and, 763 (V3)
history of, 759-760 (V3)
intravelar veloplasty in, 762-763
(V3)
outcomes in, 760-761 (V3)
palatoplasty technique in, 762 (V3)
speech evaluation and management
after, 761, 791-805 (V3)
articulation and intelligibility and,
794-795 (V3)
articulation testing in, 797 (V3)
dental and alveolar anomalies and,
791-792, 792t (V3)
intelligibility assessment and, 797
(V3)
lateral still cephalometry and, 797-
798 (V3)
multiview videofluoroscopy and,
798, 799f (V3)
nasal air emission and, 793-794
(V3)
nasal emission testing and, 796,
796f, 797b (V3)
Cleft palate repair (Continued)
nasometry and, 800-801, 801f (V3)
nostril pinch test and, 795-796
(V3)
perceptual rating scales and, 796-
797 (V3)
pressure-flow method of speech
assessment and, 798-800, 800f
(V3)
reduced intraoral air pressure and,
794 (V3)
resonance imbalance and, 793,
793f (V3)
velopharyngeal dysfunction and,
791, 792t, 801-803 (V3)
video nasoendoscopy and, 798
(V3)
vocal dysfunction and, 795 (V3)
timing of, 761 (V3)
two-flap palatoplasty for, 763-771
(V3)
fistula rates in, 765-766, 766t (V3)
growth outcomes in, 769-770 (V3)
history of, 764 (V3)
muscular reconstruction in, 768
(V3)
outcomes based on cleft type or
severity and, 768-769 (V3)
principle techniques in, 764, 764f,
765f (V3)
speech outcomes in, 766-767, 767b
(V3)
surgical procedure in, 770f, 770-
771, 771f (V3)
syndromic associations and
outcomes in, 769 (V3)
technique comparisons in, 768
(V3)
timing of, 767-768 (V3)
two-stage palate repair in, 776-778
(V3)
Cleft surgery, 697-1006 (V3)
cleft lip and palate repair in, 719-730
(V3)
cleft palate repair and, 723-727,
729f, 730f (V3)
complex facial clefting and, 727-
728, 731f (V3)
history of, 713-714 (V3)
lip adhesion and, 720 (V3)
outcome assessment in, 728-730
(V3)
presurgical taping and orthopedics
in, 719-720, 720f (V3)
primary bilateral lip repair and,
723, 724-728f (V3)
primary unilateral cleft lip repair
and, 720-723, 721-723f (V3)
treatment planning and timing in,
718t, 718-719 (V3)
in cleft maxilla, 806-812 (V3)
alveolar bone grafting technique
for, 808-810, 808-811f (V3)
grafting materials for, 806-807
(V3)
history and timing of repair in, 806
(V3)
missing teeth and crowded arches
in, 810-811, 811f (V3)
orthodontics for, 807f, 807-808
(V3)
postoperative care in, 810 (V3)
cleft palate repair in, 723-727, 729f,
730f, 759-782 (V3)
double-opposing Z-plasty in, 772-
775, 773-775f (V3)
fistulas and, 763, 765-766, 766t
(V3)
growth outcomes in, 769-770 (V3)
history of, 759-760 (V3)
intravelar veloplasty in, 762-763
(V3)
muscular reconstruction in, 768
(V3)
outcomes in, 760-761, 768-769
(V3)
palatoplasty technique in, 762
(V3)
speech evaluation in, 761 (V3)
Cleft surgery (Continued)
technique comparisons in, 768
(V3)
timing of, 761 (V3), 767-768 (V3)
two-flap palatoplasty in, 763-771,
764f, 765f, 767b, 770f, 771f
(V3)
two-stage, 776-778 (V3)
clinical facial evaluation in, 1-10
(V3)
detailed regional facial features
and, 4-8, 5-9f, 9b (V3)
facial skin age-related changes and,
8-10, 10f (V3)
facial skin health and, 2, 2t (V3)
facial skin type and, 1, 2t (V3)
general facial anthropometric
relations and, 2-4, 3f,
4f (V3)
facial skeletal growth evaluation in,
19-58 (V3)
mandibular values in, 41-57 (V3);
See also Mandibular growth
values
maxillary-midface values in, 28-40
(V3); See also Maxillary-
midface growth values
neurocranial values in, 19-27 (V3);
See also Neurocranial growth
values
facial skeleton evaluation in, 10-17
(V3)
changes with age and, 15-17, 17f
(V3)
dental relations in, 14-15, 16f (V3)
skeletal relations in, 12-14, 13-15f
(V3)
soft tissue relations in, 11-12, 12f
(V3)
functional cleft lip repair in, 752-757
(V3)
cleft model and repair in, 752f,
752-753, 753f (V3)
closure in, 755-756, 755-757f (V3)
comparison of cleft surgery
techniques, 736-737 (V3)
lip incisions in, 753-754, 754f
(V3)
nasal dissection in, 754-755 (V3)
review of studies in, 756 (V3)
Millard rotation and advancement
flap technique for unilateral cleft
lip in, 722, 737-741 (V3)
Asensio technique and, 740f, 740-
741, 741f (V3)
comparison of cleft surgery
techniques, 736 (V3)
nasal reshaping in, 741 (V3)
postoperative care in, 741 (V3)
preoperative management in, 738
(V3)
surgical technique in, 738-739,
739f, 740f (V3)
wide cleft defect and, 742f, 743f
(V3)
occlusion evaluation in, 17-19, 18b
(V3)
orofacial embryogenesis and, 697-712
(V3)
animal studies in, 705, 706-708f
(V3)
complexity of human facial
morphogenesis and, 697-705,
698f, 700-704f (V3)
orofacial clefting sites and, 705-
712, 710f, 711f (V3)
orthognathic, 813-827 (V3)
bone grafting in, 819, 820-825f
(V3)
obstructed nasal breathing and,
819 (V3)
preoperative evaluation in, 813-
814 (V3)
stabilization of mobilized cleft
maxilla and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-
819, 818f (V3)

Cleft surgery (Continued)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
presurgical dentofacial orthopedics
and, 783-790 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t
(V3)
presurgical nasoalveolar molding
and, 783 (V3)
revision surgery in, 828-847 (V3)
bone graft reconstruction of cleft
maxilla and palate in, 840
(V3)
complications of, 839 (V3)
comprehensive dental and
prosthetic rehabilitation in,
841-843, 844-845f (V3)
fistula closure in, 828-831, 830f,
832-834f (V3)
for management of submucous cleft
palate, 839-840 (V3)
for management of velopharyngeal
dysfunction, 831t, 831-835,
835f (V3)
operative techniques in, 836-839,
837f, 838f (V3)
orthognathic surgery for correction
of midfacial deficiency in, 840
(V3)
reconstruction of cleft nasal
deformity in, 840-841, 842f
(V3)
secondary surgery for cleft lip scar
revision in, 841, 843f (V3)
timing and indications for, 835-
836 (V3)
speech evaluation and management
after, 791-805 (V3)
articulation and intelligibility and,
794-795 (V3)
articulation testing in, 797 (V3)
dental and alveolar anomalies and,
791-792, 792t (V3)
intelligibility assessment and, 797
(V3)
lateral still cephalometry and, 797-
798 (V3)
multiview videofluoroscopy and,
798, 799f (V3)
nasal air emission and, 793-794
(V3)
nasal emission testing and, 796,
796f, 797b (V3)
nasometry and, 800-801,
801f (V3)
nostril pinch test and, 795-796
(V3)
perceptual rating scales and, 796-
797 (V3)
pressure-flow method of speech
assessment and, 798-800, 800f
(V3)
reduced intraoral air pressure and,
794 (V3)
resonance imbalance and, 793,
793f (V3)
velopharyngeal dysfunction and,
791, 792t, 801-803 (V3)
video nasoendoscopy and, 798
(V3)
vocal dysfunction and, 795 (V3)
Tennison-Randall triangular flap
technique in unilateral cleft lip
repair in, 722, 723f, 743-751,
744f, 745f (V3)
comparison of cleft surgery
techniques, 736 (V3)
Millard rotation and advancement
flap versus, 745 (V3)
surgical planning and markings in,
745-746, 746f, 746t, 747f
(V3)
surgical procedure in, 746-749,
747-751f (V3)
Cleidocranial dysplasia, 175-177, 176f,
177f (V1)
Clenching
anticlenching medications for, 409-
410 (V3)
postoperative, 406-407 (V3)
temporomandibular joint disorders
and, 128, 128f (V1)
Clicking after transoral vertical ramus
osteotomy, 121t (V3)
Clindamycin
effect on osteoblast, 389, 389t (V1)
in implant surgery, 388, 388b (V1)
prophylactic, 5t (V1), 383t (V3)
in sinus-lift subantral augmentation,
459, 462 (V1)
subtoxic concentration of, 390, 390t
(V1)
Clinical evaluation
in basic exodontia, 187 (V1)
in chronic facial pain, 963-966, 965f,
966t (V2)
in chronic head and neck pain, 139-
140 (V1)
facial, 1-10 (V3)
detailed regional facial features
and, 4-8, 5-9f, 9b (V3)
in facial asymmetry, 272-274, 273f
(V3)
facial skin age-related changes and,
8-10, 10f (V3)
facial skin health and, 2, 2t (V3)
facial skin type and, 1, 2t (V3)
general facial anthropometric
relations and, 2-4, 3f, 4f (V3)
in mandibular widening, 338 (V3)
in rhinoplasty, 557-560, 558-560f
(V3)
in transverse maxillary deficiency,
219-220, 220f, 221f (V3)
in preanesthetic assessment, 1-2, 2t,
69, 97 (V1)
in skin cancer, 730t, 730-733, 731b,
731-733t (V2)
in trigeminal nerve injury, 262f, 262-
264, 263f (V1)
Clinoril; See Sulindac
Clockwise rotation of
maxillomandibular complex, 252-
256 (V3)
center of rotation at anterior nasal
spine, 252, 252f, 252t (V3)
center of rotation at maxillary incisor
tip, 252, 252f, 253t (V3)
center of rotation at pogonion, 255,
255t, 256f (V3)
center of rotation at zygomatic
buttress, 255-256, 256f, 256t
(V3)
mandibular excess and, 253f, 253-
255, 254f (V3)
muscle orientation and, 266-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
stretching of soft tissues in, 267-268
(V3)
Clonazepam
for acute trigeminal nerve injury, 266
(V1)
after trigeminal nerve repair, 270
(V1)
for burning mouth syndrome, 996
(V2)
for postoperative clenching, 409-410
(V3)
for postoperative insomnia, 412 (V3)
for posttraumatic trigeminal
neuralgia, 156 (V1)
for trigeminal neuralgia, 150 (V1)
Clonidine
for complex regional pain syndrome,
158 (V1)
for postherpetic neuralgia, 152 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)
preoperative management of, 2t (V1)
Closed eruption technique for impacted
maxillary canine, 170, 170f (V1)
Closed fracture of mandible, 142 (V2)
Closed lock, 819, 931 (V2)
Closed reduction
of dentoalveolar fracture, 126, 127f
(V2)
of mandibular fracture, 146-148, 147f
(V2)
condylar, 171 (V2)
exodontia-related, 219f, 219-220,
220f (V1)
in geriatric patient, 391f, 391-392,
392f, 392t (V2)
historical overview of, 139-141,
140f, 141f (V2)
of maxillary/midface fracture, 386-
388 (V2)
of nasal fracture, 276-278, 278f, 279f
(V2)
open reduction and internal fixation
versus, 386t (V2)
Closed rhinoplasty, 561, 562f, 572-573,
573f (V3)
Closing movement of mandible, 810
(V2)
Closure
in alveolar split graft, 471 (V1)
in bone graft for implant, 420-422,
422f (V1)
in complete mandibular subapical
osteotomy, 158 (V3)
in double-opposing Z-plasty, 773-774,
774f (V3)
in endoscopic forehead and brow lift,
606 (V3)
in exodontia
basic, 190-191 (V1)
complicated, 201 (V1)
third molar, 206-207 (V1)
in functional cleft lip repair, 755-756,
755-757f (V3)
in graft harvest from mandibular
symphysis, 410-411 (V1)
in guided tissue regeneration, 431-
435, 433f, 434f (V1)
in internal derangement of
temporomandibular joint, 934,
935f (V2)
in interpositional bone graft, 472f
(V1)
in Le Fort I osteotomy, 181, 184f (V3)
in mandibular resection, 701, 701f
(V2)
in maxillectomy, 696-697, 697f, 698f
(V2)
in rhytidectomy, 505, 505f (V3)
in sagittal split ramus osteotomy, 433
(V3)
of soft tissue injury, 284, 285f, 288f
(V2)
in Tennison-Randall triangular flap
technique in unilateral cleft lip
repair, 749, 759f (V3)
in zygomatic implant, 496 (V1)
Clot formation in wound repair, 17
(V2)
Clouston’s syndrome, 177, 177f (V1)
Cloverleaf skull anomaly, 909-914,
910-914f (V3)
Cluster headache, 148-149 (V1)
Coagulation
inflammatory phase of healing and,
60 (V3)
liver disease-related alteration in, 11
(V1)
preoperative evaluation of, 16-17, 17t
(V1)
wound repair and, 17, 18f (V2)
Coated Vicryl Rapide suture, 286t (V2)
Cocaine
chemical structure of, 37f (V1)
topical, 49 (V1)
Code revision committee, 368 (V1)
Codeine
for acute postoperative pain, 81t, 82
(V1)
for chronic facial pain, 972t (V2)
in complicated exodontia, 207t (V1)
for temporomandibular disorders,
888t (V2)
INDEX I-15
Coding, 364-368 (V1)
Cognitive behavioral therapy
in burning mouth syndrome, 996
(V2)
for chronic head and neck pain, 144
(V1)
for chronic orofacial pain, 123-124
(V1)
for posttraumatic headache, 153 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)
in temporomandibular disorders, 985
(V2)
Cognitive evaluation, 380 (V2)
Cold exposure, extrinsic aging and, 513
(V3)
Cold therapy for temporomandibular
disorders, 892 (V2)
Collagen
aging-related changes in, 513 (V3)
wound repair and, 21, 21f (V2), 61
(V3)
Collagen membrane for guided bone
regeneration, 429 (V1)
selection rationale for, 433-435, 434f
(V1)
in sinus-lift subantral augmentation,
463, 463f (V1)
Collection protocol, 302 (V1)
Colloids, anaphylaxis in pediatric
anesthesia and sedation and, 107t
(V1)
Color saturation test, 75 (V2)
Columella, 554b (V3)
physical examination of, 558-559,
559f (V3)
unilateral versus bilateral oronasal
cleft deformity and, 784t (V3)
Columella-lobule angle, 558-559, 559f
(V3)
Columellar strut graft, 563, 563f (V3)
Comatose patient, reflexes examination
in, 55-56 (V2)
Combination syndrome, 186 (V1)
Combined maxillary and mandibular
osteotomies, 238-247 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
Comminuted fracture
of frontal sinus, 266, 266f, 267f (V2)
mandibular, 142 (V2)
diagnostic imaging of, 99, 99f (V2)
management of, 158-159 (V2)
Comminution of alveolar socket, 115t,
125 (V2)
Commission on Dental Accreditation,
308 (V1)
Common carotid artery, 69f (V3)
Common migraine, 146-148, 147f (V1)
Commotio retinae, 82, 82f (V2)
Communication
marketing and, 347-349, 349f (V1)
online
E-mail-based office system and, 303
(V1)
risk management and, 385 (V1)
risk management and, 378 (V1)
Community service, marketing and, 338
(V1)
Comorbid conditions
ambulatory orthognathic surgery and,
493 (V3)
geriatric patient and, 380t, 380-385
(V2)
cardiovascular disease and, 380-
381 (V2)
cardiovascular medications and,
381 (V2)
cerebrovascular and neurological
disease and, 382 (V2)
I-16 INDEX
Comorbid conditions (Continued)
dementia and postoperative
delirium and, 384-385 (V2)
diabetes mellitus and, 383-384
(V2)
hypertension and, 381-382 (V2)
respiratory disease and, 382-383
(V2)
thyroid disease and, 384 (V2)
preoperative consultation in, 389,
389t (V3)
in temporomandibular disorders, 982
(V2)
Compartment syndrome
abdominal, 45-46, 46f (V2)
in cranio-maxillofacial trauma, 11-12
(V2)
Compensation plan, 298t, 298-299,
299t (V1)
Complete blood count, 387 (V3)
Complete dentures, miniimplant
stabilization of, 567-568, 569f (V1)
Complete mandibular subapical
osteotomy, 155-171 (V3)
complications in, 158, 437f, 437-438
(V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
Complete tooth avulsion, 114t, 120-
122, 121f, 122b (V2)
Complete transfixion incision in
rhinoplasty, 561, 562f (V3)
Complex facial clefting, 727-728, 731f
(V3)
Complex fracture of mandible, 99, 142
(V2)
Complex odontoma, 173 (V1), 518,
519f (V2)
Complex pelvic fracture, 68f, 68-69, 69f
(V2)
Complex regional pain syndrome, 157-
158 (V1), 966-967, 997 (V2)
Complicated exodontia, 192-210 (V1)
bone removal in, 193-194, 194f (V1)
of canines, 196-197, 197-199f (V1)
flap design in, 192-193, 193f, 194f
(V1)
general principles of, 192 (V1)
of impacted teeth other than third
molars, 195-196 (V1)
of impacted third molar teeth, 201-
210 (V1)
bone removal and tooth sectioning
in, 205-206, 207-210f (V1)
classification of, 203, 204f (V1)
indications and contraindications
for, 202-203 (V1)
instrumentation for, 203, 203t (V1)
mandibular, 203-205, 205b, 206f
(V1)
maxillary, 207, 208-210f (V1)
postoperative instructions in, 208-
210, 209b (V1)
preoperative management in, 207t,
207-208, 208b (V1)
wound closure in, 206-207 (V1)
indications for, 192b (V1)
of premolars, 197-199, 200f (V1)
sectioning of teeth and removal in,
194-195, 195f, 196f (V1)
of teeth located in uncommon
anatomic positions, 200-201,
201f (V1)
wound closure in, 201 (V1)
Complicated fracture
of crown, 113t (V2)
mandibular, 99, 142 (V2)
Composite graft in skin cancer, 739
(V2)
Compound fracture of mandible, 99, 99f
(V2)
Compound odontoma, 173 (V1), 518,
519f (V2)
Comprehensive patient care, 395-411
(V2)
accident circumstances and, 395-396,
396f, 397f (V2)
algorithm for decision making in,
399f (V2)
final discharge planning and, 405-409
(V2)
identification of psychosocial issues
and, 400 (V2)
long-term rehabilitation and, 408-
411, 409-410f (V2)
pre-injury health and, 398-400 (V2)
preparation for postoperative events
and, 404-405, 407f (V2)
primary survey and, 396, 397b, 398f
(V2)
prioritization and integration of
surgery and, 400b, 400-401, 402f
(V2)
secondary survey and, 396-397 (V2)
surgical plan and, 401-404, 403-406f
(V2)
treatment goals in, 396b, 396t (V2)
Compression fracture of cervical spine,
63, 64f (V2)
Compressor narium minor muscle, 554f
(V3)
Computed tomography
of abnormal head shape, 856 (V3)
in ankylosis, 903 (V2)
in assessment of trauma patient, 41,
67 (V2)
in avulsive facial injury, 328 (V2)
in cervical spine injury, 63 (V2)
in chronic facial pain, 966 (V2)
in chronic orofacial pain, 118, 120f
(V1)
in condylar fracture, 168 (V2)
in facial injury, 98-99 (V2)
in frontal sinus fracture, 256-257,
260f, 261f (V2)
in head injury, 56, 57b (V2)
acute subdural hematoma and, 60,
61f (V2)
epidural hematoma and, 60, 61f
(V2)
mild closed, 56-57 (V2)
moderate closed, 57 (V2)
severe closed, 57-58 (V2)
traumatic subarachnoid
hemorrhage and, 62 (V2)
in implant surgery, 407-408, 408f,
552-564 (V1)
cone beam technology and, 554,
563-564, 564f, 565f (V1)
history of, 552-554, 553f, 554f
(V1)
for maxillary sinus augmentation,
561-563, 562f, 563f (V1)
rapid prototyping and, 555-557,
555-557f (V1)
reformatting software program and,
557-561, 557-562f (V1)
three-dimensional modeling and,
554-556, 554-556f (V1)
in internal derangement of
temporomandibular joint, 931
(V2)
of lymphoma, 762, 762f (V2)
in mandibular trauma, 98-99, 145f,
146f (V2)
of maxillofacial tumor, 690, 691f
(V2)
in midface fracture, 241f, 241-242,
242f (V2)
in nasal fracture, 274f, 274-275 (V2)
for occult vascular injuries, 69, 70f
(V2)
of odontogenic tumor, 467 (V2)
in oral cavity cancer, 710 (V2)
in orbital fracture, 209-211, 210f,
211f (V2)
in orbital trauma, 86, 86f (V2)
in osteomyelitis, 634f, 634-635, 635f
(V2)
in osteoradionecrosis, 639, 640f (V2)
in pediatric craniomaxillofacial
tumors, 961 (V3)
Computed tomography (Continued)
preoperative, 389 (V3)
in skin cancer, 732-733 (V2)
in temporomandibular disorders, 822,
822f, 823f, 839-840, 840f, 841f
(V2)
in temporomandibular joint
hypomobility, 898 (V2)
three-dimensional computer-assisted
prediction and, 377-379, 378f
(V3)
in three-dimensional radiation
treatment planning, 772-773,
773f (V2)
in transverse maxillary deficiency,
223, 223f (V3)
in trigeminal neuralgia, 991 (V2)
in tumor-related facial asymmetry,
293, 293f (V3)
in zygomatic fracture, 184-185, 185f
(V2)
for zygomatic implant, 492, 492f
(V1)
Computed tomography angiography, 92,
93f, 93t (V2)
Computer in office, 359, 360 (V1)
Computer pattern generator in laser
skin resurfacing, 515, 522 (V3)
Computer-aided design in implant
provisionalization, 528-531 (V1)
Computer-assisted cephalometric
analysis, 372 (V3)
Computer-controlled injection of local
anesthetic, 50-51 (V1)
Computerized-video imaging prediction,
375-377, 376f (V3)
Conchal cartilage, 665-666 (V3)
Davis method for conchal
hypertrophy, 670-673, 672f (V3)
excessive, 669 (V3)
Conchal cavity, 666 (V3)
Concussed tooth, 114t, 118 (V2)
Conductive hearing loss, head injury-
related, 52 (V2)
Condylar atrophy, 299-305, 303-304f,
306f (V3)
Condylar fracture, 141-142, 142f, 162-
181 (V2)
closed treatment of, 171 (V2)
conservative management of, 171
(V2)
diagnostic imaging of, 100f, 100-101,
168-170, 169f (V2)
endoscopic-assisted repair of, 172-
176, 176-180f (V2)
facial asymmetry in, 294, 295f, 296f
(V3)
facial nerve and, 164-165, 166f (V2)
geriatric, 389-391f, 390-393 (V2)
open treatment of, 171 (V2)
pediatric, 364-369, 369f (V2)
physical examination of, 168 (V2)
retromandibular approach in, 171-
172, 172-175f (V2)
retromandibular vein and, 164 (V2)
skeletal injuries in, 167, 167f, 170-
171 (V2)
soft tissue injuries in, 166-167, 170
(V2)
Spiessl and Schroll classification of,
167, 168b (V2)
superficial temporal artery and, 163-
164, 164f, 165f (V2)
temporomandibular joint anatomy
and, 162-163, 163f (V2)
treatment outcomes in, 177-179 (V2)
trigeminal nerve and, 165, 166f (V2)
Condylar hyperplasia, 868 (V2)
model surgery and, 370-371 (V3)
postoperative, 414 (V3)
Condyle, 803, 804f (V2)
abnormal biomechanics of, 817-818,
818f, 819f (V2)
anatomy of, 815-816, 816f (V2)
dislocation of, 218 (V1), 281, 281f
(V3)
displacement in bilateral sagittal split
osteotomy, 114 (V3)
mandibular asymmetry and, 99t (V3)
Condyle (Continued)
normal biomechanics of, 816-817,
817f (V2)
osteochondroma or osteoma of, 285-
291, 289-291f (V3)
pseudocyst of, 868-869 (V2)
subluxation of, 820, 820f (V2)
block graft for, 906-908f, 909 (V2)
mandibular gait in, 825, 827f (V2)
reduction of, 905-908 (V2)
unilateral adolescent internal
condylar resorption and, 299-
305, 303-304f, 306f (V3)
unilateral hyperplasia of, 284-285,
286-288f (V3)
Condylion to gonion, 46 (V3)
Condylion to pogonion, 45 (V3)
Condylotomy, 939-940 (V2)
Cone-beam computed tomography,
377-379 (V3), 554, 563-564, 564f,
565f (V1)
in temporomandibular disorders, 843,
845f, 846f (V2)
Conference room, 354, 354f (V1)
Congenital deformity
in craniofacial dysostosis syndromes,
880-921 (V3)
Apert syndrome in, 902-909, 903-
907f (V3)
Carpenter’s syndrome in, 909 (V3)
cloverleaf skull anomaly in, 909-
914, 910-914f (V3)
Crouzon syndrome in, 886-902,
887-900f (V3)
dentition and occlusion anomalies
in, 881-882 (V3)
functional considerations in, 880-
881 (V3)
genetic aspects of, 880 (V3)
morphologic considerations in,
882-883 (V3)
Pfeiffer syndrome in, 909 (V3)
Saethre-Chotzen syndrome in, 909
(V3)
surgical management of, 883-886
(V3)
in nonsyndromic craniosynostosis,
864-879 (V3)
anterior plagiocephaly in, 868-871,
871f, 872f (V3)
brachycephaly in, 874-876 (V3)
delayed diagnosis of, 867-868 (V3)
diagnosis of, 865-866 (V3)
functional consequences of, 864-
865, 865f (V3)
posterior plagiocephaly in, 874,
877f, 878f (V3)
scaphocephaly in, 868, 869-870f
(V3)
surgical considerations in, 856-858,
866-867 (V3)
syndromes associated with, 850
(V3)
timing of surgery for, 867 (V3)
trigonocephaly in, 871-874, 874-
876f (V3)
in oculoauriculovertebral spectrum,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of,
922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
maxilla and, 922-935 (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)

Congenital deformity (Continued)
zygoma and orbit reconstruction
in, 928-929 (V3)
in Treacher Collins syndrome, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
Congenital ear anomaly, otoplasty for,
665-677 (V3)
blood supply to ear and, 667-668
(V3)
complications in, 675-676 (V3)
for congenital deformities, 668-669
(V3)
for correction of protruding earlobe,
675, 675f (V3)
Davis method in, 670-673, 672f (V3)
embryology of auricle and, 665, 666f
(V3)
Farrior technique in, 673, 675f (V3)
indications and timing of, 669 (V3)
Mustard[ac]e method in, 673, 674f
(V3)
nerve supply to ear and, 668-670f
(V3)
surgical anatomy in, 665-666, 666f,
667f (V3)
techniques in, 669-670, 671f (V3)
Congenital epulis of newborn, 179 (V1)
Congenital heart disorders, 382-383,
383t (V3)
Congenital hemangioma, 579f, 579-
581, 580f (V2)
Congestive heart failure
in geriatric patient, 380-381 (V2)
perioperative management of, 382
(V3)
Conjunctiva, 581f, 582f, 585,
586f (V3)
nonperforating eye injuries and, 78
(V2)
Conjunctival incision in pediatric
craniomaxillofacial tumor, 962
(V3)
Conjunctivitis, 861 (V2)
Connective tissue disease
arthritis associated with, 865-866
(V2)
facial asymmetry and, 309-313, 310-
313f (V3)
Connective tissue grafting to improve
soft tissue health around implant,
485, 485f, 486f (V1)
Conscious sedation, 22 (V1)
Consensual pupillary reflex, 76 (V2)
Consent
for dentoalveolar surgery, 212, 213b
(V1)
for laser skin resurfacing, 519 (V3)
preoperative evaluation and,
20 (V1)
risk management and, 301-302, 379
(V1)
Conservative management
of condylar fracture, 171 (V2)
of orbital fracture, 209f, 217-220,
220f (V2)
Construction phase in building office,
362-363 (V1)
Consultation
in marketing, 322-323,
337-338 (V1)
perioperative patient management
and, 389, 389t (V3)
in rhinoplasty, 557 (V3)
Consultation room, 352, 352f (V1)
Contact dermatitis, laser skin
resurfacing-related, 539 (V3)
Contact healing, 62 (V3)
Contingency fee, 374 (V1)
Continual sedation, 22 (V1)
Continuous passive motion, arthritis
and, 851-852, 853f, 854f (V2)
Continuous positive airway pressure
for obstructive sleep apnea syndrome,
317, 319 (V3)
in speech therapy after cleft surgery,
803 (V3)
Continuous sedation, 22 (V1)
Contour Thread, 695, 696t (V3)
Contusion, gingival or mucosal, 115t,
130 (V2)
Conventional imaging in
temporomandibular disorders, 835-
836 (V2)
Conventional tomography in
temporomandibular disorders, 838-
839 (V2)
Convergence insufficiency in midface
fracture, 254 (V2)
Converse-Wood-Smith technique of
otoplasty, 670 (V3)
Cooper, A.P., 791 (V2)
COPD; See Chronic obstructive
pulmonary disease
Copy machine, 361 (V1)
Corneal injury
abrasion in, 78-79, 79f, 213, 306f,
306 (V2)
chemical burn in, 321f (V2)
in endoscopic forehead and brow lift,
606-607 (V3)
laser skin resurfacing-related, 543-544
(V3)
in midface fracture, 254 (V2)
nonperforating, 78-79, 79f (V2)
Corneal reflex, 51, 56 (V2)
Corneal shields for laser therapy, 243f
(V1)
Cornelia de Lange’s syndrome, 855-856,
856f (V3)
Coronal approach
in frontal sinus fracture, 259-262,
262f, 263f (V2)
in Le Fort III osteotomy, 206 (V3)
in nasal fracture, 279-280 (V2)
in naso-orbital-ethmoid fracture, 246,
246f (V2)
in orbital fracture, 223-224, 225f,
227f (V2)
in pediatric craniomaxillofacial
tumor, 962, 963 (V3)
in zygomatic fracture, 191-192 (V2)
Coronal defect, guided tissue
regeneration for, 436 (V1)
Coronal lift, 611t (V3)
Coronal suture, 865f (V3)
Coronal suture craniosynostosis, 868-
871, 871f, 872f (V3)
Coronectomy, 277 (V1)
Coronoid fracture, 142, 142f (V2)
diagnostic imaging of, 101 (V2)
temporomandibular joint
pseudoankylosis and, 900 (V2)
Coronoid hyperplasia, 900-901 (V2)
Coronoid process fracture, 426, 429-
431f (V3)
Correct Coding Initiative, 369 (V1)
Corrugator supercilii muscle, 244f (V2),
586f (V3)
forehead and brow lift and, 597, 598f
(V3)
Cortical autogenous bone graft, 406-427
(V1)
bone biology and, 406-407, 407f
(V1)
graft recipient site and, 419-422, 419-
422f (V1)
ilium for, 415-419, 415-419f (V1)
mandibular ramus for, 412-414, 412-
414f (V1)
mandibular symphysis for, 409-411,
410-412f (V1)
maxillary tuberosity for, 409, 409f,
410f (V1)
onlay bone graft and, 424, 424f, 425f
(V1)
patient preparation for, 409 (V1)
preoperative evaluation in, 407-408,
408f, 409f (V1)
sinus bone grafting and, 422-424,
423f (V1)
tibia for, 414f, 414-415, 415f (V1)
Corticocancellous block augmentation
of posterior mandible, 452f, 452-
453, 453f (V1)
Corticosteroids
for acute trigeminal nerve injury, 266
(V1)
for chronic facial pain, 973t, 974
(V2)
for infantile hemangioma, 580 (V2)
for laryngeal edema, 442 (V3)
for postoperative pain, 86 (V1)
for temporomandibular disorders,
886, 887t (V2)
in temporomandibular joint
arthrocentesis, 914 (V2)
topical
for aphthous stomatitis, 620 (V2)
for oral lichen planus, 619 (V2)
for pemphigoid, 624 (V2)
for pemphigus, 625 (V2)
for traumatic optic neuropathy, 85,
213 (V2)
Cortisol, preoperative evaluation of, 13,
14t (V1)
Cosmetic deformity after frontal sinus
fracture repair, 268 (V2)
Cosmetic surgery, 497-696 (V3)
blepharoplasty in, 579-594 (V3)
anterior lamella and, 582f, 582-583
(V3)
complications in, 593 (V3)
eyelid anatomy in, 580,
581f (V3)
eyelid innervation and blood
supply and, 585 (V3)
lacrimal system and, 587 (V3)
middle lamella and, 583f, 583-585,
584f (V3)
nomenclature in, 579f, 579-580
(V3)
patient evaluation in, 587-589,
588f, 589f (V3)
posterior lamella and, 585, 586f,
587f (V3)
postoperative care in, 591-593,
593f (V3)
surgical procedure in, 589-591,
590-592f (V3)
botulinum toxin injection in, 658-
661 (V3)
contraindications and adverse
effects of, 661, 662f (V3)
history and pharmacology of, 658
(V3)
preparations of, 658-659, 659t
(V3)
treatment technique for, 660-661,
661f (V3)
uses in facial cosmetics, 659f, 659-
660, 660f (V3)
cervicofacial liposuction in, 618-625
(V3)
complications of, 623-624 (V3)
history of, 618 (V3)
patient selection in, 618-620, 619f
(V3)
preoperative preparation in, 620
(V3)
INDEX I-17
Cosmetic surgery (Continued)
surgical technique in, 620-623,
620-625f (V3)
chemical peel in, 661-664, 662f, 664f
(V3)
clinical facial evaluation in, 1-10
(V3)
detailed regional facial features
and, 4-8, 5-9f, 9b (V3)
facial skin age-related changes and,
8-10, 10f (V3)
facial skin health and, 2, 2t (V3)
facial skin type and, 1, 2t (V3)
general facial anthropometric
relations and, 2-4, 3f, 4f (V3)
endoscopic forehead and brow lift in,
595-609, 596f (V3)
bone anatomy and, 595-597 (V3)
complications in, 606-607 (V3)
endoscopic anatomy and, 600-602,
601f (V3)
muscle and fascial anatomy and,
597-598, 598f (V3)
postoperative care in, 606 (V3)
preoperative evaluation in, 602t,
602-603 (V3)
technique in, 603f, 603-606, 605f
(V3)
vessel and nerve anatomy and,
598-600, 598-600f (V3)
facial implants in, 678-696 (V3)
chin position analyses and, 681-
683t (V3)
for facial skin laxity with weight
loss, 686-688, 686-688f (V3)
injectable facial fillers and, 691f,
691-692, 692f (V3)
for large nose and small chin, 679f,
679-684, 680f, 684f, 685b,
685f (V3)
lip implant in, 693-694, 694f (V3)
malar cheek implant in, 689f, 689-
690, 690f, 690t (V3)
patient selection for, 678 (V3)
thread lifts and, 695, 695t (V3)
facial skeletal growth evaluation in,
19-58 (V3)
mandibular values in, 41-57 (V3);
See also Mandibular growth
values
maxillary-midface values in, 28-40
(V3); See also Maxillary-
midface growth values
neurocranial values in, 19-27 (V3);
See also Neurocranial growth
values
facial skeleton evaluation in, 10-17
(V3)
changes with age and, 15-17, 17f
(V3)
dental relations in, 14-15, 16f (V3)
skeletal relations in, 12-14, 13-15f
(V3)
soft tissue relations in, 11-12, 12f
(V3)
hair transplantation in, 651-657 (V3)
complications of, 655-656 (V3)
current medical treatment for
alopecia and, 651 (V3)
micrograft and minigraft technique
in, 651-653, 652-655f (V3)
pathophysiology of alopecia and,
651 (V3)
rotational flaps in, 655, 655f, 656f
(V3)
scalp reduction in, 655,
656f (V3)
injectable facial fillers in, 629-650
(V3)
for augmenting wrinkles, lines, and
folds, 637-639, 638f, 639f
(V3)
complications of, 642-643, 643f,
644f (V3)
history of, 629-631, 630f, 630t,
631f (V3)
for lips, 633-637, 633-637f (V3)
for malar augmentation, 639-642,
639-642f (V3)
I-18 INDEX
Cosmetic surgery (Continued)
tissue positioning of, 631f, 631-
632, 632f (V3)
treatment considerations in, 632-
633, 633f (V3)
treatment results in, 643, 645-649f
(V3)
laser skin resurfacing in, 513-552
(V3)
anesthesia and, 521, 522f (V3)
carbon dioxide laser for, 514f, 514-
516, 515f (V3)
contact dermatitis and, 539 (V3)
dyschromias and, 541-542, 542f,
543f (V3)
erbium:YAG laser in, 532-534,
536-538f (V3)
fractional photothermolysis in,
532, 536f (V3)
history of, 513-514 (V3)
infection and, 540-541, 541f (V3)
intrinsic and extrinsic aging and,
513 (V3)
laser blepharoplasty with, 544-545,
545-547f (V3)
laser properties in, 514f, 514-516,
515f (V3)
laser settings for, 521-522, 522f
(V3)
milia and acne formation and,
539-540, 540f (V3)
ocular complications in, 543-544
(V3)
patient evaluation in, 516-519,
518b (V3)
postoperative care in, 524-529,
526-528f, 530-531f (V3)
preoperative considerations in, 519
(V3)
prolonged erythema and, 535-537,
539f (V3)
pruritus and, 537-538, 539f (V3)
resurfacing acne scars in, 529 (V3)
rhytidectomy with, 545-548, 547-
548f (V3)
scarring and, 542-543, 543f (V3)
sepsis and, 544 (V3)
single-pass resurfacing in, 529-532,
533-534f (V3)
skin preparation for, 519-521
(V3)
telangiectasias and, 538-539 (V3)
traditional technique in, 522-524,
523f, 525-526f (V3)
traumatic and surgical scars
improvement in, 529 (V3)
treatment of benign skin lesions
in, 529 (V3)
laser therapy in, 248-251, 249t (V1)
marketing strategies for, 343-345,
343-345f (V1)
occlusion evaluation in, 17-19, 18b
(V3)
otoplasty in, 665-677 (V3)
blood supply to ear and, 667-668
(V3)
complications in, 675-676 (V3)
for congenital deformities, 668-669
(V3)
for correction of protruding
earlobe, 675, 675f (V3)
Davis method in, 670-673, 672f
(V3)
embryology of auricle and, 665,
666f (V3)
Farrior technique in, 673, 675f
(V3)
indications and timing of, 669
(V3)
Mustard[ac]e method in, 673, 674f
(V3)
nerve supply to ear and, 668-670f
(V3)
surgical anatomy in, 665-666, 666f,
667f (V3)
techniques in, 669-670, 671f (V3)
rhinoplasty in, 553-578 (V3)
case reports in, 574-576,
574-576f (V3)
Cosmetic surgery (Continued)
clinical examination in, 557-560,
558-560f (V3)
closed, 572-573, 573f (V3)
complications in, 573-577 (V3)
dressings and splinting in, 573,
573f (V3)
follow-up care in, 573 (V3)
incisions in, 560-562, 561f, 562f
(V3)
initial consultation in, 557 (V3)
nasal anatomy and, 553-556, 554b,
554-557f (V3)
open, 567-572, 568-571f (V3)
tip plasty in, 562, 563f (V3)
tip projection in, 562-564, 563-
565f (V3)
tip rotation in, 564, 565f (V3)
tip shape and, 565-566, 566f (V3)
rhytidectomy in, 497-512 (V3)
complications in, 506-510, 507-
510f (V3)
patient evaluation in, 497-500,
498t, 499f, 499t (V3)
surgical technique in, 500-506,
500-506f (V3)
trichophytic forehead and brow lift
in, 610-617 (V3)
comparison of lift techniques and,
611t (V3)
complications in, 614-616, 616f,
617f (V3)
fixation techniques in, 610-611
(V3)
patient selection for, 613-614,
615f, 616f (V3)
surgical technique in, 611-614f,
612-613 (V3)
CosmoDerm, 629-630 (V3)
CosmoPlast, 629-630 (V3)
Cost effectiveness issues in trauma, 410-
411 (V2)
Costen’s syndrome, 792-793 (V2)
Cottle test, 560 (V3)
Coumadin; See Warfarin
Counterclockwise rotation of
maxillomandibular complex, 256-
260 (V3)
center of rotation at anterior nasal
spine, 256, 259f, 259t (V3)
center of rotation at posterior
nasal spine, 256-260, 260f,
260t (V3)
center of rotation at zygomatic
buttress, 256, 259f, 259t (V3)
muscle orientation and, 266-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
stretching of soft tissues in, 267-268
(V3)
in Treacher Collins syndrome, 954
(V3)
in unilateral adolescent internal
condylar resorption, 303-304f,
305, 306f (V3)
vertical maxillary deficiency and
mandibular anteroposterior
deficiency and, 257f, 257-258,
258f (V3)
vertical maxillary excess and
mandibular anteroposterior
deficiency and, 261-263, 261-
263f (V3)
Cover-uncover test, 77 (V2)
Cowley, R. Adams, 1, 2f (V2)
Cox-2 inhibitors, 86 (V1)
for skin cancer, 740 (V2)
for temporomandibular disorders,
886, 887t (V2)
CPAP; See Continuous positive airway
pressure
CPG; See Computer pattern generator
in laser skin resurfacing
CPT; See Current Procedural
Terminology
Cranial fossa dead space in
craniofacial dysotosis syndromes,
884-886 (V3)
Cranial nerve examination
in chronic head and neck pain, 140
(V1)
in chronic orofacial pain, 116-118,
119f, 120f (V1)
in head injury, 51-52 (V2)
in trigeminal neuralgia, 991 (V2)
Cranial nerve injury in ocular trauma,
85-86 (V2)
Cranial sutures, 864, 865f (V3)
Cranial vault
craniofacial dysostosis syndromes and,
880-921 (V3)
Apert syndrome in, 902-909, 903-
907f (V3)
Carpenter’s syndrome in, 909 (V3)
cloverleaf skull anomaly in, 909-
914, 910-914f (V3)
Crouzon syndrome in, 886-902,
887-900f (V3)
dentition and occlusion anomalies
in, 881-882 (V3)
functional considerations in, 880-
881 (V3)
genetic aspects of, 880 (V3)
morphologic considerations in,
882-883 (V3)
Pfeiffer syndrome in, 909 (V3)
Saethre-Chotzen syndrome in, 909
(V3)
surgical management of, 883-886
(V3)
craniosynostosis and, 864-879 (V3)
anterior plagiocephaly in, 868-871,
871f, 872f (V3)
brachycephaly in, 874-876 (V3)
delayed diagnosis of, 867-868 (V3)
diagnosis of, 865-866 (V3)
functional consequences of, 864-
865, 865f (V3)
posterior plagiocephaly in, 874,
877f, 878f (V3)
scaphocephaly in, 868, 869-870f
(V3)
surgical considerations in, 856-858,
866-867 (V3)
syndromes associated with, 850
(V3)
timing of surgery for, 867 (V3)
trigonocephaly in, 871-874, 874-
876f (V3)
growth and development of, 850-851,
852f (V3)
Cranial vault distraction osteogenesis,
1002 (V3)
Craniofacial deformity
cleft maxilla in, 806-812 (V3)
alveolar bone grafting technique
for, 808-810, 808-811f (V3)
grafting materials for, 806-807
(V3)
history and timing of repair in, 806
(V3)
missing teeth and crowded arches
in, 810-811, 811f (V3)
orthodontics for, 807f, 807-808
(V3)
postoperative care in, 810 (V3)
considerations in pediatric
craniomaxillary surgery, 848-863
(V3)
clinical evaluation of craniofacial
growth and, 856 (V3)
concepts of craniofacial skeletal
growth and development and,
849f, 849t, 849-850, 850t
(V3)
cranio-orbital dysmorphology and,
856-858 (V3)
cranium and, 850-851, 852f (V3)
mandible and, 855-856, 856f, 857f
(V3)
mandibular hyperplasia and, 859-
860, 860f (V3)
mandibular hypoplasia and, 858-
859, 859f (V3)
maxilla and, 851, 854f, 855f (V3)
maxillary hypoplasia and, 860-861
(V3)
Craniofacial deformity (Continued)
orbits and, 851, 853f (V3)
vertical maxillary excess and, 861f,
861-862 (V3)
zygoma and, 851, 853f (V3)
in craniofacial dysostosis syndromes,
880-921 (V3)
Apert syndrome in, 902-909, 903-
907f (V3)
Carpenter’s syndrome in, 909 (V3)
cloverleaf skull anomaly in, 909-
914, 910-914f (V3)
Crouzon syndrome in, 886-902,
887-900f (V3)
dentition and occlusion anomalies
in, 881-882 (V3)
functional considerations in, 880-
881 (V3)
genetic aspects of, 880 (V3)
morphologic considerations in,
882-883 (V3)
Pfeiffer syndrome in, 909 (V3)
Saethre-Chotzen syndrome in, 909
(V3)
surgical management of, 883-886
(V3)
distraction osteogenesis for, 338-363
(V3)
alveolar distraction in, 349-354,
349-354f (V3)
bone transport by, 354-360, 355-
361f (V3)
future directions in, 362 (V3)
mandibular lengthening in, 342-
346, 342-346f (V3)
mandibular widening in, 338-342,
339-342f (V3)
maxillary bone transport in, 360-
362, 362f (V3)
maxillary distraction by intraoral
devices in, 346-349, 347-349f
(V3)
Le Fort III osteotomy for, 205-218
(V3)
for craniofacial dysostosis, 205-206
(V3)
indications for, 205 (V3)
for midface deficiency, 206, 207-
210f (V3)
modified, 211-218 (V3)
subcranial, 210-211, 212-217f (V3)
technique in, 206-210 (V3)
in oculoauriculovertebral spectrum,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of, 922
(V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
in Treacher Collins syndrome, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)

Craniofacial deformity (Continued)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
Craniofacial disassembly, 967 (V3)
Craniofacial dysostosis syndromes, 851,
880-921 (V3)
Apert syndrome in, 902-909 (V3)
assessment of treatment results in,
902-909 (V3)
cranial vault expansion and, 902
(V3)
cranio-orbital reshaping in infancy
and, 902, 903-905f (V3)
orthognathic procedures in, 902
(V3)
total midface deformity and, 902,
906-907f (V3)
Carpenter’s syndrome in, 909 (V3)
cloverleaf skull anomaly in, 909-914,
910-914f (V3)
Crouzon syndrome in, 886-902 (V3)
assessment of treatment results in,
901-902 (V3)
cranial vault expansion and, 889,
890-891f (V3)
cranio-orbital reshaping in infancy
and, 886-889, 887-888f (V3)
orthognathic procedures in, 900
(V3)
total midface deformity and, 889-
900, 892-900f (V3)
dentition and occlusion anomalies in,
881-882 (V3)
functional considerations in, 880-881
(V3)
genetic aspects of, 880 (V3)
Le Fort III osteotomy in, 205-206
(V3)
morphologic considerations in, 882-
883 (V3)
Pfeiffer syndrome in, 909 (V3)
Saethre-Chotzen syndrome in, 909
(V3)
surgical management of, 883-886
(V3)
Craniofacial fibrous dysplasia, 977-980,
980-985f (V3)
Craniofacial growth and development,
352-353, 353f (V2)
Craniofacial microsomia, 855, 857f
(V3)
Craniofacial pain, 136-163 (V1)
characterization and measurement of,
139 (V1)
clinical and laboratory examination
in, 139-140 (V1)
diagnosis of, 139, 139t (V1)
incidence and demographics of, 137
(V1)
musculoskeletal, 142-146 (V1)
fibromyalgia and, 142 (V1)
myofascial pain syndromes and,
143-145 (V1)
temporomandibular arthritis and,
145-146 (V1)
neurologic, 149-158 (V1)
brain stimulation procedures for,
157 (V1)
complex regional pain syndrome
and, 157-158 (V1)
idiopathic and atypical orofacial
pain syndromes and, 158 (V1)
postherpetic neuralgia and, 151-
152 (V1)
Craniofacial pain (Continued)
posttraumatic headache and, 152-
153 (V1)
posttraumatic trigeminal neuralgia
and, 154-156 (V1)
surgical treatments for, 156-157
(V1)
trigeminal neuralgia and, 149-151
(V1)
pain definitions and, 137-138, 138t
(V1)
pathophysiology of pain and, 137f,
137-139, 138f (V1)
pharmacologic screening in, 140-141
(V1)
psychiatric disorders and, 141-142
(V1)
sleep dysfunction and, 141 (V1)
systemic disease and, 141 (V1)
vascular, 146-149 (V1)
cluster headache and
trigeminoautonomic variants
and, 148-149 (V1)
migraine and, 146-148, 147f (V1)
orofacial migraine variants and,
149 (V1)
Craniofacial skeleton
access in pediatric craniomaxillofacial
tumors and, 962-967, 963-965f
(V3)
clinical evaluation of growth, 856
(V3)
distraction osteogenesis of, 996-1006
(V3)
biologic basis of, 996-997 (V3)
cranial vault, 1002 (V3)
history of, 996 (V3)
mandibular, 998-1001f, 999-1002
(V3)
maxillary, 1002, 1003f, 1004f
(V3)
growth and development of, 849f,
849t, 849-850, 850t (V3)
growth discrepancy and, 848-849
(V3)
regions of growth, 850-856 (V3)
cranium and, 850-851, 852f (V3)
mandible and, 855-856, 856f, 857f
(V3)
maxilla and, 851, 854f, 855f (V3)
orbits and, 851, 853f (V3)
zygoma and, 851, 853f (V3)
Craniofacial surgery, 697-1006 (V3)
cleft lip and palate repair in, 719-730
(V3)
cleft palate repair and, 723-727,
729f, 730f (V3)
complex facial clefting and, 727-
728, 731f (V3)
history of, 713-714 (V3)
lip adhesion and, 720 (V3)
outcome assessment in, 728-730
(V3)
presurgical taping and orthopedics
in, 719-720, 720f (V3)
primary bilateral lip repair and,
723, 724-728f (V3)
primary unilateral cleft lip repair
and, 720-723, 721-723f (V3)
treatment planning and timing in,
718t, 718-719 (V3)
for cleft maxilla, 806-812 (V3)
alveolar bone grafting technique
for, 808-810, 808-811f (V3)
grafting materials for, 806-807
(V3)
history and timing of repair in, 806
(V3)
missing teeth and crowded arches
in, 810-811, 811f (V3)
orthodontics for, 807f, 807-808
(V3)
postoperative care in, 810 (V3)
cleft orthognathic surgery in, 813-827
(V3)
bone grafting in, 819, 820-825f
(V3)
obstructed nasal breathing and,
819 (V3)
Craniofacial surgery (Continued)
preoperative evaluation in, 813-
814 (V3)
stabilization of mobilized cleft
maxilla and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-
819, 818f (V3)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
cleft palate repair in, 723-727, 729f,
730f, 759-782 (V3)
double-opposing Z-plasty in, 772-
775, 773-775f (V3)
fistulas and, 763, 765-766, 766t
(V3)
growth outcomes in, 769-770 (V3)
history of, 759-760 (V3)
intravelar veloplasty in, 762-763
(V3)
muscular reconstruction in, 768
(V3)
outcomes in, 760-761, 768-769
(V3)
palatoplasty technique in, 762
(V3)
speech evaluation in, 761 (V3)
technique comparisons in, 768
(V3)
timing of, 761 (V3), 767-768 (V3)
two-flap palatoplasty in, 763-771,
764f, 765f, 767b, 770f, 771f
(V3)
two-stage, 776-778 (V3)
clinical facial evaluation in, 1-10
(V3)
detailed regional facial features
and, 4-8, 5-9f, 9b (V3)
facial skin age-related changes and,
8-10, 10f (V3)
facial skin health and, 2, 2t (V3)
facial skin type and, 1, 2t (V3)
general facial anthropometric
relations and, 2-4, 3f, 4f (V3)
in craniofacial dysostosis syndromes,
880-921 (V3)
Apert syndrome and, 902-909,
903-907f (V3)
Carpenter’s syndrome and, 909
(V3)
cloverleaf skull anomaly and, 909-
914, 910-914f (V3)
Crouzon syndrome and, 886-902,
887-900f (V3)
dentition and occlusion anomalies
and, 881-882 (V3)
functional considerations in, 880-
881 (V3)
genetic aspects of, 880 (V3)
morphologic considerations in,
882-883 (V3)
Pfeiffer syndrome and, 909 (V3)
Saethre-Chotzen syndrome and,
909 (V3)
in craniosynostosis, 864-879 (V3)
anterior plagiocephaly in, 868-871,
871f, 872f (V3)
brachycephaly in, 874-876 (V3)
delayed diagnosis of, 867-868 (V3)
diagnosis of, 865-866 (V3)
functional consequences of, 864-
865, 865f (V3)
posterior plagiocephaly in, 874,
877f, 878f (V3)
scaphocephaly in, 868, 869-870f
(V3)
surgical considerations in, 856-858,
866-867 (V3)
syndromes associated with, 850
(V3)
timing of surgery for, 867 (V3)
trigonocephaly in, 871-874, 874-
876f (V3)
distraction osteogenesis in, 996-1006
(V3)
biologic basis of, 996-997 (V3)
INDEX I-19
Craniofacial surgery (Continued)
cranial vault, 1002 (V3)
history of, 996 (V3)
mandibular, 998-1001f, 999-1002
(V3)
maxillary, 1002, 1003f, 1004f (V3)
facial skeletal growth evaluation in,
19-58 (V3)
mandibular values in, 41-57 (V3);
See also Mandibular growth
values
maxillary-midface values in, 28-40
(V3); See also Maxillary-
midface growth values
neurocranial values in, 19-27 (V3);
See also Neurocranial growth
values
facial skeleton evaluation in, 10-17
(V3)
changes with age and, 15-17, 17f
(V3)
dental relations in, 14-15, 16f (V3)
skeletal relations in, 12-14, 13-15f
(V3)
soft tissue relations in, 11-12, 12f
(V3)
growth and development
considerations in pediatric
patient, 848-863 (V3)
clinical evaluation of craniofacial
growth and, 856 (V3)
concepts of craniofacial skeletal
growth and development and,
849f, 849t, 849-850, 850t
(V3)
cranio-orbital dysmorphology and,
856-858 (V3)
cranium and, 850-851, 852f (V3)
growth discrepancy and
craniofacial skeleton and,
848-849 (V3)
mandible and, 855-856, 856f, 857f
(V3)
mandibular hyperplasia and, 859-
860, 860f (V3)
mandibular hypoplasia and, 858-
859, 859f (V3)
maxilla and, 851, 854f, 855f (V3)
maxillary hypoplasia and, 860-861
(V3)
orbits and, 851, 853f (V3)
vertical maxillary excess and, 861f,
861-862 (V3)
zygoma and, 851, 853f (V3)
occlusion evaluation in, 17-19, 18b
(V3)
in oculoauriculovertebral spectrum,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of,
922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
orofacial embryogenesis and, 697-712
(V3)
animal studies in, 705, 706-708f
(V3)
complexity of human facial
morphogenesis and, 697-705,
698f, 700-704f (V3)
orofacial clefting sites and, 705-
712, 710f, 711f (V3)
I-20 INDEX
Craniofacial surgery (Continued)
in pediatric tumors, 961-995 (V3)
adenomatoid odontogenic tumor
in, 968, 968f (V3)
ameloblastic fibroma in, 968-970,
970f (V3)
ameloblastic fibro-odontoma in,
970, 970f (V3)
ameloblastoma in, 967f, 967-968
(V3)
anatomic classification in, 962
(V3)
aneurysmal bone cyst in, 972, 974-
975 (V3)
central giant cell lesions in, 970-
972, 973f (V3)
craniofacial fibrous dysplasia in,
977-980, 980-985f (V3)
craniomaxillofacial access and,
962-967, 963-965f (V3)
endoscopic approaches in, 967
(V3)
imaging in, 961-962 (V3)
imaging of, 961-962 (V3)
juvenile aggressive fibromatosis in,
970, 972f (V3)
juvenile nasopharyngeal
angiofibroma in, 972-974,
976-977f (V3)
juvenile ossifying fibroma in, 974-
977, 978-979f (V3)
neurofibromatosis in, 980-984, 986f
(V3)
odontogenic myxoma in, 968, 969f
(V3)
odontoma in, 970, 971f (V3)
reconstruction in, 988-993, 991f,
992f (V3)
rhabdomyosarcoma in, 984-986,
987f (V3)
salivary gland tumor in, 987-988
(V3)
sarcomas in, 986-987, 988-990f
(V3)
presurgical dentofacial orthopedics
and, 783-790 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t
(V3)
presurgical nasoalveolar molding
and, 783 (V3)
revision surgery for cleft
malformations in, 828-847 (V3)
bone graft reconstruction of cleft
maxilla and palate in, 840
(V3)
complications of, 839 (V3)
comprehensive dental and
prosthetic rehabilitation in,
841-843, 844-845f (V3)
fistula closure in, 828-831, 830f,
832-834f (V3)
for management of submucous cleft
palate, 839-840 (V3)
for management of velopharyngeal
dysfunction, 831t, 831-835,
835f (V3)
operative techniques in, 836-839,
837f, 838f (V3)
orthognathic surgery for correction
of midfacial deficiency in, 840
(V3)
reconstruction of cleft nasal
deformity in, 840-841, 842f
(V3)
secondary surgery for cleft lip
scar revision in, 841,
843f (V3)
timing and indications for, 835-
836 (V3)
speech evaluation and management
after, 791-805 (V3)
articulation and intelligibility and,
794-795 (V3)
articulation testing in, 797 (V3)
dental and alveolar anomalies and,
791-792, 792t (V3)
Craniofacial surgery (Continued)
intelligibility assessment and, 797
(V3)
lateral still cephalometry and, 797-
798 (V3)
multiview videofluoroscopy and,
798, 799f (V3)
nasal air emission and, 793-794
(V3)
nasal emission testing and, 796,
796f, 797b (V3)
nasometry and, 800-801,
801f (V3)
nostril pinch test and, 795-796
(V3)
perceptual rating scales and, 796-
797 (V3)
pressure-flow method of speech
assessment and, 798-800,
800f (V3)
reduced intraoral air pressure and,
794 (V3)
resonance imbalance and, 793,
793f (V3)
velopharyngeal dysfunction and,
791, 792t, 801-803 (V3)
video nasoendoscopy and, 798
(V3)
vocal dysfunction and, 795 (V3)
surgical pathology and, 413-417, 415-
416f (V2)
in Treacher Collins syndrome, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
unilateral cleft lip repair in, 735-758
(V3)
comparison of surgical techniques
for, 735-737 (V3)
functional approach in, 752-757,
752-757f (V3)
Millard rotation and advancement
flap technique in, 737-741,
739-743f (V3)
Tennison triangular flap technique
in, 743-751, 744-751f (V3)
timing of, 735 (V3)
Craniomandibular articulation, 801,
802f (V2); See also
Temporomandibular joint
Craniomaxillofacial trauma, 1-411 (V2)
airway management in, 25-34 (V2)
airway assessment and, 25, 26b
(V2)
airway maneuvers and adjuncts in,
26, 26b (V2)
complications in, 33 (V2)
cricothyroidotomy in, 32f, 32-33
(V2)
endotracheal intubation in, 28-31,
31f (V2)
supraglottic airway devices for, 26-
28, 27f, 28f (V2)
Craniomaxillofacial trauma (Continued)
systematic approach to, 25 (V2)
tracheostomy in, 33 (V2)
avulsive facial injuries in, 289-290,
290f, 291f, 327-351 (V2)
Abbe flap in, 329, 330f (V2)
aesthetic and prosthetic
rehabilitation and, 346-350f
(V2)
airway management in, 327 (V2)
of alveolus, 128 (V2)
anterolateral thigh free flap for,
335, 335f (V2)
cervicofacial flap for, 329-330, 333f
(V2)
of cheek, 293f, 320, 320f (V2)
cheek defects in, 344, 345-348f
(V2)
clinical examination in, 327-328
(V2)
debridement in, 328 (V2)
of ear, 294, 297f (V2)
eyelid, 88, 308-309, 310f (V2)
facial artery musculomucosal flap
for, 329 (V2)
fibular free flap for, 333-335, 335f
(V2)
gingival, 130 (V2)
imaging in, 328 (V2)
lip defect reconstruction in, 343f,
343-344 (V2)
of lower face and mandible, 335-
340f, 336-337 (V2)
nasal, 301, 302-303f, 305f (V2)
nasal defects and, 337, 343 (V2)
optic disc, 83, 84f (V2)
paramedian forehead flap for, 329,
331-332f (V2)
pectoralis major myocutaneous flap
for, 330-331 (V2)
radial forearm flap for, 332-333,
334f (V2)
rectus abdominis free flap for, 335
(V2)
of scalp, 59, 293f, 324, 324f V2)
scalp defects and, 346 (V2)
submental island flap for, 331-332,
334f (V2)
of teeth, 114t, 120-122, 121f, 122b
(V2)
temporoparietal fascia flap for, 330
(V2)
wound assessment in, 327, 328f
(V2)
comprehensive patient care in, 395-
411 (V2)
accident circumstances and, 395-
396, 396f, 397f (V2)
algorithm for decision making in,
399f (V2)
final discharge planning and, 405-
409 (V2)
identification of psychosocial issues
and, 400 (V2)
long-term rehabilitation and, 408-
411, 409-410f (V2)
pre-injury health and, 398-400
(V2)
preparation for postoperative
events and, 404-405, 407f
(V2)
primary survey and, 396, 397b,
398f (V2)
prioritization and integration of
surgery and, 400b, 400-401,
402f (V2)
secondary survey and, 396-397
(V2)
surgical plan and, 401-404, 403-
406f (V2)
treatment goals in, 396b, 396t
(V2)
condylar fracture in, 141-142, 142f,
162-181 (V2)
closed treatment of, 171 (V2)
conservative management of, 171
(V2)
diagnostic imaging of, 100f, 100-
101, 168-170, 169f (V2)
Craniomaxillofacial trauma (Continued)
endoscopic-assisted repair of, 172-
176, 176-180f (V2)
facial nerve and, 164-165, 166f
(V2)
geriatric, 389-391f, 390-393 (V2)
open treatment of, 171 (V2)
pediatric, 364-369, 369f (V2)
physical examination of, 168 (V2)
retromandibular approach in, 171-
172, 172-175f (V2)
retromandibular vein and, 164
(V2)
skeletal injuries in, 167, 167f, 170-
171 (V2)
soft tissue injuries in, 166-167, 170
(V2)
Spiessl and Schroll classification
of, 167, 168b (V2)
superficial temporal artery and,
163-164, 164f, 165f (V2)
temporomandibular joint anatomy
and, 162-163, 163f (V2)
treatment outcomes in, 177-179
(V2)
trigeminal nerve and, 165, 166f
(V2)
dentoalveolar, 104-138, 105f, 106f
(V2)
alveolar process fracture in, 126-
128, 127f, 128f (V2)
classification of, 110-112, 111f,
112b, 113-115t (V2)
comminution of alveolar socket in,
125 (V2)
complete tooth avulsion in, 120-
122, 121f, 122b (V2)
concussed tooth in, 118 (V2)
crown fracture in, 113-118, 116-
118f (V2)
crown infraction in, 112-113
(V2)
displacement of tooth in, 118,
118b (V2)
extrusive luxation in, 118f (V2)
general considerations in, 112
(V2)
gingival injury in, 130 (V2)
history in, 105-107 (V2)
intrusive luxation in, 118, 119f
(V2)
lateral luxation of tooth in, 119-
120 (V2)
pediatric, 364 (V2)
physical examination in, 107-109,
107-109f (V2)
primary tooth injury in, 122-125,
123b, 123-126f (V2)
prognosis in, 132f, 132-135, 134f,
135f (V2)
radiographic examination in, 102,
102f, 109-110, 110f (V2)
reactions of teeth to, 130b, 130-
131, 131f, 132f (V2)
socket wall fracture in, 126 (V2)
splinting techniques for, 128-130,
129f (V2)
subluxation of tooth in, 118 (V2)
diagnostic imaging in, 91-103 (V2)
in angle of mandible fracture, 101,
101f (V2)
in avulsive facial injury, 328 (V2)
in comminuted, complicated, and
impacted fracture, 99, 99f
(V2)
in complications of treatment of
mandibular fracture, 102-103
(V2)
computed tomography in, 98-99
(V2)
in condylar fracture, 100f, 100-101,
168-170, 169f (V2)
in coronoid process and ramus
fractures, 101 (V2)
in dentoalveolar injuries, 102,
102f, 102f (V2), 109-110,
110f (V2)
in greenstick and pathologic
fractures, 99, 100f (V2)

Craniomaxillofacial trauma (Continued)
imaging techniques in, 91-92, 92f,
92t (V2)
mandibular anatomy and,
96 (V2)
in mandibular body fracture, 101,
102f (V2)
mandibular series in, 96-98, 97f
(V2)
in mandibular symphysis and
parasymphysis fractures, 101,
102f (V2)
midfacial anatomy and, 91, 92f
(V2)
in orbital fracture, 209-211, 210f,
211f (V2)
panoramic radiography in, 98, 99f
(V2)
rendering techniques in, 92-94,
93-95f (V2)
in simple and compound fractures,
99, 99f (V2)
in soft tissue trauma to neck, 94-
95, 96f (V2)
supplemental radiographs in, 98
(V2)
in zygomatic fracture, 184-185,
185f (V2)
frontal sinus fracture in, 256-269
(V2)
classification of, 257-259, 261f
(V2)
clinical evaluation in, 256, 258f,
259f (V2)
pediatric, 355, 356-357f (V2)
postoperative care in, 266-268,
268f (V2)
radiologic evaluation in, 256-257,
260f, 261f (V2)
surgical anatomy and, 256, 257f,
258f (V2)
surgical management of, 259-266,
262-269f (V2)
geriatric, 374-394 (V2)
aging of face and neck in, 377
(V2)
anesthetic management in, 385,
385b (V2)
closed versus open reduction of
fractures in, 386t (V2)
cognitive evaluation and informed
consent in, 380 (V2)
considerations in management of,
392t (V2)
epidemiology of, 374-377, 375t,
376-377f (V2)
mandibular fractures in, 389-392f,
390-393 (V2)
maxilla and midface fractures in,
386-390, 387-389f (V2)
medications and over-the-counter
drug history and, 380 (V2)
nutrition and fluid and electrolyte
management in, 379 (V2)
perioperative risk assessment of co-
morbid systemic disease in,
380t, 380-385 (V2)
social history and, 379-380 (V2)
wound healing and, 377-378, 378f
(V2)
initial assessment in, 35-42, 36t
(V2)
adjuncts to primary survey and,
39-40 (V2)
adjuncts to secondary survey and,
40-41 (V2)
airway evaluation in, 35-36 (V2)
breathing evaluation in, 36, 36f,
37f (V2)
circulation evaluation in, 37-38,
38f, 38t (V2)
definitive care and, 41 (V2)
disability evaluation in, 38-39, 39t
(V2)
exposure and environment control
in, 39, 39f (V2)
penetrating injuries and, 41-42
(V2)
secondary survey and, 40 (V2)
Craniomaxillofacial trauma (Continued)
intensive care in, 42-48, 43t (V2)
abdominal compartment syndrome
and, 45-46, 46f (V2)
acalculous cholecystitis and, 45
(V2)
acute adrenal insufficiency and, 46-
47 (V2)
acute renal failure and, 46 (V2)
acute respiratory distress syndrome
and, 43-44, 44t (V2)
adynamic ileus and, 45 (V2)
atrial fibrillation and, 44-45 (V2)
blood loss and, 46 (V2)
blunt myocardial injury and, 44
(V2)
fluids, electrolytes, and nutrition
and, 45 (V2)
infectious disease and, 47 (V2)
intensive insulin therapy and, 46-
47 (V2)
intubation and mechanical
ventilation and, 43 (V2)
pain control and sedation and, 47
(V2)
prophylaxis and, 48 (V2)
rehabilitation and, 48 (V2)
shock and, 44 (V2)
systemic inflammatory response
and multiple organ failure
syndrome and, 44, 44t (V2)
tubes and lines and, 47-48 (V2)
midface fracture in, 239-255 (V2)
anatomy in, 239, 240f (V2)
classification of, 239-240, 240f,
241f (V2)
complications in, 253-254 (V2)
geriatric, 386-390, 387-390f, 392t
(V2)
imaging of, 241f, 241-242, 242f
(V2)
Le Fort fractures in, 248-253, 250-
252f (V2)
naso-orbital-ethmoid fracture in,
243-248, 243-249f (V2)
neurologic injury in, 242-243 (V2)
pediatric, 253, 363 (V2)
multi-system trauma and, 65-73 (V2)
abdominal evaluation and, 65-67,
66f, 67f (V2)
antibiotics and, 73 (V2)
complex pelvic fractures and, 68f,
68-69, 69f (V2)
deep venous thrombosis
prophylaxis and, 72-73 (V2)
ICU considerations and, 70-72
(V2)
occult pneumothorax and, 68, 68f
(V2)
occult vascular injuries and, 69-70,
70f (V2)
preparation for rehabilitation and,
73 (V2)
steroids and, 72 (V2)
tertiary examination and, 72 (V2)
nasal fracture in, 270-283, 271f (V2)
anatomy and pathogenesis of, 270-
273, 272f, 273f (V2)
classification of, 275, 275t (V2)
closed reduction in, 276-278, 278f,
279f (V2)
complications of, 281-282 (V2)
diagnosis and evaluation of, 273-
275, 274f (V2)
medical management of, 275 (V2)
open reduction in, 278-281, 280f
(V2)
pediatric, 281, 362-363 (V2)
neurologic assessment in, 11, 49-56
(V2)
detailed evaluation in, 51-52 (V2)
grading severity of injury and, 52-
56, 54f, 54t (V2)
initial evaluation and, 49-51 (V2)
neuropathic pain after, 997 (V2)
ocular injury in, 74-90 (V2)
carotid cavernous fistula and, 89
(V2)
cranial nerve injury in, 85-86 (V2)
Craniomaxillofacial trauma (Continued)
eyelid injuries in, 88 (V2)
globe dystopia in, 88 (V2)
nasolacrimal injuries in, 88-89, 89f
(V2)
nonperforating, 78-82, 78-82f (V2)
ophthalmic assessment in, 74-78,
75-78f (V2)
orbital fractures in, 86f, 86-88, 87f
(V2)
orbital injury and, 83-85, 84f (V2)
penetrating, 83, 83f (V2)
orbital fracture in, 83-85, 84f, 202-
238 (V2)
anatomy in, 202-206, 203t, 203-
206f, 205b, 205t (V2)
associated injuries in, 211-212,
212f (V2)
clinical examination in, 207-209,
208f, 209f (V2)
conservative management of, 217-
220, 219f, 220f (V2)
diagnostic imaging of, 94, 94f (V2)
diplopia in, 214-215, 215f, 216f
(V2)
eyelid lacerations in, 215 (V2)
fracture patterns in, 206-207, 206-
208f (V2)
imaging techniques in, 209-211,
210f, 211f (V2)
indications for operative treatment
of, 220, 221f (V2)
inferior and lateral orbital
approach in, 221-222, 222f,
223f (V2)
lacrimal injuries in, 215, 217f (V2)
medial orbital approach in, 225-
228, 226f, 227f (V2)
ophthalmic assessment in, 78, 78f
(V2)
primary reconstruction in, 228-
233, 228-236f (V2)
secondary reconstruction in, 233-
236, 233-236f (V2)
superior and lateral orbital
approach in, 222-225, 224-
226f (V2)
telecanthus in, 215-217, 218f (V2)
visual disturbances in, 212-214,
212-214f (V2)
orbital injury in, 83-86 (V2)
cranial nerve injury in, 85-86 (V2)
displacement of globe in, 88 (V2)
intraorbital foreign body in, 83-84,
84f (V2)
optic disc avulsion in, 83, 84f (V2)
orbital fracture in, 86f, 86-88, 87f
(V2)
traumatic optic neuropathy in, 84-
85 (V2)
traumatic retrobulbar hemorrhage
in, 84f, 84 (V2)
pediatric, 352-373 (V2)
child abuse and, 372 (V2)
craniofacial growth and
development and, 352-353,
353f (V2)
dentoalveolar fractures in, 363-364
(V2)
epidemiology of, 353-354 (V2)
frontal bone and superior orbital
fractures in, 355 (V2)
frontal sinus and frontobasilar
injuries in, 355, 356-357f (V2)
mandibular body and angle
fractures in, 364 (V2)
mandibular condyle fractures in,
364-369, 369f (V2)
midface fractures in, 363 (V2)
nasal fractures in, 362-363 (V2)
naso-orbito-ethmoid fractures in,
355-360, 358-359f (V2)
orbital fractures in, 360-361, 360-
361f (V2)
perioperative management of, 354-
355 (V2)
prevention of, 354 (V2)
rigid internal fixation and, 369-370
(V2)
INDEX I-21
Craniomaxillofacial trauma (Continued)
Risdon cable and, 370f, 370-372
(V2)
surgical anatomy in, 353 (V2)
symphyseal and parasymphyseal
mandibular fractures in, 364,
365-367f (V2)
zygomaticomaxillary complex
fractures in, 361-362, 362-
363f (V2)
perioperative management in, 1-16,
56-73 (V2)
abdominal assessment in, 11 (V2)
abdominal evaluation and, 11, 65-
67, 66f, 67f (V2)
acute subdural hematoma and, 60,
61t (V2)
airway assessment in, 2-4, 3f, 4f
(V2)
antibiotics and, 73 (V2)
basilar skull fracture and, 59-60
(V2)
breathing assessment in, 4-6 (V2)
chest imaging studies in, 11 (V2)
chronic subdural hematoma and,
61, 62f (V2)
circulation problems and, 6-7, 7t
(V2)
complex pelvic fractures and, 68f,
68-69, 69f (V2)
deep venous thrombosis
prophylaxis and, 72-73 (V2)
diffuse axonal injury and, 62 (V2)
disability status in, 7-8, 8t (V2)
ear examination in, 9 (V2)
epidural hematoma and, 60, 61f
(V2)
exposure and environmental
control in, 8 (V2)
eye examination in, 9 (V2)
head injury and, 8-9 (V2)
historic perspective in, 1, 2f (V2)
history in, 8 (V2)
ICU considerations and, 70-72
(V2)
mild closed head injury and, 56-57,
57b (V2)
moderate closed head injury and,
57 (V2)
musculoskeletal assessment in, 11-
12 (V2)
neck examination in, 10f, 10-11
(V2)
neurologic examination in, 11
(V2)
nose and neurologic evaluation in,
9 (V2)
occult pneumothorax and, 68, 68f
(V2)
occult vascular injuries and, 69-70,
70f (V2)
perineal, rectal, and vaginal
assessment in, 11 (V2)
preparation for rehabilitation and,
73 (V2)
primary survey in, 1 (V2)
scalp injury and, 58-59 (V2)
secondary survey in, 8 (V2)
severe closed head injury and, 57-
58 (V2)
skull fracture and, 59 (V2)
steroids and, 72 (V2)
tertiary examination and, 72 (V2)
throat examination in, 9, 10f (V2)
traumatic intracerebral hematoma/
cerebral contusion and, 61-62
(V2)
traumatic intraventricular
hemorrhage and, 63 (V2)
traumatic subarachnoid
hemorrhage and, 62 (V2)
postoperative management in, 14-15,
15f, 15t (V2)
reactions of teeth to, 130b, 130-131,
131f, 132f (V2)
soft tissue injuries in, 283-326 (V2)
abrasion in, 289 (V2)
from air bag device blast, 313,
314f, 315f (V2)
I-22 INDEX
Craniomaxillofacial trauma (Continued)
anatomic considerations in, 283,
284t, 285f (V2)
anesthesia for, 284, 284 (V2)
avulsive wounds in, 289-290, 290f,
291f (V2)
bite wounds in, 290-292, 292f,
313-316, 314-317f (V2)
burn-related, 321-323, 321-323f,
322t (V2)
of cheek, 320f, 320-321, 321f (V2)
closure of, 284, 285f, 288f (V2)
of ear, 294, 297f, 310-313, 312f,
313f (V2)
of eyelid and nasolacrimal
apparatus, 292-294, 295f, 296f
(V2)
initial evaluation and early
management of, 283, 284f
(V2)
laceration in, 289, 290f (V2)
of lip, 294, 298f (V2)
nasal, 301, 302-305f (V2)
of neck, 294, 316-318, 318f (V2)
of parotid, 294 (V2)
of parotid gland, 294, 318-320,
320f (V2)
pediatric, 292, 293f, 371f, 372
(V2)
periorbital, 301-310, 306-311f
(V2)
of peripheral nerves, 318, 319f
(V2)
of scalp, 292, 293-294f, 323-324,
324f, 325f (V2)
suture materials for, 284-289, 286-
287t (V2)
wound care in, 294-299 (V2)
wound repair in, 17-24 (V2)
aberrant bone healing in, 22-23
(V2)
abnormal wound healing in, 22
(V2)
bone regeneration in, 22 (V2)
coagulation and, 17, 18f (V2)
formation of granulation tissue
and, 19-21, 20f (V2)
future directions in, 23, 23f (V2)
inflammation and, 17-19, 19f (V2)
neural control of, 21 (V2)
phases of, 17, 18f (V2)
prevention of infection in, 21-22
(V2)
remodeling phase of, 21f, 21 (V2)
zygomatic fracture in, 182-201 (V2)
anatomy in, 182-183, 183f (V2)
Carroll-Girard screw for, 186, 186f
(V2)
coronal approach in, 191-192 (V2)
eyebrow approach in, 187, 188f
(V2)
fixation in, 192, 193f (V2)
fracture patterns in, 206-207, 206-
208f (V2)
history and physical examination
in, 183b, 183-184, 184f (V2)
indications for radiographs and
surgery in, 184-185, 185f (V2)
infraorbital paresthesia and, 194-
195 (V2)
late-onset post-traumatic
enophthalmos and, 198 (V2)
lateral canthotomy in, 186-187
(V2)
lower eyelid approaches in, 187-
188, 188f (V2)
malunion of, 197f, 197-198 (V2)
persistent diplopia following, 195-
197, 196f, 196t (V2)
primary reconstruction in, 231f,
231-233, 232f (V2)
radiography in, 184-185, 185f (V2)
retrobulbar hemorrhage and, 198-
199 (V2)
soft tissue complications of, 195
(V2)
subciliary approach in, 190-191,
191f (V2)
subtarsal approach in, 191 (V2)
Craniomaxillofacial trauma (Continued)
transconjunctival approach in,
188-190, 188-190f (V2)
traumatic optic neuropathy and,
197 (V2)
upper eyelid approach in, 187, 187f
(V2)
vestibular approach in, 186 (V2)
zygomatic arch fracture and, 192-
194, 194f (V2)
Cranio-orbital complex
craniosynostosis and, 856-858 (V3)
growth and development of, 851
(V3)
oculoauriculovertebral spectrum and,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
Treacher Collins syndrome and, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
Craniopalatal line, 139, 139f,
140f (V3)
Craniosynostosis
cranial vault distraction osteogenesis
in, 1002 (V3)
in craniofacial dysostosis syndromes,
880-921 (V3)
Apert syndrome in, 902-909, 903-
907f (V3)
Carpenter’s syndrome in, 909 (V3)
cloverleaf skull anomaly in, 909-
914, 910-914f (V3)
Crouzon syndrome in, 886-902,
887-900f (V3)
dentition and occlusion anomalies
in, 881-882 (V3)
functional considerations in, 880-
881 (V3)
genetic aspects of, 880 (V3)
morphologic considerations in,
882-883 (V3)
Pfeiffer syndrome in, 909 (V3)
Craniosynostosis (Continued)
Saethre-Chotzen syndrome in, 909
(V3)
surgical management of, 883-886
(V3)
nonsyndromic, 864-879 (V3)
anterior plagiocephaly in, 868-871,
871f, 872f (V3)
brachycephaly in, 874-876 (V3)
delayed diagnosis of, 867-868 (V3)
diagnosis of, 865-866 (V3)
functional consequences of, 864-
865, 865f (V3)
posterior plagiocephaly in, 874,
877f, 878f (V3)
scaphocephaly in, 868, 869-870f
(V3)
surgical considerations in, 856-858,
866-867 (V3)
syndromes associated with, 850
(V3)
timing of surgery for, 867 (V3)
trigonocephaly in, 871-874, 874-
876f (V3)
Craniotomy
in craniofacial dysostosis syndromes
in Apert syndrome, 902 (V3)
in Crouzon syndrome, 889, 890-
891f (V3)
in frontal sinus fracture, 266, 267f
(V2)
in pediatric craniomaxillofacial
tumor, 964, 964f, 965f (V3)
Cranium
age-related changes in, 16, 17f (V3)
average growth completion of, 850t
(V3)
craniomandibular articulation and,
801, 802f (V2); See also
Temporomandibular joint
growth and development of, 850-851,
852f (V3)
CRC; See Code revision committee
Creatinine, 19t (V1), 387 (V3)
Credentialing, 307-317 (V1)
accreditation and certification and,
308-309 (V1)
adverse action in, 315-316 (V1)
appointment to medical staff in, 314-
315 (V1)
definitions and resources in, 309-313,
310-313t (V1)
privileging and, 313-314, 314f (V1)
specialty board certification and, 308
(V1)
Credit card transaction machine, 361
(V1)
Cretinism, 851 (V3)
Cricoid pressure in endotracheal
intubation, 30 (V2)
Cricothyroidotomy, 3-4, 4-5f, 32f, 32-
33 (V2)
Crohn’s disease
perioperative management of, 386-
387, 387t (V3)
preoperative evaluation of, 9 (V1)
Crossbite
facial asymmetry in, 282, 283-284f
(V3)
in transverse maxillary deficiency,
219-220, 220f, 221f (V3)
in unilateral reactive arthritis, 305
(V3)
Crouzon syndrome, 886-902 (V3)
assessment of treatment results in,
901-902 (V3)
cranial vault expansion and, 889,
890-891f (V3)
cranio-orbital reshaping in infancy
and, 886-889, 887-888f (V3)
craniosynostosis in, 850, 874 (V3)
functional considerations in, 880-881
(V3)
genetic aspects of, 880 (V3)
hearing deficits in, 882 (V3)
hydrocephalus in, 881 (V3)
Le Fort III osteotomy for midface
deformity in, 205-206, 207-210f
(V3)
Crouzon syndrome (Continued)
maxillary distraction osteogenesis in,
1002, 1003f, 1004f (V3)
maxillary hypoplasia in, 861 (V3)
orbital and midface hypoplasia in,
854-855f (V3)
orbito-naso-zygomatic deformity in,
882 (V3)
orthognathic procedures in, 900 (V3)
total midface deformity and, 889-900,
892-900f (V3)
Crown
exodontia and
aspiration during, 215 (V1)
dislodgement during, 212, 213f
(V1)
impressions at implant placement
and, 525-539 (V1)
concept of, 531 (V1)
history of immediate loading and,
525-527, 526b, 526f, 527f
(V1)
immediate extraction, implant
placement, and provisional
restoration and, 534f, 534-
535, 535f (V1)
immediate provisionalization and,
528-531, 530-531f (V1)
prefabricated ceramic abutments
and temporary crowns and,
536f, 536-537, 537f (V1)
primary bone-level impressions
and, 527-528, 529f, 530f (V1)
second-stage surgery and, 532f,
532-533, 533f (V1)
Crown fracture, 113t, 113-118, 115b
(V2)
crown-root, 116 (V2)
enamel, 113 (V2)
enamel, dentin, and pulp exposure
in, 113-114 (V2)
pulp exposure with non-vital pulp,
115-116, 116f (V2)
pulp exposure with vital pulp, 114-
115 (V2)
root, 116-117, 117f, 118f (V2)
Crown infraction, 112-113, 113t (V2)
Crown lengthening
for aesthetic purposes, 481f (V1)
laser-assisted, 254 (V1)
Crown-root fracture, 113t, 116 (V2)
Crow’s feet, Botox injection for, 659,
660f, 661f (V3)
Crude-touch detection in trigeminal
nerve injury, 262f, 263 (V1)
Cryoneurolysis, 150 (V1)
Cryoprecipitate, 385 (V3)
Cryotherapy
for odontogenic keratocyst, 438-440
(V2)
in skin cancer, 734 (V2)
for temporomandibular disorders, 892
(V2)
for trigeminal neuralgia, 993 (V2)
Crystalloids, 72 (V1)
CT; See Computed tomography
Cumulative interceptive supportive
therapy, 391, 391t (V1)
Curettage
of ameloblastoma, 500 (V2)
in Langerhans cell histiocytosis, 573,
573f, 574f (V2)
in skin cancer, 734, 735f (V2)
Current Dental Terminology, 367-368
(V1)
Current Procedural Terminology, 365
(V1)
Cushing’s syndrome, 13-14 (V1)
Cut-and-paste hand planning
cephalometric technique,
372 (V3)
Cutaneous malignancy, 724-748 (V2)
aggressive behavior of, 728-730, 729f
(V2)
basal cell carcinoma in, 725, 725f
(V2)
cryotherapy for, 734 (V2)
curettage/electrodesiccation in, 734,
735f (V2)

Cutaneous malignancy (Continued)
dermatofibrosarcoma protuberans in,
727-728, 728f (V2)
epidemiology and etiology of, 724-
725 (V2)
laser ablation and resurfacing in, 734-
735 (V2)
of lip, 742-744, 743f (V2)
lymph node involvement in, 737-739
(V2)
melanoma in, 749-757 (V2)
diagnosis of, 752t, 752-754, 753f,
753t (V2)
epidemiology of, 749, 750b (V2)
incidence and etiology of, 749-750,
750b, 750t, 750-752f, 751t
(V2)
management of regional disease in,
754 (V2)
staging of, 754-755, 755t (V2)
treatment of, 755-756 (V2)
Merkel cell carcinoma in, 727 (V2)
microcystic adnexal carcinoma in,
726-727, 727f (V2)
Mohs’ micrographic surgery in, 735-
736, 736b, 736f (V2)
photodynamic therapy for, 741 (V2)
physical examination in, 730t, 730-
733, 731b, 731-733t (V2)
radiation therapy in, 741-742 (V2)
sebaceous gland carcinoma in, 727,
727f (V2)
squamous cell carcinoma in, 725-726,
726f (V2)
staging of, 733-734 (V2)
systemic and topical medications for,
739-741 (V2)
traditional surgical excision in, 736-
737 (V2)
Cutaneous neuroendocrine carcinoma,
727 (V2)
Cutaneous pigmented lesions,
251 (V1)
Cyclic tensile strain in arthritis, 851,
851f, 852f (V2)
Cyclin D1, 708 (V2)
Cyclobenzaprine
for chronic facial pain, 974 (V2)
for myofascial pain, 144 (V1)
for temporomandibular disorders,
887, 888t, 985 (V2)
for temporomandibular osteoarthritis,
146 (V1)
Cyclooxygenase inhibitors, 83-84, 86
(V1)
for skin cancer, 740 (V2)
for temporomandibular disorders,
886, 887t (V2)
Cyclooxygenase pathway, 886f, 886
(V2)
Cyclooxygenase-2
normal inflammation and, 393 (V1)
temporomandibular disorders and,
850 (V2)
Cyclophosphamide, 763, 781t (V2)
Cymba concha, 666, 667f (V3)
Cyst(s), 418-465 (V2)
aneurysmal bone, 596-597, 597-598f,
868 (V2)
definitions in, 418 (V2)
eruption, 179-180 (V1)
general surgical considerations in,
418 (V2)
nonodontogenic, 447-460 (V2)
branchial cleft, 458-460, 458-460f
(V2)
dermoid and epidermoid, 451-455,
454f, 455f (V2)
globulomaxillary, 451 (V2)
median mandibular, 451 (V2)
median palatal, 451 (V2)
nasolabial, 447-448, 449f, 450f
(V2)
nasopalatine duct, 448-451, 451-
453f (V2)
thyroglossal duct, 455-458, 455-
458f (V2)
odontogenic, 418-447 (V2)
calcifying, 445-447, 447f (V2)
Cyst(s) (Continued)
dentigerous, 419, 424-426, 425-
428f (V2)
gingival, 180 (V1), 442, 445f (V2)
glandular, 444-445 (V2)
lateral periodontal, 442-444 (V2)
in nevoid basal cell carcinoma
syndrome, 441b, 441-442,
442t, 443f, 444f (V2)
odontogenic keratocyst, 426-441
(V2); See also Odontogenic
keratocyst
paradental, 421-424 (V2)
radicular, 419-421, 420f, 422f (V2)
residual, 421, 423f (V2)
third molar, 203 (V1)
salivary gland, 539, 540f (V2)
temporomandibular joint, 868-872
(V2)
Cystic adenomatoid odontogenic
tumors, 470-471f (V2)
ameloblastic fibrodentinoma in, 524-
527, 527f (V2)
ameloblastic fibroma in, 522-524,
523f (V2)
ameloblastic fibro-odontoma in, 524,
525f, 526f (V2)
cementoblastoma in, 510-512 (V2)
fibroma in, 508-510, 509f, 511f (V2)
intraosseous odontogenic carcinoma
in, 527-532, 528-530f (V2)
myxoma in, 512-517f, 512-518 (V2)
odontoameloblastoma in, 519-522
(V2)
odontoma in, 518-519, 519-521f
(V2)
sarcoma in, 532-533 (V2)
Cystic fibrosis, 384 (V3)
Cystic hygroma, 582 (V2)
Cytokines
in bone regeneration, 22 (V2)
temporomandibular disorders and,
849-850, 850f, 930 (V2)
wound repair and, 17-19, 18f, 19f
(V2)
Cytomegalovirus infection of salivary
glands, 543 (V2)
D 321-323, 325-327f (V3)
Dal Pont technique in bilateral sagittal
split osteotomy, 87, 88f, 106, 107t
(V3)
Dalmane; See Flurazepam
Damages in malpractice claim, 375
(V1)
Darvon; See Propoxyphene
Datril; See Acetaminophen
Davis method of otoplasty, 670-673,
672f (V3)
DDAVP; See Desmopressin
Deafferentation pain, 138 (V1)
Debridement
of animal bite wound, 315 (V2)
in avulsive facial injury, 328 (V2)
in facial soft tissue injury, 284 (V2)
in guided tissue regeneration
procedures, 430 (V1)
laser-assisted, 255 (V1)
in periimplantitis, 391 (V1)
Decadron; See Dexamethasone
Decannulation of tracheotomy, 14 (V2)
Decerebrate posturing, 54, 54f (V2)
Deciduous teeth, eruption pattern for,
165, 166t (V1)
Decompression
of glandular odontogenic cyst, 445
(V2)
in Gorlin’s syndrome, 442, 443-444f
(V2)
of odontogenic keratocyst, 440-441
(V2)
in trigeminal nerve repair, 268 (V1)
in trigeminal neuralgia, 992 (V2)
Decongestants, 410 (V3)
Decontamination of facial soft tissue
injury, 284 (V2)
Decorticate posturing, 54, 54f (V2)
Decortication in guided tissue
regeneration procedures, 430 (V1)
Dedo classification of facial profiles,
499, 499f, 499t (V3)
Deep circumflex iliac artery flap, 991-
992, 992f (V3)
Deep facial vein, 433f (V3)
Deep palmar arch, 334f (V2)
Deep peroneal artery, 335f (V2)
Deep sedation/analgesia, 22, 67 (V1)
in pediatric surgery, 105-106 (V1)
Deep temporal artery, 668f (V3)
Deep tendon reflexes, head injury and,
56 (V2)
Deep venous thrombosis
in geriatric patient, 383 (V2)
prophylaxis in intensive care of
trauma patient, 48, 72-73 (V2)
Default judgment, 376 (V1)
Defendant, 374 (V1)
Defined benefit plan, 287 (V1)
Definitive airway in trauma, 2-3, 3f, 35-
36 (V2)
Definitive radiotherapy, 771 (V2)
Deformation, defined, 849t (V3)
Degenerative joint disease
chronic orofacial pain in, 118 (V1)
diagnostic approach to, 832t (V2)
temporomandibular, 145-146 (V1),
855-857, 885 (V2)
Dehiscence
after repair of zygomatic fracture, 195
(V2)
in bilateral sagittal split osteotomy,
115-116, 116b (V3)
guided tissue regeneration for, 435-
436, 447, 447f (V1)
in sinus-lift subantral augmentation,
462 (V1)
Dehydration
in geriatric patient, 379 (V2)
in herpes simplex virus infection, 616
(V2)
in mandibular surgery, 443 (V3)
preoperative fasting in child and, 98
(V1)
Delaire architectural and structural
craniofacial analysis, 138-139,
139f, 144f (V3)
in obstructive sleep apnea syndrome,
Delaire functional cleft lip repair, 752-
757 (V3)
cleft model and repair in, 752f, 752-
753, 753f (V3)
closure in, 755-756, 755-757f (V3)
comparison of cleft surgery
techniques, 736-737 (V3)
lip incisions in, 753-754, 754f (V3)
nasal dissection in, 754-755 (V3)
review of studies in, 756 (V3)
Delayed hard palate closure, 776-778
(V3)
Delayed onset muscle soreness, 979
(V2)
Delayed repair in skin cancer, 738-739
(V2)
Delayed union of mandibular fracture,
102, 159 (V2)
Delirium tremens, liver disease-related,
11 (V1)
Delivery system requirements in office,
360 (V1)
Delta-Cortef; See Prednisolone
Deltasone; See Prednisone
Dementia in geriatric patient, 384-385
(V2)
Demerol; See Meperidine
Demineralized freeze-dried allograft,
platelet-rich plasma and, 505-506
(V1)
Dental arch discrepancy
complete mandibular subapical
osteotomy for, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
INDEX I-23
Dental arch discrepancy (Continued)
technique in, 156-158, 157-160f
(V3)
mandibular surgery complications
and, 421-422 (V3)
maxillary surgery complications and,
456-458 (V3)
surgically assisted maxillary
expansion for, 219-237 (V3)
clinical evaluation in, 219, 220-
220f, 221f (V3)
complications of, 231-232, 233f
(V3)
modification of, 232-233, 234f
(V3)
orthopedic rapid maxillary
expansion and, 224-226, 224-
226f (V3)
radiographic evaluation in, 220-
223, 221-223f (V3)
segmental maxillary osteotomy
versus, 233-235 (V3)
total maxillary segmental osteotomy
for, 192-204 (V3)
complications in, 198, 198f, 199f
(V3)
historical background of, 192 (V3)
indications for, 192-193 (V3)
for maxillary deficiency, 199-203f
(V3)
osteotomy design in, 196 (V3)
postoperative care in, 196-197,
197f (V3)
surgical planning in, 197-198 (V3)
technique in, 193-196, 194-196f
(V3)
Dental arch spacing, 401, 401f (V3)
Dental chair, 360 (V1)
Dental compensations
mandibular surgery complications
and, 419-421, 420-422f (V3)
maxillary surgery complications and,
456, 457-458f (V3)
Dental implant, 387-574 (V1)
autogenous bone grafting in, 406-427
(V1)
bone biology and, 406-407, 407f
(V1)
graft recipient site and, 419-422,
419-422f (V1)
ilium for, 415-419, 415-419f (V1)
mandibular ramus for, 412-414,
412-414f (V1)
mandibular symphysis for, 409-411,
410-412f (V1)
maxillary tuberosity for, 409, 409f,
410f (V1)
onlay bone graft and, 424, 424f,
425f (V1)
patient preparation for, 409 (V1)
preoperative evaluation in, 407-
408, 408f, 409f (V1)
sinus bone grafting and, 422-424,
423f (V1)
tibia for, 414f, 414-415, 415f (V1)
chronic facial pain after, 968 (V2)
guided tissue regeneration in, 428-
457 (V1)
for augmentation using allograft
and xenograft bone with
titanium-reinforced
membrane, 450-451, 450-451f
(V1)
for augmentation using allograft
bone putty and resorbable
collagen membrane, 448f,
448-449, 449f (V1)
for coronal defects, 436 (V1)
for corticocancellous block
augmentation of posterior
mandible, 452-453, 452-453f
(V1)
for dehiscence defects, 435-436,
447, 447f (V1)
dual-layered technique in, 445f,
445-446, 446f (V1)
for fenestration defects, 436 (V1)
flapless buccal wall reconstruction
in, 443f, 443-444, 444f (V1)
I-24 INDEX
Dental implant (Continued)
functional and design requirements
of membranes for, 429-431,
431f, 432f (V1)
to reduce postextraction bone loss,
438-440, 454f, 454-455, 455f
(V1)
ridge preservation using high-
density PTFE membrane in,
440-441f, 440-442 (V1)
in subantral augmentation, 436-
438, 437f (V1)
wound closure in, 431-435, 433f,
434f (V1)
immediate implant loading in, 511-
524 (V1)
benefits of, 522-524 (V1)
in edentulous jaw, 518-521, 519-
524f (V1)
following extraction, 540-546, 541-
545f (V1)
for single tooth or partially
edentulous restoration, 511-
517, 512-518f (V1)
impressions at implant placement
and, 525-539 (V1)
concept of, 531 (V1)
history of immediate loading and,
525-527, 526b, 526f, 527f
(V1)
immediate extraction, implant
placement, and provisional
restoration and, 534f, 534-
535, 535f (V1)
immediate provisionalization and,
528-531, 530-531f (V1)
prefabricated ceramic abutments
and temporary crowns and,
536f, 536-537, 537f (V1)
primary bone-level impressions
and, 527-528, 529f, 530f (V1)
second-stage surgery and, 532f,
532-533, 533f (V1)
laser-assisted, 245-246 (V1)
miniimplants and, 567-574, 568f
(V1)
for orthodontic anchorage, 570-
574, 572-574f (V1)
for pontic support of fixed partial
denture, 568 (V1)
for retention of obturators, 568-
569 (V1)
for single-tooth implant restoration
in narrow space, 569, 570f,
571f (V1)
for stabilization of complete
dentures, 567-568, 569f (V1)
for stabilization of removable
partial dentures, 568 (V1)
osteoperiosteal flap and, 471-478
(V1)
alveolar repositioning osteotomies
and, 473, 473f, 474f (V1)
alveolar split graft and, 471, 473f
(V1)
alveolar width distraction
osteogenesis and, 474-477,
475-478f (V1)
interpositional bone graft and, 471,
472f (V1)
pediatric, 181-183, 182f, 183f (V1)
pharmacology for, 387-405 (V1)
antibiotic prophylaxis and, 387-
388, 388b (V1)
antibiotics added to bone grafting
materials and, 388-390, 389t,
390t (V1)
bioactive fatty acids and bone
development and, 399-400
(V1)
bisphosphonates and, 395-398,
396t, 397t (V1)
mineral, hormonal, and vitamin
supplements and, 398-399,
399t (V1)
NSAIDS and bone development
and, 392-395 (V1)
periimplantitis and, 390-392, 391t
(V1)
Dental implant (Continued)
platelet-rich plasma and bone
grafting in, 501-510 (V1)
allograft and alloplastic materials
and, 504f, 504-506 (V1)
benefits of, 502-503 (V1)
bone healing and, 394, 503f, 503-
504 (V1)
case report of, 509, 509f (V1)
concept of, 501-502, 502f (V1)
processing of, 506-508, 507f, 508f
(V1)
radiographic evaluation in, 547-566
(V1)
computed tomography in, 552-564,
553-565f (V1)
digital radiography in, 549-550,
551f (V1)
linear tomography in, 552 (V1)
orthopantomogram in, 551-552,
552f, 553f (V1)
plain films in, 549-551f (V1)
principles for, 547-548, 548f, 549f
(V1)
subtraction radiography in, 551
(V1)
sinus-lift subantral augmentation in,
458-470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic
considerations in, 458-459
(V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f,
464f (V1)
elevation of schneiderian
membrane in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
trephine core membrane elevation
in, 464-468, 464-468f (V1)
vascular supply, lymphatic
drainage, and innervation in,
459 (V1)
soft tissue procedures around implant,
479-490 (V1)
aesthetic considerations and, 479-
480, 480t, 481f (V1)
AlloDerm in, 486, 487f (V1)
connective tissue grafting in, 485,
485f, 486f (V1)
epithelialized free-gingival grafting
in, 483f, 484-485 (V1)
gingivectomy in, 481-484, 484f,
485f (V1)
modified roll tissue graft in, 486,
488f (V1)
papilla regeneration technique in,
487-489, 489f (V1)
pediculated connective tissue graft
in, 486 (V1)
soft tissue health considerations
and, 479, 480f (V1)
trigeminal nerve injury and, 275-276
(V1)
zygomatic implant in, 491-500 (V1)
complications in, 498f, 498-499
(V1)
final prosthesis fabrication and,
499 (V1)
historical perspective in,
491 (V1)
patient selection for, 491-492, 492f
(V1)
postoperative care in, 498 (V1)
preoperative considerations in,
493, 493f (V1)
prosthetic conversion technique
in, 496-497, 497f, 498f (V1)
Dental implant (Continued)
radiographic evaluation in, 492,
492f (V1)
regional anatomy in, 492-493 (V1)
surgical options in, 493-494, 494f
(V1)
surgical protocol in, 494-496, 494-
497f (V1)
Dental model analysis, 364-371 (V3)
construction of intermediate splint
in, 368-369, 369f, 370f (V3)
in facial asymmetry, 277 (V3)
in mandibular widening, 338 (V3)
marking cast in, 366-367 (V3)
measurements in, 367f, 367-368 (V3)
mounting case in, 364-366, 365f,
366f (V3)
positioning of maxilla in, 368, 368f
(V3)
for segmental surgery, 369-370, 370f
(V3)
for special situations, 370-371 (V3)
Dental periapical radiography
in apexification procedure, 115-116,
116f (V2)
in dentoalveolar injury, 109 (V2)
of impacted teeth, 167, 168f (V1)
in implant surgery, 549-551f (V1)
of luxation of tooth, 119f (V2)
in mandibular trauma, 98 (V2)
Dental Practice Act, 309-312, 310-311t
(V1)
Dental procedures
applications for laser therapy in, 254-
256 (V1)
definitions and resources in, 309-313,
310-312t (V1)
endocarditis prophylaxis and, 3, 5t
(V1)
Dental pulpal blood flow
Le Fort 1 osteotomy and, 65 (V3)
segmental maxillary osteotomy and,
67, 67f (V3)
Dental rehabilitation in cleft palate,
841-843, 844-845f (V3)
Dental relations in cephalometry, 14-
15, 16f (V3)
Dental-borne appliance
in mandibular widening, 338, 340f
(V3)
in maxillary distraction by intraoral
device, 347 (V3)
Dentatus miniimplant, 568f (V1)
Dentigerous cyst, 419, 424-426, 425-
428f (V2)
Dentin, enamel fracture and, 113-117,
115b, 116-118f (V2)
Dentinoma, 524-527, 527f (V2)
Denti-patch, 49 (V1)
Dentistry
applications for laser therapy in, 254-
256 (V1)
definitions and resources in, 309-313,
310-312t (V1)
endocarditis prophylaxis and, 3, 5t
(V1)
Dentition disorders, 175-181 (V1)
cleidocranial dysplasia in, 175-177,
176f, 177f (V1)
in craniofacial dysostosis syndromes,
881-882 (V3)
Gardner’s syndrome in, 178f, 178
(V1)
generalized gingival hyperplasia in,
178-179, 179f (V1)
hereditary ectodermal dysplasia in,
177f, 177-178 (V1)
localized gingival lesions in, 179-181,
180f, 181f (V1)
Dentoalveolar asymmetry
facial asymmetry and, 282, 283-284f
(V3)
speech disorder and, 791-792, 792t
(V3)
Dentoalveolar evaluation in facial
asymmetry, 274 (V3)
Dentoalveolar surgery, 165-284 (V1)
basic exodontia in, 185-192 (V1)
complications in, 191-192 (V1)
Dentoalveolar surgery (Continued)
diagnosis and treatment planning
in, 187 (V1)
indications for, 186-187 (V1)
pain management in, 192 (V1)
principles of, 187-190, 188-190f
(V1)
socket preservation and wound
closure in, 190-191 (V1)
complicated exodontia in, 192-201
(V1)
bone removal in, 193-194, 194f
(V1)
of canines, 196-197, 197-199f (V1)
flap design in, 192-193, 193f, 194f
(V1)
general principles of, 192 (V1)
of impacted teeth other than third
molars, 195-196 (V1)
indications for, 192b (V1)
of premolars, 197-199, 200f (V1)
sectioning of teeth and removal in,
194-195, 195f, 196f (V1)
of teeth located in uncommon
anatomic positions, 200-201,
201f (V1)
wound closure in, 201 (V1)
complications of, 212-222 (V1)
alveolar osteitis in, 216 (V1)
bisphosphonate-related
osteonecrosis in, 217, 218t
(V1)
displacement of teeth and root tips
in, 213-214 (V1)
hemorrhage in, 219 (V1)
infection in, 216-217 (V1)
injuries to teeth or adjacent
structures in, 212, 213f (V1)
oroantral communication in, 214f,
214-215 (V1)
osseous injuries in, 219f, 219-220,
220f (V1)
osteoradionecrosis in, 217 (V1)
removal of wrong tooth in, 212
(V1)
residual root remnants in, 213
(V1)
sensory nerve injuries in, 215f,
215-216, 216f (V1)
soft tissue injuries in, 214 (V1)
swallowing or aspiration of teeth,
crowns, or restorations in, 215
(V1)
temporomandibular joint problems
in, 218 (V1)
tissue emphysema in, 215 (V1)
trismus, pain, and swelling in, 217-
218 (V1)
for impacted third molar teeth, 201-
210 (V1)
bone removal and tooth sectioning
in, 205-206, 207-210f (V1)
classification of, 203, 204f (V1)
indications and contraindications
for, 202-203 (V1)
instrumentation for, 203, 203t
(V1)
mandibular, 203-205, 205b, 206f
(V1)
maxillary, 207, 208-210f (V1)
postoperative instructions in, 208-
210, 209b (V1)
preoperative management in, 207t,
207-208, 208b (V1)
wound closure in, 206-207 (V1)
informed consent for, 212,
213b (V1)
laser-assisted, 237-258 (V1)
applications for general dentistry,
254-256 (V1)
bone healing and, 253-254 (V1)
for cosmetic skin procedures, 248-
251, 249t (V1)
for cutaneous pigmented lesions or
tattoos, 251 (V1)
effects on postoperative pain and
swelling, 254b, 254 (V1)
equipment in, 241-242, 242f (V1)
for hair removal, 251-252 (V1)

Dentoalveolar surgery (Continued)
implant surgery with, 245-246
(V1)
in incisional and excisional soft
tissue procedures, 244-245
(V1)
laser physics and, 237-238, 238f
(V1)
laser-scan-based registration and,
256 (V1)
low-level, 253 (V1)
in oral and maxillofacial surgery,
243-244, 244f (V1)
for oral pathologic conditions, 245
(V1)
safety issues in, 242b, 242f, 242-
243, 243f (V1)
for sleep apnea and snoring, 252-
253 (V1)
for temporomandibular disorders,
246-248 (V1)
tissue interactions in, 239t, 239-
241f, 239-241 (V1)
for vascular lesions of face, 251
(V1)
wound healing and, 253 (V1)
pediatric, 165-184 (V1)
for cleidocranial dysplasia, 175-
177, 176f, 177f (V1)
eruption pattern for deciduous and
permanent dentition, 165,
166t (V1)
for Gardner’s syndrome, 178f, 178
(V1)
for generalized gingival hyperplasia,
178-179, 179f (V1)
for hereditary ectodermal dysplasia,
177f, 177-178 (V1)
for impacted teeth, 165-173 (V1);
See also Impacted teeth
implants in, 181-183, 182f, 183f
(V1)
for localized gingival lesions, 179-
181, 180f, 181f (V1)
soft tissue procedures in, 173-174,
173-176f (V1)
skeletal anchorage for orthodontics
in, 223-236 (V1)
basic orthodontic mechanics and,
224-225 (V1)
bone plates in, 232-233, 233f, 234f
(V1)
for closure of anterior open bite,
232 (V1)
devices for, 225f, 225-226, 226f
(V1)
historical perspective of, 223-224
(V1)
mesial or distal movement of teeth
and, 226-231f (V1)
miniscrews in, 233-235 (V1)
orthopedic growth modification
and, 232 (V1)
outcomes and complications in,
235-236 (V1)
postoperative regimen in, 234-235
(V1)
for uprighting and intruding molar
teeth, 232 (V1)
trigeminal nerve injury and, 259-284
(V1)
acute, 265-266, 266f, 267f (V1)
classification of, 259-261, 260t
(V1)
clinical neurosensory testing in,
262f, 262-264, 263f (V1)
decompression in, 268 (V1)
determinants of nerve injury
responses, 261 (V1)
in facial trauma, 272-273 (V1)
function impairment assessment in,
261, 261t (V1)
impacted third molar removal-
related, 276-278 (V1)
implant-related, 275-276 (V1)
inferior alveolar nerve repairs in,
266f, 270 (V1)
infraorbital nerve repairs in, 270
(V1)
Dentoalveolar surgery (Continued)
internal neurolysis in, 268-269
(V1)
lingual nerve repairs in, 269f, 269-
270 (V1)
local anesthetic injection-related,
273-274 (V1)
medicolegal issues in, 278-279
(V1)
nerve grafting in, 269 (V1)
neuroma resection in, 268 (V1)
neurorrhaphy in, 269 (V1)
orthognathic, 275 (V1)
outcomes of repair in, 271-272 (V1)
pain and discomfort assessment in,
261t, 261-262 (V1)
patient selection for nerve repair
in, 265 (V1)
pharmacologic testing in, 264 (V1)
postoperative management of, 270-
271 (V1)
sensory reeducation and patient
follow-up in, 271 (V1)
surgical and endodontic
medicament-related, 274-275
(V1)
surgical instrumentation for, 267-
268 (V1)
timing of surgery for, 266-267 (V1)
traumatic neuropathic pain
assessment in, 264-265, 265f
(V1)
Dentofacial deformity
complete mandibular subapical
osteotomy for, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
in craniofacial dysostosis syndromes,
881-882 (V3)
genioplasty for, 137-154 (V3)
fixation devices in, 142-145, 144-
148f (V3)
functional, 137, 138f (V3)
indications for, 137-138 (V3)
results in, 148-151, 150-153f (V3)
surgical procedure in, 140-142,
141f, 142f (V3)
treatment planning in, 138-140,
139f, 140f (V3)
model surgery in, 364-371 (V3)
construction of intermediate splint
in, 368-369, 369f, 370f (V3)
in facial asymmetry, 277 (V3)
in mandibular widening, 338 (V3)
marking cast in, 366-367 (V3)
measurements in, 367f, 367-368
(V3)
mounting case in, 364-366, 365f,
366f (V3)
positioning of maxilla in, 368, 368f
(V3)
for segmental surgery, 369-370,
370f (V3)
for special situations, 370-371 (V3)
obstructive sleep apnea syndrome
and, 321f (V3)
occlusal plane rotation for, 248-271
(V3)
clockwise rotation in, 252-256,
252-256f (V3)
counterclockwise rotation in, 256-
260, 257-263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-
249, 249f, 250f (V3)
geometry of treatment design
using constructed
maxillomandibular triangle in,
261f, 261-262 (V3)
Dentofacial deformity (Continued)
linear dimensions between
maxillary length and vertical
facial height in, 250, 250f (V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-
268 (V3)
prediction of soft tissue changes in
surgery for, 372-381 (V3)
cephalometric, 372-375, 373f (V3)
computerized-video imaging, 375-
377, 376f (V3)
photographic, 375 (V3)
three-dimensional computer-
assisted, 377-379, 378f (V3)
speech disorder and, 791-792, 792t
(V3)
total maxillary segmental osteotomy
for, 192-204 (V3)
complications in, 198, 198f, 199f
(V3)
historical background of, 192 (V3)
indications for, 192-193 (V3)
for maxillary deficiency, 199-203f
(V3)
osteotomy design in, 196 (V3)
postoperative care in, 196-197,
197f (V3)
surgical planning in, 197-198 (V3)
technique in, 193-196, 194-196f
(V3)
transverse maxillary deficiency in,
219-237 (V3)
clinical evaluation in, 219, 220-
220f, 221f (V3)
incidence and origin of, 219, 220f
(V3)
orthopedic rapid maxillary
expansion for, 224-226, 224-
226f (V3)
radiographic evaluation in, 220-
223, 221-223f (V3)
surgically assisted maxillary
expansion for, 227-235, 228-
234f (V3)
Dentofacial Planner Plus software, 376,
377 (V3)
Dentures, miniimplant stabilization of,
567-568, 569f (V1)
Denver splint, 279f (V2)
Deoxyribonucleic acid, cell function
and, 648-652, 649-651f (V2)
Dependence on opioid analgesics, 81
(V1)
Deposition, lawsuit and, 377 (V1)
Depressed skull fracture, 59 (V2)
Depression
chronic head and neck pain in, 141
(V1)
surgery-related, 408 (V3)
Depressor anguli oris muscle, 174f (V3)
botulinum toxin injection into before
lip augmentation, 636, 636f,
637f (V3)
Depressor septi nasi muscle, 553, 554f
(V3)
Depressor supercilii muscle, 597, 598f
(V3)
Depth of sedation monitoring, 30b, 30-
31, 31f (V1)
Dermal graft
in internal derangement of
temporomandibular joint, 938-
939, 939f (V2)
for maxillectomy-related defect, 696,
697f (V2)
postauricular, 297f (V2)
in skin cancer, 739 (V2)
Dermatitis, laser skin resurfacing-
related, 539 (V3)
INDEX I-25
Dermatochalasia, 579, 580f (V3)
Dermatofibrosarcoma protuberans, 727-
728, 728f (V2)
Dermis, 9, 10f, 513 (V3)
Dermoid cyst, 451-455, 454f, 455f (V2)
Descending inhibitory control of pain,
963 (V2)
Descending palatine artery, 174, 175f,
555f (V3)
maxilla and, 63f, 66f, 173f (V3)
postoperative bleeding in Le Fort I
osteotomy and, 186 (V3)
Descending palatine neurovascular
bundle, 172 (V3)
Descending pharyngeal artery, 66f (V3)
Desflurane, 64t, 65 (V1)
Desipramine, 889t (V2)
Desmoplastic ameloblastoma, 481f (V2)
Desmoplastic fibroma, 606-608, 607-
608f (V2)
Desmoplastic melanoma, 751t, 752t
(V2)
Desmopressin
for hemophilia, 16 (V1)
perioperative management of, 385
(V3)
for von Willebrand disease, 17 (V1)
Desyrel; See Trazodone
Development, defined, 849t (V3)
Developmental cysts, 424-447 (V2)
dentigerous, 424-426, 425-428f (V2)
dermoid and epidermoid, 451-455,
454f, 455f (V2)
globulomaxillary, 451 (V2)
median mandibular, 451 (V2)
median palatal, 451 (V2)
nasolabial, 447-448, 449f, 450f (V2)
nasopalatine duct, 448-451, 451-453f
(V2)
nevoid basal cell carcinoma syndrome
in, 433f, 441b, 441-442, 442t,
444f (V2)
odontogenic keratocyst, 426-441
(V2)
clinical features of, 428-435, 430-
435f (V2)
etiology of, 426-428 (V2)
imaging features of, 435, 436-437f
(V2)
pathologic features of, 435f, 435-
436 (V2)
surgical management of, 437-441,
439f, 440f (V2)
ultrastructure of, 437, 438f (V2)
Developmental facial asymmetry, 282
(V3)
Developmental pharmacology, 96-97
(V1)
Dexamethasone
for acute trigeminal nerve injury, 266
(V1)
for chronic facial pain, 974 (V2)
in laser skin resurfacing, 521 (V3)
for postoperative vomiting, 108 (V1)
for temporomandibular disorders,
887t (V2)
Diabetes mellitus
ambulatory orthognathic surgery and,
493 (V3)
in geriatric patient, 383-384 (V2)
impaired healing in, 419 (V3)
intensive care of trauma patient and,
46-47 (V2)
perioperative management of, 385-
386 (V3)
preoperative evaluation of, 11-12, 12t
(V1)
salivary disease in, 556 (V2)
Diagnostic coding, 364 (V1)
Diagnostic imaging
of abnormal head shape, 856 (V3)
in ankylosis, 903 (V2)
in assessment of trauma patient, 41,
67 (V2)
in avulsive facial trauma, 328 (V2)
in cervical spine injury, 63 (V2)
in chronic facial pain, 118, 119f, 120f
(V1), 965-966 (V2)
in condylar hyperplasia, 285 (V3)
I-26 INDEX
Diagnostic imaging (Continued)
in dentoalveolar injury, 102, 102f,
109-110, 110f (V2)
documentation of, 382 (V1)
in facial asymmetry, 274-275 (V3)
in adolescent internal condylar
resorption, 305, 306f (V3)
in autoimmune and connective
tissue diseases, 309, 312-313f
(V3)
in condylar dislocation, 281, 281f
(V3)
in condylar hyperplasia, 285 (V3)
developmental, 282 (V3)
in dystonia, 281, 281f (V3)
in hemifacial microsomia, 299,
302f (V3)
iatrogenic, 294 (V3)
infection-related, 282 (V3)
in malocclusion, 278, 279-280f
(V3)
in neuromuscular disorders, 292
(V3)
in osteochondroma or osteoma of
mandible, 291, 291f (V3)
in temporomandibular joint
ankylosis, 297, 298f (V3)
tumor-related, 293, 293f (V3)
unilateral dentoalveolar asymmetry
and, 282 (V3)
in unilateral reactive arthritis, 305-
306, 309f (V3)
in facial injuries, 91-92, 98-99 (V2)
in fractures
angle of mandible, 101, 101f (V2)
comminuted, complicated, and
impacted fractures of face, 99,
99f (V2)
in complications of treatment of
mandibular fracture, 102-103
(V2)
computed tomography in, 98-99
(V2)
condylar, 100f, 100-101, 168-170,
169f (V2)
coronoid process and ramus, 101
(V2)
frontal sinus, 256-257, 260f, 261f
(V2)
greenstick and pathologic, 99, 100f
(V2)
mandibular body, 101, 102f (V2)
mandibular symphysis and
parasymphysis, 101, 102f (V2)
midface, 241f, 241-242, 242f (V2)
nasal, 274f, 274-275 (V2)
naso-orbital-ethmoid, 246 (V2)
orbital, 209-211, 210f, 211f (V2)
simple and compound, 99, 99f
(V2)
zygomatic, 184-185, 185f (V2)
in head injury, 56, 57b (V2)
acute subdural hematoma and, 60,
61f (V2)
epidural hematoma and, 60, 61f
(V2)
mild closed, 56-57 (V2)
moderate closed, 57 (V2)
severe closed, 57-58 (V2)
traumatic subarachnoid
hemorrhage and, 62 (V2)
in implant surgery, 407, 408, 408f,
547-566 (V1)
computed tomography in, 552-564,
553-565f (V1)
cone beam technology and, 554,
563-564, 564f, 565f (V1)
digital radiography in, 549-550,
551f (V1)
history of, 552-554, 553f, 554f
(V1)
linear tomography in, 552 (V1)
for maxillary sinus augmentation,
561-563, 562f, 563f (V1)
orthopantomogram in, 551-552,
552f, 553f (V1)
plain films in, 549-551f (V1)
principles for, 547-548, 548f, 549f
(V1)
Diagnostic imaging (Continued)
rapid prototyping and, 555-557,
555-557f (V1)
reformatting software program and,
557-561, 557-562f (V1)
subtraction radiography in, 551
(V1)
three-dimensional modeling and,
554-556, 554-556f (V1)
zygomatic implant and, 492, 492f
(V1)
mandibular anatomy and, 96 (V2)
mandibular series in, 96-98, 97f (V2)
in mandibular trauma, 96-99, 97f,
99f, 145f, 146f (V2)
midfacial anatomy and, 91, 92f (V2)
in obstructive sleep apnea syndrome,
319-321, 320-322f (V3)
for occult vascular injuries, 69, 70f
(V2)
in orbital trauma, 86, 86f (V2)
in osteomyelitis, 634f, 634-635, 635f
(V2)
in osteoradionecrosis, 639, 640f (V2)
panoramic radiography in, 98, 99f
(V2)
of pediatric impacted teeth, 166-168f,
167 (V1)
rendering techniques in, 92-94, 93-
95f (V2)
in soft tissue trauma to neck, 94-95,
96f (V2)
supplemental radiographs in, 98 (V2)
techniques in, 91-92, 92f, 92t (V2)
in temporomandibular disorders, 821-
823, 821-823f, 835-841 (V2)
advanced modalities in, 839 (V2)
in anterior disc displacement, 819
(V2)
computed tomography in, 839-840,
840f, 841f (V2)
cone beam computed tomography
in, 843, 845f, 846f (V2)
conventional, 835-836 (V2)
functional, 843-845 (V2)
fusion, 845 (V2)
in internal derangement of
temporomandibular joint,
931, 932f (V2)
lateral oblique views in, 837, 837f
(V2)
linear tomography in, 838 (V2)
magnetic resonance imaging in,
840-841, 842-843f (V2)
multidirectional tomography in,
838-839 (V2)
panoramic radiography in, 837-
838, 838f (V2)
reverse Towne’s projection in, 836,
837f (V2)
submentovertex projection in, 837,
837f (V2)
in temporomandibular joint
hypomobility, 898 (V2)
transcranial radiography in, 836,
836f (V2)
transmaxillary or transorbital
radiography in, 836, 836f
(V2)
tuned aperture computed
tomography in, 841-843, 844f
(V2)
ultrasonography in, 846 (V2)
three-dimensional computer-assisted
prediction and, 377-379, 378f
(V3)
in three-dimensional radiation
treatment planning, 772-773,
773f (V2)
in transverse maxillary deficiency,
220-223, 221-223f (V3)
in trigeminal neuralgia, 991 (V2)
in tumors
Ewing’s sarcoma, 687, 688f (V2)
lymphoma, 762f, 762-763 (V2)
maxillofacial, 690, 691f (V2)
odontogenic, 467 (V2)
oral cavity cancer, 710 (V2)
osteosarcoma, 680, 681f, 682f (V2)
Diagnostic imaging (Continued)
pediatric craniomaxillofacial, 961-
962 (V3)
skin cancer, 732-733, 733f (V2)
Diagnostic peritoneal lavage, 41, 65-66,
66f (V2)
Diagnostic tests
documentation of, 382 (V1)
in temporomandibular disorders,
982b, 982 (V2)
Diapedesis, 61 (V3)
Diazepam, 57-58, 58f (V1)
half-life and protein binding of, 58t
(V1)
pharmacokinetics of, 62t (V1)
for postoperative pain, 90 (V1)
for temporomandibular disorders,
889, 889t (V2)
for trigeminal neuralgia, 150 (V1)
Diclofenac, 84t, 86t (V1)
for neuropathy secondary to neuritis,
1000 (V2)
for skin cancer, 740-741 (V2)
for temporomandibular disorders,
887t (V2)
Dicodid; See Hydrocodone
DICOM; See Digital Imaging and
Communication in Medicine format
Didronel; See Etidronate
Diet, postsurgical, 408-409, 409f (V3)
Diet therapy after temporomandibular
joint surgery, 133 (V1)
Difficult airway
adjuncts for, 31 (V2)
identification in trauma patient, 25,
26b (V2)
Diffuse axonal injury, 62 (V2)
Diffuse large B-cell lymphoma, 761,
761f (V2)
Diffuse sclerosing osteomyelitis, 638,
638f (V2)
Diflunisal, 84t, 86t (V1), 887t (V2)
Digastric muscle, 808 (V2)
DiGeorge syndrome, 715 (V3)
Digital Imaging and Communication in
Medicine format, 377-379 (V3)
Digital imaging systems, office
management and, 303 (V1)
Digital radiography in implant surgery,
549-550, 551f (V1)
Digital rectal examination in cranio-
maxillofacial trauma, 11 (V2)
Dihydrocodeine, 81t (V1)
Dilantin; See Phenytoin
Dilated examination of eye, 76f, 76-77
(V2)
Dilator naris muscle, 174f, 554f (V3)
Dilaudid; See Hydromorphone
Dingman, Reed, 794 (V2)
Diode laser, 240, 241 (V1)
in periodontal therapy, 255-256 (V1)
in soft tissue recontouring procedures,
254-255 (V1)
Diphenhydramine, 538 (V3)
Diplopia
evaluation of, 77 (V2)
following blepharoplasty, 593 (V3)
in head injury, 52 (V2)
in orbital fracture, 214-215, 215f,
216f, 235-236 (V2)
in orbital injury, 86 (V2)
in zygomatic fracture, 195-197, 196f,
196t (V2)
Direct bone healing, 62 (V3), 146, 147f
(V2)
Direct costs, 298 (V1)
Direct forehead and brow lift, 611t
(V3)
Direct laryngoscopy in trauma patient,
30-31, 31f (V2)
Direct pupillary reflex, 76 (V2)
Direct skeletal anchorage techniques,
224 (V1)
Disability status in trauma, 7-8, 8f, 38-
39, 39t (V2)
Disc derangement of
temporomandibular joint
arthrocentesis in, 912-917 (V2)
outcome assessment in, 915 (V2)
Disc derangement of temporomandibular
joint (Continued)
pathophysiology of
temporomandibular disorder
and, 912-913 (V2)
prognostic and predictive factors
in, 916 (V2)
technique in, 913-915, 914f (V2)
arthroscopy for, 920-921, 921f (V2)
arthrotomy in, 929-944, 930b (V2)
capsular incisions in, 934, 934f
(V2)
condylotomy in, 939-940 (V2)
diagnostic imaging in, 931, 932f
(V2)
disk repair in, 936, 936f (V2)
disk repositioning in, 935f, 935-
936 (V2)
diskectomy in, 936 (V2)
diskectomy with replacement in,
936-939, 937-939f (V2)
endaural incision in, 933f, 933-
934, 934f (V2)
goals and criteria for surgery in,
931 (V2)
history and physical examination
in, 929-930 (V2)
pathogenesis of, 930-931 (V2)
postoperative care in, 940-941 (V2)
preauricular incision in, 932-933,
933f (V2)
preoperative therapies for, 931
(V2)
surgical complications in, 940 (V2)
wound closure in, 934, 935f (V2)
diagnostic approach to, 831t (V2)
osteoarthritis and, 856 (V2)
splint therapy for, 884-885 (V2)
Disc displacement
in condylar fracture, 168 (V2)
osteoarthritis and, 856 (V2)
Disc interference disorders
mandibular gait in, 825, 826f (V2)
stages of, 833f (V2)
Disc ligaments, 802-803, 803f (V2)
Disc perforation, laser-assisted
treatment of, 247-248 (V1)
Discharge criteria, 75-76 (V1)
in ambulatory surgery, 485 (V3)
for child, 108 (V1)
Discharge of patient from practice, 383
(V1)
Discharge planning, 405-409 (V2)
Discoloration of tooth, postsurgical, 412
(V3)
Discovery, lawsuit and, 377f (V1)
Diskectomy, 936 (V2)
Diskectomy with replacement, 936-939,
937-939f (V2)
Diskoplasty, 132-133 (V1)
Dislocated condylar fracture, 142 (V2)
Dislocation
condylar, 281, 281f (V3)
exodontia-related, 218 (V1)
lens, 213 (V2)
temporomandibular joint, 905b, 905-
908 (V2)
Displaced condylar fracture, 142 (V2)
Displacement
anterior disc, 818-821, 819-821f (V2)
advanced imaging modalities in,
839 (V2)
chronic orofacial pain in, 127 (V1)
mandibular gait in, 825, 827f (V2)
splint therapy for, 885 (V2)
anteroposterior globe, 78, 78f, 88
(V2)
condylar, in bilateral sagittal split
osteotomy, 114 (V3)
craniofacial skeletal growth and, 850
(V3)
of tooth, 118, 118b, 213-214 (V2)
primary tooth, 124-125, 125f, 126f
(V2)
Disruption, defined, 849t (V3)
Distal movement of teeth with maximal
anchorage, 226-231f (V1)
Distoangular impaction of third molar,
205-206 (V1)

Distraction histogenesis, 997 (V3)
Distraction osteogenesis, 338-363, 996-
1006 (V3)
alveolar distraction in, 349-354, 349-
354f (V3)
biologic basis of, 996-997 (V3)
bone transport by, 354-360, 355-361f
(V3)
cranial vault, 1002 (V3)
in craniofacial dysostosis syndromes,
885-886 (V3)
future directions in, 362 (V3)
history of, 996 (V3)
mandibular, 998-1001f, 998-1002 (V3)
mandibular lengthening in, 342-346,
342-346f (V3)
mandibular widening in, 338-342,
339-342f (V3)
maxillary, 1002, 1003f, 1004f (V3)
maxillary bone transport in, 360-362,
362f (V3)
maxillary distraction by intraoral
devices in, 346-349, 347-349f
(V3)
in oculoauriculovertebral spectrum
mandibular lengthening and, 928,
929-930f (V3)
temporomandibular joint
reconstruction and, 927-928
(V3)
pediatric, 858 (V3)
in temporomandibular joint
reconstruction, 904-905, 955
(V2)
in Treacher Collins syndrome, 954
(V3)
in tumor-related mandibular defect,
992 (V3)
Distraction test, 519 (V3)
Docetaxel, 779, 781t, 782t (V2)
Docking site surgery, 359-360, 360f,
361f (V3)
Documentation
of anesthesia care, 31-32, 32t (V1)
of informed consent, 379 (V1)
in nerve injury and repair, 278-279
(V1)
risk management and, 379-383 (V1)
Dog bite, 290-292, 292f, 313-316, 314-
317f (V2)
Dolobid; See Diflunisal
Dolophine; See Meperidine
Dome division, 565 (V3)
Domestic violence with facial injuries,
395 (V2)
Don Joy Pain Pump, 974 (V2)
Dorsal lingual artery, 68 (V3)
Dorsal nasal artery, 69f, 555f (V3)
Dorsal root entry zone, 992 (V2)
Dorsum, 554b (V3)
physical examination of, 558f, 558
(V3)
reduction of, 568f, 568-569 (V3)
Double dome technique, 563f, 566 (V3)
Double-jaw surgery, 238-247 (V3)
cephalometric analysis and, 375 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
model surgery and, 364-371 (V3)
construction of intermediate splint
in, 368-369, 369f, 370f (V3)
marking cast in, 366-367 (V3)
measurements in, 367f, 367-368
(V3)
mounting case in, 364-366, 365f,
366f (V3)
positioning of maxilla in, 368, 368f
(V3)
for segmental surgery, 369-370,
370f (V3)
for special situations, 370-371 (V3)
occlusal plane rotation in, 248-271
(V3)
clockwise rotation in, 252-256,
252-256f (V3)
counterclockwise rotation in, 256-
260, 257-263f (V3)
Double-jaw surgery (Continued)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-
249, 249f, 250f (V3)
geometry of treatment design using
constructed
maxillomandibular triangle in,
261f, 261-262 (V3)
linear dimensions between
maxillary length and vertical
facial height in, 250, 250f
(V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-
268 (V3)
postsurgical complications in, 396
(V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for unilateral adolescent internal
condylar resorption, 305 (V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
videocephalometric prediction and,
376 (V3)
Double-opposing Z-plasty for cleft
palate, 726, 730f, 772-775, 773-
775f (V3)
controversies in, 762 (V3)
history of, 759-760 (V3)
Down syndrome, 851 (V3)
Down-fracture of maxilla in Le Fort I
osteotomy, 179, 180f (V3)
Doxepin, 889t (V2)
Doxorubicin, 781t (V2)
Doxycycline, 392 (V1)
Doyle splint, 279f (V2)
dPTFE membrane; See High-density
polytetrafluoroethylene membrane
Dressing
in genioplasty, 142, 142f (V3)
in laser skin resurfacing, 524-529 (V3)
in Mustard[ac]e method of otoplasty,
673 (V3)
in rhinoplasty, 573, 573f (V3)
in rhytidectomy, 505 (V3)
Drug(s)
avoidance after surgery, 408 (V3)
liver disease-related alteration in
metabolism of, 11t, 11 (V1)
Drug allergy
to local anesthetics, 48 (V1)
preoperative evaluation of, 1-2, 2t
(V1)
Drug dependence
barrier to chronic pain management,
970-971 (V2)
to opioid analgesics, 81 (V1)
treatment of, 408-410 (V2)
Drug history
of geriatric patient, 380 (V2)
preoperative evaluation of, 1-2, 2t
(V1)
Drug therapy
for chronic head and neck pain, 144
(V1)
for fibromyalgia, 142 (V1)
implant dentistry pharmacology and,
387-405 (V1)
antibiotic prophylaxis and, 387-
388, 388b (V1)
antibiotics added to bone grafting
materials and, 388-390, 389t,
390t (V1)
Drug therapy (Continued)
bioactive fatty acids and bone
development and, 399-400
(V1)
bisphosphonates and, 395-398,
396t, 397t (V1)
mineral, hormonal, and vitamin
supplements and, 398-399,
399t (V1)
NSAIDS and bone development
and, 392-395 (V1)
periimplantitis and, 390-392, 391t
(V1)
for infantile hemangioma, 580 (V2)
for migraine, 148 (V1)
for myofascial pain syndromes, 144-
145 (V1)
for orofacial migraine variants, 149
(V1)
for postherpetic neuralgia, 152 (V1)
postoperative, 78-92 (V1)
assessment of, 87, 87b, 88f, 89f
(V1)
local anesthetics for, 82-83 (V1)
neuroanatomy and pathophysiology
of, 78-80, 79f, 80f (V1)
nonsteroidal antiinflammatory
drugs for, 83-86, 84t, 85b, 86t
(V1)
opioid analgesics for, 80-82, 81b,
81t, 82t (V1)
patient-controlled analgesia for, 88
(V1)
perioperative considerations in, 87,
87b (V1)
physical methods for, 88-89 (V1)
preemptive analgesia therapy for,
87-88 (V1)
reassessment of, 89-90 (V1)
in temporomandibular joint
surgery, 133-134 (V1)
for posttraumatic headache, 153 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)
preoperative management of, 2t (V1)
in skin cancer, 739-741 (V2)
in temporomandibular disorders,
885b, 885-889, 985, 986-987
(V2)
for temporomandibular osteoarthritis,
146 (V1)
for temporomandibular rheumatoid
arthritis, 145 (V1)
in trigeminal neuralgia, 150 (V1),
992, 992t (V2)
Drug-drug interaction, use of
vasoconstrictors with local
anesthetics and, 42t, 42-43 (V1)
Drug-induced gingival hyperplasia, 178-
179, 179f (V1)
Dry eyes
following blepharoplasty, 593 (V3)
in Sj[um]ogren’s syndrome,
866 (V2)
Dry mouth, radiation therapy-related,
774 (V2)
Dry socket, 209b, 216 (V1)
Dual-layered guided socket regeneration
technique, 445f, 445-446, 446f
(V1)
Dual-X-ray absorptiometry, 396 (V1)
Due process, adverse action in
privileging and, 316 (V1)
Duloxetine, 999t (V2)
DVT; See Deep venous thrombosis
Dyclonine, 37f (V1)
Dynamic sphincter pharyngoplasty,
836-838, 838f (V3)
Dynamic wrinkles, 518 (V3)
Dyschromias, laser skin resurfacing and,
518, 541-542, 542f, 543f (V3)
Dysesthesia, 966t (V2)
Dysmorphology
cranio-orbital, 856-858 (V3)
defined, 849t (V3)
in oculoauriculovertebral spectrum,
922-925, 925b (V3)
in Treacher Collins syndrome, 936-
939 (V3)
INDEX I-27
Dysostosis
craniofacial dysostosis syndromes and,
880-921 (V3)
Apert syndrome in, 902-909, 903-
907f (V3)
Carpenter’s syndrome in, 909 (V3)
cloverleaf skull anomaly in, 909-
914, 910-914f (V3)
Crouzon syndrome in, 886-902,
887-900f (V3)
dentition and occlusion anomalies
in, 881-882 (V3)
functional considerations in, 880-
881 (V3)
genetic aspects of, 880 (V3)
morphologic considerations in,
882-883 (V3)
Pfeiffer syndrome in, 909 (V3)
Saethre-Chotzen syndrome in, 909
(V3)
surgical management of, 883-886
(V3)
mandibulofacial, 936-960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in,
855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
Dysplasia
cleidocranial, 175-177, 176f, 177f
(V1)
fibrous, 600-601, 870 (V2)
florid cemento-osseous, 601, 601f
(V2)
focal cemento-osseous, 601 (V2)
hereditary ectodermal, 177f, 177-178
(V1)
periapical cemental, 601 (V2)
Dysport (botulinum toxin type A), 659
(V3)
Dystonia, facial asymmetry and, 280-
281 (V3)
Dystopia in naso-orbital-ethmoid
fracture, 245, 245f (V2)
Dystrophic form of epidermolysis
bullosa, 626-627 (V2)
E
Eagle’s syndrome, 969-970, 970f (V2)
Ear
blood supply to, 667-668 (V3)
detailed aesthetic evaluation of, 6, 8f
(V3)
embryology of, 698f, 699, 700-703f
(V3)
examination in cranio-maxillofacial
trauma, 9, 50 (V2)
innervation of, 668-670f (V3)
oculoauriculovertebral spectrum and,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
I-28 INDEX
Ear (Continued)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
maxilla and, 922-935 (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
otoplasty and, 665-677 (V3)
blood supply to ear and, 667-668
(V3)
complications in, 675-676 (V3)
for congenital deformities, 668-669
(V3)
for correction of protruding
earlobe, 675, 675f (V3)
Davis method in, 670-673, 672f
(V3)
embryology of auricle and, 665,
666f (V3)
Farrior technique in, 673, 675f
(V3)
indications and timing of, 669
(V3)
Mustard[ac]e method in, 673, 674f
(V3)
nerve supply to ear and, 668-670f
(V3)
surgical anatomy in, 665-666, 666f,
667f (V3)
techniques in, 669-670, 671f (V3)
periauricular cancer and, 728-729,
729f (V2)
reconstructive flap options for, 336b
(V2)
rhytidectomy-related deformity of,
509-510, 510f (V3)
trauma to, 294, 297f, 310-313, 312f,
313f (V2)
Treacher Collins syndrome and, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
Ear plane, 272-274, 273f (V3)
Earlobe, 667f (V3)
protruding, 675, 675f (V3)
rhytidectomy complications and,
509-510, 510f (V3)
Eastman anatomically oriented model
surgery technique, 364-371 (V3)
construction of intermediate splint
in, 368-369, 369f, 370f (V3)
marking cast in, 366-367 (V3)
Eastman anatomically oriented model
surgery technique (Continued)
measurements in, 367f, 367-368 (V3)
mounting case in, 364-366, 365f,
366f (V3)
positioning of maxilla in, 368, 368f
(V3)
for segmental surgery, 369-370, 370f
(V3)
for special situations, 370-371 (V3)
E-cadherin, 664-665 (V2)
Ecchymosis
Botox injection and, 661 (V3)
injectable facial filler and, 643 (V3)
periorbital
in basilar skull fracture, 50 (V2)
in frontal sinus fracture, 256, 259f
(V2)
in orbital fracture, 208 (V2)
postoperative, 403-404 (V3)
in bilateral sagittal split osteotomy,
111-112 (V3)
in sinus-lift subantral
augmentation, 463 (V1)
in zygomatic fracture, 184f (V2)
Ectasia, laser therapy for, 251 (V1)
Ectropion
after repair of zygomatic fracture, 195
(V2)
laser skin resurfacing-related, 543-544
(V3)
in orbital fracture, 235, 236f (V2)
Edatrexate, 779t (V2)
Edema, 403-404 (V3)
in acute traumatic arthritis of
temporomandibular joint, 855
(V2)
in chondrosarcoma, 872 (V2)
effects of laser on, 254b, 254 (V1)
injectable facial filler and, 643, 643f
(V3)
in Langerhans cell histiocytosis, 571,
571f, 572f (V2)
in osteomyelitis, 633 (V2)
in osteosarcoma, 680 (V2)
postoperative
in bilateral sagittal split osteotomy,
111 (V3)
exodontia-related, 217-218 (V1)
in mandibular orthognathic
surgery, 441-442, 442f (V3)
in rhytidectomy, 507 (V3)
in sinus-lift subantral
augmentation, 463 (V1)
temporomandibular joint and, 413
(V3)
Edentulous mandible, immediate
implant loading in, 518 (V1)
Edentulous maxilla
immediate implant loading in, 518-
519, 519-522f (V1)
zygomatic implant and, 491-500 (V1)
complications in, 498f, 498-499
(V1)
final prosthesis fabrication and,
499 (V1)
historical perspective in, 491 (V1)
patient selection for, 491-492, 492f
(V1)
postoperative care in, 498 (V1)
preoperative considerations in,
493, 493f (V1)
prosthetic conversion technique
in, 496-497, 497f, 498f (V1)
radiographic evaluation in, 492,
492f (V1)
regional anatomy in, 492-493 (V1)
surgical options in, 493-494, 494f
(V1)
surgical protocol in, 494-496, 494-
497f (V1)
Edentulous patient
cleft maxilla repair and, 810-811,
811f (V3)
impressions at implant placement
and, 525-539 (V1)
concept of, 531 (V1)
history of immediate loading and,
525-527, 526b, 526f, 527f (V1)
Edentulous patient (Continued)
immediate extraction, implant
placement, and provisional
restoration and, 534f, 534-
535, 535f (V1)
immediate provisionalization and,
528-531, 530-531f (V1)
prefabricated ceramic abutments
and temporary crowns and,
536f, 536-537, 537f (V1)
primary bone-level impressions
and, 527-528, 529f, 530f (V1)
second-stage surgery and, 532f,
532-533, 533f (V1)
restorative considerations for, 519-
521, 522-524f (V1)
Educational materials, risk management
and, 379 (V1)
Effective maxillary length: mandibular
length, 14, 14f, 15f (V3)
Effexor; See Venlafaxine
Effusion in acute traumatic arthritis of
temporomandibular joint, 855
(V2)
Eggers, G.W.N., 795 (V2)
Eicosanoids, bone development and,
399-400 (V1)
Eicosapentaenoic acid, bone
development and, 399 (V1)
Elastic bands for anchorage, 224 (V1)
Elastics, postsurgical, 400 (V3)
Elavil; See Amitriptyline
Elderly patient
maxillofacial trauma in, 374-394
(V2)
aging of face and neck in, 377
(V2)
anesthetic management in, 385,
385b (V2)
closed versus open reduction of
fractures in, 386t (V2)
cognitive evaluation and informed
consent in, 380 (V2)
considerations in management of,
392t (V2)
epidemiology of, 374-377, 375t,
376-377f (V2)
mandibular fractures in, 389-392f,
390-393 (V2)
maxilla and midface fractures in,
386-390, 387-389f (V2)
medications and over-the-counter
drug history and, 380 (V2)
nutrition and fluid and electrolyte
management in, 379 (V2)
perioperative risk assessment of co-
morbid systemic disease in,
380t, 380-385 (V2)
social history and, 379-380 (V2)
wound healing and, 377-378, 378f
(V2)
nonsteroidal antiinflammatory drugs
and, 85 (V1)
Elective lymph node dissection in
malignant melanoma, 754 (V2)
Electrical burn, 322-323 (V2)
Electrical hazards in laser therapy, 516
(V3)
Electrical stimulation for
temporomandibular disorders, 892
(V2)
Electrocardiography
as adjunct to primary survey, 39 (V2)
during anesthesia, 25 (V1)
in congenital heart disorders, 382-
383 (V3)
in pediatric anesthesia and sedation,
99 (V1)
preoperative, 19t (V1), 390 (V3)
Electrocautery
in blepharoplasty, 590 (V3)
in forehead and brow lift
endoscopic, 601 (V3)
trichophytic, 613 (V3)
Electrodesiccation in skin cancer, 734,
735f (V2)
Electroencephalography
in overnight polysomnography, 317-
318 (V3)
Electroencephalography (Continued)
in pediatric anesthesia and sedation,
99 (V1)
Electrolyte management in trauma
patient, 45, 379 (V2)
Electromagnetic spectrum, 240f (V1)
Electromyogram in overnight
polysomnography, 317-318 (V3)
Electron microscopy, 416, 416f (V2)
Electronic dental anesthesia, 51 (V1)
Electronic health record, 303 (V1)
Electrooculogram in overnight
polysomnography, 317-318 (V3)
Electrotherapy for temporomandibular
osteoarthritis, 146 (V1)
Elimination patterns, postoperative, 409
(V3)
Ellis and Davey classification of
dentoalveolar injury, 110, 111f
(V2)
ELND; See Elective lymph node
dissection
Elongation, hemimandibular
bilateral sagittal split osteotomy
for, 99t, 99-102, 102f, 104-105f
(V3)
transoral vertical ramus osteotomy
for, 121, 122f (V3)
E/M codes, 365-366 (V1)
E-mail, risk management and,
385 (V1)
E-mail-based office system, 303 (V1)
Embolism after facial fat
transplantation, 627 (V3)
Embolization
in arteriovenous malformation, 589
(V2)
in lymphatic malformation, 583 (V2)
Embryology
of auricle, 665, 666f (V3)
of cleft lip and palate, 714-715 (V3)
orofacial embryogenesis and, 697-712
(V3)
animal studies in, 705, 706-708f
(V3)
complexity of human facial
morphogenesis and, 697-705,
698f, 700-704f (V3)
orofacial clefting sites and, 705-
712, 710f, 711f (V3)
Embryonic stem cells, 23 (V2)
Emergency airway management, 25-34
(V2)
airway assessment and, 25, 26b (V2)
airway maneuvers and adjuncts in,
26, 26b (V2)
complications in, 33 (V2)
cricothyroidotomy in, 32f, 32-33
(V2)
endotracheal intubation in, 28-31,
31f (V2)
supraglottic airway devices for, 26-28,
27f, 28f (V2)
systematic approach to, 25 (V2)
tracheostomy in, 33 (V2)
Emergency Medical Treatment and
Active Labor Act, 385 (V1)
Eminectomy to limit condylar
translation, 909 (V2)
Emissary veins, 433f (V3)
EMLA cream, 49-50 (V1)
for intravenous access in child, 102
(V1)
Emphysema
geriatric patient and, 382 (V2)
orbital, 87, 87f (V2)
perioperative management of, 383-
384, 384b (V3)
Employee, hiring and firing of, 322
(V1)
Employee performance evaluation, 291,
292t (V1)
Employee relations, 323-329, 326b (V1)
Employment agreement, 299, 300t (V1)
EMTALA; See Emergency Medical
Treatment and Active Labor Act
Enamel and dentin fracture, 113-117,
115b, 116-118f (V2)
Enamel fracture, 113 (V2)

Endaural approach
in internal derangement of
temporomandibular joint, 933f,
933-934, 934f (V2)
in temporomandibular joint
arthroscopy, 923f (V2)
Endocarditis, preoperative prophylaxis
of, 3, 5t, 97 (V1)
Endocrine disorders
adrenocortical insufficiency in
perioperative management of, 386
(V3)
preoperative evaluation of, 13-14,
14t (V1)
diabetes mellitus in
ambulatory orthognathic surgery
and, 493 (V3)
in geriatric patient, 383-384 (V2)
impaired healing in, 419 (V3)
intensive care of trauma patient
and, 46-47 (V2)
perioperative management of, 385-
386 (V3)
preoperative evaluation of, 11-12,
12t (V1)
salivary disease in, 556 (V2)
perioperative management of, 385-
386 (V3)
thyroid disease in
in geriatric patient, 384 (V2)
salivary disease in, 556 (V2)
use of vasoconstrictors with local
anesthetics and, 44, 44b (V1)
Endocrine system
intensive care of trauma patient and,
46-47 (V2)
preoperative evaluation of, 11-14, 12-
14t (V1)
Endodontic therapy
chronic facial pain after, 968f, 968-
969 (V2)
neuropathic pain after, 996-997 (V2)
trigeminal nerve injury and, 267f,
274-275 (V1)
Endoscopic evaluation of upper airway,
318 (V3)
Endoscopic forehead and brow lift, 595-
609, 596f (V3)
bone anatomy and, 595-597 (V3)
comparison of lift techniques, 611t
(V3)
complications in, 606-607 (V3)
endoscopic anatomy and, 600-602,
601f (V3)
muscle and fascial anatomy and, 597-
598, 598f (V3)
postoperative care in, 606 (V3)
preoperative evaluation in, 602t, 602-
603 (V3)
technique in, 603f, 603-606, 605f
(V3)
vessel and nerve anatomy and, 598-
600, 598-600f (V3)
Endoscopic techniques
in management of craniosynostosis,
867 (V3)
for mandibular fracture, 152-156
(V2)
condylar, 172-176, 176-180f
(V2)
internal fixation modalities in,
154f, 154-155, 155f (V2)
lag screws in, 155-156, 156-158f
(V2)
miniplates in, 155 (V2)
transosseous wiring in, 156, 158f
(V2)
in pediatric craniomaxillofacial
tumors, 967 (V3)
for sialolithiasis, 544 (V2)
Endotracheal intubation
pediatric, 94 (V1)
in trauma patient, 28-31, 31f (V2)
in trigeminal nerve repair, 268 (V1)
Endovascular treatment in
arteriovenous malformation, 589-
590 (V2)
End-stage renal disease, 7, 8t, 9t (V1)
End-tidal carbon dioxide, 28 (V1)
Energy
laser production of, 237 (V1)
laser property, 514 (V3)
Enflurane, 43, 44t (V1)
Enophthalmos, 78, 78f (V2)
in blow-out fracture of orbital floor,
86 (V2)
following primary reconstruction in
orbital fracture, 234, 234f (V2)
in globe dystopia, 88 (V2)
in zygomatic fracture, 198 (V2)
Entegra implant, 567, 568f (V1)
Enteral nutrition, 15, 15t (V2)
Enterovirus diseases, 617 (V2)
Entropion, postoperative
in orbital fracture, 235 (V2)
in zygomatic fracture, 195 (V2)
Enucleation
of adenomatoid odontogenic tumor,
469-472 (V2)
of ameloblastoma, 500 (V2)
of calcifying odontogenic cyst, 447,
447f (V2)
of central giant cell granuloma, 593-
594 (V2)
of dentigerous cyst, 426, 428f, 429f
(V2)
of globulomaxillary cyst, 451 (V2)
in Gorlin’s syndrome, 442 (V2)
in Langerhans cell histiocytosis, 573,
573f, 574f (V2)
of myxoma, 517-518 (V2)
of nasopalatine duct cyst, 450-451,
451f (V2)
of odontogenic keratocyst, 437-438
(V2)
of osteoma, 605 (V2)
of radicular cyst, 421, 422f (V2)
of residual cyst, 421, 423f (V2)
Envelope flap in exodontia, 193, 193f
(V1)
Environment
control in trauma, 8, 39, 39f (V2)
in optimizing wound repair, 21-22
(V2)
EOA; See Esophageal obturator airway
Eosinophilic granuloma, 567 (V2)
Ephelides, 518 (V3)
Epidermal growth factor receptor
blockers, 782-783, 783t (V2)
for metastatic tumors, 779 (V2)
oral cavity cancer and, 707 (V2)
Epidermis
age-related changes in, 9, 513 (V3)
of eyelid, 582 (V3)
relative depth of, 10f (V3)
Epidermoid cyst, 451-455, 454f, 455f
(V2)
Epidermolysis bullosa, 626-627 (V2)
Epidural hematoma, 60, 61f (V2)
Epigenetic alteration of gene expression
in cancer cell, 655 (V2)
Epilepsy
ambulatory orthognathic surgery and,
493 (V3)
perioperative management of, 388
(V3)
Epinephrine use with local anesthetics,
39-45, 40t, 43-45t, 44b (V1)
Epiphora
after Le Fort I osteotomy, 475 (V3)
in midface fracture, 254 (V2)
in nasolacrimal injuries, 88-89 (V2)
Epistaxis
in cranio-maxillofacial trauma, 9
(V2)
in medial orbital wall fracture, 87
(V2)
Epithelial cell, wound repair and, 20f,
20-21 (V2)
Epithelial growth factor in platelet-rich
plasma, 501 (V1)
Epithelial tumors, 469-508, 725f, 725-
727, 726f (V2)
adenomatoid odontogenic tumor in,
469-472, 470-472f (V2)
ameloblastoma in, 476-502 (V2)
clinical forms and mechanisms of
growth of, 478 (V2)
Epithelial tumors (Continued)
clinicopathologic considerations
in, 477-478, 478-481f (V2)
management of, 500-502 (V2)
marked aggressive behavior and
metastases in, 492-500, 499f
(V2)
peripheral, 496-499f (V2)
solid and multicystic, 479-485,
486-495f (V2)
unicystic, 478-479, 482-484f, 486f
(V2)
calcifying epithelial odontogenic
tumor in, 473-476, 474f, 475f
(V2)
clear cell odontogenic carcinoma in,
502-508, 503-507f (V2)
intraosseous carcinoma from, 531
(V2)
squamous odontogenic tumor in,
472f, 472-473 (V2)
Epithelialized free-gingival graft, 483f,
484-485 (V1)
Epker modification of sagittal split
osteotomy, 268, 269f (V3)
Epoetin alfa, 390 (V3)
E-prescribing facilities, 303 (V1)
ePTFE membrane; See Expanded
polytetrafluoroethylene membrane
Equal share model of compensation,
298, 298t (V1)
Equal-appearing interval scale, 796-797
(V3)
Equipment
equipping and furnishing office and,
358-361, 359f, 360f (V1)
in laser therapy, 241-242, 242f (V1)
for pediatric anesthesia and sedation,
100t, 100-103, 101b, 102f (V1)
for temporomandibular joint
arthroscopy, 921-923, 922f, 924f
(V2)
Erbium:YAG laser, 240 (V1)
for skin resurfacing, 249-250 (V1),
532-534, 536-538f (V3)
for tooth preparation, 256 (V1)
Ergonomics, office design and, 361-362
(V1)
Erich arch bars, 141f (V2)
Erickson Model Table, 367, 367f (V3)
Erlotinib, 781t, 782t, 782-783 (V2)
Erosive oral lichen planus, 618-619
(V2)
Eruption cyst, 179-180 (V1)
Eruption pattern for deciduous and
permanent dentition, 165, 166t
(V1)
Erythema
chemical peel and, 664, 664f (V3)
laser skin resurfacing and, 250 (V1),
535-537, 539f (V3)
Erythema chronicum migrans, 864 (V2)
Erythema multiforme, 627-628 (V2)
Erythromycin, 389, 389t (V1)
Erythroplakia, 245 (V1)
Erythroplasia of Queyrat, 726 (V2)
Escherichia coli infection, 676 (V3)
Eschmann stylet, 31 (V2)
Esophageal obturator airway, 28, 28f,
29f (V2)
Esophageal tracheal combitube, 28, 28f,
29f (V2)
Esophageal trauma, 95 (V2)
Essential fatty acids, 399-400 (V1)
Ester local anesthetics, 36, 36t, 37f, 82-
83 (V1)
Esthetic surgery, 497-696 (V3)
blepharoplasty in, 579-594 (V3)
anterior lamella and, 582f, 582-583
(V3)
complications in, 593 (V3)
eyelid anatomy in, 580, 581f (V3)
eyelid innervation and blood
supply and, 585 (V3)
lacrimal system and, 587 (V3)
middle lamella and, 583f, 583-585,
584f (V3)
nomenclature in, 579f, 579-580
(V3)
INDEX I-29
Esthetic surgery (Continued)
patient evaluation in, 587-589,
588f, 589f (V3)
posterior lamella and, 585, 586f,
587f (V3)
postoperative care in, 591-593,
593f (V3)
surgical procedure in, 589-591,
590-592f (V3)
botulinum toxin injection in, 658-
661 (V3)
contraindications and adverse
effects of, 661, 662f (V3)
history and pharmacology of, 658
(V3)
preparations of, 658-659, 659t
(V3)
treatment technique for, 660-661,
661f (V3)
uses in facial cosmetics, 659f, 659-
660, 660f (V3)
cervicofacial liposuction in, 618-625
(V3)
complications of, 623-624 (V3)
history of, 618 (V3)
patient selection in, 618-620, 619f
(V3)
preoperative preparation in, 620
(V3)
surgical technique in, 620-623,
620-625f (V3)
chemical peel in, 661-664, 662f, 664f
(V3)
clinical facial evaluation in, 1-10
(V3)
detailed regional facial features
and, 4-8, 5-9f, 9b (V3)
facial skin age-related changes and,
8-10, 10f (V3)
facial skin health and, 2, 2t (V3)
facial skin type and, 1, 2t (V3)
general facial anthropometric
relations and, 2-4, 3f, 4f (V3)
endoscopic forehead and brow lift in,
595-609, 596f (V3)
bone anatomy and, 595-597 (V3)
complications in, 606-607 (V3)
endoscopic anatomy and, 600-602,
601f (V3)
muscle and fascial anatomy and,
597-598, 598f (V3)
postoperative care in, 606 (V3)
preoperative evaluation in, 602t,
602-603 (V3)
technique in, 603f, 603-606, 605f
(V3)
vessel and nerve anatomy and,
598-600, 598-600f (V3)
facial implants in, 678-696 (V3)
chin position analyses and, 681-
683t (V3)
for facial skin laxity with weight
loss, 686-688, 686-688f (V3)
injectable facial fillers and, 691f,
691-692, 692f (V3)
for large nose and small chin, 679f,
679-684, 680f, 684f, 685b,
685f (V3)
lip implant in, 693-694, 694f (V3)
malar cheek implant in, 689f, 689-
690, 690f, 690t (V3)
patient selection for, 678 (V3)
thread lifts and, 695, 695t (V3)
facial skeletal growth evaluation in,
19-58 (V3)
mandibular values in, 41-57 (V3);
See also Mandibular growth
values
maxillary-midface values in, 28-40
(V3); See also Maxillary-
midface growth values
neurocranial values in, 19-27 (V3);
See also Neurocranial growth
values
facial skeleton evaluation in, 10-17
(V3)
changes with age and, 15-17, 17f
(V3)
dental relations in, 14-15, 16f (V3)
I-30 INDEX
Esthetic surgery (Continued)
skeletal relations in, 12-14, 13-15f
(V3)
soft tissue relations in, 11-12, 12f
(V3)
hair transplantation in, 651-657 (V3)
complications of, 655-656 (V3)
current medical treatment for
alopecia and, 651 (V3)
micrograft and minigraft technique
in, 651-653, 652-655f (V3)
pathophysiology of alopecia and,
651 (V3)
rotational flaps in, 655, 655f, 656f
(V3)
scalp reduction in, 655, 656f (V3)
injectable facial fillers in, 629-650
(V3)
for augmenting wrinkles, lines, and
folds, 637-639, 638f, 639f
(V3)
complications of, 642-643, 643f,
644f (V3)
history of, 629-631, 630f, 630t,
631f (V3)
for lips, 633-637, 633-637f (V3)
for malar augmentation, 639-642,
639-642f (V3)
tissue positioning of, 631f, 631-
632, 632f (V3)
treatment considerations in, 632-
633, 633f (V3)
treatment results in, 643, 645-649f
(V3)
laser skin resurfacing in, 513-552
(V3)
anesthesia and, 521, 522f (V3)
carbon dioxide laser for, 514f, 514-
516, 515f (V3)
contact dermatitis and, 539 (V3)
dyschromias and, 541-542, 542f,
543f (V3)
erbium:YAG laser in, 532-534,
536-538f (V3)
fractional photothermolysis in,
532, 536f (V3)
history of, 513-514 (V3)
infection and, 540-541, 541f (V3)
intrinsic and extrinsic aging and,
513 (V3)
laser blepharoplasty with, 544-545,
545-547f (V3)
laser properties in, 514f, 514-516,
515f (V3)
laser settings for, 521-522, 522f
(V3)
milia and acne formation and,
539-540, 540f (V3)
ocular complications in, 543-544
(V3)
patient evaluation in, 516-519,
518b (V3)
postoperative care in, 524-529,
526-528f, 530-531f (V3)
preoperative considerations in, 519
(V3)
prolonged erythema and, 535-537,
539f (V3)
pruritus and, 537-538, 539f (V3)
resurfacing acne scars in, 529 (V3)
rhytidectomy with, 545-548, 547-
548f (V3)
scarring and, 542-543, 543f (V3)
sepsis and, 544 (V3)
single-pass resurfacing in, 529-532,
533-534f (V3)
skin preparation for, 519-521 (V3)
telangiectasias and, 538-539 (V3)
traditional technique in, 522-524,
523f, 525-526f (V3)
traumatic and surgical scars
improvement in, 529 (V3)
treatment of benign skin lesions
in, 529 (V3)
in midface avulsive injury, 346, 349-
350f (V2)
occlusion evaluation in, 17-19, 18b
(V3)
otoplasty in, 665-677 (V3)
Esthetic surgery (Continued)
blood supply to ear and, 667-668
(V3)
complications in, 675-676 (V3)
for congenital deformities, 668-669
(V3)
for correction of protruding
earlobe, 675, 675f (V3)
Davis method in, 670-673, 672f
(V3)
embryology of auricle and, 665,
666f (V3)
Farrior technique in, 673, 675f
(V3)
indications and timing of, 669
(V3)
Mustard[ac]e method in, 673, 674f
(V3)
nerve supply to ear and, 668-670f
(V3)
surgical anatomy in, 665-666, 666f,
667f (V3)
techniques in, 669-670, 671f (V3)
rhinoplasty in, 553-578 (V3)
case reports in, 574-576, 574-576f
(V3)
clinical examination in, 557-560,
558-560f (V3)
closed, 572-573, 573f (V3)
complications in, 573-577 (V3)
dressings and splinting in, 573,
573f (V3)
follow-up care in, 573 (V3)
incisions in, 560-562, 561f, 562f
(V3)
initial consultation in, 557 (V3)
nasal anatomy and, 553-556, 554b,
554-557f (V3)
open, 567-572, 568-571f (V3)
tip plasty in, 562, 563f (V3)
tip projection in, 562-564, 563-
565f (V3)
tip rotation in, 564, 565f (V3)
tip shape and, 565-566, 566f (V3)
rhytidectomy in, 497-512 (V3)
complications in, 506-510, 507-
510f (V3)
patient evaluation in, 497-500,
498t, 499f, 499t (V3)
surgical technique in, 500-506,
500-506f (V3)
soft tissue procedures around implant
in, 479-490, 480t (V1)
AlloDerm in, 486, 487f (V1)
connective tissue grafting in, 485,
485f, 486f (V1)
epithelialized free-gingival grafting
in, 483f, 484-485 (V1)
gingivectomy in, 481-484, 484f,
485f (V1)
modified roll tissue graft in, 486,
488f (V1)
papilla regeneration technique in,
487-489, 489f (V1)
pediculated connective tissue graft
in, 486 (V1)
soft tissue health considerations
and, 479, 480f (V1)
trichophytic forehead and brow lift
in, 610-617 (V3)
comparison of lift techniques and,
611t (V3)
complications in, 614-616, 616f,
617f (V3)
fixation techniques in, 610-611
(V3)
patient selection for, 613-614,
615f, 616f (V3)
surgical technique in, 611-614f,
612-613 (V3)
Estimated blood loss, 389 (V3)
Estrogen for postmenopausal bone loss,
398-399, 399t (V1)
ETC; See Esophageal tracheal
combitube
Ethibond Excel polyester fiber suture,
287t (V2)
Ethilon Nurolon nylon suture, 287t
(V2)
Ethmoid, naso-orbital-ethmoid fracture
and, 207, 207f, 243-248 (V2)
anatomy in, 243f, 243-244, 244f (V2)
clinical findings in, 244-246, 245f
(V2)
computed tomography of, 214f (V2)
identification of medial canthal
tendon and, 246 (V2)
injury classification in, 244, 245f
(V2)
nasal fracture and, 276, 276f, 278-
280 (V2)
nasal reconstruction in, 248, 249f
(V2)
nasolacrimal apparatus repair in, 248
(V2)
pediatric, 355-360, 358-359f (V2)
primary reconstruction in, 233 (V2)
radiographic evaluation in, 246 (V2)
reconstruction of medial orbital rims
in, 246-247, 247f (V2)
reconstruction of medial orbital wall
in, 247, 247f (V2)
soft tissue readaptation in, 248, 248f
(V2)
surgical approaches in, 246, 246f
(V2)
transnasal canthopexy in, 247-248
(V2)
Ethmoid sinus, 257f (V2)
Ethyl chloride, 50 (V1)
Etidocaine
for acute postoperative pain, 83 (V1)
chemical structure of, 37f (V1)
pH effects on, 37t (V1)
Etidronate, 558t (V2)
Etodolac, 84t, 86t (V1)
for neuropathy secondary to neuritis,
1000 (V2)
for temporomandibular disorders,
887t (V2)
Etomidate, 29 (V2)
Eustachian tube, surgery-related
dysfunction of, 406 (V3)
Eutectic mixture of local anesthetics,
49-50 (V1)
for intravenous access in child, 102
(V1)
Evaluation and management codes,
365-366 (V1)
Ewing’s sarcoma, 687, 688f, 689f (V2),
986 (V3)
Exarticulation of tooth, 114t, 120-122,
121f, 122b (V2)
Excision
in arteriovenous malformation, 590
(V2)
of branchial cleft cyst, 460 (V2)
of calcifying odontogenic cyst, 447
(V2)
in dermatofibrosarcoma protuberans,
728 (V2)
of dermoid and epidermoid cysts, 455
(V2)
in juvenile ossifying fibroma, 600,
600f (V2)
of median palatal cyst, 451 (V2)
in melanoma, 754 (V2)
of nasolabial cyst, 448, 450f (V2)
in neurofibroma, 602 (V2)
in odontoma, 519 (V2)
in ossifying fibroma, 598, 599f (V2)
in osteoma, 605 (V2)
in osteosarcoma, 683 (V2)
in sebaceous gland carcinoma, 727
(V2)
in skin cancer, 736-737 (V2)
in squamous odontogenic tumor, 473
(V2)
in submandibular sialolithiasis, 543,
546f (V2)
of thyroglossal duct cyst, 456 (V2)
Excisional biopsy, 467-468, 731f (V2)
in lymphoma, 758 (V2)
in malignant melanoma, 753 (V2)
in skin cancer, 731, 732 (V2)
Excisional uncovering of impacted
maxillary canine, 169f, 169 (V1)
Excyclotorsion, 85 (V2)
Exercise
postoperative, 411 (V3)
in temporomandibular disorders, 891,
985f, 985-986 (V2)
Exfoliative cytology, 415 (V2)
Exodontia, 185-211 (V1)
alveolar ridge preservation after, 438-
440 (V1)
autotransplantation of impacted
tooth versus, 171-172 (V1)
basic, 185-192 (V1)
complications in, 191-192 (V1)
diagnosis and treatment planning
in, 187 (V1)
indications for, 186-187 (V1)
pain management in, 192 (V1)
principles of, 187-190, 188-190f
(V1)
socket preservation and wound
closure in, 190-191 (V1)
complicated, 192-201 (V1)
bone removal in, 193-194, 194f
(V1)
of canines, 196-197, 197-199f (V1)
flap design in, 192-193, 193f, 194f
(V1)
general principles of, 192 (V1)
of impacted teeth other than third
molars, 195-196 (V1)
indications for, 192b (V1)
of premolars, 197-199, 200f (V1)
sectioning of teeth and removal in,
194-195, 195f, 196f (V1)
of teeth located in uncommon
anatomic positions, 200-201,
201f (V1)
wound closure in, 201 (V1)
complications of, 212-222 (V1)
alveolar osteitis in, 216 (V1)
bisphosphonate-related
osteonecrosis in, 217, 218t
(V1)
displacement of teeth and root tips
in, 213-214 (V1)
hemorrhage in, 219 (V1)
infection in, 216-217 (V1)
injuries to teeth or adjacent
structures in, 212, 213f (V1)
oroantral communication in, 214f,
214-215 (V1)
osseous injuries in, 219f, 219i-220,
220f (V1)
osteoradionecrosis in, 217 (V1)
removal of wrong tooth in, 212
(V1)
residual root remnants in, 213
(V1)
sensory nerve injuries in, 215f,
215-216, 216f (V1)
soft tissue injuries in, 214 (V1)
swallowing or aspiration of teeth,
crowns, or restorations in, 215
(V1)
temporomandibular joint problems
in, 218 (V1)
tissue emphysema in, 215 (V1)
trismus, pain, and swelling in, 217-
218 (V1)
immediate implant loading following,
534f, 534-535, 535f, 540-546
(V1)
adaptive morphology of maxillary
alveolar process and, 541
(V1)
atraumatic extraction techniques
and, 541, 542f (V1)
bone loss following extraction and,
541, 541f (V1)
classification of extraction socket
defects and, 541, 543f (V1)
clinical situations for, 542-544,
544f, 545f (V1)
healing of extraction socket and,
540-541 (V1)
of impacted third molar teeth, 201-
210 (V1)
bone removal and tooth sectioning
in, 205-206, 207-210f (V1)
classification of, 203, 204f (V1)

Exodontia (Continued)
indications and contraindications
for, 202-203 (V1)
instrumentation for, 203, 203t
(V1)
mandibular, 203-205, 205b, 206f
(V1)
maxillary, 207, 208-210f (V1)
postoperative instructions in, 208-
210, 209b (V1)
preoperative management in, 207t,
207-208, 208b (V1)
trigeminal nerve injury and, 276-
278 (V1)
wound closure in, 206-207 (V1)
informed consent for, 212, 213b (V1)
open technique in guided bone
regeneration in, 454f, 454-455,
455f (V1)
Exophthalmos, 78, 78f (V2)
Exotropia, 881 (V3)
Expanded polytetrafluoroethylene
membrane, 429 (V1)
postoperative considerations in, 432
(V1)
primary closure in, 431 (V1)
to reduced postextraction bone loss,
439 (V1)
selection rationale for, 432-435, 433f
(V1)
in subantral augmentation, 437 (V1)
Exposure control in trauma, 8, 39, 39f
(V2)
Exposure keratosis, laser skin
resurfacing-related, 543-544 (V3)
Exposure time in laser therapy, 238
(V1)
Extended neck dissection, 719t (V2)
External auditory meatus
condylar head and, 163f (V2)
constriction of, 676 (V3)
Treacher Collins syndrome and, 938-
939, 956 (V3)
External carotid artery
ear and, 667 (V3)
eyelid and, 585 (V3)
forehead and brow and, 598 (V3)
mandibular orthognathic surgery and,
68, 69f (V3)
maxilla and, 63, 63f, 173f, 175f (V3)
nose and, 553-554 (V3)
temporomandibular joint and, 163,
163f, 165f (V2)
External ear reconstruction in Treacher
Collins syndrome, 955-956 (V3)
External fixation
of mandibular fracture, 148 (V2)
in mandibular resection, 701, 702f
(V2)
External jugular vein, 433f (V3)
External nasal artery, 69f (V3)
External nasal branch of anterior
ethmoidal artery, 555f (V3)
External nasal branch of anterior
ethmoidal nerve, 557f (V3)
External nasal valve, 560, 560f (V3)
External neurolysis in trigeminal nerve
repair, 268 (V1)
External pelvic fixator, 69f (V2)
External pin fixation of mandibular
fracture, 139, 140f, 391-392 (V2)
Extracapsular disorders, 825-826, 825-
828f (V2)
Extracapsular fracture, 100f, 100-101
(V2)
Extracapsular ligaments of
temporomandibular joint, 803-804,
804f (V2)
Extracellular matrix, articular cartilage
and, 849-850, 850f (V2)
Extraction, 185-211 (V1)
alveolar ridge preservation after, 438-
440 (V1)
autotransplantation of impacted
tooth versus, 171-172 (V1)
basic, 185-192 (V1)
complications in, 191-192 (V1)
diagnosis and treatment planning
in, 187 (V1)
Extraction (Continued)
indications for, 186-187 (V1)
pain management in, 192 (V1)
principles of, 187-190, 188-190f
(V1)
socket preservation and wound
closure in, 190-191 (V1)
complicated, 192-201 (V1)
bone removal in, 193-194,
194f (V1)
of canines, 196-197, 197-199f
(V1)
flap design in, 192-193, 193f, 194f
(V1)
general principles of, 192 (V1)
of impacted teeth other than third
molars, 195-196 (V1)
indications for, 192b (V1)
of premolars, 197-199, 200f (V1)
sectioning of teeth and removal in,
194-195, 195f, 196f (V1)
of teeth located in uncommon
anatomic positions, 200-201,
201f (V1)
wound closure in, 201 (V1)
complications of, 212-222 (V1)
alveolar osteitis in, 216 (V1)
bisphosphonate-related
osteonecrosis in, 217, 218t
(V1)
displacement of teeth and root tips
in, 213-214 (V1)
hemorrhage in, 219 (V1)
infection in, 216-217 (V1)
injuries to teeth or adjacent
structures in, 212, 213f (V1)
oroantral communication in, 214f,
214-215 (V1)
osseous injuries in, 219f, 219i-220,
220f (V1)
osteoradionecrosis in, 217 (V1)
removal of wrong tooth in, 212
(V1)
residual root remnants in, 213
(V1)
sensory nerve injuries in, 215f,
215-216, 216f (V1)
soft tissue injuries in, 214 (V1)
swallowing or aspiration of teeth,
crowns, or restorations in, 215
(V1)
temporomandibular joint problems
in, 218 (V1)
tissue emphysema in, 215 (V1)
trismus, pain, and swelling in, 217-
218 (V1)
immediate implant loading following,
534f, 534-535, 535f, 540-546
(V1)
adaptive morphology of maxillary
alveolar process and, 541
(V1)
atraumatic extraction techniques
and, 541, 542f (V1)
bone loss following extraction and,
541, 541f (V1)
classification of extraction socket
defects and, 541, 543f (V1)
clinical situations for, 542-544,
544f, 545f (V1)
healing of extraction socket and,
540-541 (V1)
of impacted third molar teeth, 201-
210 (V1)
bone removal and tooth sectioning
in, 205-206, 207-210f (V1)
classification of, 203, 204f (V1)
indications and contraindications
for, 202-203 (V1)
instrumentation for, 203, 203t
(V1)
mandibular, 203-205, 205b, 206f
(V1)
maxillary, 207, 208-210f (V1)
postoperative instructions in, 208-
210, 209b (V1)
preoperative management in, 207t,
207-208, 208b (V1)
wound closure in, 206-207 (V1)
Extraction (Continued)
informed consent for, 212, 213b (V1)
open technique in guided bone
regeneration in, 454f, 454-455,
455f (V1)
Extraction socket
classification of defects of, 541, 543f
(V1)
preoperative evaluation of, 543-544,
544f (V1)
Extranodal marginal zone B-cell
lymphoma, 760-761, 761f (V2)
Extraocular muscles
actions and innervation of, 196t (V2)
assessment of
in initial evaluation in head injury,
50-51 (V2)
in ocular trauma, 77f, 77-78 (V2)
in orbital fracture, 209f, 209 (V2)
in zygomatic fracture, 183, 184f
(V2)
entrapment in midface fracture, 254
(V2)
traumatic disorders of, 85-86 (V2)
Extraoral anchorage techniques, 224
(V1)
Extraoral approach in endoscopic repair
of condylar fracture, 178f (V2)
Extraoral implant, 685t (V3)
Extraoral miniplate fixation in bilateral
sagittal split osteotomy, 109-110
(V3)
Extremities, initial assessment in
trauma, 11-12, 42 (V2)
Extrinsic aging, 513 (V3)
Extrusive luxation of tooth, 114t, 118
(V2)
Eye
corneal abrasion in endoscopic
forehead and brow lift, 606-607
(V3)
craniofacial dysostosis syndromes and,
881 (V3)
embryology of, 698f, 699, 700-703f
(V3)
examination in cranio-maxillofacial
trauma, 9 (V2)
laser skin resurfacing complications
of, 543-544 (V3)
orbital fracture and, 86f, 86-88, 87f,
212-217 (V2)
diplopia in, 214-215, 215f, 216f
(V2)
eyelid lacerations in, 215 (V2)
lacrimal injuries in, 215, 217f (V2)
telecanthus in, 215-217, 218f (V2)
visual disturbances in, 212-214,
212-214f (V2)
periorbital soft tissue injuries and,
301-310, 306-311f (V2)
profile evaluation and, 3 (V3)
safety regulations in laser therapy,
516 (V3)
trauma to, 74-90, 295f, 296f (V2)
carotid cavernous fistula and, 89
(V2)
chemical burn in, 321f (V2)
cranial nerve injury in, 85-86 (V2)
eyelid injuries in, 88 (V2)
globe dystopia in, 88 (V2)
nasolacrimal injuries in, 88-89,
89f (V2)
nonperforating, 78-82, 78-82f
(V2)
ophthalmic assessment in, 74-78,
75-78f (V2)
orbital fracture in, 86f, 86-88, 87f,
212-217, 212-218f (V2)
orbital injury and, 83-85, 84f (V2)
penetrating, 83, 83f (V2)
temporomandibular joint
arthroscopy-related, 927 (V2)
Treacher Collins syndrome and, 939
(V3)
Eye fissure height, 4, 5f (V3)
Eye glasses for laser therapy,
243f (V1)
Eyebrow, reconstructive flap options for,
336b (V2)
INDEX I-31
Eyebrow approach
in orbital fracture, 223, 224f (V2)
in zygomatic fracture, 187, 188f (V2)
Eyelet loops, 148 (V2)
Eyelid
anatomy of, 182, 204-205, 205t, 206f
(V2), 580-587, 581f (V3)
anterior lamella and, 582f, 582-583
(V3)
innervation and blood supply in,
585 (V3)
lacrimal system and, 587 (V3)
middle lamella and, 583f, 583-585,
584f (V3)
posterior lamella and, 585, 586f,
587f (V3)
blepharoplasty and, 579-594 (V3)
anterior lamella and, 582f, 582-583
(V3)
complications in, 593 (V3)
eyelid anatomy in, 580, 581f (V3)
eyelid innervation and blood
supply and, 585 (V3)
lacrimal system and, 587 (V3)
middle lamella and, 583f, 583-585,
584f (V3)
nomenclature in, 579f, 579-580
(V3)
patient evaluation in, 587-589,
588f, 589f (V3)
posterior lamella and, 585, 586f,
587f (V3)
postoperative care in, 591-593,
593f (V3)
surgical procedure in, 589-591,
590-592f (V3)
orbital fracture and, 208, 208f, 215
(V2)
preoperative evaluation in laser skin
resurfacing, 519 (V3)
surgical approaches to, 205f (V2)
trauma to, 88, 292-294, 295f, 296f
(V2)
avulsion in, 308-310, 310f (V2)
laceration in, 306-307, 307f, 308f
(V2)
F
Face
aging of, 377 (V2)
anthropometric relations of, 2-8 (V3)
detailed, 4-8, 5-9f, 9b (V3)
general, 2-4, 3f, 4f (V3)
botulinum toxin and, 658-661 (V3)
contraindications and adverse
effects of, 661, 662f (V3)
history and pharmacology of, 658
(V3)
preparations of, 658-659, 659t
(V3)
treatment technique for, 660-661,
661f (V3)
uses in facial cosmetics, 659f, 659-
660, 660f (V3)
cervicofacial liposuction and, 618-
625 (V3)
complications of, 623-624 (V3)
history of, 618 (V3)
patient selection in, 618-620, 619f
(V3)
preoperative preparation in, 620
(V3)
surgical technique in, 620-623,
620-625f (V3)
Dedo classification of facial profiles
and, 499, 499f, 499t (V3)
endoscopic forehead and brow lift
and, 595-609, 596f (V3)
bone anatomy and, 595-597 (V3)
complications in, 606-607 (V3)
endoscopic anatomy and, 600-602,
601f (V3)
muscle and fascial anatomy and,
597-598, 598f (V3)
postoperative care in, 606 (V3)
preoperative evaluation in, 602t,
602-603 (V3)
technique in, 603f, 603-606, 605f
(V3)
I-32 INDEX
Face (Continued)
vessel and nerve anatomy and,
598-600, 598-600f (V3)
evaluation of; See Facial evaluation
healing by secondary intention, 735,
735f (V2)
laser skin resurfacing of, 248-251,
249t (V1), 513-552 (V3)
anesthesia and, 521, 522f (V3)
carbon dioxide laser in, 514f, 514-
516, 515f (V3)
contact dermatitis and, 539 (V3)
dyschromias and, 541-542, 542f,
543f (V3)
erbium:YAG laser in, 532-534,
536-538f (V3)
fractional photothermolysis in,
532, 536f (V3)
history of, 513-514 (V3)
infection and, 540-541, 541f (V3)
intrinsic and extrinsic aging and,
513 (V3)
laser blepharoplasty with, 544-545,
545-547f (V3)
laser properties in, 514f, 514-516,
515f (V3)
laser settings for, 521-522, 522f
(V3)
milia and acne formation and,
539-540, 540f (V3)
ocular complications in, 543-544
(V3)
patient evaluation in, 516-519,
518b (V3)
postoperative care in, 524-529,
526-528f, 530-531f (V3)
preoperative considerations in, 519
(V3)
prolonged erythema and, 535-537,
539f (V3)
pruritus and, 537-538, 539f (V3)
resurfacing acne scars in, 529 (V3)
rhytidectomy with, 545-548, 547-
548f (V3)
scarring and, 542-543, 543f (V3)
sepsis and, 544 (V3)
single-pass resurfacing in, 529-532,
533-534f (V3)
skin preparation for, 519-521 (V3)
telangiectasias and, 538-539 (V3)
traditional technique in, 522-524,
523f, 525-526f (V3)
traumatic and surgical scars
improvement in, 529 (V3)
treatment of benign skin lesions
in, 529 (V3)
malignant melanoma of, 749-757
(V2)
diagnosis of, 752t, 752-754, 753f,
753t (V2)
epidemiology of, 749, 750b (V2)
incidence and etiology of, 749-750,
750b, 750t, 750-752f, 751t
(V2)
management of regional disease in,
754 (V2)
staging of, 754-755, 755t (V2)
treatment of, 755-756 (V2)
orofacial embryogenesis and, 697-712
(V3)
animal studies in, 705, 706-708f
(V3)
complexity of human facial
morphogenesis and, 697-705,
698f, 700-704f (V3)
orofacial clefting sites and, 705-
712, 710f, 711f (V3)
resting skin tension lines of, 732,
732f (V2)
trichophytic forehead and brow lift
and, 610-617 (V3)
comparison of lift techniques and,
611t (V3)
complications in, 614-616, 616f,
617f (V3)
fixation techniques in, 610-611
(V3)
patient selection for, 613-614,
615f, 616f (V3)
Face (Continued)
surgical technique in, 611-614f,
612-613 (V3)
vascular anomalies of, 577-591 (V2)
arteriovenous malformation in,
588-590, 589f (V2)
binary classification of, 578b (V2)
capillary malformation in, 581,
581f (V2)
congenital hemangioma in, 579f,
579-581, 580f (V2)
infantile hemangioma in, 577-579,
578f (V2)
lymphatic malformation in, 581-
583, 582-585f (V2)
venous malformation in, 585-588,
586-588f (V2)
Face height
bilateral sagittal split osteotomy and
long face and, 95f, 95-96, 96f, 97,
97b (V3)
normal face and, 90-92, 90-92f, 97,
97b (V3)
short face and, 93f, 93-94, 94f, 97,
97b (V3)
combined maxillary and mandibular
osteotomies and, 238-247 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
complete mandibular subapical
osteotomy and, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
forehead and, 595 (V3)
occlusal plane rotation and, 248-271
(V3)
clockwise rotation in, 252-256,
252-256f (V3)
counterclockwise rotation in, 256-
260, 257-263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-
249, 249f, 250f (V3)
geometry of treatment design using
constructed
maxillomandibular triangle in,
261f, 261-262 (V3)
linear dimensions between
maxillary length and vertical
facial height in, 250, 250f
(V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-
268 (V3)
Treacher Collins syndrome and, 938
(V3)
Facebow transfer in mounting maxillary
cast, 365, 366, 366f (V3)
Facelift surgery, 497-512 (V3)
complications in, 506-510, 507-510f
(V3)
Facelift surgery (Continued)
patient evaluation in, 497-500, 498t,
499f, 499t (V3)
surgical technique in, 500-506, 500-
506f (V3)
Facial artery, 69f (V3), 165f (V2)
bleeding in bilateral sagittal split
osteotomy and, 115 (V3)
eyelid and, 585 (V3)
hemorrhage in sagittal split ramus
osteotomy and, 429-430 (V3)
mandibular orthognathic surgery and,
68 (V3)
maxilla and, 63f, 175f (V3)
nose and, 272 (V2), 555f (V3)
Facial artery musculomucosal flap, 329
(V2)
for lip defect, 343 (V2)
Facial asymmetry, 272-315 (V3)
categories of, 278 (V3)
clinical evaluation in, 272-274, 273f
(V3)
dentoalveolar and occlusal assessment
in, 274 (V3)
dentoalveolar asymmetry and, 282,
283-284f (V3)
developmental, 282 (V3)
diagnostic and treatment
considerations in, 275-277, 276f
(V3)
genioplasty for, 137-154 (V3)
fixation devices in, 142-145, 144-
148f (V3)
functional, 137, 138f (V3)
indications for, 137-138 (V3)
results in, 148-151, 150-153f (V3)
surgical procedure in, 140-142,
141f, 142f (V3)
treatment planning in, 138-140,
139f, 140f (V3)
imaging in, 274-275 (V3)
mandibular prognathism and
maxillary retrognathism and,
130f, 130-131, 131f (V3)
in oculoauriculovertebral spectrum,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
facial asymmetry in, 298-299, 300-
302f (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
maxilla and, 922-935 (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
overdevelopment and, 282-293 (V3)
in mandibular condylar
osteochondroma or osteoma,
285-291, 289-291f (V3)
in muscle hypertrophy, 291-292
(V3)
in neuromuscular disorders, 292,
292f (V3)
in tumor, 293, 293f (V3)
in unilateral condylar hyperplasia,
284-285, 286-288f (V3)
postoperative, 414-415 (V3)
presurgical patient preparation and,
277-278 (V3)
pseudoasymmetry and, 278-282
(V3)
condylar dislocation and, 281, 281f
(V3)
infection and, 281-282 (V3)
Facial asymmetry (Continued)
malocclusion and, 278-280, 279-
280f (V3)
muscle dysfunction and, 280-281
(V3)
torticollis and, 853f (V3)
in Treacher Collins syndrome, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
unilateral facial underdevelopment or
degeneration and, 294-313 (V3)
in adolescent internal condylar
resorption, 299-305, 303-304f,
306f (V3)
in autoimmune and connective
tissue diseases, 309-313, 310-
313f (V3)
in hemifacial microsomia, 298-299,
300-302f (V3)
iatrogenic, 294 (V3)
in reactive arthritis, 305-309, 307-
309f (V3)
in temporomandibular joint
ankylosis, 294-298, 297f, 298f
(V3)
trauma-related, 294, 295f, 296f
(V3)
Facial axis angle, 12-13, 13f (V3)
Facial bones, 15-17, 17f (V3)
Facial chemical peel, 661-664, 662f,
664f (V3)
Facial cleft
cleft lip and palate in, 713-734 (V3)
classification of, 715-716, 716f,
717f (V3)
embryology of, 714-715 (V3)
feeding child with, 717-718 (V3)
genetics and etiology of, 715 (V3)
history of cleft lip and palate repair
and, 713-714 (V3)
prenatal counseling and, 716-717
(V3)
repair of; See Cleft lip and palate
repair
treatment planning and timing,
718t, 718-719 (V3)
cleft lip and palate repair in, 719-730
(V3)
cleft palate repair and, 723-727,
729f, 730f (V3)
complex facial clefting and, 727-
728, 731f (V3)
history of, 713-714 (V3)
lip adhesion and, 720 (V3)
outcome assessment in, 728-730
(V3)
presurgical taping and orthopedics
in, 719-720, 720f (V3)
primary bilateral lip repair and,
723, 724-728f (V3)
primary unilateral cleft lip repair
and, 720-723, 721-723f (V3)

Facial cleft (Continued)
treatment planning and timing in,
718t, 718-719 (V3)
cleft maxilla in, 806-812 (V3)
alveolar bone grafting technique
for, 808-810, 808-811f (V3)
grafting materials for, 806-807
(V3)
history and timing of repair in, 806
(V3)
missing teeth and crowded arches
in, 810-811, 811f (V3)
orthodontics for, 807f, 807-808
(V3)
postoperative care in, 810 (V3)
cleft orthognathic surgery in, 813-827
(V3)
bone grafting in, 819, 820-825f
(V3)
obstructed nasal breathing and,
819 (V3)
preoperative evaluation in, 813-
814 (V3)
stabilization of mobilized cleft
maxilla and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-
819, 818f (V3)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
in oculoauriculovertebral spectrum,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of,
922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
maxilla and, 922-935 (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
velopharyngeal insufficiency in,
927 (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
orofacial embryogenesis and, 697-712
(V3)
animal studies in, 705, 706-708f
(V3)
complexity of human facial
morphogenesis and, 697-705,
698f, 700-704f (V3)
orofacial clefting sites and, 705-
712, 710f, 711f (V3)
revision surgery for, 828-847 (V3)
bone graft reconstruction of cleft
maxilla and palate in, 840
(V3)
complications of, 839 (V3)
comprehensive dental and
prosthetic rehabilitation in,
841-843, 844-845f (V3)
fistula closure in, 828-831, 830f,
832-834f (V3)
for management of submucous cleft
palate, 839-840 (V3)
for management of velopharyngeal
dysfunction, 831t, 831-835,
835f (V3)
operative techniques in, 836-839,
837f, 838f (V3)
orthognathic surgery for correction
of midfacial deficiency in, 840
(V3)
reconstruction of cleft nasal
deformity in, 840-841, 842f
(V3)
Facial cleft (Continued)
secondary surgery for cleft lip scar
revision in, 841, 843f (V3)
timing and indications for, 835-
836 (V3)
unilateral cleft lip repair in, 735-758
(V3)
comparison of surgical techniques
for, 735-737 (V3)
functional approach in, 752-757,
752-757f (V3)
Millard rotation and advancement
flap technique in, 737-741,
739-743f (V3)
Tennison triangular flap technique
in, 743-751, 744-751f (V3)
timing of, 735 (V3)
Facial convexity, 13-14, 14f (V3)
Facial deformity
considerations in pediatric
craniomaxillary surgery, 848-863
(V3)
clinical evaluation of craniofacial
growth and, 856 (V3)
concepts of craniofacial skeletal
growth and development and,
849f, 849t, 849-850, 850t
(V3)
cranio-orbital dysmorphology and,
856-858 (V3)
cranium and, 850-851, 852f (V3)
mandible and, 855-856, 856f, 857f
(V3)
mandibular hyperplasia and, 859-
860, 860f (V3)
mandibular hypoplasia and, 858-
859, 859f (V3)
maxilla and, 851, 854f, 855f (V3)
maxillary hypoplasia and, 860-861
(V3)
orbits and, 851, 853f (V3)
vertical maxillary excess and, 861f,
861-862 (V3)
zygoma and, 851, 853f (V3)
in craniofacial dysostosis syndromes,
880-921 (V3)
Apert syndrome in, 902-909, 903-
907f (V3)
Carpenter’s syndrome in, 909 (V3)
cloverleaf skull anomaly in, 909-
914, 910-914f (V3)
Crouzon syndrome in, 886-902,
887-900f (V3)
dentition and occlusion anomalies
in, 881-882 (V3)
functional considerations in, 880-
881 (V3)
genetic aspects of, 880 (V3)
morphologic considerations in,
882-883 (V3)
Pfeiffer syndrome in, 909 (V3)
Saethre-Chotzen syndrome in, 909
(V3)
surgical management of, 883-886
(V3)
distraction osteogenesis for, 338-363
(V3)
alveolar distraction in, 349-354,
349-354f (V3)
bone transport by, 354-360, 355-
361f (V3)
future directions in, 362 (V3)
mandibular lengthening in, 342-
346, 342-346f (V3)
mandibular widening in, 338-342,
339-342f (V3)
maxillary bone transport in, 360-
362, 362f (V3)
maxillary distraction by intraoral
devices in, 346-349, 347-349f
(V3)
Le Fort III osteotomy for, 205-218
(V3)
for craniofacial dysostosis, 205-206
(V3)
indications for, 205 (V3)
for midface deficiency, 206, 207-
210f (V3)
modified, 211-218 (V3)
Facial deformity (Continued)
subcranial, 210-211, 212-217f (V3)
technique in, 206-210 (V3)
mandibular deficiency and
pediatric surgical considerations in,
858-859, 859f (V3)
videocephalometric prediction in,
376, 376f (V3)
in naso-orbital-ethmoid fracture, 244-
246, 245f (V2)
in oculoauriculovertebral spectrum,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
in Treacher Collins syndrome, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956 (V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
Facial depth angle, 13, 13f (V3)
Facial evaluation, 1-59 (V3)
analysis for determining chin
position, 681-683t (V3)
clinical, 1-10 (V3)
detailed regional facial features
and, 4-8, 5-9f, 9b (V3)
facial skin age-related changes and,
8-10, 10f (V3)
facial skin health and, 2, 2t (V3)
facial skin type and, 1, 2t (V3)
general facial anthropometric
relations and, 2-4, 3f, 4f (V3)
in rhinoplasty, 557-560, 558-560f
(V3)
Dedo classification of facial profiles
and, 499, 499f, 499t (V3)
facial skeletal growth, 19-58 (V3)
mandibular values in, 41-57 (V3);
See also Mandibular growth
values
maxillary-midface values in, 28-40
(V3); See also Maxillary-
midface growth values
neurocranial values in, 19-27 (V3);
See also Neurocranial growth
values
INDEX I-33
Facial evaluation (Continued)
indications for special evaluations, 19
(V3)
initial examination in head injury, 50
(V2)
occlusion evaluation in, 17-19, 18b
(V3)
before orthognathic surgery, 459
(V3)
in rhytidectomy, 497-500, 498t, 499f,
499t (V3)
skeletal, 10-17 (V3)
changes with age and, 15-17, 17f
(V3)
dental relations in, 14-15, 16f (V3)
skeletal relations in, 12-14, 13-15f
(V3)
soft tissue relations in, 11-12, 12f
(V3)
Facial fat transplantation, 625-627,
626-628f (V3)
Facial filler augmentation, 629-650,
691f, 691-692, 692f (V3)
for augmenting wrinkles, lines, and
folds, 637-639, 638f, 639f (V3)
complications of, 642-643, 643f, 644f
(V3)
history of, 629-631, 630f, 630t, 631f
(V3)
for lips, 633-637, 633-637f (V3)
for malar augmentation, 639-642,
639-642f (V3)
tissue positioning of, 631f, 631-632,
632f (V3)
treatment considerations in, 632-633,
633f (V3)
treatment results in, 643, 645-649f
(V3)
Facial fracture
facial asymmetry in, 294, 295f, 296f
(V3)
mandibular, 95-103, 139-161 (V2)
atrophic, 156-158 (V2)
in bilateral sagittal split osteotomy,
114-115 (V3)
bone healing and, 144-146, 146f,
147f (V2)
classification of, 141-143, 142-144f
(V2)
closed treatment of, 146-148, 147f
(V2)
comminuted, 158-159 (V2)
in complete mandibular subapical
osteotomy, 158 (V3)
complications of, 159-160 (V2)
complications of treatment of, 102-
103 (V2)
condylar and subcondylar, 141-
142, 142f, 162-181 (V2); See
also Condylar fracture
dentoalveolar injury and, 115t,
127f (V2)
epidemiology of, 141 (V2)
facial asymmetry in, 294, 295f,
296f (V3)
geriatric, 389-391f, 390-393 (V2)
historical overview of management
of, 139-141, 140f, 141f (V2)
imaging of complications of
treatment, 102-103 (V2)
internal fixation modalities in,
154f, 154-155, 155f (V2)
lag screws in, 155-156, 156-158f
(V2)
management of teeth in line of
fracture, 156 (V2)
mandibular anatomy and, 96 (V2)
of mandibular body, 101, 102f
(V2)
mandibular series in, 96-98, 97f
(V2)
miniplates in, 155 (V2)
open treatment of, 148-152, 149-
152f (V2)
panoramic radiography in, 98, 99f
(V2)
pediatric, 364-369, 369f (V2)
physical examination in, 143-144
(V2)
I-34 INDEX
Facial fracture (Continued)
reconstruction in, 336-337, 336-
340f (V2)
in sagittal split ramus osteotomy,
424-426, 425-431f (V3)
simple and compound, 99, 99f
(V2)
supplemental radiographs in, 98
(V2)
of symphysis and parasymphysis,
101, 102f (V2)
transosseous wiring in, 156, 158f
(V2)
maxillary
dentoalveolar injury and, 115t
(V2)
in geriatric patient, 386-390, 387-
390f, 392t (V2)
midface, 239-255 (V2)
anatomy in, 239, 240f (V2)
classification of, 239-240, 240f,
241f (V2)
complications in, 253-254 (V2)
geriatric, 386-390, 387-390f, 392t
(V2)
imaging of, 241f, 241-242, 242f
(V2)
Le Fort fractures in, 248-253, 250-
252f (V2)
naso-orbital-ethmoid fracture in,
243-248, 243-249f (V2)
neurologic injury in, 242-243 (V2)
pediatric, 253, 363 (V2)
nasal, 270-283, 271f (V2)
anatomy and pathogenesis of, 270-
273, 272f, 273f (V2)
classification of, 275, 275t (V2)
closed reduction in, 276-278, 278f,
279f (V2)
complications of, 281-282 (V2)
diagnosis and evaluation of, 273-
275, 274f (V2)
medical management of, 275 (V2)
open reduction in, 278-281, 280f
(V2)
pediatric, 281, 362-363 (V2)
naso-orbital-ethmoid, 207, 207f, 243-
248 (V2)
anatomy in, 243f, 243-244, 244f
(V2)
clinical findings in, 244-246, 245f
(V2)
computed tomography of, 214f
(V2)
identification of medial canthal
tendon and, 246 (V2)
injury classification in, 244, 245f
(V2)
nasal fracture and, 276, 276f, 278-
280 (V2)
nasal reconstruction in, 248, 249f
(V2)
nasolacrimal apparatus repair in,
248 (V2)
pediatric, 355-360, 358-359f (V2)
primary reconstruction in, 233
(V2)
radiographic evaluation in, 246
(V2)
reconstruction of medial orbital
rims in, 246-247, 247f (V2)
reconstruction of medial orbital
wall in, 247, 247f (V2)
soft tissue readaptation in, 248,
248f (V2)
surgical approaches in, 246, 246f
(V2)
transnasal canthopexy in, 247-248
(V2)
Facial implants, 678-696 (V3)
chin position analyses and, 681-683t
(V3)
for facial skin laxity with weight loss,
686-688, 686-688f (V3)
injectable facial fillers and, 691f, 691-
692, 692f (V3)
for large nose and small chin, 679f,
679-684, 680f, 684f, 685b, 685f
(V3)
Facial implants (Continued)
lip implant in, 693-694, 694f (V3)
malar cheek implant in, 689f, 689-
690, 690f, 690t (V3)
patient selection for, 678 (V3)
thread lifts and, 695, 695t (V3)
Facial morphogenesis, 697-712 (V3)
animal studies in, 705, 706-708f (V3)
complexity of, 697-705, 698f, 700-
704f (V3)
orofacial clefting sites and, 705-712,
710f, 711f (V3)
Facial nerve
evaluation of
in chronic orofacial pain, 117 (V1)
in head injury, 52 (V2)
facial soft tissue injury and, 283,
284t, 285f, 318, 319, 319f (V2)
forehead and, 599-600, 600f (V3)
high-grade malignant tumor of
salivary gland and, 550, 552f
(V2)
injury of
in arthrotomy, 940 (V2)
condylar fracture and, 164-165,
166f (V2)
endoscopic forehead and brow lift-
related, 606 (V3)
local anesthetic-related, 47 (V1)
in mandibular surgery, 444-445
(V3)
postoperative management of, 405-
406 (V3)
in rhytidectomy, 507-508, 508f
(V3)
in skin cancer, 729, 729f (V2)
in temporomandibular joint
surgery, 905 (V2)
rhytidectomy and, 502 (V3)
types of dysfunction of, 118, 119f (V1)
Facial pain, 961-978 (V2)
antidepressants for, 973 (V2)
atypical, 967-968 (V2)
barriers to management of, 970-971
(V2)
botulinum toxin injection for, 974-
975 (V2)
of cardiac origin, 969 (V2)
central mechanisms of, 963 (V2)
clinically based comprehensive pain
management program for, 975
(V2)
complex regional pain syndrome and,
966-967 (V2)
Eagle’s syndrome and, 969-970, 970f
(V2)
evaluation of, 963-966, 965f, 966t
(V2)
future directions in management of,
975-976 (V2)
muscle relaxants for, 974 (V2)
nerve injury from dental procedures
and, 968f, 968-969 (V2)
neuralgia-inducing cavitational
osteonecrosis and, 967 (V2)
neuropathic agents for, 973-974 (V2)
nonsteroidal antiinflammatory drugs
for, 972-973, 973t (V2)
opioid therapy for, 971-972, 972t
(V2)
osteonecrosis-related, 970 (V2)
peripheral mechanisms of, 962, 963f
(V2)
physical therapy for, 971 (V2)
surgical intervention for, 975 (V2)
therapeutic injections for, 974 (V2)
topical capsaicin for, 975 (V2)
trigeminal anatomy and, 961-962,
962f (V2)
Facial paralysis
endoscopic forehead and brow lift-
related, 606 (V3)
local anesthetic-related, 47 (V1)
tumor-related, 293f (V3)
Facial skeletal growth evaluation, 19-58
(V3)
mandibular, 41-57 (V3)
anterior alveolar height in, 48
(V3)
Facial skeletal growth evaluation
(Continued)
antigonial width in, 51 (V3)
basion to B-point in, 54 (V3)
condylion to gonion in, 46 (V3)
condylion to pogonion in, 45 (V3)
gonion to pogonion in, 42 (V3)
lower canine to lower canine in,
53 (V3)
lower molar to lower molar in, 52
(V3)
mandibular plane to lower incisor
in, 50 (V3)
mandibular plane to lower molar
in, 49 (V3)
nasion to menton in, 57 (V3)
pogonion to N-B line in, 44 (V3)
posterior alveolar height in, 47
(V3)
ramus width at occlusal plane in,
43 (V3)
sella to gnathion in, 55 (V3)
sella to gonion in, 56 (V3)
maxillary-midface, 28-40 (V3)
anterior alveolar height in, 31
(V3)
basion to A-point in, 37 (V3)
bizygomatic width in, 36 (V3)
maxillary width in, 34 (V3)
nasion to anterior nasal spine in,
40 (V3)
palatal plane to upper incisor in,
33 (V3)
palatal plane to upper molar in, 32
(V3)
posterior alveolar height in, 30
(V3)
pterygoid fissure to A-point in, 29
(V3)
sella to anterior nasal spine in, 38
(V3)
sella to posterior nasal spine in, 39
(V3)
skeletal nasal width in, 35 (V3)
neurocranial, 19-27 (V3)
basion to nasion in, 27 (V3)
bony interorbital distance in, 24
(V3)
head breadth in, 23 (V3)
head circumference in, 20 (V3)
head height in, 22 (V3)
head length in, 21 (V3)
sella to basion in, 26 (V3)
sella to nasion in, 25 (V3)
Facial skeletal surgery; See Orthognathic
surgery
Facial skeleton evaluation,
10-17 (V3)
age-related changes and, 15-17, 17f
(V3)
dental relations in, 14-15, 16f (V3)
skeletal relations in, 12-14, 13-15f
(V3)
soft tissue relations in, 11-12, 12f
(V3)
Facial skin
botulinum toxin injection and, 658-
661 (V3)
contraindications and adverse
effects of, 661, 662f (V3)
before filler injection in lip, 636,
636f (V3)
history and pharmacology of, 658
(V3)
for persistent rhytidectomy-related
parotid sialocele, 509 (V3)
preoperative use in laser skin
resurfacing, 521 (V3)
preparations of, 658-659, 659t
(V3)
treatment technique for, 660-661,
661f (V3)
uses in facial cosmetics, 659f, 659-
660, 660f (V3)
evaluation of
age-related changes in, 8-10, 10f,
513 (V3)
skin health and, 2, 2t (V3)
skin type and, 1, 2t (V3)
Facial skin (Continued)
implant in facial skin laxity with
weight loss, 686-688, 686-688f
(V3)
laser resurfacing of, 513-552 (V3)
anesthesia and, 521, 522f (V3)
carbon dioxide laser in, 514f, 514-
516, 515f (V3)
contact dermatitis and, 539 (V3)
dyschromias and, 541-542, 542f,
543f (V3)
erbium:YAG laser in, 532-534,
536-538f (V3)
fractional photothermolysis in,
532, 536f (V3)
history of, 513-514 (V3)
infection and, 540-541, 541f (V3)
intrinsic and extrinsic aging and,
513 (V3)
laser blepharoplasty with, 544-545,
545-547f (V3)
laser properties in, 514f, 514-516,
515f (V3)
laser settings for, 521-522, 522f
(V3)
milia and acne formation and,
539-540, 540f (V3)
ocular complications in, 543-544
(V3)
patient evaluation in, 516-519,
518b (V3)
postoperative care in, 524-529,
526-528f, 530-531f (V3)
preoperative considerations in, 519
(V3)
prolonged erythema and, 535-537,
539f (V3)
pruritus and, 537-538, 539f (V3)
resurfacing acne scars in,
529 (V3)
rhytidectomy with, 545-548, 547-
548f (V3)
scarring and, 542-543, 543f (V3)
sepsis and, 544 (V3)
single-pass resurfacing in, 529-532,
533-534f (V3)
skin preparation for, 519-521 (V3)
telangiectasias and, 538-539 (V3)
traditional technique in, 522-524,
523f, 525-526f (V3)
traumatic and surgical scars
improvement in, 529 (V3)
treatment of benign skin lesions
in, 529 (V3)
orthognathic surgery-related changes
in, 75 (V3)
Facial swelling
exodontia-related, 217-218 (V1)
injectable facial filler and, 643, 643f
(V3)
in Langerhans cell histiocytosis, 571,
571f, 572f (V2)
in osteomyelitis, 633 (V2)
in rhytidectomy, 507 (V3)
in sinus-lift subantral augmentation,
463 (V1)
Facial trauma, 1-411 (V2)
airway management in, 25-34 (V2)
airway assessment and, 25, 26b
(V2)
airway maneuvers and adjuncts in,
26, 26b (V2)
complications in, 33 (V2)
cricothyroidotomy in, 32f, 32-33
(V2)
endotracheal intubation in, 28-31,
31f (V2)
supraglottic airway devices for, 26-
28, 27f, 28f (V2)
systematic approach to, 25 (V2)
tracheostomy in, 33 (V2)
avulsive, 327-351 (V2)
Abbe flap in, 329, 330f (V2)
aesthetic and prosthetic
rehabilitation and, 346-350f
(V2)
airway management in, 327 (V2)
anterolateral thigh free flap in,
335, 335f (V2)

Facial trauma (Continued)
cervicofacial flap in, 329-330, 333f
(V2)
of cheek defects, 344, 345-348f
(V2)
clinical examination in, 327-328
(V2)
debridement in, 328 (V2)
facial artery musculomucosal flap
in, 329 (V2)
fibular free flap in, 333-335, 335f
(V2)
imaging in, 328 (V2)
of lip defects, 343f, 343-344 (V2)
of lower face and mandible, 335-
340f, 336-337 (V2)
of nasal defects, 337, 343 (V2)
paramedian forehead flap in, 329,
331-332f (V2)
pectoralis major myocutaneous flap
in, 330-331 (V2)
radial forearm flap in, 332-333,
334f (V2)
rectus abdominis free flap in, 335
(V2)
of scalp defects, 346 (V2)
submental island flap in, 331-332,
334f (V2)
temporoparietal fascia flap in, 330
(V2)
wound assessment in, 317, 328f
(V2)
comprehensive patient care in, 395-
411 (V2)
accident circumstances and, 395-
396, 396f, 397f (V2)
algorithm for decision making in,
399f (V2)
final discharge planning and, 405-
409 (V2)
identification of psychosocial issues
and, 400 (V2)
long-term rehabilitation and, 408-
411, 409-410f (V2)
pre-injury health and, 398-400
(V2)
preparation for postoperative
events and, 404-405, 407f
(V2)
primary survey and, 396, 397b,
398f (V2)
prioritization and integration of
surgery and, 400b, 400-401,
402f (V2)
secondary survey and, 396-397
(V2)
surgical plan and, 401-404, 403-
406f (V2)
treatment goals in, 396b, 396t
(V2)
condylar fracture in, 141-142, 142f,
162-181 (V2)
closed treatment of, 171 (V2)
conservative management of, 171
(V2)
diagnostic imaging of, 100f, 100-
101, 168-170, 169f (V2)
endoscopic-assisted repair of, 172-
176, 176-180f (V2)
facial nerve and, 164-165, 166f
(V2)
geriatric, 389-391f, 390-393 (V2)
open treatment of, 171 (V2)
pediatric, 364-369, 369f (V2)
physical examination of, 168 (V2)
retromandibular approach in, 171-
172, 172-175f (V2)
retromandibular vein and, 164
(V2)
skeletal injuries in, 167, 167f, 170-
171 (V2)
soft tissue injuries in, 166-167, 170
(V2)
Spiessl and Schroll classification
of, 167, 168b (V2)
superficial temporal artery and,
163-164, 164f, 165f (V2)
temporomandibular joint anatomy
and, 162-163, 163f (V2)
Facial trauma (Continued)
treatment outcomes in, 177-179
(V2)
trigeminal nerve and, 165, 166f
(V2)
dentoalveolar injuries in, 104-138,
105f, 106f (V2)
alveolar process fracture in, 126-
128, 127f, 128f (V2)
classification of, 110-112, 111f,
112b, 113-115t (V2)
comminution of alveolar socket in,
125 (V2)
complete tooth avulsion in, 120-
122, 121f, 122b (V2)
concussed tooth in, 118 (V2)
crown fracture in, 113-118, 116-
118f (V2)
crown infraction in, 112-113 (V2)
displacement of tooth in, 118,
118b (V2)
extrusive luxation in, 118f (V2)
general considerations in, 112
(V2)
gingival injury in, 130 (V2)
history in, 105-107 (V2)
intrusive luxation in, 118, 119f
(V2)
lateral luxation of tooth in, 119-
120 (V2)
pediatric, 364 (V2)
physical examination in, 107-109,
107-109f (V2)
primary tooth injury in, 122-125,
123b, 123-126f (V2)
prognosis in, 132f, 132-135, 134f,
135f (V2)
radiographic examination in, 102,
102f, 109-110, 110f (V2)
reactions of teeth to, 130b, 130-
131, 131f, 132f (V2)
socket wall fracture in, 126 (V2)
splinting techniques for, 128-130,
129f (V2)
subluxation of tooth in, 118 (V2)
diagnostic imaging in, 91-103 (V2)
in angle of mandible fracture, 101,
101f (V2)
in avulsive facial injury, 328 (V2)
in comminuted, complicated, and
impacted fracture, 99, 99f
(V2)
in complications of treatment of
mandibular fracture, 102-103
(V2)
computed tomography in, 98-99
(V2)
in condylar fracture, 100f, 100-101,
168-170, 169f (V2)
in coronoid process and ramus
fractures, 101 (V2)
in dentoalveolar injuries, 102,
102f, 109-110, 110f (V2)
in greenstick and pathologic
fractures, 99, 100f (V2)
imaging techniques in, 91-92, 92f,
92t (V2)
mandibular anatomy and, 96 (V2)
in mandibular body fracture, 101,
102f (V2)
mandibular series in, 96-98, 97f
(V2)
in mandibular symphysis and
parasymphysis fractures, 101,
102f (V2)
midfacial anatomy and, 91, 92f
(V2)
in orbital fracture, 209-211, 210f,
211f (V2)
panoramic radiography in, 98, 99f
(V2)
rendering techniques in, 92-94, 93-
95f (V2)
in simple and compound fractures,
99, 99f (V2)
in soft tissue trauma to neck, 94-
95, 96f (V2)
supplemental radiographs in, 98
(V2)
Facial trauma (Continued)
in zygomatic fracture, 184-185,
185f (V2)
facial asymmetry after, 294, 295f,
296f (V3)
frontal sinus fracture in, 256-269
(V2)
classification of, 257-259, 261f
(V2)
clinical evaluation in, 256, 258f,
259f (V2)
pediatric, 355, 356-357f (V2)
postoperative care in, 266-268,
268f (V2)
radiologic evaluation in, 256-257,
260f, 261f (V2)
surgical anatomy and, 256, 257f,
258f (V2)
surgical management of, 259-266,
262-269f (V2)
in geriatric patient, 374-394 (V2)
aging of face and neck in, 377
(V2)
anesthetic management in, 385,
385b (V2)
closed versus open reduction of
fractures in, 386t (V2)
cognitive evaluation and informed
consent in, 380 (V2)
considerations in management of,
392t (V2)
epidemiology of, 374-377, 375t,
376-377f (V2)
mandibular fractures in, 389-392f,
390-393 (V2)
maxilla and midface fractures in,
386-390, 387-389f (V2)
medications and over-the-counter
drug history and, 380 (V2)
nutrition and fluid and electrolyte
management in, 379 (V2)
perioperative risk assessment of co-
morbid systemic disease in,
380t, 380-385 (V2)
social history and, 379-380 (V2)
wound healing and, 377-378, 378f
(V2)
initial assessment in, 35-42, 36t (V2)
adjuncts to primary survey and, 39-
40 (V2)
adjuncts to secondary survey and,
40-41 (V2)
airway evaluation in, 35-36 (V2)
breathing evaluation in, 36, 36f,
37f (V2)
circulation evaluation in, 37-38,
38f, 38t (V2)
definitive care and, 41 (V2)
disability evaluation in, 38-39, 39t
(V2)
exposure and environment control
in, 39, 39f (V2)
penetrating injuries and, 41-42
(V2)
secondary survey and, 40 (V2)
intensive care in, 42-48, 43t (V2)
abdominal compartment syndrome
and, 45-46, 46f (V2)
acalculous cholecystitis and, 45
(V2)
acute adrenal insufficiency and, 46-
47 (V2)
acute renal failure and, 46 (V2)
acute respiratory distress syndrome
and, 43-44, 44t (V2)
adynamic ileus and, 45 (V2)
atrial fibrillation and, 44-45 (V2)
blood loss and, 46 (V2)
blunt myocardial injury and, 44
(V2)
fluids, electrolytes, and nutrition
and, 45 (V2)
infectious disease and, 47 (V2)
intensive insulin therapy and, 46-
47 (V2)
intubation and mechanical
ventilation and, 43 (V2)
pain control and sedation and, 47
(V2)
INDEX I-35
Facial trauma (Continued)
prophylaxis and, 48 (V2)
rehabilitation and, 48 (V2)
shock and, 44 (V2)
systemic inflammatory response
and multiple organ failure
syndrome and, 44, 44t (V2)
tubes and lines and, 47-48 (V2)
mandibular fracture in; See
Mandibular fracture
midface fracture in, 239-255 (V2)
anatomy in, 239, 240f (V2)
classification of, 239-240, 240f,
241f (V2)
complications in, 253-254 (V2)
geriatric, 386-390, 387-390f, 392t
(V2)
imaging of, 241f, 241-242, 242f
(V2)
Le Fort fractures in, 248-253, 250-
252f (V2)
naso-orbital-ethmoid fracture in,
243-248, 243-249f (V2)
neurologic injury in, 242-243
(V2)
pediatric, 253, 363 (V2)
multi-system trauma and, 65-73 (V2)
abdominal evaluation and, 65-67,
66f, 67f (V2)
antibiotics and, 73 (V2)
complex pelvic fractures and, 68f,
68-69, 69f (V2)
deep venous thrombosis
prophylaxis and, 72-73 (V2)
ICU considerations and, 70-72
(V2)
occult pneumothorax and, 68, 68f
(V2)
occult vascular injuries and, 69-70,
70f (V2)
preparation for rehabilitation and,
73 (V2)
steroids and, 72 (V2)
tertiary examination and, 72 (V2)
nasal fracture in, 270-283, 271f (V2)
anatomy and pathogenesis of, 270-
273, 272f, 273f (V2)
classification of, 275, 275t (V2)
closed reduction in, 276-278, 278f,
279f (V2)
complications of, 281-282 (V2)
diagnosis and evaluation of, 273-
275, 274f (V2)
medical management of, 275 (V2)
open reduction in, 278-281, 280f
(V2)
pediatric, 281, 362-363 (V2)
neurologic assessment in, 11, 49-56
(V2)
detailed evaluation in, 51-52 (V2)
grading severity of injury and, 52-
56, 54f, 54t (V2)
initial evaluation and, 49-51 (V2)
ocular injury in, 74-90 (V2)
carotid cavernous fistula and, 89
(V2)
cranial nerve injury in, 85-86 (V2)
eyelid injuries in, 88 (V2)
globe dystopia in, 88 (V2)
nasolacrimal injuries in, 88-89, 89f
(V2)
nonperforating, 78-82, 78-82f (V2)
ophthalmic assessment in, 74-78,
75-78f (V2)
orbital fractures in, 86f, 86-88, 87f
(V2)
orbital injury and, 83-85, 84f (V2)
penetrating, 83, 83f (V2)
orbital fracture in, 83-85, 84f, 202-
238 (V2)
anatomy in, 202-206, 203t, 203-
206f, 205b, 205t (V2)
associated injuries in, 211-212,
212f (V2)
clinical examination in, 207-209,
208f, 209f (V2)
conservative management of, 217-
220, 219f, 220f (V2)
diagnostic imaging of, 94, 94f (V2)
I-36 INDEX
Facial trauma (Continued)
diplopia in, 214-215, 215f, 216f
(V2)
eyelid lacerations in, 215 (V2)
fracture patterns in, 206-207, 206-
208f (V2)
imaging techniques in, 209-211,
210f, 211f (V2)
indications for operative treatment
of, 220, 221f (V2)
inferior and lateral orbital
approach in, 221-222, 222f,
223f (V2)
lacrimal injuries in, 215, 217f (V2)
medial orbital approach in, 225-
228, 226f, 227f (V2)
ophthalmic assessment in, 78, 78f
(V2)
primary reconstruction in, 228-
233, 228-236f (V2)
secondary reconstruction in, 233-
236, 233-236f (V2)
superior and lateral orbital
approach in, 222-225, 224-
226f (V2)
telecanthus in, 215-217, 218f (V2)
visual disturbances in, 212-214,
212-214f (V2)
orbital injury in, 83-86 (V2)
cranial nerve injury in, 85-86 (V2)
displacement of globe in, 88 (V2)
intraorbital foreign body in, 83-84,
84f (V2)
optic disc avulsion in, 83, 84f (V2)
orbital fracture in, 86f, 86-88, 87f
(V2)
traumatic optic neuropathy in, 84-
85 (V2)
traumatic retrobulbar hemorrhage
in, 84f, 84 (V2)
pediatric, 352-373 (V2)
child abuse and, 372 (V2)
craniofacial growth and
development and, 352-353,
353f (V2)
dentoalveolar fractures in, 363-364
(V2)
epidemiology of, 353-354 (V2)
frontal bone and superior orbital
fractures in, 355 (V2)
frontal sinus and frontobasilar
injuries in, 355, 356-357f (V2)
mandibular body and angle
fractures in, 364 (V2)
mandibular condyle fractures in,
364-369, 369f (V2)
midface fractures in, 363 (V2)
nasal fractures in, 362-363 (V2)
naso-orbito-ethmoid fractures in,
355-360, 358-359f (V2)
orbital fractures in, 360-361, 360-
361f (V2)
perioperative management of, 354-
355 (V2)
prevention of, 354 (V2)
rigid internal fixation and, 369-370
(V2)
Risdon cable and, 370f, 370-372
(V2)
surgical anatomy in, 353 (V2)
symphyseal and parasymphyseal
mandibular fractures in, 364,
365-367f (V2)
zygomaticomaxillary complex
fractures in, 361-362, 362-
363f (V2)
perioperative management of, 1-16
(V2)
abdominal assessment in, 11 (V2)
airway assessment in, 2-4, 3f, 4f
(V2)
breathing assessment in, 4-6 (V2)
chest imaging studies in, 11 (V2)
circulation problems and, 6-7, 7t
(V2)
disability status in, 7-8, 8t (V2)
ear examination in, 9 (V2)
exposure and environmental
control in, 8 (V2)
Facial trauma (Continued)
eye examination in, 9 (V2)
head injury and, 8-9 (V2)
historic perspective in, 1, 2f (V2)
history in, 8 (V2)
musculoskeletal assessment in, 11-
12 (V2)
neck examination in, 10f, 10-11
(V2)
neurologic examination in, 11
(V2)
nose and neurologic evaluation in,
9 (V2)
perineal, rectal, and vaginal
assessment in, 11 (V2)
primary survey in, 1 (V2)
secondary survey in, 8 (V2)
throat examination in, 9, 10f (V2)
postoperative management of, 14-15,
15f, 15t (V2)
reactions of teeth to, 130b, 130-131,
131f, 132f (V2)
soft tissue injuries in, 283-326 (V2)
abrasion in, 289 (V2)
from air bag device blast, 313,
314f, 315f (V2)
anatomic considerations in, 283,
284t, 285f (V2)
anesthesia for, 284, 284 (V2)
avulsive wounds in, 289-290, 290f,
291f (V2)
bite wounds in, 290-292, 292f,
313-316, 314-317f (V2)
burn-related, 321-323, 321-323f,
322t (V2)
of cheek, 320f, 320-321, 321f (V2)
closure of, 284, 285f, 288f (V2)
of ear, 294, 297f, 310-313, 312f,
313f (V2)
of eyelid and nasolacrimal
apparatus, 292-294, 295f, 296f
(V2)
initial evaluation and early
management of, 283, 284f
(V2)
laceration in, 289, 290f (V2)
of lip, 294, 298f (V2)
nasal, 301, 302-305f (V2)
of neck, 294, 316-318, 318f (V2)
of parotid, 294 (V2)
of parotid gland, 294, 318-320,
320f (V2)
pediatric, 292, 293f, 371f, 372
(V2)
periorbital, 301-310, 306-311f
(V2)
of peripheral nerves, 318, 319f
(V2)
of scalp, 292, 293-294f, 323-324,
324f, 325f (V2)
suture materials for, 284-289, 286-
287t (V2)
wound care in, 294-299 (V2)
trigeminal nerve injury in, 272-273
(V1)
wound repair in, 17-24 (V2)
aberrant bone healing in, 22-23
(V2)
abnormal wound healing in, 22
(V2)
bone regeneration in, 22 (V2)
coagulation and, 17, 18f (V2)
formation of granulation tissue
and, 19-21, 20f (V2)
future directions in, 23, 23f (V2)
inflammation and, 17-19, 19f (V2)
neural control of, 21 (V2)
phases of, 17, 18f (V2)
prevention of infection in, 21-22
(V2)
remodeling phase of, 21f, 21 (V2)
zygomatic fracture in, 182-201 (V2)
anatomy in, 182-183, 183f (V2)
Carroll-Girard screw for, 186, 186f
(V2)
coronal approach in, 191-192 (V2)
eyebrow approach in, 187, 188f
(V2)
fixation in, 192, 193f (V2)
Facial trauma (Continued)
fracture patterns in, 206-207, 206-
208f (V2)
history and physical examination
in, 183b, 183-184, 184f (V2)
indications for radiographs and
surgery in, 184-185, 185f (V2)
infraorbital paresthesia and, 194-
195 (V2)
late-onset post-traumatic
enophthalmos and, 198 (V2)
lateral canthotomy in, 186-187
(V2)
lower eyelid approaches in, 187-
188, 188f (V2)
malunion of, 197f, 197-198 (V2)
persistent diplopia following, 195-
197, 196f, 196t (V2)
primary reconstruction in, 231f,
231-233, 232f (V2)
radiography in, 184-185, 185f (V2)
retrobulbar hemorrhage and, 198-
199 (V2)
soft tissue complications of, 195
(V2)
subciliary approach in, 190-191,
191f (V2)
subtarsal approach in, 191 (V2)
transconjunctival approach in,
188-190, 188-190f (V2)
traumatic optic neuropathy and,
197 (V2)
upper eyelid approach in, 187, 187f
(V2)
vestibular approach in, 186 (V2)
zygomatic arch fracture and, 192-
194, 194f (V2)
Facial vein, 433f (V3)
maxillary sinus and, 459 (V1)
nose and, 555 (V3)
Facility for ambulatory orthognathic
surgery, 490-492, 491f, 492f (V3)
Factor IX, 16 (V1)
Factor VIII, 16 (V1)
Falls, geriatric population and, 375,
376-377f (V2)
Famiciclovir
for herpes simplex virus infection,
614-615 (V2)
for herpetic lesions, 520 (V3)
for laser skin resurfacing-related viral
infection, 541 (V3)
FAMM flap; See Facial artery
musculomucosal flap
Farrior technique in otoplasty, 673,
675f (V3)
FAST; See Focused abdominal
sonogram for trauma
Fast absorbable surgical gut, 286t (V2)
Fast-flow vascular malformation, 588-
590, 589f (V2)
Fat embolism, 40 (V2)
Fat injection, 641, 642f (V3)
Fatigue, postsurgical, 405 (V3)
Fatty acids, bone development and,
399-400 (V1)
Fax machine, 361 (V1)
FDA; See Food and Drug
Administration
Feeding child with cleft lip and palate,
717-718 (V3)
Feeding devices, 408-409, 409f (V3)
Feeding tube in ICU patient, 72 (V2)
Felbamate, 150 (V1)
Feldene; See Piroxicam
Female
mandibular growth evaluation and,
41-57 (V3)
anterior alveolar height in, 48
(V3)
antigonial width in, 51 (V3)
basion to B-point in, 54 (V3)
condylion to gonion in, 46 (V3)
condylion to pogonion in, 45 (V3)
gonion to pogonion in, 42 (V3)
lower canine to lower canine in,
53 (V3)
lower molar to lower molar in, 52
(V3)
Female (Continued)
mandibular plane to lower incisor
in, 50 (V3)
mandibular plane to lower molar
in, 49 (V3)
nasion to menton in, 57 (V3)
pogonion to N-B line in, 44 (V3)
posterior alveolar height in, 47
(V3)
ramus width at occlusal plane in,
43 (V3)
sella to gnathion in, 55 (V3)
sella to gonion in, 56 (V3)
maxillary-midface growth evaluation
and, 28-40 (V3)
anterior alveolar height in, 31
(V3)
basion to A-point in, 37 (V3)
bizygomatic width in, 36 (V3)
maxillary width in, 34 (V3)
nasion to anterior nasal spine in,
40 (V3)
palatal plane to upper incisor in,
33 (V3)
palatal plane to upper molar in, 32
(V3)
posterior alveolar height in, 30
(V3)
pterygoid fissure to A-point in, 29
(V3)
sella to anterior nasal spine in, 38
(V3)
sella to posterior nasal spine in, 39
(V3)
skeletal nasal width in, 35 (V3)
neurocranial growth evaluation and
anterior cranial base in, 25 (V3)
basion to nasion in, 27 (V3)
bony interorbital distance in, 24
(V3)
head breadth in, 23 (V3)
head circumference in, 20 (V3)
head height in, 22 (V3)
head length in, 21 (V3)
posterior cranial base in, 26 (V3)
sella to basion in, 26 (V3)
sella to nasion in, 25 (V3)
total cranial base in, 27 (V3)
pregnancy and
gingival enlargement during, 179
(V1)
nonsteroidal antiinflammatory drug
use during, 85 (V1)
use of local anesthetics during, 45t,
45 (V1)
pregnancy test for, 19t (V1), 389-390
(V3)
Femoral artery, anterolateral thigh flap
and, 335f (V2)
Femoral nerve, anterolateral thigh flap
and, 335f (V2)
Femoral vein, anterolateral thigh flap
and, 335f (V2)
Fenamic acids, 887t (V2)
Fenestration defect, 436 (V1)
Fentanyl, 60 (V1)
for acute postoperative pain, 82 (V1)
for chronic facial pain, 972, 972t
(V2)
in laser skin resurfacing, 521 (V3)
midazolam with, 74 (V1)
for pediatric anesthesia and sedation,
104, 105t (V1)
in rapid-sequence intubation, 29
(V2)
Festooning, 205 (V2)
Fever, intensive care of trauma patient
and, 47 (V2)
Fiberoptic nasoendoscopy for speech
assessment, 767 (V3)
Fibrin, wound repair and, 20f, 20-21
(V2)
Fibrin clot formation, 60 (V3)
Fibrin glue, 501 (V1)
in rhytidectomy, 505 (V3)
for sinus obliteration in frontal sinus
fracture, 264, 265f (V2)
Fibroblast, wound repair and, 20, 20f
(V2)

Fibroma
ameloblastic, 522-524, 523f (V2)
desmoplastic, 606-608, 607-608f (V2)
juvenile ossifying, 599-600, 600f
(V2)
neurofibroma, 602, 604f (V2)
odontogenic, 508-510, 509f, 511f
(V2)
ossifying, 598, 599f (V2)
peripheral ossifying, 180, 180f (V1)
Fibromyalgia, 118 (V1), 142 (V1), 964
(V2)
Fibro-osseous lesions, 598-601 (V2)
cemento-osseous dysplasias in, 601,
601f (V2)
fibrous dysplasia in, 600-601 (V2)
juvenile ossifying fibroma in, 599-
600, 600f (V2)
ossifying fibroma in, 598, 599f (V2)
Fibroplasia, 61 (V3)
Fibrous cortical defect, 870 (V2)
Fibrous dysplasia, 600-601, 870 (V2)
Fibrous orbital septum, 205 (V2)
Fibular free flap, 333-335, 335f (V2)
in mandibular reconstruction, 337-
339f (V2)
for midface defect, 346-350f (V2)
Filing cabinet, 361 (V1)
Financial considerations in discharge
planning, 405-408 (V2)
Financial management, 291-299 (V1)
accounting in, 293 (V1)
budgeting in, 291-293, 294t (V1)
compensation plans in, 298t, 298-
299, 299t (V1)
financial policy in, 295 (V1)
financial reporting in, 297-298 (V1)
financial statement trend analysis in,
295 (V1)
financial statements in, 295, 295t,
296t (V1)
patient payment options and, 342
(V1)
projections and feasibility in office
design and, 352 (V1)
revenue cycle and, 293-295 (V1)
third party payers and, 369-370
(V1)
Financial policy, 295 (V1)
Financial reporting, 297-298 (V1)
Financial statement, 295, 295t, 296t
(V1)
Financial statement trend analysis, 295
(V1)
Financing of office building, 362 (V1)
Finasteride, 651 (V3)
Fine needle aspiration, 414f, 414-415,
415f (V2)
in lymphoma, 758 (V2)
in parotid gland tumor, 547 (V2)
Fine-touch discrimination
in chronic head and neck pain, 140
(V1)
in trigeminal nerve injury, 262f, 262-
263 (V1)
Finite element method, 377 (V3)
Fire hazards in laser therapy, 243 (V1),
516 (V3)
Firing of employee, 322 (V1)
First intention healing, 62 (V3)
First molar
bilateral sagittal split osteotomy and,
106-108 (V3)
impacted, 171 (V1)
First premolar
complete mandibular subapical
osteotomy and, 156 (V3)
extraction for orthodontics, 185-186
(V1)
sectioning in extraction of, 194, 195f,
196f (V1)
First-degree burn, 322t (V2)
Fistula
carotid cavernous, 89 (V2)
cleft palate repair and, 763, 765-766,
766t (V3)
closure in secondary cleft lip and
palate reconstruction, 828-831,
830f, 832-834f (V3)
Fistula (Continued)
maxillary surgery-related, 480 (V3)
salivary, rhytidectomy-related, 509
(V3)
Fitzpatrick classification of skin types, 1,
2t, 249, 249t (V1), 518, 518b (V3)
malignant melanoma and, 749, 750t
(V2)
non-melanoma skin cancer and, 730,
730t (V2)
Five-wall extraction socket defect, 541,
543f (V1)
Fixation
in bilateral sagittal split osteotomy,
109-111, 110f, 111b (V3)
bone plate
in cleft orthognathic surgery, 819
(V3)
in complete mandibular subapical
osteotomy, 158, 160f, 168f,
170f (V3)
in Le Fort I osteotomy, 180, 182f
(V3)
in Le Fort III osteotomy, 211 (V3)
in modified Le Fort III osteotomy,
211-212 (V3)
in chin implant, 687f, 687-688 (V3)
in forehead and brow lift
endoscopic, 605-606 (V3)
trichophytic, 610-611 (V3)
in genioplasty, 142-145, 144-148f
(V3)
in Le Fort I osteotomy, 180-184, 182f
(V3)
in mandibular fracture
external, 148 (V2)
external pin, 139, 140f (V2)
internal, 154f, 154-155, 155f (V2)
maxillomandibular, 366-369 (V2)
open reduction and internal
fixation, 391f, 391-392, 392f,
392t (V2)
in mandibular lengthening by
distraction osteogenesis, 343f
(V3)
in mandibular widening, 341, 341f
(V3)
maxillomandibular, 146-148, 147f
(V2)
ambulatory surgery and, 494
(V3)
in bilateral sagittal split osteotomy,
109 (V3)
in condylar fracture, 171 (V2)
in internal derangement of
temporomandibular joint, 940
(V2)
in mandibular condyle fracture,
366-369 (V2)
Risdon cable and, 370f, 370-372
(V2)
for skeletal anchorage, 225 (V1)
in symphyseal and parasymphyseal
fractures, 364 (V2)
tracheotomy and, 12-14, 12-14f
(V2)
in transoral vertical ramus
osteotomy, 128-129 (V3)
miniplate
in bilateral sagittal split osteotomy,
109-111 (V3)
in genioplasty, 143, 145f, 149f
(V3)
for impacted teeth, 172 (V1)
in mandibular fracture, 155 (V2)
in nasal fracture, 280 (V2)
in naso-orbital-ethmoid fracture, 247
(V2)
open reduction and internal fixation
in mandibular fracture, 391f, 391-
392, 392f, 392t (V2)
in maxillary/midface fracture, 386t,
387-389f, 388-390 (V2)
in otoplasty, 673 (V3)
screw
in bilateral sagittal split osteotomy,
109, 110f (V3)
at bone graft site, 420, 420f (V1)
in chin implant, 688 (V3)
Fixation (Continued)
in cleft orthognathic surgery, 819
(V3)
in complete mandibular subapical
osteotomy, 158, 160f, 168f,
170f (V3)
in genioplasty, 143, 145f (V3)
in implant placement in onlay
bone graft, 424, 424f (V1)
in mandibular lengthening by
distraction osteogenesis, 343f
(V3)
in mandibular symphysis bone graft
harvest, 412f (V1)
in modified Le Fort III osteotomy,
211-212 (V3)
wire
in bilateral sagittal split osteotomy,
109 (V3)
in genioplasty, 143, 149f (V3)
in mandibular fracture, 391, 391f,
391f (V2)
in mandibular lengthening by
distraction osteogenesis, 343f
(V3)
in mandibular widening, 341, 341f
(V3)
in maxillary/midface fracture, 386-
388 (V2)
in naso-orbital-ethmoid fracture,
247 (V2)
of palatal splint, 397t, 398, 398f
(V3)
in zygomatic fracture, 192, 193f
(V2)
Fixed costs, 298 (V1)
Fixed implant restorations classification,
479, 480t (V1)
Fixed partial denture, miniimplant
stabilization of, 568 (V1)
Fixed provisional prosthesis in bone
graft for implant, 422 (V1)
Flail mandible, 2, 3f (V2)
Flap
in avulsive facial injury, 329-350
(V2)
Abbe flap in, 329, 330f (V2)
aesthetic and prosthetic
rehabilitation and, 346, 349-
350f (V2)
anterolateral thigh free flap in,
335, 335f (V2)
cervicofacial flap in, 329-330, 333f
(V2)
of cheek, 344, 345-348f (V2)
facial artery musculomucosal flap
in, 329 (V2)
fibular free flap in, 333-335, 335f
(V2)
of lip, 343f, 343-344 (V2)
of nose, 343 (V2)
paramedian forehead flap in, 329,
331-332f (V2)
pectoralis major myocutaneous flap
in, 330-331 (V2)
radial forearm flap in, 332-333,
334f (V2)
rectus abdominis free flap in, 332-
333, 334f (V2)
of scalp, 346 (V2)
submental island flap in, 331-332,
334f (V2)
temporoparietal fascia flap in, 330
(V2)
Blair preauricular incision and, 933,
933f (V2)
in bone graft for implant, 420-422,
422f (V1)
buccal
in impacted maxillary canine, 197,
198f (V1)
in mandibular resection, 700-701,
701f (V2)
cheek
in mandibular resection, 700-701,
701f (V2)
in rhytidectomy, 502, 503f (V3)
in complicated exodontia, 192-193,
193f, 194f (V1)
INDEX I-37
Flap (Continued)
for impacted mandibular second
premolar, 197-199 (V1)
for impacted mandibular third
molar, 206f (V1)
for impacted maxillary canine,
196, 196f, 197f, 199f (V1)
for impacted maxillary premolar,
199, 200f (V1)
root tip displacement and, 214
(V1)
designs to improve aesthetics of soft
tissue around implant and, 487-
489, 488f, 489f (V1)
in guided tissue regeneration
procedures, 430 (V1)
in hair replacement, 655, 655f, 656f
(V3)
mucoperiosteal
in alveolar bone grafting for cleft
maxilla, 808 (V3)
in antral membrane balloon
elevation, 465, 467f (V1)
in complete mandibular subapical
osteotomy, 156 (V3)
in complicated exodontia, 192-
193, 193-195f, 199f, 206f
(V1)
in lingual nerve repair, 269-270
(V1)
in mandibular lengthening by
distraction osteogenesis, 344
(V3)
in palatoplasty, 762 (V3)
in residual palatal fistula closure,
830, 830f (V3)
in sinus-lift subantral
augmentation, 459, 459f (V1)
in trephine bone core sinus
elevation, 464, 464f (V1)
nasal
in primary bilateral cleft lip and
palate repair and, 724f (V3)
in primary unilateral cleft lip
repair, 721f, 722f (V3)
osteoperiosteal, 471-478 (V1)
alveolar repositioning osteotomies
and, 473, 473f, 474f (V1)
alveolar split graft and, 471, 473f
(V1)
alveolar width distraction
osteogenesis and, 474-477,
475-478f (V1)
interpositional bone graft and, 471,
472f (V1)
pharyngeal
in cleft orthognathic surgery, 826
(V3)
in primary palatoplasty procedure,
726-727 (V3)
in residual palatal fistula closure,
830 (V3)
in surgical management of
velopharyngeal insufficiency,
836 (V3)
in rhytidectomy, 502, 503f (V3)
in rotation and advancement flap
technique for unilateral cleft lip,
722, 737-741 (V3)
Asensio technique and, 740f, 740-
741, 741f (V3)
comparison of cleft surgery
techniques, 736 (V3)
nasal reshaping in, 741 (V3)
postoperative care in, 741 (V3)
preoperative management in, 738
(V3)
surgical technique in, 738-739,
739f, 740f (V3)
wide cleft defect and, 742f, 743f
(V3)
in skin cancer repair, 738, 739 (V2)
in trichophytic forehead and brow
lift, 613 (V3)
Flapless buccal wall reconstruction in
guided tissue regeneration, 443f,
443-444, 444f (V1)
Flashscanning in laser therapy, 238
(V1)
I-38 INDEX
Flat plane splint, 984 (V2)
Flexeril; See Cyclobenzaprine
Flexzan, 526 (V3)
Floor of mouth, 705 (V2)
lymphatic malformation of, 582, 583-
585f (V2)
squamous cell carcinoma of, 714,
714f, 715f (V2)
Floor plan in office design, 352-358
(V1)
additional space requirements in,
358, 358f, 359f (V1)
business office area in, 355f, 355-356,
356f (V1)
conference room in, 354, 354f (V1)
consultation room in, 352, 352f (V1)
laboratory in, 356-357 (V1)
lunchroom in, 357, 357f (V1)
patient reception and waiting area in,
355, 355f (V1)
physician’s office in, 356, 357f (V1)
posttreatment area in, 353-355, 354f
(V1)
pretreatment area in, 353 (V1)
radiology suite in, 352 (V1)
restrooms in, 356, 356f (V1)
staff office in, 357-358, 358f (V1)
surgical treatment area in, 352-353,
353f (V1)
Florid cemento-osseous dysplasia, 601,
601f (V2)
Flow cytometry, 416-417 (V2)
Fluconazole, 520 (V3)
Fluence, 238 (V1), 514 (V3)
Fluid administration during anesthesia,
72 (V1)
child and, 102-103 (V1)
Fluid analysis, temporomandibular joint
arthroscopy and, 921 (V2)
Fluid compartmentalization, 72 (V1)
Fluid management in trauma patient,
45 (V2)
geriatric, 379 (V2)
pediatric, 354-355 (V2)
Flumazenil, 58t, 59 (V1)
Fluoroquinolones, 389, 389t (V1)
5-Fluorouracil, 781t (V2)
cisplatin and taxanes with, 778 (V2)
for metastatic tumors, 779, 779t (V2)
radiation therapy with, 771, 772
(V2)
for skin cancer, 740 (V2)
Fluoxetine
for myofascial pain, 144 (V1)
for posttraumatic headache, 153 (V1)
for temporomandibular disorders,
889t (V2)
Flurazepam, 889t (V2)
Flurbiprofen
bone healing and, 394, 395 (V1)
for temporomandibular disorders,
887t (V2)
Focal cemento-osseous dysplasia, 601
(V2)
Focused abdominal sonogram for
trauma, 41, 66-67, 67f (V2)
Follicular ameloblastoma, 477, 480f,
485f, 488f (V2)
Follicular lymphoma, 760-761 (V2)
Follicular unit, 652 (V3)
Food and Drug Administration laser
safety and compliance, 515-516
(V3)
Food avoidance after surgery, 408 (V3)
Forced duction test, 77-78 (V2)
Forehead
Botox injection in, 659, 659f, 661f
(V3)
endoscopic forehead and brow lift
and, 595-609, 596f (V3)
bone anatomy and, 595-597 (V3)
complications in, 606-607 (V3)
endoscopic anatomy and, 600-602,
601f (V3)
muscle and fascial anatomy and,
597-598, 598f (V3)
postoperative care in, 606 (V3)
preoperative evaluation in, 602t,
602-603 (V3)
Forehead (Continued)
technique in, 603f, 603-606, 605f
(V3)
vessel and nerve anatomy and,
598-600, 598-600f (V3)
evaluation before blepharoplasty, 587
(V3)
frontal face evaluation and, 1-2, 2f
(V3)
lymphatic malformation in, 582 (V2)
malformation in craniofacial
dysostosis syndromes, 882 (V3)
trichophytic forehead and brow lift
and, 610-617 (V3)
comparison of lift techniques and,
611t (V3)
complications in, 614-616, 616f,
617f (V3)
fixation techniques in, 610-611
(V3)
patient selection for, 613-614,
615f, 616f (V3)
surgical technique in, 611-614f,
612-613 (V3)
Foreign body
intraorbital, 83-84, 84f (V2)
ocular, 78, 306 (V2)
Fornix incision of lower lid, 205f, 227f
(V2)
Fosamax; See Alendronate
Fospropofol, 61 (V1)
Fourth cranial nerve palsy, 85 (V2)
Fourth-degree burn, 322t (V2)
Four-wall extraction socket defect, 541,
543f (V1)
Fractional excretion of sodium, 46 (V2)
Fractional laser skin resurfacing, 532,
536f (V3)
Fracture
alveolar process, 126-128, 127f, 128f
(V2)
alveolar socket wall, 115t, 126 (V2)
cervical spine, 63, 64f (V2)
condylar, 141-142, 142f, 162-181
(V2)
closed treatment of, 171 (V2)
conservative management of, 171
(V2)
diagnostic imaging of, 100f, 100-
101, 168-170, 169f (V2)
endoscopic-assisted repair of, 172-
176, 176-180f (V2)
facial nerve and, 164-165, 166f
(V2)
geriatric, 389-391f, 390-393 (V2)
open treatment of, 171 (V2)
pediatric, 364-369, 369f (V2)
physical examination of, 168 (V2)
retromandibular approach in, 171-
172, 172-175f (V2)
retromandibular vein and, 164
(V2)
skeletal injuries in, 167, 167f, 170-
171 (V2)
soft tissue injuries in, 166-167, 170
(V2)
Spiessl and Schroll classification
of, 167, 168b (V2)
superficial temporal artery and,
163-164, 164f, 165f (V2)
temporomandibular joint anatomy
and, 162-163, 163f (V2)
treatment outcomes in, 177-179
(V2)
trigeminal nerve and, 165, 166f
(V2)
diagnostic imaging of, 93-94, 93-95f
(V2)
exodontia-related, 219f, 219-220,
220f (V1)
frontal bone, 355 (V2)
frontal sinus, 256-269 (V2)
classification of, 257-259, 261f
(V2)
clinical evaluation in, 256, 258f,
259f (V2)
pediatric, 355, 356-357f (V2)
postoperative care in, 266-268,
268f (V2)
Fracture (Continued)
radiologic evaluation in, 256-257,
260f, 261f (V2)
surgical anatomy and, 256, 257f,
258f (V2)
surgical management of, 259-266,
262-269f (V2)
in geriatric patient, 374-394 (V2)
aging of face and neck in, 377
(V2)
anesthetic management in, 385,
385b (V2)
closed versus open reduction of
fractures in, 386t (V2)
cognitive evaluation and informed
consent in, 380 (V2)
considerations in management of,
392t (V2)
epidemiology of, 374-377, 375t,
376-377f (V2)
mandibular fractures in, 389-392f,
390-393 (V2)
maxilla and midface fractures in,
386-390, 387-389f (V2)
medications and over-the-counter
drug history and, 380 (V2)
nutrition and fluid and electrolyte
management in, 379 (V2)
perioperative risk assessment of co-
morbid systemic disease in,
380t, 380-385 (V2)
social history and, 379-380 (V2)
wound healing and, 377-378, 378f
(V2)
mandibular, 95-103 (V2); See also
Mandibular fracture
in bilateral sagittal split osteotomy,
114-115 (V3)
in complete mandibular subapical
osteotomy, 158 (V3)
complications of treatment of, 102-
103 (V2)
facial asymmetry in, 294, 295f,
296f (V3)
geriatric, 389-391f, 390-393 (V2)
mandibular anatomy and, 96 (V2)
of mandibular body, 101, 102f
(V2)
mandibular series in, 96-98, 97f
(V2)
panoramic radiography in, 98, 99f
(V2)
pediatric, 364-369, 369f (V2)
in sagittal split ramus osteotomy,
424-426, 425-431f (V3)
simple and compound, 99, 99f
(V2)
supplemental radiography in, 98
(V2)
of symphysis and parasymphysis,
101, 102f (V2)
maxillary
dentoalveolar injury and, 115t
(V2)
in geriatric patient, 386-390, 387-
390f, 392t (V2)
midface, 239-255 (V2)
anatomy in, 239, 240f (V2)
classification of, 239-240, 240f,
241f (V2)
complications in, 253-254 (V2)
geriatric, 386-390, 387-390f, 392t
(V2)
imaging of, 241f, 241-242, 242f
(V2)
Le Fort fractures in, 248-253, 250-
252f (V2)
naso-orbital-ethmoid fracture in,
243-248, 243-249f (V2)
neurologic injury in, 242-243
(V2)
pediatric, 253, 363 (V2)
nasal, 270-283, 271f (V2)
anatomy and pathogenesis of, 270-
273, 272f, 273f (V2)
classification of, 275, 275t (V2)
closed reduction in, 276-278, 278f,
279f (V2)
complications of, 281-282 (V2)
Fracture (Continued)
diagnosis and evaluation of, 273-
275, 274f (V2)
medical management of, 275 (V2)
open reduction in, 278-281, 280f
(V2)
pediatric, 281, 362-363 (V2)
naso-orbital-ethmoid, 207, 207f, 243-
248 (V2)
anatomy in, 243f, 243-244, 244f
(V2)
clinical findings in, 244-246, 245f
(V2)
computed tomography of, 214f
(V2)
identification of medial canthal
tendon and, 246 (V2)
injury classification in, 244, 245f
(V2)
nasal reconstruction in, 248, 249f
(V2)
nasolacrimal apparatus repair in,
248 (V2)
pediatric, 355-360, 358-359f (V2)
primary reconstruction in, 233
(V2)
radiographic evaluation in, 246
(V2)
reconstruction of medial orbital
rims in, 246-247, 247f (V2)
reconstruction of medial orbital
wall in, 247, 247f (V2)
soft tissue readaptation in, 248,
248f (V2)
surgical approaches in, 246, 246f
(V2)
transnasal canthopexy in, 247-248
(V2)
orbital, 83-88, 84f, 86f, 87f, 202-238
(V2)
anatomy in, 202-206, 203t, 203-
206f, 205b, 205t (V2)
associated injuries in, 211-212,
212f (V2)
clinical examination in, 207-209,
208f, 209f (V2)
conservative management of, 217-
220, 219f, 220f (V2)
diagnostic imaging of, 94, 94f (V2)
diplopia in, 214-215, 215f, 216f
(V2)
eyelid lacerations in, 215 (V2)
fracture patterns in, 206-207, 206-
208f (V2)
imaging techniques in, 209-211,
210f, 211f (V2)
indications for operative treatment
of, 220, 221f (V2)
inferior and lateral orbital
approach in, 221-222, 222f,
223f (V2)
lacrimal injuries in, 215, 217f (V2)
medial orbital approach in, 225-
228, 226f, 227f (V2)
ophthalmic assessment in, 78, 78f
(V2)
primary reconstruction in, 228-
233, 228-236f (V2)
secondary reconstruction in, 233-
236, 233-236f (V2)
superior and lateral orbital
approach in, 222-225, 224-
226f (V2)
telecanthus in, 215-217, 218f
(V2)
visual disturbances in, 212-214,
212-214f (V2)
pelvic, 68f, 68-69, 69f (V2)
of primary tooth, 123, 123f, 124f
(V2)
skull
initial assessment of, 50 (V2)
management of, 59-60 (V2)
orbital fracture and, 212 (V2)
of tooth crown, 113-118 (V2)
crown-root, 116 (V2)
enamel, 113-114 (V2)
pulp exposure with non-vital pulp,
115-116, 116f (V2)

Fracture (Continued)
pulp exposure with vital pulp, 114-
115 (V2)
root, 116-117, 117f, 118f (V2)
treatment of, 115b (V2)
zygomatic, 182-201 (V2)
anatomy in, 182-183, 183f (V2)
Carroll-Girard screw for, 186, 186f
(V2)
coronal approach in, 191-192 (V2)
eyebrow approach in, 187, 188f
(V2)
fixation in, 192, 193f (V2)
history and physical examination
in, 183b, 183-184, 184f (V2)
indications for radiographs and
surgery in, 184-185, 185f (V2)
infraorbital paresthesia and, 194-
195 (V2)
late-onset post-traumatic
enophthalmos and, 198 (V2)
lateral canthotomy in, 186-187
(V2)
lower eyelid approaches in, 187-
188, 188f (V2)
malunion of, 197f, 197-198 (V2)
pediatric, 361-362, 362-363f (V2)
persistent diplopia following, 195-
197, 196f, 196t (V2)
retrobulbar hemorrhage and, 198-
199 (V2)
soft tissue complications of, 195
(V2)
subciliary approach in, 190-191,
191f (V2)
subtarsal approach in, 191 (V2)
transconjunctival approach in,
188-190, 188-190f (V2)
traumatic optic neuropathy and,
197 (V2)
upper eyelid approach in, 187, 187f
(V2)
vestibular approach in, 186 (V2)
zygomatic arch fracture and, 192-
194, 194f (V2)
zygomatic arch, 192-194, 194f (V2)
Frankfort horizontal plane
horizontal relations measured parallel
to, 12, 12f (V3)
in profile view in facial asymmetry,
273f, 274 (V3)
vertical relations measured
perpendicular to, 11-12, 12f (V3)
Fraudulent health care claim
submission, 371 (V1)
Freckles, 518 (V3)
Free base form of local anesthetic, 37-
38, 38f (V1)
Free flap in avulsive facial injury, 332-
335, 334f, 335f (V2)
Free gingival graft, 408, 409f (V1)
Free radicals, 435 (V1)
Freeze-dried bone allograft, 505-506
(V1)
Frenectomy
laser, 244 (V1)
lingual, 174, 175f, 176f (V1)
maxillary labial, 173-174, 174f (V1)
Front desk staff, 346-347 (V1)
Frontal artery, 668f (V3)
Frontal bone
forehead and brow lift and, 595 (V3)
pediatric fracture of, 355 (V2)
Frontal face evaluation, 1-2, 2f, 272-
274, 273f (V3)
Frontal nerve
eyelid and, 584f, 585 (V3)
forehead and, 599-600, 600f (V3)
Frontal process of zygoma, 182 (V2)
Frontal sinus
fracture of, 256-269 (V2)
classification of, 257-259, 261f (V2)
clinical evaluation in, 256, 258f,
259f (V2)
pediatric, 355, 356-357f (V2)
postoperative care in, 266-268,
268f (V2)
radiologic evaluation in, 256-257,
260f, 261f (V2)
Frontal sinus (Continued)
surgical anatomy and, 256, 257f,
258f (V2)
surgical management of, 259-266,
262-269f (V2)
ossifying fibroma of, 965f, 966f (V3)
Frontalis muscle
Botox injection into, 659, 659f (V3)
eyelid and, 581f, 586f (V3)
forehead and, 597 (V3)
Frontobasilar injury, 355, 356-357f (V2)
Fronto-zygomatic suture line, 596 (V3)
Frost suture
in ectropion deformity repair, 236f
(V2)
in orbital fracture, 222, 224f (V2)
in zygomatic fracture, 191, 191f, 195
(V2)
Frozen section, 414 (V2)
FulFil lip implant, 693 (V3)
Full histologic periosteal refixation, 605
(V3)
Full-coverage splint, 984 (V2)
Full-thickness burn, 322t (V2)
Full-thickness skin graft
in internal derangement of
temporomandibular joint, 939
(V2)
in skin cancer, 739 (V2)
Functional cleft lip repair, 752-757
(V3)
cleft model and repair in, 752f, 752-
753, 753f (V3)
closure in, 755-756, 755-757f (V3)
comparison of cleft surgery
techniques, 736-737 (V3)
lip incisions in, 753-754, 754f (V3)
nasal dissection in, 754-755 (V3)
review of studies in, 756 (V3)
Functional evaluation of occlusion, 17,
18b (V3)
Functional genioplasty, 137, 138f (V3)
Functional imaging in
temporomandibular disorders, 843-
845 (V2)
Functional impairment assessment in
trigeminal nerve injury, 261, 261t
(V1)
Functional magnetic resonance imaging
in chronic facial pain, 966 (V2)
Functional residual capacity
of child, 96, 96t (V1)
patient positioning and, 75 (V1)
Functional temporomandibular
disorders, 898-911 (V2)
hypermobility in, 905b, 905-908f,
905-909 (V2)
hypomobility in, 898-905 (V2)
ankylosis and, 901-905 (V2)
complications of, 905 (V2)
imaging in, 898 (V2)
pseudoankylosis and, 899-901 (V2)
treatment of, 905 (V2)
trismus and, 898-899 (V2)
Funduscopic examination
in orbital fracture, 209 (V2)
in periorbital soft tissue injury, 306
(V2)
Fungal infection, laser skin resurfacing-
related, 538, 540-541, 541f (V3)
Furlow double-opposing Z-plasty for
cleft palate, 726, 730f, 772-775,
773-775f (V3)
advantages in initial palate repair,
833 (V3)
controversies in, 762 (V3)
history of, 759-760 (V3)
Furnishing of office, 358-361, 359f, 360f
(V1)
Fusiform biopsy, 731f (V2)
Fusion imaging in temporomandibular
disorders, 845 (V2)
G localized gingival lesions in, 179-181,
Gabapentin
after trigeminal nerve repair, 271
(V1)
for chronic facial pain, 973f, 973-974
(V2)
Gabapentin (Continued)
for complex regional pain syndrome,
158 (V1)
for myofascial pain, 144 (V1)
for neuropathic orofacial pain, 999
(V2)
for postherpetic neuralgia, 152 (V1)
for posttraumatic headache, 153 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)
for trigeminal neuralgia, 150 (V1),
992, 992t (V2)
Gag reflex, 51 (V2)
Gamma knife stereotactic radiosurgery
in orofacial pain, 975 (V2)
for posttraumatic trigeminal
neuralgia, 157 (V1)
for trigeminal neuralgia, 151 (V1),
993 (V2)
Gamma-aminobutyric acid,
benzodiazepines and, 56 (V1)
Ganglion, 869 (V2)
Gap arthroplasty, 903 (V2)
Gap healing, 62 (V3)
Gardner’s syndrome, 178f, 178 (V1),
605 (V2)
Garr[ac]e’s osteomyelitis, 874 (V2)
Gasserian ganglion procedures, 151
(V1)
Gastric contents aspiration, 107 (V1)
Gastroesophageal reflux disease, 7-8
(V1)
Gastrointestinal disorders, 386-387,
387t (V3)
Gastrointestinal system
effects of nonsteroidal
antiinflammatory drugs on, 84
(V1)
effects of thyroid disorders on, 13t
(V1)
intensive care of trauma patient and,
45-46, 46f (V2)
involvement in extranodal
lymphoma, 760 (V2)
liver disease-related alteration in, 11
(V1)
preoperative evaluation of, 7-11, 9-
11t, 10f (V1)
GBR; See Guided bone regeneration
Gefitinib, 781t, 782t, 783 (V2)
Gelatin sponge, 274 (V1)
GELCLAIR, 616 (V2)
Gemcitabine, 781t (V2)
Gene amplification, 652, 653f (V2)
Gene regulation of cell function, 648-
652, 649-651f (V2)
Gene therapy for oral cavity cancer,
713 (V2)
General anesthesia, 22, 67 (V1)
for child, 103-106, 105t (V1)
for geriatric patient, 385, 385b (V2)
laryngeal mask airway and, 70 (V1)
in open rhinoplasty, 567 (V3)
in trigeminal nerve repair, 268 (V1)
General damages in malpractice lawsuit,
375 (V1)
General dentistry
definitions and resources in, 309-313,
310-312t (V1)
laser therapy applications for, 254-
256 (V1)
General partnership, 285-286, 286t
(V1)
Generalized disorders of dentition, 175-
181 (V1)
cleidocranial dysplasia in, 175-177,
176f, 177f (V1)
Gardner’s syndrome in, 178f, 178
(V1)
generalized gingival hyperplasia in,
178-179, 179f (V1)
hereditary ectodermal dysplasia in,
177f, 177-178 (V1)
180f, 181f (V1)
Generalized gingival hyperplasia, 178-
179, 179f (V1)
Genetics
in cancer, 647-666, 648f (V2)
INDEX I-39
Genetics (Continued)
cancer cell evasion of apoptosis
and, 660-662, 661f (V2)
cancer cell insensitivity to growth
inhibitory signals and, 658-
660, 659f (V2)
cancer cell release from growth
signal requirement and, 655-
658, 657f (V2)
chromosomal abnormalities in
cancer cells and, 652-653,
653-655f (V2)
epigenetic alteration of gene
expression in cancer cells and,
655 (V2)
gene regulation of cell function
and, 648-652, 649-651f (V2)
immortalization of cancer cell and,
662-664, 663f (V2)
neovascularization and, 664, 665f
(V2)
nevoid basal cell carcinoma
syndrome and, 441 (V2)
nucleotide sequence abnormalities
in cancer cells and, 653-655,
656f (V2)
oral cavity cancer and, 707-708
(V2)
osteosarcoma and, 683 (V2)
tissue invasion and metastases and,
664-666, 666f (V2)
in cleft lip and palate, 715 (V3)
in craniofacial dysostosis syndromes,
880 (V3)
in oculoauriculovertebral spectrum,
922 (V3)
in Treacher Collins syndrome, 936
(V3)
in venous malformation, 585-586
(V2)
Geniohyoid muscle, 808, 809f (V2)
Genioplasty, 137-154 (V3)
advantages and disadvantages of, 685t
(V3)
cephalometric analysis and, 373
(V3)
before complete mandibular subapical
osteotomy, 162f, 163f (V3)
fixation devices in, 142-145, 144-
148f (V3)
functional, 137, 138f (V3)
indications for, 137-138 (V3)
Le Fort I segmental osteotomy with,
199-203f (V3)
mandibular relapse in, 446-451, 449-
452f (V3)
mandibular widening with, 339-341,
340f, 341f (V3)
for obstructive sleep apnea syndrome,
325-327, 329f (V3)
in oculoauriculovertebral spectrum,
931 (V3)
outpatient, 493 (V3)
results in, 148-151, 150-153f (V3)
surgical procedure in, 140-142, 141f,
142f (V3)
treatment planning in, 138-140, 139f,
140f (V3)
Genioplasty incision, 197 (V1)
Gentamicin, 389-390 (V1)
Geographic Practice Cost Index, 370-
371 (V1)
Gerdy’s tubercle of tibia, bone graft
harvest from, 414, 414f (V1)
Geriatric patient
maxillofacial trauma in, 6, 374-394
(V2)
aging of face and neck in, 377
(V2)
anesthetic management in, 385,
385b (V2)
closed versus open reduction of
fractures in, 386t (V2)
cognitive evaluation and informed
consent in, 380 (V2)
considerations in management of,
392t (V2)
epidemiology of, 374-377, 375t,
376-377f (V2)
I-40 INDEX
Geriatric patient (Continued)
mandibular fractures in, 389-392f,
390-393 (V2)
maxilla and midface fractures in,
386-390, 387-389f (V2)
medications and over-the-counter
drug history and, 380 (V2)
nutrition and fluid and electrolyte
management in, 379 (V2)
perioperative risk assessment of co-
morbid systemic disease in,
380t, 380-385 (V2)
social history and, 379-380 (V2)
wound healing and, 377-378, 378f
(V2)
nonsteroidal antiinflammatory drugs
and, 85 (V1)
Giant cell arteritis, 899 (V2)
Giant cell granuloma, 180-181 (V1)
Giant cell tumor, 594, 869, 871 (V2)
Gillies approach to zygomatic arch
fracture, 194, 194f (V2)
Gingiva
laser-assisted removal of, 254-255
(V1)
Le Fort 1 osteotomy and, 64-65 (V3)
localized lesions of, 179-181, 180f,
181f (V1)
trauma to, 115t (V2), 130
Gingival augmentation procedures, 481-
484, 481-485f (V1)
Gingival cyst, 442, 445f (V2)
Gingival cyst of newborn, 180 (V1)
Gingival graft, 408, 409f, 484-486, 485-
488f (V1)
Gingival plexus, 175f
Gingivectomy, 481-484, 484f, 485f
(V1)
Gingivolabial sulcus incision, 197 (V1)
Gingivoperiosteoplasty, 720 (V3)
Glabella, 554b (V3)
Botox injection in, 659, 659f, 661f
(V3)
endoscopic forehead and brow lift
and, 601 (V3)
motor innervation of, 599-600 (V3)
Glands of Krause, 581f, 587 (V3)
Glands of Wolfring, 587 (V3)
Glandular odontogenic cyst, 444-445
(V2)
Glasgow Coma Scale, 8, 8t, 38, 39t
(V2)
acute subdural hematoma and, 60
(V2)
epidural hematoma and, 60 (V2)
grading severity of injury and, 52-56,
54f, 54t (V2)
mild closed head injury and, 56-57
(V2)
moderate closed head injury and, 57
(V2)
severe closed head injury and, 57-58
(V2)
traumatic subarachnoid hemorrhage
and, 62 (V2)
Glaucoma, post-traumatic, 81 (V2)
Glenoid fossa, 802, 802f (V2)
Glenoid fossa prosthesis, 796f (V2)
Glial-derived growth factor, chronic
facial pain and, 976 (V2)
Globe dystopia, 88 (V2)
Globe injury
in midface fracture, 254 (V2)
in orbital fracture, 213 (V2)
Globulomaxillary cyst, 451 (V2)
Glogau skin classification, 2, 2t, 248,
249t (V1), 517 (V3)
Glomerular filtration rate, 387 (V3)
Glossopharyngeal nerve evaluation
in chronic orofacial pain, 118 (V1)
in head injury, 52 (V2)
Glossopharyngeal neuralgia, 993-994
(V2)
Glucocorticoid deficiency, 13,
14t (V1)
Glucose, preoperative testing of, 19t
(V1)
Glucose-6-phosphate dehydrogenase
deficiency, 2 (V1)
Glutamate
central sensitization and, 963 (V2)
ketamine and, 62 (V1)
posttraumatic trigeminal neuralgia
and, 155 (V1)
Glycolic acid
for chemical peel, 663 (V3)
for milia, 540 (V3)
for skin preparation in laser skin
resurfacing, 520 (V3)
Glycosaminoglycans, 849 (V2)
Goldenhar syndrome, 298-299, 300-
302f (V3)
Goldman Cardiac Risk Index, 382, 383t
(V3)
Goldman criteria, 3, 3t (V1)
Goldman tip, 565-566, 566f (V3)
Goldman visual field test, 216f (V2)
Gonion to pogonion, 42 (V3)
Goode’s method of nasal projection,
558, 559f, 682t (V3)
Gordon, S.D., 795 (V2)
Gorlin’s syndrome, 433f, 441b, 441-442,
442t, 444f, 725 (V2)
Gout in temporomandibular joint, 865
(V2)
GPCI; See Geographic Practice Cost
Index
Graft recipient site, 419-422, 419-422f
(V1)
Granular cell ameloblastoma, 481f (V2)
Granulation tissue formation, 19-21,
20f (V2), 61 (V3)
Granuloma
central giant cell, 592-594, 593f, 593t
(V2)
peripheral giant cell, 180-181 (V1)
pyogenic gingival, 180, 180f (V1)
Gray line alignment, 310, 311f (V2)
Grayson nasoalveolar molding
appliance, 720, 720f, 783-790 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t (V3)
Great auricular nerve, 668 (V3)
injury in rhytidectomy, 503, 508,
508f (V3)
Greater palatine artery
maxilla and, 63f, 66f, 173f, 175f, 555f
(V3)
Greenstick fracture
mandibular, 142 (V2)
condylar process, 171 (V2)
diagnostic imaging of, 99, 100f
(V2)
nasal, 278 (V2)
Gross collection ratio, 297-298 (V1)
Group practice, 290 (V1)
Growth, defined, 849t (V3)
Growth and development
considerations in pediatric
craniomaxillary surgery, 848-863
(V3)
clinical evaluation of craniofacial
growth and, 856 (V3)
concepts of craniofacial skeletal
growth and development
and, 849f, 849t, 849-850,
850t (V3)
cranio-orbital dysmorphology and,
856-858 (V3)
cranium and, 850-851, 852f (V3)
mandible and, 855-856, 856f, 857f
(V3)
mandibular hyperplasia and, 859-860,
860f (V3)
mandibular hypoplasia and, 858-859,
859f (V3)
maxilla and, 851, 854f, 855f (V3)
maxillary hypoplasia and, 860-861
(V3)
orbits and, 851, 853f (V3)
vertical maxillary excess and, 861f,
861-862 (V3)
zygoma and, 851, 853f (V3)
Growth factors
central sensitization and, 963 (V2)
chronic facial pain and, 976 (V2)
Growth factors (Continued)
in platelet-rich plasma, 501, 503
(V1)
temporomandibular disorders and,
849-850, 850f (V2)
Growth outcomes in cleft palate repair,
769-770, 775 (V3)
GTR; See Guided tissue regeneration
Guided bone regeneration, 428-429
(V1)
platelet-rich plasma and, 505-506
(V1)
Guided tissue regeneration, 428-457
(V1)
for alveolar ridge augmentation
using allograft and xenograft bone
with titanium-reinforced
membrane, 450-451, 450-451f
(V1)
using allograft bone putty and
resorbable collagen
membrane, 448f, 448-449,
449f (V1)
for coronal defects, 436 (V1)
in corticocancellous block
augmentation of posterior
mandible, 452-453, 452-453f
(V1)
for dehiscence defects, 435-436, 447,
447f (V1)
dual-layered technique in, 445f, 445-
446, 446f (V1)
for fenestration defects, 436 (V1)
flapless buccal wall reconstruction in,
443f, 443-444, 444f (V1)
functional and design requirements of
membranes for, 429-431, 431f,
432f (V1)
to reduce postextraction bone loss,
438-440, 454f, 454-455, 455f
(V1)
ridge preservation using high-density
PTFE membrane in, 440-441f,
440-442 (V1)
in sinus-lift subantral augmentation,
463, 463f (V1)
in subantral augmentation, 436-438,
437f (V1)
wound closure in, 431-435, 433f,
434f (V1)
Gum elastic bougie stylet, 31 (V2)
Gunning splint, 140f (V2), 371 (V3)
in mandibular fracture, 391 (V2)
in maxillary/midface fracture, 386
(V2)
Gunshot wound
avulsive injury in, 290, 291f (V2)
reconstruction in avulsive facial
injury, 327-351 (V2)
Abbe flap in, 329, 330f (V2)
aesthetic and prosthetic
rehabilitation and, 346-350f
(V2)
airway management in, 327 (V2)
anterolateral thigh free flap in,
335, 335f (V2)
cervicofacial flap in, 329-330, 333f
(V2)
of cheek defects, 344, 345-348f
(V2)
clinical examination in, 327-328
(V2)
debridement in, 328 (V2)
facial artery musculomucosal flap
in, 329 (V2)
fibular free flap in, 333-335, 335f
(V2)
imaging in, 328 (V2)
of lip defects, 343f, 343-344
(V2)
of lower face and mandible, 335-
340f, 336-337 (V2)
of nasal defects, 337, 343 (V2)
paramedian forehead flap in, 329,
331-332f (V2)
pectoralis major myocutaneous flap
in, 330-331 (V2)
radial forearm flap in, 332-333,
334f (V2)
Gunshot wound (Continued)
rectus abdominis free flap in, 335
(V2)
of scalp defects, 346 (V2)
submental island flap in, 331-332,
334f (V2)
temporoparietal fascia flap in, 330
(V2)
wound assessment in, 317, 328f
(V2)
Gutta percha, 274 (V1)
H
Haas appliance, 224, 225f, 226f 228f,
232f (V3)
Hair
laser-assisted removal of, 251-252
(V1)
radiation therapy-related loss of, 774
(V2)
rhytidectomy and, 501-502, 502f
(V3)
trichophytic forehead and brow lift
and, 612 (V3)
Hair follicle stem cells, 23, 23f (V2)
Hair transplantation, 651-657 (V3)
complications of, 655-656 (V3)
current medical treatment for
alopecia and, 651 (V3)
micrograft and minigraft technique
in, 651-653, 652-655f (V3)
pathophysiology of alopecia and, 651
(V3)
rotational flaps in, 655, 655f, 656f
(V3)
scalp reduction in, 655, 656f (V3)
Halcion; See Triazolam
Halothane, 43, 44t, 64t (V1)
Hand, arterial supply to, 334f (V2)
Hand/palm method of burn estimation,
321 (V2)
Hand-Sch[um]uller-Christian disease,
567 (V2)
Hand-wrist plain film, 856 (V3)
Hangman’s fracture, 63, 64f (V2)
Hanks Balanced Salt Solution, 120,
121f (V2)
Hapsburg jaw, 97, 98f (V3)
Hard equipment in office, 359f, 359-
360, 360f (V1)
Hard palate, 706 (V2)
alveolar distraction and, 349-354,
349-354f (V3)
embryology of, 701-705, 704t (V3)
maxilla and, 173f (V3)
miniimplant for orthodontic
anchorage in, 570-574, 572-574f
(V1)
squamous cell carcinoma of, 716-719
(V2)
surgically assisted maxillary
expansion and, 67f, 67-68, 219-
237 (V3)
clinical evaluation in, 219, 220-
220f, 221f (V3)
complications of, 231-232, 233f
(V3)
incidence and origin of transverse
maxillary deficiency and, 219,
220f (V3)
modification of, 232-233, 234f
(V3)
orthopedic rapid maxillary
expansion and, 224-226, 224-
226f (V3)
radiographic evaluation in, 220-
223, 221-223f (V3)
segmental maxillary osteotomy
versus, 233-235 (V3)
technique in, 227-231, 228-232f
(V3)
Harris-Benedict equation, 15, 45 (V2)
Hashimoto-Pritzker syndrome, 567 (V2)
Haversian remodeling, 62 (V3)
Hawley type retainer, 401, 402f (V3)
Hayflick limit, 662 (V2)
HBO; See Hyperbaric oxygen therapy
HCFAC; See Health Care Fraud and
Abuse Control Program

HCPCS; See Healthcare Common
Procedure Coding System
Head
abnormal shape of, 865-866 (V3)
arteriovenous malformation in, 588-
590, 589f (V2)
embryology of, 697-705, 698f, 700-
704f (V3)
infantile hemangioma-related
structural anomaly of, 577-579,
578f (V2)
resting skin tension lines of, 732,
732f (V2)
secondary survey of, 40 (V2)
Head and neck cancer, 680-788 (V2),
984-993 (V3)
chemotherapy in, 777-788 (V2)
background of, 777, 778f (V2)
epidemiology and, 777 (V2)
epidermal growth factor receptor
blockers and, 782-783, 783t
(V2)
induction, 777-778 (V2)
for metastatic carcinoma, 778-781,
779t, 781t, 782t (V2)
salivary gland cancers and, 783-
785, 785f (V2)
taxanes in, 781-782 (V2)
lymphoma in, 758-766, 759b (V2)
angiocentric, 761-762 (V2)
diagnosis of, 758-759, 759f, 760f
(V2)
Hodgkin’s, 759-760, 760f (V2)
non-Hodgkin’s, 760-761, 761f
(V2)
prognosis of, 763-764, 764b (V2)
radiographic evaluation of, 762f,
762-763 (V2)
treatment of, 763 (V2)
melanoma in, 749-757 (V2)
diagnosis of, 752t, 752-754, 753f,
753t (V2)
epidemiology of, 749, 750b (V2)
incidence and etiology of, 749-750,
750b, 750t, 750-752f, 751t
(V2)
management of regional disease in,
754 (V2)
staging of, 754-755, 755t (V2)
treatment of, 755-756 (V2)
non-melanoma skin cancer in, 724-
748 (V2)
aggressive behavior of, 728-730,
729f (V2)
basal cell carcinoma in, 725, 725f
(V2)
cryotherapy for, 734 (V2)
curettage/electrodesiccation in,
734, 735f (V2)
dermatofibrosarcoma protuberans
in, 727-728, 728f (V2)
epidemiology and etiology of, 724-
725 (V2)
laser ablation and resurfacing in,
734-735 (V2)
of lip, 742-744, 743f (V2)
lymph node involvement in, 737-
739 (V2)
Merkel cell carcinoma in, 727
(V2)
microcystic adnexal carcinoma in,
726-727, 727f (V2)
Mohs’ micrographic surgery in,
735-736, 736b, 736f (V2)
photodynamic therapy for, 741
(V2)
physical examination in, 730t,
730-733, 731b, 731-733t (V2)
radiation therapy in, 741-742 (V2)
sebaceous gland carcinoma in, 727,
727f (V2)
squamous cell carcinoma in, 725-
726, 726f (V2)
staging of, 733-734 (V2)
systemic and topical medications
for, 739-741 (V2)
traditional surgical excision in,
736-737 (V2)
radiation therapy in, 767-776 (V2)
Head and neck cancer (Continued)
altered radiation fractionation
schemes and, 772 (V2)
complications of, 773-774 (V2)
definitive radiotherapy and, 771
(V2)
histologies and, 767-768 (V2)
preoperative and postoperative,
771-772 (V2)
sites of disease and, 768t, 768-771,
769f, 770f, 770t, 771t (V2)
systemic therapy with, 772, 772t
(V2)
techniques in, 772-773, 773f (V2)
reconstruction in, 988-993, 991f,
992f (V3)
rhabdomyosarcoma in, 984-986, 987f
(V3)
salivary gland tumor in, 987-988
(V3)
sarcoma of jaws in, 680-704 (V2)
chondrosarcoma in, 684f, 684-685
(V2)
Ewing’s sarcoma in, 687, 688f, 689f
(V2)
mandibular approaches in, 699-
702, 701f, 702f (V2)
maxillectomy in, 692-699, 694f,
695f, 697-699f (V2)
metastatic tumors to jaw and, 687-
689 (V2)
multiple myeloma and, 685-687,
686f, 687f (V2)
osteosarcoma in, 680-684, 681f,
682f (V2)
patient evaluation in, 689-692,
690t, 691f (V2)
radiation-induced, 685 (V2)
sarcomas in, 986-987, 988-990f (V3)
squamous cell carcinoma in, 705-723
(V2)
anatomy in, 705-706 (V2)
buccal mucosa cancer and, 714-
715, 715f, 716f (V2)
diagnostic adjuncts in, 708-709,
709f (V2)
floor of mouth cancer and, 714,
714f, 715f (V2)
follow-up care in, 719-720 (V2)
genetic abnormalities in, 707-708
(V2)
non-surgical management of, 710-
713 (V2)
pretreatment evaluation in, 710
(V2)
primary tumor and, 713-714 (V2)
retromolar trigone, alveolar ridge,
and palate cancer and, 716-
719 (V2)
risk factors for, 706-707 (V2)
salivary gland cancer and, 549-550,
552f (V2)
screening for, 708 (V2)
staging of, 710, 711t (V2)
tongue cancer and, 716-717, 716-
718f (V2)
types of neck dissection in, 719,
719t, 720f (V2)
Head and neck pain, 136-163 (V1)
characterization and measurement of,
139 (V1)
clinical and laboratory examination
in, 139-140 (V1)
diagnosis of, 139, 139t (V1)
incidence and demographics of, 137
(V1)
musculoskeletal, 142-146 (V1)
fibromyalgia and, 142 (V1)
myofascial pain syndromes and,
143-145 (V1)
temporomandibular arthritis and,
145-146 (V1)
neurologic, 149-158 (V1)
brain stimulation procedures for,
157 (V1)
complex regional pain syndrome
and, 157-158 (V1)
idiopathic and atypical orofacial
pain syndromes and, 158 (V1)
Head and neck pain (Continued)
postherpetic neuralgia and, 151-
152 (V1)
posttraumatic headache and, 152-
153 (V1)
posttraumatic trigeminal neuralgia
and, 154-156 (V1)
surgical treatments for, 156-157
(V1)
trigeminal neuralgia and, 149-151
(V1)
pain definitions and, 137-138, 138t
(V1)
pathophysiology of pain and, 137f,
137-139, 138f (V1)
pharmacologic screening in, 140-141
(V1)
psychiatric disorders and, 141-142
(V1)
sleep dysfunction and, 141 (V1)
systemic disease and, 141 (V1)
vascular, 146-149 (V1)
cluster headache and
trigeminoautonomic variants
and, 148-149 (V1)
migraine and, 146-148, 147f (V1)
orofacial migraine variants and,
149 (V1)
Head breadth, 23 (V3)
Head circumference
abnormal, 865-866 (V3)
neurocranial growth value, 20 (V3)
Head height, 22 (V3)
Head injury, 56-63 (V2)
acute subdural hematoma in, 60, 61t
(V2)
basilar skull fracture in, 59-60 (V2)
chronic subdural hematoma in, 61,
62f (V2)
in cranio-maxillofacial trauma, 8-9
(V2)
diffuse axonal injury in, 62 (V2)
epidural hematoma in, 60, 61f (V2)
frontal sinus fracture in, 256-269
(V2)
classification of, 257-259, 261f (V2)
clinical evaluation in, 256, 258f,
259f (V2)
postoperative care in, 266-268,
268f (V2)
radiologic evaluation in, 256-257,
260f, 261f (V2)
surgical anatomy and, 256, 257f,
258f (V2)
surgical management of, 259-266,
262-269f (V2)
mild closed, 56-57, 57b (V2)
moderate closed, 57 (V2)
nasal fracture in, 270-283, 271f (V2)
anatomy and pathogenesis of, 270-
273, 272f, 273f (V2)
classification of, 275, 275t (V2)
closed reduction in, 276-278, 278f,
279f (V2)
complications of, 281-282 (V2)
diagnosis and evaluation of, 273-
275, 274f (V2)
medical management of, 275 (V2)
open reduction in, 278-281, 280f
(V2)
pediatric, 281 (V2)
ophthalmic consequences of, 74-90
(V2)
carotid cavernous fistula and, 89
(V2)
cranial nerve injury in, 85-86 (V2)
eyelid injuries in, 88 (V2)
globe dystopia in, 88 (V2)
nasolacrimal injuries in, 88-89, 89f
(V2)
nonperforating ocular trauma in,
78-82, 78-82f (V2)
ophthalmic assessment in, 74-78,
75-78f (V2)
orbital fractures in, 86f, 86-88, 87f
(V2)
orbital injury in, 83-85, 84f (V2)
penetrating ocular trauma in, 83,
83f (V2)
INDEX I-41
Head injury (Continued)
pediatric, 352-373 (V2)
child abuse and, 372 (V2)
craniofacial growth and
development and, 352-353,
353f (V2)
dentoalveolar fractures in, 363-364
(V2)
epidemiology of, 353-354 (V2)
frontal bone and superior orbital
fractures in, 355 (V2)
frontal sinus and frontobasilar
injuries in, 355, 356-357f
(V2)
mandibular body and angle
fractures in, 364 (V2)
mandibular condyle fractures in,
364-369, 369f (V2)
midface fractures in, 363 (V2)
nasal fractures and, 362-363 (V2)
naso-orbito-ethmoid fractures in,
355-360, 358-359f (V2)
orbital fractures in, 360-361, 360-
361f (V2)
perioperative management of, 354-
355 (V2)
prevention of, 354 (V2)
rigid internal fixation and, 369-370
(V2)
Risdon cable and, 370f, 370-372
(V2)
surgical anatomy in, 353 (V2)
symphyseal and parasymphyseal
mandibular fractures in, 364,
365-367f (V2)
zygomaticomaxillary complex
fractures in, 361-362, 362-
363f (V2)
penetrating, 42 (V2)
scalp injury in, 58-59 (V2)
severe closed, 57-58 (V2)
skull fracture in, 59 (V2)
traumatic intracerebral hematoma/
cerebral contusion in, 61-62 (V2)
traumatic intraventricular
hemorrhage in, 63 (V2)
traumatic subarachnoid hemorrhage
in, 62 (V2)
Head length, 21 (V3)
Head posture, orthognathic surgery-
related changes in, 75 (V3)
Headache
after frontal sinus fracture repair, 268
(V2)
cervicogenic, 143 (V1)
cluster, 148-149 (V1)
migraine, 146-148, 147f (V1)
orofacial migraine variants, 149 (V1)
posttraumatic, 152-153 (V1)
tension-type, 148 (V1)
Healing
after laser skin resurfacing, 250 (V1)
of bone graft in implant surgery, 424,
425f (V1)
effects of aging on, 377-378, 378f
(V2)
effects of smoking on, 71 (V1)
of extraction socket, 540-541 (V1)
laser therapy and, 253 (V1)
of mandibular fracture, 144-146,
146f, 147f (V2)
in orthognathic surgery, 60-71, 403t,
403-408 (V3)
airway obstruction and, 404 (V3)
bone healing and, 62 (V3)
categorization of, 62 (V3)
genioplasty and, 71 (V3)
Le Fort 1 osteotomy and, 63-68,
64-67f (V3)
mandibular osteotomy and, 68-70f,
68-71 (V3)
maxillary surgery and, 62-63, 63f
(V3)
phases of, 60-62, 61f, 62f (V3)
psychological factors in, 404 (V3)
swelling and ecchymosis and, 403-
404 (V3)
platelet-rich plasma for, 501-510
(V1)
I-42 INDEX
Healing (Continued)
allograft and alloplastic materials
and, 504f, 504-506 (V1)
benefits of, 502-503 (V1)
case report of, 509, 509f (V1)
concept of, 501-502, 502f (V1)
processing of, 506-508, 507f, 508f
(V1)
by secondary intention in skin
cancer, 735, 735f, 738 (V2)
of traumatic injuries, 17-24 (V2)
aberrant bone healing in, 22-23
(V2)
abnormal wound healing in, 22
(V2)
bone regeneration in, 22 (V2)
coagulation and, 17, 18f (V2)
dentoalveolar, 133-135, 134f, 135f
(V2)
formation of granulation tissue
and, 19-21, 20f (V2)
future directions in, 23, 23f (V2)
inflammation and, 17-19, 19f (V2)
neural control of, 21 (V2)
prevention of infection in, 21-22
(V2)
remodeling phase and, 21f, 21
(V2)
wound repair phases in, 17, 18f
(V2)
Health Care Fraud and Abuse Control
Program, 371 (V1)
Health Care Quality Improvement Act,
316 (V1)
Health Insurance Portability and
Accountability Act
compliance with, 302 (V1)
risk management and, 384 (V1)
Healthcare Common Procedure Coding
System, 368 (V1)
Hearing loss
in craniofacial dysostosis syndromes,
882 (V3)
in oculoauriculovertebral spectrum,
930 (V3)
in Treacher Collins syndrome, 938-
939 (V3)
Heart
cardiotoxicity of local anesthetics, 47
(V1)
of child, 93-94, 94t (V1)
effects of thyroid disorders on, 13t
(V1)
preoperative cardiac assessment, 2-3,
3t, 4f, 5t (V1)
Heart disease
ambulatory orthognathic surgery and,
493 (V3)
use of vasoconstrictors with local
anesthetics and, 41, 44, 44b (V1)
Heart rate, age-related values, 94t (V1)
Heating, ventilation, and air
conditioning in office, 360 (V1)
Helical crus of external ear, 667f (V3)
Helical defect, 297f (V2)
Hemangioma, 577 (V2)
congenital, 579f, 579-581, 580f (V2)
infantile, 577-579, 578f (V2)
laser therapy for, 251 (V1)
management of, 580-581 (V2)
of temporomandibular joint, 869-870
(V2)
Hemarthrosis in condylar fracture, 168
(V2)
Hematocrit, 387 (V3)
Hematologic disorders, 384-385 (V3)
Hematologic system
effects of thyroid disorders on, 13t
(V1)
intensive care of trauma patient and,
46 (V2)
preoperative evaluation of, 14-17, 14-
17t, 15f (V1)
Hematoma, 442-443 (V3)
after repair of zygomatic fracture, 195
(V2)
auricular, 9 (V2)
in bilateral sagittal split osteotomy,
113 (V3)
Hematoma (Continued)
in ear laceration, 310, 313f (V2)
in endoscopic forehead and brow lift,
606 (V3)
epidural, 60, 61f (V2)
exodontia-related, 219 (V1)
injectable facial filler and, 643, 643f
(V3)
local anesthetic-related, 47 (V1)
in orbital fracture, 212f, 212-213
(V2)
in otoplasty, 675-676 (V3)
in rhinoplasty, 573-577 (V3)
in rhytidectomy, 507, 507f (V3)
septal, 273-274, 274f, 281-282 (V2)
subdural
acute, 60, 61f (V2)
chronic, 61, 62f (V2)
third nerve palsy and, 85-86 (V2)
Hemidesmosomal epidermolysis bullosa,
626-627 (V2)
Hemifacial microsomia, 859f (V3)
facial asymmetry in, 298-299, 300-
302f (V3)
model surgery and, 370-371 (V3)
in oculoauriculovertebral spectrum,
922-925 (V3)
in Treacher Collins syndrome, 942,
943f (V3)
Hemimandibular elongation, 285-291,
289-291f (V3), 868 (V2)
bilateral sagittal split osteotomy for,
99t, 99-102, 102f, 104-105f (V3)
model surgery and, 370-371 (V3)
transoral vertical ramus osteotomy
for, 121, 122f (V3)
Hemimandibular hyperplasia, 285-291,
289-291f (V3)
Hemimaxillectomy, miniimplant-
retained obturators and, 568-569
(V1)
Hemiparesis, 51 (V2)
Hemitransfixion incision in rhinoplasty,
561 (V3)
Hemoglobin, 19t (V1)
Hemophilia
perioperative management of, 385
(V3)
preoperative evaluation of, 16 (V1)
Hemorrhage
intra-abdominal, 65-67, 66f,
67f (V2)
intraventricular, 63 (V2)
postoperative, 442-443 (V3)
arthroscopic-related, 926 (V2)
in arthrotomy, 940 (V2)
in bilateral sagittal split osteotomy,
115, 115b (V3)
exodontia-related, 219 (V1)
in genioplasty, 439 (V3)
in intraoral vertical ramus
osteotomy, 435, 435f (V3)
in Le Fort I osteotomy, 185-186
(V3)
in sagittal split ramus osteotomy,
429-431, 433f (V3)
retrobulbar
after repair of zygomatic fracture,
198-199 (V2)
traumatic, 84, 84f (V2)
subarachnoid
traumatic, 62 (V2)
vitreous hemorrhage with, 82, 82f
(V2)
subconjunctival, 78, 83, 83f (V2)
in trauma, 6t, 6-7, 37-38, 38t (V2)
vitreous, 82, 82f, 213 (V2)
Hemorrhagic bone cyst, 869 (V2)
Hemorrhagic shock, 6-7, 7t, 37-38, 38t
(V2)
Hemothorax, 36, 42 (V2)
Hemotympanum, 59 (V2)
Henderson-Hasselbalch equation, 38
(V1)
Heparin
preoperative evaluation of, 17, 17t
(V1)
prophylactic, 383 (V2)
Hepatic disorders, 9, 10f, 10t (V1)
Hereditary ectodermal dysplasia, 177f,
177-178, 181 (V1)
Herlitz’s type epidermolysis bullosa,
626-627 (V2)
Herpangina, 617t, 617-618 (V2)
Herpes simplex virus infection, 612-
617, 613f (V2)
injectable facial filler and, 644f (V3)
laser resurfacing and, 517, 520, 541,
541f (V3)
oral cavity cancer and, 706 (V2)
oral mucositis and, 785 (V2)
pediatric, 615-617 (V2)
primary herpetic gingivostomatitis in,
612-613, 613f (V2)
secondary herpes in, 613-614 (V2)
systemic agents for, 614-615 (V2)
Herpes zoster infection
neuropathic orofacial pain in, 994
(V2)
postherpetic neuralgia and, 151-152
(V1)
Herpetiform aphthae, 620 (V2)
Hertel exophthalmometry in orbital
fracture, 220, 220f (V2)
Heteroaryl acetic acids, 84t (V1)
Heterotopic bone formation in
temporomandibular joint, 874-875
(V2)
Hexafluoropropylene suture, 287t (V2)
Hidrotic form hereditary ectodermal
dysplasia, 177 (V1)
Hierarchy of stability in Le Fort I
osteotomy, 184 (V3)
High condylectomy, 285, 288f (V3)
High-density polytetrafluoroethylene
membrane, 429 (V1)
in alveolar ridge augmentation, 450f,
450-451, 451f (V1)
in corticocancellous block
augmentation of posterior
mandible, 452f, 452-453, 453f
(V1)
in dual-layered guided socket
regeneration technique, 445f,
445-446, 446f (V1)
in flapless buccal wall reconstruction,
443f, 443-444, 444f (V1)
in open technique in guided bone
regeneration in extraction site,
454f, 454-455, 455f (V1)
postoperative considerations in, 432
(V1)
ridge preservation and, 440-441f,
440-442 (V1)
selection rationale for, 432-435, 433f,
434f (V1)
wound closure in, 431 (V1)
High-grade malignant tumor of parotid,
549-550, 552f (V2)
Hinderer analysis for malar implant,
690t (V3)
Hinge articulator in model surgery, 364-
365, 365f (V3)
HIPAA privacy and security
compliance with, 302 (V1)
risk management and, 384 (V1)
Hiring and firing employee, 322 (V1)
Histamine
chronic facial pain and, 962, 963f
(V2)
opiates and opioids stimulation of,
59-60 (V1)
wound repair and, 18, 18f (V2)
Histiocytosis X, 567 (V2)
Histology
in Le Fort 1 osteotomy, 64, 64f, 65f
(V3)
of skin, 10f (V3)
History
in abnormal head shape, 856 (V3)
in ankylosis, 903 (V2)
in blepharoplasty, 587 (V3)
in cervicofacial liposuction, 620 (V3)
in chronic orofacial pain, 112-113
(V1)
in condylar fracture, 167-168 (V2)
in craniomaxillofacial trauma, 8, 49
(V2)
History (Continued)
in dentoalveolar injury, 105-107
(V2)
for exodontia treatment planning,
187 (V1)
in internal derangement of
temporomandibular joint, 929-
930 (V2)
in laser skin resurfacing, 517 (V3)
in maxillofacial tumor, 689 (V2)
in ophthalmic assessment, 74 (V2)
in orbital fracture, 207-208 (V2)
in pediatric preanesthetic assessment,
97 (V1)
potential nerve injuries and, 278
(V1)
in preanesthetic assessment, 69 (V1)
preoperative, 1-2, 2t (V1)
in rhytidectomy, 497-498 (V3)
in temporomandibular joint
hypomobility, 898, 899b (V2)
in zygomatic fracture, 183b, 183-184,
184f (V2)
HMB-45 immunohistochemical marker
for melanoma, 752t (V2)
Hodgkin cell, 759, 760f (V2)
Hodgkin’s lymphoma, 759-760, 760f,
767 (V2)
Holdaway technique for determining
chin position, 683t (V3)
Holmium:YAG laser
in arthroscopic temporomandibular
joint surgery, 246-247 (V1)
in synovial surgery, 247 (V1)
Horizontal impaction of third molar,
206, 209f (V1)
Horizontal maxillary bone transport,
360, 362f (V3)
Horizontal maxillary deficiency,
combined maxillary and
mandibular osteotomies for, 238-
247 (V3)
indications for, 238-239 (V3)
mandibular excess and, 244f, 244-
245, 245f (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
Horizontal proportions of face, 4 (V3)
ear, 8f (V3)
nose, 7f (V3)
perioral, 8f (V3)
periorbital, 5f (V3)
Horizontal ramus osteotomy, 963, 963f
(V3)
Hormones
implant dentistry pharmacology and,
398-399, 399t (V1)
surgery-related imbalance of, 408
(V3)
Horner’s muscle, 227f (V2)
Hospital privileging, 307-317 (V1)
accreditation and certification and,
308-309 (V1)
adverse action in, 315-316 (V1)
appointment to medical staff in, 314-
315 (V1)
credentialing and, 313-314, 314f
(V1)
definitions and resources in, 309-313,
310-313t (V1)
specialty board certification and, 308
(V1)
Hounsfield unit, 839 (V2)
Human chromosome, 648 (V2)
Human growth hormone, bone
development and, 398 (V1)
Human immunodeficiency virus
infection, 543 (V2)
Human mesenchymal stem cell, 389,
389t (V1)
Human papillomavirus, oral cavity
cancer and, 706-707, 777 (V2)
Human resources, office management
and, 290b, 290-291, 291-294t (V1)

Hundshuck technique in bilateral
sagittal split osteotomy, 87, 88f,
106, 107t (V3)
Hutchinson pupil, 86 (V2)
Hutchinson’s sign, 613 (V2)
Hyaluronic acid for facial augmentation,
629 (V3)
Hybrid or base plus bonus model of
compensation, 298-299, 299t (V1)
Hydrocephalus
in craniofacial dysostosis syndromes,
881 (V3)
in craniosynostosis, 864-865 (V3)
Hydrocodone
for acute postoperative pain, 81t, 82
(V1)
for chronic facial pain, 972, 973t
(V2)
in complicated exodontia, 207t (V1)
for temporomandibular disorders,
887t, 888t (V2)
Hydrocortisone
preoperative, 14t (V1)
for prolonged erythema in laser skin
resurfacing, 537 (V3)
Hydromorphone
for chronic facial pain, 972t (V2)
for temporomandibular disorders,
888t (V2)
Hydroquinone
as skin lightener, 250 (V1)
for skin preparation in laser skin
resurfacing, 520 (V3)
Hydroxydaunorubicin, 763 (V2)
Hydroxyurea, 781t (V2)
Hydroxyzine, 889t (V2)
Hygiene, postoperative, 410-411, 411f
(V3)
Hylaform, 630 (V3)
Hyoid advancement for obstructive
sleep apnea syndrome, 316 (V3)
Hyoid bone, 8 (V3)
Hyperalgesia, 140 (V1), 966t (V2)
in posttraumatic trigeminal neuralgia,
154 (V1)
in trigeminal nerve injury, 262f, 263-
264 (V1)
Hyperbaric oxygen therapy
in ear laceration, 310 (V2)
for osteomyelitis, 638, 638b (V2)
in osteoradionecrosis, 639-641 (V2)
in total maxillary segmental
osteotomy, 198 (V3)
Hyperesthesia, 966t (V2)
in posttraumatic trigeminal neuralgia,
154 (V1)
in trigeminal nerve injury, 262f, 263
(V1)
in trigeminal traumatic neuralgia,
264-265 (V1)
Hyperglycemia, 72 (V1)
Hyperkalemia, 387 (V3)
Hyperkeratosis, 245 (V1)
Hypermobility of temporomandibular
joint, 905b, 905-908f, 905-909 (V2)
Hypernasal speech
after cleft surgery, 793 (V3)
after maxillary advancement, 822-
826 (V3)
revision surgery for, 835-836 (V3)
Hyperparathyroidism, 594f, 594-595
(V2)
Hyperpathia, 140 (V1), 966t (V2)
in trigeminal nerve injury, 262f, 263
(V1)
Hyperpigmentation, laser skin
resurfacing and, 250 (V1)
postoperative complication in, 541-
542, 542f (V3)
preoperative evaluation of, 518 (V3)
Hyperplasia
condylar
model surgery and, 370-371 (V3)
postoperative, 414 (V3)
unilateral, 284-285, 286-288f (V3)
defined, 849t (V3)
hemimandibular, 285-291, 289-291f
(V3)
mandibular; See Mandibular excess
Hypersensitivity to local anesthetics, 48
(V1)
Hypertension
in geriatric patient, 381-382 (V2)
trigeminal neuralgia and, 991 (V2)
Hyperthyroidism
in geriatric patient, 384 (V2)
preoperative evaluation of, 12, 13t
(V1)
Hypertrophic orbicularis oculi, 579
(V3)
Hypertrophic scarring, 22 (V2)
in eyelid avulsive laceration, 311f
(V2)
in laser skin resurfacing, 250 (V1),
542-543, 543f (V3)
in otoplasty, 676 (V3)
in rhytidectomy, 509, 509f (V3)
Hypertrophy
defined, 849t (V3)
hemimandibular
bilateral sagittal split osteotomy
for, 99t, 99-102, 103f (V3)
model surgery and, 370-371 (V3)
Hyperventilation in head-injured
patient, 49 (V2)
Hyphema, 79f, 79-80 (V2)
in orbital fracture, 213 (V2)
Hypoalgesia, 966t (V2)
Hypoesthesia, 966t (V2)
in trigeminal nerve injury, 262f, 263,
264 (V1)
Hypoglossal nerve
chronic orofacial pain and, 118 (V1)
head injury and, 52 (V2)
injury in resection of lymphatic
malformation, 582 (V2)
Hypoglycemia, 383 (V2)
Hypomobility of temporomandibular
joint, 898-905 (V2)
ankylosis and, 901-905 (V2)
in bilateral sagittal split osteotomy,
112 (V3)
complications of, 905 (V2)
imaging in, 898 (V2)
postoperative, 414, 445 (V3)
pseudoankylosis and, 899-901 (V2)
treatment of, 905 (V2)
trismus and, 898-899 (V2)
Hyponasality after cleft surgery, 793
(V3)
Hypopharyngeal cancer, 770, 771t (V2)
Hypopigmentation, laser skin
resurfacing and, 250 (V1)
postoperative complication in, 541-
542, 543f (V3)
preoperative evaluation of, 518 (V3)
Hypoplasia
mandibular; See Mandibular
deficiency
maxillary; See Maxillary deficiency
Hypopnea, 318 (V3)
Hypotension, 6, 37-38, 38t, 49 (V2)
Hypotensive anesthesia
for blood loss management, 392 (V3)
in total maxillary segmental
osteotomy, 193 (V3)
Hypothermia
child and, 355 (V2)
during ICU resuscitation, 71 (V2)
trauma and, 39, 39f (V2)
Hypothyroidism
in geriatric patient, 384 (V2)
preoperative evaluation of, 12-13, 13t
(V1)
Hypotony, 81 (V2)
Hypovolemia, 387 (V3)
Hypoxia, 49, 70 (V2)
Hyrax appliance, 224, 225f (V3)
H-zone, 728 (V2)
I comminuted, complicated, and
Iatrogenic facial asymmetry, 294 (V3)
Ibandronate, 395, 396t (V1), 558t
(V2)
Ibuprofen, 84t, 86t (V1)
for acute postoperative pain
in complicated exodontia, 207t
(V1)
Ibuprofen (Continued)
in sinus-lift subantral
augmentation, 462 (V1)
bone healing and, 394 (V1)
for chronic facial pain, 972, 973t
(V2)
for myofascial pain, 144 (V1)
for neuropathy secondary to neuritis,
1000 (V2)
for temporomandibular disorders, 130
(V1), 887t (V2)
for temporomandibular osteoarthritis,
146 (V1)
ICD-10; See International Classification of
Diseases
Ice for topical anesthesia, 50 (V1)
ICP; See Increased intracranial pressure
Ideal weight, 391 (V3)
Idiopathic bone cavity cyst, 869 (V2)
Idiopathic condylar resorption, 299-305,
303-304f, 306f (V3)
after mandibular surgery, 453-454
(V3)
Idiopathic condylysis, 299-305, 303-
304f, 306f (V3)
postoperative, 414, 415f (V3)
Idiopathic facial pain, 158 (V1)
Idiopathic orofacial pain syndromes,
149, 158 (V1)
Idiopathic trigeminal neuralgia, 149-
151 (V1)
Ifosfamide, 781t (V2)
Ilium for bone graft
harvesting of, 415-419, 415-419f (V1)
in sinus-lift subantral augmentation,
468-469, 469f (V1)
Image, marketing and, 331, 331f (V1)
Imaging
of abnormal head shape, 856 (V3)
in ankylosis, 903 (V2)
in assessment of trauma patient, 41,
67 (V2)
in avulsive facial trauma, 328 (V2)
in cervical spine injury, 63 (V2)
in chronic facial pain, 118, 119f, 120f
(V1), 965-966 (V2)
in condylar hyperplasia, 285 (V3)
in dentoalveolar injury, 102, 102f,
109-110, 110f (V2)
documentation of, 382 (V1)
in facial asymmetry, 274-275 (V3)
in adolescent internal condylar
resorption, 305, 306f (V3)
in autoimmune and connective
tissue diseases, 309, 312-313f
(V3)
in condylar dislocation, 281, 281f
(V3)
in condylar hyperplasia, 285 (V3)
developmental, 282 (V3)
in dystonia, 281, 281f (V3)
in hemifacial microsomia, 299,
302f (V3)
iatrogenic, 294 (V3)
infection-related, 282 (V3)
in malocclusion, 278, 279-280f
(V3)
in neuromuscular disorders, 292
(V3)
in osteochondroma or osteoma of
mandible, 291, 291f (V3)
in temporomandibular joint
ankylosis, 297, 298f (V3)
tumor-related, 293, 293f (V3)
unilateral dentoalveolar asymmetry
and, 282 (V3)
in unilateral reactive arthritis,
305-306, 309f (V3)
in facial injuries, 91-92, 98-99 (V2)
in fractures
angle of mandible, 101, 101f (V2)
impacted fractures of face, 99,
99f (V2)
in complications of treatment of
mandibular fracture, 102-103
(V2)
computed tomography in, 98-99
(V2)
INDEX I-43
Imaging (Continued)
condylar, 100f, 100-101, 168-170,
169f (V2)
coronoid process and ramus, 101
(V2)
frontal sinus, 256-257, 260f, 261f
(V2)
greenstick and pathologic, 99, 100f
(V2)
mandibular body, 101, 102f (V2)
mandibular symphysis and
parasymphysis, 101, 102f (V2)
midface, 241f, 241-242, 242f (V2)
nasal, 274f, 274-275 (V2)
naso-orbital-ethmoid, 246 (V2)
orbital, 209-211, 210f, 211f (V2)
simple and compound, 99, 99f
(V2)
zygomatic, 184-185, 185f (V2)
in head injury, 56, 57b (V2)
acute subdural hematoma and, 60,
61f (V2)
epidural hematoma and, 60, 61f
(V2)
mild closed, 56-57 (V2)
moderate closed, 57 (V2)
severe closed, 57-58 (V2)
traumatic subarachnoid
hemorrhage and, 62 (V2)
in implant surgery, 407, 408, 408f,
547-566 (V1)
computed tomography in, 552-564,
553-565f (V1)
cone beam technology and, 554,
563-564, 564f, 565f (V1)
digital radiography in, 549-550,
551f (V1)
history of, 552-554, 553f, 554f
(V1)
linear tomography in, 552 (V1)
for maxillary sinus augmentation,
561-563, 562f, 563f (V1)
orthopantomogram in, 551-552,
552f, 553f (V1)
plain films in, 549-551f (V1)
principles for, 547-548, 548f, 549f
(V1)
rapid prototyping and, 555-557,
555-557f (V1)
reformatting software program and,
557-561, 557-562f (V1)
subtraction radiography in, 551
(V1)
three-dimensional modeling and,
554-556, 554-556f (V1)
zygomatic implant and, 492, 492f
(V1)
mandibular anatomy and, 96 (V2)
mandibular series in, 96-98, 97f (V2)
in mandibular trauma, 96-99, 97f,
99f, 145f, 146f (V2)
midfacial anatomy and, 91, 92f (V2)
in obstructive sleep apnea syndrome,
319-321, 320-322f (V3)
for occult vascular injuries, 69, 70f
(V2)
in orbital trauma, 86, 86f (V2)
in osteomyelitis, 634f, 634-635, 635f
(V2)
in osteoradionecrosis, 639, 640f (V2)
panoramic radiography in, 98, 99f
(V2)
of pediatric impacted teeth, 166-168f,
167 (V1)
rendering techniques in, 92-94, 93-
95f (V2)
in soft tissue trauma to neck, 94-95,
96f (V2)
supplemental radiographs in, 98 (V2)
techniques in, 91-92, 92f, 92t (V2)
in temporomandibular disorders, 821-
823, 821-823f, 835-841 (V2)
advanced modalities in, 839 (V2)
in anterior disc displacement, 819
(V2)
computed tomography in, 839-840,
840f, 841f (V2)
cone beam computed tomography
in, 843, 845f, 846f (V2)
I-44 INDEX
Imaging (Continued)
conventional, 835-836 (V2)
functional, 843-845 (V2)
fusion, 845 (V2)
in internal derangement of
temporomandibular joint,
931, 932f (V2)
lateral oblique views in, 837, 837f
(V2)
linear tomography in, 838 (V2)
magnetic resonance imaging in,
840-841, 842-843f (V2)
multidirectional tomography in,
838-839 (V2)
panoramic radiography in, 837-
838, 838f (V2)
reverse Towne’s projection in, 836,
837f (V2)
submentovertex projection in, 837,
837f (V2)
in temporomandibular joint
hypomobility, 898 (V2)
transcranial radiography in, 836,
836f (V2)
transmaxillary or transorbital
radiography in, 836, 836f
(V2)
tuned aperture computed
tomography in, 841-843, 844f
(V2)
ultrasonography in, 846 (V2)
three-dimensional computer-assisted
prediction and, 377-379, 378f
(V3)
in three-dimensional radiation
treatment planning, 772-773,
773f (V2)
in transverse maxillary deficiency,
220-223, 221-223f (V3)
in trigeminal neuralgia, 991 (V2)
in tumors
Ewing’s sarcoma, 687, 688f (V2)
lymphoma, 762f, 762-763 (V2)
maxillofacial, 690, 691f (V2)
odontogenic, 467 (V2)
oral cavity cancer, 710 (V2)
osteosarcoma, 680, 681f,
682f (V2)
pediatric craniomaxillofacial, 961-
962 (V3)
skin cancer, 732-733, 733f (V2)
Imbrication in rhytidectomy, 504, 504f,
505f (V3)
Imipramine
for complex regional pain syndrome,
158 (V1)
for neuropathic orofacial pain, 999t
(V2)
for temporomandibular disorders,
889t (V2)
Imiquimod, 741 (V2)
Immediate implant loading, 511-524
(V1)
benefits of, 522-524, 542 (V1)
contraindications for, 542 (V1)
in edentulous jaw, 518-521, 519-524f
(V1)
following tooth extraction, 540-546
(V1)
adaptive morphology of maxillary
alveolar process and, 541
(V1)
atraumatic extraction techniques
and, 541, 542f (V1)
bone loss following extraction and,
541, 541f (V1)
classification of extraction
socket defects and, 541,
543f (V1)
clinical situations for, 542-544,
544f, 545f (V1)
healing of extraction socket and,
540-541 (V1)
impressions at implant placement
and, 525-539 (V1)
concept of, 531 (V1)
history of immediate loading and,
525-527, 526b, 526f, 527f
(V1)
Immediate implant loading (Continued)
immediate extraction, implant
placement, and provisional
restoration and, 534f, 534-
535, 535f (V1)
immediate provisionalization and,
528-531, 530-531f (V1)
prefabricated ceramic abutments
and temporary crowns and,
536f, 536-537, 537f (V1)
primary bone-level impressions
and, 527-528, 529f, 530f (V1)
second-stage surgery and, 532f,
532-533, 533f (V1)
for single tooth or partially
edentulous restoration, 511-517,
512-518f (V1)
Immediate provisionalization, 528-531,
530-531f (V1)
Immobilization
in bone graft for implant, 422 (V1)
continuous passive motion versus,
851-852, 853f, 854f (V2)
Immortalization of cancer cell, 662-664,
663f (V2)
Immune system
cancer and, 645 (V2)
effects of aging on, 378 (V2)
preoperative evaluation of, 18-19 (V1)
Immunohistochemical markers for
melanoma, 752, 752t (V2)
Immunohistochemistry, 415f, 415-416,
416f (V2)
Immunosuppressed patient
antiyeast medications for, 410 (V3)
perioperative management of, 387-
388 (V3)
Immunotherapy for oral cavity cancer,
713 (V2)
Impacted fracture, mandibular, 99, 142
(V2)
Impacted teeth
angulation classification of, 204f (V1)
basic exodontia for, 185-192 (V1)
complications in, 191-192 (V1)
diagnosis and treatment planning
in, 187 (V1)
indications for, 186-187 (V1)
pain management in, 192 (V1)
principles of, 187-190, 188-190f
(V1)
socket preservation and wound
closure in, 190-191 (V1)
complicated exodontia for, 192-210
(V1)
bone removal in, 193-194, 194f
(V1)
canines, 196-197, 197-199f (V1)
flap design in, 192-193, 193f, 194f
(V1)
general principles of, 192 (V1)
impacted teeth other than third
molars, 195-196 (V1)
indications for, 192b (V1)
premolars, 197-199, 200f (V1)
sectioning of teeth and removal in,
194-195, 195f, 196f (V1)
teeth located in uncommon
anatomic positions, 200-201,
201f (V1)
wound closure in, 201 (V1)
pediatric, 165-173 (V1)
advances in orthodontic anchorage
and, 172 (V1)
autotransplantation versus
extraction in, 171-172 (V1)
etiology of, 166f, 166 (V1)
evaluation of, 166-167, 167f, 168f
(V1)
incidence of, 165-166 (V1)
incisors, 171 (V1)
maxillary canines, 167-170, 169f,
170f (V1)
molars, 171 (V1)
odontomas and, 173 (V1)
premolars, 170-171, 171f (V1)
supernumerary teeth, 172-173,
173f (V1)
treatment options for, 167 (V1)
Impacted teeth (Continued)
third molar, 201-210 (V1)
bone removal and tooth sectioning
in, 205-206, 207-210f (V1)
classification of, 203, 204f (V1)
indications and contraindications
for, 202-203 (V1)
instrumentation for, 203, 203t
(V1)
mandibular, 203-205, 205b, 206f
(V1)
mandibular fracture in bilateral
sagittal split osteotomy and,
114-115 (V3)
maxillary, 207, 208-210f (V1)
outpatient surgery and, 494 (V3)
postoperative instructions in, 208-
210, 209b (V1)
preoperative management in, 207t,
207-208, 208b (V1)
removal-related trigeminal nerve
injury in, 276-278 (V1)
trigeminal nerve injury and, 276
(V1)
wound closure in, 206-207 (V1)
Implant repositioning osteotomy, 473,
474f (V1)
Implant surgery, 387-574 (V1)
alveolar distraction in, 349-354, 349-
354f (V3)
autogenous bone grafting in, 406-427
(V1)
bone biology and, 406-407, 407f
(V1)
graft recipient site and, 419-422,
419-422f (V1)
ilium for, 415-419, 415-419f (V1)
mandibular ramus for, 412-414,
412-414f (V1)
mandibular symphysis for, 409-411,
410-412f (V1)
maxillary tuberosity for, 409, 409f,
410f (V1)
onlay bone graft and, 424, 424f,
425f (V1)
patient preparation for, 409 (V1)
preoperative evaluation in, 407-
408, 408f, 409f (V1)
sinus bone grafting and, 422-424,
423f (V1)
tibia for, 414f, 414-415, 415f (V1)
chronic facial pain after, 968 (V2)
facial, 678-696 (V3)
chin position analyses and, 681-
683t (V3)
for facial skin laxity with weight
loss, 686-688, 686-688f (V3)
injectable facial fillers and, 691f,
691-692, 692f (V3)
for large nose and small chin, 679f,
679-684, 680f, 684f, 685b,
685f (V3)
lip implant in, 693-694, 694f
(V3)
malar cheek implant in, 689f, 689-
690, 690f, 690t (V3)
patient selection for, 678 (V3)
thread lifts and, 695, 695t (V3)
guided tissue regeneration in, 428-
457 (V1)
for augmentation using allograft
and xenograft bone with
titanium-reinforced
membrane, 450-451, 450-451f
(V1)
for augmentation using allograft
bone putty and resorbable
collagen membrane, 448f,
448-449, 449f (V1)
for coronal defects, 436 (V1)
for corticocancellous block
augmentation of posterior
mandible, 452-453, 452-453f
(V1)
for dehiscence defects, 435-436,
447, 447f (V1)
dual-layered technique in, 445f,
445-446, 446f (V1)
for fenestration defects, 436 (V1)
Implant surgery (Continued)
flapless buccal wall reconstruction
in, 443f, 443-444, 444f (V1)
functional and design requirements
of membranes for, 429-431,
431f, 432f (V1)
to reduce postextraction bone loss,
438-440, 454f, 454-455, 455f
(V1)
ridge preservation using high-
density PTFE membrane in,
440-441f, 440-442 (V1)
in subantral augmentation, 436-
438, 437f (V1)
wound closure in, 431-435, 433f,
434f (V1)
immediate implant loading in, 511-
524 (V1)
benefits of, 522-524 (V1)
in edentulous jaw, 518-521, 519-
524f (V1)
following extraction, 540-546, 541-
545f (V1)
history of, 525-527, 526b, 526f,
527f (V1)
for single tooth or partially
edentulous restoration, 511-
517, 512-518f (V1)
impressions at implant placement
and, 525-539 (V1)
concept of, 531 (V1)
immediate extraction, implant
placement, and provisional
restoration and, 534f, 534-
535, 535f (V1)
immediate provisionalization and,
528-531, 530-531f (V1)
prefabricated ceramic abutments
and temporary crowns and,
536f, 536-537, 537f (V1)
primary bone-level impressions
and, 527-528, 529f, 530f (V1)
second-stage surgery and, 532f,
532-533, 533f (V1)
laser-assisted, 245-246 (V1)
lingual nerve injury in, 275-276 (V1)
miniimplants in, 567-574, 568f (V1)
for orthodontic anchorage, 570-
574, 572-574f (V1)
for pontic support of fixed partial
denture, 568 (V1)
for retention of obturators, 568-
569 (V1)
for single-tooth implant restoration
in narrow space, 569, 570f,
571f (V1)
for stabilization of complete
dentures, 567-568, 569f (V1)
for stabilization of removable
partial dentures, 568 (V1)
osteoperiosteal flap and, 471-478
(V1)
alveolar repositioning osteotomies
and, 473, 473f, 474f (V1)
alveolar split graft and, 471, 473f
(V1)
alveolar width distraction
osteogenesis and, 474-477,
475-478f (V1)
interpositional bone graft and, 471,
472f (V1)
pediatric, 181-183, 182f,
183f (V1)
pharmacology for, 387-405 (V1)
antibiotic prophylaxis and, 387-
388, 388b (V1)
antibiotics added to bone grafting
materials and, 388-390, 389t,
390t (V1)
bioactive fatty acids and bone
development and, 399-400
(V1)
bisphosphonates and, 395-398,
396t, 397t (V1)
mineral, hormonal, and vitamin
supplements and, 398-399,
399t (V1)
NSAIDS and bone development
and, 392-395 (V1)

Implant surgery (Continued)
periimplantitis and, 390-392, 391t
(V1)
platelet-rich plasma and bone
grafting in, 501-510 (V1)
allograft and alloplastic materials
and, 504f, 504-506 (V1)
benefits of, 502-503 (V1)
bone healing and, 394, 503f, 503-
504 (V1)
case report of, 509, 509f (V1)
concept of, 501-502, 502f (V1)
processing of, 506-508, 507f, 508f
(V1)
radiographic evaluation in, 547-566
(V1)
computed tomography in, 552-564,
553-565f (V1)
digital radiography in, 549-550,
551f (V1)
linear tomography in, 552 (V1)
orthopantomogram in, 551-552,
552f, 553f (V1)
plain films in, 549-551f (V1)
principles for, 547-548, 548f, 549f
(V1)
subtraction radiography in, 551
(V1)
sinus-lift subantral augmentation in,
458-470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic
considerations in, 458-459
(V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f,
464f (V1)
elevation of schneiderian
membrane in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
trephine core membrane elevation
in, 464-468, 464-468f (V1)
vascular supply, lymphatic
drainage, and innervation in,
459 (V1)
soft tissue procedures around implant
and, 479-490 (V1)
aesthetic considerations and, 479-
480, 480t, 481f (V1)
AlloDerm in, 486, 487f (V1)
connective tissue grafting in, 485,
485f, 486f (V1)
epithelialized free-gingival grafting
in, 483f, 484-485 (V1)
gingivectomy in, 481-484, 484f,
485f (V1)
modified roll tissue graft in, 486,
488f (V1)
papilla regeneration technique in,
487-489, 489f (V1)
pediculated connective tissue graft
in, 486 (V1)
soft tissue health considerations
and, 479, 480f (V1)
trigeminal nerve injury and, 275-276
(V1)
zygomatic implant in, 491-500 (V1)
complications in, 498f, 498-499
(V1)
final prosthesis fabrication and,
499 (V1)
historical perspective in,
491 (V1)
patient selection for, 491-492, 492f
(V1)
postoperative care in, 498 (V1)
preoperative considerations in,
493, 493f (V1)
Implant surgery (Continued)
prosthetic conversion technique
in, 496-497, 497f, 498f (V1)
radiographic evaluation in, 492,
492f (V1)
regional anatomy in, 492-493 (V1)
surgical options in, 493-494, 494f
(V1)
surgical protocol in, 494-496, 494-
497f (V1)
Impression at implant placement,
525-539 (V1)
concept of, 531 (V1)
history of immediate loading and,
525-527, 526b, 526f, 527f (V1)
immediate extraction, implant
placement, and provisional
restoration and, 534f, 534-535,
535f (V1)
immediate provisionalization and,
528-531, 530-531f (V1)
prefabricated ceramic abutments and
temporary crowns and, 536f,
536-537, 537f (V1)
primary bone-level impressions and,
527-528, 529f, 530f (V1)
second-stage surgery and, 532f, 532-
533, 533f (V1)
Incident reporting, 375-376 (V1)
Incision
in alveolar bone grafting for cleft
maxilla, 808-810 (V3)
in alveolar distraction, 350-351, 351f
(V3)
in alveolar split graft, 471, 473f (V1)
in antral membrane balloon
elevation, 465, 465f (V1)
apron-style, 963 (V3)
in auricular cartilage graft, 938, 938f
(V2)
in bilateral sagittal split osteotomy,
102-106, 106f (V3)
for extraoral miniplate fixation,
109-110 (V3)
Blair preauricular, 932-933, 933f (V2)
in blepharoplasty, 590, 591f (V3)
in bone graft harvest
from mandibular ramus, 413, 413f
(V1)
from mandibular symphysis, 410
(V1)
from maxillary tuberosity, 409
(V1)
from tibia, 414, 414f (V1)
in cervicofacial liposuction, 620-621,
621f (V3)
in cleft palate repair
in double-opposing Z-plasty, 772-
775, 773-775f (V3)
two-flap palatoplasty and, 770f,
770-771, 771f (V3)
in complete mandibular subapical
osteotomy, 156 (V3)
in exodontia
genioplasty, 197 (V1)
sulcular with vertical release, 193f,
193-194, 194f (V1)
for tooth located in uncommon
anatomic positions, 200, 201f
(V1)
trapezoidal, 198f (V1)
in forehead and brow lift
endoscopic, 603, 603f (V3)
trichophytic, 612-613 (V3)
in genioplasty, 141, 141f, 142 (V3)
gingivolabial sulcus, 197 (V1)
at graft recipient site, 419 (V1)
in guided tissue regeneration
procedures, 430 (V1)
in implant surgery
facial skin laxity with weight loss
and, 686-688, 686-688f (V3)
immediate implant loading and,
512 (V1)
implant placement in onlay bone
graft and, 424 (V1)
sinus-lift subantral augmentation
and, 459, 459f (V1)
zygomatic, 494, 494f (V1)
Incision (Continued)
in internal derangement of
temporomandibular joint, 932-
934, 933f, 934f (V2)
capsular, 934, 934f (V2)
endaural, 933f, 933-934, 934f (V2)
preauricular, 932-933, 933f (V2)
Killian, 562, 562f (V3)
in Le Fort fracture, 252 (V2)
in Le Fort I osteotomy, 65-66 (V3)
in cleft lip and palate, 818, 818f
(V3)
in craniofacial dysotosis syndromes,
884 (V3)
design and closure of, 459-464
(V3)
in Le Fort III osteotomy, 206 (V3)
of lower lid, 205f, 227f (V2)
Lynch
in nasal fracture, 279 (V2)
in naso-orbital-ethmoid fracture,
246, 246f (V2)
in mandibular lengthening by
distraction osteogenesis, 342
(V3)
in mandibular resection, 700-701,
701f (V2)
in mandibular widening, 339 (V3)
in maxillectomy, 694-695, 695f, 697,
697f (V2)
subtotal anterior, 698, 699f (V2)
subtotal inferior, 697f, 697-698
(V2)
medial canthal-lateral nasal, 227-228,
228f (V2)
modified Blair, 549f (V2)
mucoperiosteal
in alveolar distraction, 350-351
(V3)
in transoral vertical ramus
osteotomy, 123 (V3)
mucosal
in pediatric craniomaxillofacial
tumor, 962-963 (V3)
in transoral vertical ramus
osteotomy, 123 (V3)
Murphy’s, 790, 790f (V2)
in naso-orbital-ethmoid fracture, 246,
246f (V2)
in orbital fracture, 227f (V2)
in parotidectomy, 549f (V2)
in pediatric craniomaxillofacial
tumor, 962-967, 963-965f (V3)
in radicular cyst enucleation, 421,
422f (V2)
in rhinoplasty, 560-562, 561f, 562f
(V3)
open, 567-572, 568-571f (V3)
in rhytidectomy, 500-506, 500-506f
(V3)
in sagittal split ramus osteotomy, 433
(V3)
in total maxillary segmental
osteotomy, 193 (V3)
transcolumellar, 561, 561f,
567 (V3)
in transoral vertical ramus osteotomy,
123 (V3)
in trephine bone core sinus elevation,
464, 464f (V1)
in unilateral cleft lip repair
Asensio technique and, 740f, 740-
741, 741f (V3)
functional cleft lip repair and, 753-
754, 754f (V3)
Millard technique and, 739, 739f
(V3)
Tennison-Randall technique and,
746-749, 747-750f (V3)
vestibular
in alveolar distraction, 350-351,
351f (V3)
in genioplasty, 141, 142 (V3)
in pediatric craniomaxillofacial
tumor, 962 (V3)
in total maxillary segmental
osteotomy, 193 (V3)
Weber-Ferguson, 963f, 965f (V3)
Incisional biopsy, 467, 731t (V2)
INDEX I-45
Incisor
impacted, 171 (V1)
simple extraction of, 188, 189f (V1)
Increased intracranial pressure
in acute subdural hematoma, 60 (V2)
in chronic subdural hematoma, 61,
62f (V2)
in craniofacial dysostosis syndromes,
880-881 (V3)
in craniosynostosis, 864, 865f (V3)
in epidural hematoma, 60 (V2)
in severe closed head injury, 58 (V2)
in traumatic intracerebral hematoma/
cerebral contusion, 62 (V2)
Independent practitioner association,
307-308 (V1)
Indirect bone healing, 62 (V3), 144-
146, 146f (V2)
Indirect mandibular fracture, 142 (V2)
Indirect skeletal anchorage techniques,
224 (V1)
Individual Retirement Account, 287
(V1)
Indocin; See Indomethacin
Indoleacetic acids, 84t, 86t (V1)
Indomethacin, 86t (V1)
bone healing and, 393, 394 (V1)
for chronic facial pain, 972, 973t
(V2)
for temporomandibular disorders,
887t (V2)
Inducible form of nitrous oxide
synthase, 850 (V2)
Induction agents in rapid-sequence
intubation, 29 (V2)
Induction chemotherapy, 777-778 (V2)
Infant
cleft lip and palate in, 713-734 (V3)
classification of, 715-716, 716f,
717f (V3)
embryology of, 714-715 (V3)
feeding child with, 717-718 (V3)
genetics and etiology of, 715 (V3)
prenatal counseling and, 716-717
(V3)
cleft lip and palate repair in, 719-730
(V3)
cleft palate repair and, 723-727,
729f, 730f (V3)
complex facial clefting and, 727-
728, 731f (V3)
history of, 713-714 (V3)
lip adhesion and, 720 (V3)
outcome assessment in, 728-730
(V3)
presurgical taping and orthopedics
in, 719-720, 720f (V3)
primary bilateral lip repair and,
723, 724-728f (V3)
primary unilateral cleft lip repair
and, 720-723, 721-723f (V3)
treatment planning and timing in,
718t, 718-719 (V3)
cleft palate repair in, 723-727, 729f,
730f, 759-782 (V3)
double-opposing Z-plasty in, 772-
775, 773-775f (V3)
fistulas and, 763 (V3)
history of, 759-760 (V3)
intravelar veloplasty in, 762-763
(V3)
outcomes in, 760-761 (V3)
palatoplasty technique in, 762
(V3)
speech evaluation in, 761 (V3)
timing of, 761 (V3)
two-flap palatoplasty for, 763-771,
764-765f, 766t, 767b, 770f,
771f (V3)
two-stage palate repair in, 776-778
(V3)
congenital heart disease in, 382-383,
383t (V3)
craniofacial dysostosis syndromes in,
880-921 (V3)
Apert syndrome in, 902-909, 903-
907f (V3)
Carpenter’s syndrome in,
909 (V3)
I-46 INDEX
Infant (Continued)
cloverleaf skull anomaly in, 909-
914, 910-914f (V3)
Crouzon syndrome in, 886-902,
887-900f (V3)
dentition and occlusion anomalies
in, 881-882 (V3)
functional considerations in, 880-
881 (V3)
genetic aspects of, 880 (V3)
morphologic considerations in,
882-883 (V3)
Pfeiffer syndrome in, 909 (V3)
Saethre-Chotzen syndrome in, 909
(V3)
surgical management of, 883-886
(V3)
craniosynostosis in, 864-879 (V3)
anterior plagiocephaly in, 868-871,
871f, 872f (V3)
brachycephaly in, 874-876 (V3)
delayed diagnosis of, 867-868 (V3)
diagnosis of, 865-866 (V3)
functional consequences of, 864-
865, 865f (V3)
posterior plagiocephaly in, 874,
877f, 878f (V3)
scaphocephaly in, 868, 869-870f
(V3)
surgical considerations in, 856-858,
866-867 (V3)
syndromes associated with, 850
(V3)
timing of surgery for, 867 (V3)
trigonocephaly in, 871-874, 874-
876f (V3)
gingival cyst in, 442, 445f (V2)
herpes simplex virus infection in,
615-617 (V2)
infantile hemangioma in, 577-579,
578f (V2)
melanotic neuroectodermal tumor of
infancy and, 181, 181f (V1)
presurgical dentofacial orthopedics
for, 783-790 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t
(V3)
presurgical nasoalveolar molding
and, 783 (V3)
Infantile hemangioma, 577-579, 578f
(V2)
Infection
animal bite-related, 313-314 (V2)
exodontia-related, 216-217 (V1)
facial asymmetry after, 281-282 (V3)
osteomyelitis and, 633-639 (V2)
classifications of, 633, 634b (V2)
clinical and radiographic
presentation of, 633-635, 634-
636f (V2)
pathogenesis of, 633 (V2)
risk factors for, 634b (V2)
treatment of, 635-638, 636t, 637f
(V2)
unique complications in, 638b,
638f, 638-639 (V2)
postoperative, 412 (V3)
in bilateral sagittal split osteotomy,
115, 116b (V3)
chemical peel and, 664 (V3)
in facial fat transplantation, 627
(V3)
in frontal sinus fracture, 267 (V2)
in laser skin resurfacing, 540-541,
541f (V3)
in mandibular fracture, 159 (V2)
in mandibular surgery, 443 (V3)
in otoplasty, 676 (V3)
in rhinoplasty, 573 (V3)
in rhytidectomy, 508-509 (V3)
prevention in wound repair, 21-22
(V2)
salivary gland, 540-543, 541f, 542f
(V2)
sinus-lift subantral augmentation-
related, 464 (V1)
Infection (Continued)
temporomandibular joint ankylosis
and, 901 (V2)
trismus and, 899 (V2)
Infection control area, 354, 354f (V1)
Infectious arthritis of
temporomandibular joint, 861-864,
862-863f (V2)
Infectious disease, intensive care unit
and, 47 (V2)
Inferior alveolar artery, 174, 175f (V3)
bleeding in intraoral vertical ramus
osteotomy and, 435 (V3)
Inferior alveolar nerve, 165, 166f (V2)
complete mandibular subapical
osteotomy and, 156-157 (V3)
injury of
in bilateral sagittal split osteotomy,
112-113, 113b (V3), 275 (V1)
in intraoral vertical ramus
osteotomy, 434-435, 435f
(V3)
laceration in, 318 (V2)
postoperative management of, 405
(V3)
in sagittal split ramus osteotomy,
426-429, 432f, 444 (V3)
third molar removal-related, 276-
277 (V1)
in total alveolar subapical
osteotomy, 438 (V3)
odontogenic keratocyst impingement
of, 429 (V2)
radiographic evaluation and, 548f
(V1)
transoral vertical ramus osteotomy
and, 126 (V3)
Inferior alveolar nerve block in
zygomatic implant, 493 (V1)
Inferior alveolar nerve repair, 266f, 270
(V1)
Inferior alveolar vein, 433f (V3)
Inferior and lateral approaches to
orbital floor, 221-222, 222f, 223f
(V2)
Inferior compartment of
temporomandibular joint,
arthroscopy and, 920, 920f (V2)
Inferior depressor oris muscle, 174f
(V3)
Inferior division of oculomotor nerve,
584f (V3)
Inferior facial buttress, 91 (V2)
Inferior fornix incision in orbital
fracture, 227f (V2)
Inferior mandibular transverse buttress,
91 (V2)
Inferior oblique muscle, 581f, 584f (V3)
Inferior ophthalmic vein, 433f (V3)
Inferior orbital fissure, 203f, 203t (V2)
Inferior puncta, 206f (V2)
Inferior rectus muscle, 196t (V2), 581f,
584f (V3)
Inferior tarsal muscle, 581f (V3)
Inferior tarsal plate, 586f (V3)
Inferior thyroid artery, 69f (V3)
Inferior turbinate, 257f (V2)
Inferior turbinectomy in Le Fort I
osteotomy, 180, 182f (V3)
Inferolateral approach in
temporomandibular joint
arthroscopy, 923, 923f (V2)
Inflammation
cyclooxygenase-2 and, 393 (V1)
postoperative pain and, 80 (V1)
in temporomandibular joint disorders,
130-131 (V1)
wound repair and, 17-19, 19f (V2)
Inflammatory arthritis of
temporomandibular joint, 857-861
(V2)
ankylosing spondylitis in, 860-861
(V2)
juvenile rheumatoid arthritis in, 859
(V2)
psoriatic arthritis in, 859-860 (V2)
Reiter syndrome in, 861 (V2)
rheumatoid arthritis in, 857b, 857-
858 (V2)
Inflammatory arthritis of
temporomandibular joint
(Continued)
temporomandibular joint
reconstruction in, 950-952, 952f
(V2)
Inflammatory bowel disease
perioperative management of, 386-
387, 387t (V3)
preoperative evaluation of, 9 (V1)
Inflammatory conditions
osteomyelitis in, 633-639 (V2)
classifications of, 633, 634b (V2)
clinical and radiographic
presentation of, 633-635, 634-
636f (V2)
pathogenesis of, 633 (V2)
risk factors for, 634b (V2)
treatment of, 635-638, 636t, 637f
(V2)
unique complications in, 638b,
638f, 638-639 (V2)
of salivary gland, 540-543, 541f, 542f
(V2)
Inflammatory cysts, 418-424, 419b,
419f, 420f (V2)
paradental, 421-424 (V2)
radicular, 419-421, 420f, 422f (V2)
residual, 421, 423f (V2)
Inflammatory mediators
in bone regeneration, 22 (V2)
chronic facial pain and, 962, 963f (V2)
in synovial fluid, 850 (V2)
in temporomandibular disorders, 930
(V2)
in tissue healing, 17-19, 19f (V2)
Inflammatory mucocutaneous diseases,
618f, 618-619 (V2)
Inflammatory phase of healing, 60-61
(V3)
Information technology, office
management and, 303 (V1)
Informed consent
for dentoalveolar surgery, 212, 213b
(V1)
geriatric patient and, 380 (V2)
for laser skin resurfacing, 519 (V3)
potential nerve injuries and, 278 (V1)
risk management and, 301-302, 379
(V1)
Infraorbital approach to orbital floor,
221 (V2)
Infraorbital artery, 69f, 174, 175f, 555f
(V3)
eyelid and, 585 (V3)
maxilla and, 63, 63f, 66f (V3)
maxillary sinus and, 459 (V1)
Infraorbital foramen, 172, 173f (V3)
Infraorbital groove, 203, 203f (V2)
Infraorbital nerve
eyelid and, 585 (V3)
injury of, 87 (V2), 405 (V3)
nose and, 556, 557f (V3)
Infraorbital nerve repair, 270 (V1)
Infraorbital paresthesia, zygomatic
fracture-related, 194-195 (V2)
Infraorbital rim, surgical approaches to,
187-191 (V2)
lower eyelid, 187-188, 188f (V2)
subciliary, 190-191, 191f (V2)
subtarsal, 191 (V2)
transconjunctival, 188-190, 188-190f
(V2)
Infraorbital vein, 469f (V3)
Infratemporal fossa
exodontia-related displacement of
tooth into, 213 (V1)
maxillectomy and, 693 (V2)
Infratip lobule, 554b (V3)
Infratrochlear nerve, 557f (V3)
Inhalation anesthesia
pediatric, 104-105 (V1)
pharmacology of, 63-65, 64t (V1)
Initial assessment in trauma, 35-42, 36t
(V2)
adjuncts to primary survey and, 39-40
(V2)
adjuncts to secondary survey and, 40-
41 (V2)
Initial assessment in trauma (Continued)
airway evaluation in, 35-36 (V2)
breathing evaluation in, 36, 36f, 37f
(V2)
of child, 354-355 (V2)
circulation evaluation in, 37-38, 38f,
38t (V2)
definitive care and, 41 (V2)
disability evaluation in, 38-39, 39t
(V2)
exposure and environment control
in, 39, 39f (V2)
in facial gunshot wound, 327-328
(V2)
in head injury, 49-51 (V2)
in penetrating injuries, 41-42 (V2)
secondary survey and, 40 (V2)
in soft tissue injuries, 283, 284f (V2)
Injectable facial fillers, 629-650, 691f,
691-692, 692f (V3)
for augmenting wrinkles, lines, and
folds, 637-639, 638f, 639f (V3)
complications of, 642-643, 643f, 644f
(V3)
history of, 629-631, 630f, 630t, 631f
(V3)
for lips, 633-637, 633-637f (V3)
for malar augmentation, 639-642,
639-642f (V3)
tissue positioning of, 631f, 631-632,
632f (V3)
treatment considerations in, 632-633,
633f (V3)
treatment results in, 643, 645-649f
(V3)
Injectable local anesthetics, 39t (V1)
Inner office e-mail, 303 (V1)
Innervation
of ear, 668-670f (V3)
of eyelid, 585 (V3)
of forehead and brow, 598-600, 598-
600f (V3)
of maxillary sinus, 459 (V1)
of nose, 273, 273f (V2), 556, 557f
(V3)
of temporomandibular joint, 809,
809f (V2)
In-office operating room, 490-492, 491t,
492f (V3)
Inpatient consultation, coding
requirements for, 367 (V1)
Instrumentation
for exodontia
of impacted third molar, 203, 203t
(V1)
simple extraction, 187-188, 188f
(V1)
third molar, 203, 203t (V1)
for temporomandibular joint
arthroscopy, 921-923, 922f, 924f
(V2)
for trigeminal nerve repair, 267-268
(V1)
Insulin therapy
geriatric patient and, 383 (V2)
intensive care unit and, 46-47 (V2)
perioperative management of, 386
(V3)
preoperative management of, 2t (V1)
Insurance, 368-369 (V1)
incidents and claims and, 375-376
(V1)
risk management and, 377 (V1)
Insurance broker, 287 (V1)
Insurance coverage, 302-303 (V1)
Intelligibility after cleft surgery, 794-
795, 797 (V3)
Intensity modulated radiation therapy,
773, 773f (V2)
Intensive care of trauma patient, 42-48,
43t (V2)
abdominal compartment syndrome
and, 45-46, 46f (V2)
acalculous cholecystitis and, 45 (V2)
acute adrenal insufficiency and, 46-47
(V2)
acute renal failure and, 46 (V2)
acute respiratory distress syndrome
and, 43-44, 44t (V2)

Intensive care of trauma patient
(Continued)
adynamic ileus and, 45 (V2)
atrial fibrillation and, 44-45 (V2)
blood loss and, 46 (V2)
blunt myocardial injury and, 44 (V2)
fluids, electrolytes, and nutrition and,
45 (V2)
infectious disease and, 47 (V2)
intensive insulin therapy and, 46-47
(V2)
intubation and mechanical
ventilation and, 43 (V2)
pain control and sedation and, 47
(V2)
preparation for surgery and, 70-72
(V2)
prophylaxis and, 48 (V2)
rehabilitation and, 48 (V2)
shock and, 44, 70 (V2)
systemic inflammatory response and
multiple organ failure syndrome
and, 44, 44t (V2)
tubes and lines and, 47-48 (V2)
use of steroids in, 72 (V2)
Intensive insulin therapy, 46-47 (V2)
Interarch relations in occlusion
evaluation, 18, 18b (V3)
Intercartilaginous incision
in pediatric craniomaxillofacial
tumor, 962, 963f (V3)
in rhinoplasty, 561, 562f (V3)
Interdental osteotomy
in complete mandibular subapical
osteotomy, 158, 159f (V3)
in total maxillary segmental
osteotomy, 197 (V3)
unfavorable results in segmental
maxillary surgery, 473-474f (V3)
Interferon therapy
in central giant cell granuloma, 593-
594 (V2)
in malignant melanoma, 756 (V2)
Interincisal angle, 15, 16f (V3)
Interlabial distance, 12 (V3)
Interleukins
bone homeostasis and, 394 (V1)
chronic facial pain and, 962, 963f
(V2)
cyclic tensile strain in arthritis and,
851, 851f, 852f (V2)
temporomandibular disorders and,
849, 850f, 930 (V2)
Intermaxillary fixation in midface
fracture, 386-388 (V2)
Intermaxillary screws, 139, 141f, 147-
148 (V2)
Intermediate crus of nose, 556 (V3)
Intermediate splint, 364, 368-369, 369f,
370f (V3)
Internal carotid artery, 69f (V3)
eyelid and, 585 (V3)
forehead and brow and, 598 (V3)
injury in Le Fort I osteotomy, 469,
469f (V3)
nose and, 553 (V3)
Internal derangement of
temporomandibular joint
arthrocentesis in, 912-917 (V2)
outcome assessment in, 915 (V2)
pathophysiology of
temporomandibular disorder
and, 912-913 (V2)
prognostic and predictive factors
in, 916 (V2)
technique in, 913-915, 914f (V2)
arthroscopy for, 920-921, 921f (V2)
arthrotomy in, 929-944, 930b (V2)
capsular incisions in, 934, 934f
(V2)
condylotomy in, 939-940 (V2)
diagnostic imaging in, 931, 932f
(V2)
disk repair in, 936, 936f (V2)
disk repositioning in, 935f, 935-
936 (V2)
diskectomy in, 936 (V2)
diskectomy with replacement in,
936-939, 937-939f (V2)
Internal derangement of
temporomandibular joint
(Continued)
endaural incision in, 933f, 933-
934, 934f (V2)
goals and criteria for surgery in,
931 (V2)
history and physical examination
in, 929-930 (V2)
pathogenesis of, 930-931 (V2)
postoperative care in, 940-941 (V2)
preauricular incision in, 932-933,
933f (V2)
preoperative therapies for, 931 (V2)
surgical complications in, 940 (V2)
wound closure in, 934, 935f (V2)
diagnostic approach to, 831t (V2)
osteoarthritis and, 856 (V2)
splint therapy for, 884-885 (V2)
Internal derangement theory of
temporomandibular joint disorders,
126-127, 128f (V1)
Internal fixation of mandibular fracture,
154f, 154-155, 155f (V2)
pediatric, 369-370 (V2)
Internal jugular vein, 433f (V3)
Internal marketing, 339t, 339-340, 340f
(V1)
Internal maxillary artery, 66f, 174, 175f,
554 (V3)
Internal nasal nerve, 556, 557f (V3)
Internal nasal valve, 560, 560f (V3)
Internal neurolysis in trigeminal nerve
repair, 268-269 (V1)
International Classification of Diseases,
364-365 (V1)
Interpositional bone graft, 471, 472f (V1)
Interrogatory, lawsuit and, 377 (V1)
Interviewing potential employee, 325-
326, 326b (V1)
Intra-abdominal hemorrhage, 65-67,
66f, 67f (V2)
Intraalveolar split graft, 471 (V1)
Intraalveolar vessels, 175f (V3)
in maxillary central incisor, 67f (V3)
Intraarch relations in occlusion
evaluation, 18, 18b (V3)
Intracapsular adhesions, 820 (V2)
arthroscopic removal of, 924 (V2)
Intracapsular fracture, 141 (V2)
Intracapsular pathofunctional disorders,
818-821, 819-821f (V2)
mandibular gait in, 825-826, 825-
828f (V2)
mandibular range of motion in, 824-
825 (V2)
Intracartilaginous incision in
rhinoplasty, 561, 562f (V3)
Intracerebral hematoma, 61-62 (V2)
Intracranial pressure elevation
in acute subdural hematoma, 60 (V2)
craniofacial dysostosis syndromes and,
880-881 (V3)
craniosynostosis and, 864, 865f (V3)
in epidural hematoma, 60 (V2)
in severe closed head injury, 58 (V2)
in traumatic intracerebral hematoma/
cerebral contusion, 62 (V2)
Intracranial tumor, 992 (V2)
INTRA-LOCK miniimplant, 567, 568f
(V1)
Intranasal lidocaine
for cluster headache, 149 (V1)
for migraine, 148 (V1)
Intranasal splint, 302f (V2)
Intranasal wiring in nasal fracture, 280
(V2)
Intraocular pressure, post-traumatic
change in, 81 (V2)
Intraoffice communication system, 359,
359f (V1)
Intraoperative complications, 423-441
(V3)
in genioplasty, 439-441, 440f, 441f
(V3)
in intraoral vertical ramus osteotomy,
433-436, 434f, 435f (V3)
in inverted L and C osteotomies,
436-437 (V3)
Intraoperative complications
(Continued)
in maxillary surgery, 459-472 (V3)
bleeding in, 467-469f, 467-470
(V3)
bradycardia in, 470 (V3)
improper maxillary repositioning
in, 470-471, 471f (V3)
incision design and closure and,
459-464 (V3)
technical difficulties and, 471-472,
472f (V3)
unfavorable osteotomy in, 464-467,
465f, 466f (V3)
in sagittal split ramus osteotomy,
423-433 (V3)
intraoperative bleeding in, 429-
431, 433f (V3)
minor technical difficulties in, 433
(V3)
nerve injury in, 426-429, 432f (V3)
proximal segment malpositioning
in, 431-432 (V3)
relapse in, 445, 446f (V3)
unfavorable osteotomy in, 423-426,
424-434f (V3)
in subapical osteotomies, 437f, 437-
438 (V3)
Intraoperative fluids, 72 (V1)
pediatric anesthesia and sedation
and, 102-103 (V1)
Intraoperative patient management,
382-395 (V3)
antibiotics and, 392-393 (V3)
asplenia and, 387-388 (V3)
blood loss management and, 392
(V3)
cardiovascular disorders and, 382,
383b (V3)
congenital heart disorders and, 382-
383, 383t (V3)
consultation and, 389, 389t (V3)
in cranio-maxillofacial trauma, 12-14,
12-14f (V2)
endocrine disorders and, 385-386
(V3)
epoetin alfa and, 390 (V3)
gastrointestinal disorders and, 386-
387, 387t (V3)
hematologic disorders and, 384-385
(V3)
imaging and, 389 (V3)
laboratory tests and, 389-390 (V3)
neurologic disorders and, 388-389
(V3)
nutrition and, 390-391 (V3)
patient positioning and, 391-392
(V3)
postoperative nausea and vomiting
and, 393 (V3)
preoperative interview and, 391,
391b (V3)
pulmonary disorders and, 383-384,
384b, 384t (V3)
single kidney and, 387 (V3)
social factors in, 391 (V3)
steroids and, 393 (V3)
Intraoral air pressure after cleft surgery,
794 (V3)
Intraoral anchorage techniques, 224
(V1)
Intraoral approach in endoscopic repair
of condylar fracture, 178f (V2)
Intraoral distraction osteogenesis, 338-
363 (V3)
alveolar distraction in, 349-354, 349-
354f (V3)
bone transport by, 354-360, 355-361f
(V3)
future directions in, 362 (V3)
mandibular lengthening in, 342-346,
342-346f (V3)
mandibular widening in, 338-342,
339-342f (V3)
maxillary bone transport in, 360-362,
362f (V3)
maxillary distraction by intraoral
devices in, 346-349, 347-349f
(V3)
INDEX I-47
Intraoral implant
allograft, 685t (V3)
for facial skin laxity with weight loss,
687f, 687-688 (V3)
Intraoral soft tissue examination, 107,
107f (V2)
Intraoral subcondylar osteotomy, 119
(V3)
Intraoral vertical ramus osteotomy, 70-
71, 119-136 (V3)
advantages and disadvantages of,
120-121, 121t, 122f (V3)
complications in, 433-436, 434f, 435f
(V3)
facial nerve injury in, 444 (V3)
historical background of, 68, 119
(V3)
indications and contraindications for,
121-122 (V3)
intraoperative procedure in, 123-128,
125-127f (V3)
Le Fort I segmental osteotomy with,
199-203f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe facial asymmetry, 130f,
130-131, 131f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe open bite, 132-135, 132-
135f (V3)
mandibular relapse in, 445-446, 446-
449f (V3)
postoperative physiotherapy in, 128f,
128-129 (V3)
sagittal split ramus osteotomy versus,
119, 120f, 120t (V3)
surgical treatment objectives in, 123,
124f, 125f (V3)
Intraorbital bleeding after maxillary
osteotomy, 474 (V3)
Intraorbital foreign body, 83-84, 84f
(V2)
Intraosseous anesthesia, 50 (V1)
Intraosseous hemangioma, 869 (V2)
Intraosseous infusion, 6 (V2)
Intraosseous odontogenic carcinoma,
527-532, 528-530f (V2)
Intravelar veloplasty
controversies in, 762-763 (V3)
in two-flap palatoplasty, 770f, 770-
771, 771f (V3)
Intravenous access in pediatric
anesthesia and sedation, 102, 102f
(V1)
Intravenous lidocaine testing
in chronic head and neck pain, 140-
141 (V1)
in trigeminal nerve injury, 264 (V1)
Intravenous sedative-hypnotics, 60-62,
62t (V1)
Intraventricular hemorrhage, 63 (V2)
Intrinsic aging, 513 (V3)
Intruding tooth, skeletal anchorage for,
232 (V1)
Intrusive luxation of tooth, 114t, 118,
119f (V2)
Intubation
complications of, 33 (V2)
equipment for, 26b (V2)
in Le Fort III osteotomy, 206 (V3)
in maxillectomy, 694, 694f, 695f
(V2)
nasotracheal, 31 (V2)
pediatric, 94 (V1)
in trauma, 28-31, 31f (V2)
cranio-maxillofacial, 3-4, 4-5f (V2)
intensive care unit and, 43 (V2)
in trigeminal nerve repair, 268 (V1)
Inverted C osteotomy, 436-439, 437f
(V3)
Inverted L osteotomy, 436-439, 437f
(V3)
Iontophoresis, 50 (V1), 892 (V2)
Iontophoresis-phonophoresis, 146 (V1)
Iridodialysis, 80f, 80-81 (V2)
Irinotecan, 781t, 782t (V2)
Iris, nonperforating injury of, 80f, 80-81
(V2)
I-48 INDEX
Iron, postoperative, 391 (V3)
Irrigation of animal bite wound, 315
(V2)
Irritant dermatitis, laser skin
resurfacing-related, 539 (V3)
Ischemic complications
in Le Fort I osteotomy, 64, 187, 475
(V3)
radiation therapy-related, 774 (V2)
in total maxillary segmental
osteotomy, 198, 198f (V3)
Isocarboxazid, 2t (V1)
Isoflurane, 43, 44t, 64t, 65 (V1)
Isolated anterior table fracture, 259,
261f (V2)
Isolated posterior table fracture, 259,
261f (V2)
Isotretinoin
for skin cancer, 740 (V2)
usage history in laser skin resurfacing,
517 (V3)
Isovolemic degradation, 629 (V3)
Itching, laser skin resurfacing and, 537-
538, 539f (V3)
IVRO; See Intraoral vertical ramus
osteotomy
J for pediatric anesthesia and sedation,
Jaw exercises in temporomandibular
disorders, 985, 985f (V2)
Jaw instability after surgery, 406, 413-
415, 414-417f (V3)
JCAHO; See Joint Commission on
Accreditation of Health Care
Organizations
Jefferson fracture, 63, 64f (V2)
Jerusalem approach in cleidocranial
dysplasia, 177 (V1)
Jessner’s solution, 663 (V3)
Job description, 291, 293t, 294t (V1)
Joffe and Morgan management strategy
for elective surgery, 382, 383b
(V3)
Joining or starting practice, 285 (V1)
Joint Commission on Accreditation of
Health Care Organizations
accreditation of surgicenter and, 304,
305t (V1)
on laser safety and compliance, 515-
516 (V3)
on medical licensure, 307 (V1)
Joint effusion in acute traumatic
arthritis of temporomandibular
joint, 855 (V2)
Joint space adhesions
arthroscopic removal of, 924 (V2)
laser treatment of, 247 (V1)
Jowl region, cervicofacial liposuction
and, 618-625 (V3)
complications of, 623-624 (V3)
history of, 618 (V3)
patient selection in, 618-620, 619f
(V3)
preoperative preparation in,
620 (V3)
surgical technique in, 620-623, 620-
625f (V3)
Jugular lymph nodes, neck dissection
and, 711t (V2)
Jugular neck dissection, 720f (V2)
Jugular vein, 163f (V2)
Juri flap, 655, 655f, 656f (V3)
Juvederm 24HV, 630 (V3)
Juvenile active ossifying fibroma, 599-
600, 600f (V2)
Juvenile aggressive fibromatosis, 970,
972f (V3)
Juvenile aggressive ossifying fibroma,
599-600, 600f (V2)
Juvenile nasopharyngeal angiofibroma,
972-974, 976-977f (V3)
Juvenile ossifying fibroma, 599-600,
600f (V2), 974-977, 978-979f (V3)
Juvenile rheumatoid arthritis
facial asymmetry in, 309 (V3)
of temporomandibular joint, 859
(V2)
temporomandibular joint ankylosis
and, 902 (V2)
Juvenile rheumatoid arthritis Lacrimal apparatus, 587 (V3)
(Continued) cancer arising near medial canthus
temporomandibular joint and, 728 (V2)
reconstruction in, 961-962 (V2) injury of
Juxtacortical osteosarcoma, 683-684 in Le Fort I osteotomy, 475 (V3)
(V2) in naso-orbital-ethmoid fracture,
244 (V2)
K in orbital fracture, 215, 217f (V2)
Kaban’s classification of Lacrimal gland, 583, 584f, 587f, 587
oculoauriculovertebral spectrum, (V3)
925 (V3) prolapsed, 579 (V3)
Kasabach-Merritt coagulopathy, 577 Lacrimal nerve, 585 (V3)
(V2) Lacrimal sac, 206, 244f (V2)
Keen approach to zygomatic arch Lactate, 70 (V2)
fracture, 194 (V2) Lactation
Keflex; See Cephalexin nonsteroidal antiinflammatory drug
Keloid formation, 22, 298 (V2) use during, 85 (V1)
in otoplasty, 676 (V3) use of local anesthetics during, 45
in rhytidectomy, 509, 509f (V3) (V1)
Keratoacanthoma, 726 (V2) Lactic acid for chemical peel, 663 (V3)
Keratoconjunctival herpes, 615-616 Lag screws in mandibular fracture, 155-
(V2) 156, 156-158f (V2)
Keratoderma blennorrhagicum, 861 (V2) Lambdoid suture, 865f (V3)
Kessler scale, 79b, 80 (V3) Lambdoid suture craniosynostosis, 874,
Ketamine, 62t, 62-63 (V1) 877f, 878f (V3)
in laser skin resurfacing, 521 (V3) Lamina papyracea, 204 (V2)
for office-based anesthesia, 74 (V1) Laminar freeze-dried bone for guided
bone regeneration, 429 (V1)
104, 105t (V1) Lamotrigine, 150 (V1), 992, 992t (V2)
in rapid-sequence intubation, 29-30 Langerhans cell, 513 (V3), 568-569,
(V2) 569f (V2)
Ketoprofen, 84t, 86t (V1), 887t (V2) Langerhans cell granulomatosis, 567
Ketorolac, 84t, 86t (V1) (V2)
Kidney Langerhans cell histiocytosis, 567-576,
effects of thyroid disorders on, 13t (V1) 568f (V2)
intensive care of trauma patient and, classification of, 569b, 569-570 (V2)
46 (V2) clonality of, 570 (V2)
liver disease-related alteration in diagnosis, treatment, and prognosis
function of, 11 (V1) of, 571-575, 571-575f (V2)
pediatric anesthesia and sedation histopathology of, 570, 570f (V2)
and, 96 (V1) Langerhans cell and, 568-569, 569f
perioperative management of renal (V2)
disorders and, 387 (V3) temporomandibular joint
preoperative evaluation of, 7-9t (V1) involvement in, 874 (V2)
preoperative management of renal Lanz, Otto, 791, 791f (V2)
failure and, 8t, 9t (V1) Large vessel occlusive disease, 18 (V1)
Kiesselbach’s plexus, 554, 556f (V3) Laryngeal cancer, 768-770, 770f, 770t
Killian incision, 562, 562f (V3) (V2)
Kinogen, 17 (V2) Laryngeal edema, 442 (V3)
Kleeblattsch[um]adel anomaly, 909-914, Laryngeal mask airway, 26, 27f, 28f
910-914f (V3) (V2), 70 (V1)
Klonopin; See Clonazepam in pediatric anesthesia and sedation,
Kufner’s operation, 211-218 (V3) 100-102 (V1)
sizes and inflation volume of, 100t
L (V1)
Labial frenulum, soft tissue procedures Laryngoscope, 30-31, 31f (V2)
of, 173-174, 174f (V1) Laryngoscopy, 30-31, 31f (V2)
Labiomental fold Laryngospasm, 106-107 (V1)
macrogenia and, 167f, 169f (V3) Larynx of child, 94, 95f (V1)
profile evaluation and, 4 (V3) Laser blepharoplasty, 544-545, 545-547f
Laboratory, floor plan in office design (V3)
and, 356-357 (V1) Laser frenectomy, 244 (V1)
Laboratory equipment, 360 (V1) Laser skin resurfacing, 513-552 (V3)
Laboratory testing carbon dioxide laser in, 521-532
in chronic head and neck pain, 139- (V3)
140 (V1) anesthesia and, 521, 522f (V3)
documentation of, 382 (V1) fractional photothermolysis in,
preoperative, 9t (V1), 389-390 (V3) 532, 536f (V3)
Laceration, 289, 290f (V2) laser properties in, 514f, 514-516,
canalicular, 88-89, 89f (V2) 515f (V3)
canthal tendon, 308-309f (V2) laser settings for, 521-522, 522f
of cheek, 320, 320f (V2) (V3)
corneoscleral, 83, 83f (V2) postoperative care in, 524-529,
of ear, 310-313, 312f, 313f (V2) 526-528f, 530-531f (V3)
during exodontia, 214 (V1) resurfacing acne scars in,
eyelid, 88, 306-307, 307f, 308f (V2) 529 (V3)
of facial nerve, 318, 319, 319f (V2) single-pass resurfacing in, 529-532,
in frontal sinus fracture, 256, 258f, 533-534f (V3)
262f (V2) traditional technique in, 522-524,
gingival, 107 (V2), 115t, 130 (V2) 523f, 525-526f (V3)
of lip, 294, 298f (V2) traumatic and surgical scars
mucosal, 115t (V2) improvement in, 529 (V3)
nasal, 275, 301, 304f (V2) treatment of benign skin lesions
in orbital fracture, 208, 208f, 215 in, 529 (V3)
(V2) complications of, 534-544 (V3)
pericardial, 42 (V2) contact dermatitis in, 539 (V3)
of scalp, 323-324, 324f, 325f (V2) dyschromias in, 541-542, 542f,
initial assessment of, 50 (V2) 543f (V3)
management of, 58-59 (V2) infection in, 540-541, 541f (V3)
Laser skin resurfacing (Continued)
milia and acne formation in, 539-
540, 540f (V3)
ocular, 543-544 (V3)
prolonged erythema in, 535-537,
539f (V3)
pruritus in, 537-538, 539f (V3)
scarring in, 542-543, 543f (V3)
sepsis in, 544 (V3)
telangiectasias in, 538-539 (V3)
erbium:YAG laser in, 532-534, 536-
538f (V3)
history of, 513-514 (V3)
intrinsic and extrinsic aging and, 513
(V3)
laser blepharoplasty with, 544-545,
545-547f (V3)
patient evaluation in, 516-519, 518b
(V3)
preoperative considerations in, 519
(V3)
rhytidectomy with, 545-548, 547-
548f (V3)
skin preparation for, 519-521 (V3)
Laser therapy, 237-258 (V1)
for aphthous stomatitis, 620 (V2)
applications for general dentistry,
254-256 (V1)
in arthroscopic disk repositioning,
925-926 (V2)
bone healing and, 253-254 (V1)
in capillary malformation, 581 (V2)
for cosmetic skin procedures, 248-
251, 249t (V1)
for cutaneous pigmented lesions or
tattoos, 251 (V1)
effects on postoperative pain and
swelling, 254b, 254 (V1)
equipment in, 241-242, 242f (V1)
for hair removal, 251-252 (V1)
implant surgery with, 245-246 (V1)
in incisional and excisional soft tissue
procedures, 244-245 (V1)
for infantile hemangioma, 580 (V2)
laser physics and, 237-238,
238f (V1)
laser-scan-based registration and, 256
(V1)
low-level, 253 (V1)
for lymphatic malformation, 583
(V2)
in oral and maxillofacial surgery,
243-244, 244f (V1)
for oral pathologic conditions, 245
(V1)
safety issues in, 242b, 242f, 242-243,
243f (V1)
for skin cancer, 734-735 (V2)
for sleep apnea and snoring, 252-253
(V1)
for temporomandibular disorders,
246-248 (V1)
tissue interactions in, 239t, 239-241f,
239-241 (V1)
for vascular lesions of face,
251 (V1)
wound healing and, 253 (V1)
Laser-scan-based surface registration,
256 (V1)
Late-onset post-traumatic
enophthalmos, 198 (V2)
Lateral branch of posterior ethmoidal
artery, 555f (V3)
Lateral canthal tendon, 583f, 586f, 587f
(V3)
Lateral canthotomy
in orbital fracture, 222 (V2)
in zygomatic fracture, 186-187 (V2)
Lateral canthus, 585 (V3)
Botox injection and, 659, 660f, 661f
(V3)
Lateral capsular release, 924 (V2)
Lateral cephalometrics, 11-15 (V3)
dental relations in, 14-15, 16f (V3)
in facial asymmetry, 274-275 (V3)
skeletal relations in, 12-14, 13-15f
(V3)
soft tissue relations in, 11-12, 12f
(V3)

Lateral crura of nasal cartilage, 556
(V3)
Goldman tip and, 565-566 (V3)
tip plasty and, 563f, 564 (V3)
Lateral crural pull up method, 566 (V3)
Lateral crural steal, 563, 564f (V3)
Lateral horn levator, 586f, 587f (V3)
Lateral internal nasal branch of anterior
ethmoid artery, 555f (V3)
Lateral luxation of tooth, 114t, 119-120
(V2)
Lateral nasal artery, 69f, 555f (V3)
Lateral nasal osteotomy, 569, 569f (V3)
Lateral neck dissection, 720f (V2)
Lateral oblique view
of mandible, 96-97, 97f, 145f (V2)
in temporomandibular disorders, 837,
837f (V2)
Lateral orbital fat pad, 584f (V3)
Lateral periodontal cyst, 442-444 (V2)
Lateral polar ligament, 804 (V2)
Lateral pterygoid muscle, 163 (V2),
807-808, 808f (V2)
Lateral pterygoid nerve, 809 (V2)
Lateral rectus muscle, 196t (V2), 584f
(V3)
Lateral retinaculum, 585, 587f (V3)
Lateral shift of mandible, 811 (V2)
Lateral still cephalometry, 797-798
(V3)
Latex anaphylaxis, 107t (V1)
Latex rubber dam for guided bone
regeneration, 429 (V1)
Latham appliance, 720, 738 (V3)
Lavage of adhesions in
temporomandibular joint
arthroscopy, 924, 924f (V2)
Law screw technique in bilateral sagittal
split osteotomy, 109, 110f (V3)
Lawsuit process, 376-378 (V1)
Le Fort fracture, 248-253 (V2)
anatomy in, 249 (V2)
classification system of, 95f, 239-240,
240f, 241f, 249 (V2)
clinical findings in, 250f, 250-251
(V2)
examination considerations in, 251,
251f (V2)
neurologic injury in, 242-243 (V2)
radiographic evaluation in, 94, 251
(V2)
treatment of, 251-253, 252f (V2)
Le Fort I fracture, 239, 240f, 250, 250f
(V2)
Le Fort I osteotomy, 63-68, 172-191
(V3)
ambulatory, 494 (V3)
in cleft orthognathic surgery, 815-
819, 818f (V3)
before complete mandibular subapical
osteotomy, 162f (V3)
complications of, 185-189 (V3)
in craniofacial dysotosis syndromes,
884, 885 (V3)
fixation of, 181-184 (V3)
hierarchy of stability in, 184 (V3)
historical background of, 63, 172,
173f (V3)
intraoperative complications in, 459-
472 (V3)
bleeding in, 467-469f, 467-470
(V3)
bradycardia in, 470 (V3)
improper maxillary repositioning
in, 470-471, 471f (V3)
incision design and closure and,
459-464 (V3)
technical difficulties and, 471-472,
472f (V3)
unfavorable osteotomy in, 464-467,
465f, 466f (V3)
Le Fort III osteotomy with,
211 (V3)
in maxillary bone transport, 360
(V3)
in maxillary distraction by intraoral
devices, 347, 348f (V3)
maxillomandibular complex rotation
and, 266, 267f (V3)
Le Fort I osteotomy (Continued)
for obstructive sleep apnea syndrome,
323-330, 327-332f (V3)
in oculoauriculovertebral spectrum,
931, 931f (V3)
in pediatric craniomaxillofacial
tumor, 963-964 (V3)
postoperative complications in, 473-
480 (V3)
antral or nasal fistulas in, 480 (V3)
atrophic rhinitis in, 480 (V3)
dental and periodontal problems
in, 475, 477f (V3)
nasal septal deviation in, 478-480,
479f (V3)
nerve injury in, 477 (V3)
ophthalmic disorders in, 473-475,
476f (V3)
prevention of, 480t (V3)
relapse in, 480 (V3)
unfavorable nasolabial esthetics in,
477-478 (V3)
vascular compromise in, 475 (V3)
postoperative management of, 184
(V3)
preoperative issues in, 454-480 (V3)
accurate presurgical records and,
459, 460-463f (V3)
dental compensations and, 456,
457-458f (V3)
leveling and root divergence in
segmental cases and, 458-459
(V3)
psychologic preparation and, 459
(V3)
systematic aesthetic analysis and,
459 (V3)
tooth size discrepancies and, 458
(V3)
transverse discrepancies and, 456-
458 (V3)
revascularization and healing in, 63-
65, 64f, 65f (V3)
segmental, 66-67, 67f, 192-204 (V3)
complications in, 198, 198f, 199f,
472-473 (V3)
historical background of, 192 (V3)
indications for, 192-193 (V3)
for maxillary deficiency, 199-203f
(V3)
osteotomy design in, 196 (V3)
postoperative care in, 196-197,
197f (V3)
surgical planning in, 197-198 (V3)
technique in, 193-196, 194-196f
(V3)
unfavorable interdental osteotomy
in, 473-475f (V3)
soft tissue changes in, 184-185, 185-
188f (V3)
soft tissue incision in, 65-66 (V3)
surgical anatomy in, 172-174, 173f,
174f (V3)
surgical technique in, 176-181, 176-
184f (V3)
in surgically assisted maxillary
expansion, 67f, 67-68, 227, 228-
230f (V3)
in Treacher Collins syndrome, 954
(V3)
in two-jaw surgery, 239 (V3)
vascular anatomy in, 174-175, 176f
(V3)
Le Fort II fracture, 239, 240f, 250 (V2)
Le Fort III fracture, 239, 241f, 250f,
250-251 (V2)
Le Fort III osteotomy, 205-218 (V3)
for craniofacial dysostosis, 205-206
(V3)
indications for, 205 (V3)
in maxillary distraction by intraoral
devices, 347, 348f (V3)
for midface deficiency, 206, 207-210f
(V3)
modified, 211-218 (V3)
subcranial, 210-211, 212-217f (V3)
technique in, 206-210 (V3)
Lease agreement, 301 (V1)
Leg, vascular supply to, 335f (V2)
Legal documents, office management
and, 299-301, 300t, 301t (V1)
Legal entities, 285-286, 286t (V1)
Legal issues
in adverse action in privileging, 315-
316 (V1)
chart documentation and, 368 (V1)
claims adjudication and, 370 (V1)
coding and, 364-368 (V1)
fraudulent claims submission and,
371 (V1)
insurance and, 368-369 (V1)
Medicare fees and, 370-371 (V1)
risk management and, 373-386 (V1)
Americans with Disabilities Act
and, 383-384 (V1)
discharging patient from practice
and, 383 (V1)
documentation and legible records
and, 379-383 (V1)
Emergency Medical Treatment and
Active Labor Act and, 385
(V1)
HIPAA privacy and security and,
384 (V1)
incidents and claims and, 375-376
(V1)
informed consent and, 379 (V1)
lawsuit process and, 376-378 (V1)
limited English proficiency and,
384-385 (V1)
malpractice and, 374-375 (V1)
online communication and, 385
(V1)
patient rapport and, 378-379 (V1)
release of records and, 384 (V1)
telemedicine and, 385 (V1)
third-party payers and, 369-370 (V1)
in trigeminal nerve injury, 278-279
(V1)
Legan’s angle for determining chin
position, 681t (V3)
Legibility of documentation, 379-383
(V1)
Lekholm and Zarb bone quality system,
547-548 (V1)
Lens
dislocation in orbital fracture, 213
(V2)
nonperforating eye injuries and, 81,
81f (V2)
Lentigines, 518 (V3)
Lentigo maligna, 751f, 751t, 752t (V2)
Lesser palatine artery
maxilla and, 63f, 66f, 173f, 175f, 555f
(V3)
LET topical anesthetic, 50 (V1)
Lethal midline granuloma, 761-762
(V2)
Letterer-Siwe disease, 567 (V2)
Leucovorin, 779t (V2)
Leukemia, 179 (V1)
Leukocyte, wound healing and, 60-61,
61f (V3)
Leukoplakia, 245 (V1)
Leukotrienes, 400 (V1)
Levator anguli oris muscle, 174, 174f
(V3)
Levator aponeurosis, 581f, 583f, 585,
586f (V3)
Levator labii superioris alaeque nasi
muscle, 174, 174f (V3), 554f (V3)
Levator labii superioris muscle, 174,
174f (V3)
Levator muscle, 581f (V3)
Levator palpebral aponeurosis, 585,
586f (V3)
Levator palpebral superioris muscle, 205
(V2), 582, 584f (V3)
Levator veli palatini muscle, 831t, 835f
(V3)
Leveling and root divergence in
segmental cases
mandibular surgery complications
and, 423 (V3)
maxillary surgery complications and,
458-459 (V3)
Levonordefrin, 39-45, 40t, 43-45t, 44b
(V1)
INDEX I-49
Levorphanol, 888t (V2)
Liberation from mechanical ventilation,
43 (V2)
Librium; See Chlordiazepoxide
Licensed independent practitioner, 307
(V1)
Lichen planus, 245 (V1), 618f, 618-619
(V2)
Lid retractors, 585, 586f (V3)
Lidocaine
for acute postoperative pain, 83 (V1)
chemical structure of, 37f (V1)
for cluster headache, 149 (V1)
duration of action of, 39t (V1)
iontophoresis for, 50 (V1)
lipid solubility of, 38t (V1)
for migraine, 148 (V1)
pH effects on, 37t (V1)
for postherpetic neuralgia, 152 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)
prolonged sensory alteration with, 46t
(V1)
in rapid-sequence intubation, 29
(V2)
in rhytidectomy, 500 (V3)
topical, 48-49 (V1)
vasoconstrictors with, 41 (V1)
Lidocaine, epinephrine, tetracaine
combination, 50 (V1)
Lidocaine testing
in chronic head and neck pain, 140-
141 (V1)
in trigeminal nerve injury, 264 (V1)
Life insurance, 303 (V1)
Lifting after surgery, 412 (V3)
Ligaments of temporomandibular joint,
162 (V2)
Light, laser generation of, 237-238 (V1)
Light intensity test, 75 (V2)
Lighted stylet, 31 (V2)
Limited English proficiency, 384-385
(V1)
Limited liability company, 285-286,
286t (V1)
Limited licensed practitioner, 307 (V1)
Limited mouth opening after simple
extraction, 191 (V1)
Limited partnership, 285-286, 286t
(V1)
Lincomycin, 389t, 390 (V1)
Lindhal classification of condylar
process fractures, 168b (V2)
Line of theoretical facial height, 139-
140 (V3)
Linear IgA disease, 625-626 (V2)
Linear skull fracture, 59 (V2)
Linear tomography
in implant surgery, 552 (V1)
in temporomandibular disorders, 838
(V2)
Lingual artery, 69f (V3)
Lingual flap, 277 (V1)
Lingual frenectomy, 174, 175f, 176f
(V1)
Lingual nerve, 165 (V2)
injury of
in bilateral sagittal split osteotomy,
113, 113b (V3)
during exodontia, 216 (V1)
laceration in, 318 (V2)
local anesthetic injection-related,
273 (V1)
in mandibular endosseous implant
surgery, 275-276 (V1)
in mandibular surgery, 444 (V3)
orthognathic surgery-related, 275
(V1)
third molar removal-related, 276-
277 (V1)
Lingual nerve repair, 269f, 269-270 (V1)
Lingual splint, 148 (V2)
Linoleic acid, 399-400 (V1)
Linolenic acid, 399-400 (V1)
Lioresal; See Baclofen
Lip
Botox injection in, 660 (V3)
changes following Le Fort I
osteotomy, 185 (V3)
I-50 INDEX
Lip (Continued)
cleft lip and palate repair and, 719-
730 (V3)
cleft palate repair and, 723-727,
729f, 730f (V3)
complex facial clefting and, 727-
728, 731f (V3)
history of, 713-714 (V3)
lip adhesion and, 720 (V3)
lip revision after, 719 (V3)
outcome assessment in, 728-730
(V3)
presurgical taping and orthopedics
in, 719-720, 720f (V3)
primary bilateral lip repair and,
723, 724-728f (V3)
primary unilateral cleft lip repair
and, 720-723, 721-723f (V3)
treatment planning and timing in,
718t, 718-719 (V3)
detailed aesthetic evaluation of, 6-7,
8f (V3)
embryology of, 699, 701f (V3)
herpes simplex virus infection of,
613 (V2)
injectable filler for, 633-637, 633-
637f (V3)
lateral cephalometrics of, 11 (V3)
profile evaluation and, 4 (V3)
secondary cleft lip scar revision and,
841, 843f (V3)
unilateral cleft lip repair and, 735-
758 (V3)
comparison of surgical techniques
for, 735-737 (V3)
functional approach in, 752-757,
752-757f (V3)
Millard rotation and advancement
flap technique in, 737-741,
739-743f (V3)
Tennison triangular flap technique
in, 743-751, 744-751f (V3)
timing of, 735 (V3)
Lip adhesion procedure, 720,
738 (V3)
Lip cancer
basal cell carcinoma in, 725, 725f
(V2)
malignant melanoma in, 751f (V2)
squamous cell carcinoma in, 742-744,
743f (V2)
Lip implant, 693f, 693-694, 694f (V3)
Lip trauma, 294, 298f (V2)
laceration in, 290f, 291f (V2)
reconstructive flaps for, 336b, 343f,
343-344 (V2)
Lipectomy in rhytidectomy, 502 (V3)
Lipid solubility of local anesthetics, 38t,
38-39 (V1)
Lipomatosis, 8 (V3)
Liposuction
cervicofacial, 618-625 (V3)
complications of, 623-624 (V3)
history of, 618 (V3)
patient selection in, 618-620, 619f
(V3)
preoperative preparation in, 620
(V3)
surgical technique in, 620-623,
620-625f (V3)
in rhytidectomy, 502 (V3)
Liquid crystal thermometer, 29 (V1)
Liquid silicone injection, 639-641, 641f,
649f (V3)
Lithium, 2t (V1)
Lithotripsy for sialolithiasis, 544 (V2)
Little’s area, 554, 556f (V3)
Liver
pediatric anesthesia and sedation
and, 96 (V1)
preoperative evaluation of, 9, 10f, 10t
(V1)
Liver enzymes, 71 (V1)
LLLT; See Low-level laser therapy
LMA; See Laryngeal mask airway
LMX topical anesthetic, 49 (V1)
Local anesthesia, 35-55 (V1)
for acute postoperative pain, 82-83
(V1)
Local anesthesia (Continued)
in acute trigeminal nerve injury, 266
(V1)
in arthrocentesis of
temporomandibular joint, 913
(V2)
in bone graft harvest
from mandibular ramus, 412 (V1)
from mandibular symphysis, 410
(V1)
from tibia, 414 (V1)
in cervicofacial liposuction, 621-622
(V3)
in chemical peel, 663 (V3)
chemistry of, 36t, 36-37, 37f (V1)
chronic facial pain after, 969 (V2)
for chronic orofacial pain, 114-115,
115-117f (V1), 974 (V2)
efficacy and duration of action of,
39t, 39 (V1)
in endoscopic forehead and brow lift,
603 (V3)
for facial soft tissue injury, 284 (V2)
historical perspective of, 35-36 (V1)
injection-related trigeminal nerve
injury and, 267f, 273-274 (V1)
in laser skin resurfacing, 521, 522f
(V3)
latest development and future
direction of, 50-51 (V1)
in Le Fort I osteotomy, 176 (V3)
localized complications of, 45-47, 46f,
46t (V1)
mechanism of action of, 38 (V1)
in Moh’s micrographic surgery, 735
(V2)
in Mustard[ac]e method of otoplasty,
673 (V3)
in open rhinoplasty, 567 (V3)
pH effects on, 37t, 37-38, 38f (V1)
for placement of skeletal anchorage
miniscrews, 234 (V1)
potency of, 38t, 38-39 (V1)
in rhytidectomy, 500 (V3)
in sinus-lift subantral augmentation,
459 (V1)
for skeletal anchorage plate
placement, 233 (V1)
systemic complications of, 47-48
(V1)
topical, 48-50 (V1)
use of vasoconstrictors with, 39-45,
40t, 43-45t, 44b (V1)
in zygomatic implant, 493 (V1)
Local flap
in avulsive facial injury, 329-332
(V2)
Abbe flap in, 329, 330f (V2)
cervicofacial flap in, 329-330, 333f
(V2)
facial artery musculomucosal flap
in, 329 (V2)
paramedian forehead flap in, 329,
331-332f (V2)
pectoralis major myocutaneous flap
in, 330-331 (V2)
submental island flap in, 331-332,
334f (V2)
temporoparietal fascia flap in, 330
(V2)
in skin cancer repair, 738 (V2)
Local myalgia, 832t (V2)
Localized bone defects, guided tissue
regeneration for, 428-457 (V1)
in augmentation using allograft and
xenograft bone with titanium-
reinforced membrane, 450-451,
450-451f (V1)
in augmentation using allograft bone
putty and resorbable collagen
membrane, 448f, 448-449, 449f
(V1)
in coronal defects, 436 (V1)
in corticocancellous block
augmentation of posterior
mandible, 452-453, 452-453f
(V1)
in dehiscence defects, 435-436, 447,
447f (V1)
Localized bone defects, guided tissue
regeneration for (Continued)
dual-layered technique in, 445f,
445-446, 446f (V1)
in fenestration defects, 436 (V1)
flapless buccal wall reconstruction in,
443f, 443-444, 444f (V1)
functional and design requirements of
membranes for, 429-431, 431f,
432f (V1)
to reduce postextraction bone loss,
438-440, 454f, 454-455, 455f
(V1)
ridge preservation using high-density
PTFE membrane in, 440-441f,
440-442 (V1)
in subantral augmentation, 436-438,
437f (V1)
wound closure in, 431-435, 433f,
434f (V1)
Localized gingival lesions, 179-181,
180f, 181f (V1)
Locking plates/screws for mandibular
fracture, 154f, 155 (V2)
Locking running suture, 288f (V2)
Lockwood’s ligament, 204, 205 (V2),
585, 586f, 587f (V3)
Lodine; See Etodolac
Logo, marketing and, 331, 331f (V1)
Long-term rehabilitation, 400-411, 409-
410f (V2)
Lorazepam, 58 (V1)
half-life and protein binding of, 58t
(V1)
for temporomandibular disorders,
889t (V2)
Loss of business insurance, 303 (V1)
Loss ratio, 377 (V1)
Low-dose doxycycline, 392 (V1)
Low-energy diode laser, 244, 244f (V1)
Lower canine to lower canine, 53 (V3)
Lower compartment of
temporomandibular joint,
arthroscopy and, 920, 920f (V2)
Lower eyelid
anatomy of, 581f (V3)
approaches in zygomatic fracture,
187-188, 188f (V2)
blepharoplasty of, 544-545, 545f,
590-591, 592f (V3)
malposition of, 579-580, 580f (V3)
physical examination of, 588, 589f
(V3)
Lower incisor inclination, 15, 16f (V3)
Lower incisor protrusion, 15, 16f (V3)
Lower lid crease incision, 205f (V2)
Lower lid height, 4, 5f (V3)
Lower molar to lower molar, 52 (V3)
Lower third of face
considerations in pediatric
craniomaxillary surgery, 848-863
(V3)
clinical evaluation of craniofacial
growth and, 856 (V3)
concepts of craniofacial skeletal
growth and development and,
849f, 849t, 849-850, 850t (V3)
cranio-orbital dysmorphology and,
856-858 (V3)
cranium and, 850-851, 852f (V3)
mandible and, 855-856, 856f, 857f
(V3)
mandibular hyperplasia and, 859-
860, 860f (V3)
mandibular hypoplasia and, 858-
859, 859f (V3)
maxilla and, 851, 854f,
855f (V3)
maxillary hypoplasia and, 860-861
(V3)
orbits and, 851, 853f (V3)
vertical maxillary excess and, 861f,
861-862 (V3)
zygoma and, 851, 853f (V3)
Dedo classification of facial profiles
and, 499, 499f, 499t (V3)
genioplasty and, 137-154 (V3)
advantages and disadvantages of,
685t (V3)
Lower third of face (Continued)
cephalometric analysis and, 373
(V3)
before complete mandibular
subapical osteotomy, 162f,
163f (V3)
fixation devices in, 142-145, 144-
148f (V3)
functional, 137, 138f (V3)
indications for, 137-138 (V3)
Le Fort I segmental osteotomy
with, 199-203f (V3)
mandibular relapse in, 446-451,
449-452f (V3)
mandibular widening with, 339-
341, 340f, 341f (V3)
for obstructive sleep apnea
syndrome, 325-327, 329f (V3)
in oculoauriculovertebral spectrum,
931 (V3)
outpatient, 493 (V3)
results in, 148-151, 150-153f (V3)
surgical procedure in, 140-142,
141f, 142f (V3)
treatment planning in, 138-140,
139f, 140f (V3)
profile evaluation and, 4 (V3)
Low-grade malignant tumor of parotid,
549 (V2)
Low-grade osteosarcoma, 682 (V2)
Low-level laser therapy, 253, 254b (V1)
in temporomandibular joint disorders,
248 (V1)
Lunchroom, floor plan in office design
and, 357, 357f (V1)
Lund and Browder burn estimate, 321
(V2)
Lung
of child, 95-96, 96t (V1)
effects of thyroid disorders on, 13t
(V1)
preoperative evaluation of, 3-6, 5-7t
(V1)
Lye ingestion, 323f (V2)
Lyme disease-associated arthritis of
temporomandibular joint, 864
(V2)
Lymphangioma, 581-582 (V2)
Lymphatics
of ear, 668 (V3)
involvement in cancer
lymphoma and, 758 (V2)
radiation therapy and, 771, 771t
(V2)
skin cancer and, 730-731, 737-739
(V2)
of maxillary sinus, 459 (V1)
nasal, 273 (V2)
oral cavity, 705 (V2)
Lymphedema after repair of zygomatic
fracture, 195 (V2)
Lymphoepithelial cyst of parotid gland,
539, 540f (V2)
Lymphoma, 758-766, 759b (V2)
angiocentric, 761-762 (V2)
diagnosis of, 758-759, 759f, 760f
(V2)
Hodgkin’s, 759-760, 760f (V2)
non-Hodgkin’s, 760-761, 761f (V2)
of parotid gland, 551, 556 (V2)
prognosis of, 763-764, 764b (V2)
radiation therapy in, 767 (V2)
radiographic evaluation of, 762f, 762-
763 (V2)
treatment of, 763 (V2)
Lymphomatoid granulomatosis, 761-762
(V2)
Lymphoplasmacytic lymphoma, 760-761
(V2)
Lynch incision
in nasal fracture, 279 (V2)
in naso-orbital-ethmoid fracture, 246,
246f (V2)
Lypophilized dura mater for guided
bone regeneration, 429 (V1)
Lyrica; See Pregabalin
Lysis of adhesions in
temporomandibular joint
arthroscopy, 924, 924f (V2)

M gonion to pogonion in, 42 (V3)
Macrocystic lymphatic malformation,
582 (V2)
Macrogenia, complete mandibular
subapical osteotomy for, 155-171
(V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
Macroglossia, 582 (V2)
Macrophage
platelet-rich plasma and, 504 (V1)
wound healing and, 19, 19f (V2) 61,
61f (V3)
Magnesium supplementation for
preventing bone loss, 398, 399t
(V1)
Magnetic resonance angiography
for detection of occult vascular
injuries, 69-70 (V2)
in pediatric craniomaxillofacial
tumors, 961-962 (V3)
in trigeminal neuralgia, 991 (V2)
Magnetic resonance imaging
in cervical spine injury, 63 (V2)
in chronic orofacial pain, 118, 119f
(V1)
in facial asymmetry
in adolescent internal condylar
resorption, 306f (V3)
in condylar hyperplasia, 285 (V3)
tumor-related, 293 (V3)
in unilateral reactive arthritis, 305-
306, 309f (V3)
in fracture
condylar, 170 (V2)
midface, 242 (V2)
orbital, 211 (V2)
in osteomyelitis, 634 (V2)
in temporomandibular disorders, 822-
823, 823f, 840-841, 842-843f
(V2)
in anterior disc displacement, 819
(V2)
in internal derangement of
temporomandibular joint,
931, 932f (V2)
in temporomandibular joint
hypomobility, 898 (V2)
in trigeminal neuralgia, 991 (V2)
in tumors
lymphoma, 762 (V2)
maxillofacial, 690 (V2)
odontogenic, 467 (V2)
oral cavity cancer, 710 (V2)
pediatric craniomaxillofacial, 961
(V3)
skin cancer, 733 (V2)
Malar augmentation with injectable
fillers, 639-643, 639-644f (V3)
Malar cheek implant, 689f, 689-690,
690f, 690t (V3)
Male
hair transplantation in, 651-657 (V3)
complications of, 655-656 (V3)
current medical treatment for
alopecia and, 651 (V3)
micrograft and minigraft technique
in, 651-653, 652-655f (V3)
pathophysiology of alopecia and,
651 (V3)
rotational flaps in, 655, 655f, 656f
(V3)
scalp reduction in, 655, 656f (V3)
mandibular growth evaluation and,
41-57 (V3)
anterior alveolar height in, 48
(V3)
antigonial width in, 51 (V3)
basion to B-point in, 54 (V3)
condylion to gonion in, 46 (V3)
condylion to pogonion in, 45 (V3)
Male (Continued)
lower canine to lower canine in,
53 (V3)
lower molar to lower molar in, 52
(V3)
mandibular plane to lower incisor
in, 50 (V3)
mandibular plane to lower molar
in, 49 (V3)
nasion to menton in, 57 (V3)
pogonion to N-B line in, 44 (V3)
posterior alveolar height in, 47
(V3)
ramus width at occlusal plane in,
43 (V3)
sella to gnathion in, 55 (V3)
sella to gonion in, 56 (V3)
maxillary-midface growth evaluation
and, 28-40 (V3)
anterior alveolar height in, 31
(V3)
basion to A-point in, 37 (V3)
bizygomatic width in, 36 (V3)
maxillary width in, 34 (V3)
nasion to anterior nasal spine in,
40 (V3)
palatal plane to upper incisor in,
33 (V3)
palatal plane to upper molar in, 32
(V3)
posterior alveolar height in, 30
(V3)
pterygoid fissure to A-point in, 29
(V3)
sella to anterior nasal spine in, 38
(V3)
sella to posterior nasal spine in, 39
(V3)
skeletal nasal width in, 35 (V3)
neurocranial growth evaluation and,
19-27 (V3)
basion to nasion in, 27 (V3)
bony interorbital distance in, 24
(V3)
head breadth in, 23 (V3)
head circumference in, 20 (V3)
head height in, 22 (V3)
head length in, 21 (V3)
sella to basion in, 26 (V3)
sella to nasion in, 25 (V3)
trichophytic forehead and brow lift
in, 614, 616f, 617f (V3)
Malformation, defined, 849t (V3)
Malignant bone disease,
bisphosphonates for, 558 (V2)
Malignant change
branchial cleft cyst and, 460 (V2)
thyroglossal duct cyst and, 456-458,
457f (V2)
Malignant hyperthermia
in child, 107-108 (V1)
local anesthetic-related, 48 (V1)
preoperative identification of, 2 (V1)
Malignant melanoma, 749-757 (V2)
diagnosis of, 752t, 752-754, 753f,
753t (V2)
epidemiology of, 749, 750b (V2)
incidence and etiology of, 749-750,
750b, 750t, 750-752f, 751t (V2)
management of regional disease in,
754 (V2)
staging of, 754-755, 755t (V2)
treatment of, 755-756 (V2)
Malignant midline reticulosis, 761-762
(V2)
Malignant tumors, 984-993 (V3)
reconstruction in, 988-993, 991f,
992f (V3)
rhabdomyosarcoma in, 984-986, 987f
(V3)
salivary gland tumor in, 987-988
(V3)
sarcomas in, 986-987, 988-990f (V3)
Malignant tumors of jaw, 680-704 (V2)
chondrosarcoma in, 684f, 684-685,
872 (V2)
Ewing’s sarcoma in, 687, 688f, 689f
(V2)
Malignant tumors of jaw (Continued)
mandibular approaches in, 699-702,
701f, 702f (V2)
maxillectomy in, 692-699 (V2)
airway management in, 694, 694f,
695f (V2)
critical anatomic regions in, 693
(V2)
postoperative considerations in,
699 (V2)
subtotal anterior, 698-699, 699f
(V2)
subtotal inferior, 697f, 697-698,
698f (V2)
surgical anatomic features in, 692
(V2)
technique in, 694-697, 695f, 697f
(V2)
metastatic, 687-689, 874 (V2)
multiple myeloma and, 685-687,
686f, 687f, 873-874 (V2)
osteosarcoma in, 680-684, 681f, 682f,
873 (V2)
patient evaluation in, 689-692, 690t,
691f (V2)
radiation-induced, 685 (V2)
synovial chondrosarcoma in, 872-873
(V2)
synovial sarcoma in, 873 (V2)
Mallampati classification, 69, 69t, 97-
98, 98f (V1), 419 (V3)
Malnutrition
in cranio-maxillofacial trauma
patient, 14-15, 15t (V2)
in geriatric patient, 379 (V2)
Malocclusion
after mandibular fracture, 160 (V2)
complete mandibular subapical
osteotomy for, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
facial asymmetry and, 278-280, 279-
280f (V3)
Malposition of lower eyelid, 579-580,
580f (V3)
Malpositioning of mobilized segment
in genioplasty, 439 (V3)
in total alveolar subapical osteotomy,
438 (V3)
Malpositioning of proximal segment
in intraoral vertical ramus osteotomy,
435-436, 436f (V3)
in sagittal split ramus osteotomy,
431-432 (V3)
Malpractice claim, 374-375 (V1)
Malpractice insurance, 302-303 (V1)
MALT lymphoma, 760-761, 763 (V2)
Malunion
of mandibular fracture, 102 (V2)
of midface fracture, 253 (V2)
of nasal fracture, 282 (V2)
of zygomatic fracture, 197f, 197-198
(V2)
Managed care, marketing and, 345-346
(V1)
Managed care contracting, 301, 302b
(V1)
Managing partner, 290 (V1)
Mandible
age-related changes in, 17 (V3)
alveolar repositioning osteotomies
and, 473, 473f, 474f (V1)
alveolar width distraction
osteogenesis and, 474-477, 475-
478f (V1)
anatomy of, 96 (V2)
average growth completion of, 850t
(V3)
benign nonodontogenic tumors of,
592-610 (V2)
aneurysmal bone cyst in, 596-597,
597-598f (V2)
INDEX I-51
Mandible (Continued)
central giant cell granuloma in,
592-594, 593f, 593t (V2),
970-972, 973f (V3)
cherubism in, 595-596, 596f (V2)
chondroma in, 605-606 (V2)
desmoplastic fibroma in, 606-608,
607-608f (V2)
fibrous dysplasia in, 600-601 (V2)
florid cemento-osseous dysplasia in,
601, 601f (V2)
focal cemento-osseous dysplasia in,
601 (V2)
giant cell tumor in, 594 (V2)
hyperparathyroidism lesion in,
594f, 594-595 (V2)
juvenile ossifying fibroma in, 599-
600, 600f (V2)
neurofibroma in, 602, 604f (V2)
ossifying fibroma in, 598, 599f
(V2)
osteoblastoma in, 602-604, 605f
(V2)
osteochondroma in, 606 (V2)
osteoid osteoma in, 602 (V2)
osteoma in, 604-605, 606f (V2)
periapical cemental dysplasia in,
601 (V2)
schwannoma in, 601-602, 603f (V2)
bisphosphonate-related osteonecrosis
of, 395-396 (V1), 557-566 (V2)
clinical presentation of, 559-560,
560f, 561f (V2)
clinical use of bisphosphonates
and, 558-559 (V2)
future research in, 564 (V2)
mechanism of action of
bisphosphonates and, 557-
558, 558f, 558t (V2)
pathophysiology and risk factors
for, 559 (V2)
staging of, 560-561, 561t (V2)
treatment outlines for, 561-564,
563f, 563t, 564f (V2)
for bone graft harvest, 412-414, 412-
414f (V1)
combined maxillary and mandibular
osteotomies and, 238-247 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
complete mandibular subapical
osteotomy and, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
corticocancellous block augmentation
of, 452f, 452-453, 453f (V1)
embryology of, 698f, 699, 700-703f
(V3)
examination in dentoalveolar injury,
107 (V2)
exodontia-related fracture of, 219f,
219-220, 220f (V1)
facial skeletal growth evaluation and,
41-57 (V3)
anterior alveolar height in, 48
(V3)
antigonial width in, 51 (V3)
basion to B-point in, 54 (V3)
condylion to gonion in, 46 (V3)
condylion to pogonion in, 45 (V3)
gonion to pogonion in, 42 (V3)
lower canine to lower canine in,
53 (V3)
I-52 INDEX
Mandible (Continued)
lower molar to lower molar in, 52
(V3)
mandibular plane to lower incisor
in, 50 (V3)
mandibular plane to lower molar
in, 49 (V3)
nasion to menton in, 57 (V3)
pogonion to N-B line in, 44 (V3)
posterior alveolar height in, 47
(V3)
ramus width at occlusal plane in,
43 (V3)
sella to gnathion in, 55 (V3)
sella to gonion in, 56 (V3)
free movements of, 810-811 (V2)
gait of, 825-826, 825-828f (V2)
genioplasty and, 137-154 (V3)
fixation devices in, 142-145, 144-
148f (V3)
functional, 137, 138f (V3)
indications for, 137-138 (V3)
results in, 148-151, 150-153f (V3)
surgical procedure in, 140-142,
141f, 142f (V3)
treatment planning in, 138-140,
139f, 140f (V3)
growth and development of, 855-856,
856f, 857f (V3)
hypermobility of, 905b, 905-908f,
905-909 (V2)
hypomobility of, 898-905 (V2)
ankylosis and, 901-905 (V2)
complications of, 905 (V2)
imaging in, 898 (V2)
pseudoankylosis and, 899-901 (V2)
treatment of, 905 (V2)
trismus and, 898-899 (V2)
immediate implant loading and, 518-
521, 519-524f (V1)
improper position after surgery, 413
(V3)
inadequate stabilization after surgery,
413 (V3)
interpositional bone graft and, 471,
472f (V1)
intraoral distraction osteogenesis and,
338-363, 998-1001f, 998-1002
(V3)
alveolar distraction in, 349-354,
349-354f (V3)
bone transport by, 354-360, 355-
361f (V3)
future directions in, 362 (V3)
mandibular lengthening in, 342-
346, 342-346f (V3)
mandibular widening in, 338-342,
339-342f (V3)
maxillary bone transport in, 360-
362, 362f (V3)
maxillary distraction by intraoral
devices in, 346-349, 347-349f
(V3)
Langerhans cell histiocytosis and,
567-576, 568f (V2)
classification of, 569b, 569-570 (V2)
clonality of, 570 (V2)
diagnosis, treatment, and prognosis
of, 571-575, 571-575f (V2)
histopathology of, 570, 570f (V2)
Langerhans cell and, 568-569, 569f
(V2)
masticatory movements of, 811-812
(V2)
model surgery and, 364-371 (V3)
construction of intermediate splint
in, 368-369, 369f, 370f (V3)
in facial asymmetry, 277 (V3)
in mandibular widening, 338 (V3)
marking cast in, 366-367 (V3)
measurements in, 367f, 367-368
(V3)
mounting case in, 364-366, 365f,
366f (V3)
positioning of maxilla in, 368, 368f
(V3)
for segmental surgery, 369-370,
370f (V3)
for special situations, 370-371 (V3)
Mandible (Continued)
non-Hodgkin’s lymphoma and, 763
(V2)
nonodontogenic cysts in, 447-460
(V2)
branchial cleft, 458-460, 458-460f
(V2)
dermoid and epidermoid, 451-455,
454f, 455f (V2)
globulomaxillary, 451 (V2)
median mandibular, 451 (V2)
median palatal, 451 (V2)
nasolabial, 447-448, 449f, 450f
(V2)
nasopalatine duct, 448-451, 451-
453f (V2)
thyroglossal duct, 455-458, 455-
458f (V2)
occlusal plane rotation and, 248-271
(V3)
clockwise rotation in, 252-256,
252-256f (V3)
counterclockwise rotation in, 256-
260, 257-263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-
249, 249f, 250f (V3)
geometry of treatment design using
constructed
maxillomandibular triangle in,
261f, 261-262 (V3)
linear dimensions between
maxillary length and vertical
facial height in, 250, 250f
(V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-
268 (V3)
oculoauriculovertebral spectrum and,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
odontogenic cysts in, 418-447 (V2)
calcifying, 445-447, 447f (V2)
dentigerous, 424-426, 425-428f
(V2)
gingival, 442, 445f (V2)
glandular, 444-445 (V2)
lateral periodontal, 442-444 (V2)
in nevoid basal cell carcinoma
syndrome, 441b, 441-442,
442t, 443f, 444f (V2)
paradental, 421-424 (V2)
radicular, 419-421, 420f, 422f (V2)
residual, 421, 423f (V2)
sites of, 420f (V2)
odontogenic keratocyst of, 426-441
(V2)
Mandible (Continued)
clinical features of, 428-435, 430-
435f (V2)
etiology of, 426-428 (V2)
imaging features of, 435, 436-437f
(V2)
pathologic features of, 435f, 435-
436 (V2)
surgical management of, 437-441,
439f, 440f (V2)
ultrastructure of, 437, 438f (V2)
odontogenic tumors of, 466-538 (V2)
adenomatoid, 469-472, 470-472f
(V2)
ameloblastic fibrodentinoma in,
524-527, 527f (V2)
ameloblastic fibroma in, 522-524,
523f (V2)
ameloblastic fibro-odontoma in,
524, 525f, 526f (V2)
ameloblastoma in, 476-502 (V2);
See also Ameloblastoma
biopsy of, 467-468 (V2)
calcifying, 473-476, 474f, 475f
(V2)
cementoblastoma in, 510-512 (V2)
classification of, 466-467 (V2)
clear cell, 502-508, 503-507f (V2)
clinical considerations in, 467
(V2)
fibroma in, 508-510, 509f, 511f
(V2)
imaging of, 467 (V2)
intraosseous odontogenic
carcinoma in, 527-532, 528-
530f (V2)
management objectives in, 468-
469 (V2)
myxoma in, 512-517f, 512-518
(V2)
odontoameloblastoma in, 519-522
(V2)
odontoma in, 518-519, 519-521f
(V2)
sarcoma in, 532-533 (V2)
squamous, 472f, 472-473 (V2)
osteochondroma of, 285-291, 289-
291f (V3)
osteomyelitis in, 633-639 (V2)
classifications of, 633, 634b (V2)
clinical and radiographic
presentation of, 633-635, 634-
636f (V2)
pathogenesis of, 633 (V2)
risk factors for, 634b (V2)
treatment of, 635-638, 636t, 637f
(V2)
unique complications in, 638b,
638f, 638-639 (V2)
pediatric, 352-353, 353f (V2)
pediatric tumors of
ameloblastic fibroma in, 968-970,
970f (V3)
ameloblastic fibro-odontoma in,
970, 970f (V3)
juvenile ossifying fibroma in, 974-
977, 978-979f (V3)
odontogenic myxoma in, 968, 969f
(V3)
reconstruction in, 988-993, 991f,
992f (V3)
placement of skeletal anchorage plate
in, 233, 234f (V1)
postoperative hypomobility of, 414,
445 (V3)
in bilateral sagittal split osteotomy,
112 (V3)
postoperative nonunion of,
414 (V3)
range of motion of, 824-825 (V2)
reconstructive flap options for, 336b
(V2)
sarcomas of, 680-704 (V2)
chondrosarcoma in, 684f, 684-685
(V2)
Ewing’s sarcoma in, 687, 688f, 689f
(V2)
mandibular approaches in, 699-
702, 701f, 702f (V2)
Mandible (Continued)
metastatic tumors to jaw and, 687-
689 (V2)
multiple myeloma and, 685-687,
686f, 687f (V2)
osteosarcoma in, 680-684, 681f,
682f (V2)
patient evaluation in, 689-692,
690t, 691f (V2)
radiation-induced, 685 (V2)
temporomandibular joint of, 801-814,
810b (V2); See also
Temporomandibular joint
articular disc and, 802-803, 803f
(V2)
capsule and extracapsular
ligaments and, 803-804, 804f
(V2)
condyle and, 803, 804f (V2)
developmental perspective of, 801
(V2)
digastric muscle and, 808 (V2)
free movements of mandible and,
810-811 (V2)
geniohyoid muscle and, 808, 809f
(V2)
glenoid fossa and, 802, 802f (V2)
innervation and blood supply in,
809, 809f (V2)
lateral pterygoid muscle and, 807-
808, 808f (V2)
masseter muscle and, 805f, 805-
806 (V2)
masticatory movements of
mandible and, 811-812 (V2)
medial pterygoid muscle and, 807,
807f (V2)
mylohyoid muscle and, 808, 808f
(V2)
sphenomandibular ligament and,
804-805 (V2)
stylomandibular ligament and, 805
(V2)
synovial membrane and, 803 (V2)
temporalis muscle and, 806f, 806-
807 (V2)
Treacher Collins syndrome and, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
unilateral condylar hyperplasia of,
284-285, 286-288f (V3)
vectors of growth of, 183, 183f (V1)
Mandibular anchor plate, 230-231f
(V1)
Mandibular angles and inferior borders
detailed aesthetic evaluation of, 7, 9f
(V3)
mandibular asymmetry and, 99t (V3)
profile evaluation and, 4 (V3)
Mandibular canine extraction
complicated, 196-197, 197-199f (V1)
simple, 188, 189f (V1)

Mandibular condyle, 803, 804f (V2)
abnormal biomechanics of, 817-818,
818f, 819f (V2)
anatomy of, 815-816, 816f (V2)
dislocation of, 281, 281f (V3)
exodontia-related, 218 (V1)
displacement and resorption in
bilateral sagittal split osteotomy,
114 (V3)
fracture of, 141-142, 142f, 162-181
(V2)
closed treatment of, 171 (V2)
conservative management of, 171
(V2)
diagnostic imaging of, 100f, 100-
101, 168-170, 169f (V2)
endoscopic-assisted repair of, 172-
176, 176-180f (V2)
facial asymmetry in, 294, 295f,
296f (V3)
facial nerve and, 164-165, 166f
(V2)
geriatric, 389-391f, 390-393 (V2)
open treatment of, 171 (V2)
pediatric, 364-369, 369f (V2)
physical examination of, 168 (V2)
retromandibular approach in, 171-
172, 172-175f (V2)
retromandibular vein and, 164
(V2)
skeletal injuries in, 167, 167f, 170-
171 (V2)
soft tissue injuries in, 166-167, 170
(V2)
Spiessl and Schroll classification
of, 167, 168b (V2)
superficial temporal artery and,
163-164, 164f, 165f (V2)
temporomandibular joint anatomy
and, 162-163, 163f (V2)
treatment outcomes in, 177-179
(V2)
trigeminal nerve and, 165, 166f
(V2)
mandibular asymmetry and, 99t (V3)
normal biomechanics of, 816-817,
817f (V2)
osteochondroma of, 285-291, 289-
291f (V3)
postoperative hyperplasia of, 414
(V3)
pseudocyst of, 868-869 (V2)
subluxation of, 820, 820f (V2)
unilateral adolescent internal
condylar resorption and, 299-
305, 303-304f, 306f (V3)
Mandibular deficiency
bilateral sagittal split osteotomy for,
89b, 89-97 (V3)
with long face, 95f, 95-96, 96f, 97,
97b (V3)
with normal face height, 90-92,
90-92f, 97, 97b (V3)
with short face, 93f, 93-94, 94f, 97,
97b (V3)
complete mandibular subapical
osteotomy for, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
counterclockwise rotation of
maxillomandibular complex for,
257f, 257-258, 258f (V3)
mandibular lengthening by
distraction osteogenesis for, 342-
346, 342-346f, 998-1001f, 998-
1002 (V3)
videocephalometric prediction in,
376, 376f (V3)
Mandibular excess
after cleft palate repair, 769 (V3)
bilateral sagittal split osteotomy for,
97-99, 98f (V3)
Mandibular excess (Continued)
with long face, 99, 99b, 101f (V3)
with short face, 98-99, 99b, 100f
(V3)
cephalometric analysis and, 373 (V3)
clockwise occlusal plane rotation for,
253f, 253-255, 254f (V3)
combined maxillary and mandibular
osteotomies for, 238-247 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
counterclockwise occlusal plane
rotation for, 257f, 257-258, 258f
(V3)
genioplasty for, 137-154 (V3)
fixation devices in, 142-145, 144-
148f (V3)
functional, 137, 138f (V3)
indications for, 137-138 (V3)
results in, 148-151, 150-153f (V3)
surgical procedure in, 140-142,
141f, 142f (V3)
treatment planning in, 138-140,
139f, 140f (V3)
pediatric surgical considerations in,
859-860, 860f (V3)
transoral vertical ramus osteotomy
for, 119-136 (V3), 130-135
(V3)
advantages and disadvantages of,
120-121, 121t, 122f (V3)
historical background of, 119 (V3)
indications and contraindications
for, 121-122 (V3)
intraoperative procedure in, 123-
128, 125-127f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe facial asymmetry, 130f,
130-131, 131f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe open bite, 132-135,
132-135f (V3)
postoperative physiotherapy in,
128f, 128-129 (V3)
sagittal split ramus osteotomy
versus, 119, 120f, 120t (V3)
with severe facial asymmetry, 130f,
130-131, 131f (V3)
with severe open bite, 132-135,
132-135f (V3)
surgical treatment objectives in,
123, 124f, 125f (V3)
videocephalometric prediction and,
376 (V3)
Mandibular fossa, 802, 802f (V2)
Mandibular fracture, 139-161 (V2)
atrophic, 156-158 (V2)
in bilateral sagittal split osteotomy,
114-115 (V3)
bone healing and, 144-146, 146f,
147f (V2)
classification of, 141-143, 142-144f
(V2)
closed treatment of, 146-148, 147f
(V2)
comminuted, 158-159 (V2)
in complete mandibular subapical
osteotomy, 158 (V3)
complications of, 159-160 (V2)
condylar and subcondylar, 141-142,
142f, 162-181 (V2)
closed treatment of, 171 (V2)
conservative management of, 171
(V2)
diagnostic imaging of, 100f, 100-
101, 168-170, 169f (V2)
endoscopic-assisted repair of, 172-
176, 176-180f (V2)
Mandibular fracture (Continued)
facial nerve and, 164-165, 166f
(V2)
open treatment of, 171 (V2)
pediatric, 364-369, 369f (V2)
physical examination of, 168 (V2)
retromandibular approach in, 171-
172, 172-175f (V2)
retromandibular vein and, 164
(V2)
skeletal injuries in, 167, 167f, 170-
171 (V2)
soft tissue injuries in, 166-167, 170
(V2)
Spiessl and Schroll classification
of, 167, 168b (V2)
superficial temporal artery and,
163-164, 164f, 165f (V2)
temporomandibular joint anatomy
and, 162-163, 163f (V2)
treatment outcomes in, 177-179
(V2)
trigeminal nerve and, 165, 166f
(V2)
dentoalveolar injury and, 115t, 127f
(V2)
diagnostic imaging of, 95-103, 144-
145f (V2)
in complications of treatment,
102-103 (V2)
mandibular anatomy and, 96 (V2)
in mandibular body fracture, 101,
102f (V2)
mandibular series in, 96-98, 97f
(V2)
in mandibular symphysis and
parasymphysis fractures, 101,
102f (V2)
panoramic radiography in, 98, 99f
(V2)
in simple and compound fractures,
99, 99f (V2)
supplemental radiographs in, 98
(V2)
endoscopic techniques in, 152-156
(V2)
internal fixation modalities in,
154f, 154-155, 155f (V2)
lag screws in, 155-156, 156-158f
(V2)
miniplates in, 155 (V2)
transosseous wiring in, 156, 158f
(V2)
epidemiology of, 141 (V2)
facial asymmetry in, 294, 295f, 296f
(V3)
geriatric, 389-391f, 390-393 (V2)
historical overview of management
of, 139-141, 140f, 141f (V2)
management of teeth in line of
fracture, 156 (V2)
open treatment of, 148-152 (V2)
transcervical-retromandibular
approach in, 152, 152f, 153f
(V2)
transcervical-submandibular
approach in, 150-152, 150-
152f (V2)
transoral/transbuccal approach in,
148-150, 149f, 150f (V2)
pediatric, 364-369, 369f (V2)
physical examination of, 143-144 (V2)
reconstruction in, 336-337, 336-340f
(V2)
in sagittal split ramus osteotomy,
424-426, 425-431f (V3)
trigeminal nerve injury in, 272-273
(V1)
Mandibular growth values, 41-57 (V3)
anterior alveolar height in, 48 (V3)
antigonial width in, 51 (V3)
basion to B-point in, 54 (V3)
condylion to gonion in, 46 (V3)
condylion to pogonion in, 45 (V3)
gonion to pogonion in, 42 (V3)
lower canine to lower canine in, 53
(V3)
lower molar to lower molar in, 52
(V3)
INDEX I-53
Mandibular growth values (Continued)
mandibular plane to lower incisor in,
50 (V3)
mandibular plane to lower molar in,
49 (V3)
nasion to menton in, 57 (V3)
pogonion to N-B line in, 44 (V3)
posterior alveolar height in, 47 (V3)
ramus width at occlusal plane in, 43
(V3)
sella to gnathion in, 55 (V3)
sella to gonion in, 56 (V3)
Mandibular lengthening, 342-346, 342-
346f (V3)
in oculoauriculovertebral spectrum,
928, 929-930f (V3)
Mandibular molar extraction
sectioning in, 194, 195f (V1)
simple, 188, 190f (V1)
Mandibular nerve, 163f (V2)
Mandibular nerve block
acute trigeminal nerve symptoms
after, 273 (V1)
in bone graft harvest
from mandibular ramus, 412 (V1)
from mandibular symphysis, 410
(V1)
chronic facial pain after, 969 (V2)
Mandibular orthognathic surgery, 68-71
(V3)
bilateral sagittal split osteotomy in,
71, 87-118 (V3)
characteristics and advantages of,
89, 89b (V3)
hemorrhage in, 115, 115b (V3)
for mandibular asymmetry, 99t, 99-
102, 102-105f (V3)
for mandibular deficiency, 89b, 89-
97, 90-96f, 97b (V3)
for mandibular prognathism, 97-99,
98f, 99b, 100f, 101f (V3)
nerve injury in, 112-113, 113b
(V3)
osteosynthesis in, 109-111, 110f,
111b (V3)
osteotomy in, 106-109, 107f, 107t,
108f, 109b (V3)
postoperative sequelae in, 111-112
(V3)
postoperative wound infection in,
115, 116b (V3)
rare complications in, 116, 116b
(V3)
relapse in, 115-116, 116b (V3)
soft tissue dissection in, 102-106,
106f (V3)
temporomandibular joint
dysfunction after, 113-114
(V3)
unfavorable bony split in, 114b,
114-115 (V3)
cephalometric analysis and, 373, 374f
(V3)
complications in, 419-454 (V3)
dental and periodontal problems
in, 453 (V3)
dental compensations and, 419-
421, 420-422f (V3)
excessive swelling in, 441-442,
442f (V3)
hemorrhage and hematoma in,
442-443 (V3)
idiopathic condylar resorption in,
453-454 (V3)
infection in, 443 (V3)
leveling and root divergence
in segmental cases and,
423 (V3)
loss of gonial projection in, 454,
455-456f (V3)
mandibular dysfunction in, 445,
453 (V3)
neurologic dysfunction in, 444-
445, 453 (V3)
patient dissatisfaction and, 423
(V3)
postoperative nausea, vomiting,
and dehydration in, 443 (V3)
prevention of, 454t (V3)
I-54 INDEX
Mandibular orthognathic surgery
(Continued)
tooth size discrepancies and, 422-
423, 423f (V3)
transverse discrepancies and, 421-
422 (V3)
genioplasty in, 137-154 (V3)
cephalometric analysis and, 373
(V3)
before complete mandibular
subapical osteotomy, 162f,
163f (V3)
complications in, 439-441, 440f,
441f, 446-451, 449-452f (V3)
fixation devices in, 142-145, 144-
148f (V3)
functional, 137, 138f (V3)
indications for, 137-138 (V3)
Le Fort I segmental osteotomy
with, 199-203f (V3)
mandibular widening with, 339-
341, 340f, 341f (V3)
for obstructive sleep apnea
syndrome, 325-327, 329f (V3)
outpatient, 493 (V3)
results in, 148-151, 150-153f (V3)
surgical procedure in, 140-142,
141f, 142f (V3)
treatment planning in, 138-140,
139f, 140f (V3)
historical background of, 68, 68f (V3)
intraoral vertical ramus osteotomy in,
70-71, 119-136 (V3)
advantages and disadvantages of,
120-121, 121t, 122f (V3)
historical background of, 68, 119
(V3)
indications and contraindications
for, 121-122 (V3)
intraoperative procedure in, 123-
128, 125-127f (V3)
Le Fort I segmental osteotomy
with, 199-203f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe facial asymmetry, 130f,
130-131, 131f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe open bite, 132-135,
132-135f (V3)
postoperative physiotherapy in,
128f, 128-129 (V3)
sagittal split ramus osteotomy
versus, 119, 120f, 120t
(V3)
surgical treatment objectives in,
123, 124f, 125f (V3)
inverted L and C osteotomies in,
436-439, 437f (V3)
maxillary osteotomy with, 238-247
(V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
pediatric, 858 (V3)
revascularization and healing in, 68-
70, 70f (V3)
sagittal split ramus osteotomy in, 70,
70f, 423-433 (V3)
intraoperative bleeding in, 429-
431, 433f (V3)
minor technical difficulties in, 433
(V3)
nerve injury in, 426-429, 432f
(V3)
proximal segment malpositioning
in, 431-432 (V3)
relapse in, 445, 446f (V3)
in rotation of maxillomandibular
complex, 268, 268f, 269f (V3)
Mandibular orthognathic surgery
(Continued)
transoral vertical ramus osteotomy
versus, 119, 120t, 121 (V3)
in two-jaw surgery, 240 (V3)
unfavorable osteotomy in, 423-426,
424-434f (V3)
transoral vertical ramus osteotomy in,
119-136 (V3)
advantages and disadvantages of,
120-121, 121t, 122f (V3)
complications in, 433-436, 434-
436f, 445-446, 446-449f (V3)
historical background of, 119 (V3)
indications and contraindications
for, 121-122 (V3)
intraoperative procedure in, 123-
128, 125-127f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe facial asymmetry, 130f,
130-131, 131f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe open bite, 132-135,
132-135f (V3)
postoperative physiotherapy in,
128f, 128-129 (V3)
sagittal split ramus osteotomy
versus, 119, 120f, 120t (V3)
surgical treatment objectives in,
123, 124f, 125f (V3)
vascular anatomic considerations in,
68, 69f (V3)
Mandibular plane angle, 13, 13f (V3)
Mandibular plane to lower incisor, 50
(V3)
Mandibular plane to lower molar, 49 (V3)
Mandibular ramus
bilateral sagittal split osteotomy and,
106-108, 107f, 108f, 114, 114b
(V3)
for bone graft harvest, 412-414, 412-
414f (V1)
mandibular asymmetry and, 99t (V3)
transoral vertical ramus osteotomy
and, 119-136 (V3)
advantages and disadvantages of,
120-121, 121t, 122f (V3)
historical background of, 119 (V3)
indications and contraindications
for, 121-122 (V3)
intraoperative procedure in, 123-
128, 125-127f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe facial asymmetry, 130f,
130-131, 131f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe open bite, 132-135,
132-135f (V3)
postoperative physiotherapy in,
128f, 128-129 (V3)
sagittal split ramus osteotomy
versus, 119, 120f, 120t (V3)
surgical treatment objectives in,
123, 124f, 125f (V3)
Mandibular resection technique, 700-
702, 701f, 702f (V2)
Mandibular second molar, bilateral
sagittal split osteotomy and, 106-
108 (V3)
Mandibular second premolar,
complicated extraction of, 197-
199, 200f (V1)
Mandibular series, 96-98, 97f, 144,
144f, 145f (V2)
Mandibular splint, 398-399, 399f (V3)
Mandibular symphyseal osteotomy, 137-
154 (V3)
cephalometric analysis and, 373 (V3)
before complete mandibular subapical
osteotomy, 162f, 163f (V3)
complications in, 439-441, 440f, 441f
(V3)
fixation devices in, 142-145, 144-
148f (V3)
functional, 137, 138f (V3)
Mandibular symphyseal osteotomy
(Continued)
indications for, 137-138 (V3)
Le Fort I segmental osteotomy with,
199-203f (V3)
mandibular widening with, 339-341,
340f, 341f (V3)
for obstructive sleep apnea syndrome,
325-327, 329f (V3)
outpatient, 493 (V3)
relapse in, 446-451, 449-452f (V3)
results in, 148-151, 150-153f (V3)
surgical procedure in, 140-142, 141f,
142f (V3)
treatment planning in, 138-140, 139f,
140f (V3)
Mandibular symphysis for bone graft
harvest, 409-411, 410-412f (V1)
Mandibular third molar impaction
chronic orofacial pain and, 125-126
(V1)
complicated exodontia for, 201-210
(V1)
bone removal and tooth sectioning
in, 205-206, 207-210f (V1)
classification of, 203, 204f (V1)
indications and contraindications
for, 202-203 (V1)
instrumentation for, 203, 203t (V1)
postoperative instructions in, 208-
210, 209b (V1)
preoperative management in, 207t,
207-208, 208b (V1)
surgical technique in, 203-205,
205b, 206f (V1)
trauma to temporomandibular joint
and, 218 (V1)
wound closure in, 206-207 (V1)
mandibular fracture in bilateral
sagittal split osteotomy and,
114-115 (V3)
Mandibular widening, 338-342, 339-
342f (V3)
Mandibulofacial dysostosis, 936-960,
937f (V3)
classification of temporomandibular
joint-mandibular malformation
in, 939-943, 943-944f (V3)
considerations during infancy and
early childhood, 939, 943f (V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956 (V3)
external ear reconstruction in, 955-
956 (V3)
facial growth potential in, 939, 940-
942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction in,
948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital reconstruction
in, 943-948, 944-948f (V3)
zygomatic deformity in, 851 (V3)
Manipulation of occlusal plane, 248-
271 (V3)
clockwise rotation in, 252-256
(V3)
center of rotation at anterior nasal
spine, 252, 252f, 252t (V3)
center of rotation at maxillary
incisor tip, 252, 252f, 253t
(V3)
center of rotation at pogonion,
255, 255t, 256f (V3)
center of rotation at zygomatic
buttress, 255-256, 256f, 256t
(V3)
mandibular excess and, 253f, 253-
255, 254f (V3)
counterclockwise rotation in, 256-
260 (V3)
center of rotation at anterior nasal
spine, 256, 259f, 259t (V3)
Manipulation of occlusal plane
(Continued)
center of rotation at posterior nasal
spine, 256-260, 260f, 260t
(V3)
center of rotation at zygomatic
buttress, 256, 259f, 259t (V3)
in Treacher Collins syndrome, 954
(V3)
in unilateral adolescent internal
condylar resorption, 303-304f,
305, 306f (V3)
vertical maxillary deficiency and
mandibular anteroposterior
deficiency and, 257f, 257-258,
258f (V3)
vertical maxillary excess and
mandibular anteroposterior
deficiency and, 261-263, 261-
263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-249,
249f, 250f (V3)
geometry of treatment design using
constructed maxillomandibular
triangle in, 261f, 261-262 (V3)
linear dimensions between maxillary
length and vertical facial height
in, 250, 250f (V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f (V3)
stretching of soft tissues in, 267-268
(V3)
Manson facial fracture system, 241 (V2)
Mantle cell lymphoma, 760-761, 763
(V2)
Marcaine; See Bupivacaine
Marcus-Gunn pupil, 55 (V2)
Margin reflex distance-1, 588, 588f
(V3)
Margin reflex distance-3, 588 (V3)
Marginal incision in rhinoplasty, 561,
561f (V3)
closed, 572 (V3)
open, 567-568 (V3)
Margination in wound healing, 61 (V3)
Marie-Str[um]upell disease, 860-861
(V2)
Marketing, 287, 318-350 (V1)
academic, 319 (V1)
activity sponsorship in, 345 (V1)
business lunches and, 337 (V1)
calling postoperative patients and,
345 (V1)
communication and, 347-349, 349f
(V1)
community service and, 338 (V1)
cosmetic surgery, 343-345, 343-345f
(V1)
descriptive name in, 318-319 (V1)
employee relations and, 323-329,
326b (V1)
front desk staff and, 346-347 (V1)
hiring and firing and, 322 (V1)
identification of target market in, 334
(V1)
image and logo and, 331, 331f (V1)
initiation of marketing plan in, 329-
331, 330f (V1)
internal, 339t, 339-340, 340f (V1)
lessons from big business in, 319-320
(V1)
managed care and, 345-346 (V1)
media networking and, 341-342, 342f
(V1)
newsletters and media packs in, 340-
341, 341f (V1)
office environment and, 333-334
(V1)

Marketing (Continued)
outside professional consultation in,
322-323, 337-338 (V1)
patient call-on-hold devices in, 345
(V1)
patient payment options and, 342 (V1)
patient surveys in, 336-337 (V1)
patient-surgeon interaction and, 331-
333, 332f (V1)
preentry materials in, 334-335 (V1)
procedure-specific, 338-339 (V1)
synergy in, 335-336, 336b (V1)
uniformity in, 331b (V1)
vision in, 321-322 (V1)
waiting patient and, 333 (V1)
yellow pages advertising in, 342 (V1)
Marking of cast in model surgery, 366-
367 (V3)
Markowitz classification of naso-orbital-
ethmoid fracture injuries, 244, 245f
(V2)
Marsupialization of odontogenic
keratocyst, 440-441 (V2)
MART-1/Melan-A
immunohistochemical marker for
melanoma, 752t (V2)
Massage of temporomandibular joint,
891 (V2)
Masseter muscle, 163, 805f, 805-806
(V2)
attachments of, 269f (V3)
bleeding in bilateral sagittal split
osteotomy and, 115, 115b (V3)
innervation and blood supply to, 809,
809f (V2)
maxillomandibular rotation and, 270f
(V3)
surgery-related dysfunction of, 406
(V3)
Masseteric artery, 174, 175f (V3)
bleeding in intraoral vertical ramus
osteotomy and, 435 (V3)
Masseteric nerve, 809 (V2)
Massive osteolysis, 875 (V2)
Mast cell, wound repair and, 17-18, 18f
(V2)
Mastication, 811-812 (V2)
Masticatory muscle(s)
bilateral sagittal split osteotomy and,
89 (V3)
hypertrophy-related facial asymmetry
and, 291-292 (V3)
passive stretching of, 986 (V2)
surgery-related dysfunction of, 406
(V3)
Masticatory muscle pain, 961-978 (V2)
antidepressants for, 973 (V2)
atypical facial pain and, 967-968
(V2)
barriers to management of, 970-971
(V2)
botulinum toxin injection for, 974-
975 (V2)
of cardiac origin, 969 (V2)
central mechanisms of, 963 (V2)
chronic, 131 (V1)
clinically based comprehensive pain
management program for, 975
(V2)
complex regional pain syndrome and,
966-967 (V2)
diagnostic approach to, 126 (V1),
832t (V2)
Eagle’s syndrome and, 969-970, 970f
(V2)
evaluation of, 963-966, 965f, 966t
(V2)
future directions in management of,
975-976 (V2)
muscle relaxants for, 974 (V2)
nerve injury from dental procedures
and, 968f, 968-969 (V2)
neuralgia-inducing cavitational
osteonecrosis and, 967 (V2)
neuropathic agents for, 973-974 (V2)
nonsteroidal antiinflammatory drugs
for, 972-973, 973t (V2)
opioid therapy for, 971-972, 972t
(V2)
Masticatory muscle pain (Continued)
orthognathic surgery-related, 72-73
(V3)
osteonecrosis-related, 970 (V2)
peripheral mechanisms of, 962, 963f
(V2)
physical therapy for, 971 (V2)
surgical intervention for, 975 (V2)
therapeutic injections for, 974 (V2)
topical capsaicin for, 975 (V2)
trigeminal anatomy and, 961-962,
962f (V2)
Mastoid fontanel, 865f (V3)
Material risks of proposed procedure,
379 (V1)
Matrix metalloproteinases
periimplantitis and, 392 (V1)
temporomandibular disorders and,
850, 930 (V2)
Maxilla
adaptive morphology of, 541 (V1)
age-related changes in, 16, 17f (V3)
alveolar vertical distraction
osteogenesis and, 477, 477f, 478f
(V1)
average growth completion of, 850t
(V3)
benign nonodontogenic tumors of,
592-610 (V2)
aneurysmal bone cyst in, 596-597,
597-598f (V2)
central giant cell granuloma in,
592-594, 593f, 593t (V2),
970-972, 973f (V3)
cherubism in, 595-596, 596f (V2)
chondroma in, 605-606 (V2)
desmoplastic fibroma in, 606-608,
607-608f (V2)
fibrous dysplasia in, 600-601 (V2)
florid cemento-osseous dysplasia in,
601, 601f (V2)
focal cemento-osseous dysplasia in,
601 (V2)
giant cell tumor in, 594 (V2)
hyperparathyroidism lesion in,
594f, 594-595 (V2)
juvenile ossifying fibroma in, 599-
600, 600f (V2)
neurofibroma in, 602, 604f (V2)
ossifying fibroma in, 598, 599f (V2)
osteoblastoma in, 602-604, 605f
(V2)
osteochondroma in, 606 (V2)
osteoid osteoma in, 602 (V2)
osteoma in, 604-605, 606f (V2)
periapical cemental dysplasia in,
601 (V2)
schwannoma in, 601-602, 603f
(V2)
bisphosphonate-related osteonecrosis
of, 557-566 (V2)
clinical presentation of, 559-560,
560f, 561f (V2)
clinical use of bisphosphonates
and, 558-559 (V2)
future research in, 564 (V2)
mechanism of action of
bisphosphonates and, 557-
558, 558f, 558t (V2)
pathophysiology and risk factors
for, 559 (V2)
staging of, 560-561, 561t (V2)
treatment outlines for, 561-564,
563f, 563t, 564f (V2)
cephalometric analysis of, 13-14, 14f
(V3)
cleft, 806-812, 840 (V3)
alveolar bone grafting technique
for, 808-810, 808-811f (V3)
cleft orthognathic surgery and, 819
(V3)
grafting materials for, 806-807 (V3)
history and timing of repair in, 806
(V3)
missing teeth and crowded arches
in, 810-811, 811f (V3)
orthodontics for, 807f, 807-808
(V3)
postoperative care in, 810 (V3)
Maxilla (Continued)
combined maxillary and mandibular
osteotomies and, 238-247 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
deformity in craniofacial dysostosis
syndromes, 882-883 (V3)
embryology of, 698f, 699, 700-703f
(V3)
exodontia-related fracture of, 219-
220 (V1)
forehead and brow lift and, 595 (V3)
growth and development of, 851,
854f, 855f (V3)
improper position after surgery, 413
(V3)
improper repositioning in Le Fort I
osteotomy, 470-471, 471f (V3)
inadequate stabilization after surgery,
413 (V3)
intraoral distraction osteogenesis and,
338-363 (V3)
alveolar distraction in, 349-354,
349-354f (V3)
bone transport by, 354-360, 355-
361f (V3)
future directions in, 362 (V3)
mandibular lengthening in, 342-
346, 342-346f (V3)
mandibular widening in, 338-342,
339-342f (V3)
maxillary bone transport in, 360-
362, 362f (V3)
maxillary distraction by intraoral
devices in, 346-349, 347-349f
(V3)
Langerhans cell histiocytosis and,
567-576, 568f (V2)
classification of, 569b, 569-570
(V2)
clonality of, 570 (V2)
diagnosis, treatment, and prognosis
of, 571-575, 571-575f (V2)
histopathology of, 570, 570f (V2)
Langerhans cell and, 568-569, 569f
(V2)
maxillary-midface growth evaluation
and, 28-40 (V3)
anterior alveolar height in, 31
(V3)
basion to A-point in, 37 (V3)
bizygomatic width in, 36 (V3)
maxillary width in, 34 (V3)
nasion to anterior nasal spine in,
40 (V3)
palatal plane to upper incisor in,
33 (V3)
palatal plane to upper molar in, 32
(V3)
posterior alveolar height in, 30 (V3)
pterygoid fissure to A-point in, 29
(V3)
sella to anterior nasal spine in, 38
(V3)
sella to posterior nasal spine in, 39
(V3)
skeletal nasal width in, 35 (V3)
non-Hodgkin’s lymphoma and, 763
(V2)
nonodontogenic cysts in, 447-460
(V2)
branchial cleft, 458-460, 458-460f
(V2)
dermoid and epidermoid, 451-455,
454f, 455f (V2)
globulomaxillary, 451 (V2)
median mandibular, 451 (V2)
median palatal, 451 (V2)
nasolabial, 447-448, 449f, 450f
(V2)
INDEX I-55
Maxilla (Continued)
nasopalatine duct, 448-451, 451-
453f (V2)
thyroglossal duct, 455-458, 455-
458f (V2)
occlusal plane rotation and, 248-271
(V3)
clockwise rotation in, 252-256,
252-256f (V3)
counterclockwise rotation in, 256-
260, 257-263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-
249, 249f, 250f (V3)
geometry of treatment design using
constructed
maxillomandibular triangle in,
261f, 261-262 (V3)
linear dimensions between
maxillary length and vertical
facial height in, 250, 250f
(V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-
268 (V3)
oculoauriculovertebral spectrum and
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
odontogenic cysts in, 418-447 (V2)
calcifying, 445-447, 447f (V2)
dentigerous, 424-426, 425-428f
(V2)
gingival, 442, 445f (V2)
glandular, 444-445 (V2)
lateral periodontal, 442-444 (V2)
in nevoid basal cell carcinoma
syndrome, 441b, 441-442,
442t, 443f, 444f (V2)
odontogenic keratocyst, 426-441
(V2); See also Odontogenic
keratocyst
paradental, 421-424 (V2)
radicular, 419-421, 420f, 422f (V2)
residual, 421, 423f (V2)
sites of, 420f (V2)
odontogenic tumors of, 466-538
(V2)
adenomatoid, 469-472, 470-472f
(V2)
ameloblastic fibrodentinoma in,
524-527, 527f (V2)
ameloblastic fibroma in, 522-524,
523f (V2)
ameloblastic fibro-odontoma in,
524, 525f, 526f (V2)
ameloblastoma in, 476-502 (V2);
See also Ameloblastoma
biopsy of, 467-468 (V2)
I-56 INDEX
Maxilla (Continued)
calcifying, 473-476, 474f, 475f
(V2)
cementoblastoma in, 510-512 (V2)
classification of, 466-467 (V2)
clear cell, 502-508, 503-507f (V2)
clinical considerations in, 467
(V2)
fibroma in, 508-510, 509f, 511f
(V2)
imaging of, 467 (V2)
intraosseous odontogenic
carcinoma in, 527-532, 528-
530f (V2)
management objectives in, 468-
469 (V2)
myxoma in, 512-517f, 512-518
(V2)
odontoameloblastoma in, 519-522
(V2)
odontoma in, 518-519, 519-521f
(V2)
sarcoma in, 532-533 (V2)
squamous, 472f, 472-473 (V2)
placement of skeletal anchorage plate
in, 232-233, 233f (V1)
postoperative nonunion of, 414 (V3)
reconstructive flap options for, 336b
(V2)
sarcomas of, 680-704 (V2)
chondrosarcoma in, 684f, 684-685
(V2)
Ewing’s sarcoma in, 687, 688f, 689f
(V2)
maxillectomy in, 692-699, 694f,
695f, 697-699f (V2)
metastatic tumors to jaw and, 687-
689 (V2)
multiple myeloma and, 685-687,
686f, 687f (V2)
osteosarcoma in, 680-684, 681f,
682f (V2)
patient evaluation in, 689-692,
690t, 691f (V2)
radiation-induced, 685 (V2)
sinus-lift subantral augmentation and,
458-470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic
considerations in, 458-459
(V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f,
464f (V1)
elevation of schneiderian
membrane in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
trephine core membrane elevation
in, 464-468, 464-468f (V1)
vascular supply, lymphatic
drainage, and innervation in,
459 (V1)
subantral bone augmentation and,
436-438, 437f (V1)
transverse deficiency of, 219-237
(V3)
clinical evaluation in, 219, 220-
220f, 221f (V3)
incidence and origin of, 219, 220f
(V3)
orthopedic rapid maxillary
expansion for, 224-226, 224-
226f (V3)
radiographic evaluation in, 220-
223, 221-223f (V3)
surgically assisted maxillary
expansion for, 227-235, 228-
234f (V3)
Maxilla (Continued)
tumors of
adenomatoid odontogenic, 968,
968f (V3)
ameloblastic fibro-odontoma in,
970, 970f (V3)
juvenile ossifying fibroma in, 974-
977, 978-979f (V3)
odontogenic myxoma in, 968, 969f
(V3)
reconstruction in, 988-993, 991f,
992f (V3)
unilateral versus bilateral oronasal
cleft deformity and, 784t (V3)
vectors of growth of, 183, 183f (V1)
zygomatic implant and, 491-500 (V1)
complications in, 498f, 498-499
(V1)
final prosthesis fabrication and,
499 (V1)
historical perspective in, 491 (V1)
patient selection for, 491-492, 492f
(V1)
postoperative care in, 498 (V1)
preoperative considerations in,
493, 493f (V1)
prosthetic conversion technique
in, 496-497, 497f, 498f (V1)
radiographic evaluation in, 492,
492f (V1)
regional anatomy in, 492-493 (V1)
surgical options in, 493-494, 494f
(V1)
surgical protocol in, 494-496, 494-
497f (V1)
Maxillary anchor plate, 226t, 226 (V1)
Maxillary anchor screw, 225f (V1)
Maxillary artery, 69f, 174, 175f (V3)
condylar fracture and, 163-164, 164f,
165f (V2)
hemorrhage and
in intraoral vertical ramus
osteotomy and, 435 (V3)
in Le Fort I osteotomy, 468 (V3)
in sagittal split ramus osteotomy,
430-431, 433f (V3)
mandibular orthognathic surgery and,
68 (V3)
maxilla and, 63f, 173f (V3)
maxillary sinus and, 459 (V1)
transoral vertical ramus osteotomy
and, 126-127, 127f (V3)
Maxillary bone transport, 360-362, 362f
(V3)
Maxillary buttresses, 227, 227f (V3)
Maxillary canine
complicated extraction of, 196-197,
197-199f (V1)
impacted, 167-170, 169f, 170f (V1)
simple extraction of, 188, 189f (V1)
Maxillary central incisor, blood vessels
in, 67f (V3)
Maxillary deficiency
cephalometric analysis and, 373-375
(V3)
cleft orthognathic surgery in, 813-827
(V3)
bone grafting in, 819, 820-825f (V3)
obstructed nasal breathing and,
819 (V3)
preoperative evaluation in, 813-
814 (V3)
stabilization of mobilized cleft
maxilla and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-
819, 818f (V3)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
clinical evaluation in, 219, 220-220f,
221f (V3)
combined maxillary and mandibular
osteotomies for, 238-247 (V3)
in horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
Maxillary deficiency (Continued)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
in vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
incidence and origin of, 219, 220f
(V3)
maxillary distraction by intraoral
devices for, 346-349, 347-349f
(V3)
orthopedic rapid maxillary expansion
for, 224-226, 224-226f (V3)
pediatric surgical considerations in,
860-861 (V3)
radiographic evaluation in, 220-223,
221-223f (V3)
surgically assisted maxillary
expansion for, 227-231, 228-
232f (V3)
complications of, 231-232, 233f
(V3)
modification of, 232-233, 234f
(V3)
segmental maxillary osteotomy
versus, 233-235 (V3)
transoral vertical ramus osteotomy
for, 130-135 (V3)
with severe facial asymmetry, 130f,
130-131, 131f (V3)
with severe open bite, 132-135,
132-135f (V3)
vertical
combined maxillary and
mandibular osteotomies for,
244f, 244-245, 245f (V3)
counterclockwise rotation of
maxillomandibular complex
for, 257f, 257-258, 258f (V3)
total maxillary segmental
osteotomy for, 199-203f (V3)
Maxillary depth angle, 13, 14f (V3)
Maxillary distraction by intraoral
devices, 346-349, 347-349f (V3)
Maxillary distraction osteogenesis,
1002, 1003f, 1004f (V3)
Maxillary excess
clockwise occlusal plane rotation for,
253f, 253-255, 254f (V3)
pediatric surgical considerations in,
861f, 861-862 (V3)
Maxillary fracture
dentoalveolar injury and, 115t (V2)
in geriatric patient, 386-390, 387-
390f, 392t (V2)
Maxillary incisor
clockwise rotation of
maxillomandibular complex at,
252, 252f, 253t (V3)
impacted, 171 (V1)
implant in pediatric trauma, 181,
182f (V1)
Maxillary labial frenectomy, 173-174,
174f (V1)
Maxillary length to mandibular length,
14, 14f (V3)
Maxillary molar extraction
oroantral communication in, 214f,
214-215 (V1)
sectioning in, 194, 195f, 196f (V1)
simple, 188, 190f (V1)
Maxillary nerve, eyelid and, 585 (V3)
Maxillary osteotomy, 63-68, 172-204
(V3)
ambulatory, 494 (V3)
arch wire change and, 400 (V3)
cephalometric analysis and, 373-375
(V3)
in cleft orthognathic surgery, 815-
819, 818f (V3)
before complete mandibular subapical
osteotomy, 162f (V3)
complications of, 185-189 (V3)
in craniofacial dysotosis syndromes,
884 (V3)
fixation of, 181-184 (V3)
Maxillary osteotomy (Continued)
hierarchy of stability in, 184 (V3)
historical background of, 62-63, 172,
173f (V3)
mandibular osteotomy with, 238-247
(V3)
in horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
in vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
in maxillary bone transport, 360
(V3)
maxillomandibular complex rotation
and, 266, 267f (V3)
model surgery and, 364-371 (V3)
construction of intermediate splint
in, 368-369, 369f, 370f (V3)
in facial asymmetry, 277 (V3)
in mandibular widening, 338 (V3)
marking cast in, 366-367 (V3)
measurements in, 367f, 367-368
(V3)
mounting case in, 364-366, 365f,
366f (V3)
positioning of maxilla in, 368, 368f
(V3)
for segmental surgery, 369-370,
370f (V3)
for special situations, 370-371 (V3)
for obstructive sleep apnea syndrome,
323-330, 327-332f (V3)
in oculoauriculovertebral spectrum,
931, 931f (V3)
in pediatric craniomaxillofacial
tumor, 963-964 (V3)
postoperative management of, 184
(V3)
postoperative nasal bleeding and, 404
(V3)
postoperative sensory nerve deficit
and, 405 (V3)
postsurgical airway obstruction and,
404 (V3)
revascularization and healing in, 63-
65, 64f, 65f (V3)
segmental, 66-67, 67f, 192-204 (V3)
complications in, 198, 198f, 199f
(V3)
historical background of,
192 (V3)
indications for, 192-193 (V3)
for maxillary deficiency, 199-203f
(V3)
osteotomy design in, 196 (V3)
postoperative care in, 196-197,
197f (V3)
surgical planning in, 197-198 (V3)
surgically assisted maxillary
expansion versus, 233-235
(V3)
technique in, 193-196, 194-196f
(V3)
soft tissue changes in, 184-185, 185-
188f (V3)
soft tissue incision in, 65-66 (V3)
surgical anatomy in, 172-174, 173f,
174f (V3)
surgical technique in, 176-181, 176-
184f (V3)
surgically assisted maxillary
expansion in, 67f, 67-68 (V3)
in Treacher Collins syndrome, 954
(V3)
vascular anatomy in, 174-175, 176f
(V3)
Maxillary premolar extraction
complicated, 199, 200f (V1)
simple, 188, 189f (V1)
Maxillary process of zygoma, 182 (V2)
Maxillary sinus
effect of Le Fort 1 osteotomy on, 65
(V3)

Maxillary sinus (Continued)
exodontia-related displacement of
tooth into, 213 (V1)
location in maxilla, 172 (V3)
oroantral communication in
maxillary molar extraction, 214f,
214-215 (V1)
orthognathic surgery-related changes
in, 76 (V3)
osteoma and, 605 (V2)
radiographic evaluation and, 549f
(V1)
sinus-lift subantral augmentation and,
458-470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic
considerations in, 458-459
(V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f,
464f (V1)
computed tomography in, 561-563,
562f, 563f (V1)
elevation of schneiderian
membrane in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
trephine core membrane
elevation in, 464-468,
464-468f (V1)
vascular supply, lymphatic
drainage, and innervation in,
459 (V1)
three-dimensional treatment
planning and, 560-561, 561-562f
(V1)
zygomatic implant and, 494, 494f
(V1)
Maxillary splint, 397f, 397-398, 398f
(V3)
Maxillary surgery complications, 454-
480 (V3)
accurate presurgical records and, 459,
460-463f (V3)
antral or nasal fistulas in, 480 (V3)
atrophic rhinitis in, 480 (V3)
bleeding in, 467-469f, 467-470 (V3)
bradycardia in, 470 (V3)
dental and periodontal problems in,
475, 477f (V3)
dental compensations and, 456, 457-
458f (V3)
improper maxillary repositioning in,
470-471, 471f (V3)
incision design and closure and,
459-464 (V3)
leveling and root divergence in
segmental cases and, 458-459
(V3)
nasal septal deviation in, 478-480,
479f (V3)
nerve injury in, 477 (V3)
ophthalmic disorders in, 473-475,
476f (V3)
prevention of, 480t (V3)
psychologic preparation and, 459
(V3)
relapse in, 480 (V3)
in segmental surgery, 472-473 (V3)
systematic aesthetic analysis and, 459
(V3)
technical difficulties and, 471-472,
472f (V3)
tooth size discrepancies and, 458
(V3)
transverse discrepancies and, 456-458
(V3)
unfavorable interdental osteotomy in,
473-475f (V3)
Maxillary surgery complications
(Continued)
unfavorable nasolabial esthetics in,
477-478 (V3)
unfavorable osteotomy in, 464-467,
465f, 466f (V3)
vascular compromise in, 475 (V3)
Maxillary third molar exodontia for
impaction, 201-210 (V1)
bone removal and tooth sectioning
in, 205-206, 207-210f (V1)
classification of, 203, 204f (V1)
indications and contraindications for,
202-203 (V1)
instrumentation for, 203, 203t (V1)
postoperative instructions in, 208-
210, 209b (V1)
preoperative management in, 207t,
207-208, 208b (V1)
surgical technique in, 207, 208-210f
(V1)
wound closure in, 206-207 (V1)
Maxillary tuberosity, 173 (V3)
for bone graft harvest, 409, 409f, 410f
(V1)
Maxillary vein, 433f (V3)
Maxillary-midface growth values, 28-40
(V3)
anterior alveolar height in, 31 (V3)
basion to A-point in, 37 (V3)
bizygomatic width in, 36 (V3)
maxillary width in, 34 (V3)
nasion to anterior nasal spine in, 40
(V3)
palatal plane to upper incisor in, 33
(V3)
palatal plane to upper molar in, 32
(V3)
posterior alveolar height in, 30 (V3)
pterygoid fissure to A-point in, 29
(V3)
sella to anterior nasal spine in, 38
(V3)
sella to posterior nasal spine in, 39
(V3)
skeletal nasal width in, 35 (V3)
Maxillectomy, 692-699 (V2)
airway management in, 694, 694f,
695f (V2)
critical anatomic regions in, 693 (V2)
postoperative considerations in, 699
(V2)
subtotal anterior, 698-699, 699f (V2)
subtotal inferior, 697f, 697-698, 698f
(V2)
surgical anatomic features in, 692 (V2)
technique in, 694-697, 695f, 697f
(V2)
Maxillofacial cysts, 418-465 (V2)
definitions in, 418 (V2)
general surgical considerations in,
418 (V2)
nonodontogenic, 447-460 (V2)
branchial cleft, 458-460, 458-460f
(V2)
dermoid and epidermoid, 451-455,
454f, 455f (V2)
globulomaxillary, 451 (V2)
median mandibular, 451 (V2)
median palatal, 451 (V2)
nasolabial, 447-448, 449f, 450f
(V2)
nasopalatine duct, 448-451, 451-
453f (V2)
thyroglossal duct, 455-458, 455-
458f (V2)
odontogenic, 418-447 (V2)
calcifying, 445-447, 447f (V2)
dentigerous, 424-426, 425-428f
(V2)
gingival, 442, 445f (V2)
glandular, 444-445 (V2)
lateral periodontal, 442-444 (V2)
in nevoid basal cell carcinoma
syndrome, 441b, 441-442,
442t, 443f, 444f (V2)
odontogenic keratocyst, 426-441
(V2); See also Odontogenic
keratocyst
Maxillofacial cysts (Continued)
paradental, 421-424 (V2)
radicular, 419-421, 420f, 422f (V2)
residual, 421, 423f (V2)
Maxillofacial deformity
Le Fort III osteotomy for, 205-218
(V3)
in craniofacial dysostosis, 205-206
(V3)
indications for, 205 (V3)
in midface deficiency, 206, 207-
210f (V3)
modified, 211-218 (V3)
subcranial, 210-211, 212-217f (V3)
technique in, 206-210 (V3)
in Treacher Collins syndrome, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
Maxillofacial region
Langerhans cell histiocytosis in, 567-
576, 568f (V2)
classification of, 569b, 569-570
(V2)
clonality of, 570 (V2)
diagnosis, treatment, and prognosis
of, 571-575, 571-575f (V2)
histopathology of, 570, 570f (V2)
Langerhans cell and, 568-569, 569f
(V2)
osteomyelitis in, 633-639 (V2)
classifications of, 633, 634b (V2)
clinical and radiographic
presentation of, 633-635, 634-
636f (V2)
pathogenesis of, 633 (V2)
risk factors for, 634b (V2)
treatment of, 635-638, 636t, 637f
(V2)
unique complications in, 638b,
638f, 638-639 (V2)
squamous cell carcinoma of, 705-723
(V2)
anatomy in, 705-706 (V2)
buccal mucosa, 714-715, 715f, 716f
(V2)
diagnostic adjuncts in, 708-709,
709f (V2)
floor of mouth, 714, 714f, 715f
(V2)
follow-up in, 719-720 (V2)
genetic abnormalities in, 707-708
(V2)
non-surgical management of, 710-
713 (V2)
pretreatment evaluation in, 710
(V2)
primary tumor and, 713-714 (V2)
retromolar trigone, alveolar ridge,
and palate, 716-719 (V2)
risk factors for, 706-707 (V2)
screening for, 708 (V2)
staging of, 710, 711t (V2)
INDEX I-57
Maxillofacial region (Continued)
tongue, 716-717, 716-718f (V2)
types of neck dissection in, 719,
719t, 720f (V2)
vascular anomalies of, 577-591 (V2)
arteriovenous malformation in,
588-590, 589f (V2)
binary classification of, 578b (V2)
capillary malformation in, 581,
581f (V2)
congenital hemangioma in, 579f,
579-581, 580f (V2)
infantile hemangioma in, 577-579,
578f (V2)
lymphatic malformation in, 581-
583, 582-585f (V2)
venous malformation in, 585-588,
586-588f (V2)
Maxillofacial trauma, 1-411 (V2)
airway management in, 25-34 (V2)
airway assessment and, 25, 26b
(V2)
airway maneuvers and adjuncts in,
26, 26b (V2)
complications in, 33 (V2)
cricothyroidotomy in, 32f, 32-33
(V2)
endotracheal intubation in, 28-31,
31f (V2)
supraglottic airway devices for, 26-
28, 27f, 28f (V2)
systematic approach to, 25 (V2)
tracheostomy in, 33 (V2)
avulsive facial injuries in, 289-290,
290f, 291f, 327-351 (V2)
Abbe flap in, 329, 330f (V2)
aesthetic and prosthetic
rehabilitation and, 346-350f
(V2)
airway management in, 327 (V2)
of alveolus, 128 (V2)
anterolateral thigh free flap for,
335, 335f (V2)
cervicofacial flap for, 329-330, 333f
(V2)
of cheek, 293f, 320, 320f (V2)
cheek defects in, 344, 345-348f
(V2)
clinical examination in, 327-328
(V2)
debridement in, 328 (V2)
of ear, 294, 297f (V2)
eyelid, 88, 308-309, 310f (V2)
facial artery musculomucosal flap
for, 329 (V2)
fibular free flap for, 333-335, 335f
(V2)
gingival, 130 (V2)
imaging in, 328 (V2)
lip defect reconstruction in, 343f,
343-344 (V2)
of lower face and mandible, 335-
340f, 336-337 (V2)
nasal, 301, 302-303f, 305f (V2)
nasal defects and, 337, 343 (V2)
optic disc, 83, 84f (V2)
paramedian forehead flap for, 329,
331-332f (V2)
pectoralis major myocutaneous flap
for, 330-331 (V2)
radial forearm flap for, 332-333,
334f (V2)
rectus abdominis free flap for, 335
(V2)
of scalp, 59, 293t, 324,
324f (V2)
scalp defects and, 346 (V2)
submental island flap for, 331-332,
334f (V2)
of teeth, 114t, 120-122, 121f, 122b
(V2)
temporoparietal fascia flap for, 330
(V2)
wound assessment in, 327, 328f
(V2)
comprehensive patient care in, 395-
411 (V2)
accident circumstances and,
395-396, 396f, 397f (V2)
I-58 INDEX
Maxillofacial trauma (Continued)
algorithm for decision making in,
399f (V2)
final discharge planning and, 405-
409 (V2)
identification of psychosocial issues
and, 400 (V2)
long-term rehabilitation and, 408-
411, 409-410f (V2)
pre-injury health and, 398-400
(V2)
preparation for postoperative
events and, 404-405, 407f
(V2)
primary survey and, 396, 397b,
398f (V2)
prioritization and integration of
surgery and, 400b, 400-401,
402f (V2)
secondary survey and, 396-397
(V2)
surgical plan and, 401-404, 403-
406f (V2)
treatment goals in, 396b, 396t
(V2)
condylar fracture in, 141-142, 142f,
162-181 (V2)
closed treatment of, 171 (V2)
conservative management of, 171
(V2)
diagnostic imaging of, 100f, 100-
101, 168-170, 169f (V2)
endoscopic-assisted repair of, 172-
176, 176-180f (V2)
facial nerve and, 164-165, 166f
(V2)
geriatric, 389-391f, 390-393 (V2)
open treatment of, 171 (V2)
pediatric, 364-369, 369f (V2)
physical examination of, 168 (V2)
retromandibular approach in, 171-
172, 172-175f (V2)
retromandibular vein and, 164
(V2)
skeletal injuries in, 167, 167f, 170-
171 (V2)
soft tissue injuries in, 166-167, 170
(V2)
Spiessl and Schroll classification
of, 167, 168b (V2)
superficial temporal artery and,
163-164, 164f, 165f (V2)
temporomandibular joint anatomy
and, 162-163, 163f (V2)
treatment outcomes in, 177-179
(V2)
trigeminal nerve and, 165, 166f
(V2)
dentoalveolar injury in, 104-138,
105f, 106f (V2)
alveolar process fracture in, 126-
128, 127f, 128f (V2)
classification of, 110-112, 111f,
112b, 113-115t (V2)
comminution of alveolar socket in,
125 (V2)
complete tooth avulsion in, 120-
122, 121f, 122b (V2)
concussed tooth in, 118 (V2)
crown fracture in, 113-118, 116-
118f (V2)
crown infraction in, 112-113
(V2)
displacement of tooth in, 118,
118b (V2)
extrusive luxation in, 118f (V2)
general considerations in, 112
(V2)
gingival injury in, 130 (V2)
history in, 105-107 (V2)
intrusive luxation in, 118, 119f
(V2)
lateral luxation of tooth in, 119-
120 (V2)
pediatric, 364 (V2)
physical examination in, 107-109,
107-109f (V2)
primary tooth injury in, 122-125,
123b, 123-126f (V2)
Maxillofacial trauma (Continued)
prognosis in, 132f, 132-135, 134f,
135f (V2)
radiographic examination in, 102,
102f, 109-110, 110f (V2)
reactions of teeth to, 130b, 130-
131, 131f, 132f (V2)
socket wall fracture in, 126 (V2)
splinting techniques for, 128-130,
129f (V2)
subluxation of tooth in, 118 (V2)
diagnostic imaging in, 91-103 (V2)
in angle of mandible fracture, 101,
101f (V2)
in avulsive facial injury, 328 (V2)
in comminuted, complicated, and
impacted fracture, 99, 99f
(V2)
in complications of treatment of
mandibular fracture, 102-103
(V2)
computed tomography in, 98-99
(V2)
in condylar fracture, 100f, 100-101,
168-170, 169f (V2)
in coronoid process and ramus
fractures, 101 (V2)
in dentoalveolar injuries, 102,
102f, 102f (V2), 109-110,
110f (V2)
in greenstick and pathologic
fractures, 99, 100f (V2)
imaging techniques in, 91-92, 92f,
92t (V2)
mandibular anatomy and, 96 (V2)
in mandibular body fracture, 101,
102f (V2)
mandibular series in, 96-98, 97f
(V2)
in mandibular symphysis and
parasymphysis fractures, 101,
102f (V2)
midfacial anatomy and, 91, 92f
(V2)
in orbital fracture, 209-211, 210f,
211f (V2)
panoramic radiography in, 98, 99f
(V2)
rendering techniques in, 92-94, 93-
95f (V2)
in simple and compound fractures,
99, 99f (V2)
in soft tissue trauma to neck,
94-95, 96f (V2)
supplemental radiographs in, 98
(V2)
in zygomatic fracture, 184-185,
185f (V2)
frontal sinus fracture in, 256-269 (V2)
classification of, 257-259, 261f
(V2)
clinical evaluation in, 256, 258f,
259f (V2)
pediatric, 355, 356-357f (V2)
postoperative care in, 266-268,
268f (V2)
radiologic evaluation in, 256-257,
260f, 261f (V2)
surgical anatomy and, 256, 257f,
258f (V2)
surgical management of, 259-266,
262-269f (V2)
geriatric, 374-394 (V2)
aging of face and neck in, 377
(V2)
anesthetic management in, 385,
385b (V2)
closed versus open reduction of
fractures in, 386t (V2)
cognitive evaluation and informed
consent in, 380 (V2)
considerations in management of,
392t (V2)
epidemiology of, 374-377, 375t,
376-377f (V2)
mandibular fractures in, 389-392f,
390-393 (V2)
maxilla and midface fractures in,
386-390, 387-389f (V2)
Maxillofacial trauma (Continued)
medications and over-the-counter
drug history and, 380 (V2)
nutrition and fluid and electrolyte
management in, 379 (V2)
perioperative risk assessment of co-
morbid systemic disease in,
380t, 380-385 (V2)
social history and, 379-380 (V2)
wound healing and, 377-378, 378f
(V2)
initial assessment in, 35-42, 36t (V2)
adjuncts to primary survey and, 39-
40 (V2)
adjuncts to secondary survey and,
40-41 (V2)
airway evaluation in, 35-36 (V2)
breathing evaluation in, 36, 36f,
37f (V2)
circulation evaluation in, 37-38,
38f, 38t (V2)
definitive care and, 41 (V2)
disability evaluation in, 38-39, 39t
(V2)
exposure and environment control
in, 39, 39f (V2)
penetrating injuries and, 41-42
(V2)
secondary survey and, 40 (V2)
intensive care in, 42-48, 43t (V2)
abdominal compartment syndrome
and, 45-46, 46f (V2)
acalculous cholecystitis and, 45
(V2)
acute adrenal insufficiency and, 46-
47 (V2)
acute renal failure and, 46 (V2)
acute respiratory distress syndrome
and, 43-44, 44t (V2)
adynamic ileus and, 45 (V2)
atrial fibrillation and, 44-45 (V2)
blood loss and, 46 (V2)
blunt myocardial injury and, 44
(V2)
fluids, electrolytes, and nutrition
and, 45 (V2)
infectious disease and, 47 (V2)
intensive insulin therapy and, 46-
47 (V2)
intubation and mechanical
ventilation and, 43 (V2)
pain control and sedation and, 47
(V2)
prophylaxis and, 48 (V2)
rehabilitation and, 48 (V2)
shock and, 44 (V2)
systemic inflammatory response
and multiple organ failure
syndrome and, 44, 44t (V2)
tubes and lines and, 47-48 (V2)
midface fracture in, 239-255 (V2)
anatomy in, 239, 240f (V2)
classification of, 239-240, 240f,
241f (V2)
complications in, 253-254 (V2)
geriatric, 386-390, 387-390f, 392t
(V2)
imaging of, 241f, 241-242, 242f
(V2)
Le Fort fractures in, 248-253, 250-
252f (V2)
naso-orbital-ethmoid fracture in,
243-248, 243-249f (V2)
neurologic injury in, 242-243 (V2)
pediatric, 253, 363 (V2)
multi-system trauma and, 65-73 (V2)
abdominal evaluation and, 65-67,
66f, 67f (V2)
antibiotics and, 73 (V2)
complex pelvic fractures and, 68f,
68-69, 69f (V2)
deep venous thrombosis
prophylaxis and, 72-73 (V2)
ICU considerations and, 70-72
(V2)
occult pneumothorax and, 68, 68f
(V2)
occult vascular injuries and, 69-70,
70f (V2)
Maxillofacial trauma (Continued)
preparation for rehabilitation and,
73 (V2)
steroids and, 72 (V2)
tertiary examination and, 72 (V2)
nasal fracture in, 270-283, 271f (V2)
anatomy and pathogenesis of, 270-
273, 272f, 273f (V2)
classification of, 275, 275t (V2)
closed reduction in, 276-278, 278f,
279f (V2)
complications of, 281-282 (V2)
diagnosis and evaluation of, 273-
275, 274f (V2)
medical management of, 275 (V2)
open reduction in, 278-281, 280f
(V2)
pediatric, 281, 362-363 (V2)
neurologic assessment in, 11, 49-56
(V2)
detailed evaluation in, 51-52 (V2)
grading severity of injury and, 52-
56, 54f, 54t (V2)
initial evaluation and, 49-51 (V2)
ocular injury in, 74-90 (V2)
carotid cavernous fistula and, 89
(V2)
cranial nerve injury in, 85-86 (V2)
eyelid injuries in, 88 (V2)
globe dystopia in, 88 (V2)
nasolacrimal injuries in, 88-89, 89f
(V2)
nonperforating, 78-82, 78-82f (V2)
ophthalmic assessment in, 74-78,
75-78f (V2)
orbital fractures in, 86f, 86-88, 87f
(V2)
orbital injury and, 83-85, 84f (V2)
penetrating, 83, 83f (V2)
orbital fracture in, 83-85, 84f, 202-
238 (V2)
anatomy in, 202-206, 203t, 203-
206f, 205b, 205t (V2)
associated injuries in, 211-212,
212f (V2)
clinical examination in, 207-209,
208f, 209f (V2)
conservative management of, 217-
220, 219f, 220f (V2)
diagnostic imaging of, 94, 94f (V2)
diplopia in, 214-215, 215f, 216f
(V2)
eyelid lacerations in, 215 (V2)
fracture patterns in, 206-207, 206-
208f (V2)
imaging techniques in, 209-211,
210f, 211f (V2)
indications for operative treatment
of, 220, 221f (V2)
inferior and lateral orbital
approach in, 221-222, 222f,
223f (V2)
lacrimal injuries in, 215, 217f (V2)
medial orbital approach in, 225-
228, 226f, 227f (V2)
ophthalmic assessment in, 78, 78f
(V2)
primary reconstruction in, 228-
233, 228-236f (V2)
secondary reconstruction in, 233-
236, 233-236f (V2)
superior and lateral orbital
approach in, 222-225, 224-
226f (V2)
telecanthus in, 215-217, 218f (V2)
visual disturbances in, 212-214,
212-214f (V2)
orbital injury in, 83-86 (V2)
cranial nerve injury in, 85-86 (V2)
displacement of globe in, 88 (V2)
intraorbital foreign body in, 83-84,
84f (V2)
optic disc avulsion in, 83, 84f (V2)
orbital fracture in, 86f, 86-88, 87f
(V2)
traumatic optic neuropathy in, 84-
85 (V2)
traumatic retrobulbar hemorrhage
in, 84f, 84 (V2)

Maxillofacial trauma (Continued)
pediatric, 352-373 (V2)
child abuse and, 372 (V2)
craniofacial growth and
development and, 352-353,
353f (V2)
dentoalveolar fractures in, 363-364
(V2)
epidemiology of, 353-354 (V2)
frontal bone and superior orbital
fractures in, 355 (V2)
frontal sinus and frontobasilar
injuries in, 355, 356-357f
(V2)
mandibular body and angle
fractures in, 364 (V2)
mandibular condyle fractures in,
364-369, 369f (V2)
midface fractures in, 363 (V2)
nasal fractures in, 362-363 (V2)
naso-orbito-ethmoid fractures in,
355-360, 358-359f (V2)
orbital fractures in, 360-361, 360-
361f (V2)
perioperative management of, 354-
355 (V2)
prevention of, 354 (V2)
rigid internal fixation and, 369-370
(V2)
Risdon cable and, 370f, 370-372
(V2)
surgical anatomy in, 353 (V2)
symphyseal and parasymphyseal
mandibular fractures in, 364,
365-367f (V2)
zygomaticomaxillary complex
fractures in, 361-362, 362-
363f (V2)
perioperative management in, 1-16,
56-73 (V2)
abdominal assessment in, 11 (V2)
abdominal evaluation and, 11, 65-
67, 66f, 67f (V2)
acute subdural hematoma and, 60,
61t (V2)
airway assessment in, 2-4, 3f, 4f
(V2)
antibiotics and, 73 (V2)
basilar skull fracture and, 59-60
(V2)
breathing assessment in, 4-6 (V2)
chest imaging studies in, 11 (V2)
chronic subdural hematoma and,
61, 62f (V2)
circulation problems and, 6-7, 7t
(V2)
complex pelvic fractures and, 68f,
68-69, 69f (V2)
deep venous thrombosis
prophylaxis and, 72-73 (V2)
diffuse axonal injury and, 62 (V2)
disability status in, 7-8, 8t (V2)
ear examination in, 9 (V2)
epidural hematoma and, 60, 61f
(V2)
exposure and environmental
control in, 8 (V2)
eye examination in, 9 (V2)
head injury and, 8-9 (V2)
historic perspective in, 1, 2f (V2)
history in, 8 (V2)
ICU considerations and, 70-72
(V2)
mild closed head injury and, 56-57,
57b (V2)
moderate closed head injury and,
57 (V2)
musculoskeletal assessment in, 11-
12 (V2)
neck examination in, 10f, 10-11
(V2)
neurologic examination in, 11
(V2)
nose and neurologic evaluation in,
9 (V2)
occult pneumothorax and, 68, 68f
(V2)
occult vascular injuries and, 69-70,
70f (V2)
Maxillofacial trauma (Continued)
perineal, rectal, and vaginal
assessment in, 11 (V2)
preparation for rehabilitation and,
73 (V2)
primary survey in, 1 (V2)
scalp injury and, 58-59 (V2)
secondary survey in, 8 (V2)
severe closed head injury and, 57-
58 (V2)
skull fracture and, 59 (V2)
steroids and, 72 (V2)
tertiary examination and, 72 (V2)
throat examination in, 9, 10f (V2)
traumatic intracerebral hematoma/
cerebral contusion and, 61-62
(V2)
traumatic intraventricular
hemorrhage and, 63 (V2)
traumatic subarachnoid
hemorrhage and, 62 (V2)
postoperative management in, 14-15,
15f, 15t (V2)
reactions of teeth to, 130b, 130-131,
131f, 132f (V2)
soft tissue injuries in, 283-326 (V2)
abrasion in, 289 (V2)
from air bag device blast, 313,
314f, 315f (V2)
anatomic considerations in, 283,
284t, 285f (V2)
anesthesia for, 284, 284 (V2)
avulsive wounds in, 289-290, 290f,
291f (V2)
bite wounds in, 290-292, 292f,
313-316, 314-317f (V2)
burn-related, 321-323, 321-323f,
322t (V2)
of cheek, 320f, 320-321, 321f (V2)
closure of, 284, 285f, 288f (V2)
of ear, 294, 297f, 310-313, 312f,
313f (V2)
of eyelid and nasolacrimal
apparatus, 292-294, 295f, 296f
(V2)
initial evaluation and early
management of, 283, 284f
(V2)
laceration in, 289, 290f (V2)
of lip, 294, 298f (V2)
nasal, 301, 302-305f (V2)
of neck, 294, 316-318, 318f (V2)
of parotid, 294 (V2)
of parotid gland, 294, 318-320,
320f (V2)
pediatric, 292, 293f, 371f, 372 (V2)
periorbital, 301-310, 306-311f
(V2)
of peripheral nerves, 318, 319f
(V2)
of scalp, 292, 293-294f, 323-324,
324f, 325f (V2)
suture materials for, 284-289, 286-
287t (V2)
wound care in, 294-299 (V2)
temporomandibular joint ankylosis
and, 901 (V2)
temporomandibular joint
pseudoankylosis and, 900 (V2)
wound repair in, 17-24 (V2)
aberrant bone healing in, 22-23
(V2)
abnormal wound healing in, 22
(V2)
bone regeneration in, 22 (V2)
coagulation and, 17, 18f (V2)
formation of granulation tissue
and, 19-21, 20f (V2)
future directions in, 23, 23f (V2)
inflammation and, 17-19, 19f (V2)
neural control of, 21 (V2)
phases of, 17, 18f (V2)
prevention of infection in, 21-22
(V2)
remodeling phase of, 21f, 21 (V2)
zygomatic fracture in, 182-201 (V2)
anatomy in, 182-183, 183f (V2)
Carroll-Girard screw for, 186, 186f
(V2)
Maxillofacial trauma (Continued)
coronal approach in, 191-192 (V2)
eyebrow approach in, 187, 188f
(V2)
fixation in, 192, 193f (V2)
fracture patterns in, 206-207, 206-
208f (V2)
history and physical examination
in, 183b, 183-184, 184f (V2)
indications for radiographs and
surgery in, 184-185, 185f (V2)
infraorbital paresthesia and, 194-
195 (V2)
late-onset post-traumatic
enophthalmos and, 198 (V2)
lateral canthotomy in, 186-187
(V2)
lower eyelid approaches in, 187-
188, 188f (V2)
malunion of, 197f, 197-198 (V2)
persistent diplopia following, 195-
197, 196f, 196t (V2)
primary reconstruction in, 231f,
231-233, 232f (V2)
radiography in, 184-185,
185f (V2)
retrobulbar hemorrhage and, 198-
199 (V2)
soft tissue complications of, 195
(V2)
subciliary approach in, 190-191,
191f (V2)
subtarsal approach in, 191 (V2)
transconjunctival approach in,
188-190, 188-190f (V2)
traumatic optic neuropathy and,
197 (V2)
upper eyelid approach in, 187, 187f
(V2)
vestibular approach in, 186 (V2)
zygomatic arch fracture and, 192-
194, 194f (V2)
Maxillofacial tumors, 680-704 (V2)
chondrosarcoma in, 684f, 684-685
(V2)
Ewing’s sarcoma in, 687, 688f, 689f
(V2)
mandibular approaches in, 699-702,
701f, 702f (V2)
maxillectomy in, 692-699 (V2)
airway management in, 694, 694f,
695f (V2)
critical anatomic regions in, 693
(V2)
postoperative considerations in,
699 (V2)
subtotal anterior, 698-699, 699f
(V2)
subtotal inferior, 697f, 697-698,
698f (V2)
surgical anatomic features in, 692
(V2)
technique in, 694-697, 695f, 697f
(V2)
metastatic tumors to jaw and, 687-
689 (V2)
multiple myeloma and, 685-687,
686f, 687f (V2)
osteosarcoma in, 680-684, 681f, 682f
(V2)
patient evaluation in, 689-692, 690t,
691f (V2)
radiation-induced, 685 (V2)
Maxillomandibular advancement
cephalometric analysis and, 373, 374f
(V3)
mandibular lengthening by
distraction osteogenesis in, 342-
346, 342-346f (V3)
for obstructive sleep apnea syndrome,
316-337 (V3)
Delaire cephalometric analysis in,
321-323, 325-327f (V3)
diagnosis and treatment planning
in, 319-321, 322-324f (V3)
pathophysiology of, 316-318, 318f
(V3)
patient outcomes in, 330-336, 333-
335f (V3)
INDEX I-59
Maxillomandibular advancement
(Continued)
surgical technique in, 323-330,
327-332f (V3)
treatment options for, 318-319,
320-322f (V3)
Maxillomandibular complex
Le Fort I osteotomy and, 179-180,
181f (V3)
model surgery and, 364 (V3)
Treacher Collins syndrome and, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
Maxillomandibular complex rotation,
248-271 (V3)
clockwise rotation in, 252-256 (V3)
center of rotation at anterior nasal
spine, 252, 252f, 252t (V3)
center of rotation at maxillary
incisor tip, 252, 252f, 253t
(V3)
center of rotation at pogonion,
255, 255t, 256f (V3)
center of rotation at zygomatic
buttress, 255-256, 256f, 256t
(V3)
mandibular excess and, 253f, 253-
255, 254f (V3)
counterclockwise rotation in, 256-
260 (V3)
center of rotation at anterior nasal
spine, 256, 259f, 259t (V3)
center of rotation at posterior nasal
spine, 256-260, 260f, 260t
(V3)
center of rotation at zygomatic
buttress, 256, 259f, 259t (V3)
in Treacher Collins syndrome, 954
(V3)
in unilateral adolescent internal
condylar resorption, 303-304f,
305, 306f (V3)
vertical maxillary deficiency and
mandibular anteroposterior
deficiency and, 257f, 257-258,
258f (V3)
vertical maxillary excess and
mandibular anteroposterior
deficiency and, 261-263, 261-
263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-249,
249f, 250f (V3)
geometry of treatment design using
constructed maxillomandibular
triangle in, 261f, 261-262 (V3)
linear dimensions between maxillary
length and vertical facial height
in, 250, 250f (V3)
I-60 INDEX
Maxillomandibular complex rotation
(Continued)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-268
(V3)
Maxillomandibular fixation, 146-148,
147f (V2)
ambulatory surgery and, 494 (V3)
in bilateral sagittal split osteotomy,
109 (V3)
in condylar fracture, 171 (V2)
in internal derangement of
temporomandibular joint, 940
(V2)
pediatric
in mandibular condyle fracture,
366-369 (V2)
Risdon cable and, 370f, 370-372
(V2)
in symphyseal and parasymphyseal
fractures, 364 (V2)
for skeletal anchorage, 225 (V1)
tracheotomy and, 12-14, 12-14f (V2)
in transoral vertical ramus osteotomy,
128-129 (V3)
Maxillomandibular pain, chronic, 136-
163 (V1)
brain stimulation procedures for, 157
(V1)
characterization and measurement of,
139 (V1)
clinical and laboratory examination
in, 139-140 (V1)
cluster headache and
trigeminoautonomic variants
and, 148-149 (V1)
complex regional pain syndrome and,
157-158 (V1)
diagnosis of, 139, 139t (V1)
fibromyalgia and, 142 (V1)
idiopathic and atypical orofacial pain
syndromes and, 158 (V1)
incidence and demographics of, 137
(V1)
migraine and, 146-148, 147f (V1)
myofascial pain syndromes and,
143-145 (V1)
orofacial migraine variants and, 149
(V1)
pain definitions and, 137-138, 138t
(V1)
pathophysiology of pain and, 137f,
137-139, 138f (V1)
pharmacologic screening in, 140-141
(V1)
postherpetic neuralgia and, 151-152
(V1)
posttraumatic headache and, 152-153
(V1)
posttraumatic trigeminal neuralgia
and, 154-156 (V1)
psychiatric disorders and, 141-142
(V1)
sleep dysfunction and, 141 (V1)
surgical treatments for, 156-157 (V1)
systemic disease and, 141 (V1)
temporomandibular arthritis and,
145-146 (V1)
trigeminal neuralgia and, 149-151
(V1)
Maxillomandibular transverse
differential index, 221-223, 222f
(V3)
Maxillomandibular triangle, 249, 250f
(V3)
Maxillomandibular width differential,
222f, 223 (V3)
McCune-Albright syndrome, 600 (V2),
977-980, 980-985f (V3)
McGill pain inventory, 139 (V1)
MDCT; See Multi-detector computed
tomography
MDI; See Mini dental implant
Mean arterial pressure of child, 94 (V1)
Mechanical debridement in
periimplantitis, 391 (V1)
Mechanical ventilation in intensive
care unit, 43 (V2)
Meclofenamate, 887t (V2)
Media networking, 341-342, 342f (V1)
Media pack, marketing and, 340-341,
341f (V1)
Medial canthal ligament, 205 (V2)
Medial canthal tendon, 583f, 586f (V3)
naso-orbital-ethmoid fracture and,
243f, 243-244, 244f, 246 (V2)
Medial canthal-lateral nasal incision,
227-228, 228f (V2)
Medial canthus, 206f (V2), 585 (V3)
cancer near, 728 (V2)
widening of, 88 (V2)
Medial crura of nasal cartilage, 556
(V3)
Goldman tip and, 565-566 (V3)
tip plasty and, 563f, 564 (V3)
Medial internal branch of anterior
ethmoidal artery, 556f (V3)
Medial nasal osteotomy, 569, 570f (V3)
Medial orbital approach in orbital
fracture, 225-228, 226f, 227f (V2)
Medial orbital fat pad, 583-585, 584f
(V3)
Medial orbital wall fracture, 87f, 87-88,
247, 247f (V2)
Medial palpebral fissure, Le Fort I
osteotomy and, 176-177 (V3)
Medial pterygoid muscle, 163, 807, 807f
(V2)
Medial pterygoid nerve, 809 (V2)
Medial rectus muscle, 196t (V2), 584f
(V3)
Medial zygomatic-temporal vein, 596,
598 (V3)
Median mandibular cyst, 451 (V2)
Median palatal cyst, 451 (V2)
Mediastinal box, 38f (V2)
Medical licensure, 307-317 (V1)
accreditation and certification and,
308-309 (V1)
adverse action in, 315-316 (V1)
appointment to medical staff in, 314-
315 (V1)
definitions and resources in, 309-313,
310-313t (V1)
process of, 313-314, 314f (V1)
specialty board certification and, 308
(V1)
Medical necessity, 379 (V1)
Medical oncology in head and neck
cancer, 777-788 (V2)
background of, 777, 778f (V2)
chemotherapy for metastatic
carcinoma and, 778-781, 779t,
781t, 782t (V2)
epidemiology and, 777 (V2)
epidermal growth factor receptors
and, 782-783, 783t (V2)
induction chemotherapy and, 777-
778 (V2)
salivary gland cancers and, 783-785,
785f (V2)
taxanes in, 781-782 (V2)
Medicare
claims submission to, 368-369 (V1)
fee schedule of, 370-371 (V1)
licensure of surgicenter and, 304-306,
305t (V1)
Medication history
of geriatric patient, 380 (V2)
preoperative evaluation of, 1-2, 2t
(V1)
Medicolegal issues
in adverse action in privileging, 315-
316 (V1)
chart documentation and, 368 (V1)
claims adjudication and, 370 (V1)
coding and, 364-368 (V1)
fraudulent claims submission and,
371 (V1)
Medicolegal issues (Continued)
insurance and, 368-369 (V1)
Medicare fees and, 370-371 (V1)
risk management and, 373-386 (V1)
Americans with Disabilities Act
and, 383-384 (V1)
discharging patient from practice
and, 383 (V1)
documentation and legible records
and, 379-383 (V1)
Emergency Medical Treatment and
Active Labor Act and, 385
(V1)
HIPAA privacy and security and,
384 (V1)
incidents and claims and, 375-376
(V1)
informed consent and, 379 (V1)
lawsuit process and, 376-378 (V1)
limited English proficiency and,
384-385 (V1)
malpractice and, 374-375 (V1)
online communication and, 385
(V1)
patient rapport and, 378-379 (V1)
release of records and, 384 (V1)
telemedicine and, 385 (V1)
third-party payers and, 369-370 (V1)
in trigeminal nerve injury, 278-279
(V1)
Mefenamic acid, 887t (V2)
Meissner’s corpuscle, 962 (V2)
Melanocyte, aging-related changes in,
513 (V3)
Melanoma, 749-757 (V2)
diagnosis of, 752t, 752-754, 753f,
753t (V2)
epidemiology of, 749, 750b (V2)
incidence and etiology of, 749-750,
750b, 750t, 750-752f, 751t (V2)
management of regional disease in,
754 (V2)
radiation therapy in, 768 (V2)
staging of, 754-755, 755t (V2)
treatment of, 755-756 (V2)
Melanotic neuroectodermal tumor of
infancy, 181, 181f (V1)
Melasma, 518 (V3)
Melatonin, bone development and, 398
(V1)
Melker cricothyroidotomy kit,
33 (V2)
Meloxicam, 887t (V2)
Membrane guided techniques for bone
defects, 428-457 (V1)
for alveolar ridge augmentation
using allograft and xenograft bone
with titanium-reinforced
membrane, 450-451, 450-451f
(V1)
using allograft bone putty and
resorbable collagen
membrane, 448f, 448-449,
449f (V1)
for coronal defects, 436 (V1)
in corticocancellous block
augmentation of posterior
mandible, 452-453, 452-453f
(V1)
for dehiscence defects, 435-436, 447,
447f (V1)
dual-layered technique in, 445f, 445-
446, 446f (V1)
for fenestration defects, 436 (V1)
flapless buccal wall reconstruction in,
443f, 443-444, 444f (V1)
functional and design requirements of
membranes for, 429-431, 431f,
432f (V1)
to reduce postextraction bone loss,
438-440, 454f, 454-455, 455f
(V1)
ridge preservation using high-density
PTFE membrane in, 440-441f,
440-442 (V1)
in subantral augmentation, 436-438,
437f (V1)
wound closure in, 431-435, 433f,
434f (V1)
Meningeal branch of mandibular nerve,
163f (V2)
Meningioma, trigeminal neuralgia in,
992 (V2)
Meningitis after frontal sinus fracture
repair, 267 (V2)
Mental artery, 69f (V3)
Mental nerve injury
during exodontia, 216 (V1)
in genioplasty, 439, 441f (V3)
Mental status
in head injury, 49-50, 51 (V2)
in hemorrhagic shock, 7 (V2)
Mentalis muscle, 174f (V3)
Meperidine, 60 (V1)
for acute postoperative pain, 82 (V1)
for chronic facial pain, 972t (V2)
in laser skin resurfacing, 521 (V3)
for temporomandibular disorders,
888t (V2)
Mepivacaine
for acute postoperative pain, 83 (V1)
chemical structure of, 37f (V1)
for chronic orofacial pain, 115 (V1)
duration of action, 39t (V1)
lipid solubility of, 38t (V1)
pH effects on, 37t (V1)
prolonged sensory alteration with, 46t
(V1)
Meprobamate, 889t (V2)
Merkel cell carcinoma, 727 (V2)
Merkel’s corpuscle, 962 (V2)
Merrifield Z-angle for determining chin
position, 681t (V3)
Mersilene polyester fiber suture, 287t
(V2)
Mesenchymal tumors, 508-518 (V2)
cementoblastoma in, 510-512 (V2)
chondrosarcoma in, 685 (V2)
myxoma in, 512-517f, 512-518 (V2)
odontogenic fibroma in, 508-510,
509f, 511f (V2)
Mesial movement of teeth with
maximal anchorage, 226-231f (V1)
Mesioangular impaction of third molar,
205, 207f (V1)
Messenger ribonucleic acid, 648, 649f,
651 (V2)
Metabolic arthritis, 865 (V2)
Metabolism
of benzodiazepines, 57-59, 58f, 58t
(V1)
of ketamine, 63 (V1)
of sedative-hypnotics, 61-62, 62t
(V1)
Metastasis, 664-666, 666f (V2)
adenoid cystic carcinoma and, 549
(V2)
ameloblastoma and, 492-500, 499f
(V2)
basal cell carcinoma and, 725 (V2)
in dermatofibrosarcoma protuberans,
728 (V2)
in melanoma, 754-755 (V2)
in osteosarcoma, 682 (V2)
Metastatic tumors
chemotherapy for, 778-781, 779t,
781t, 782t (V2)
to jaw, 687-689 (V2)
temporomandibular joint and, 874
(V2)
Methadone, 972t (V2)
Methemoglobinemia, 47-48 (V1)
Methocarbamol, 887, 888t (V2)
Methohexital, 61 (V1)
for office-based anesthesia, 74 (V1)
pharmacokinetics of, 62t (V1)
Methotrexate, 779, 779t, 781t (V2)
N-Methyl-[e2]D[/e2]-aspartate
central sensitization and, 963 (V2)
chronic pain and, 138 (V1)
ketamine and, 62 (V1)
Methylprednisolone
for chronic facial pain, 974 (V2)
for traumatic optic neuropathy, 85,
213 (V2)
Metopic suture, 865f (V3)
Metopic suture craniosynostosis, 852f,
871-874, 874-876f (V3)

Metronidazole, 391-392 (V1)
Microcystic adnexal carcinoma, 726-
727, 727f (V2)
Microcystic lymphatic malformation,
581-582 (V2)
Micrognathia in juvenile rheumatoid
arthritis, 859 (V2)
Micrograft technique in hair
transplantation, 651-653, 652-655f
(V3)
Microhyphema, 79 (V2)
Microparticulate formulations of local
anesthetics, 50 (V1)
Microsatellite instability, 653-655 (V2)
Microvascular decompression in
trigeminal neuralgia, 151 (V1),
993 (V2)
Microvascular free flap, 332-335, 334f,
335f (V2)
Midazolam, 58b (V1)
fentanyl with, 74 (V1)
half-life and protein binding of, 58t
(V1)
in laser skin resurfacing, 521 (V3)
for pediatric anesthesia and sedation,
103-104, 105t (V1)
pharmacokinetics of, 62t (V1)
in rapid-sequence intubation, 29
(V2)
Middle ear, Treacher Collins syndrome
and
dysmorphology of, 938-939 (V3)
reconstruction of, 956 (V3)
Middle lamella, 583f, 583-585, 584f
(V3)
Middle meningeal artery, 163f (V2),
174 (V3)
Middle meningeal vein, 163f (V2)
Middle superior alveolar nerve, 459
(V1)
Middle third facial height to lower third
facial height, 11 (V3)
Middle transverse buttress, 91 (V2)
Middle turbinate, 257f (V2)
Midface
age-related changes in, 16, 17f (V3)
augmentation with injectable fillers,
639-643, 639-644f (V3)
cleft orthognathic surgery and, 813-
827, 840 (V3)
bone grafting in, 819, 820-825f
(V3)
obstructed nasal breathing and,
819 (V3)
preoperative evaluation in, 813-
814 (V3)
stabilization of mobilized cleft
maxilla and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-
819, 818f (V3)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
lateral cephalometrics of, 11 (V3)
maxillary-midface growth evaluation
and, 28-40 (V3)
anterior alveolar height in, 31
(V3)
basion to A-point in, 37 (V3)
bizygomatic width in, 36 (V3)
maxillary width in, 34 (V3)
nasion to anterior nasal spine in,
40 (V3)
palatal plane to upper incisor in,
33 (V3)
palatal plane to upper molar in, 32
(V3)
posterior alveolar height in, 30 (V3)
pterygoid fissure to A-point in, 29
(V3)
sella to anterior nasal spine in, 38
(V3)
sella to posterior nasal spine in, 39
(V3)
skeletal nasal width in, 35 (V3)
profile evaluation and, 3, 3f (V3)
Midface deficiency
complete mandibular subapical
osteotomy for, 161-167f (V3)
in craniofacial dysostosis syndromes,
881, 884-886 (V3)
in Apert syndrome, 902, 906-907f
(V3)
in Crouzon syndrome, 889-900,
892-900f (V3)
Le Fort III osteotomy for, 205-218
(V3)
for craniofacial dysostosis, 205-206
(V3)
indications for, 205 (V3)
for midface deficiency, 206, 207-
210f (V3)
modified, 211-218 (V3)
subcranial, 210-211, 212-217f (V3)
technique in, 206-210 (V3)
maxillary bone transport for, 360-
362, 362f (V3)
maxillary growth and development
discrepancy in, 851, 854f, 855f
(V3)
Midface fracture, 239-255 (V2)
anatomy in, 239, 240f (V2)
classification of, 239-240, 240f, 241f
(V2)
complications in, 253-254 (V2)
geriatric, 386-390, 387-390f, 392t
(V2)
imaging of, 241f, 241-242, 242f (V2)
Le Fort fractures in, 248-253 (V2)
anatomy in, 249 (V2)
classification of injury in, 249 (V2)
clinical findings in, 250f, 250-251
(V2)
examination considerations in,
251, 251f (V2)
radiographic evaluation in, 251
(V2)
treatment of, 251-253, 252f (V2)
naso-orbital-ethmoid fracture in, 243-
248 (V2)
anatomy in, 243f, 243-244, 244f
(V2)
clinical findings in, 244-246, 245f
(V2)
identification of medial canthal
tendon and, 246 (V2)
injury classification in, 244, 245f
(V2)
nasal reconstruction in, 248, 249f
(V2)
nasolacrimal apparatus repair in,
248 (V2)
radiographic evaluation in, 246
(V2)
reconstruction of medial orbital
rims in, 246-247, 247f (V2)
reconstruction of medial orbital
wall in, 247, 247f (V2)
soft tissue readaptation in, 248,
248f (V2)
surgical approaches in, 246, 246f
(V2)
transnasal canthopexy in, 247-248
(V2)
neurologic injury in, 242-243 (V2)
pediatric, 253, 363 (V2)
Midfacial degloving approach in
subtotal anterior maxillectomy,
698, 699f (V2)
Midfacial injuries
pediatric, 355-363 (V2)
frontal bone and superior orbital
fractures in, 355 (V2)
frontal sinus and frontobasilar
injuries in, 355, 356-357f
(V2)
midface fractures in, 363 (V2)
nasal fractures in, 362-363 (V2)
naso-orbito-ethmoid fractures in,
355-360, 358-359f (V2)
orbital fractures in, 360-361, 360-
361f (V2)
zygomaticomaxillary complex
fractures in, 361-362, 362-
363f (V2)
Midfacial injuries (Continued)
reconstruction in, 337-350, 341-342f
(V2)
aesthetic and prosthetic
rehabilitation and, 346-350f
(V2)
cheek defects and, 344, 345-348f
(V2)
lip defects and, 343f, 343-344 (V2)
nasal defects and, 337, 343 (V2)
scalp defects and, 346 (V2)
Mid-forehead lift, 611t (V3)
Midline main facial line, cheek trauma
and, 320 (V2)
Migraine, 146-148, 147f (V1)
Mild closed head injury, 56-57, 57b
(V2)
Milia
chemical peel and, 664 (V3)
laser skin resurfacing and, 539-540,
540f (V3)
Millard rotation and advancement flap
technique for unilateral cleft lip,
722, 737-741 (V3)
Asensio technique and, 740f, 740-
741, 741f (V3)
comparison of cleft surgery
techniques, 736 (V3)
nasal reshaping in, 741 (V3)
postoperative care in, 741 (V3)
preoperative management in, 738
(V3)
surgical procedure in, 738-739, 739f,
740f (V3)
Tennison-Randall triangular flap
technique versus, 745 (V3)
wide cleft defect and, 742f, 743f (V3)
Miltown; See Meprobamate
Mineralization, platelet-rich plasma
and, 503 (V1)
Minerals, implant dentistry
pharmacology and, 398-399, 399t
(V1)
Mini dental implant, 567-574, 568f
(V1)
for orthodontic anchorage, 570-574,
572-574f (V1)
for pontic support of fixed partial
denture, 568 (V1)
for retention of obturators, 568-569
(V1)
for single-tooth implant restoration
in narrow space, 569, 570f, 571f
(V1)
for stabilization of complete dentures,
567-568, 569f (V1)
for stabilization of removable partial
dentures, 568 (V1)
Minigraft technique in hair
transplantation, 651-653, 652-655f
(V3)
Miniimplant-retained obturator, 568-
569 (V1)
Minimal sedation, 22, 67 (V1)
Minimally invasive treatment,
798 (V2)
Minimum ventilation, pediatric versus
adult, 96t (V1)
Miniplate fixation
in bilateral sagittal split osteotomy,
109-111 (V3)
in genioplasty, 143, 145f, 149f (V3)
for impacted teeth, 172 (V1)
in mandibular fracture, 155 (V2)
in nasal fracture, 280 (V2)
Miniscrews for orthodontic skeletal
anchorage, 233-235 (V1)
Minnesota Multiphasic Personality
Inventory, 142 (V1)
Minocycline
for pemphigoid, 624 (V2)
for periimplantitis, 392 (V1)
Minor salivary gland
mucocele of, 539 (V2)
nonsalivary tumor of, 552-555, 554f,
555f (V2)
sialolithiasis of, 543 (V2)
Minor technical difficulties
in genioplasty, 439-441, 441f (V3)
INDEX I-61
Minor technical difficulties (Continued)
in intraoral vertical ramus osteotomy,
436 (V3)
in Le Fort I osteotomy, 439-441, 441f
(V3)
in sagittal split ramus osteotomy, 433
(V3)
in segmental mandibular surgery,
438-439 (V3)
Minoxidil, 651 (V3)
Misch classification system, 479 (V1)
Mitek anchor, 275, 276f, 306-309 (V3)
Mitten deformity, 627 (V2)
Mixed connective tissue disease
facial asymmetry in, 309 (V3)
temporomandibular joint
involvement in, 866 (V2)
Mixed odontogenic tumors, 518-533
(V2)
ameloblastic fibrodentinoma in, 524-
527, 527f (V2)
ameloblastic fibroma in, 522-524,
523f (V2)
ameloblastic fibro-odontoma in, 524,
525f, 526f (V2)
intraosseous odontogenic carcinoma
in, 527-532, 528-530f (V2)
odontoameloblastoma in, 519-522
(V2)
odontogenic sarcoma in, 532-533
(V2)
odontoma in, 518-519, 519-521f
(V2)
MMF; See Maxillomandibular fixation
MMPs; See Matrix metalloproteinases
Mobicox; See Meloxicam
Mobius syndrome, 292 (V3)
Model surgery, 364-371 (V3)
construction of intermediate splint
in, 368-369, 369f, 370f (V3)
in facial asymmetry, 277 (V3)
in mandibular widening, 338 (V3)
marking cast in, 366-367 (V3)
measurements in, 367f, 367-368 (V3)
mounting case in, 364-366, 365f,
366f (V3)
positioning of maxilla in, 368, 368f
(V3)
for segmental surgery, 369-370, 370f
(V3)
for special situations, 370-371 (V3)
Moderate closed head injury, 57 (V2)
Moderate sedation/analgesia, 67 (V1)
Modified Aldrete Scoring System, 33t
(V1)
Modified Blair incision, 549f (V2)
Modified Le Fort III osteotomy, 211-
218 (V3)
Modified Mallampati test, 69 (V1)
Modified radical neck dissection, 719t,
720f (V2)
Modified roll tissue graft, 486, 488f (V1)
Modified sagittal splitting of mandibular
ramus, 70, 70f (V3)
Modified surgically assisted maxillary
expansion, 232-233, 234f (V3)
Mohs’ micrographic surgery
in dermatofibrosarcoma protuberans,
728 (V2)
in sebaceous gland carcinoma, 727,
727f (V2)
in skin cancer, 735-736, 736b, 736f
(V2)
traditional surgical excision versus,
737 (V2)
Molar
impacted, 171 (V1)
simple extraction of, 188, 190f (V1)
skeletal anchorage devices for, 232
(V1)
Molding helmet, 867 (V3)
Molecular biologic testing, 417 (V2)
Molecular biology of cancer, 645-679
(V2)
cancer cell evasion of apoptosis and,
660-662, 661f (V2)
cancer cell insensitivity to growth
inhibitory signals and, 658-660,
659f (V2)
I-62 INDEX
Molecular biology of cancer (Continued)
cancer cell release from growth signal
requirement and, 655-658, 657f
(V2)
cancer cell versus normal cell and,
646-647, 647f (V2)
chromosomal abnormalities in cancer
cells and, 652-653, 653-655f
(V2)
epigenetic alteration of gene
expression in cancer cells and,
655 (V2)
gene regulation of cell function and,
648-652, 649-651f (V2)
immortalization of cancer cell and,
662-664, 663f (V2)
molecular diagnostics in oncology
and, 666-669, 667f (V2)
neovascularization and, 664, 665f
(V2)
nucleotide sequence abnormalities in
cancer cells and, 653-655, 656f
(V2)
in osteosarcoma, 683 (V2)
strategies of cancer-related molecular
therapeutics and, 669-671, 670f
(V2)
stromal changes in cells and, 645,
646f (V2)
targeted therapy based on tumor
behavior and, 671-673 (V2)
tissue invasion and metastases and,
664-666, 666f (V2)
Molecular diagnostics in oncology, 666-
669, 667f (V2)
Molecular therapeutics in oncology,
669-673 (V2)
biologically based cancer treatments
and, 669-671, 670f (V2)
targeted therapy based on tumor
behavior, 671-673 (V2)
Monitoring, 22-34 (V1)
anesthesia record and, 31-32, 32t
(V1)
of body temperature, 29 (V1)
of circulatory system, 24-25 (V1)
definitions in, 22 (V1)
of depth of sedation, 30b, 30-31, 31f,
72-73 (V1)
history and evolution of guidelines
for, 22-24, 23b (V1)
of neuromuscular blockade, 29-30
(V1)
in pediatric anesthesia and sedation,
99-100 (V1)
during recovery, 32-33, 33t, 75-76
(V1)
of respiratory system, 25-29, 26f, 28f
(V1)
Monitoring devices, 360 (V1)
Monoamine oxidase inhibitors
interaction with local anesthetics
with vasoconstrictors, 42t, 42-43
(V1)
preoperative management of, 2t (V1)
Monobloc osteotomy in craniofacial
dysotosis syndromes, 885, 901-902
(V3)
Monocanalicular stent, 307-308, 308f
(V2)
Monocryl suture, 286t (V2)
Monocyte, wound healing and, 19, 19f
(V2), 61, 61f (V3)
Monostotic fibrous dysplasia, 600 (V2)
Monro-Kellie doctrine, 41 (V2)
Mood swings, surgery-related, 408 (V3)
Morning jaw stiffness, 855 (V2)
Morphine
for acute postoperative pain, 81t, 81-
82 (V1)
for chronic facial pain, 972t (V2)
for temporomandibular disorders,
888t (V2)
Morris, John H., 792, 793f (V2)
Motor examination in head injury, 51,
52, 53t (V2)
Motor nerve deficit, postoperative
management of, 405-406 (V3)
Motrin; See Ibuprofen
Mouth
electrical burn of, 322-323 (V2)
limited opening after simple
extraction, 191 (V1)
soft tissue injury of, 320-321, 321f
(V2)
Moxifloxacin, 389, 389t (V1)
M-plasty biopsy, 731f (V2)
MRA; See Magnetic resonance
angiography
MRI; See Magnetic resonance imaging
MS Contin; See Morphine
Mucocele, 539 (V2)
after frontal sinus fracture repair,
267-268 (V2)
Mucocutaneous lesions
aphthous stomatitis in, 619f, 619-620
(V2)
in Beh[ced]cet’s syndrome, 620-622
(V2)
epidermolysis bullosa in, 626-627
(V2)
erythema multiforme in, 627-628
(V2)
herpangina in, 617f, 617-618 (V2)
herpes simplex virus infections in,
612-617, 613f (V2)
pediatric, 615-617 (V2)
primary herpetic gingivostomatitis
in, 612-613, 613f (V2)
secondary herpes in, 613-614 (V2)
systemic agents for, 614-615 (V2)
lichen planus in, 618f, 618-619 (V2)
linear IgA disease in, 625-626 (V2)
pemphigoid in, 622-624, 623f (V2)
pemphigus in, 624-625, 625f (V2)
in Reiter syndrome, 622 (V2)
Mucoepidermoid carcinoma, 784 (V2)
of minor salivary gland, 553-555,
555f (V2)
of parotid gland, 549-550 (V2)
Mucoperiosteal flap
in alveolar bone grafting for cleft
maxilla, 808 (V3)
in antral membrane balloon
elevation, 465, 467f (V1)
in complete mandibular subapical
osteotomy, 156 (V3)
in complicated exodontia, 192-193,
193-195f, 199f, 206f (V1)
in lingual nerve repair, 269-270 (V1)
in mandibular lengthening by
distraction osteogenesis, 344 (V3)
in palatoplasty, 762 (V3)
in residual palatal fistula closure, 830,
830f (V3)
in sinus-lift subantral augmentation,
459, 459f (V1)
in trephine bone core sinus elevation,
464, 464f (V1)
Mucoperiosteal incision
in alveolar distraction, 350-351 (V3)
in transoral vertical ramus osteotomy,
123 (V3)
Mucopyocele after frontal sinus fracture
repair, 267-268 (V2)
Mucosa-associated lymphoid tissue
lymphoma, 760-761, 763 (V2)
Mucosal flap in cleft maxilla repair,
811f (V3)
Mucosal incision
in pediatric craniomaxillofacial
tumor, 962-963 (V3)
in transoral vertical ramus osteotomy,
123 (V3)
Mucosal injury, 115t (V2)
Mucosal lesion, laser therapy for, 244-
245 (V1)
Mucositis
phases of, 785, 785f (V2)
radiation therapy-related, 774 (V2)
treatment and management of, 784-
785 (V2)
Mucous membrane pemphigoid, 623
(V2)
Mueller’s maneuver, 318 (V3)
Muenke syndrome, 880 (V3)
M[um]uller’s muscle, 205 (V2), 581f,
585, 586f (V3)
Multicenter Selective
Lymphadenectomy Trial, 756 (V2)
Multicentric basal cell carcinoma, 725
(V2)
Multicystic ameloblastoma, 479-485,
486-495f, 500-501 (V2)
Multi-detector computed tomography,
92, 93t (V2)
Multidirectional tomography, 838-839
(V2)
Multifocal distraction in bone transport
by distraction osteogenesis, 356-
359 (V3)
Multinucleated giant cell lesions, 592-
597 (V2)
aneurysmal bone cyst in, 596-597,
597-598f (V2)
central giant cell granuloma in, 592-
594, 593f, 593t (V2)
in cherubism, 595-596, 596f (V2)
giant cell tumor in, 594 (V2)
in hyperparathyroidism, 594f, 594-
595 (V2)
Multiplanar reformatting in computed
tomography, 839 (V2)
Multiple fracture of mandible, 142 (V2)
Multiple myeloma, 685-687, 686f, 687f
(V2)
bisphosphonates for, 558 (V2)
temporomandibular joint
involvement in, 873-874 (V2)
Multiple organ failure syndrome, 44, 44t
(V2)
Multiple sclerosis
preoperative evaluation of, 18 (V1)
trigeminal neuralgia and, 149 (V1),
991 (V2)
Multiview videofluoroscopy, 798, 799f
(V3)
Mumps, 542 (V2)
Murine hair follicle stem cells, 23, 23f
(V2)
Murphy, John, 789-790, 790f,
792 (V2)
Murphy’s bony landmarks and skin
incision, 790, 790f (V2)
Muscle(s)
adaptation in maxillomandibular
rotation, 268-271, 270f (V3)
facial asymmetry and, 280-281, 291-
292 (V3)
of facial expression, surgery-related
dysfunction of, 406 (V3)
of forehead and brow, 597-598, 598f
(V3)
of maxilla, 174, 174f (V3)
of nose, 270 (V2), 553, 554f (V3)
reconstruction in cleft palate repair,
768 (V3)
of temporomandibular joint, 162-163,
805-808 (V2)
digastric muscle in, 808 (V2)
geniohyoid muscle in, 808, 809f
(V2)
lateral pterygoid muscle in, 807-
808, 808f (V2)
main actions of, 810b (V2)
masseter muscle in, 805f, 805-806
(V2)
medial pterygoid muscle in, 807,
807f (V2)
mylohyoid muscle in, 808, 808f
(V2)
temporalis muscle in, 806f, 806-
807 (V2)
tenderness in temporomandibular
joint disorders, 980, 981f (V2)
in velopharyngeal mechanism, 831t
(V3)
zygoma, 182 (V2)
Muscle contracture, 979, 982b (V2)
Muscle exercises in temporomandibular
disorders, 891, 985f, 985-986 (V2)
Muscle pain disorders, 961-978 (V2)
antidepressants for, 973 (V2)
atypical facial pain and, 967-968
(V2)
barriers to management of, 970-971
(V2)
Muscle pain disorders (Continued)
botulinum toxin injection for, 974-
975 (V2)
of cardiac origin, 969 (V2)
central mechanisms of, 963 (V2)
clinically based comprehensive pain
management program for, 975
(V2)
complex regional pain syndrome and,
966-967 (V2)
Eagle’s syndrome and, 969-970, 970f
(V2)
evaluation of, 963-966, 965f, 966t
(V2)
future directions in management of,
975-976 (V2)
muscle relaxants for, 974 (V2)
nerve injury from dental procedures
and, 968f, 968-969 (V2)
neuralgia-inducing cavitational
osteonecrosis and, 967 (V2)
neuropathic agents for, 973-974 (V2)
nonsteroidal antiinflammatory drugs
for, 972-973, 973t (V2)
opioid therapy for, 971-972, 972t
(V2)
osteonecrosis-related, 970 (V2)
peripheral mechanisms of, 962, 963f
(V2)
physical therapy for, 971 (V2)
surgical intervention for, 975 (V2)
therapeutic injections for, 974 (V2)
topical capsaicin for, 975 (V2)
trigeminal anatomy and, 961-962,
962f (V2)
Muscle relaxants
anaphylaxis in pediatric anesthesia
and sedation and, 107t (V1)
benzodiazepines in, 57 (V1)
for chronic facial pain, 973t, 974
(V2)
for myofascial pain, 144-145 (V1)
for sleep management, 131 (V1)
for temporomandibular disorders,
887-888, 888t (V2)
in trigeminal nerve repair,
268 (V1)
Muscle spasm, 979 (V2), 982b (V2)
Muscle tone evaluation in head injury,
56 (V2)
Muscles of mastication
evaluation of, 829 (V2)
hypertrophy-related facial asymmetry
and, 291-292 (V3)
passive stretching of, 986 (V2)
surgery-related dysfunction of, 406
(V3)
Muscular dystrophy, 388-389 (V3)
Musculoskeletal assessment
in cranio-maxillofacial trauma, 11-12
(V2)
in secondary survey, 40 (V2)
Musculoskeletal head and neck pain,
142-146 (V1)
clinical examination in, 139-140
(V1)
fibromyalgia and, 142 (V1)
myofascial pain syndromes and, 143-
145 (V1)
temporomandibular arthritis and,
145-146 (V1)
Musculoskeletal strain in cervical spine
injury, 63 (V2)
Musculoskeletal system
effects of thyroid disorders on, 13t
(V1)
involvement in Lyme disease, 864
(V2)
Musculoskeletal tender-point block
therapy, 145 (V1)
Musculus uvulus muscle, 831t (V3)
Mustarde’s procedure, 306, 307t (V2),
673, 674f (V3)
Myalgia, 961-978 (V2)
antidepressants for, 973 (V2)
atypical facial pain and, 967-968
(V2)
barriers to management of, 970-971
(V2)

Myalgia (Continued)
botulinum toxin injection for, 974-
975 (V2)
of cardiac origin, 969 (V2)
central mechanisms of, 963 (V2)
clinically based comprehensive pain
management program for, 975
(V2)
complex regional pain syndrome and,
966-967 (V2)
diagnostic approach to, 832t (V2)
Eagle’s syndrome and, 969-970, 970f
(V2)
evaluation of, 963-966, 965f, 966t
(V2)
future directions in management of,
975-976 (V2)
muscle relaxants for, 974 (V2)
nerve injury from dental procedures
and, 968f, 968-969 (V2)
neuralgia-inducing cavitational
osteonecrosis and, 967 (V2)
neuropathic agents for, 973-974 (V2)
nonsteroidal antiinflammatory drugs
for, 972-973, 973t (V2)
opioid therapy for, 971-972, 972t
(V2)
osteonecrosis-related, 970 (V2)
peripheral mechanisms of, 962, 963f
(V2)
physical therapy for, 971 (V2)
surgical intervention for, 975 (V2)
therapeutic injections for, 974 (V2)
topical capsaicin for, 975 (V2)
trigeminal anatomy and, 961-962,
962f (V2)
Myasthenia gravis, 17-18, 18t (V1)
Mycophenolate mofetil, 625 (V2)
Mylohyoid muscle, 808, 808f (V2)
Mylohyoid nerve, 809 (V2)
Myobloc (botulinum toxin type B), 659
(V3)
Myocardial infarction, chronic orofacial
pain in, 118 (V1)
Myofascial pain, 961-978 (V2)
antidepressants for, 973 (V2)
atypical facial pain and, 967-968
(V2)
barriers to management of, 970-971
(V2)
botulinum toxin injection for, 974-
975 (V2)
of cardiac origin, 969 (V2)
central mechanisms of, 963 (V2)
chronic head and neck pain and,
143-145 (V1)
clinically based comprehensive pain
management program for, 975
(V2)
complex regional pain syndrome and,
966-967 (V2)
diagnostic approach to, 832t (V2)
Eagle’s syndrome and, 969-970, 970f
(V2)
evaluation of, 963-966, 965f, 966t
(V2)
future directions in management of,
975-976 (V2)
lidocaine block for, 141 (V1)
muscle relaxants for, 974 (V2)
nerve injury from dental procedures
and, 968f, 968-969 (V2)
neuralgia-inducing cavitational
osteonecrosis and, 967 (V2)
neuropathic agents for, 973-974 (V2)
nonsteroidal antiinflammatory drugs
for, 972-973, 973t (V2)
opioid therapy for, 971-972, 972t
(V2)
osteonecrosis-related, 970 (V2)
peripheral mechanisms of, 962, 963f
(V2)
physical therapy for, 971 (V2)
splint therapy for, 884 (V2)
surgical intervention for, 975 (V2)
therapeutic injections for, 974 (V2)
topical capsaicin for, 975 (V2)
trigeminal anatomy and, 961-962,
962f (V2)
Myofibroma, 182f (V1)
Myofibrotic contracture, 815, 832t (V2)
Myositis, 832t, 979, 982b (V2)
Myositis ossificans traumatica, 900 (V2)
Myospasm, 815, 832t (V2)
Myxedema coma, 12-13 (V1)
Myxofibroma, 512-517f, 512-518 (V2)
Myxoma, 512-517f, 512-518 (V2)
odontogenic, 968, 969f (V3)
N open, 567-572, 568-571f (V3)
Nager syndrome, 939, 943f (V3)
mandibular deformity in, 855 (V3)
mandibular distraction osteogenesis
in, 998-1001f, 999-1002 (V3)
Nail polish, accuracy of pulse oximetry
measurements and, 27 (V1)
Naloxone, 60, 80 (V1)
Nambumetone, 887t (V2)
Nance button appliance, 224 (V1)
Naphthylalkanones, 887t (V2)
Naproxen sodium, 84t, 86t (V1)
bone healing and, 394 (V1)
for chronic facial pain, 972, 973t
(V2)
for temporomandibular disorders, 130
(V1), 887t (V2)
Narcan; See Naloxone
Narcotic analgesics
for acute postoperative pain, 80-82,
81b, 81t, 82t (V1)
anaphylaxis in pediatric anesthesia
and sedation and, 107t (V1)
for bone grafting in implant surgery,
422 (V1)
for chronic facial pain, 971-972, 972t
(V2)
for chronic orofacial pain, 120-121
(V1)
for myofascial pain, 144-145 (V1)
for neuropathic orofacial pain, 999
(V2)
for pain in bone graft harvest, 415
(V1)
pharmacology of, 59-60 (V1)
for temporomandibular osteoarthritis,
146 (V1)
Nasal airway obstruction
cleft orthognathic surgery and, 819
(V3)
postsurgical, 404 (V3)
Nasal airway resistance, orthognathic
surgery-related changes in, 73-74
(V3)
Nasal bleeding
postsurgical, 404 (V3)
in rhinoplasty, 573 (V3)
Nasal bones, 270-272 (V2), 555-556,
595 (V3)
Nasal capsaicin
for cluster headache, 149 (V1)
for postherpetic neuralgia, 152 (V1)
Nasal cartilage, 272 (V2), 556, 556f
(V3)
cephalic strip technique and, 566
(V3)
closed rhinoplasty and, 572-573 (V3)
dorsal reduction and, 568f, 568-569
(V3)
septoplasty and, 570 (V3)
tip plasty and, 562-563, 563f (V3)
unilateral versus bilateral oronasal
cleft deformity and, 784t (V3)
Nasal deformity
presurgical dentofacial orthopedics in
clefting and, 783-790 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t
(V3)
presurgical nasoalveolar molding
and, 783 (V3)
rhinoplasty for, 553-578 (V3)
case reports in, 574-576, 574-576f
(V3)
clinical examination in, 557-560,
558-560f (V3)
closed, 572-573, 573f (V3)
Nasal deformity (Continued)
complications in, 573-577 (V3)
dressings and splinting in, 573,
573f (V3)
follow-up care in, 573 (V3)
incisions in, 560-562, 561f, 562f
(V3)
initial consultation in, 557 (V3)
nasal anatomy and, 553-556, 554b,
554-557f (V3)
tip plasty in, 562, 563f (V3)
tip projection in, 562-564, 563-
565f (V3)
tip rotation in, 564, 565f (V3)
tip shape and, 565-566, 566f (V3)
secondary cleft-nasal reconstruction
and, 840-841, 842f (V3)
in Treacher Collins syndrome, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956 (V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
unilateral cleft lip repair and,
735-758 (V3)
comparison of surgical techniques
for, 735-737 (V3)
functional approach in, 752-757,
752-757f (V3)
Millard rotation and advancement
flap technique in, 737-741,
739-743f (V3)
Tennison triangular flap technique
in, 743-751, 744-751f (V3)
timing of, 735 (V3)
Nasal emission testing, 796, 796f, 797b
(V3)
Nasal fistula, maxillary surgery-related,
480 (V3)
Nasal flap
in primary bilateral cleft lip and
palate repair and, 724f (V3)
in primary unilateral cleft lip repair,
721f, 722f (V3)
Nasal fracture, 270-283, 271f (V2)
anatomy and pathogenesis of, 270-
273, 272f, 273f (V2)
classification of, 275, 275t (V2)
complications of, 281-282 (V2)
diagnosis and evaluation of, 273-275,
274f (V2)
medical management of, 275 (V2)
pediatric, 281, 362-363 (V2)
surgical management of, 275-281,
276f, 277f (V2)
closed reduction in, 276-278, 278f,
279f (V2)
open reduction in, 278-281, 280f
(V2)
Nasal muscles, 270 (V2)
Nasal osteotomy, 569, 569f, 570f (V3)
Nasal packing
in nasal fracture, 275 (V2)
in nasal soft tissue injury, 301, 302f
(V2)
INDEX I-63
Nasal ram pressure, 800 (V3)
Nasal respiration
cleft orthognathic surgery and, 819
(V3)
craniofacial dysostosis syndromes and,
881 (V3)
orthognathic surgery-related changes
in, 73, 74 (V3)
Nasal septum, 272 (V2), 556 (V3)
deviation of
following Le Fort I osteotomy,
186-187 (V3)
maxillary surgery-related, 478-480,
479f (V3)
harvesting in rhinoplasty, 570, 571f
(V3)
maxilla and, 172, 173f (V3)
unilateral versus bilateral oronasal
cleft deformity and, 784t (V3)
Nasal splint, 278, 301, 302f, 304f (V2)
Nasal spray
after Le Fort I osteotomy, 184 (V3)
after Le Fort III osteotomy, 218 (V3)
Nasal stent
in functional cleft lip repair, 755f,
755-756 (V3)
in nasoalveolar molding, 786 (V3)
Nasal stuffiness after surgery, 411, 411f
(V3)
Nasal tip, 556 (V3)
physical examination of, 558-559,
559f (V3)
primary herpetic gingivostomatitis
and, 613 (V2)
rhinoplasty and
tip plasty in, 562, 563f (V3)
tip projection in, 562-564, 563-
565f (V3)
tip rotation in, 564, 565f (V3)
tip shape in, 565-566, 566f (V3)
unilateral versus bilateral oronasal
cleft deformity and, 784t (V3)
Nasal tip width, 6, 7f (V3)
Nasal trauma, reconstruction in, 337,
343 (V2)
Nasalis muscle, 174f (V3)
Nasion to anterior nasal spine, 40 (V3)
genioplasty and, 137, 138f (V3)
Treacher Collins syndrome and, 938
(V3)
Nasion to menton, 57 (V3)
Nasoalveolar molding, 783-790 (V3)
in cleft maxilla, 807 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
in Millard rotation and advancement
flap technique for unilateral cleft
lip, 738 (V3)
nasal deformity and, 783, 784t (V3)
Nasociliary nerve, 584f, 585 (V3)
Nasoendoscopy for speech assessment,
767, 798 (V3)
Naso-endotracheal intubation, 206
(V3)
Nasofrontal angle, 6, 7f, 554b, 596 (V3)
Nasofrontal buttress, 91, 92f (V2)
Nasofrontal ducts
anatomy of, 256, 257f, 258f (V2)
frontal sinus fracture and, 262-266,
263f, 265f, 266f (V2)
Nasofrontal suture line, 596 (V3)
Nasogastric tube, 404-405 (V3)
Nasolabial angle, 554b (V3)
Nasolabial confluence with mesiolabial
crease, 320 (V2)
Nasolabial cyst, 447-448, 449f, 450f
(V2)
Nasolabial esthetics after maxillary
surgery, 477-478 (V3)
Nasolabial fold
Botox injection in, 660 (V3)
injectable facial filler for, 637-638,
638f (V3)
Nasolacrimal apparatus repair, 248 (V2)
Nasolacrimal duct, 206 (V2)
Le Fort I osteotomy-related injury of,
475 (V3)
maxilla and, 172-173 (V3)
I-64 INDEX
Nasolacrimal fossa, 203t (V2)
Nasolacrimal trauma, 88-89, 89f, 292-
294, 295f, 296f (V2)
Nasomaxillary buttress, 227, 227f (V3)
Nasomaxillary complex, 851 (V3)
Nasometry, 800-801, 801f (V3)
Naso-orbital-ethmoid fracture, 207,
207f, 243-248 (V2)
anatomy in, 243f, 243-244, 244f (V2)
clinical findings in, 244-246, 245f
(V2)
computed tomography of, 214f (V2)
identification of medial canthal
tendon and, 246 (V2)
injury classification in, 244, 245f
(V2)
nasal fracture and, 276, 276f, 278-
280 (V2)
nasal reconstruction in, 248, 249f
(V2)
nasolacrimal apparatus repair in, 248
(V2)
pediatric, 355-360, 358-359f (V2)
primary reconstruction in, 233 (V2)
radiographic evaluation in, 246 (V2)
reconstruction of medial orbital rims
in, 246-247, 247f (V2)
reconstruction of medial orbital wall
in, 247, 247f (V2)
soft tissue readaptation in, 248, 248f
(V2)
surgical approaches in, 246, 246f (V2)
transnasal canthopexy in, 247-248
(V2)
Nasopalatine artery, 63, 63f, 173f (V3)
Nasopalatine duct cyst, 448-451, 451-
453f (V2)
Nasopalatine nerve, 556, 557f (V3)
Nasopharyngeal cancer, 770-771, 771t
(V2)
Nasopharyngoscopy, 835 (V3)
Nasotracheal intubation, 31 (V2)
National Correct Coding Initiative
Edits, 369 (V1)
National Highway Traffic Safety
Administration, 354 (V2)
National Provider Identifier, 370 (V1)
Nausea, postoperative, 393, 404-405
(V3)
in mandibular surgery, 443 (V3)
medications for, 410 (V3)
Nd:YAG laser, 240 (V1)
for hair removal, 251-252 (V1)
for tattoo removal, 251 (V1)
ND:YAGKTP laser, 240 (V1)
Neck
aging of, 377 (V2)
arteriovenous malformation in, 588-
590, 589f (V2)
Botox injection in, 660 (V3)
cervicofacial liposuction and, 618-
625 (V3)
complications of, 623-624 (V3)
history of, 618 (V3)
patient selection in, 618-620, 619f
(V3)
preoperative preparation in, 620
(V3)
surgical technique in, 620-623,
620-625f (V3)
characteristics of ideal, 619f (V3)
Dedo classification of facial profiles
and, 499, 499f, 499t (V3)
developmental cysts of, 451-460 (V2)
branchial cleft, 458-460, 458-460f
(V2)
dermoid and epidermoid, 451-455,
454f, 455f (V2)
thyroglossal duct, 455-458, 455-
458f (V2)
embryology of, 697-705, 698f, 700-
704f (V3)
evaluation of mass in, 758-759, 760f
(V2)
examination in cranio-maxillofacial
trauma, 10f, 10-11 (V2)
infantile hemangioma-related
structural anomaly of, 577-579,
578f (V2)
Neck (Continued)
lymphoma in, 758-766, 759b (V2)
angiocentric, 761-762 (V2)
diagnosis of, 758-759, 759f, 760f
(V2)
Hodgkin’s, 759-760, 760f (V2)
non-Hodgkin’s, 760-761, 761f
(V2)
prognosis of, 763-764, 764b (V2)
radiographic evaluation of, 762f,
762-763 (V2)
treatment of, 763 (V2)
mandibular asymmetry and, 99t (V3)
melanoma of, 749-757 (V2)
diagnosis of, 752t, 752-754, 753f,
753t (V2)
epidemiology of, 749, 750b (V2)
incidence and etiology of, 749-750,
750b, 750t, 750-752f, 751t
(V2)
management of regional disease in,
754 (V2)
staging of, 754-755, 755t (V2)
treatment of, 755-756 (V2)
non-melanoma skin cancer of, 724-
748 (V2)
aggressive behavior of, 728-730,
729f (V2)
basal cell carcinoma in, 725, 725f
(V2)
cryotherapy for, 734 (V2)
curettage/electrodesiccation in,
734, 735f (V2)
dermatofibrosarcoma protuberans
in, 727-728, 728f (V2)
epidemiology and etiology of, 724-
725 (V2)
laser ablation and resurfacing in,
734-735 (V2)
of lip, 742-744, 743f (V2)
lymph node involvement in, 737-
739 (V2)
Merkel cell carcinoma in, 727
(V2)
microcystic adnexal carcinoma in,
726-727, 727f (V2)
Mohs’ micrographic surgery in,
735-736, 736b, 736f (V2)
photodynamic therapy for, 741
(V2)
physical examination in, 730t,
730-733, 731b, 731-733t (V2)
radiation therapy in, 741-742 (V2)
sebaceous gland carcinoma in, 727,
727f (V2)
squamous cell carcinoma in, 725-
726, 726f (V2)
staging of, 733-734 (V2)
systemic and topical medications
for, 739-741 (V2)
traditional surgical excision in,
736-737 (V2)
preoperative evaluation in laser skin
resurfacing, 518 (V3)
resting skin tension lines of, 732,
732f (V2)
secondary survey of, 40 (V2)
squamous cell carcinoma of, 705-723
(V2)
anatomy in, 705-706 (V2)
buccal mucosa cancer and, 714-
715, 715f, 716f (V2)
diagnostic adjuncts in, 708-709,
709f (V2)
floor of mouth cancer and, 714,
714f, 715f (V2)
follow-up care in, 719-720 (V2)
genetic abnormalities in, 707-708
(V2)
non-surgical management of, 710-
713 (V2)
pretreatment evaluation in, 710
(V2)
primary tumor and, 713-714
(V2)
retromolar trigone, alveolar ridge,
and palate cancer and, 716-
719 (V2)
risk factors for, 706-707 (V2)
Neck (Continued)
salivary gland cancer and, 549-550,
552f (V2)
screening for, 708 (V2)
staging of, 710, 711t (V2)
tongue cancer and, 716-717, 716-
718f (V2)
types of neck dissection in, 719,
719t, 720f (V2)
trauma to, 294 (V2)
initial assessment of, 42 (V2)
multi-detector computed
tomography in, 92, 93t (V2)
radiographic and imaging
evaluation of, 94-95, 96f (V2)
soft tissue injury in, 316-318, 318f
(V2)
Neck dissection in head and neck
squamous cell carcinoma, 713-720
(V2)
buccal mucosa cancer and, 714-715,
715f, 716f (V2)
floor of mouth cancer and, 714, 714f,
715f (V2)
follow-up in, 719-720 (V2)
lip cancer and, 744 (V2)
lymph node groups in, 711t (V2)
primary tumor and, 713-714 (V2)
retromolar trigone, alveolar ridge,
and palate cancer and, 716-719
(V2)
tongue cancer and, 716-717, 716-
718f (V2)
types of, 719, 719t, 720f (V2)
Neck pain, 136-163 (V1)
brain stimulation procedures for, 157
(V1)
characterization and measurement of,
139 (V1)
clinical and laboratory examination
in, 139-140 (V1)
cluster headache and
trigeminoautonomic variants
and, 148-149 (V1)
complex regional pain syndrome and,
157-158 (V1)
diagnosis of, 139, 139t (V1)
fibromyalgia and, 142 (V1)
idiopathic and atypical orofacial pain
syndromes and, 158 (V1)
incidence and demographics of, 137
(V1)
migraine and, 146-148, 147f (V1)
myofascial pain syndromes and, 143-
145 (V1)
orofacial migraine variants and, 149
(V1)
pain definitions and, 137-138, 138t
(V1)
pathophysiology of pain and, 137f,
137-139, 138f (V1)
pharmacologic screening in,
140-141 (V1)
postherpetic neuralgia and,
151-152 (V1)
posttraumatic headache and,
152-153 (V1)
posttraumatic trigeminal neuralgia
and, 154-156 (V1)
psychiatric disorders and, 141-142
(V1)
sleep dysfunction and, 141 (V1)
surgical treatments for, 156-157
(V1)
systemic disease and, 141 (V1)
temporomandibular arthritis and,
145-146 (V1)
trigeminal neuralgia and, 149-151
(V1)
Neck-chin angle and length, 4 (V3)
Needle breakage on injection of local
anesthetic, 47 (V1)
Needle cricothyroidotomy, 3 (V2)
Needle decompression of tension
pneumothorax, 36, 37f (V2)
Needle electrode electromyography, 829
(V2)
Needleless injection of local anesthetic,
51 (V1)
Negligence-malpractice insurance, 302-
303 (V1)
NEMB; See Notice of exclusion from
Medicare benefits
NemoCeph NX 2005 software, 374f,
376, 376f (V3)
Neoadjuvant preoperative radiation
therapy, 771-772 (V2)
Neoplasm; See Tumor
Neovascularization, cancer and, 664,
665f (V2)
Nepotism, 325 (V1)
Nerve block
in cervicofacial liposuction, 621-622
(V3)
in chemical peel, 663 (V3)
in endoscopic forehead and brow lift,
603 (V3)
for facial soft tissue injury, 284 (V2)
in laser skin resurfacing, 521, 522f
(V3)
in Le Fort I osteotomy, 176 (V3)
in Mustard[ac]e method of otoplasty,
673 (V3)
in open rhinoplasty, 567 (V3)
in rhytidectomy, 500 (V3)
in temporomandibular joint
arthrocentesis, 914 (V2)
for trigeminal neuralgia, 150 (V1)
in zygomatic implant, 493 (V1)
Nerve block testing
in chronic head and neck pain, 140-
141 (V1)
in trigeminal nerve injury, 264 (V1)
Nerve graft in trigeminal nerve repair,
269 (V1)
Nerve growth factor, chronic facial pain
and, 976 (V2)
Nerve injury
in bilateral sagittal split osteotomy,
111-113, 113b (V3)
chronic facial pain and, 968f, 968-
969 (V2)
during exodontia, 215f, 215-216, 216f
(V1)
in genioplasty, 439, 441f (V3)
in intraoral vertical ramus osteotomy,
434, 434f (V3)
local anesthetic-related, 45-46, 46f
(V1)
mandibular fracture-related, 159-160
(V2)
in mandibular surgery, 444-445, 453
(V3)
in mandibular symphysis bone graft
harvest, 411 (V1)
in maxillary surgery, 477 (V3)
in midface fracture, 242-243 (V2)
in orthognathic surgery, 75-76 (V3)
in osteomyelitis, 638-639 (V2)
patient positioning-related, 75 (V1)
posttraumatic trigeminal neuralgia
and, 154-156 (V1)
in repair of zygomatic fracture, 197
(V2)
in rhytidectomy, 507-508, 508f (V3)
in sagittal split ramus osteotomy,
426-429, 432f (V3)
in skin cancer, 729f, 729-730 (V2)
in total alveolar subapical osteotomy,
438 (V3)
trigeminal, 259-284 (V1)
acute, 265-266, 266f, 267f (V1)
classification of, 259-261, 260t (V1)
clinical neurosensory testing in,
262f, 262-264, 263f (V1)
decompression in, 268 (V1)
determinants of nerve injury
responses, 261 (V1)
in facial trauma, 272-273 (V1)
function impairment assessment in,
261, 261t (V1)
impacted third molar removal-
related, 276-278 (V1)
implant-related, 275-276 (V1)
inferior alveolar nerve repairs in,
266f, 270 (V1)
infraorbital nerve repairs in, 270
(V1)

Nerve injury (Continued)
internal neurolysis in, 268-269
(V1)
lingual nerve repairs in, 269f, 269-
270 (V1)
local anesthetic injection-related,
273-274 (V1)
medicolegal issues in, 278-279
(V1)
nerve grafting in, 269 (V1)
neuroma resection in, 268 (V1)
neurorrhaphy in, 269 (V1)
orthognathic, 275 (V1)
outcomes of repair in, 271-272
(V1)
pain and discomfort assessment in,
261t, 261-262 (V1)
patient selection for nerve repair
in, 265 (V1)
pharmacologic testing in, 264 (V1)
postoperative management of, 270-
271 (V1)
sensory reeducation and patient
follow-up in, 271 (V1)
surgical and endodontic
medicament-related, 274-275
(V1)
surgical instrumentation for, 267-
268 (V1)
timing of surgery for, 266-267 (V1)
traumatic neuropathic pain
assessment in, 264-265, 265f
(V1)
Nerve repair surgery, trigeminal nerve,
265-272 (V1)
decompression in, 268 (V1)
inferior alveolar nerve repairs and,
266f, 270 (V1)
infraorbital nerve repairs and, 270
(V1)
internal neurolysis in, 268-269 (V1)
lingual nerve repairs and, 269f, 269-
270 (V1)
nerve grafting in, 269 (V1)
neuroma resection in, 268 (V1)
neurorrhaphy in, 269 (V1)
outcomes of, 271-272 (V1)
postoperative management in, 270-
271 (V1)
for posttraumatic trigeminal
neuralgia, 156-157 (V1)
sensory reeducation and patient
follow-up in, 271 (V1)
surgical instrumentation for, 267-268
(V1)
timing of, 266-267 (V1)
Nerve supply
of ear, 668-670f (V3)
of eyelid, 585 (V3)
of forehead and brow, 598-600, 598-
600f (V3)
of nose, 556, 557f (V3)
Net collection ratio, 298 (V1)
Neuralgia, 966t (V2)
glossopharyngeal, 993-994 (V2)
trigeminal, 990-992t, 990-993 (V2)
chronic head and neck pain in,
149-151 (V1)
chronic orofacial pain in, 118 (V1)
postherpetic, 994 (V2)
posttraumatic, 154-156 (V1)
Neuralgia-inducing cavitational
osteonecrosis, 967 (V2)
Neurapraxia
classification of, 260, 260t (V1)
during exodontia, 216 (V1)
Neurectomy
for posttraumatic trigeminal
neuralgia, 157 (V1)
for trigeminal neuralgia, 150-151
(V1)
Neurilemmoma, 601-602, 603f (V2)
Neuritis, 1000 (V2)
Neurocranial growth values, 19-27 (V3)
basion to nasion, 27 (V3)
bony interorbital distance, 24 (V3)
head breadth, 23 (V3)
head circumference, 20 (V3)
head height, 22 (V3)
Neurocranial growth values (Continued)
head length, 21 (V3)
sella to basion, 26 (V3)
sella to nasion, 25 (V3)
Neurocranium
growth and development of, 850-851,
852f (V3)
Treacher Collins syndrome and, 936
(V3)
Neurofibroma, 602, 604f (V2)
Neurofibromatosis, 980-984, 986f (V3)
Neurogenic tumors, 601-602, 603f, 604f
(V2)
Neurokinin-1, 963 (V2)
Neurologic assessment
in head injury, 7-8, 8t, 9, 11, 49-56
(V2)
detailed evaluation and, 51-52, 53f
(V2)
grading severity of injury in, 52-56,
54f, 54t (V2)
initial assessment and, 49-51 (V2)
in maxillofacial tumor, 690 (V2)
of trauma victim, 38-39, 39t (V2)
Neurologic deficits
after frontal sinus fracture repair, 268
(V2)
local anesthetic-related, 45-46, 46f
(V1)
Neurologic disease
in geriatric patient, 382 (V2)
perioperative management of, 388-
389 (V3)
Neurologic head and neck pain, 149-
158 (V1)
brain stimulation procedures for, 157
(V1)
clinical examination in, 140 (V1)
complex regional pain syndrome and,
157-158 (V1)
idiopathic and atypical orofacial pain
syndromes and, 158 (V1)
postherpetic neuralgia and, 151-152
(V1)
posttraumatic headache and, 152-153
(V1)
posttraumatic trigeminal neuralgia
and, 154-156 (V1)
surgical treatments for, 156-157 (V1)
trigeminal neuralgia and, 149-151
(V1)
Neurologic system
in control of wound repair, 21 (V2)
effects of thyroid disorders on, 13t
(V1)
liver disease-related alteration in, 11
(V1)
preoperative evaluation of, 17-18, 18t
(V1)
Neuroma
acoustic, 120f (V1)
resection in trigeminal nerve repair,
268 (V1)
traumatic, 154-155 (V1)
Neuromuscular blocking agents, 30 (V2)
Neuromuscular disorders, facial
asymmetry in, 292, 292f (V3)
Neuromuscular transmission monitor,
29-30 (V1)
Neurontin; See Gabapentin
Neuropathic agents, 973t, 973-974 (V2)
Neuropathic pain, 137 (V1), 966t (V2)
orofacial, 989-1004 (V2)
burning mouth syndrome in, 995-
996 (V2)
central poststroke pain in, 994-995
(V2)
diagnosis of, 989-990 (V2)
glossopharyngeal neuralgia in, 993-
994 (V2)
herpes zoster and, 994 (V2)
secondary to neuritis, 1000 (V2)
traumatic orofacial neuropathies
in, 996-999, 998t, 999t (V2)
trigeminal neuralgia in, 990-992t,
990-993 (V2)
posttraumatic, 152-156 (V1)
complex regional pain syndrome
in, 157-158 (V1)
Neuropathic pain (Continued)
idiopathic and atypical orofacial
pain syndromes in, 158 (V1)
posttraumatic headache in, 152-
153 (V1)
posttraumatic trigeminal neuralgia
in, 154-156 (V1)
surgical treatments for, 156-157
(V1)
trigeminal nerve injury and, 264
(V1)
Neuropathy, 966t (V2)
optic, 197 (V2)
traumatic orofacial, 996-999, 998t,
999t (V2)
Neurophysiologic hypothesis of
myogenous pain, 980 (V2)
Neuropraxia, 998t (V2)
in bilateral sagittal split osteotomy,
112 (V3)
Neurorrhaphy, 266f, 269 (V1)
Neurosensory disturbances
orthognathic surgery-related, 75-76
(V3), 275 (V1)
in rhytidectomy, 508 (V3)
Neurosensory testing in trigeminal
nerve injury, 262f, 262-264, 263f
(V1)
Neurotmesis, 998t (V2)
in bilateral sagittal split osteotomy,
112 (V3)
classification of, 260t, 260-261 (V1)
during exodontia, 216 (V1)
Neurotropism, 729 (V2)
Neurovascular bundle
bilateral sagittal split osteotomy and,
108 (V3)
complete mandibular subapical
osteotomy and, 157 (V3)
transoral vertical ramus osteotomy
and, 126 (V3)
Neutrophil, wound healing and, 19, 19f
(V2), 61, 61f (V3)
Nevoid basal cell carcinoma syndrome,
433f, 441b, 441-442, 442t, 444f
(V2)
Nevus evaluation in laser skin
resurfacing, 518 (V3)
New procedures, office management
and, 287-288 (V1)
Newborn
congenital epulis of, 179 (V1)
gingival cyst of, 180 (V1)
NewFill, 631 (V3)
Newsletter, marketing and, 340-341,
341f (V1)
Newton’s third law, orthodontic tooth
movement and, 224 (V1)
NHL; See Non-Hodgkin’s lymphoma
NICO lesions, 149 (V1)
Nicotine interaction with estrogen, 398
(V1)
Nicotine stomatitis, 245 (V1)
Nieden, H., 791 (V2)
Nitric oxide, 930 (V2)
Nitrogen balance, 15 (V2)
Nitrogenous bisphosphonates, 395-398,
396t, 397t (V1)
Nitrous oxide, 63-65, 64t (V1)
delivery system for, 360 (V1)
for office-based anesthesia, 74 (V1)
for pediatric anesthesia and sedation,
104-105 (V1)
temporomandibular joint
inflammation and, 850, 851f
(V2)
Nitrous oxide synthase, 850 (V2)
NMDA; See
N-methyl-[e2]D[/e2]-aspartate
Nociception, 78-79 (V1)
Nociceptive pain, 137 (V1)
Nociceptor, 137 (V1)
Nodular basal cell carcinoma, 725 (V2)
Nodular melanoma, 751f, 751t, 752t
(V2)
Nodule after facial fat transplantation,
627 (V3)
NOE fracture; See Naso-orbital-ethmoid
fracture
INDEX I-65
Nonepithelial cancers, 727-728, 728f
(V2)
Nonfunctional immediate loading, 515-
517, 517f (V1)
Non-Hodgkin’s lymphoma, 760-761,
761f, 767 (V2)
Noninvoluting congenital hemangioma,
579-581, 580f (V2)
Nonlipid reticuloendotheliosis, 567
(V2)
Nonlocking plates/screws for
mandibular fracture, 154f, 154-155,
155f (V2)
Non-melanoma skin cancer, 724-748
(V2)
aggressive behavior of, 728-730, 729f
(V2)
basal cell carcinoma in, 725, 725f
(V2)
cryotherapy for, 734 (V2)
curettage/electrodesiccation in, 734,
735f (V2)
dermatofibrosarcoma protuberans in,
727-728, 728f (V2)
epidemiology and etiology of, 724-
725 (V2)
laser ablation and resurfacing in, 734-
735 (V2)
of lip, 742-744, 743f (V2)
lymph node involvement in, 737-739
(V2)
Merkel cell carcinoma in, 727 (V2)
microcystic adnexal carcinoma in,
726-727, 727f (V2)
Mohs’ micrographic surgery in, 735-
736, 736b, 736f (V2)
photodynamic therapy for, 741 (V2)
physical examination in, 730t, 730-
733, 731b, 731-733t (V2)
radiation therapy in, 741-742 (V2)
sebaceous gland carcinoma in, 727,
727f (V2)
squamous cell carcinoma in, 725-726,
726f (V2)
staging of, 733-734 (V2)
systemic and topical medications for,
739-741 (V2)
traditional surgical excision in, 736-
737 (V2)
Non-odontogenic cysts, 447-460 (V2)
branchial cleft, 458-460, 458-460f
(V2)
dermoid and epidermoid, 451-455,
454f, 455f (V2)
globulomaxillary, 451 (V2)
median mandibular, 451 (V2)
median palatal, 451 (V2)
nasolabial, 447-448, 449f, 450f (V2)
nasopalatine duct, 448-451, 451-453f
(V2)
thyroglossal duct, 455-458, 455-458f
(V2)
Non-odontogenic tumors, 592-610
(V2), 970-984 (V3)
aneurysmal bone cyst in, 596-597,
597-598f (V2), 972, 974-975
(V3)
central giant cell granuloma in, 592-
594, 593f, 593t (V2), 970-972,
973f (V3)
cherubism in, 595-596, 596f
(V2)
chondroma in, 605-606 (V2)
craniofacial fibrous dysplasia in, 977-
980, 980-985f (V3)
desmoplastic fibroma in, 606-608,
607-608f (V2)
fibrous dysplasia in, 600-601 (V2)
florid cemento-osseous dysplasia in,
601, 601f (V2)
focal cemento-osseous dysplasia in,
601 (V2)
giant cell tumor in, 594 (V2)
hyperparathyroidism lesion in, 594f,
594-595 (V2)
juvenile aggressive fibromatosis in,
970, 972f (V3)
juvenile nasopharyngeal angiofibroma
in, 972-974, 976-977f (V3)
I-66 INDEX
Non-odontogenic tumors (Continued)
juvenile ossifying fibroma in, 599-
600, 600f (V2), 974-977, 978-
979f (V3)
neurofibroma in, 602, 604f (V2)
neurofibromatosis in, 980-984, 986f
(V3)
ossifying fibroma in, 598, 599f (V2)
osteoblastoma in, 602-604, 605f (V2)
osteochondroma in, 606 (V2)
osteoid osteoma in, 602 (V2)
osteoma in, 604-605, 606f (V2)
periapical cemental dysplasia in, 601
(V2)
schwannoma in, 601-602, 603f (V2)
Nonopioid mediated analgesia, 83, 84t
(V1)
Nonossifying fibroma, 870 (V2)
Nonperforating eye injuries, 78-82, 78-
82f (V2)
Nonsteroidal antiinflammatory drugs
for acute postoperative pain, 83-86,
84t, 85b, 86t (V1)
bone development and, 392-395
(V1)
for bone graft for implant, 422 (V1)
for chronic facial pain, 972-973, 973t
(V2)
geriatric patient and, 381 (V2)
for myofascial pain, 144 (V1)
for neuropathy secondary to neuritis,
1000 (V2)
for temporomandibular disorders, 130
(V1), 885-886, 886f, 887t, 985
(V2)
for temporomandibular osteoarthritis,
146 (V1)
Nonsurgical management of
temporomandibular disorders, 881-
897 (V2)
in internal derangement of
temporomandibular joint, 931
(V2)
occlusal management in, 889-890
(V2)
pharmacotherapy in, 885b, 885-889
(V2)
philosophies of treatment and, 881
(V2)
physical therapy in, 890-892, 891t
(V2)
splint therapy in, 881-885, 882b,
883f, 884f (V2)
Nonsyndromic craniosynostosis, 864-
879 (V3)
anterior plagiocephaly in, 868-871,
871f, 872f (V3)
brachycephaly in, 874-876 (V3)
delayed diagnosis of, 867-868 (V3)
diagnosis of, 865-866 (V3)
functional consequences of, 864-865,
865f (V3)
posterior plagiocephaly in, 874, 877f,
878f (V3)
scaphocephaly in, 868, 869-870f (V3)
surgical considerations in, 866-867
(V3)
timing of surgery for, 867 (V3)
trigonocephaly in, 871-874, 874-876f
(V3)
Nonunion, 414 (V3)
of mandibular fracture, 102, 159 (V2)
Noonan’s syndrome, 228-229f (V1)
Norepinephrine use with local
anesthetics, 40, 40t (V1)
Norpramin; See Desipramine
Nortriptyline, 889t, 986 (V2)
Norwood classification of male pattern
baldness, 654f (V3)
Nose
age-related changes in, 16, 17f (V3)
anatomy of, 553-556, 554b, 554-557f
(V3)
cleft lip and palate repair and
nasal revision after, 719, 840-841,
842f (V3)
presurgical dentofacial orthopedics
for, 783-790, 784t, 785t, 788f,
789f (V3)
Nose (Continued)
primary unilateral cleft lip repair
and, 722-723 (V3)
detailed aesthetic evaluation of, 6, 7f
(V3)
embryology of, 698f, 699, 700-703f,
701 (V3)
evaluation in cranio-maxillofacial
trauma, 9, 50 (V2)
fracture of, 270-283, 271f (V2)
anatomy and pathogenesis of, 270-
273, 272f, 273f (V2)
classification of, 275, 275t (V2)
closed reduction in, 276-278, 278f,
279f (V2)
complications of, 281-282 (V2)
diagnosis and evaluation of, 273-
275, 274f (V2)
medical management of, 275 (V2)
open reduction in, 278-281, 280f
(V2)
pediatric, 281, 362-363 (V2)
implants for large nose and small
chin, 679f, 679-684, 680f, 684f,
685b, 685f (V3)
lateral cephalometrics of, 11 (V3)
lymphoma of, 762 (V2)
malformation in craniofacial
dysostosis syndromes, 882-883
(V3)
maxilla and, 172 (V3)
naso-orbital-ethmoid fracture and,
207, 207f, 243-248 (V2)
anatomy in, 243f, 243-244, 244f
(V2)
clinical findings in, 244-246, 245f
(V2)
computed tomography of, 214f
(V2)
identification of medial canthal
tendon and, 246 (V2)
injury classification in, 244, 245f
(V2)
nasal fracture and, 276, 276f, 278-
280 (V2)
nasal reconstruction in, 248, 249f
(V2)
nasolacrimal apparatus repair in,
248 (V2)
pediatric, 355-360, 358-359f (V2)
primary reconstruction in, 233 (V2)
radiographic evaluation in, 246
(V2)
reconstruction of medial orbital
rims in, 246-247, 247f (V2)
reconstruction of medial orbital
wall in, 247, 247f (V2)
soft tissue readaptation in, 248,
248f (V2)
surgical approaches in, 246, 246f
(V2)
transnasal canthopexy in, 247-248
(V2)
profile evaluation and, 3, 3f (V3)
reconstruction in Treacher Collins
syndrome, 954-955 (V3)
rhinoplasty of, 553-578 (V3)
case reports in, 574-576, 574-576f
(V3)
clinical examination in, 557-560,
558-560f (V3)
closed, 572-573, 573f (V3)
complications in, 573-577 (V3)
dressings and splinting in, 573,
573f (V3)
follow-up care in, 573 (V3)
incisions in, 560-562, 561f, 562f
(V3)
initial consultation in, 557 (V3)
nasal anatomy and, 553-556, 554b,
554-557f (V3)
open, 567-572, 568-571f (V3)
tip plasty in, 562, 563f (V3)
tip projection in, 562-564, 563-
565f (V3)
tip rotation in, 564, 565f (V3)
tip shape and, 565-566, 566f (V3)
soft tissue injury of, 301, 302-305f
(V2)
Nose (Continued)
laceration in, 290f (V2)
reconstructive flap options for,
336b (V2)
unilateral cleft lip repair and, 735-
758 (V3)
comparison of surgical techniques
for, 735-737 (V3)
functional approach in, 752-757,
752-757f (V3)
Millard rotation and advancement
flap technique in, 737-741,
739-743f (V3)
Tennison triangular flap technique
in, 743-751, 744-751f (V3)
timing of, 735 (V3)
Nose blowing after surgery, 411, 411f
(V3)
Nostril pinch test, 795-796 (V3)
Notice of exclusion from Medicare
benefits, 370 (V1)
Noxious-stimulus pain, 140 (V1)
NPI; See National Provider Identifier
NTX; See Type 1 collagen cross-linked
N-telopeptide
Nuclear factor, 850 (V2)
Nucleic acid dysregulation in cancer,
652-655, 653-656f (V2)
Nucleotide sequence abnormalities in
cancer cell, 653-655, 656-657f
(V2)
Numbness
in chronic orofacial pain, 118 (V1)
in posttraumatic trigeminal neuralgia,
154 (V1)
Nutrition, perioperative patient
management and, 390-391 (V3)
Nutritional deficiency, oral cavity
cancer and, 707 (V2)
Nutritional support for trauma patient,
14-15, 15t (V2)
geriatric, 379 (V2)
intensive care unit and, 45 (V2)
Nylon suture, 287t (V2)
Nystatin, 410 (V3)
O vertical maxillary excess and
Obagi skin classification, 248, 249t
(V1)
Obesity
ambulatory orthognathic surgery and,
493 (V3)
obstructive sleep apnea syndrome
and, 318 (V3)
perioperative management of, 386
(V3)
preanesthetic airway assessment and,
69-70 (V1)
preoperative evaluation of, 6 (V1)
Obstructive disease of salivary gland,
543-546, 544-547f (V2)
Obstructive sleep apnea, 316-337
(V3)
in craniofacial dysostosis syndromes,
881 (V3)
Delaire cephalometric analysis in,
321-323, 325-327f (V3)
diagnosis and treatment planning in,
319-321, 322-324f (V3)
mandibular distraction osteogenesis
for, 342-346, 342-346f, 998-
1001f, 999-1002 (V3)
maxillary and mandibular
advancement for, 323-330, 327-
332f (V3)
pathophysiology of, 316-318, 318f
(V3)
patient outcomes in, 330-336, 333-
335f (V3)
preanesthetic airway assessment and,
70 (V1)
treatment options for, 318-319, 320-
322f (V3)
Obturator, miniimplant-retained, 568-
569 (V1)
Obwegeser bilateral sagittal split
osteotomy, 87, 88f, 106,
107t (V3)
Occipital artery, 69f (V3)
Occlusal assessment
in facial asymmetry, 273f, 274 (V3)
before maxillary surgery, 459, 460-
463f (V3)
Occlusal coverage retainer, 401, 402f
(V3)
Occlusal coverage splint, 398, 398f
(V3)
Occlusal instability after surgery, 413-
415, 414-417f (V3)
Occlusal plane
facial asymmetry and, 273f, 274 (V3)
mandibular asymmetry and, 99t (V3)
Occlusal Plane Indicator, 277, 365 (V3)
Occlusal plane rotation, 248-271 (V3)
clockwise rotation in, 252-256 (V3)
center of rotation at anterior nasal
spine, 252, 252f, 252t (V3)
center of rotation at maxillary
incisor tip, 252, 252f, 253t
(V3)
center of rotation at pogonion,
255, 255t, 256f (V3)
center of rotation at zygomatic
buttress, 255-256, 256f, 256t
(V3)
mandibular excess and, 253f, 253-
255, 254f (V3)
counterclockwise rotation in, 256-
260 (V3)
center of rotation at anterior nasal
spine, 256, 259f, 259t (V3)
center of rotation at posterior nasal
spine, 256-260, 260f, 260t
(V3)
center of rotation at zygomatic
buttress, 256, 259f, 259t (V3)
in Treacher Collins syndrome, 954
(V3)
in unilateral adolescent internal
condylar resorption, 303-304f,
305, 306f (V3)
vertical maxillary deficiency and
mandibular anteroposterior
deficiency and, 257f, 257-258,
258f (V3)
mandibular anteroposterior
deficiency and, 261-263, 261-
263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-249,
249f, 250f (V3)
geometry of treatment design using
constructed maxillomandibular
triangle in, 261f, 261-262 (V3)
linear dimensions between maxillary
length and vertical facial height
in, 250, 250f (V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-268
(V3)
Occlusal radiograph
of avulsed tooth, 121f (V2)
in dentoalveolar injury, 109 (V2)
in implant surgery, 549-551f (V1)
of intruded primary tooth, 126f (V2)
in mandibular trauma, 98 (V2)
of primary tooth fracture, 124f (V2)
Occlusal relations, postsurgical, 399
(V3)
Occlusal splint therapy in
temporomandibular disorders, 881-
885, 882b, 883f, 884f, 984 (V2)
Occlusion
anomalies in craniofacial dysostosis
syndromes, 881-882 (V3)

Occlusion (Continued)
discrepancy in midface deficiency,
206, 207-210f (V3)
evaluation of, 17-19, 18b (V3)
Le Fort fracture repair and, 252 (V2)
temporomandibular disorders and,
792-793, 793b (V2)
transoral vertical ramus osteotomy
and, 128f, 128-129 (V3)
Occult pneumothorax, 68, 68f (V2)
Occult vascular injuries, 69-70, 70f
(V2)
Occupational Safety and Health
Administration
accreditation of surgicenter and, 304
(V1)
on laser safety and compliance, 515-
516 (V3)
practice compliance with, 302 (V1)
Occurrence policy, 377 (V1)
Ocular injuries, 74-90 (V2)
carotid cavernous fistula and, 89
(V2)
cranial nerve injury in, 85-86 (V2)
eyelid injuries in, 88 (V2)
globe dystopia in, 88 (V2)
nasolacrimal injuries in, 88-89, 89f
(V2)
nonperforating, 78-82, 78-82f (V2)
ophthalmic assessment in, 74-78, 75-
78f (V2)
orbital fractures in, 86f, 86-88, 87f
(V2)
orbital injury and, 83-85, 84f (V2)
penetrating, 83, 83f (V2)
Oculoauriculovertebral spectrum, 922-
935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency in,
927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
facial asymmetry in, 298-299, 300-
302f (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in, 928,
929-930f (V3)
maxilla and, 922-935 (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928, 928f
(V3)
zygoma and orbit reconstruction in,
928-929 (V3)
Oculocephalic reflex, 51, 55 (V2)
Oculomotor nerve, 584f (V3)
evaluation of
in chronic orofacial pain, 117 (V1)
in head injury, 51-52 (V2)
Oculovestibular reflex, 51, 55-56 (V2)
Odontoameloblastoma, 519-522 (V2)
Odontogenesis, 418 (V2)
Odontogenic cysts, 418-447 (V2)
calcifying, 445-447, 447f (V2)
dentigerous, 424-426, 425-428f (V2)
gingival, 442, 445f (V2)
glandular, 444-445 (V2)
intraosseous carcinoma from, 531
(V2)
lateral periodontal, 442-444 (V2)
in nevoid basal cell carcinoma
syndrome, 441b, 441-442, 442t,
443f, 444f (V2)
odontogenic keratocyst, 426-441
(V2); See also Odontogenic
keratocyst
paradental, 421-424 (V2)
radicular, 419-421, 420f, 422f (V2)
residual, 421, 423f (V2)
third molar, 203 (V1)
Odontogenic epithelial hamartoma, 510
(V2)
Odontogenic fibroma, 508-510, 509f,
511f (V2)
Odontogenic keratocyst, 426-441 (V2)
clinical features of, 428-435, 430-
435f (V2)
etiology of, 426-428 (V2)
imaging features of, 435, 436-437f
(V2)
pathologic features of, 435f, 435-436
(V2)
surgical management of, 437-441,
439f, 440f (V2)
ultrastructure of, 437, 438f (V2)
Odontogenic myxoma, 512-517f, 512-
518 (V2), 968, 969f (V3)
Odontogenic sarcoma, 532-533 (V2)
Odontogenic tumors, 466-538 (V2),
967-970 (V3)
adenomatoid, 181 (V1), 469-472,
470-472f (V2), 968, 968f (V3)
ameloblastic fibrodentinoma in, 524-
527, 527f (V2)
ameloblastic fibroma in, 522-524,
523f (V2), 968-970, 970f (V3)
ameloblastic fibro-odontoma in, 524,
525f, 526f (V2), 970, 970f (V3)
ameloblastoma in, 476-502 (V2),
964f (V3)
clinical forms and mechanisms of
growth, 478 (V2)
clinicopathologic considerations
in, 477-478, 478-481f (V2)
management of, 500-502 (V2)
marked aggressive behavior and
metastases in, 492-500, 499f
(V2)
pediatric, 967f, 967-968 (V3)
peripheral, 485-492, 496-499f (V2)
solid and multicystic, 479-485,
486-495f (V2)
unicystic, 478-479, 482-484f, 486f
(V2)
biopsy of, 467-468 (V2)
calcifying, 473-476, 474f, 475f (V2)
cementoblastoma in, 510-512 (V2)
classification of, 466-467 (V2)
clear cell, 502-508, 503-507f (V2)
clinical considerations in, 467 (V2)
fibroma in, 508-510, 509f, 511f (V2)
imaging of, 467 (V2)
intraosseous odontogenic carcinoma
in, 527-532, 528-530f (V2)
management objectives in, 468-469
(V2)
myxoma in, 512-517f, 512-518 (V2)
odontoameloblastoma in, 519-522
(V2)
odontogenic myxoma in, 968, 969f
(V3)
odontoma in, 518-519, 519-521f
(V2), 970, 971f (V3)
sarcoma in, 532-533 (V2)
squamous, 472f, 472-473 (V2)
third molar, 203 (V1)
Odontoid fracture, 63, 64f (V2)
Odontoma, 518-519, 519-521f (V2),
970, 971f (V3)
pediatric impacted tooth and, 173
(V1)
Office design, 351-363 (V1)
construction phase and, 362-363
(V1)
defining goals in, 351 (V1)
equipping and furnishing and, 358-
361, 359f, 360f (V1)
ergonomics and, 361-362 (V1)
financial projections and feasibility
in, 352 (V1)
financing of project and, 362 (V1)
floor plan in, 352-358 (V1)
additional space requirements and,
358, 358f, 359f (V1)
business office area and, 355f, 355-
356, 356f (V1)
conference room and, 354, 354f
(V1)
consultation room and, 352, 352f
(V1)
laboratory and, 356-357 (V1)
Office design (Continued)
lunchroom and, 357, 357f (V1)
patient reception and waiting area
and, 355, 355f (V1)
physician’s office and, 356, 357f
(V1)
posttreatment area and, 353-355,
354f (V1)
pretreatment area and, 353 (V1)
radiology suite and, 352 (V1)
restrooms and, 356, 356f (V1)
staff office and, 357-358, 358f (V1)
surgical treatment area and, 352-
353, 353f (V1)
project consultant team and, 361
(V1)
Office environment, marketing and,
333-334 (V1)
Office furniture, 361 (V1)
Office management, 285-303 (V1)
financial management and, 291-299
(V1)
accounting in, 293 (V1)
budgeting in, 291-293, 294t (V1)
compensation plans in, 298t, 298-
299, 299t (V1)
financial policy in, 295 (V1)
financial reporting in, 297-298
(V1)
financial statement trend analysis
in, 295 (V1)
financial statements in, 295, 295t,
296t (V1)
revenue cycle and, 293-295 (V1)
human resources and, 290b, 290-291,
291-294t (V1)
information technology and, 303
(V1)
joining or starting practice and, 285
(V1)
legal documents and, 299-301, 300t,
301t (V1)
legal entities and, 285-286, 286t (V1)
organizational styles and, 288-290
(V1)
patient first impressions and, 333-334
(V1)
practice advisors and, 286-287 (V1)
practice evaluation and, 287-288,
288t, 289t (V1)
risk management and, 301-303 (V1)
Office policy manual, 290b, 290 (V1)
Office-based anesthesia, 67-77 (V1)
airway assessment and, 69t, 69-70
(V1)
concept of rescue in, 68-69 (V1)
fluid administration and, 72 (V1)
goals of sedation in, 67-68 (V1)
laryngeal mask airway and, 70 (V1)
levels of sedation in, 67 (V1)
patient positioning and, 75 (V1)
pharmacology of drugs in, 56-66 (V1)
benzodiazepines and, 56-59, 58t,
59f (V1)
inhalation anesthetics and, 63-65,
64t (V1)
intravenous sedative-hypnotics
and, 60-62, 62t (V1)
ketamine and, 62-63 (V1)
opiates and opioids and, 59-60
(V1)
postoperative recovery and discharge
and, 75-76 (V1)
preoperative fasting and, 71-72
(V1)
smoking and, 70-71 (V1)
Office-based surgical facility, 490-492,
491f, 492f (V3)
Older adult
maxillofacial trauma in, 6, 374-394
(V2)
aging of face and neck in, 377
(V2)
anesthetic management in, 385,
385b (V2)
closed versus open reduction of
fractures in, 386t (V2)
cognitive evaluation and informed
consent in, 380 (V2)
INDEX I-67
Older adult (Continued)
considerations in management of,
392t (V2)
epidemiology of, 374-377, 375t,
376-377f (V2)
mandibular fractures in, 389-392f,
390-393 (V2)
maxilla and midface fractures in,
386-390, 387-389f (V2)
medications and over-the-counter
drug history and, 380 (V2)
nutrition and fluid and electrolyte
management in, 379 (V2)
perioperative risk assessment of co-
morbid systemic disease in,
380t, 380-385 (V2)
social history and, 379-380 (V2)
wound healing and, 377-378, 378f
(V2)
nonsteroidal antiinflammatory drugs
and, 85 (V1)
Olfaction, orthognathic surgery-related
changes in, 74 (V3)
Olfactory nerve evaluation
in chronic orofacial pain, 117 (V1)
in head injury, 51 (V2)
Omega-3 fatty acids, 399-400 (V1)
Omega-6 fatty acids, 399 (V1)
OMENS classification system for
oculoauriculovertebral spectrum,
925, 925b (V3)
Omiderm in laser skin resurfacing, 528
(V3)
OMS National Insurance Company,
373 (V1)
Oncogene, 647, 776f (V2)
Oncoproteins, 655 (V2)
One-wall extraction socket defect, 541,
543f (V1)
Onlay bone graft, implant placement
on, 424, 424f, 425f (V1)
Online communication
E-mail-based office system and, 303
(V1)
risk management and, 385 (V1)
Onplant system, 225 (V1)
On-Q Pain Management System, 974
(V2)
Open bite
genioplasty and, 140 (V3)
mandibular lengthening by
distraction osteogenesis and, 345
(V3)
postoperative, 414 (V3)
skeletal anchorage devices for, 232
(V1)
transoral vertical ramus osteotomy
and, 123, 124f, 132-135, 132-
135f (V3)
Open fracture, mandibular, 142 (V2)
Open investigation claim, 376 (V1)
Open joint surgery
history of, 796-797, 797f (V2)
in temporomandibular joint disorders,
132 (V1)
Open pneumothorax, 36 (V2)
Open reduction
of condylar fracture, 171 (V2)
of mandibular fracture, 148-152 (V2)
displaced mandibular dentoalveolar
fracture, 128f, 128 (V2)
in geriatric patient, 391f, 391-392,
392f, 392t (V2)
historical overview of, 139-141,
140f, 141f (V2)
transcervical-retromandibular
approach in, 152, 152f, 153f
(V2)
transcervical-submandibular
approach in, 150-152, 150-
152f (V2)
transoral/transbuccal approach in,
148-150, 149f, 150f (V2)
of nasal fracture, 278-281, 280f (V2)
Open reduction and internal fixation
in mandibular fracture, 391f, 391-
392, 392f, 392t (V2)
in maxillary/midface fracture, 386t,
387-389f, 388-390 (V2)
I-68 INDEX
Open rhinoplasty, 280, 281f (V2), 567-
572, 568-571f (V3)
anesthesia in, 567 (V3)
case reports in, 574-576, 574-576f
(V3)
incisions in, 560-562, 561f, 562f
(V3)
Open skull fracture, 59 (V2)
Open technique in guided bone
regeneration in extraction site,
454f, 454-455, 455f (V1)
Open tracheostomy, 33 (V2)
Opening movement of mandible, 810
(V2)
Opening-to-lateral excursion ratio, 826f
(V2)
Operating agreement, 299 (V1)
Ophthalmic artery
eyelid and, 584f, 585 (V3)
nose and, 553 (V3)
Ophthalmic assessment, 74-78, 75-78f
(V2)
in orbital fracture, 207-209, 208f,
209f (V2)
in zygomatic fracture, 183-184 (V2)
Ophthalmic disorders
after maxillary osteotomy, 473-475,
476f (V3)
in craniosynostosis, 865 (V3)
Ophthalmic nerve, 585 (V3)
Ophthalmic vein, 555 (V3)
OPI; See Occlusal Plane Indicator
Opioid analgesics
for acute postoperative pain, 80-82,
81b, 81t, 82t (V1)
anaphylaxis in pediatric anesthesia
and sedation and, 107t (V1)
for bone grafting in implant surgery,
422 (V1)
for chronic facial pain, 971-972, 972t
(V2)
for chronic orofacial pain, 120-121
(V1)
for myofascial pain, 144-145 (V1)
for neuropathic orofacial pain, 999
(V2)
for pain in bone graft harvest, 415
(V1)
pharmacology of, 59-60 (V1)
for temporomandibular osteoarthritis,
146 (V1)
Opioid receptors, 80-81 (V1)
Optic canal, 203t (V2)
Optic chiasm trauma, 85 (V2)
Optic disc avulsion, 83, 84f (V2)
Optic foramen, 203f, 203t (V2)
Optic nerve
evaluation of
in chronic orofacial pain, 117 (V1)
in head injury, 50, 51 (V2)
eyelid and, 584f (V3)
injury in orbit fracture, 213-214, 214f
(V2)
Optic neuropathy
after zygomatic fracture repair, 197
(V2)
traumatic, 84-85 (V2)
Oral anticoagulant therapy, 17, 17t
(V1)
Oral appliance for obstructive sleep
apnea syndrome, 319 (V3)
Oral cavity assessment in cranio-
maxillofacial trauma, 9, 10f (V2)
Oral cavity cancer, 705-723 (V2)
anatomy in, 705-706 (V2)
diagnostic adjuncts in, 708-709, 709f
(V2)
genetic abnormalities in, 707-708
(V2)
lymphoma in, 758, 759f, 762 (V2)
malignant melanoma in, 749, 750f
(V2)
non-surgical management of, 710-713
(V2)
pretreatment evaluation in, 710 (V2)
radiation therapy in, 768, 768t, 769f
(V2)
risk factors for, 706-707 (V2)
screening for, 708 (V2)
Oral cavity cancer (Continued)
staging of, 710, 711t (V2)
surgical management of, 713-720
(V2)
buccal mucosa cancer and, 714-
715, 715f, 716f (V2)
floor of mouth cancer and, 714,
714f, 715f (V2)
follow-up in, 719-720 (V2)
primary tumor and, 713-714 (V2)
retromolar trigone, alveolar ridge,
and palate cancer and, 716-
719 (V2)
tongue cancer and, 716-717, 716-
718f (V2)
types of neck dissection in, 719,
719t, 720f (V2)
trismus and, 899 (V2)
Oral commissure injection, 636f, 636-
637, 637f (V3)
Oral dysesthesia, 967-968, 995-996
(V2)
Oral exfoliative cytology, 415 (V2)
Oral hygiene, postoperative, 410 (V3)
Oral lesions
laser therapy for, 245 (V1)
in vesiculobullous diseases, 611-632
(V2)
aphthous stomatitis in, 619f, 619-
620 (V2)
Beh[ced]cet’s syndrome in, 620-
622 (V2)
epidermolysis bullosa in, 626-627
(V2)
erythema multiforme in, 627-628
(V2)
herpangina in, 617t, 617-618 (V2)
lichen planus in, 618f, 618-619
(V2)
linear IgA disease in, 625-626
(V2)
pediatric herpes simplex infection
in, 615-617 (V2)
pemphigoid in, 622-624, 623f (V2)
pemphigus in, 624-625, 625f (V2)
primary herpetic gingivostomatitis
in, 612-613, 613f (V2)
Reiter syndrome in, 622 (V2)
secondary herpes in, 613-614 (V2)
Oral membrane protection during laser
therapy, 243 (V1)
Oral mucositis
phases of, 785, 785f (V2)
radiation therapy-related, 774 (V2)
treatment and management of, 784-
785 (V2)
Oral region
Langerhans cell histiocytosis in, 567-
576, 568f (V2)
classification of, 569b, 569-570
(V2)
clonality of, 570 (V2)
diagnosis, treatment, and
prognosis of, 571-575,
571-575f (V2)
histopathology of, 570, 570f (V2)
Langerhans cell and, 568-569, 569f
(V2)
vascular anomalies of, 577-591 (V2)
arteriovenous malformation in,
588-590, 589f (V2)
binary classification of, 578b (V2)
capillary malformation in, 581,
581f (V2)
congenital hemangioma in, 579f,
579-581, 580f (V2)
infantile hemangioma in, 577-579,
578f (V2)
lymphatic malformation in, 581-
583, 582-585f (V2)
venous malformation in, 585-588,
586-588f (V2)
Oral region cysts, 418-465 (V2)
definitions in, 418 (V2)
general surgical considerations in,
418 (V2)
nonodontogenic, 447-460 (V2)
branchial cleft, 458-460, 458-460f
(V2)
Oral region cysts (Continued)
dermoid and epidermoid, 451-455,
454f, 455f (V2)
globulomaxillary, 451 (V2)
median mandibular, 451 (V2)
median palatal, 451 (V2)
nasolabial, 447-448, 449f, 450f
(V2)
nasopalatine duct, 448-451, 451-
453f (V2)
thyroglossal duct, 455-458, 455-
458f (V2)
odontogenic, 418-447 (V2)
calcifying, 445-447, 447f (V2)
dentigerous, 424-426, 425-428f
(V2)
gingival, 442, 445f (V2)
glandular, 444-445 (V2)
lateral periodontal, 442-444 (V2)
in nevoid basal cell carcinoma
syndrome, 441b, 441-442,
442t, 443f, 444f (V2)
odontogenic keratocyst, 426-441
(V2); See also Odontogenic
keratocyst
paradental, 421-424 (V2)
radicular, 419-421, 420f, 422f (V2)
residual, 421, 423f (V2)
Oral yeast infection, 410 (V3)
OralCDx, 709 (V2)
Orasone; See Prednisone
Orbicularis oculi muscle, 174f, 205
(V2), 582f, 582-583, 586f (V3)
forehead and brow lift and, 597 (V3)
hypertrophic, 579 (V3)
medial canthal tendon and, 244f
(V2)
Orbicularis oris muscle, 554f (V3)
primary bilateral cleft lip and palate
repair and, 724f (V3)
primary unilateral cleft lip repair and,
721f (V3)
Orbicularis-temporal ligament, 601
(V3)
Orbit
average growth completion of, 850t
(V3)
bony anatomy of, 183f (V2)
cancer arising near medial canthus
and, 728 (V2)
forehead and brow lift and, 596 (V3)
growth and development of, 851,
853f (V3)
malformation in craniofacial
dysostosis syndromes, 882 (V3)
maxilla and, 172 (V3)
maxillectomy and, 693 (V2)
oculoauriculovertebral spectrum and,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
maxilla and, 922-935 (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
pediatric, 352, 353f (V2)
psammomatoid variant of juvenile
ossifying fibroma and, 599 (V2)
trauma of, 83-86 (V2)
cranial nerve injury in, 85-86 (V2)
displacement of globe in, 88 (V2)
intraorbital foreign body in, 83-84,
84f (V2)
Orbit (Continued)
optic disc avulsion in, 83, 84f (V2)
orbital fracture in, 86f, 86-88, 87f
(V2); See also Orbital fracture
traumatic optic neuropathy in, 84-
85 (V2)
traumatic retrobulbar hemorrhage
in, 84f, 84 (V2)
Treacher Collins syndrome and, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
tumor of, 986 (V3)
Orbit height, 4, 5f (V3)
Orbital cleft, 728 (V3)
Orbital dysmorphology, 851 (V3)
Orbital emphysema, 87, 87f (V2)
Orbital fat pads, 583-585, 584f (V3)
prolapsed, 579, 580f (V3)
Orbital fissures, 203t (V2)
Orbital floor
anatomy of, 203 (V2)
blow-out fracture of, 86f, 86-87, 87f,
207, 207f (V2)
pediatric, 360-361, 360-361f (V2)
primary reconstruction of, 230f,
230-231 (V2)
surgical approaches to, 187-191 (V2)
lower eyelid, 187-188, 188f (V2)
subciliary, 190-191, 191f,
221 (V2)
subtarsal, 191 (V2)
transconjunctival, 188-190, 188-
190f (V2)
Orbital fracture, 83-85, 84f, 202-238
(V2)
anatomy in, 202-206, 203t, 203-206f,
205b, 205t (V2)
associated injuries in, 211-212, 212f
(V2)
clinical examination in, 207-209,
208f, 209f (V2)
conservative management of, 217-
220, 219f, 220f (V2)
diagnostic imaging of, 94, 94f (V2)
fracture patterns in, 206-207, 206-
208f (V2)
imaging techniques in, 209-211, 210f,
211f (V2)
indications for operative treatment
of, 220, 221f (V2)
naso-orbital-ethmoid, 207, 207f,
243-248 (V2)
anatomy in, 243f, 243-244, 244f
(V2)
clinical findings in, 244-246, 245f
(V2)
computed tomography of, 214f
(V2)
identification of medial canthal
tendon and, 246 (V2)
injury classification in, 244, 245f
(V2)

Orbital fracture (Continued)
nasal fracture and, 276, 276f, 278-
280 (V2)
nasal reconstruction in, 248, 249f
(V2)
nasolacrimal apparatus repair in,
248 (V2)
pediatric, 355-360, 358-359f (V2)
primary reconstruction in, 233
(V2)
radiographic evaluation in, 246
(V2)
reconstruction of medial orbital
rims in, 246-247, 247f (V2)
reconstruction of medial orbital
wall in, 247, 247f (V2)
soft tissue readaptation in, 248,
248f (V2)
surgical approaches in, 246, 246f
(V2)
transnasal canthopexy in, 247-248
(V2)
ophthalmic aspects of, 212-217 (V2)
diplopia in, 214-215, 215f, 216f
(V2)
eyelid lacerations in, 215 (V2)
lacrimal injuries in, 215, 217f (V2)
telecanthus in, 215-217, 218f (V2)
visual disturbances in, 212-214,
212-214f (V2)
ophthalmic assessment in, 78, 78f
(V2)
pediatric, 360-361, 360-361f (V2)
primary reconstruction in, 228-233
(V2)
internal orbital fracture and, 228-
230f, 228-231 (V2)
naso-orbital-ethmoid fracture and,
233 (V2)
zygomatic complex fracture and,
231f, 231-233, 232f (V2)
secondary reconstruction in, 233-236,
233-236f (V2)
surgical approaches in,
220-228 (V2)
inferior and lateral orbital, 221-
222, 222f, 223f (V2)
medial orbital, 225-228, 226f, 227f
(V2)
superior and lateral orbital, 222-
225, 224-226f (V2)
Orbital hypertelorism
in Apert syndrome, 881 (V3)
in midface deficiency, 206, 207-210f
(V3)
Orbital ligament, 597 (V3)
Orbital roof
anatomy of, 203 (V2)
fracture of, 88 (V2)
Orbital septum, 581f, 583, 583f, 586f,
587f (V3)
Orbitozygomatic fracture patterns, 206-
207, 206-208f (V2)
Organization of labor and
compensation, 291, 291t (V1)
Organizational styles, 288-290 (V1)
ORIF; See Open reduction and internal
fixation
ORME; See Orthopedic rapid maxillary
expansion
Oroantral communication
maxillary molar extraction and, 214f,
214-215 (V1)
simple extraction and, 191-192 (V1)
Oroantral fistula, maxillary surgery-
related, 480 (V3)
Orofacial cleft
cleft lip and palate, 713-734 (V3)
classification of, 715-716, 716f,
717f (V3)
embryology of, 714-715 (V3)
feeding child with, 717-718 (V3)
genetics and etiology of, 715 (V3)
history of cleft lip and palate repair
and, 713-714 (V3)
prenatal counseling and, 716-717
(V3)
repair of; See Cleft lip and palate
repair
Orofacial cleft (Continued)
treatment planning and timing,
718t, 718-719 (V3)
cleft lip and palate repair in, 719-730
(V3)
cleft palate repair and, 723-727,
729f, 730f (V3)
complex facial clefting and, 727-
728, 731f (V3)
history of, 713-714 (V3)
lip adhesion and, 720 (V3)
outcome assessment in, 728-730
(V3)
presurgical taping and orthopedics
in, 719-720, 720f (V3)
primary bilateral lip repair and,
723, 724-728f (V3)
primary unilateral cleft lip repair
and, 720-723, 721-723f (V3)
treatment planning and timing in,
718t, 718-719 (V3)
cleft maxilla in, 806-812, 840 (V3)
alveolar bone grafting technique
for, 808-810, 808-811f (V3)
grafting materials for, 806-807
(V3)
history and timing of repair in, 806
(V3)
missing teeth and crowded arches
in, 810-811, 811f (V3)
orthodontics for, 807f, 807-808
(V3)
postoperative care in, 810 (V3)
cleft orthognathic surgery in, 813-827
(V3)
bone grafting in, 819, 820-825f
(V3)
obstructed nasal breathing and,
819 (V3)
preoperative evaluation in, 813-
814 (V3)
stabilization of mobilized cleft
maxilla and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-
819, 818f (V3)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
orofacial embryogenesis and, 697-712
(V3)
animal studies in, 705, 706-708f
(V3)
complexity of human facial
morphogenesis and, 697-705,
698f, 700-704f (V3)
orofacial clefting sites and, 705-
712, 710f, 711f (V3)
revision surgery for, 828-847 (V3)
bone graft reconstruction of cleft
maxilla and palate in, 840
(V3)
complications of, 839 (V3)
comprehensive dental and
prosthetic rehabilitation in,
841-843, 844-845f (V3)
fistula closure in, 828-831, 830f,
832-834f (V3)
for management of submucous cleft
palate, 839-840 (V3)
for management of velopharyngeal
dysfunction, 831t, 831-835,
835f (V3)
operative techniques in, 836-839,
837f, 838f (V3)
orthognathic surgery for correction
of midfacial deficiency in, 840
(V3)
reconstruction of cleft nasal
deformity in, 840-841, 842f
(V3)
secondary surgery for cleft lip scar
revision in, 841, 843f (V3)
timing and indications for, 835-
836 (V3)
unilateral cleft lip repair in, 735-758
(V3)
Orofacial cleft (Continued)
comparison of surgical techniques
for, 735-737 (V3)
functional approach in, 752-757,
752-757f (V3)
Millard rotation and advancement
flap technique in, 737-741,
739-743f (V3)
Tennison triangular flap technique
in, 743-751, 744-751f (V3)
timing of, 735 (V3)
Orofacial embryogenesis, 697-712 (V3)
animal studies in, 705, 706-708f (V3)
cleft lip and palate and, 714-715
(V3)
complexity of human facial
morphogenesis and, 697-705,
698f, 700-704f (V3)
orofacial clefting sites and, 705-712,
710f, 711f (V3)
Orofacial migraine variants, 149 (V1)
Orofacial pain, 961-978 (V2)
acute postoperative, 78-92 (V1)
assessment of, 87, 87b, 88f, 89f
(V1)
local anesthetics for, 82-83 (V1)
neuroanatomy and pathophysiology
of, 78-80, 79f, 80f (V1)
nonsteroidal antiinflammatory
drugs for, 83-86, 84t, 85b, 86t
(V1)
opioid analgesics for, 80-82, 81b,
81t, 82t (V1)
patient-controlled analgesia for, 88
(V1)
perioperative considerations in, 87,
87b (V1)
physical methods for, 88-89 (V1)
preemptive analgesia therapy for,
87-88 (V1)
reassessment of, 89-90 (V1)
antidepressants for, 973 (V2)
atypical facial pain and, 158 (V1),
967-968 (V2)
barriers to management of, 970-971
(V2)
botulinum toxin injection for, 974-
975 (V2)
of cardiac origin, 969 (V2)
central mechanisms of, 963 (V2)
chronic, 112-135 (V1)
changing treatment of, 121-122
(V1)
cranial nerve examination in, 116-
118, 119f, 120f (V1)
flexible diagnoses-management
concept in, 113-114 (V1)
follow-up visits for, 121 (V1)
individualized pain management
in, 122-124, 123f, 124f (V1)
initial visit for, 112-113 (V1)
local anesthetic injections for,
114-115, 115-117f (V1)
localized pathologic conditions
and, 115-116 (V1)
peripheral and central mediated
pain in, 120-121 (V1)
prevention of progression to, 124-
126 (V1)
reevaluation of diagnoses in, 121
(V1)
systemic pathologic conditions
and, 118 (V1)
in temporomandibular joint
disorders, 126-134, 128f,
129f (V1); See also
Temporomandibular
disorders
temporomandibular joint
protection during surgical
procedures and, 125 (V1)
third molar pathologic conditions
and, 125-126 (V1)
third molar surgery and, 125 (V1)
clinically based comprehensive pain
management program for, 975
(V2)
complex regional pain syndrome and,
966-967 (V2)
INDEX I-69
Orofacial pain (Continued)
Eagle’s syndrome and, 969-970, 970f
(V2)
evaluation of, 824, 824b, 963-966,
965f, 966t (V2)
future directions in management of,
975-976 (V2)
muscle relaxants for, 974 (V2)
nerve injury from dental procedures
and, 968f, 968-969 (V2)
neuralgia-inducing cavitational
osteonecrosis and, 967 (V2)
neuropathic, 989-1004 (V2)
burning mouth syndrome in, 995-
996 (V2)
central poststroke pain in, 994-995
(V2)
diagnosis of, 989-990 (V2)
glossopharyngeal neuralgia in, 993-
994 (V2)
herpes zoster and, 994 (V2)
secondary to neuritis, 1000 (V2)
traumatic orofacial neuropathies
in, 996-999, 998t, 999t (V2)
trigeminal neuralgia in, 990-992t,
990-993 (V2)
neuropathic agents for, 973-974 (V2)
nonsteroidal antiinflammatory drugs
for, 972-973, 973t (V2)
opioid therapy for, 971-972, 972t
(V2)
osteonecrosis-related, 970 (V2)
peripheral mechanisms of, 962, 963f
(V2)
physical therapy for, 971 (V2)
surgical intervention for, 975 (V2)
in temporomandibular disorders, 815
(V2)
therapeutic injections for, 974 (V2)
topical capsaicin for, 975 (V2)
trigeminal anatomy and, 961-962,
962f (V2)
Oronasal fistula, maxillary surgery-
related, 480 (V3)
Oropharyngeal airway, 100-102 (V1)
Oropharyngeal cancer, 768, 768t, 769f
(V2)
Orthodontic appliance
in mandibular widening, 338, 340f
(V3)
in maxillary distraction by intraoral
device, 347 (V3)
postsurgical management of, 401
(V3)
Orthodontic bracket arch wire splint,
130 (V2)
Orthodontic instability after surgery,
413 (V3)
Orthodontic therapy
basic exodontia before, 185-186
(V1)
in cleft maxilla, 807f, 807-808 (V3)
distraction osteogenesis and, 338-363
(V3)
alveolar distraction in, 349-354,
349-354f (V3)
bone transport by, 354-360, 355-
361f (V3)
future directions in, 362 (V3)
mandibular lengthening in, 342-
346, 342-346f (V3)
mandibular widening in, 338-342,
339-342f (V3)
maxillary bone transport in, 360-
362, 362f (V3)
maxillary distraction by intraoral
devices in, 346-349, 347-349f
(V3)
in facial asymmetry, 277 (V3)
developmental, 282 (V3)
unilateral dentoalveolar asymmetry
and, 282, 283-284f (V3)
laser-assisted soft tissue procedures in,
255 (V1)
maxillomandibular complex rotation
and, 266-267 (V3)
orthognathic surgery and, 72 (V3)
postsurgical, 399-402, 401f, 402f
(V3)
I-70 INDEX
Orthodontic therapy (Continued)
surgical factors to enhance, 396-
399, 398-399f (V3)
skeletal anchorage for, 223-236 (V1)
basic orthodontic mechanics and,
224-225 (V1)
bone plates in, 232-233, 233f, 234f
(V1)
for closure of anterior open bite,
232 (V1)
devices for, 225f, 225-226, 226f
(V1)
historical perspective of, 223-224
(V1)
impacted teeth and, 172 (V1)
mesial or distal movement of teeth
and, 226-231f (V1)
miniimplants in, 570-574, 572-
574f (V1)
miniscrews in, 233-235 (V1)
orthopedic growth modification
and, 232 (V1)
outcomes and complications in,
235-236 (V1)
postoperative regimen in, 234-235
(V1)
for uprighting and intruding molar
teeth, 232 (V1)
for transverse maxillary deficiency,
224 (V3)
Orthognathic surgery
after cleft lip and palate repair, 719,
840 (V3)
ambulatory, 490-496 (V3)
absolute contraindications for, 494
(V3)
airway evaluation and, 492-493
(V3)
comorbidities and, 493 (V3)
complexity of surgical procedure
and, 494-495 (V3)
facility for, 490-492, 491f, 492f
(V3)
patient selection and, 492 (V3)
postoperative care and, 495-496,
496t (V3)
surgeon skill and comfort level
and, 494 (V3)
bilateral sagittal split osteotomy in,
71, 87-118 (V3)
characteristics and advantages of,
89, 89b (V3)
hemorrhage in, 115, 115b (V3)
for mandibular asymmetry, 99t, 99-
102, 102-105f (V3)
for mandibular deficiency, 89b, 89-
97, 90-96f, 97b (V3)
for mandibular prognathism, 97-99,
98f, 99b, 100f, 101f (V3)
nerve injury in, 112-113, 113b
(V3)
osteosynthesis in, 109-111, 110f,
111b (V3)
osteotomy in, 106-109, 107f, 107t,
108f, 109b (V3)
postoperative sequelae in, 111-112
(V3)
postoperative wound infection in,
115, 116b (V3)
rare complications in, 116, 116b
(V3)
relapse in, 115-116, 116b (V3)
soft tissue dissection in, 102-106,
106f (V3)
temporomandibular joint
dysfunction after, 113-114
(V3)
unfavorable bony split in, 114b,
114-115 (V3)
cleft, 813-827 (V3)
bone grafting in, 819, 820-825f
(V3)
for comprehensive dental and
prosthetic rehabilitation, 841-
843, 844-845f (V3)
obstructed nasal breathing and,
819 (V3)
preoperative evaluation in, 813-
814 (V3)
Orthognathic surgery (Continued)
stabilization of mobilized cleft
maxilla and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-
819, 818f (V3)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
clinical facial evaluation in, 1-10 (V3)
detailed regional facial features
and, 4-8, 5-9f, 9b (V3)
facial skin age-related changes and,
8-10, 10f (V3)
facial skin health and, 2, 2t (V3)
facial skin type and, 1, 2t (V3)
general facial anthropometric
relations and, 2-4, 3f, 4f (V3)
combined maxillary and mandibular
osteotomies in, 238-247 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
complete mandibular subapical
osteotomy in, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
complications of; See Orthognathic
surgery complications
in craniofacial dysostosis syndromes
in Apert syndrome, 902 (V3)
in Crouzon syndrome, 900 (V3)
exacerbation of mandibular
hypomobility and, 902 (V2)
in facial asymmetry, 272-315 (V3)
in adolescent internal condylar
resorption, 299-305, 303-304f,
306f (V3)
in autoimmune and connective
tissue diseases, 309-313, 310-
313f (V3)
categories of, 278 (V3)
clinical evaluation in, 272-274,
273f (V3)
dentoalveolar and occlusal
assessment in, 274 (V3)
dentoalveolar asymmetry and, 282,
283-284f (V3)
developmental, 282 (V3)
diagnostic and treatment
considerations in, 275-277,
276f (V3)
in hemifacial microsomia, 298-299,
300-302f (V3)
iatrogenic, 294 (V3)
imaging in, 274-275 (V3)
in mandibular condylar
osteochondroma or osteoma,
285-291, 289-291f (V3)
in muscle hypertrophy, 291-292
(V3)
in neuromuscular disorders, 292,
292f (V3)
presurgical patient preparation
and, 277-278 (V3)
pseudoasymmetry and, 278-282,
279-281f (V3)
in reactive arthritis, 305-309, 307-
309f (V3)
in temporomandibular joint
ankylosis, 294-298, 297f, 298f
(V3)
Orthognathic surgery (Continued)
trauma-related, 294, 295f, 296f
(V3)
in tumor, 293, 293f (V3)
in unilateral condylar hyperplasia,
284-285, 286-288f (V3)
unilateral facial underdevelopment
or degeneration and, 294-313
(V3)
facial skeletal growth evaluation in,
19-58 (V3)
mandibular values in, 41-57 (V3);
See also Mandibular growth
values
maxillary-midface values in, 28-40
(V3); See also Maxillary-
midface growth values
neurocranial values in, 19-27 (V3);
See also Neurocranial growth
values
facial skeleton evaluation in, 10-17
(V3)
changes with age and, 15-17, 17f
(V3)
dental relations in, 14-15, 16f (V3)
skeletal relations in, 12-14, 13-15f
(V3)
soft tissue relations in, 11-12, 12f
(V3)
genioplasty in, 71, 137-154 (V3)
fixation devices in, 142-145, 144-
148f (V3)
functional, 137, 138f (V3)
indications for, 137-138 (V3)
results in, 148-151, 150-153f (V3)
surgical procedure in, 140-142,
141f, 142f (V3)
treatment planning in, 138-140,
139f, 140f (V3)
intraoral distraction osteogenesis in,
338-363 (V3)
alveolar distraction in, 349-354,
349-354f (V3)
bone transport by, 354-360, 355-
361f (V3)
future directions in, 362 (V3)
mandibular lengthening in, 342-
346, 342-346f (V3)
mandibular widening in, 338-342,
339-342f (V3)
maxillary bone transport in, 360-
362, 362f (V3)
maxillary distraction by intraoral
devices in, 346-349, 347-349f
(V3)
Le Fort I osteotomy in, 63-68, 172-
191 (V3); See also Le Fort I
osteotomy
ambulatory, 494 (V3)
in cleft orthognathic surgery, 815-
819, 818f (V3)
before complete mandibular
subapical osteotomy, 162f
(V3)
complications of, 185-189 (V3)
in craniofacial dysotosis syndromes,
884, 885 (V3)
fixation of, 181-184 (V3)
hierarchy of stability in, 184 (V3)
historical background of, 63, 172,
173f (V3)
Le Fort III osteotomy with, 211
(V3)
in maxillary bone transport, 360
(V3)
in maxillary distraction by
intraoral devices, 347, 348f
(V3)
maxillomandibular complex
rotation and, 266, 267f (V3)
for obstructive sleep apnea
syndrome, 323-330, 327-332f
(V3)
in oculoauriculovertebral spectrum,
931, 931f (V3)
in pediatric craniomaxillofacial
tumor, 963-964 (V3)
postoperative management of, 184
(V3)
Orthognathic surgery (Continued)
revascularization and healing in,
63-65, 64f, 65f (V3)
soft tissue changes in, 184-185,
185-188f (V3)
soft tissue incision in, 65-66 (V3)
surgical anatomy in, 172-174, 173f,
174f (V3)
surgical technique in, 176-181,
176-184f (V3)
in surgically assisted maxillary
expansion, 67f, 67-68, 227,
228-230f (V3)
in Treacher Collins syndrome, 954
(V3)
in two-jaw surgery, 239 (V3)
vascular anatomy in, 174-175, 176f
(V3)
Le Fort I segmental osteotomy in
complications in, 198, 198f, 199f
(V3)
historical background of, 192 (V3)
indications for, 192-193 (V3)
for maxillary deficiency, 199-203f
(V3)
osteotomy design in, 196 (V3)
postoperative care in, 196-197,
197f (V3)
surgical planning in, 197-198 (V3)
technique in, 193-196, 194-196f
(V3)
Le Fort III osteotomy in, 205-218 (V3)
for craniofacial dysostosis, 205-206
(V3)
indications for, 205 (V3)
in maxillary distraction by
intraoral devices, 347, 348f
(V3)
for midface deficiency, 206, 207-
210f (V3)
modified, 211-218 (V3)
subcranial, 210-211, 212-217f (V3)
technique in, 206-210 (V3)
model surgery and, 364-371 (V3)
construction of intermediate splint
in, 368-369, 369f, 370f (V3)
in facial asymmetry, 277 (V3)
in mandibular widening, 338 (V3)
marking cast in, 366-367 (V3)
measurements in, 367f, 367-368
(V3)
mounting case in, 364-366, 365f,
366f (V3)
positioning of maxilla in, 368, 368f
(V3)
for segmental surgery, 369-370,
370f (V3)
for special situations, 370-371 (V3)
for obstructive sleep apnea syndrome,
316-337 (V3)
Delaire cephalometric analysis in,
321-323, 325-327f (V3)
diagnosis and treatment planning
in, 319-321, 322-324f (V3)
maxillary and mandibular
advancement for, 323-330,
327-332f (V3)
pathophysiology of, 316-318, 318f
(V3)
patient outcomes in, 330-336, 333-
335f (V3)
treatment options for, 318-319,
320-322f (V3)
occlusal plane rotation in, 248-271
(V3)
clockwise rotation in, 252-256,
252-256f (V3)
counterclockwise rotation in, 256-
260, 257-263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-
249, 249f, 250f (V3)
geometry of treatment design using
constructed
maxillomandibular triangle in,
261f, 261-262 (V3)

Orthognathic surgery (Continued)
linear dimensions between
maxillary length and vertical
facial height in, 250, 250f
(V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-
268 (V3)
occlusion evaluation in, 17-19, 18b
(V3)
in oculoauriculovertebral spectrum,
930-934, 931-933f (V3)
perioperative patient management in,
382-395 (V3)
antibiotics and, 392-393 (V3)
asplenia and, 387-388 (V3)
blood loss management and, 392
(V3)
cardiovascular disorders and, 382,
383b (V3)
congenital heart disorders and,
382-383, 383t (V3)
consultation and, 389, 389t (V3)
endocrine disorders and, 385-386
(V3)
epoetin alfa and, 390 (V3)
gastrointestinal disorders and, 386-
387, 387t (V3)
hematologic disorders and, 384-
385 (V3)
imaging and, 389 (V3)
laboratory tests and, 389-390 (V3)
neurologic disorders and, 388-389
(V3)
nutrition and, 390-391 (V3)
patient positioning and, 391-392
(V3)
postoperative nausea and vomiting
and, 393 (V3)
preoperative interview and, 391,
391b (V3)
pulmonary disorders and, 383-384,
384b, 384t (V3)
single kidney and, 387 (V3)
social factors in, 391 (V3)
steroids and, 393 (V3)
physiologic consequences of, 72-76
(V3)
biting differences in, 72 (V3)
head posture and, 75 (V3)
nasal airway resistance and, 73-74
(V3)
nasal and oral respiratory patterns
and, 74 (V3)
neurosensory changes in, 75-76
(V3)
olfaction and, 74 (V3)
respiration and, 73 (V3)
sinus function and, 76 (V3)
speech and, 74-75 (V3)
temporomandibular joint
dysfunction and masticatory
muscle pain in, 72-73 (V3)
tongue posture and function and,
75 (V3)
velopharyngeal function and, 73
(V3)
postsurgical patient management in,
396-418 (V3)
airway obstruction and, 404 (V3)
anticlenching medications and,
409-410 (V3)
antinausea medications and, 410
(V3)
in bone transport by distraction
osteogenesis, 360 (V3)
clenching and bruxism and, 406-
407 (V3)
decongestants and antihistamines
and, 410 (V3)
Orthognathic surgery (Continued)
dietary considerations in, 408-409,
409f (V3)
elimination patterns and, 409 (V3)
fatigue and, 405 (V3)
hormone imbalance and, 408 (V3)
jaw and occlusal instability and,
413-415, 414-417f (V3)
jaw function and, 406 (V3)
in Le Fort I osteotomy, 184 (V3)
in mandibular lengthening by
distraction osteogenesis, 345-
346 (V3)
in mandibular widening, 341-342
(V3)
masseter muscles recovery and, 406
(V3)
middle ear dysfunction and, 406
(V3)
in modified Le Fort III osteotomy,
212-218 (V3)
motor nerve deficit and, 405-406
(V3)
muscles of facial expression issues
and, 406 (V3)
nasal bleeding and, 404 (V3)
nausea and, 404-405 (V3)
nose blowing and, 411, 411f (V3)
oral hygiene and, 410 (V3)
pain and, 405, 409b (V3)
physical activities and, 411-412
(V3)
postsurgical orthodontics and, 399-
402, 401f, 402f (V3)
prophylactic antibiotics and, 410
(V3)
psychosocial issues in, 404 (V3)
scarring reduction medications
and, 410 (V3)
sensory nerve deficit and,
405 (V3)
showers and baths and, 411 (V3)
surgical factors to enhance
postsurgical orthodontics,
396-399, 397-399f (V3)
swelling and ecchymosis and, 403-
404 (V3)
temporomandibular joint function
and, 406, 407f (V3)
therapeutic clenching and, 407
(V3)
tooth ankylosis and, 412-413 (V3)
tooth discoloration and, 412 (V3)
in total maxillary segmental
osteotomy, 196-197, 197f
(V3)
in transoral vertical ramus
osteotomy, 128f, 128-129
(V3)
wound infection and, 412 (V3)
prediction of soft tissue changes in,
372-381 (V3)
cephalometric, 372-375, 373f (V3)
computerized-video imaging, 375-
377, 376f (V3)
photographic, 375 (V3)
three-dimensional computer-
assisted, 377-379, 378f (V3)
prevention of complications in, 419
(V3)
psychosocial aspects of, 76-81, 77f,
78f, 79b (V3)
revascularization and healing in, 60-
71 (V3)
bone healing and, 62 (V3)
categorization of, 62 (V3)
genioplasty and, 71 (V3)
Le Fort 1 osteotomy and, 63-68,
64-67f (V3)
mandibular osteotomy and, 68-70f,
68-71 (V3)
maxillary surgery and, 62-63, 63f
(V3)
phases of, 60-62, 61f, 62f (V3)
surgically assisted maxillary
expansion in, 67f, 67-68, 219-
237 (V3)
clinical evaluation in, 219, 220-
220f, 221f (V3)
Orthognathic surgery (Continued)
complications of, 231-232, 233f
(V3)
incidence and origin of transverse
maxillary deficiency and, 219,
220f (V3)
modification of, 232-233, 234f
(V3)
orthopedic rapid maxillary
expansion and, 224-226, 224-
226f (V3)
radiographic evaluation in, 220-
223, 221-223f (V3)
segmental maxillary osteotomy
versus, 233-235 (V3)
technique in, 227-231, 228-232f
(V3)
transoral vertical ramus osteotomy in,
119-136 (V3)
advantages and disadvantages of,
120-121, 121t, 122f (V3)
historical background of, 119 (V3)
indications and contraindications
for, 121-122 (V3)
intraoperative procedure in, 123-
128, 125-127f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe facial asymmetry, 130f,
130-131, 131f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe open bite, 132-135,
132-135f (V3)
postoperative physiotherapy in,
128f, 128-129 (V3)
sagittal split ramus osteotomy
versus, 119, 120f, 120t (V3)
surgical treatment objectives in,
123, 124f, 125f (V3)
in Treacher Collins syndrome, 954
(V3)
trigeminal nerve injury and, 275
(V1)
venous malformation and, 588 (V2)
Orthognathic surgery complications,
419-489 (V3)
in genioplasty, 439-441, 440f, 441f,
446-451, 449-452f (V3)
in inverted L and C osteotomies,
436-439, 437f (V3)
in mandibular surgery, 419-454 (V3)
dental and periodontal problems
in, 453 (V3)
dental compensations and, 419-
421, 420-422f (V3)
excessive swelling in, 441-442,
442f (V3)
hemorrhage and hematoma in,
442-443 (V3)
idiopathic condylar resorption in,
453-454 (V3)
infection in, 443 (V3)
leveling and root divergence in
segmental cases and, 423 (V3)
loss of gonial projection in, 454,
455-456f (V3)
mandibular dysfunction in, 445,
453 (V3)
neurologic dysfunction in, 444-
445, 453 (V3)
patient dissatisfaction and, 423
(V3)
postoperative nausea, vomiting,
and dehydration in,
443 (V3)
prevention of, 454t (V3)
tooth size discrepancies and, 422-
423, 423f (V3)
transverse discrepancies and, 421-
422 (V3)
in maxillary surgery, 454-480 (V3)
accurate presurgical records and,
459, 460-463f (V3)
antral or nasal fistulas in, 480 (V3)
atrophic rhinitis in, 480 (V3)
bleeding in, 467-469f, 467-470
(V3)
bradycardia in, 470 (V3)
INDEX I-71
Orthognathic surgery complications
(Continued)
dental and periodontal problems
in, 475, 477f (V3)
dental compensations and, 456,
457-458f (V3)
improper maxillary repositioning
in, 470-471, 471f (V3)
incision design and closure and,
459-464 (V3)
leveling and root divergence in
segmental cases and, 458-459
(V3)
nasal septal deviation in, 478-480,
479f (V3)
nerve injury in, 477 (V3)
ophthalmic disorders in, 473-475,
476f (V3)
prevention of, 480t (V3)
psychologic preparation and, 459
(V3)
relapse in, 480 (V3)
in segmental maxillary surgery,
472-473 (V3)
systematic aesthetic analysis and,
459 (V3)
technical difficulties and, 471-472,
472f (V3)
tooth size discrepancies and, 458
(V3)
transverse discrepancies and, 456-
458 (V3)
unfavorable interdental osteotomy
in, 473-475f (V3)
unfavorable nasolabial esthetics in,
477-478 (V3)
unfavorable osteotomy in, 464-467,
465f, 466f (V3)
vascular compromise in, 475 (V3)
prevention of, 419 (V3)
in sagittal ramus osteotomy, 423-433
(V3)
intraoperative bleeding in, 429-
431, 433f (V3)
minor technical difficulties in, 433
(V3)
nerve injury in, 426-429, 432f (V3)
proximal segment malpositioning
in, 431-432 (V3)
relapse in, 445, 446f (V3)
unfavorable osteotomy in, 423-426,
424-434f (V3)
in vertical subcondylar ramus
osteotomy, 433-436, 434-436f,
445-446, 446-449f (V3)
Orthopantomogram, 548f, 551-552,
552f, 553f (V1)
in chronic facial pain, 965-966 (V2)
in implant surgery, 551-552, 552f,
553f (V1)
Orthopedic growth modification,
skeletal anchorage for, 232 (V1)
Orthopedic intraoral splint, 984-985
(V2)
Orthopedic rapid maxillary expansion,
224-226, 224-226f (V3)
Orthopedics before cleft lip and palate
repair, 710-720, 720f, 783-790
(V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t (V3)
presurgical nasoalveolar molding and,
783 (V3)
Orudis; See Ketoprofen
Orzel, 781t (V2)
OSHA; See Occupational Safety and
Health Administration
Osseous resection of odontogenic
keratocyst, 438, 439f (V2)
Ossicle deformity in Treacher Collins
syndrome, 938-939 (V3)
Ossifying fibroma, 598, 599f (V2)
of frontal sinus, 965f, 966f (V3)
peripheral, 180, 180f (V1)
Ostectomy in complete mandibular
subapical osteotomy, 158, 159f
(V3)
I-72 INDEX
Osteitis after nasal fracture repair, 282
(V2)
Osteoarthritis
chronic orofacial pain in, 118 (V1)
diagnostic approach to, 832t (V2)
temporomandibular, 145-146 (V1),
855-857, 885 (V2)
Osteoblast
bone healing and, 62 (V3)
bone regeneration and, 22 (V2)
effect of antibiotics on, 389t, 389-390
(V1)
platelet-rich plasma and, 503, 504
(V1)
Osteoblastoma, 602-604, 605f, 871
(V2)
Osteocartilaginous exostosis, 871 (V2)
Osteochondroma, 606, 871 (V2)
mandibular, 285-291, 289-291f, 416f
(V3)
Osteochondromatosis, 872 (V2)
Osteoclast
bisphosphonates and, 557-558 (V2)
bone healing and, 62 (V3)
bone regeneration and, 22 (V2)
Osteogenesis
intraoral distraction, 338-363 (V3)
alveolar distraction in, 349-354,
349-354f (V3)
bone transport by, 354-360, 355-
361f (V3)
future directions in, 362 (V3)
mandibular lengthening in, 342-
346, 342-346f (V3)
mandibular widening in, 338-342,
339-342f (V3)
maxillary bone transport in, 360-
362, 362f (V3)
pediatric, 858 (V3)
platelet-rich plasma and, 502 (V1)
Osteogenic sarcoma, 680-684, 681f,
682f (V2)
Osteoid osteoma, 602, 871 (V2)
Osteoma, 604-605, 606f (V2)
mandibular, 285-291, 289-291f, 416f
(V3)
osteoid, 602 (V2)
of temporomandibular joint, 871
(V2)
Osteomyelitis, 633-639 (V2)
classifications of, 633, 634b (V2)
clinical and radiographic presentation
of, 633-635, 634-636f (V2)
pathogenesis of, 633 (V2)
risk factors for, 634b (V2)
treatment of, 635-638, 636t, 637f
(V2)
unique complications in, 638b, 638f,
638-639 (V2)
Osteonecrosis
bisphosphonate-related, 217, 218t,
395-396 (V1), 557-566 (V2)
chronic facial pain and, 970 (V2)
clinical presentation of, 559-560,
560f, 561f (V2)
clinical use of bisphosphonates
and, 558-559 (V2)
future research in, 564 (V2)
mechanism of action of
bisphosphonates and, 557-
558, 558f, 558t (V2)
pathophysiology and risk factors
for, 559 (V2)
staging of, 560-561, 561t (V2)
treatment outlines for, 561-564,
563f, 563t, 564f (V2)
chronic facial pain and, 970 (V2)
neuralgia-inducing cavitational, 967
(V2)
Osteoperiosteal flap, 471-478 (V1)
alveolar repositioning osteotomies
and, 473, 473f, 474f (V1)
alveolar split graft and, 471, 473f
(V1)
alveolar width distraction
osteogenesis and, 474-477, 475-
478f (V1)
interpositional bone graft and, 471,
472f (V1)
Osteoporosis, 395 (V1), 558-559 (V2)
Osteoradionecrosis, 639-642, 774 (V2)
clinical and radiographic diagnosis of,
639, 639f, 640f (V2)
exodontia and, 217 (V1)
hyperbaric oxygen therapy for, 639-
641 (V2)
prevention and maintenance of, 641-
642, 642f (V2)
treatment of, 639, 640f, 641b, 641t
(V2)
Osteosarcoma, 680-684, 681f, 682f
(V2), 986 (V3)
of temporomandibular joint, 873
(V2)
Osteosynthesis in bilateral sagittal split
osteotomy, 109-111, 110f, 111b
(V3)
Osteotomy
alveolar repositioning, 473, 473f,
474f (V1)
in antral membrane balloon
elevation, 465-466, 466f (V1)
bilateral sagittal split, 71, 87-118
(V3)
characteristics and advantages of,
89, 89b (V3)
hemorrhage in, 115, 115b (V3)
for mandibular asymmetry, 99t, 99-
102, 102-105f (V3)
for mandibular deficiency, 89b, 89-
97, 90-96f, 97b (V3)
for mandibular prognathism, 97-99,
98f, 99b, 100f, 101f (V3)
nerve injury in, 112-113, 113b
(V3)
for obstructive sleep apnea
syndrome, 323-330, 327-332f
(V3)
osteosynthesis in, 109-111, 110f,
111b (V3)
osteotomy in, 106-109, 107f, 107t,
108f, 109b (V3)
postoperative sequelae in, 111-112
(V3)
postoperative wound infection in,
115, 116b (V3)
rare complications in, 116, 116b
(V3)
relapse in, 115-116, 116b (V3)
soft tissue dissection in, 102-106,
106f (V3)
temporomandibular joint
dysfunction after, 113-114
(V3)
unfavorable bony split in, 114b,
114-115 (V3)
in bone graft harvest
from ilium, 418, 418f (V1)
from mandibular ramus, 412f, 412-
413 (V1)
from mandibular symphysis, 410,
410f (V1)
complete mandibular subapical, 155-
171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
in distraction osteogenesis, 997 (V3)
genioplasty, 71, 137-154 (V3)
fixation devices in, 142-145, 144-
148f (V3)
functional, 137, 138f (V3)
indications for, 137-138 (V3)
results in, 148-151, 150-153f (V3)
surgical procedure in, 140-142,
141f, 142f (V3)
treatment planning in, 138-140,
139f, 140f (V3)
implant repositioning, 473, 474f (V1)
in internal derangement of
temporomandibular joint, 940
(V2)
Osteotomy (Continued)
in interpositional bone graft, 471,
472f (V1)
Le Fort I, 63-68, 172-191 (V3); See
also Le Fort I osteotomy
ambulatory, 494 (V3)
in cleft orthognathic surgery, 815-
819, 818f (V3)
before complete mandibular
subapical osteotomy, 162f
(V3)
complications of, 185-189 (V3)
in craniofacial dysotosis syndromes,
884, 885 (V3)
fixation of, 181-184 (V3)
hierarchy of stability in, 184 (V3)
historical background of, 63, 172,
173f (V3)
in maxillary bone transport, 360
(V3)
in maxillary distraction by
intraoral devices, 347, 348f
(V3)
for obstructive sleep apnea
syndrome, 323-330, 327-332f
(V3)
in oculoauriculovertebral spectrum,
931, 931f (V3)
in pediatric craniomaxillofacial
tumor, 963-964 (V3)
postoperative management of, 184
(V3)
revascularization and healing in,
63-65, 64f, 65f (V3)
segmental, 66-67, 67f (V3)
soft tissue changes in, 184-185,
185-188f (V3)
soft tissue incision in, 65-66 (V3)
surgical anatomy in, 172-174, 173f,
174f (V3)
surgical technique in, 176-181,
176-184f (V3)
surgically assisted maxillary
expansion in, 67f, 67-68 (V3)
in Treacher Collins syndrome, 954
(V3)
vascular anatomy in, 174-175, 176f
(V3)
Le Fort I segmental, 66-67, 67f, 192-
204 (V3)
complications in, 198, 198f, 199f
(V3)
historical background of, 192 (V3)
indications for, 192-193 (V3)
for maxillary deficiency, 199-203f
(V3)
osteotomy design in, 196 (V3)
postoperative care in, 196-197,
197f (V3)
surgical planning in, 197-198 (V3)
technique in, 193-196, 194-196f
(V3)
Le Fort III, 205-218 (V3)
for craniofacial dysostosis, 205-206
(V3)
indications for, 205 (V3)
in maxillary distraction by
intraoral devices, 347, 348f
(V3)
for midface deficiency, 206, 207-
210f (V3)
modified, 211-218 (V3)
subcranial, 210-211, 212-217f (V3)
technique in, 206-210 (V3)
in mandibular lengthening by
distraction osteogenesis, 342,
343f (V3)
in mandibular widening, 339, 340f
(V3)
in maxillectomy, 696 (V2)
nasal, 569, 569f (V3)
sagittal split ramus, 70, 70f (V3)
in rotation of maxillomandibular
complex, 268, 268f, 269f (V3)
transoral vertical ramus osteotomy
versus, 119, 120t, 121 (V3)
in two-jaw surgery, 240 (V3)
in sinus-lift subantral augmentation,
459-460, 460f (V1)
Osteotomy (Continued)
in surgically assisted maxillary
expansion, 67f, 67-68, 219-237
(V3)
clinical evaluation in, 219, 220-
220f, 221f (V3)
complications of, 231-232, 233f
(V3)
incidence and origin of transverse
maxillary deficiency and, 219,
220f (V3)
modification of, 232-233, 234f
(V3)
orthopedic rapid maxillary
expansion and, 224-226, 224-
226f (V3)
radiographic evaluation in, 220-
223, 221-223f (V3)
segmental maxillary osteotomy
versus, 233-235 (V3)
technique in, 227-231, 228-232f
(V3)
transoral vertical ramus, 119-136
(V3)
advantages and disadvantages of,
120-121, 121t, 122f (V3)
historical background of, 119 (V3)
indications and contraindications
for, 121-122 (V3)
intraoperative procedure in, 123-
128, 125-127f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe facial asymmetry, 130f,
130-131, 131f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe open bite, 132-135,
132-135f (V3)
postoperative physiotherapy in,
128f, 128-129 (V3)
sagittal split ramus osteotomy
versus, 119, 120f, 120t (V3)
surgical treatment objectives in,
123, 124f, 125f (V3)
zygomatic arch, 909 (V2)
in zygomatic implant, 494-495, 495f
(V1)
Os-zygomaticum, zygomatic implant
and, 492-493 (V1)
Otitis media
Apert syndrome and, 882 (V3)
speech impairment and, 792 (V3)
Otoplasty, 665-677 (V3)
blood supply to ear and, 667-668
(V3)
complications in, 675-676 (V3)
for congenital deformities, 668-669
(V3)
for correction of protruding earlobe,
675, 675f (V3)
Davis method in, 670-673, 672f (V3)
embryology of auricle and, 665, 666f
(V3)
Farrior technique in, 673, 675f (V3)
indications and timing of, 669 (V3)
Mustard[ac]e method in, 673, 674f
(V3)
nerve supply to ear and, 668-670f
(V3)
surgical anatomy in, 665-666, 666f,
667f (V3)
techniques in, 669-670, 671f (V3)
Otorrhea in basilar skull fracture, 59-60
(V2)
Outcome assessment in cleft lip and
palate repair, 728-730 (V3)
Outpatient orthognathic surgery, 490-
496 (V3)
absolute contraindications for, 494
(V3)
airway evaluation and, 492-493 (V3)
comorbidities and, 493 (V3)
complexity of surgical procedure and,
494-495 (V3)
facility for, 490-492, 491f, 492f (V3)
patient selection and, 492 (V3)
postoperative care and, 495-496, 496t
(V3)

Outpatient orthognathic surgery
(Continued)
surgeon skill and comfort level and,
494 (V3)
Outside professional consultation in
marketing, 322-323, 337-338 (V1)
Overdevelopment of face, 282-293 (V3)
in mandibular condylar
osteochondroma or osteoma,
285-291, 289-291f (V3)
in muscle hypertrophy, 291-292 (V3)
in neuromuscular disorders, 292, 292f
(V3)
in tumor, 293, 293f (V3)
in unilateral condylar hyperplasia,
284-285, 286-288f (V3)
Overhead ratio, 298 (V1)
Overnight polysomnography, 317-318
(V3)
Over-the-counter drug use, 380 (V2)
Oxaliplatin, 779, 781t (V2)
Oxazepam, 889t (V2)
Oxcarbazepine, 992, 992t (V2)
Oxicams, 887t (V2)
Oxycodone
for acute postoperative pain, 81t, 82
(V1)
for chronic facial pain, 972t, 973t (V2)
in complicated exodontia, 207t (V1)
for temporomandibular disorders,
888t (V2)
Oxygen partial pressure of child, 96
(V1)
P 153 (V1)
p53 tumor suppressor gene, 662 (V2)
oral cavity cancer and, 707 (V2)
Pacinian corpuscle, 962 (V2)
Paclitaxel, 779, 781t, 782t (V2)
Pain, 78-163 (V1)
anatomic and mechanisms-based
classification of, 137f, 139t (V1)
in ankylosing spondylitis, 860 (V2)
in basic exodontia, 192 (V1)
in chondroblastoma, 868 (V2)
chronic facial, 961-978 (V2)
antidepressants for, 973 (V2)
atypical facial pain and, 967-968
(V2)
barriers to management of, 970-
971 (V2)
botulinum toxin injection for, 974-
975 (V2)
of cardiac origin, 969 (V2)
central mechanisms of, 963 (V2)
clinically based comprehensive
pain management program
for, 975 (V2)
complex regional pain syndrome
and, 966-967 (V2)
Eagle’s syndrome and, 969-970,
970f (V2)
evaluation of, 963-966, 965f, 966t
(V2)
future directions in management
of, 975-976 (V2)
muscle relaxants for, 974 (V2)
nerve injury from dental
procedures and, 968f, 968-969
(V2)
neuralgia-inducing cavitational
osteonecrosis and, 967 (V2)
neuropathic agents for, 973-974
(V2)
nonsteroidal antiinflammatory
drugs for, 972-973, 973t (V2)
opioid therapy for, 971-972, 972t
(V2)
osteonecrosis-related, 970 (V2)
peripheral mechanisms of, 962,
963f (V2)
physical therapy for, 971 (V2)
surgical intervention for,
975 (V2)
therapeutic injections for, 974
(V2)
topical capsaicin for, 975 (V2)
trigeminal anatomy and, 961-962,
962f (V2)
Pain (Continued)
chronic head and neck, 136-163
(V1)
brain stimulation procedures for,
157 (V1)
characterization and measurement
of, 139 (V1)
clinical and laboratory
examination in, 139-140 (V1)
cluster headache and
trigeminoautonomic variants
and, 148-149 (V1)
complex regional pain syndrome
and, 157-158 (V1)
diagnosis of, 139, 139t (V1)
fibromyalgia and, 142 (V1)
idiopathic and atypical orofacial
pain syndromes and, 158 (V1)
incidence and demographics of,
137 (V1)
migraine and, 146-148, 147f (V1)
myofascial pain syndromes and,
143-145 (V1)
orofacial migraine variants and,
149 (V1)
pain definitions and, 137-138, 138t
(V1)
pathophysiology of, 137f, 137-139,
138f (V1)
pharmacologic screening in, 140-
141 (V1)
postherpetic neuralgia and, 151-
152 (V1)
posttraumatic headache and, 152-
posttraumatic trigeminal neuralgia
and, 154-156 (V1)
psychiatric disorders and, 141-142
(V1)
sleep dysfunction and, 141 (V1)
surgical treatments for, 156-157
(V1)
systemic disease and, 141 (V1)
temporomandibular arthritis and,
145-146 (V1)
trigeminal neuralgia and, 149-151
(V1)
chronic orofacial, 112-135 (V1)
changing treatment of, 121-122
(V1)
cranial nerve examination in, 116-
118, 119f, 120f (V1)
flexible diagnoses-management
concept in, 113-114 (V1)
follow-up visits for, 121 (V1)
individualized pain management
in, 122-124, 123f, 124f (V1)
initial visit for, 112-113 (V1)
local anesthetic injections for, 114-
115, 115-117f (V1)
localized pathologic conditions
and, 115-116 (V1)
peripheral and central mediated
pain in, 120-121 (V1)
prevention of progression to, 124-
126 (V1)
reevaluation of diagnoses in, 121
(V1)
systemic pathologic conditions
and, 118 (V1)
in temporomandibular joint
disorders, 126-134, 128f, 129f
(V1)
temporomandibular joint
protection during surgical
procedures and, 125 (V1)
third molar pathologic conditions
and, 125-126 (V1)
third molar surgery and, 125 (V1)
in fibromyalgia, 142 (V1)
in idiopathic and atypical orofacial
pain syndromes, 158 (V1)
on injection of local anesthetic, 47
(V1)
intensive care unit control of, 47
(V2)
in Langerhans cell histiocytosis, 571
(V2)
in mandibular fracture, 143-144 (V2)
Pain (Continued)
in maxillofacial tumor, 690 (V2)
in migraine, 148 (V1)
in multiple myeloma, 686 (V2)
in myofascial pain syndromes, 144-
145 (V1)
neuropathic orofacial, 989-1004 (V2)
burning mouth syndrome in, 995-
996 (V2)
central poststroke pain in, 994-995
(V2)
diagnosis of, 989-990 (V2)
glossopharyngeal neuralgia in, 993-
994 (V2)
herpes zoster and, 994 (V2)
secondary to neuritis, 1000 (V2)
traumatic orofacial neuropathies
in, 996-999, 998t, 999t (V2)
trigeminal neuralgia in, 990-992t,
990-993 (V2)
neurophysiology of, 961-962, 962f,
963f (V2)
in orofacial migraine variants, 149
(V1)
in osteomyelitis, 633 (V2)
in osteosarcoma, 680 (V2)
in postherpetic neuralgia, 152 (V1)
postoperative, 78-92 (V1), 405, 409
(V3)
assessment of, 87, 87b, 88f, 89f
(V1)
in bone graft for implant, 422 (V1)
in bone graft harvest, 415 (V1)
in endoscopic forehead and brow
lift, 606 (V3)
in exodontia, 217-218 (V1)
laser therapy and, 254b, 254 (V1)
local anesthetics for, 82-83 (V1)
neuroanatomy and pathophysiology
of, 78-80, 79f, 80f (V1)
nonsteroidal antiinflammatory
drugs for, 83-86, 84t, 85b, 86t
(V1)
opioid analgesics for, 80-82, 81b,
81t, 82t (V1)
patient-controlled analgesia for, 88
(V1)
perioperative considerations in, 87,
87b (V1)
physical methods for, 88-89 (V1)
preemptive analgesia therapy for,
87-88 (V1)
reassessment of, 89-90 (V1)
in rhytidectomy, 507 (V3)
in sinus-lift subantral
augmentation, 462 (V1)
in temporomandibular joint
surgery, 133-134 (V1)
in transoral vertical ramus
osteotomy, 121t (V3)
in posttraumatic headache, 153 (V1)
in posttraumatic trigeminal neuralgia,
156 (V1)
in synovial chondromatosis, 872 (V2)
in temporomandibular disorders, 130-
131 (V1), 975, 980, 987 (V2)
in temporomandibular joint
pseudoankylosis, 899 (V2)
in temporomandibular osteoarthritis,
146 (V1)
in temporomandibular rheumatoid
arthritis, 145 (V1)
in trigeminal nerve injury, 261t, 261-
262, 279 (V1)
in trigeminal neuralgia, 150 (V1)
Pain Buster Pain Management System,
974 (V2)
Pain descriptors, 965, 966t (V2)
Palacci and Ericsson defect classification
scheme, 479 (V1)
Palatal fistula after cleft surgery, 829-
831, 830f, 832-834f (V3)
Palatal flap in extraction
of maxillary canine, 196, 196f, 197f
(V1)
of maxillary premolar, 199, 200f (V1)
Palatal lift appliance, 802 (V3)
Palatal plane to upper incisor, 33 (V3)
Palatal plane to upper molar, 32 (V3)
INDEX I-73
Palatal splint, 184, 397t, 397-398 (V3)
Palatal torus, 232-233 (V3)
Palate
alveolar distraction and, 349-354,
349-354f (V3)
cleft lip and palate repair and, 719-
730 (V3)
cleft palate repair and, 723-727,
729f, 730f (V3)
complex facial clefting and, 727-
728, 731f (V3)
history of, 713-714 (V3)
lip adhesion and, 720 (V3)
outcome assessment in, 728-730
(V3)
presurgical taping and orthopedics
in, 719-720, 720f (V3)
primary bilateral lip repair and,
723, 724-728f (V3)
primary unilateral cleft lip repair
and, 720-723, 721-723f (V3)
treatment planning and timing in,
718t, 718-719 (V3)
cleft palate repair and, 723-727, 729f,
730f, 759-782 (V3)
double-opposing Z-plasty in, 772-
775, 773-775f (V3)
fistulas and, 763, 765-766, 766t
(V3)
growth outcomes in, 769-770 (V3)
history of, 759-760 (V3)
intravelar veloplasty in, 762-763
(V3)
muscular reconstruction in, 768
(V3)
outcomes in, 760-761, 768-769
(V3)
palatoplasty technique in, 762
(V3)
speech evaluation in, 761 (V3)
technique comparisons in, 768
(V3)
timing of, 761 (V3), 767-768 (V3)
two-flap palatoplasty in, 763-771,
764f, 765f, 767b, 770f, 771f
(V3)
two-stage, 776-778 (V3)
embryology of, 701-705, 704t (V3)
herpangina of, 617t, 617-618 (V2)
herpes simplex virus infection of,
613, 613f (V2)
lymphoma of, 758, 759f (V2)
miniimplant for orthodontic
anchorage in, 570-574, 572-574f
(V1)
revision surgery for cleft
malformations and, 828-847
(V3)
bone graft reconstruction of cleft
maxilla and palate in, 840
(V3)
complications of, 839 (V3)
comprehensive dental and
prosthetic rehabilitation in,
841-843, 844-845f (V3)
fistula closure in, 828-831, 830f,
832-834f (V3)
for management of submucous cleft
palate, 839-840 (V3)
for management of velopharyngeal
dysfunction, 831t, 831-835,
835f (V3)
operative techniques in, 836-839,
837f, 838f (V3)
orthognathic surgery for correction
of midfacial deficiency in, 840
(V3)
reconstruction of cleft nasal
deformity in, 840-841, 842f
(V3)
secondary surgery for cleft lip scar
revision in, 841, 843f (V3)
timing and indications for, 835-
836 (V3)
squamous cell carcinoma of, 716-719
(V2)
surgically assisted maxillary
expansion and, 67f, 67-68, 219-
237 (V3)
I-74 INDEX
Palate (Continued)
clinical evaluation in, 219, 220-
220f, 221f (V3)
complications of, 231-232, 233f
(V3)
incidence and origin of transverse
maxillary deficiency and, 219,
220f (V3)
modification of, 232-233, 234f (V3)
orthopedic rapid maxillary
expansion and, 224-226, 224-
226f (V3)
radiographic evaluation in, 220-
223, 221-223f (V3)
segmental maxillary osteotomy
versus, 233-235 (V3)
technique in, 227-231, 228-232f
(V3)
Palatoglossus muscle, 831t, 835f (V3)
Palatopharyngeus muscle, 831t, 835f
(V3)
Palatoplasty
Bardach two-flap, 726, 729f, 763-771
(V3)
fistula rates in, 765-766, 766t (V3)
growth outcomes in, 769-770 (V3)
history of, 764 (V3)
muscular reconstruction in, 768
(V3)
outcomes based on cleft type or
severity and, 768-769 (V3)
principle techniques in, 764, 764f,
765f (V3)
in residual palatal fistula closure,
830, 830f (V3)
speech outcomes in, 766-767, 767b
(V3)
surgical procedure in, 770f, 770-
771, 771f (V3)
syndromic associations and
outcomes in, 769 (V3)
technique comparisons in, 768
(V3)
timing of, 767-768 (V3)
controversies in, 762 (V3)
for residual fistula closure, 828-831,
830f, 832-834f (V3)
revisional, 838-839 (V3)
Palpation
of muscles of mastication, 829 (V2)
of temporomandibular joint, 828f,
828-829, 829f (V2)
Palpebral line angles from palpebral lid
crease, 320 (V2)
Palpebral-based conjunctival
transpositional flap, 306 (V2)
Pamelor; See Nortriptyline
Pamidronate, 395, 396t (V1), 558t (V2)
Panadol; See Acetaminophen
Panoramic radiography
in ankylosis, 903 (V2)
in chronic facial pain, 965f (V2)
in condylar fracture, 168, 169f (V2)
in dentoalveolar injury, 110f, 110
(V2)
in mandibular trauma, 98, 99f, 144f
(V2)
in temporomandibular disorders, 821,
821f, 822f, 837-838, 838f (V2)
in temporomandibular joint
hypomobility, 898 (V2)
Papilla regeneration technique, 487-
489, 489f (V1)
Papillary thyroid carcinoma, 456-458,
457f (V2)
Paradental cyst, 421-424 (V2)
Paraflex; See Chlorzoxazone
Paralingual approach in lingual nerve
repair, 269-270 (V1)
Paramedian forehead flap, 329, 331-
332f, 342f (V2)
Paramedian mandibulotomy, 963 (V3)
Parameningeal tumor, 986 (V3)
Paranasal sinuses
ameloblastoma of, 964f (V3)
lymphoma of, 762-763 (V2)
osteoma of, 605 (V2)
psammomatoid variant of juvenile
ossifying fibroma and, 599 (V2)
Parasymphyseal mandibular fracture,
141, 142f (V2)
diagnostic imaging of, 101, 102f (V2)
pediatric, 364, 365-367f (V2)
Parathyroid hormone
for bone loss, 398, 399t (V1)
hyperparathyroidism and, 594f, 594-
595 (V2)
Parathyroid hormone-related protein,
ameloblastoma expression of, 485
(V2)
Parenteral nutrition, 15, 15t (V2)
Paresis of upward glance, 51 (V2)
Paresthesia, 966t (V2)
after repair of zygomatic fracture,
194-195 (V2)
local anesthetic-related, 45 (V1)
in trigeminal traumatic neuralgia,
264-265 (V1)
Parietal artery, 668f (V3)
Parietal bone, 595 (V3)
Parkinson’s disease, 18 (V1), 382 (V2)
Parosteal osteogenic sarcoma, 683-684
(V2)
Parotid duct, 283 (V2)
Parotid gland
acute suppurative parotitis of, 540-
541, 541f, 542f (V2)
chronic obstructive sialoadenitis of,
545-546, 547f (V2)
lymphoepithelial cyst of, 539, 540f
(V2)
rhytidectomy-related sialocele of, 509
(V3)
sialolithiasis of, 544-545, 547f (V2)
trauma to, 294, 318-320, 320f (V2)
tumor of, 546-547, 548f (V2)
adenocarcinoma and, 119f (V1)
lymphoma and, 763 (V2)
nonsalivary, 550-551 (V2)
viral infection of, 542-543 (V2)
Parotidectomy
in lymphoepithelial cyst, 539 (V2)
in pleomorphic adenoma, 547-549,
549f (V2)
Paroxetine
for burning mouth syndrome, 996
(V2)
for chronic facial pain, 973t (V2)
for temporomandibular disorders,
889t (V2)
Partial coverage splint, 984-985 (V2)
Partial odontectomy, 277 (V1)
Partial prothrombin time, 19t (V1)
Partial transfixion incision in
rhinoplasty, 561, 562f (V3)
Partial-thickness burn, 322t (V2)
Partial-thickness skin graft in internal
derangement of
temporomandibular joint, 939
(V2)
Participation contract, 369 (V1)
Partnership, 285-286, 286t (V1)
Passive motion exercises after
temporomandibular joint surgery,
133 (V1)
Passive range of motion, 825 (V2)
Passive smoke exposure, 70-71 (V1)
Passive stretching of masticatory
muscles, 986 (V2)
Patent ductus arteriosus, 382-383 (V3)
Pathologic mandibular fracture, 99,
100f, 142 (V2)
Patient call-on-hold device, 345 (V1)
Patient cancellation, 346 (V1)
Patient care, 395-411 (V2)
accident circumstances and, 395-396,
396f, 397f (V2)
algorithm for decision making in,
399f (V2)
final discharge planning and, 405-409
(V2)
identification of psychosocial issues
and, 400 (V2)
long-term rehabilitation and, 408-
411, 409-410f (V2)
pre-injury health and, 398-400 (V2)
preparation for postoperative events
and, 404-405, 407f (V2)
Patient care (Continued)
primary survey and, 396, 397b, 398f
(V2)
prioritization and integration of
surgery and, 400b, 400-401, 402f
(V2)
secondary survey and, 396-397 (V2)
surgical plan and, 401-404, 403-406f
(V2)
treatment goals in, 396b, 396t (V2)
Patient evaluation
in blepharoplasty, 587-589, 588f,
589f (V3)
in facial asymmetry, 272-275, 273f
(V3)
in laser skin resurfacing, 516-519,
518b (V3)
in rhytidectomy, 497-500, 498t, 499f,
499t (V3)
in sarcoma of jaw, 689-692, 690t,
691f (V2)
Patient history
in abnormal head shape, 856 (V3)
in ankylosis, 903 (V2)
in blepharoplasty, 587 (V3)
in cervicofacial liposuction, 620 (V3)
in chronic orofacial pain, 112-113
(V1)
in condylar fracture, 167-168 (V2)
in craniomaxillofacial trauma, 8, 49
(V2)
in dentoalveolar injury, 105-107
(V2)
for exodontia treatment planning,
187 (V1)
in internal derangement of
temporomandibular joint, 929-
930 (V2)
in laser skin resurfacing, 517 (V3)
in maxillofacial tumor, 689 (V2)
in ophthalmic assessment, 74 (V2)
in orbital fracture, 207-208 (V2)
in pediatric preanesthetic assessment,
97 (V1)
potential nerve injuries and, 278
(V1)
in preanesthetic assessment, 69 (V1)
preoperative, 1-2, 2t (V1)
in rhytidectomy, 497-498 (V3)
in temporomandibular joint
hypomobility, 898, 899b (V2)
in zygomatic fracture, 183b, 183-184,
184f (V2)
Patient payment options, 342 (V1)
Patient positioning
anesthesia and, 75 (V1)
in combined maxillary and
mandibular osteotomies, 241
(V3)
for Le Fort I osteotomy, 176 (V3)
surgical considerations in, 391-392
(V3)
Patient preparation, 382-395 (V3)
in ambulatory orthognathic surgery,
492-494 (V3)
antibiotics and, 392-393 (V3)
asplenia and, 387-388 (V3)
for autogenous bone graft, 409 (V1)
blood loss management and, 392
(V3)
cardiovascular disorders and, 382,
383b (V3)
in cervicofacial liposuction, 620 (V3)
in complicated exodontia, 207t, 207-
208, 208b (V1)
congenital heart disorders and, 382-
383, 383t (V3)
consultation and, 389, 389t (V3)
endocrine disorders and, 385-386
(V3)
in endoscopic forehead and brow lift,
602f, 602-603 (V3)
epoetin alfa and, 390 (V3)
in facial asymmetry correction, 277-
278 (V3)
gastrointestinal disorders and, 386-
387, 387t (V3)
for guided tissue regeneration, 429-
430 (V1)
Patient preparation (Continued)
hematologic disorders and, 384-385
(V3)
imaging and, 389 (V3)
laboratory tests and, 389-390 (V3)
in laser skin resurfacing, 519 (V3)
neurologic disorders and, 388-389
(V3)
nutrition and, 390-391 (V3)
patient positioning and, 391-392
(V3)
postoperative nausea and vomiting
and, 393 (V3)
preoperative evaluation and, 20 (V1)
preoperative interview and, 391,
391b (V3)
pulmonary disorders and, 383-384,
384b, 384t (V3)
in rhinoplasty, 557 (V3)
in rhytidectomy, 497-500, 498t, 499f,
499t (V3)
single kidney and, 387 (V3)
in sinus-lift subantral augmentation,
459 (V1)
social factors in, 391 (V3)
steroids and, 393 (V3)
in zygomatic implant, 493, 493f (V1)
Patient rapport, risk management and,
378-379 (V1)
Patient reception and waiting area, 355,
355f (V1)
Patient selection
for ambulatory orthognathic surgery,
492 (V3)
for cervicofacial liposuction, 618-620,
619f (V3)
for guided tissue regeneration, 429-
430 (V1)
for trichophytic forehead and brow
lift, 613-614, 615f, 616f (V3)
for trigeminal nerve injury repair,
265 (V1)
for zygomatic implant, 491-492, 492f
(V1)
Patient survey
marketing and, 336-337 (V1)
office management and, 287, 289t
(V1)
Patient-controlled analgesia, 88 (V1)
Patient-controlled sedation, 74 (V1)
Patient-related risk factors for
postoperative pulmonary
complications, 4-6 (V1)
Patient-surgeon interaction, marketing
and, 331-333, 332f (V1)
Pauciarticular juvenile rheumatoid
arthritis, 859 (V2)
Paxil; See Paroxetine
Pay ranges, 291, 291t (V1)
Payment options, 342 (V1)
PBF; See Pulpal blood flow
PCTG; See Pediculated connective
tissue graft
PDL; See Pulsed dye laser
Peck and Peck analysis for determining
chin position, 683t (V3)
Peck graft, 563 (V3)
Pectoralis major myocutaneous flap,
330-331 (V2)
for cheek reconstruction, 344 (V2)
Pediatric Advanced Life Support, 99
(V1)
Pediatric anesthesia and sedation, 93-
111 (V1)
airway equipment preparation for,
100t, 100-102 (V1)
anaphylaxis and, 107t, 107 (V1)
bronchospasm and, 107 (V1)
cardiovascular system and, 93-94, 94t
(V1)
developmental pharmacology and,
96-97 (V1)
fentanyl for, 104 (V1)
gastric contents aspiration and, 107
(V1)
inhalation anesthesia for, 104-105
(V1)
intraoperative fluids and, 102-103
(V1)

Pediatric anesthesia and sedation
(Continued)
intravenous access and, 102, 102f (V1)
ketamine for, 104 (V1)
laryngospasm and, 106-107 (V1)
liver function and, 96 (V1)
malignant hyperthermia and, 107-
108 (V1)
midazolam for, 103-104 (V1)
monitoring during, 99-100 (V1)
Pediatric Anesthesia Worksheet for,
101b (V1)
preanesthetic assessment and, 97-99,
98f (V1)
premedication for fear and anxiety
in, 103 (V1)
propofol for, 104, 105t (V1)
recovery and discharge in, 108 (V1)
renal system and, 96 (V1)
respiratory system and, 94-96, 95f,
96t (V1)
techniques for, 105-106 (V1)
thermoregulation and, 96 (V1)
Pediatric Anesthesia Worksheet, 101b
(V1)
Pediatric dentoalveolar surgery, 165-184
(V1)
eruption pattern for deciduous and
permanent dentition, 165, 166t
(V1)
for generalized disorders of dentition,
175-181 (V1)
cleidocranial dysplasia in, 175-177,
176f, 177f (V1)
Gardner’s syndrome in, 178f, 178
(V1)
generalized gingival hyperplasia in,
178-179, 179f (V1)
hereditary ectodermal dysplasia in,
177t, 177-178 (V1)
localized gingival lesions in,
179-181, 180f, 181f (V1)
for impacted teeth, 165-173 (V1)
advances in orthodontic anchorage
and, 172 (V1)
autotransplantation versus
extraction in, 171-172 (V1)
etiology of, 166f, 166 (V1)
evaluation of, 166-167, 167f, 168f
(V1)
incidence of, 165-166 (V1)
incisors, 171 (V1)
maxillary canines, 167-170, 169f,
170f (V1)
molars, 171 (V1)
odontomas and, 173 (V1)
premolars, 170-171, 171f (V1)
supernumerary teeth, 172-173,
173f (V1)
treatment options for, 167 (V1)
implants in, 181-183, 182f, 183f (V1)
soft tissue procedures in, 173-174,
173-176f (V1)
Pediculated connective tissue graft, 486
(V1)
Peeling agents, 663 (V3)
PEG; See Percutaneous gastrostomy tube
Pelvis
fracture of, 68f, 68-69, 69f (V2)
secondary survey of, 40 (V2)
Pemphigoid, 622-624, 623f (V2)
Pemphigus, 624-625, 625f (V2)
Penetrating injury
in frontal sinus fracture, 256, 258f
(V2)
initial assessment of, 41-42 (V2)
mediastinal box and, 38f (V2)
ocular, 83, 83f (V2)
in orbital fracture, 213 (V2)
Penicillin
effect on osteoblast, 390 (V1)
for osteomyelitis, 636 (V2)
in sinus-lift subantral augmentation,
459 (V1)
Penicillin G, 392 (V3)
Pension plan, 287 (V1)
Pentazocine
for acute postoperative pain, 81t, 82
(V1)
Pentazocine (Continued)
for temporomandibular disorders,
888t (V2)
Peptic ulcer disease
perioperative management of, 386-
387, 387t (V3)
preoperative evaluation of, 8-9 (V1)
Perceptual rating scales for speech
evaluation, 796-797 (V3)
Percodan; See Oxycodone
Percutaneous gastrostomy tube, 72 (V2)
Percutaneous tracheostomy, 33 (V2)
Percutaneous trigeminal rhizotomy, 993
(V2)
Performance evaluation, 291, 292t (V1)
Periadenitis mucosa necrotica recurrens,
620 (V2)
Periapical cemental dysplasia, 601 (V2)
Periapical cyst, 419-421, 420f, 422f
(V2)
Periapical radiography
in apexification procedure, 115-116,
116f (V2)
in dentoalveolar injury, 109 (V2)
of impacted teeth, 167, 168f (V1)
in implant surgery, 549-551f (V1)
of luxation of tooth, 119f (V2)
in mandibular trauma, 98 (V2)
Periauricular cancer, 728-729, 729f
(V2)
Pericardial laceration, 42 (V2)
Perichondritis, 676 (V3)
Pericoronitis, 202 (V1)
Periimplantitis, 246, 390-392, 391t
(V1)
Perineal assessment
in cranio-maxillofacial trauma, 11
(V2)
in secondary survey, 40 (V2)
Perineural invasion of skin cancer, 729-
730, 739f (V2)
Periocular trauma, 76 (V2)
Periodontal disease, 185 (V1)
Periodontal plexus, 67f, 175f (V3)
Periodontal problems
after genioplasty, 450-451, 452f (V3)
after Le Fort I osteotomy, 475, 477f
(V3)
after mandibular surgery, 453 (V3)
at interdental osteotomy site, 198,
199f (V3)
Periodontal therapy, laser-assisted, 255-
256 (V1)
Periodontal tissue trauma, 114t, 118-
122 (V2)
calcium hydroxide root canal fill for,
119, 119f (V2)
complete tooth avulsion in, 120-122,
121f, 122b (V2)
concussed tooth in, 118 (V2)
displacement of tooth in, 118, 118b
(V2)
extrusive luxation in, 118f (V2)
intrusive luxation in, 118, 119f (V2)
lateral luxation of tooth in, 119-120
(V2)
subluxation of tooth in, 118 (V2)
Perioperative patient management, 382-
395 (V3)
antibiotics and, 392-393 (V3)
asplenia and, 387-388 (V3)
blood loss management and, 392
(V3)
cardiovascular disorders and, 382,
383b (V3)
congenital heart disorders and, 382-
383, 383t (V3)
consultation and, 389, 389t (V3)
in cranio-maxillofacial trauma, 1-16
(V2)
abdominal assessment in, 11 (V2)
airway assessment in, 2-4, 3f, 4f
(V2)
breathing assessment in, 4-6 (V2)
chest imaging studies in, 11 (V2)
in child, 354-355 (V2)
circulation problems and, 6-7, 7t
(V2)
disability status in, 7-8, 8t (V2)
Perioperative patient management
(Continued)
ear examination in, 9 (V2)
exposure and environmental
control in, 8 (V2)
eye examination in, 9 (V2)
head injury and, 8-9 (V2)
historic perspective in, 1, 2f (V2)
history in, 8 (V2)
intraoperative management and,
12-14, 12-14f (V2)
musculoskeletal assessment in, 11-
12 (V2)
neck examination in, 10f, 10-11
(V2)
neurologic examination in, 11
(V2)
nose and neurologic evaluation in,
9 (V2)
perineal, rectal, and vaginal
assessment in, 11 (V2)
postoperative management and, 9,
10f (V2)
primary survey in, 1 (V2)
secondary survey in, 8 (V2)
throat examination in, 9, 10f (V2)
endocrine disorders and, 385-386
(V3)
epoetin alfa and, 390 (V3)
gastrointestinal disorders and, 386-
387, 387t (V3)
geriatric patient and, 378-385 (V2)
cardiovascular disease and, 380-
381 (V2)
cardiovascular medications and,
381 (V2)
cerebrovascular and neurological
disease and, 382 (V2)
cognitive evaluation and informed
consent in, 380 (V2)
dementia and postoperative
delirium and, 384-385 (V2)
diabetes mellitus and, 383-384
(V2)
hypertension and, 381-382 (V2)
medication and over-the-counter
drug history in, 380 (V2)
nutrition and fluid electrolyte
management in, 379 (V2)
respiratory disease and, 382-383
(V2)
risk assessment of co-morbid
systemic disease in, 380, 380t
(V2)
social history and, 379-380 (V2)
thyroid disease and, 384 (V2)
hematologic disorders and, 384-385
(V3)
imaging and, 389 (V3)
laboratory tests and, 389-390 (V3)
neurologic disorders and, 388-389 (V3)
nutrition and, 390-391 (V3)
patient positioning and, 391-392 (V3)
postoperative nausea and vomiting
and, 393 (V3)
preoperative interview and, 391,
391b (V3)
pulmonary disorders and, 383-384,
384b, 384t (V3)
single kidney and, 387 (V3)
social factors in, 391 (V3)
steroids and, 393 (V3)
Periorbital area
detailed aesthetic evaluation of, 4, 5f
(V3)
oculoauriculovertebral spectrum and,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
INDEX I-75
Periorbital area (Continued)
maxilla and, 922-935 (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
soft tissue injuries in, 301-310, 306-
311f (V2)
Periorbital ecchymosis
in basilar skull fracture, 50 (V2)
in frontal sinus fracture, 256, 259f
(V2)
in orbital fracture, 208 (V2)
Periorbital fat pads, 584f (V3)
Periostat; See Low-dose doxycycline
Periosteal osteosarcoma, 683-684 (V2)
Periotome for atraumatic extraction,
541, 542f (V1)
Peripheral ameloblastoma, 485-492,
496-498f, 502 (V2)
Peripheral giant cell granuloma, 180-
181 (V1)
Peripheral mechanisms of chronic facial
pain, 962, 963f (V2)
Peripheral nerve fiber, 962 (V2)
Peripheral nerve injury, 318,
319f (V2)
Peripheral nerve procedures for
trigeminal neuralgia, 150-151
(V1), 993 (V2)
Peripheral neuritis, 1000 (V2)
Peripheral odontogenic fibroma, 510
(V2)
Peripheral ossifying fibroma, 180, 180f
(V1)
Peripheral radiofrequency neurolysis,
151 (V1)
Peripheral visual field assessment, 75-76
(V2)
Peripherally inserted central catheter, 6
(V2)
Peripherally mediated pain, 120-121
(V1)
Perma-Hand silk suture, 287t (V2)
PermaLip implant, 693 (V3)
Permanent teeth, eruption pattern for,
165, 166t (V1)
Peroneal artery, 335f (V2)
PET; See Positron emission
tomography
Petrotympanic fissure, 802 (V2)
Pfeiffer syndrome, 909 (V3)
craniosynostosis in, 850, 874 (V3)
functional considerations in, 880-881
(V3)
genetic aspects of, 880 (V3)
Le Fort III osteotomy for midface
deformity in, 205-206 (V3)
maxillary distraction osteogenesis in,
1002, 1003f, 1004f (V3)
pH effects on local anesthetics, 37t, 37-
38, 38f (V1)
PHACES acronym, 579 (V2)
Phantom bone disease, 875 (V2)
Phantom tooth odontalgia, 149, 158
(V1)
Pharmacodynamics of benzodiazepines,
56-57 (V1)
Pharmacokinetics
of benzodiazepines, 57-59, 58f, 58t
(V1)
of ketamine, 63, 63t (V1)
liver disease-related alteration in, 11,
11t (V1)
of sedative-hypnotics, 61-62, 62t
(V1)
Pharmacologic testing
in chronic head and neck pain,
140-141 (V1)
in posttraumatic trigeminal neuralgia,
155 (V1)
in trigeminal nerve injury, 264 (V1)
Pharmacology
developmental, 96-97 (V1)
I-76 INDEX
Pharmacology (Continued)
for implant dentistry, 387-405 (V1)
antibiotic prophylaxis and, 387-
388, 388b (V1)
antibiotics added to bone grafting
materials and, 388-390, 389t,
390t (V1)
bioactive fatty acids and bone
development and, 399-400
(V1)
bisphosphonates and, 395-398,
396t, 397t (V1)
mineral, hormonal, and vitamin
supplements and, 398-399,
399t (V1)
NSAIDS and bone development
and, 392-395 (V1)
periimplantitis and, 390-392, 391t
(V1)
Pharmacotherapy
for chronic head and neck pain, 144
(V1)
for fibromyalgia, 142 (V1)
for infantile hemangioma, 580 (V2)
for migraine, 148 (V1)
for myofascial pain syndromes, 144-
145 (V1)
for orofacial migraine variants, 149
(V1)
for postherpetic neuralgia, 152 (V1)
postoperative, 78-92 (V1)
assessment of, 87, 87b, 88f, 89f
(V1)
local anesthetics for, 82-83 (V1)
neuroanatomy and pathophysiology
of, 78-80, 79f, 80f (V1)
nonsteroidal antiinflammatory
drugs for, 83-86, 84t, 85b, 86t
(V1)
opioid analgesics for, 80-82, 81b,
81t, 82t (V1)
patient-controlled analgesia for, 88
(V1)
perioperative considerations in, 87,
87b (V1)
physical methods for, 88-89 (V1)
preemptive analgesia therapy for,
87-88 (V1)
reassessment of, 89-90 (V1)
in temporomandibular joint
surgery, 133-134 (V1)
for posttraumatic headache, 153 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)
preoperative management of, 2t (V1)
in skin cancer, 739-741 (V2)
in temporomandibular disorders,
885b, 885-889, 985, 986-987
(V2)
for temporomandibular osteoarthritis,
146 (V1)
for temporomandibular rheumatoid
arthritis, 145 (V1)
in trigeminal neuralgia, 150 (V1),
992, 992t (V2)
Pharyngeal airway
combined maxillary and mandibular
osteotomies and, 239 (V3)
maxillomandibular advancement and,
335-336 (V3)
Pharyngeal arch embryology, 701, 701f
(V3)
Pharyngeal flap
in cleft orthognathic surgery, 826
(V3)
in primary palatoplasty procedure,
726-727 (V3)
in residual palatal fistula closure, 830
(V3)
in surgical management of
velopharyngeal insufficiency,
836, 837f (V3)
Pharyngeal tonsil lymphoma, 758 (V2)
Pharyngoplasty, 836-838, 838f (V3)
Phenelzine, 2t (V1)
Phenergan; See Promethazine
Phenol for chemical peel, 663 (V3)
Phenylephrine, 40, 40t (V1)
Phenytoin, 150 (V1)
Pheochromocytoma, 14, 14t (V1)
Philtrum
bilateral cleft lip and palate repair
and, 724f (V3)
filler injection in, 636-637, 637f (V3)
Phlebotomy for platelet-rich plasma,
506-507, 507f (V1)
Phonating cephalograph, 797-798 (V3)
Phoneme-specific nasal emission, 794
(V3)
Photoablation reaction in laser therapy,
239-240 (V1)
Photoaging, 513 (V3)
laser-assisted skin procedures for,
248-249 (V1)
Photochemical reaction in laser
therapy, 239 (V1)
Photodynamic therapy
for oral cavity cancer, 712 (V2)
for skin cancer, 741 (V2)
Photographic soft-tissue profile planning
technique, 375 (V3)
Photography, preoperative
in blepharoplasty, 589 (V3)
in endoscopic forehead and brow lift,
603 (V3)
in laser skin resurfacing, 519 (V3)
in rhinoplasty, 557 (V3)
in rhytidectomy, 499 (V3)
Phototherapy for prolonged erythema in
laser skin resurfacing, 537 (V3)
Phototherapy low-level laser therapy,
248 (V1)
Photothermolysis, 514, 514f (V3)
Physical examination
in abnormal head shape, 856 (V3)
in avulsive facial injury, 327-328 (V2)
in basic exodontia, 187 (V1)
in chronic head and neck pain, 139-
140 (V1)
in condylar fracture, 168 (V2)
in dentoalveolar injury, 107-109,
107-109f (V2)
in frontal sinus fracture, 256, 258f,
259f (V2)
in internal derangement of
temporomandibular joint, 929-
930 (V2)
in laser skin resurfacing, 517-519,
518b (V3)
in mandibular fracture, 143-144 (V2)
in maxillofacial trauma, 49, 55-56
(V2)
in maxillofacial tumor, 689-692,
690f, 691f (V2)
in nasal fracture, 273-274 (V2)
pediatric, 97 (V1)
in preanesthetic assessment, 1-2, 2t,
69 (V1)
in rhinoplasty, 557-560, 558-560f
(V3)
in rhytidectomy, 497-499, 499f, 499t
(V3)
in skin cancer, 730t, 730-733, 731b,
731-733t (V2)
in temporomandibular joint
hypomobility, 898, 899b (V2)
in zygomatic fracture, 183b, 183-184,
184f (V2)
Physical medicine and rehabilitation
service, 73 (V2)
Physical methods of pain management,
88-89 (V1)
Physical therapy
after temporomandibular joint
arthroscopy, 927 (V2)
for chronic facial pain, 971 (V2)
for chronic head and neck pain, 144
(V1)
in internal derangement of
temporomandibular joint, 940-
941 (V2)
needs after trauma, 408 (V2)
in temporomandibular disorders, 130
(V1), 890-892, 891t (V2)
Physician’s office, 356, 357f (V1)
Physics of laser, 237-238, 238f (V1)
Pierre-Robin sequence, 998-1001f, 998-
1002 (V3)
Piezosurgery, 460, 461f (V1)
Pigmentation, laser skin resurfacing and
postoperative complication in, 541-
542, 542f, 543f (V3)
preoperative evaluation of, 518 (V3)
Pigmented skin lesion
basal cell carcinoma and, 725 (V2)
laser therapy for, 251 (V1)
malignant melanoma and, 750 (V2)
Pigmented villonodular synovitis, 871-
872 (V2)
Pigmented villonodular tenosynovitis,
871 (V2)
Pindborg tumor, 473-476, 474f, 475f
(V2)
Pinhole occluder, 74, 75f (V2)
Pin-touch detection in chronic head
and neck pain, 140 (V1)
Piroxicam, 887t (V2)
Pitch, term, 365f (V3)
Pittsburgh Quality of Life Inventory,
142 (V1)
Pittsburgh Weighted Speech Score, 767
(V3)
Pivot splint, 883, 883f (V2)
Pixie ear deformity in rhytidectomy,
509-510, 510f (V3)
Plagiocephaly
anterior, 868-871, 871f, 872f (V3)
posterior, 874, 877f, 878f (V3)
Plain film
in implant surgery, 549-551f (V1)
in midface fracture, 241 (V2)
Plaintiff, 374 (V1)
Planimetry, 321 (V2)
Plasma cell tumor, 686 (V2)
Plasma exchange in myasthenic crisis,
18 (V1)
Plasmacytoma, 686 (V2)
Plasmapheresis for pemphigus, 625 (V2)
Plasmin, wound repair and, 20f, 20-21
(V2)
Plate fixation
in complete mandibular subapical
osteotomy, 158, 160f, 168f, 170f
(V3)
in Le Fort I osteotomy, 180, 182f
(V3)
in Le Fort III osteotomy, 211 (V3)
in mandibular fracture, 154f, 154-
155, 155f (V2)
pediatric, 369-370 (V2)
Plate system for orthodontic mechanics,
226, 226f (V1)
mandibular anchor plate and, 230-
231f (V1)
placement of, 232-233, 233f, 234f
(V1)
Platelet, wound repair and, 17, 18f (V2)
Platelet count, 19t (V1)
Platelet transfusion, 16 (V1)
Platelet-derived growth factors in
platelet-rich plasma, 501, 503 (V1)
Platelet-poor plasma, 501-502, 502f
(V1)
Platelet-rich plasma, 501-510 (V1)
added to autogenous cancellous bone
graft, 406-407, 407f, 504-505
(V1)
in allograft and alloplastic materials,
504f, 504-506 (V1)
benefits of, 502-503 (V1)
for bisphosphonate-related
osteonecrosis, 396 (V1)
bone healing and, 394, 503f, 503-504
(V1)
case report of, 509, 509f (V1)
concept of, 501-502, 502f (V1)
processing of, 506-508, 507f, 508f
(V1)
for soft tissue healing, 479 (V1)
Platysmal manipulation in
rhytidectomy, 502, 503f (V3)
Pleomorphic adenoma, 547-549, 549-
551f (V2)
of submandibular gland, 551-552,
553f, 554f (V2)
Plexiform ameloblastoma, 477, 480f,
485f (V2)
Plexiform neurofibroma, 551 (V2), 983
(V3)
Plica semilunaris, 206f (V2)
Plication
in rhytidectomy, 504, 504f, 505f
(V3)
in temporomandibular joint
dislocation, 908 (V2)
Pneumonia, 47 (V2)
Pneumothorax
occult, 68, 68f (V2)
in trauma patient, 36, 36f, 37f (V2)
Pogonion
clockwise rotation of
maxillomandibular complex at,
255, 255t, 256f (V3)
maxillomandibular triangle and, 249,
250f (V3)
Pogonion to N-B line, 44 (V3)
Policy manual, 290b, 290 (V1)
Poliglecaprone suture, 286t (V2)
Pollution hazards in laser therapy, 516
(V3)
Polyactic acid membrane, 435 (V1)
Polyactide and polyglycolide copolymer
membrane, 429, 435 (V1)
Polyarthritis, 831t (V2)
Polyarticular juvenile rheumatoid
arthritis, 859 (V2)
Polyether rubber base impression
materials, 527 (V1)
Polyglactin 910 suture, 286t (V2)
Polyglycolic acid fixation device, 111
(V3)
Polyglycolic acid membrane, 435, 437
(V1)
Polylactic acid-polyglycolic acid co-
polymer fixation device, 111 (V3)
Polymorphic reticulosis, 761-762 (V2)
Polyostotic craniofacial fibrous
dysplasia, 980 (V3)
Polysomnogram for sleep apnea, 252
(V1)
Polysulfide rubber base impression
materials, 527 (V1)
Polysyndactyly in craniofacial dysostosis
syndromes, 882 (V3)
Polytetrafluoroethylene membrane
expanded, 429 (V1)
postoperative considerations in,
432 (V1)
primary closure in, 431 (V1)
to reduced postextraction bone
loss, 439 (V1)
selection rationale for, 432-435,
433f (V1)
in subantral augmentation, 437
(V1)
high-density, 429 (V1)
in alveolar ridge augmentation,
450f, 450-451, 451f (V1)
in corticocancellous block
augmentation of posterior
mandible, 452f, 452-453, 453f
(V1)
in dual-layered guided socket
regeneration technique, 445f,
445-446, 446f (V1)
in flapless buccal wall
reconstruction, 443f, 443-444,
444f (V1)
in open technique in guided bone
regeneration in extraction
site, 454f, 454-455, 455f (V1)
postoperative considerations in,
432 (V1)
ridge preservation and, 440-441f,
440-442 (V1)
selection rationale for, 432-435,
433f, 434f (V1)
wound closure in, 431 (V1)
Ponstel; See Mefenamic acid
Popliteal artery, 335f (V2)
Porcine collagen membrane, 429, 433-
435, 434f (V1)
Porphyromonas gingivalis, 391 (V1)
Porphyromonas intermedia, 391 (V1)
Portex Crico Kit 6mm, 33 (V2)
Portrait Planner software, 376 (V3)

Positioning
anesthesia and, 75 (V1)
in combined maxillary and
mandibular osteotomies, 241
(V3)
for Le Fort I osteotomy, 176 (V3)
surgical considerations in, 391-392
(V3)
Positive pressure ventilation,
pneumothorax and, 36 (V2)
Positron emission tomography
in odontogenic tumors, 467 (V2)
in oral cavity cancer, 710 (V2)
in osteomyelitis, 635f, 635-636, 636f
(V2)
in pediatric craniomaxillofacial
tumors, 961 (V3)
in temporomandibular disorders, 843-
845 (V2)
Postage machine, 361 (V1)
Postanesthesia care unit, 485 (V3)
Postanesthesia Discharge Scoring
System, 32, 33t (V1)
Postauricular approach to
temporomandibular joint, 934
(V2)
Postauricular skin graft, 297f (V2)
Post-closed head injury syndrome, 152-
153 (V1)
Postconcussion syndrome, 152-153
(V1)
Posterior alveolar height
mandibular growth value, 47 (V3)
maxillary-midface growth value, 30
(V3)
Posterior articular lip, 802 (V2)
Posterior auricular artery, 63f, 69f, 175f,
667, 668f (V3)
Posterior auricular muscle, 668f (V3)
Posterior auricular vein, 433f (V3)
Posterior cranial fossa tumor, 992 (V2)
Posterior descending palatine artery,
63f, 175f (V3)
Posterior ethmoid artery, 553-554 (V3)
Posterior ethmoid foramen, 203t, 204
(V2)
Posterior fontanel, 865f (V3)
Posterior lacrimal crest, 203f (V2)
Posterior lamella, 582f, 585, 586f, 587f
(V3)
Posterior lateral nasal artery, 459 (V1)
Posterior mandible
alveolar width distraction
osteogenesis and, 474-477, 475-
478f (V1)
for bone graft harvest, 412-414, 412-
414f (V1)
corticocancellous block augmentation
of, 452f, 452-453, 453f (V1)
interpositional bone graft and, 471,
472f (V1)
Posterior mandibular alveolar
distraction, 354, 354f (V3)
Posterior margin preauricular crease,
320 (V2)
Posterior maxilla
sinus-lift subantral augmentation and,
458-470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic
considerations in, 458-459
(V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f,
464f (V1)
elevation of schneiderian
membrane in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
Posterior maxilla (Continued)
trephine core membrane elevation
in, 464-468, 464-468f (V1)
vascular supply, lymphatic
drainage, and innervation in,
459 (V1)
subantral bone augmentation and,
436-438, 437f (V1)
Posterior nasal spine
counterclockwise rotation of
maxillomandibular complex at,
256-260, 260f, 260t (V3)
maxillomandibular triangle and, 249,
250f (V3)
Posterior plagiocephaly, 874, 877f, 878f
(V3)
Posterior segment trauma, 76f, 76-77
(V2)
Posterior septal branch of
sphenopalatine artery, 556f (V3)
Posterior superior alveolar artery, 63,
63f, 66f, 175f (V3)
Posterior table fracture, 259, 261f, 264-
266, 266f (V2)
Posterior tibial artery, 335f (V2)
Posterior triangle lymph nodes, 711t
(V2)
Posterior wall fracture, 259 (V2)
Posteroanterior cephalometric
evaluation, 18-19 (V3)
Posteroanterior view of mandible, 97,
97f (V2)
Postextraction bone loss, guided tissue
regeneration for, 438-440, 454f,
454-455, 455f (V1)
Postherpetic neuralgia
chronic head and neck pain in, 151-
152 (V1)
chronic orofacial pain in, 118 (V1)
trigeminal, 994 (V2)
Post-intubation care, 31 (V2)
Postoperative bleeding, 442-443 (V3)
in bilateral sagittal split osteotomy,
115, 115b (V3)
in exodontia, 219 (V1)
in genioplasty, 439 (V3)
in intraoral vertical ramus osteotomy,
435, 435f (V3)
in Le Fort I osteotomy, 185-186, 467-
469f, 467-470 (V3)
nasal, 404 (V3)
in nasal fracture, 275 (V2)
in sagittal split ramus osteotomy,
429-431, 433f (V3)
simple extraction and, 191 (V1)
Postoperative care, 396-418 (V3)
airway obstruction and, 404 (V3)
ambulatory orthognathic surgery and,
495-496, 496t (V3)
anticlenching medications and, 409-
410 (V3)
antinausea medications and, 410
(V3)
in blepharoplasty, 591-593, 593f
(V3)
in bone transport by distraction
osteogenesis, 360 (V3)
in chemical peel, 663, 664f (V3)
in cleft maxilla repair, 810 (V3)
clenching and bruxism and, 406-407
(V3)
in complicated exodontia, 208, 209b
(V1)
in cranio-maxillofacial trauma, 14-15,
15f, 15t (V2)
decongestants and antihistamines
and, 410 (V3)
dietary considerations in, 408-409,
409f (V3)
elimination patterns and, 409 (V3)
in endoscopic forehead and brow lift,
606 (V3)
in facial soft tissue injuries, 294-299
(V2)
fatigue and, 405 (V3)
in frontal sinus fracture, 266-268,
268f (V2)
in guided bone regeneration, 431-432
(V1)
Postoperative care (Continued)
in hair transplantation, 653 (V3)
hormone imbalance and, 408 (V3)
in immediate implant loading, 517,
518f (V1)
in internal derangement of
temporomandibular joint, 940-
941 (V2)
jaw and occlusal instability and, 413-
415, 414-417f (V3)
jaw function and, 406 (V3)
in laser skin resurfacing, 524-529,
526-528f, 530-531f (V3)
in Le Fort I osteotomy, 184 (V3)
in mandibular lengthening by
distraction osteogenesis, 345-346
(V3)
in mandibular widening, 341-342
(V3)
masseter muscles recovery and, 406
(V3)
in maxillectomy, 699 (V2)
middle ear dysfunction and, 406 (V3)
in Millard rotation and advancement
flap technique for unilateral cleft
lip, 741 (V3)
in modified Le Fort III osteotomy,
212-218 (V3)
motor nerve deficit and, 405-406
(V3)
muscles of facial expression issues
and, 406 (V3)
nasal bleeding and, 404 (V3)
nausea and, 404-405 (V3)
nose blowing and, 411, 411f (V3)
oral hygiene and, 410 (V3)
in orthodontic skeletal anchorage,
234-235 (V1)
pain and, 405, 409b (V3)
physical activities and, 411-412 (V3)
planning for, 404-405, 407f (V2)
postsurgical orthodontics and, 396-
402, 397-399f, 401f, 402f (V3)
prophylactic antibiotics and, 410
(V3)
psychosocial issues in, 404 (V3)
recovery and discharge in office-based
surgery and, 75-76 (V1)
in rhinoplasty, 573 (V3)
scarring reduction medications and,
410 (V3)
sensory nerve deficit and, 405 (V3)
showers and baths and, 411 (V3)
in sinus-lift subantral augmentation,
462 (V1)
swelling and ecchymosis and, 403-
404 (V3)
in temporomandibular joint
arthroscopy, 927 (V2)
temporomandibular joint function
and, 406, 407f (V3)
therapeutic clenching and, 407 (V3)
tooth ankylosis and, 412-413 (V3)
tooth discoloration and, 412 (V3)
in total maxillary segmental
osteotomy, 196-197, 197f (V3)
in transoral vertical ramus osteotomy,
128f, 128-129 (V3)
in trigeminal nerve repair, 270-271
(V1)
wound infection and, 412 (V3)
in zygomatic implant, 498 (V1)
Postoperative complications
in mandibular surgery, 441-454 (V3)
dental and periodontal problems
in, 453 (V3)
excessive swelling in, 441-442,
442f (V3)
hemorrhage and hematoma in,
442-443 (V3)
idiopathic condylar resorption in,
453-454 (V3)
infection in, 443 (V3)
loss of gonial projection in, 454,
455-456f (V3)
nausea, vomiting, and dehydration
in, 443 (V3)
neurologic dysfunction in, 444-
445, 453 (V3)
INDEX I-77
Postoperative complications (Continued)
prevention of, 454t (V3)
relapse in, 445-451, 446-452f (V3)
temporomandibular joint
dysfunction in, 445, 453 (V3)
in maxillary surgery, 473-480 (V3)
antral or nasal fistulas in, 480 (V3)
atrophic rhinitis in, 480 (V3)
dental and periodontal problems
in, 475, 477f (V3)
nasal septal deviation in, 478-480,
479f (V3)
nerve injury in, 477 (V3)
ophthalmic disorders in, 473-475,
476f (V3)
prevention of, 480t (V3)
relapse in, 480 (V3)
unfavorable nasolabial esthetics in,
477-478 (V3)
vascular compromise in, 475 (V3)
Postoperative delirium, 384-385 (V2)
Postoperative infection, 412 (V3)
in bilateral sagittal split osteotomy,
115, 116b (V3)
in chemical peel, 664 (V3)
in exodontia, 216-217 (V1)
in facial fat transplantation, 627
(V3)
in laser skin resurfacing, 540-541,
541f (V3)
in mandibular surgery, 443 (V3)
in otoplasty, 676 (V3)
prophylactic antibiotics and, 392-393
(V3)
in rhinoplasty, 573 (V3)
in rhytidectomy, 508-509 (V3)
in sinus-lift subantral augmentation,
464 (V1)
Postoperative nausea and vomiting, 393
(V3)
child and, 108 (V1)
in mandibular surgery, 443 (V3)
Postoperative pain, 78-92 (V1), 405
(V3)
assessment of, 87, 87b, 88f, 89f (V1)
in bone graft for implant, 422 (V1)
in bone graft harvest, 415 (V1)
effects of lasers on, 254b, 254 (V1)
in endoscopic forehead and brow lift,
606 (V3)
in exodontia, 217-218 (V1)
local anesthetics for, 82-83 (V1)
neuroanatomy and pathophysiology
of, 78-80, 79f, 80f (V1)
nonsteroidal antiinflammatory drugs
for, 83-86, 84t, 85b, 86t (V1)
opioid analgesics for, 80-82, 81b, 81t,
82t (V1)
patient-controlled analgesia for, 88
(V1)
perioperative considerations in, 87,
87b (V1)
physical methods for, 88-89 (V1)
preemptive analgesia therapy for, 87-
88 (V1)
reassessment of, 89-90 (V1)
in rhytidectomy, 507 (V3)
in sinus-lift subantral augmentation,
462 (V1)
Postoperative radiation therapy, 771-
772 (V2)
Postoperative rehabilitation in
temporomandibular joint disorders,
133-134 (V1)
Post-septal fat, 581f, 586f (V3)
Postsurgical orthodontics, 396-402, 398-
399f, 401f, 402f (V3)
Posttraumatic headache, 152-153 (V1)
Posttraumatic neuropathic pain, 152-
156 (V1)
complex regional pain syndrome in,
157-158 (V1)
idiopathic and atypical orofacial pain
syndromes in, 158 (V1)
posttraumatic headache in, 152-153
(V1)
posttraumatic trigeminal neuralgia in,
154-156 (V1)
surgical treatments for, 156-157 (V1)
I-78 INDEX
Posttraumatic stress disorder, 395 (V2)
Posttraumatic temporomandibular joint
ankylosis, 901 (V2)
Posttraumatic trigeminal neuralgia, 154-
156 (V1)
Posttreatment area in office design,
353-355, 354f (V1)
Postural exercises in temporomandibular
disorders, 986 (V2)
Postural strain, temporomandibular pain
and, 979 (V2)
Powell analysis for malar implant, 690t
(V3)
Powell and Humphreys technique for
determining chin position, 683t
(V3)
Power bleaching of teeth, laser-assisted,
256 (V1)
Practice administrator, 287 (V1)
Practice advisor, 286-287 (V1)
Practice evaluation, 287-288, 288t, 289t
(V1)
Practice management, 285-386 (V1)
accreditation of surgicenter and, 304-
306, 305t (V1)
chart documentation and, 358 (V1)
claims adjudication and, 370 (V1)
coding and, 364-368 (V1)
credentialing and privileging, 307-
317 (V1)
accreditation and certification and,
308-309 (V1)
adverse action in, 315-316 (V1)
appointment to medical staff in,
314-315 (V1)
definitions and resources in, 309-
313, 310-313t (V1)
process of, 313-314, 314f (V1)
specialty board certification and,
308 (V1)
fraudulent health care claim
submission and, 371 (V1)
insurance and, 368-369 (V1)
marketing and, 287, 318-350 (V1)
academic, 319 (V1)
activity sponsorship in, 345 (V1)
business lunches and, 337 (V1)
calling postoperative patients and,
345 (V1)
communication and, 347-349, 349f
(V1)
community service and, 338 (V1)
cosmetic surgery, 343-345, 343-
345f (V1)
descriptive name in, 318-319 (V1)
employee relations and, 323-329,
326b (V1)
front desk staff and, 346-347 (V1)
hiring and firing and, 322 (V1)
identification of target market in,
334 (V1)
image and logo and, 331, 331f
(V1)
initiation of marketing plan in,
329-331, 330f (V1)
internal, 339t, 339-340, 340f (V1)
lessons from big business in, 319-
320 (V1)
managed care and, 345-346 (V1)
media networking and, 341-342,
342f (V1)
newsletters and media packs in,
340-341, 341f (V1)
office environment and, 333-334
(V1)
outside professional consultation
in, 322-323, 337-338 (V1)
patient call-on-hold devices in,
345 (V1)
patient payment options and, 342
(V1)
patient surveys in, 336-337 (V1)
patient-surgeon interaction and,
331-333, 332f (V1)
preentry materials in, 334-335
(V1)
procedure-specific, 338-339 (V1)
synergy in, 335-336, 336b (V1)
uniformity in, 331b (V1)
Practice management (Continued)
vision in, 321-322 (V1)
waiting patient and, 333 (V1)
yellow pages advertising in, 342
(V1)
Medicare fees and, 370-371 (V1)
office design and, 351-363 (V1)
additional space requirements in,
358, 358f, 359f (V1)
business office area in, 355f, 355-
356, 356f (V1)
conference room in, 354, 354f
(V1)
construction phase and, 362-363
(V1)
consultation room in, 352, 352f
(V1)
defining goals in, 351 (V1)
equipping and furnishing and, 358-
361, 359f, 360f (V1)
ergonomics and, 361-362 (V1)
financial projections and feasibility
in, 352 (V1)
financing of project and, 362 (V1)
laboratory in, 356-357 (V1)
lunchroom in, 357, 357f (V1)
patient reception and waiting area
in, 355, 355f (V1)
physician’s office in, 356, 357f
(V1)
posttreatment area in, 353-355,
354f (V1)
pretreatment area in, 353 (V1)
project consultant team in, 361
(V1)
radiology suite in, 352 (V1)
restrooms in, 356, 356f (V1)
staff office in, 357-358, 358f (V1)
surgical treatment area in, 352-
353, 353f (V1)
office management in, 285-303 (V1)
accounting in, 293 (V1)
budgeting in, 291-293, 294t (V1)
compensation plans in, 298t, 298-
299, 299t (V1)
financial policy in, 295 (V1)
financial reporting in, 297-298
(V1)
financial statement trend analysis
in, 295 (V1)
financial statements in, 295, 295t,
296t (V1)
human resources and, 290b, 290-
291, 291-294t (V1)
information technology and, 303
(V1)
joining or starting practice and,
285 (V1)
legal documents and, 299-301,
300t, 301t (V1)
legal entities and, 285-286, 286t
(V1)
organizational styles and, 288-290
(V1)
practice advisors and, 286-287
(V1)
practice evaluation and, 287-288,
288t, 289t (V1)
revenue cycle and, 293-295 (V1)
risk management and, 301-303
(V1)
risk management and, 373-386 (V1)
Americans with Disabilities Act
and, 383-384 (V1)
discharging patient from practice
and, 383 (V1)
documentation and legible records
and, 379-383 (V1)
Emergency Medical Treatment and
Active Labor Act and, 385
(V1)
HIPAA privacy and security and,
384 (V1)
incidents and claims and, 375-376
(V1)
informed consent and, 379 (V1)
lawsuit process and, 376-378 (V1)
limited English proficiency and,
384-385 (V1)
Practice management (Continued)
malpractice and, 374-375 (V1)
online communication and, 385
(V1)
patient rapport and, 378-379 (V1)
release of records and, 384 (V1)
telemedicine and, 385 (V1)
third-party companies and, 369-370
(V1)
Practice net revenue, 298 (V1)
Prazepam, 889t (V2)
Prealbumin, 390 (V3)
Preanesthetic assessment, 68-69 (V1)
pediatric, 97-99, 98f (V1)
Preaponeurotic orbital fat pads, 583,
584f (V3)
Preauricular approach
in internal derangement of
temporomandibular joint, 932-
933, 933f (V2)
in pediatric craniomaxillofacial
tumor, 963 (V3)
Precordial/pretracheal stethoscope, 25-
26, 26f, 99 (V1)
Prednisolone
for lymphoma, 763 (V2)
for temporomandibular disorders,
887t (V2)
Prednisone
for neuropathy secondary to neuritis,
1000 (V2)
for temporomandibular disorders,
887t (V2)
Preemptive analgesia therapy, 87-88
(V1)
Preentry materials in marketing, 334-
335 (V1)
Prefabricated ceramic abutment,
temporary crown and, 536f, 536-
537, 537f (V1)
Preferred provider organization, 307-
308 (V1)
Pregabalin
after trigeminal nerve repair, 271
(V1)
for complex regional pain syndrome,
158 (V1)
for neuropathic orofacial pain, 999
(V2)
for postherpetic neuralgia, 152 (V1)
for posttraumatic headache, 153 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)
for trigeminal neuralgia, 150 (V1),
992, 992t (V2)
Pregnancy
gingival enlargement during, 179
(V1)
nonsteroidal antiinflammatory drug
use during, 85 (V1)
use of local anesthetics during, 45t,
45 (V1)
Pregnancy test, 19t (V1), 389-390 (V3)
Preinjury health considerations, 398-
400 (V2)
Premaxillary implant, zygoma insert
and, 495-496, 496f (V1)
Premises insurance, 303 (V1)
Premolar
extraction of
complicated, 197-199, 200f (V1)
simple, 188, 189f (V1)
impacted, 170-171, 171f (V1)
Prenatal counseling in cleft lip and
palate, 716-717 (V3)
Prenatal diagnosis
of lymphatic malformation, 582 (V2)
of Treacher Collins syndrome, 936
(V3)
Preoperative complications
in mandibular surgery, 419-423 (V3)
dental compensations and, 419-
421, 420-422f (V3)
failure to manage transverse
discrepancies and, 421-422
(V3)
leveling and root divergence in
segmental cases and, 423 (V3)
patient expectations and, 423 (V3)
Preoperative complications (Continued)
tooth size discrepancies and, 422-
423, 423f (V3)
in maxillary surgery, 454-480 (V3)
accurate presurgical records and,
459, 460-463f (V3)
dental compensations and, 456,
457-458f (V3)
leveling and root divergence in
segmental cases and, 458-459
(V3)
psychologic preparation and, 459
(V3)
systematic aesthetic analysis and,
459 (V3)
tooth size discrepancies and, 458
(V3)
transverse discrepancies and, 456-
458 (V3)
Preoperative evaluation, 1-21 (V1)
in cleft orthognathic surgery, 813-814
(V3)
consent and preoperative preparation
and, 20 (V1)
history and physical examination in,
1-2, 2t (V1)
in implant surgery
autogenous bone graft and, 407-
408, 408f, 409f (V1)
of potential immediate implant
site, 543-544, 544f (V1)
in oral cavity cancer, 710 (V2)
potential nerve injuries and, 278
(V1)
preanesthetic assessment in, 68-69
(V1)
in child, 97-99, 98f (V1)
preoperative fasting and, 71-72 (V1)
preoperative testing and, 19t, 19-20
(V1)
in rhinoplasty, 557 (V3)
system approach in, 2-19 (V1)
cardiovascular system and, 2-3, 3t,
4f, 5t (V1)
endocrine system and, 11-14, 12-
14t (V1)
gastrointestinal system and, 7-11,
9-11t, 10f (V1)
hematologic system and, 14-17,
14-17t, 15f (V1)
immune system and, 18-19 (V1)
neurologic system and, 17-18, 18t
(V1)
pulmonary system and, 3-6, 5-7t
(V1)
renal system and, 7-9t (V1)
Preoperative fasting, 71-72 (V1)
child and, 98, 98t (V1)
Preoperative interview, 391, 391b (V3)
Preoperative medications
in exodontia, 217 (V1)
nonsteroidal antiinflammatory drugs
in, 85, 85b (V1)
pediatric anesthesia and sedation
and, 103 (V1)
in rapid-sequence intubation, 29
(V2)
Preoperative model surgery, 364-371
(V3)
construction of intermediate splint
in, 368-369, 369f, 370f (V3)
in facial asymmetry, 277 (V3)
in mandibular widening, 338 (V3)
marking cast in, 366-367 (V3)
measurements in, 367f, 367-368 (V3)
mounting case in, 364-366, 365f,
366f (V3)
positioning of maxilla in, 368, 368f
(V3)
for segmental surgery, 369-370, 370f
(V3)
for special situations, 370-371 (V3)
Preoperative orthodontics
to elimination dental compensations,
419-421, 420-422f (V3)
leveling and root divergence in
segmental cases and, 423 (V3)
Preoperative patient management, 382-
395 (V3)

Preoperative patient management
(Continued)
in ambulatory orthognathic surgery,
492-494 (V3)
antibiotics and, 392-393 (V3)
asplenia and, 387-388 (V3)
blood loss management and, 392 (V3)
cardiovascular disorders and, 382,
383b (V3)
in cervicofacial liposuction, 620 (V3)
in cleft lip and palate repair, 710-
720, 720f (V3)
congenital heart disorders and, 382-
383, 383t (V3)
consultation and, 389, 389t (V3)
dentofacial orthopedics for clefting
and, 783-790 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t
(V3)
presurgical nasoalveolar molding
and, 783 (V3)
endocrine disorders and, 385-386
(V3)
in endoscopic forehead and brow lift,
602t, 602-603 (V3)
epoetin alfa and, 390 (V3)
in facial asymmetry correction, 277-
278 (V3)
gastrointestinal disorders and, 386-
387, 387t (V3)
hematologic disorders and, 384-385
(V3)
imaging and, 389 (V3)
in internal derangement of
temporomandibular joint, 931
(V2)
laboratory tests and, 389-390 (V3)
in laser skin resurfacing, 519 (V3)
in Millard rotation and advancement
flap technique for unilateral cleft
lip, 738 (V3)
neurologic disorders and, 388-389
(V3)
nutrition and, 390-391 (V3)
patient positioning and, 391-392
(V3)
postoperative nausea and vomiting
and, 393 (V3)
preoperative interview and, 391,
391b (V3)
pulmonary disorders and, 383-384,
384b, 384t (V3)
in rhinoplasty, 557 (V3)
in rhytidectomy, 497-500, 498t, 499f,
499t (V3)
single kidney and, 387 (V3)
social factors in, 391 (V3)
steroids and, 393 (V3)
Preoperative photography
in endoscopic forehead and brow lift,
603 (V3)
in laser skin resurfacing, 519 (V3)
in rhinoplasty, 557 (V3)
in rhytidectomy, 499 (V3)
Preoperative prophylaxis of
endocarditis, 3, 5t (V1)
in child with congenital heart
defects, 97 (V1)
Preoperative radiation therapy, 771-772
(V2)
Preoperative Risk Stratification, 389t
(V3)
Preoperative testing, 19t, 19-20 (V1)
Preprosthetic preparation in basic
exodontia, 186 (V1)
Prerenal failure, 46 (V2)
Prescription, documentation of, 382 (V1)
Prescription Planner/Portrait software,
376 (V3)
Preseptal orbicularis muscle, 244f (V2),
581f (V3)
Pressure algometry, 829 (V2)
Pressure dressing in genioplasty, 142,
142f (V3)
Pressure-flow method of speech
assessment, 798-800, 800f (V3)
Presurgical dentofacial orthopedics for
clefting, 783-790 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t (V3)
presurgical nasoalveolar molding and,
783 (V3)
Presurgical orthopedic appliance, 710-
720, 720f (V3)
Pretarsal orbicularis muscle, 244f (V2),
581f (V3), 587f (V3)
Pretragal incision in rhytidectomy, 501,
501f (V3)
Pretreatment area in office design, 353
(V1)
Pretrigeminal neuralgia, 991 (V2)
Prilocaine
chemical structure of, 37f (V1)
duration of action of, 39t (V1)
lipid solubility of, 38t (V1)
pH effects on, 37t (V1)
prolonged sensory alteration with, 46t
(V1)
Primary afferent nerve fiber, 962 (V2)
Primary bilateral lip repair, 723, 724-
728f (V3)
Primary bone healing, 146, 147f (V2)
Primary bone-level impression, 527-528,
529f, 530f (V1)
Primary brain decompression
in Apert syndrome, 902, 903-905f
(V3)
in Crouzon syndrome, 886-889, 887-
888f (V3)
Primary dentition, eruption pattern of,
165, 166t (V1)
Primary herpetic gingivostomatitis, 612-
613, 613f (V2)
Primary palate, 723, 828 (V3)
Primary reconstruction in orbital
fracture, 228-233 (V2)
internal orbital fracture and, 228-
230f, 228-231 (V2)
naso-orbital-ethmoid fracture and,
233 (V2)
zygomatic complex fracture and,
231f, 231-233, 232f (V2)
Primary survey, 35-39, 36t (V2)
adjuncts to, 39-40 (V2)
airway evaluation in, 35-36 (V2)
breathing assessment in, 36, 36f, 37f
(V2)
circulation assessment in, 37-38, 38f,
38t (V2)
comprehensive patient care and, 396,
397b, 398f (V2)
in cranio-maxillofacial trauma, 1
(V2)
neurologic assessment in, 38-39, 39t
(V2)
Primary tooth injury, 122-125, 123b,
123-126f (V2)
prognosis of, 132f, 132-133 (V2)
reactions of teeth to, 130b, 130-131,
131f, 132f (V2)
Primary unilateral cleft lip repair, 720-
723, 721-723f (V3)
Primordial cyst, 419 (V2)
Pringle, J.H., 791 (V2)
Privileged communication, 376-377
(V1)
Privileging, 307-317 (V1)
accreditation and certification and,
308-309 (V1)
adverse action in, 315-316 (V1)
appointment to medical staff in, 314-
315 (V1)
credentialing and, 313-314, 314f
(V1)
definitions and resources in, 309-313,
310-313t (V1)
specialty board certification and, 308
(V1)
Procaine
chemical structure of, 37f (V1)
pH effects on, 37t (V1)
Procedure-specific marketing, 338-339
(V1)
Procerus muscle, 174f, 554f (V3)
forehead and brow lift and, 597, 598f
(V3)
Production-based model of
compensation, 298 (V1)
Professional consultation in marketing,
322-323, 337-338 (V1)
Professional negligence-malpractice
insurance, 302-303 (V1)
Profile evaluation, 3f, 3-4 (V3)
Profile view in facial asymmetry, 273f,
274 (V3)
Profiling of trauma victims, 400 (V2)
Profit and loss statement, 295, 296-297t
(V1)
Progenia, complete mandibular
subapical osteotomy for, 155-171
(V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
in mandibular alveolar deficiency,
166-170f (V3)
in midface deficiency and mandibular
dentoalveolar protrusion, 161-
165f (V3)
technique in, 156-158, 157-160f (V3)
Prognathism
after cleft palate repair, 769 (V3)
bilateral sagittal split osteotomy for,
97-99, 98f (V3)
with long face, 99, 99b, 101f (V3)
with short face, 98-99, 99b, 100f
(V3)
cephalometric analysis and, 373 (V3)
clockwise occlusal plane rotation for,
253f, 253-255, 254f (V3)
combined maxillary and mandibular
osteotomies for, 238-247 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f,
242-243, 243f (V3)
counterclockwise occlusal plane
rotation for, 257f, 257-258, 258f
(V3)
pediatric surgical considerations in,
859-860, 860f (V3)
transoral vertical ramus osteotomy
for, 119-136 (V3)
advantages and disadvantages of,
120-121, 121t, 122f (V3)
historical background of, 119 (V3)
indications and contraindications
for, 121-122 (V3)
intraoperative procedure in, 123-
128, 125-127f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe facial asymmetry, 130f,
130-131, 131f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe open bite, 132-135,
132-135f (V3)
postoperative physiotherapy in,
128f, 128-129 (V3)
sagittal split ramus osteotomy
versus, 119, 120f, 120t (V3)
with severe facial asymmetry, 130f,
130-131, 131f (V3)
with severe open bite, 132-135,
132-135f (V3)
surgical treatment objectives in,
123, 124f, 125f (V3)
videocephalometric prediction and,
376 (V3)
Progressive condylar resorption, 299-
305, 303-304f, 306f (V3)
Progressive systemic sclerosis, 865-866
(V2)
Project consultant team in office design,
361 (V1)
INDEX I-79
Prolapsed fat pads, 579, 580f (V3)
Prolapsed lacrimal gland, 579 (V3)
Prolene polypropylene suture, 287t (V2)
Proliferation phase of wound healing,
19-21, 20f (V2), 61 (V3)
Prolonged sensory alteration, local
anesthetic-related, 45-46, 46t (V1)
Promethazine, 889t (V2)
Prominent lingual frenulum, 174, 175f,
176f (V1)
Pronasale, 554b (V3)
Pronova Poly suture, 287t (V2)
Prophylaxis
in animal bite, 315 (V2)
antibiotics for, 392-393, 410 (V3)
in implant surgery, 387-388, 388b
(V1)
autogenous bone graft and, 409,
422 (V1)
guided tissue generation and, 430
(V1)
sinus-lift subantral augmentation
and, 459 (V1)
intensive care unit and, 48, 72-73
(V2)
in laser skin resurfacing, 249 (V1),
520 (V3)
in mandibular surgery, 443 (V3)
for migraine, 148 (V1)
in modified Le Fort III osteotomy,
212 (V3)
skeletal anchorage and, 235 (V1)
for surgical geriatric patient with
diabetes mellitus, 383-384 (V2)
for trauma patient, 73 (V2)
Propionic acid derivatives, 84t, 86t
(V1)
Propionic acids, 887t (V2)
Propofol, 61-62, 62t (V1)
for office-based anesthesia, 74 (V1)
for pediatric anesthesia and sedation,
104, 105t (V1)
pharmacokinetics of, 62t (V1)
in rapid-sequence intubation, 29
(V2)
Propoxycaine, 37f, 37t (V1)
Propoxyphene
for acute postoperative pain, 81t, 82
(V1)
for temporomandibular disorders,
888t (V2)
Propranolol, 148 (V1)
Proptosis
in blow-out fracture of orbital floor,
86 (V2)
in cranio-maxillofacial trauma, 9 (V2)
Prostaglandin(s), 83 (V1)
central sensitization and, 963 (V2)
chronic facial pain and, 962, 963f
(V2)
Prostaglandin E2
bone formation and, 399 (V1)
nonsteroidal antiinflammatory drug
blockage of, 394 (V1)
Prosthesis
in bone graft for implant, 422 (V1)
glenoid fossa, 796f (V2)
in guided bone regeneration, 431-432
(V1)
temporomandibular joint, 904 (V2)
in zygomatic implant, 496-497, 497f,
498f, 499 (V1)
Prosthetic rehabilitation
in cleft palate, 841-843, 844-845f
(V3)
in midface avulsive injury, 346, 349-
350f (V2)
Prosthodontic classification, 480t (V1)
Protectan, 641-642 (V2)
Protein
alterations leading to cancer, 655-
666, 657f (V2)
evasion of apoptosis and, 660-662,
661f (V2)
immortalization and, 662-664, 663f
(V2)
insensitivity to growth inhibitory
signals and, 658-660, 659f
(V2)
I-80 INDEX
Protein (Continued)
neovascularization and, 664, 665f
(V2)
release from growth signal
requirement and, 655-658,
657f (V2)
tissue invasion and metastases and,
664-666, 666f (V2)
cell function and, 651 (V2)
postsurgical intake of, 408 (V3)
Protein energy malnutrition,
379 (V2)
Prothrombin time, 19t (V1)
Protruding ear, otoplasty for, 665-677
(V3)
blood supply to ear and, 667-668
(V3)
complications in, 675-676 (V3)
for congenital deformities, 668-669
(V3)
for correction of protruding earlobe,
675, 675f (V3)
Davis method in, 670-673,
672f (V3)
embryology of auricle and, 665, 666f
(V3)
Farrior technique in, 673, 675f (V3)
indications and timing of, 669 (V3)
Mustard[ac]e method in, 673, 674f
(V3)
nerve supply to ear and, 668-670f
(V3)
surgical anatomy in, 665-666, 666f,
667f (V3)
techniques in, 669-670, 671f (V3)
Protruding earlobe correction, 675, 675f
(V3)
Protrusion of mandible, 810-811 (V2)
Provisionalization of implant, 528-531,
530-531f (V1)
Proximal segment fracture in sagittal
split ramus osteotomy, 424-426,
425-428f (V3)
Proximal segment malpositioning
in intraoral vertical ramus osteotomy,
435-436, 436f (V3)
in sagittal split ramus osteotomy,
431-432 (V3)
Proximal segment rotation after
bilateral sagittal split osteotomy,
454, 455-456f (V3)
Proximate cause of injury, 374-375
(V1)
Prozac; See Fluoxetine
PRP; See Platelet-rich plasma
Pruritus, laser skin resurfacing and, 537-
538, 539f (V3)
Psammomatoid variant of juvenile
ossifying fibroma, 599 (V2)
Pseudoaneurysm after Le Fort I
osteotomy, 187 (V3)
Pseudoankylosis of temporomandibular
joint, 899-901 (V2)
Pseudoarthrosis, 159 (V2)
Pseudoasymmetry, 278-282 (V3)
condylar dislocation and, 281, 281f
(V3)
infection and, 281-282 (V3)
malocclusion and, 278-280, 279-280f
(V3)
muscle dysfunction and, 280-281
(V3)
Pseudocholinesterase abnormalities, 2
(V1)
Pseudocyst, 418, 868-869 (V2)
Pseudogout in temporomandibular
joint, 865 (V2)
Pseudomonas infection
in laser skin resurfacing, 540 (V3)
in otoplasty, 676 (V3)
in rhinoplasty, 573 (V3)
PSO; See Presurgical orthopedic
appliance
Psoriatic arthritis
facial asymmetry in, 309 (V3)
temporomandibular joint, 859-860
(V2)
temporomandibular joint ankylosis
and, 901-902 (V2)
Psychiatric disorders
ambulatory orthognathic surgery and,
493 (V3)
chronic head and neck pain and,
141-142 (V1)
Psychologic assessment
in chronic orofacial pain, 123-124
(V1)
in laser skin resurfacing, 517 (V3)
prevention of complications and,
419, 459 (V3)
in rhinoplasty, 557 (V3)
in rhytidectomy, 498 (V3)
Psychosocial aspects
of cleft orthognathic surgery, 814
(V3)
of orthognathic surgery, 76-81, 77f,
78f, 79b (V3)
of trauma, 400, 408 (V2)
Pterygoid fissure to A-point, 29 (V3)
Pterygoid fovea, 807 (V2)
Pterygoid plexus, 174 (V3)
blood loss in Le Fort I osteotomy
and, 468-469, 469f (V3)
Pterygoideus medialis muscle bleeding
in bilateral sagittal split osteotomy,
115 (V3)
Pterygomasseteric sling, 805 (V2)
Pterygomaxillary buttress, 91, 92f (V2)
maxillary osteotomy and, 227, 227f
(V3)
Pterygomaxillary fissure, 173-174 (V3)
Pterygopalatine fossa, maxillectomy
and, 693 (V2)
Public relations, 287 (V1)
activity sponsorship and, 345 (V1)
business lunches and, 337 (V1)
calling postoperative patients and,
345 (V1)
community service and, 338 (V1)
media networking and, 341-342, 342f
(V1)
newsletters and media packs and,
340-341, 341f (V1)
telephone call-on-hold devices and,
345 (V1)
Pulfrich phenomenon, 254 (V2)
Pulmonary artery catheter
intensive care and, 48 (V2)
trauma patient and, 70-71 (V2)
Pulmonary aspiration, preoperative
fasting and, 71 (V1)
Pulmonary disease
ambulatory orthognathic surgery and,
493 (V3)
geriatric patient and, 382-383 (V2)
perioperative management of, 383-
384, 384b, 384t (V3)
Pulmonary edema, laryngospasm in
anesthetized child and, 106-107
(V1)
Pulmonary Risk index, 384b (V3)
Pulmonary system
effects of thyroid disorders on, 13t
(V1)
preoperative evaluation of, 3-6, 5-7t
(V1)
Pulp testing, 108-109 (V2)
Pulp trauma, 112-117, 113t, 115b (V2)
crown infraction and, 112-113 (V2)
crown-root fracture and, 116 (V2)
enamel, dentin, and pulp exposure
in, 113-114 (V2)
enamel fracture and, 113 (V2)
healing in, 133-134, 134f, 135f (V2)
pulp exposure with non-vital pulp in,
115-116, 116f (V2)
pulp exposure with vital pulp in, 114-
115 (V2)
root fracture and, 116-117, 117f, 118f
(V2)
Pulp vessels, 67f, 175f (V3)
Pulpal blood flow, 175, 175f (V3)
Le Fort 1 osteotomy and, 65 (V3)
segmental maxillary osteotomy and,
67, 67f (V3)
Pulse oximetry, 26-27, 99 (V1)
Pulsed dye laser
in capillary malformation, 581 (V2)
Pulsed dye laser (Continued)
in infantile hemangioma, 580 (V2)
for resurfacing of traumatic and
surgical scars, 528 (V3)
for vascular lesions of face, 251 (V1)
Punch biopsy in skin cancer, 732 (V2)
Punched-out lesions in multiple
myeloma, 686, 686f (V2)
Puncture crushing, mandible and, 812
(V2)
Puncture wound during exodontia, 214
(V1)
Punitive damages in malpractice
lawsuit, 375 (V1)
Pupil assessment
in head injury, 50, 55 (V2)
in ocular trauma, 76 (V2)
in orbital fracture, 209 (V2)
Pupillary plane, 272-274, 273f (V3)
Pupillary sphincter defect, 80, 80f (V2)
Pure cutaneous histiocytosis, 567 (V2)
Pure poly-L-lactic acid fixation device,
111 (V3)
Purtscher’s retinopathy, 82, 83f (V2)
Pyogenic granuloma of gingiva, 180,
180f (V1)
Pyranocarboxylic acids, 887t (V2)
Pyrophosphate(s), 611 (V2)
Pyrophosphate arthropathy, 865 (V2)
Q orthopantomogram in, 551-552,
QST; See Quantitative sensory testing
Q-switching in laser therapy, 238 (V1)
Quadrilateral buccal osteotomy in
sinus-lift subantral augmentation,
459-460, 460f (V1)
Quality assurance, 302 (V1)
Quantitative sensory testing
in chronic head and neck pain, 140
(V1)
in neuropathic orofacial pain, 989-
990 (V2)
in posttraumatic trigeminal neuralgia,
155 (V1)
in trigeminal nerve injury, 262f, 262-
264, 263f, 279 (V1)
Quick analysis of chin, 683t (V3)
Quick Ceph Image software, 376 (V3)
R of pediatric impacted teeth, 166-168f,
Rabies virus exposure, 314-315 (V2)
Radial artery, 334f (V2)
Radial forearm flap, 332-333, 334f (V2)
for cheek reconstruction, 344 (V2)
Radial nerve, 334f (V2)
Radiance FN injection, 631, 647f (V3)
Radiation therapy, 767-776 (V2)
altered radiation fractionation
schemes and, 772 (V2)
basic exodontia and, 186-187 (V1)
complications of, 773-774 (V2)
definitive radiotherapy and, 771 (V2)
in desmoplastic fibroma, 608 (V2)
histologies and, 767-768 (V2)
in Langerhans cell histiocytosis, 573
(V2)
in lymphoma, 763 (V2)
in malignant melanoma, 756 (V2)
osteoradionecrosis and, 639-642 (V2)
clinical and radiographic diagnosis
of, 639, 639f, 640f (V2)
hyperbaric oxygen therapy for,
639-641 (V2)
prevention and maintenance of,
641-642, 642f (V2)
treatment of, 639, 640f, 641b, 641t
(V2)
in osteosarcoma, 683 (V2)
preoperative and postoperative, 771-
772 (V2)
sites of disease and, 768t, 768-771,
769f, 770f, 770t, 771t (V2)
in skin cancer, 741-742 (V2)
systemic therapy with, 772, 772t
(V2)
techniques in, 772-773, 773f (V2)
temporomandibular joint
pseudoankylosis and,
900 (V2)
Radiation-induced sarcoma of jaw, 685
(V2)
Radical neck dissection, 719, 719t, 720f
(V2)
Radicular cyst, 419-421, 420f, 422f
(V2)
Radiesse injection, 630f, 630-631, 648f,
691f, 691-692, 692f (V3)
Radiofrequency ganglionolysis for
trigeminal neuralgia, 151 (V1)
Radiofrequency neurolysis, for
trigeminal neuralgia, 151 (V1)
Radiographic coding, 367 (V1)
Radiographic evaluation
of abnormal head shape, 856 (V3)
in ankylosis, 903 (V2)
in condylar fracture, 168-170, 169f
(V2)
in condylar hyperplasia, 285 (V3)
in dentoalveolar injury, 102, 102f,
109-110, 110f (V2)
documentation of, 382 (V1)
in Ewing’s sarcoma, 687, 688f (V2)
in facial injuries, 91-92 (V2)
in implantology, 547-566 (V1)
computed tomography in, 552-564,
553-565f (V1)
digital radiography in, 549-550,
551f (V1)
linear tomography in, 552 (V1)
552f, 553f (V1)
plain films in, 549-551f (V1)
principles for, 547-548, 548f, 549f
(V1)
subtraction radiography in, 551
(V1)
in lymphoma, 762f, 762-763 (V2)
in mandibular trauma, 96-99, 97f, 99f
(V2)
in midface fracture, 241 (V2)
in naso-orbital-ethmoid fracture, 246
(V2)
in obstructive sleep apnea syndrome,
319-321, 320-322f (V3)
in orbital fracture, 209, 210f (V2)
in osteoradionecrosis, 639, 640f (V2)
in osteosarcoma, 680, 681f, 682f
(V2)
167 (V1)
preoperative, 389 (V3)
in temporomandibular disorders, 835-
836 (V2)
in temporomandibular joint
hypomobility, 898 (V2)
in transverse maxillary deficiency,
220-223, 221-223f (V3)
for zygomatic implant, 492, 492f
(V1)
Radiology equipment, 359-360 (V1)
Radiology suite in office design, 352
(V1)
Radix, 554b, 558 (V3)
Ralitrexed, 779t (V2)
Ramsay Sedation Scale, 30, 30b (V1)
Ramsey-Hunt syndrome, 292 (V3)
Ramus
bilateral sagittal split osteotomy and,
106-108, 107f, 108f, 114, 114b
(V3)
fracture of, 101, 141, 142f (V2)
mandibular asymmetry and,
99t (V3)
transoral vertical ramus osteotomy
and, 119-136 (V3)
advantages and disadvantages of,
120-121, 121t, 122f (V3)
ambulatory, 494 (V3)
historical background of,
119 (V3)
indications and contraindications
for, 121-122 (V3)
intraoperative procedure in, 123-
128, 125-127f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe facial asymmetry, 130f,
130-131, 131f (V3)

Ramus (Continued)
for mandibular prognathism and
maxillary retrognathism with
severe open bite, 132-135,
132-135f (V3)
postoperative physiotherapy in,
128f, 128-129 (V3)
sagittal split ramus osteotomy
versus, 119, 120f, 120t (V3)
surgical treatment objectives in,
123, 124f, 125f (V3)
Ramus width at occlusal plane, 43 (V3)
Range of motion
of mandible, 824-825 (V2)
in temporomandibular disorders, 912,
980 (V2)
Ranula, 244-245 (V1), 539, 540f (V2)
Rapid maxillary expansion for
transverse maxillomandibular
discrepancy, 219 (V3)
Rapid prototyping in computed
tomography, 555-557, 555-557f
(V1)
Rapid shallow breathing index, 43 (V2)
Rapidly involuting congenital
hemangioma, 579f, 579-581 (V2)
Rapid-sequence intubation, 28-31, 31f
(V2)
Ratio analysis of financial statements,
297 (V1)
Ratio of patient height to thyromental
distance, 419 (V3)
RBRVS; See Resource Based Relative
Value Scale
Reactive arthritis, 305-309, 307-309f
(V3), 622 (V2)
Reactive oxygen species, 435 (V1)
REAL classification of lymphoid
neoplasms, 758, 759b (V2)
Receptionist, 324, 346-347 (V1)
Reclast; See Zoledronate
Reconstruction
alveolar
alveolar distraction in, 349-354,
349-354f (V3)
in cleft maxilla, 808-810, 808-811f
(V3)
in avulsive facial injuries, 327-351
(V2)
Abbe flap in, 329, 330f (V2)
aesthetic and prosthetic
rehabilitation and, 346-350f
(V2)
airway management in, 327 (V2)
anterolateral thigh free flap in,
335, 335f (V2)
cervicofacial flap in, 329-330, 333f
(V2)
of cheek defects, 344, 345-348f
(V2)
clinical examination in, 327-328
(V2)
debridement in, 328 (V2)
facial artery musculomucosal flap
in, 329 (V2)
fibular free flap in, 333-335, 335f
(V2)
imaging in, 328 (V2)
of lip defects, 343f, 343-344 (V2)
of lower face and mandible, 335-
340f, 336-337 (V2)
of nasal defects, 337, 343 (V2)
paramedian forehead flap in, 329,
331-332f (V2)
pectoralis major myocutaneous flap
in, 330-331 (V2)
radial forearm flap in, 332-333,
334f (V2)
rectus abdominis free flap in, 335
(V2)
of scalp defects, 346 (V2)
submental island flap in, 331-332,
334f (V2)
temporoparietal fascia flap in, 330
(V2)
wound assessment in, 327, 328f
(V2)
cleft lip and palate repair in, 719-730
(V3)
Reconstruction (Continued)
cleft palate repair and, 723-727,
729f, 730f (V3)
complex facial clefting and, 727-
728, 731f (V3)
history of, 713-714 (V3)
lip adhesion and, 720 (V3)
outcome assessment in, 728-730
(V3)
presurgical taping and orthopedics
in, 719-720, 720f (V3)
primary bilateral lip repair and,
723, 724-728f (V3)
primary unilateral cleft lip repair
and, 720-723, 721-723f (V3)
treatment planning and timing in,
718t, 718-719 (V3)
cleft orthognathic surgery in, 814-
815, 815b, 816-817f (V3)
bone grafting in, 819, 820-825f
(V3)
obstructed nasal breathing and,
819 (V3)
preoperative evaluation in, 813-
814 (V3)
stabilization of mobilized cleft
maxilla and, 819 (V3)
surgical reconstruction in, 814-815,
815b, 816-817f (V3)
technical considerations in, 815-
819, 818f (V3)
timing and psychosocial
considerations in, 814 (V3)
velopharyngeal considerations in,
819-826 (V3)
in craniofacial dysostosis syndromes,
880-921 (V3)
Apert syndrome in, 902-909, 903-
907f (V3)
Carpenter’s syndrome in, 909 (V3)
cloverleaf skull anomaly in, 909-
914, 910-914f (V3)
Crouzon syndrome in, 886-902,
887-900f (V3)
dentition and occlusion anomalies
in, 881-882 (V3)
functional considerations in, 880-
881 (V3)
genetic aspects of, 880 (V3)
morphologic considerations in,
882-883 (V3)
Pfeiffer syndrome in, 909 (V3)
Saethre-Chotzen syndrome in, 909
(V3)
surgical management of, 883-886
(V3)
in craniosynostosis, 864-879 (V3)
anterior plagiocephaly in, 868-871,
871f, 872f (V3)
brachycephaly in, 874-876 (V3)
delayed diagnosis of, 867-868 (V3)
diagnosis of, 865-866 (V3)
functional consequences of, 864-
865, 865f (V3)
posterior plagiocephaly in, 874,
877f, 878f (V3)
scaphocephaly in, 868, 869-870f
(V3)
surgical considerations in, 856-858,
866-867 (V3)
syndromes associated with, 850 (V3)
timing of surgery for, 867 (V3)
trigonocephaly in, 871-874, 874-
876f (V3)
in naso-orbital-ethmoid fracture
medial orbital rim and, 246-247,
247f (V2)
medial orbital wall and, 247, 247f
(V2)
nasal, 248, 248f (V2)
in oculoauriculovertebral spectrum,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
Reconstruction (Continued)
ear reconstruction in, 930 (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
maxilla and, 922-935 (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
926t (V3)
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
in, 928-929 (V3)
in orbital fracture, 228-233 (V2)
internal orbital fracture and, 228-
230f, 228-231 (V2)
naso-orbital-ethmoid fracture and,
233 (V2)
pediatric, 361 (V2)
zygomatic complex fracture and,
231f, 231-233, 232f (V2)
in osteoradionecrosis, 639 (V2)
in pediatric craniomaxillofacial
tumors, 988-993, 991f, 992f
(V3)
secondary
in orbital fracture, 233-236, 233-
236f (V2)
in periorbital soft tissue injury,
306, 307f (V2)
secondary cleft lip and palate
reconstruction in, 828-847 (V3)
bone graft reconstruction of cleft
maxilla and palate in, 840
(V3)
complications of, 839 (V3)
comprehensive dental and
prosthetic rehabilitation in,
841-843, 844-845f (V3)
fistula closure in, 828-831, 830f,
832-834f (V3)
for management of submucous cleft
palate, 839-840 (V3)
for management of velopharyngeal
dysfunction, 831t, 831-835,
835f (V3)
operative techniques in, 836-839,
837f, 838f (V3)
orthognathic surgery for correction
of midfacial deficiency in, 840
(V3)
reconstruction of cleft nasal
deformity in, 840-841, 842f
(V3)
secondary surgery for cleft lip scar
revision in, 841, 843f (V3)
timing and indications for, 835-
836 (V3)
temporomandibular joint, 945-960
(V2)
in ankylosis, 904 (V2)
distraction osteogenesis and, 955
(V2)
in failed alloplastic joint
reconstruction, 954, 954f
(V2)
in failed tissue grafts, 953-954,
954f (V2)
historic perspective of, 945-950,
946-950f (V2)
in inflammatory arthritis, 950-952,
952f (V2)
in loss of vertical mandibular
height and occlusal
relationship, 954-955, 955f
(V2)
in recurrent fibrosis and bony
ankylosis, 952-953, 953f, 953t
(V2)
tissue engineering and, 955 (V2)
in Treacher Collins syndrome, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
INDEX I-81
Reconstruction (Continued)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
Recontouring of gingiva, 481-484, 484f,
485f (V1)
Record keeping standards, 380 (V1)
Recording of prescription, 382 (V1)
Records
alterations of, 381 (V1)
legibility of, 379-383 (V1)
release of, 384 (V1)
Records request, 376-378 (V1)
Recovery facility in ambulatory
orthognathic surgery, 490, 492f
(V3)
Recovery period
child and, 108 (V1)
monitoring during, 32-33, 33t (V1)
Rectal assessment
in cranio-maxillofacial trauma, 11
(V2)
in secondary survey, 40 (V2)
Rectus abdominis free flap, 335 (V2)
for cheek reconstruction, 344, 345f
(V2)
Rectus femoris muscle, anterolateral
thigh flap and, 335f (V2)
Recurrent cellulitis in lymphatic
malformation, 582 (V2)
Red blood cell transfusion, 15t (V1)
Red reflex, 306 (V2)
Red-glass test, 77 (V2)
Reduction
of condylar fracture, 171 (V2)
of dentoalveolar fracture, 126, 127f
(V2)
of exodontia-related mandibular
fracture, 219f, 219-220, 220f
(V1)
of mandibular fracture, 146-148,
147f, 391f, 391-392, 392f, 392t
(V2)
of maxillary/midface fracture, 386-
388 (V2)
of nasal fracture, 276-278, 278f, 279f
(V2)
of naso-orbital-ethmoid fracture,
246-247, 247f (V2)
of temporomandibular joint
dislocation, 905-908 (V2)
Reed-Sternberg cell, 759, 760f (V2)
Referral
in chronic orofacial pain, 122-123
(V1)
obtaining of, 335 (V1)
for secondary nerve injury care, 279
(V1)
Referral survey, 287, 288t (V1)
Referring staff, 340-341 (V1)
Reflection, laser property, 514 (V3)
Reflex sympathetic dystrophy, 967, 997
(V2)
Reflexes, initial evaluation in head
injury and, 51 (V2)
Reformatting software program for
computed tomography, 557-561,
557-562f (V1)
I-82 INDEX
Regeneration of bone, 22 (V2)
Regional flap
in avulsive facial injury, 329-332
(V2)
Abbe flap in, 329, 330f (V2)
cervicofacial flap in, 329-330, 333f
(V2)
facial artery musculomucosal flap
in, 329 (V2)
paramedian forehead flap in, 329,
331-332f (V2)
pectoralis major myocutaneous flap
in, 330-331 (V2)
submental island flap in, 331-332,
334f (V2)
temporoparietal fascia flap in, 330
(V2)
in skin cancer repair, 739 (V2)
Rehabilitation, 48 (V2)
in temporomandibular joint disorders,
133-134 (V1)
trauma patient preparation for, 73
(V2)
Reiter syndrome, 622, 861 (V2)
Rejuvenation procedures, laser-assisted,
249 (V1)
Rela; See Carisoprodol
Relafen; See Nambumetone
Relapse
in mandibular surgery, 445-451 (V3)
in bilateral sagittal split osteotomy,
115-116, 116b (V3)
in genioplasty, 446-451, 449-452f
(V3)
idiopathic condylar resorption and,
453-454 (V3)
in intraoral vertical ramus
osteotomy, 445-446, 446-449f
(V3)
in sagittal ramus osteotomy, 445,
446f (V3)
in maxillary surgery, 480 (V3)
Relative value unit, 369 (V1)
Release of records, 384 (V1)
Remifentanil, 60, 74-75 (V1)
Remodeling phase of wound healing,
21, 21f, 61-62 (V3), 145-146 (V2)
Removable partial dentures,
miniimplant stabilization of, 568
(V1)
Removable prosthesis
in bone graft for implant, 422 (V1)
in guided bone regeneration, 431-432
(V1)
Removal of wrong tooth, 212 (V1)
Renal disorders, 387 (V3)
Renal failure, 8t, 9t (V1)
Renal function
liver disease-related alteration in, 11
(V1)
pediatric anesthesia and sedation
and, 96 (V1)
preoperative tests of, 7-9t (V1), 387
(V3)
Renal system
effects of thyroid disorders on, 13t
(V1)
intensive care of trauma patient and,
46 (V2)
Repetitive microtrauma
myofascial pain syndromes and, 143
(V1)
office ergonomics and, 362 (V1)
Repetitive strain hypothesis of
myogenous pain, 980 (V2)
Replantation of avulsed tooth, 120-122,
121f, 122b (V2)
Repositioning splint, 883, 883f, 984
(V2)
Request for records, 376 (V1)
Res ipsa loquitur, 374 (V1)
Rescue therapies in anesthetic crisis, 68
(V1)
Resection
in ameloblastic fibroma, 524 (V2)
of ankylotic bone and fibrous tissue,
903-904 (V2)
in arteriovenous malformation, 589
(V2)
Resection (Continued)
in calcifying epithelial odontogenic
tumor, 476 (V2)
in chondroma, 606 (V2)
in desmoplastic fibroma, 608 (V2)
in infantile hemangioma, 580-581
(V2)
in juvenile ossifying fibroma, 600,
600f (V2)
in Langerhans cell histiocytosis, 573,
575f (V2)
in lymphatic malformation, 582-583
(V2)
mandibular, 700-702, 701f, 702f (V2)
in myxoma, 518 (V2)
in osteoblastoma, 604 (V2)
in osteoradionecrosis, 639 (V2)
of peripheral ameloblastoma, 502
(V2)
in squamous cell carcinoma of
mandible, 717-719 (V2)
of unicystic ameloblastoma, 501-502
(V2)
in venous malformation, 587-588
(V2)
Residual cyst, 421, 423f (V2)
Residual root remnants, 213 (V1)
Resonance imbalance after cleft surgery,
793, 793f (V3)
Resorbable fixation
in bilateral sagittal split osteotomy,
111, 111b (V3)
in Le Fort I osteotomy, 182 (V3)
Resorbable sutures in exodontia, 201
(V1)
Resource Based Relative Value Scale,
370 (V1)
Respiration
age-related values, 94t (V1)
head injury and, 50 (V2)
orthognathic surgery-related changes
in, 73, 74 (V3)
Respiratory depression
benzodiazepines and, 57 (V1)
ketamine and, 63 (V1)
opiates and opioids and, 59 (V1)
Respiratory disease
ambulatory orthognathic surgery and,
493 (V3)
in geriatric patient, 382-383 (V2)
Respiratory distress, predictors of, 398b
(V2)
Respiratory disturbance index
oral appliance and, 319 (V3)
for sleep apnea, 252 (V1)
Respiratory system
effects of smoking on, 70 (V1)
intensive care and, 43-44, 44t (V2)
monitoring of
during anesthesia, 25-29, 26f, 28f
(V1)
postoperative, 75 (V1)
pediatric anesthesia and sedation
and, 94-96, 95f, 96t (V1)
predictors of respiratory distress, 398b
(V2)
preoperative evaluation of, 3-6, 5-7t
(V1)
Respiratory tract infection, 5, 98 (V1)
Resting condyle, 811 (V2)
Resting skin tension lines, 732, 732f
(V2)
Restoration, 387-574 (V1)
autogenous bone grafting in, 406-427
(V1)
bone biology and, 406-407, 407f
(V1)
graft recipient site and, 419-422,
419-422f (V1)
ilium for, 415-419, 415-419f
(V1)
mandibular ramus for, 412-414,
412-414f (V1)
mandibular symphysis for, 409-411,
410-412f (V1)
maxillary tuberosity for, 409, 409f,
410f (V1)
onlay bone graft and, 424, 424f,
425f (V1)
Restoration (Continued)
patient preparation for, 409 (V1)
preoperative evaluation in, 407-
408, 408f, 409f (V1)
sinus bone grafting and, 422-424,
423f (V1)
tibia for, 414f, 414-415, 415f (V1)
guided tissue regeneration and, 428-
457 (V1)
for augmentation using allograft
and xenograft bone with
titanium-reinforced
membrane, 450-451, 450-451f
(V1)
for augmentation using allograft
bone putty and resorbable
collagen membrane, 448f,
448-449, 449f (V1)
for coronal defects, 436 (V1)
for corticocancellous block
augmentation of posterior
mandible, 452-453, 452-453f
(V1)
for dehiscence defects, 435-436,
447, 447f (V1)
dual-layered technique in, 445f,
445-446, 446f (V1)
for fenestration defects, 436 (V1)
flapless buccal wall reconstruction
in, 443f, 443-444, 444f (V1)
functional and design requirements
of membranes for, 429-431,
431f, 432f (V1)
to reduce postextraction bone loss,
438-440, 454f, 454-455, 455f
(V1)
ridge preservation using high-
density PTFE membrane in,
440-441f, 440-442 (V1)
in subantral augmentation, 436-
438, 437f (V1)
wound closure in, 431-435, 433f,
434f (V1)
immediate implant loading in, 511-
524 (V1)
benefits of, 522-524 (V1)
in edentulous jaw, 518-521, 519-
524f (V1)
following extraction, 540-546, 541-
545f (V1)
history of, 525-527, 526b, 526f,
527f (V1)
for single tooth or partially
edentulous restoration, 511-
517, 512-518f (V1)
impressions at implant placement
and, 525-539 (V1)
concept of, 531 (V1)
history of immediate loading and,
525-527, 526b, 526f, 527f
(V1)
immediate extraction, implant
placement, and provisional
restoration and, 534f, 534-
535, 535f (V1)
immediate provisionalization and,
528-531, 530-531f (V1)
prefabricated ceramic abutments
and temporary crowns and,
536f, 536-537, 537f (V1)
primary bone-level impressions
and, 527-528, 529f, 530f (V1)
second-stage surgery and, 532f,
532-533, 533f (V1)
laser-assisted, 245-246 (V1)
miniimplants for, 567-574, 568f (V1)
for orthodontic anchorage, 570-
574, 572-574f (V1)
for pontic support of fixed partial
denture, 568 (V1)
for retention of obturators, 568-
569 (V1)
for single-tooth implant restoration
in narrow space, 569, 570f,
571f (V1)
for stabilization of complete
dentures, 567-568, 569f (V1)
for stabilization of removable
partial dentures, 568 (V1)
Restoration (Continued)
osteoperiosteal flap and, 471-478
(V1)
alveolar repositioning osteotomies
and, 473, 473f, 474f (V1)
alveolar split graft and, 471, 473f
(V1)
alveolar width distraction
osteogenesis and, 474-477,
475-478f (V1)
interpositional bone graft and, 471,
472f (V1)
pediatric, 181-183, 182f, 183f (V1)
pharmacology for, 387-405 (V1)
antibiotic prophylaxis and, 387-
388, 388b (V1)
antibiotics added to bone grafting
materials and, 388-390, 389t,
390t (V1)
bioactive fatty acids and bone
development and, 399-400
(V1)
bisphosphonates and, 395-398,
396t, 397t (V1)
mineral, hormonal, and vitamin
supplements and, 398-399,
399t (V1)
NSAIDS and bone development
and, 392-395 (V1)
periimplantitis and, 390-392, 391t
(V1)
platelet-rich plasma and bone
grafting in, 501-510 (V1)
allograft and alloplastic materials
and, 504f, 504-506 (V1)
benefits of, 502-503 (V1)
bone healing and, 394, 503f, 503-
504 (V1)
case report of, 509, 509f (V1)
concept of, 501-502, 502f (V1)
processing of, 506-508, 507f, 508f
(V1)
radiographic evaluation in, 547-566
(V1)
computed tomography in, 552-564,
553-565f (V1)
digital radiography in, 549-550,
551f (V1)
linear tomography in, 552 (V1)
orthopantomogram in, 551-552,
552f, 553f (V1)
plain films in, 549-551f (V1)
principles for, 547-548, 548f, 549f
(V1)
subtraction radiography in, 551
(V1)
sinus-lift subantral augmentation in,
458-470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic
considerations in, 458-459
(V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f,
464f (V1)
elevation of schneiderian
membrane in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
trephine core membrane elevation
in, 464-468, 464-468f (V1)
vascular supply, lymphatic
drainage, and innervation in,
459 (V1)
soft tissue procedures around implant
in, 479-490 (V1)
aesthetic considerations and, 479-
480, 480t, 481f (V1)
AlloDerm in, 486, 487f (V1)

Restoration (Continued)
connective tissue grafting in, 485,
485f, 486f (V1)
epithelialized free-gingival grafting
in, 483f, 484-485 (V1)
gingivectomy in, 481-484, 484f,
485f (V1)
modified roll tissue graft in, 486,
488f (V1)
papilla regeneration technique in,
487-489, 489f (V1)
pediculated connective tissue graft
in, 486 (V1)
soft tissue health considerations
and, 479, 480f (V1)
trigeminal nerve injury and, 275-276
(V1)
zygomatic implant in, 491-500 (V1)
complications in, 498f, 498-499
(V1)
final prosthesis fabrication and,
499 (V1)
historical perspective in, 491 (V1)
patient selection for, 491-492, 492f
(V1)
postoperative care in, 498 (V1)
preoperative considerations in,
493, 493f (V1)
prosthetic conversion technique
in, 496-497, 497f, 498f (V1)
radiographic evaluation in, 492,
492f (V1)
regional anatomy in, 492-493 (V1)
surgical options in, 493-494, 494f
(V1)
surgical protocol in, 494-496, 494-
497f (V1)
Restoril; See Temazepam
Restroom, floor plan in office design
and, 356, 356f (V1)
Restylane injection, 629, 645-648f (V3)
Resurfacing procedures, 513-552 (V3)
botulinum toxin in, 658-661 (V3)
contraindications and adverse
effects of, 661, 662f (V3)
history and pharmacology of, 658
(V3)
preparations of, 658-659, 659t
(V3)
treatment technique for, 660-661,
661f (V3)
uses in facial cosmetics, 659f, 659-
660, 660f (V3)
carbon dioxide laser in, 521-532
(V3)
anesthesia and, 521, 522f (V3)
fractional photothermolysis in,
532, 536f (V3)
laser properties in, 514f, 514-516,
515f (V3)
laser settings for, 521-522, 522f
(V3)
postoperative care in, 524-529,
526-528f, 530-531f (V3)
resurfacing acne scars in, 529 (V3)
single-pass resurfacing in, 529-532,
533-534f (V3)
traditional technique in, 522-524,
523f, 525-526f (V3)
traumatic and surgical scars
improvement in, 529 (V3)
treatment of benign skin lesions
in, 529 (V3)
chemical peel in, 661-664, 662f, 664f
(V3)
complications of, 534-544 (V3)
contact dermatitis in, 539 (V3)
dyschromias in, 541-542, 542f,
543f (V3)
infection in, 540-541, 541f (V3)
milia and acne formation in, 539-
540, 540f (V3)
ocular, 543-544 (V3)
prolonged erythema in, 535-537,
539f (V3)
pruritus in, 537-538, 539f (V3)
scarring in, 542-543, 543f (V3)
sepsis in, 544 (V3)
telangiectasias in, 538-539 (V3)
Resurfacing procedures (Continued)
erbium:YAG laser in, 532-534, 536-
538f (V3)
history of, 513-514 (V3)
intrinsic and extrinsic aging and, 513
(V3)
laser blepharoplasty with, 544-545,
545-547f (V3)
patient evaluation in, 516-519, 518b
(V3)
preoperative considerations in, 519
(V3)
rhytidectomy with, 545-548, 547-
548f (V3)
in skin cancer, 734-735 (V2)
skin preparation for, 519-521 (V3)
Retainer, postsurgical management of,
401, 402f (V3)
Reticular formation, 962, 962f (V2)
Reticular oral lichen planus, 618-619
(V2)
Retin-A; See Tretinoin
Retina, nonperforating eye injuries and,
81-82, 81-83f (V2)
Retinal detachment, 81f (V2), 81-82
in orbital fracture, 213, 213b (V2)
Retinoic acid
for milia, 540 (V3)
for skin preparation in laser skin
resurfacing, 520 (V3)
Retinoid dermatitis, 520 (V3)
Retinoids for skin cancer, 740 (V2)
Retirement plan administrator, 287
(V1)
Retrobulbar bleeding
after repair of zygomatic fracture,
198-199 (V2)
following blepharoplasty, 593 (V3)
traumatic, 84, 84f (V2)
Retrobulbar hematoma in orbital
fracture, 212f, 212-213 (V2)
Retrognathism
bilateral sagittal split osteotomy for,
89b, 89-97 (V3)
with long face, 95f, 95-96, 96f, 97,
97b (V3)
with normal face height, 90-92,
90-92f, 97, 97b (V3)
with short face, 93f, 93-94, 94f, 97,
97b (V3)
complete mandibular subapical
osteotomy for, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
counterclockwise rotation of
maxillomandibular complex for,
257f, 257-258, 258f (V3)
mandibular lengthening by
distraction osteogenesis for, 342-
346, 342-346f, 998-1001f, 998-
1002 (V3)
videocephalometric prediction in,
376, 376f (V3)
Retromandibular approach in
condylar fracture, 171-172, 172-
175f (V2)
Retromandibular vein, 433f (V3)
condylar fracture and, 164 (V2)
Retromolar trigone, 705-706 (V2)
squamous cell carcinoma of, 716-719
(V2)
Retromolar vertical osteotomy, 157-
158, 158f (V3)
Retrusion of mandible, 811 (V2)
Revascularization in orthognathic
surgery, 60-71 (V3)
bone healing and, 62 (V3)
categorization of healing and, 62
(V3)
genioplasty and, 71 (V3)
Le Fort 1 osteotomy and, 63-68, 64-
67f (V3)
Revascularization in orthognathic
surgery (Continued)
mandibular osteotomy and, 68-70f,
68-71 (V3)
maxillary surgery and, 62-63, 63f
(V3)
wound healing phases and, 60-62,
61f, 62f (V3)
Revenue cycle, financial policy and,
293-295 (V1)
Reverse Towne’s projection in
temporomandibular disorders, 144,
145f, 836, 837f (V2)
Reversible pulpitis, 186 (V1)
Revised European-American
Classification of Lymphoid
Neoplasms, 758, 759b (V2)
Revision surgery for cleft malformations,
828-847 (V3)
bone graft reconstruction of cleft
maxilla and palate in, 840 (V3)
complications of, 839 (V3)
comprehensive dental and prosthetic
rehabilitation in, 841-843, 844-
845f (V3)
fistula closure in, 828-831, 830f, 832-
834f (V3)
for management of submucous cleft
palate, 839-840 (V3)
for management of velopharyngeal
dysfunction, 831t, 831-835, 835f
(V3)
operative techniques in, 836-839,
837f, 838f (V3)
orthognathic surgery for correction of
midfacial deficiency in, 840 (V3)
reconstruction of cleft nasal
deformity in, 840-841, 842f
(V3)
secondary surgery for cleft lip scar
revision in, 841, 843f (V3)
timing and indications for, 835-836
(V3)
Revisional palatoplasty, 838-839 (V3)
Rhabdomyosarcoma, 984-986, 987f (V3)
Rheumatoid arthritis
chronic orofacial pain in, 118 (V1)
facial asymmetry in, 309 (V3)
temporomandibular, 145 (V1)
of temporomandibular joint, 145
(V1), 857b, 857-858 (V2)
temporomandibular joint ankylosis
and, 901-902 (V2)
Rheumatoid factor, 858 (V2)
Rhinion, 554b (V3)
Rhinophyma, 529 (V3)
Rhinoplasty, 553-578 (V3)
case reports in, 574-576, 574-576f
(V3)
clinical examination in, 557-560,
558-560f (V3)
closed, 572-573, 573f (V3)
complications in, 573-577 (V3)
dressings and splinting in, 573, 573f
(V3)
follow-up care in, 573 (V3)
incisions in, 560-562, 561f, 562f
(V3)
initial consultation in, 557 (V3)
nasal anatomy and, 553-556, 554b,
554-557f (V3)
open, 567-572, 568-571f (V3)
tip plasty in, 562, 563f (V3)
tip projection in, 562-564, 563-565f
(V3)
tip rotation in, 564, 565f (V3)
tip shape and, 565-566, 566f (V3)
Rhinorrhea, 59-60 (V2)
Rhizotomy, percutaneous trigeminal,
993 (V2)
Rhytidectomy, 497-512 (V3)
complications in, 506-510, 507-510f
(V3)
laser skin resurfacing with, 545-548,
547-548f (V3)
patient evaluation in, 497-500, 498t,
499f, 499t (V3)
surgical technique in, 500-506, 500-
506f (V3)
INDEX I-83
Rib cage of child, 95, 95f (V1)
Ridge preservation, guided tissue
regeneration in, 440-441f, 440-442
(V1)
Ridge resorption after tooth extraction,
190 (V1)
Rifampin, 389 (V1)
Rigid internal fixation
ambulatory surgery and, 494 (V3)
in cleft orthognathic surgery, 819 (V3)
in genioplasty, 142-145, 144-148f
(V3)
in Le Fort I osteotomy, 181-184 (V3)
Rim incision of lower lid, 205f (V2)
Risdon cable, 370f, 370-372 (V2)
Risedronate, 395, 396t (V1), 558t (V2)
Rish technique for determining chin
position, 681t (V3)
Risk assessment of co-morbid systemic
disease, 380t, 380-385 (V2)
cardiovascular disease and, 380-381
(V2)
cardiovascular medications and, 381
(V2)
cerebrovascular and neurological
disease and, 382 (V2)
dementia and postoperative delirium
and, 384-385 (V2)
diabetes mellitus and, 383-384 (V2)
hypertension and, 381-382 (V2)
respiratory disease and, 382-383 (V2)
thyroid disease and, 384 (V2)
Risk management, 373-386 (V1)
accreditation of surgicenter and, 304-
306, 305t (V1)
Americans with Disabilities Act and,
383-384 (V1)
discharging patient from practice
and, 383 (V1)
documentation and legible records
and, 379-383 (V1)
Emergency Medical Treatment and
Active Labor Act and, 385 (V1)
HIPAA privacy and security and,
384 (V1)
incidents and claims and, 375-376
(V1)
informed consent and, 379 (V1)
lawsuit process and, 376-378 (V1)
limited English proficiency and, 384-
385 (V1)
malpractice and, 374-375 (V1)
office management and, 301-303 (V1)
online communication and, 385 (V1)
patient rapport and, 378-379 (V1)
release of records and, 384 (V1)
telemedicine and, 385 (V1)
Risorius muscle, 174f (V3)
Robaxin; See Methocarbamol
Rocker deformity, 569, 570f (V3)
Rocuronium
for laryngospasm in anesthetized
child, 106 (V1)
in rapid-sequence intubation, 30 (V2)
Rodent ulcer, 725 (V2)
Roll, term, 365f (V3)
Rongetti endaural incision, 933f, 933-
934, 934f (V2)
Room preparation for pediatric
anesthesia and sedation, 100t, 100-
103, 101b, 102f (V1)
Root canal therapy
basic exodontia versus, 186 (V1)
calcium hydroxide in, 119, 119f (V2)
in intrusive luxation of tooth, 118
(V2)
in root fracture, 117 (V2)
Root fracture, 113t, 114t, 116-117,
117f, 118f (V2)
of primary tooth, 123, 124f, 133 (V2)
Root of tooth
damage in orthodontic skeletal
anchorage, 235-236 (V1)
exodontia and
displacement during, 213-214 (V1)
residual root remnants and, 213
(V1)
resorption after Le Fort I osteotomy,
475 (V3)
I-84 INDEX
Rotation and advancement flap
technique for unilateral cleft lip,
722, 737-741 (V3)
Asensio technique and, 740f, 740-
741, 741f (V3)
comparison of cleft surgery
techniques, 736 (V3)
nasal reshaping in, 741 (V3)
postoperative care in, 741 (V3)
preoperative management in, 738
(V3)
surgical technique in, 738-739, 739f,
740f (V3)
wide cleft defect and, 742f, 743f (V3)
Rotation of occlusal plane, 248-271
(V3)
clockwise rotation in, 252-256 (V3)
center of rotation at anterior nasal
spine, 252, 252f, 252t (V3)
center of rotation at maxillary
incisor tip, 252, 252f, 253t
(V3)
center of rotation at pogonion,
255, 255t, 256f (V3)
center of rotation at zygomatic
buttress, 255-256, 256f, 256t
(V3)
mandibular excess and, 253f, 253-
255, 254f (V3)
counterclockwise rotation in, 256-
260 (V3)
center of rotation at anterior nasal
spine, 256, 259f, 259t (V3)
center of rotation at posterior nasal
spine, 256-260, 260f, 260t
(V3)
center of rotation at zygomatic
buttress, 256, 259f, 259t (V3)
in Treacher Collins syndrome, 954
(V3)
in unilateral adolescent internal
condylar resorption, 303-304f,
305, 306f (V3)
vertical maxillary deficiency and
mandibular anteroposterior
deficiency and, 257f, 257-258,
258f (V3)
vertical maxillary excess and
mandibular anteroposterior
deficiency and, 261-263, 261-
263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-249,
249f, 250f (V3)
geometry of treatment design using
constructed maxillomandibular
triangle in, 261f, 261-262 (V3)
linear dimensions between maxillary
length and vertical facial height
in, 250, 250f (V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-268
(V3)
Rotational flap in hair replacement,
655, 655f, 656f (V3)
Roxithromycin, 389, 389t (V1)
RSBI; See Rapid shallow breathing
index
RSI; See Rapid-sequence intubation
Ruby laser
for hair removal, 251-252 (V1)
for tattoo removal, 251 (V1)
Ruffini’s corpuscle, 962 (V2)
Rule of nines, 321 (V2)
Rule of tens in cleft lip repair, 718, 735
(V3)
RVU; See Relative value unit
S of jaws, 680-704 (V2)
S corporation, 285-286, 286t (V1)
S-100 immunohistochemical marker for
melanoma, 752t (V2)
Saethre-Chotzen syndrome, 909 (V3)
craniosynostosis in, 852f, 874 (V3)
functional considerations in, 880-881
(V3)
Le Fort III osteotomy for midface
deformity in, 205-206 (V3)
Safety in laser therapy, 242b, 242f, 242-
243, 243f (V1), 515-516 (V3)
Sagittal osteotomy in inferior alveolar
nerve repair, 266f, 270 (V1)
Sagittal split ramus osteotomy, 70, 70f
(V3)
intraoperative complications in, 423-
433 (V3)
bleeding in, 429-431, 433f (V3)
minor technical difficulties in, 433
(V3)
nerve injury in, 426-429, 432f
(V3)
proximal segment malpositioning
in, 431-432 (V3)
relapse in, 445, 446f (V3)
unfavorable osteotomy in, 423-426,
424-434f (V3)
mandibular relapse in, 445, 446f (V3)
nerve injury in, 444-445 (V3)
pediatric, 858 (V3)
postoperative hematoma in, 442 (V3)
in rotation of maxillomandibular
complex, 268, 268f, 269f (V3)
transoral vertical ramus osteotomy
versus, 119, 120t, 121 (V3)
in two-jaw surgery, 240 (V3)
Sagittal suture, 865f (V3)
Sagittal suture craniosynostosis, 868,
869-870f (V3)
Salaried position, 290 (V1)
Salicylates, 887t (V2)
Salicylic acid derivatives, 84t (V1)
Salivary duct carcinoma, 784 (V2)
Salivary fistula, rhytidectomy-related,
509 (V3)
Salivary gland, 539-556 (V2)
acute suppurative infection of
submandibular gland and, 541-
542, 542f (V2)
acute suppurative parotitis and, 540-
541, 541f, 542f (V2)
chronic obstructive sialoadenitis and,
545-546, 547f (V2)
cystic conditions of, 539, 540f (V2)
cytomegalovirus infection of, 543
(V2)
HIV-related infection of, 543 (V2)
mumps and, 542 (V2)
sialolithiasis and, 543-545, 544-547f
(V2)
systemic disease associated with
disease of, 555-556 (V2)
trauma to, 294, 318-320, 320f (V2)
Salivary gland tumors, 546-555 (V2)
benign, 547-549, 549-551f (V2)
chemotherapy for, 783-785, 785f
(V2)
high-grade malignant, 549-550, 552f
(V2)
low-grade malignant, 549 (V2)
lymphoma in, 763 (V2)
nonsalivary, 550-555, 553-556f
(V2)
parotid gland, 546-547, 548f (V2)
pediatric, 987-988 (V3)
Salivary pellicle, 611 (V2)
Salpingopharyngeus muscle,
831t (V3)
SAM Occlusal Plane Indicator, 277,
365 (V3)
SAME; See Surgically assisted maxillary
expansion
Same lingual-opposite buccal rule, 196
(V1)
Sanders classification of dentoalveolar
injury, 110-111, 112b (V2)
Sarcoidosis, 556 (V2)
Sarcoma, 986-987, 988-990f (V3)
chondrosarcoma in, 684f, 684-685
(V2)
Ewing’s sarcoma in, 687, 688f, 689f
(V2)
mandibular approaches in, 699-
702, 701f, 702f (V2)
maxillectomy in, 692-699, 694f,
695f, 697-699f (V2)
metastatic tumors to jaw and, 687-
689 (V2)
multiple myeloma and, 685-687,
686f, 687f (V2)
osteosarcoma in, 680-684, 681f,
682f (V2)
patient evaluation in, 689-692,
690t, 691f (V2)
radiation-induced, 685 (V2)
odontogenic, 532-533 (V2)
radiation therapy in, 767 (V2)
rhabdomyosarcoma, 984-986, 987f
(V3)
Sartorius muscle, anterolateral thigh
flap and, 335f (V2)
Saturation monitoring, 39 (V2)
Scaling and root planing, laser-assisted,
255 (V1)
Scalp
anatomy of, 182 (V2)
reconstructive flap options for, 336b
(V2)
reduction of, 655, 656f (V3)
trauma to, 58-59, 323-324, 324f, 325f
(V2)
initial assessment of, 50 (V2)
management of, 292, 293-294f
(V2)
reconstruction in, 346 (V2)
Scapha, 666 (V3)
Scapha-conchal angle, 665 (V3)
Scaphal buckling, 676 (V3)
Scaphocephaly, 868, 869-870f (V3)
Scaphoid fossa of external ear, 667f
(V3)
Scar revision, laser-assisted, 250 (V1)
Scarring
after repair of zygomatic fracture, 195
(V2)
chemical peel and, 664, 664f (V3)
in cleft palate repair, 769-770 (V3)
in epidermolysis bullosa, 627 (V2)
in eyelid avulsive laceration, 311f
(V2)
in facial soft tissue injury, 298-299
(V2)
laser skin resurfacing of, 529 (V3)
laser skin resurfacing-related, 542-
543, 543f (V3)
medications for, 410 (V3)
in otoplasty, 676 (V3)
in rhytidectomy, 509, 509f (V3)
secondary cleft lip scar revision and,
841, 843f (V3)
ulcerated cutaneous hemangioma
and, 580 (V2)
Schirmer test, 589 (V3)
Schneiderian membrane elevation
in sinus-lift subantral augmentation,
460-462f (V1)
in zygomatic implant, 494, 494f (V1)
Schobinger clinical staging system for
arteriovenous malformations, 589
(V2)
Schoenrock analysis for malar implant,
690t (V3)
School attendance after surgery, 411
(V3)
Schultz, Louis, 795 (V2)
Schwannoma, 601-602, 603f (V2)
Schwartz, Laszlo, 795 (V2)
Schweckendiek two-stage palate
repair for cleft palate,
776-778 (V3)
Scintigraphy in temporomandibular
disorders, 843-845 (V2)
Scleral buckle in orbital fracture, 213,
213b (V2)
Scleral rupture, 83, 83f (V2)
Scleroderma
facial asymmetry in, 309 (V3)
temporomandibular joint
involvement in, 865-866 (V2)
Sclerosing basal cell carcinoma, 725
(V2)
Sclerotherapy
in arteriovenous malformation, 589
(V2)
in lymphatic malformation, 582 (V2)
in venous malformation, 587, 587f
(V2)
Screening
for oral cavity cancer, 708 (V2)
for skin cancer, 730t, 730-733, 731b,
731-733t (V2)
for temporomandibular disorders,
824, 824t (V2)
Screw fixation
in bilateral sagittal split osteotomy,
109, 110f (V3)
at bone graft site, 420, 420f (V1)
in chin implant for facial skin laxity
with weight loss, 688 (V3)
in cleft orthognathic surgery, 819
(V3)
in complete mandibular subapical
osteotomy, 158, 160f, 168f, 170f
(V3)
in genioplasty, 143, 145f (V3)
in implant placement in onlay bone
graft, 424, 424f (V1)
in mandibular lengthening by
distraction osteogenesis, 343f
(V3)
in mandibular symphysis bone graft
harvest, 412f (V1)
in modified Le Fort III osteotomy,
211-212 (V3)
for orthodontic mechanics, 225 (V1)
Screw system for orthodontic skeletal
anchorage, 225f, 225-226, 233-235
(V1)
Scroll, 556, 556f (V3)
Sculptra, 631, 631f (V3)
SDE; See Slow dentoalveolar expansion
SDI; See Small diameter implant
Sebaceous apparatus, 10 (V3)
Sebaceous gland carcinoma, 727, 727f
(V2)
Seborrheic keratosis, 518 (V3)
Second intention healing, 62 (V3)
Second molar
bilateral sagittal split osteotomy and,
106-108 (V3)
impacted, 171 (V1)
Secondary bone healing, 144-146, 146f
(V2)
Secondary cleft lip and palate
reconstruction, 828-847 (V3)
bone graft reconstruction of cleft
maxilla and palate in, 840 (V3)
complications of, 839 (V3)
comprehensive dental and prosthetic
rehabilitation in, 841-843, 844-
845f (V3)
fistula closure in, 828-831, 830f, 832-
834f (V3)
for management of submucous cleft
palate, 839-840 (V3)
for management of velopharyngeal
dysfunction, 831t, 831-835, 835f
(V3)
operative techniques in, 836-839,
837f, 838f (V3)
orthognathic surgery for correction of
midfacial deficiency in, 840
(V3)
reconstruction of cleft nasal
deformity in, 840-841, 842f
(V3)
secondary surgery for cleft lip scar
revision in, 841, 843f (V3)
timing and indications for, 835-836
(V3)
Secondary herpes, 613-614 (V2)
Secondary hyperalgesia, 140 (V1)
Secondary osteosarcoma, 663 (V2)
Secondary palate, 723, 828 (V3)

Secondary reconstruction
in avulsive wound, 289 (V2)
in orbital fracture, 233-236, 233-236f
(V2)
in periorbital soft tissue injury, 306,
307f (V2)
Secondary surgery
in iatrogenic facial asymmetry, 294
(V3)
in trigeminal nerve injury, 267 (V1)
in velopharyngeal dysfunction after
cleft surgery, 801-802 (V3)
Secondary survey, 40 (V2)
adjuncts to, 40-41 (V2)
comprehensive patient care and, 396-
397 (V2)
in cranio-maxillofacial trauma, 8
(V2)
Second-degree burn, 322t (V2)
Sectioning of tooth
impacted third molar and, 205-206,
207-210f (V1)
in simple extraction, 194-195, 195f,
196f (V1)
Security system of office, 359 (V1)
Sedation
benzodiazepines and, 57 (V1)
in cervicofacial liposuction, 621 (V3)
correlation of BIS value with level of,
73, 73t (V1)
goals of, 67-68 (V1)
intensive care unit and, 47 (V2)
in laser skin resurfacing, 521 (V3)
levels in anesthesia, 67 (V1)
patient-controlled, 74 (V1)
pediatric, 67-68, 93-111 (V1)
airway equipment preparation for,
100t, 100-102 (V1)
anaphylaxis and, 107t, 107 (V1)
bronchospasm and, 107 (V1)
carbon dioxide monitoring during,
28 (V1)
cardiovascular system and, 93-94,
94t (V1)
developmental pharmacology and,
96-97 (V1)
fentanyl for, 104 (V1)
gastric contents aspiration and,
107 (V1)
inhalation anesthesia for, 104-105
(V1)
intraoperative fluids and, 102-103
(V1)
intravenous access and, 102, 102f
(V1)
ketamine for, 104 (V1)
laryngospasm and, 106-107 (V1)
liver function and, 96 (V1)
malignant hyperthermia and, 107-
108 (V1)
midazolam for, 103-104 (V1)
monitoring during, 99-100 (V1)
Pediatric Anesthesia Worksheet
for, 101b (V1)
preanesthetic assessment and, 97-
99, 98f (V1)
premedication for fear and anxiety
in, 103 (V1)
propofol for, 104, 105t (V1)
renal system and, 96 (V1)
respiratory system and, 94-96, 95f,
96t (V1)
techniques for, 105-106 (V1)
thermoregulation and, 96 (V1)
Sedative-hypnotics, 60-62, 62t (V1)
anaphylaxis in pediatric anesthesia
and sedation and, 107t (V1)
Seddon classification of nerve injury,
216, 260t, 260-261 (V1)
Segmental maxillary osteotomy, 66-67,
67f, 192-204 (V3)
ambulatory, 494 (V3)
arch wire change and, 400 (V3)
complications in, 198, 198f, 199f,
472-473 (V3)
historical background of, 192 (V3)
indications for, 192-193 (V3)
for maxillary deficiency, 199-203f
(V3)
Segmental maxillary osteotomy
(Continued)
model surgery and, 369-370, 370f
(V3)
osteotomy design in, 196 (V3)
postoperative care in, 196-197, 197f
(V3)
surgical planning in, 197-198 (V3)
surgically assisted maxillary
expansion versus, 233-235 (V3)
technique in, 193-196, 194-196f
(V3)
in transverse maxillary deficiency,
224 (V3)
unfavorable interdental osteotomy in,
473-474f (V3)
Seizure
ambulatory orthognathic surgery and,
493 (V3)
perioperative management of, 388
(V3)
preoperative evaluation of, 18, 18t
(V1)
Selective neck dissection, 719, 719t
(V2)
Selective serotonin reuptake inhibitors
for burning mouth syndrome, 996
(V2)
for chronic facial pain, 973, 973t
(V2)
interaction with local anesthetics
with vasoconstrictors, 42t, 42-43
(V1)
for myofascial pain, 144 (V1)
for posttraumatic headache, 153 (V1)
for temporomandibular disorders,
888, 889t (V2)
Self-care in temporomandibular
disorders, 984, 984b (V2)
Self-employed pension plan, 287 (V1)
Self-healing histiocytosis, 567 (V2)
Self-report of incident, 375 (V1)
Sella to anterior nasal spine, 38 (V3)
Sella to basion, 26 (V3)
Sella to gnathion, 55 (V3)
Sella to gonion, 56 (V3)
Sella to nasion
neurocranial growth value, 25 (V3)
Treacher Collins syndrome and, 938
(V3)
Sella to posterior nasal spine, 39 (V3)
Sellick maneuver, 30 (V2)
Semiadjustable articulator in model
surgery, 364-365, 365f (V3)
Semi-rigid fixation in mandibular
fracture, 155 (V2)
Semmes-Weinstein test, 140 (V1)
Sensitization, chronic pain and, 137-
138 (V1)
Sensorineural hearing loss, head injury-
related, 52 (V2)
Sensory disturbances
postoperative, 405 (V3)
in endoscopic forehead and brow
lift, 607 (V3)
orthognathic surgery-related, 75-76
(V3)
in rhytidectomy, 508 (V3)
in trichophytic forehead and brow
lift, 607 (V3)
in trigeminal neuralgia, 991 (V2)
Sensory examination in head injury, 51,
52 (V2)
Sensory reeducation after trigeminal
nerve repair, 271 (V1)
Sentinel lymph node biopsy
in malignant melanoma, 754 (V2)
in skin cancer, 737-738 (V2)
Sentinel vein, 596, 598 (V3)
Sepsis, laser skin resurfacing-related,
544 (V3)
Septal branch of posterior ethmoidal
artery, 556f (V3)
Septal branch of superior labial artery,
556f (V3)
Septal cartilage, 173f (V3)
Septal fracture, 275f, 275-281 (V2)
Septal hematoma, 273-274, 274f, 281-
282 (V2)
Septic arthritis of temporomandibular
joint, 861-864, 862-863f (V2)
Septoplasty
in closed rhinoplasty, 572 (V3)
in open rhinoplasty, 570, 571 (V3)
Septorhinoplasty, 280, 281f (V2)
Serax; See Oxazepam
Seroma, 195 (V2)
Seronegative spondylitis, 860-861 (V2)
Serotonin, chronic facial pain and, 962,
963f (V2)
Sertraline
for burning mouth syndrome, 996
(V2)
for chronic facial pain, 973t (V2)
for myofascial pain, 144 (V1)
for posttraumatic headache, 153 (V1)
for temporomandibular disorders,
889t (V2)
Serum albumin, 390-391 (V3)
Serum potassium, 387 (V3)
Serum prealbumin, 390 (V3)
Severe closed head injury, 57-58 (V2)
Sevoflurane, 64t, 65, 105 (V1)
Shaded-surface display in facial injury,
92-93 (V2)
Shave biopsy in skin cancer, 731-732
(V2)
Shield graft, 563-564, 564f (V3)
Shock, trauma-related, 6-7, 7t, 70 (V2)
intensive care unit and, 44 (V2)
primary survey and, 37-38, 38f, 38t
(V2)
Showering after surgery, 411 (V3)
Shprintzen syndrome, 769 (V3)
Shredder, 361 (V1)
Sialolith excision, laser-assisted, 245
(V1)
Sialolithiasis, 543-545, 544-547f (V2)
Sicher, Harry, 793 (V2)
Sickle cell crisis, 385 (V3)
Sickle cell disease, 15-16 (V1), 385
(V3)
Sideburns, rhytidectomy and, 502, 502f
(V3)
Silhouette Suture, 695, 696t (V3)
Silicone impression materials,
527 (V1)
Silicone sheet for guided bone
regeneration, 429 (V1)
Silikon 1000, 640 (V3)
Silk suture, 287t (V2)
Silon TSR in laser skin resurfacing,
524, 528 (V3)
Silver and Guilden analysis for malar
implant, 690t (V3)
Simon’s method of nasal projection,
558 (V3)
SimPlant Master, 557-558, 557-559f
(V1)
Simple bone cyst, 869 (V2)
Simple exodontia, 185-192 (V1)
complications in, 191-192 (V1)
diagnosis and treatment planning in,
187 (V1)
indications for, 186-187 (V1)
pain management in, 192 (V1)
principles of, 187-190, 188-190f (V1)
socket preservation and wound
closure in, 190-191 (V1)
Simple fracture, mandibular, 99, 99f
(V2)
Simple hinge articulator in model
surgery, 364-365, 365f (V3)
Simple interrupted suture, 288f (V2)
Simple lentigines, 518 (V3)
Simple running suture, 288f (V2)
Simplex form of epidermolysis bullosa,
626-627 (V2)
Sinequan; See Doxepin
Single kidney, perioperative
management of, 387 (V3)
Single photon emission computed
tomography
in chronic facial pain, 966 (V2)
in temporomandibular disorders, 845
(V2)
Single-pass resurfacing, 529-532, 533-
534f (V3)
INDEX I-85
Single-word speech intelligibility test,
797 (V3)
Sinus bone grafting, 422-424, 423f (V1)
mandibular symphysis for, 409-411,
410-412f (V1)
Sinus disease
effect of Le Fort 1 osteotomy on, 65
(V3)
maxillary osteotomy and, 76 (V3)
Sinus obliteration in frontal sinus
fracture, 263-264, 264f, 265f (V2)
Sinusitis
after Le Fort 1 osteotomy, 65 (V3)
chronic orofacial pain in, 116 (V1)
trauma resuscitation process and, 71-
72 (V2)
zygomatic implant-related, 498 (V1)
Sinus-lift subantral augmentation, 458-
470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic considerations
in, 458-459 (V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f, 464f
(V1)
elevation of schneiderian membrane
in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
trephine core membrane elevation in,
464-468, 464-468f (V1)
vascular supply, lymphatic drainage,
and innervation in, 459 (V1)
Sixth cranial nerve palsy, 85 (V2)
Sj[um]ogren’s syndrome, 551, 556 (V2)
facial asymmetry in, 309 (V3)
temporomandibular joint
involvement in, 866 (V2)
Skeletal anchorage for orthodontics,
223-236 (V1)
basic orthodontic mechanics and,
224-225 (V1)
bone plates in, 232-233, 233f, 234f
(V1)
for closure of anterior open bite, 232
(V1)
devices for, 225f, 225-226, 226f (V1)
historical perspective of, 223-224
(V1)
mesial or distal movement of teeth
and, 226-231f (V1)
miniimplants in, 570-574, 572-574f
(V1)
miniscrews in, 233-235 (V1)
orthopedic growth modification and,
232 (V1)
outcomes and complications in, 235-
236 (V1)
postoperative regimen in, 234-235
(V1)
for uprighting and intruding molar
teeth, 232 (V1)
Skeletal facial deformity
in cleft lip and palate, 815, 815b,
816-817f (V3)
combined maxillary and
mandibular osteotomies for,
238-247 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
I-86 INDEX
Skeletal facial deformity (Continued)
considerations in pediatric
craniomaxillary surgery, 848-863
(V3)
clinical evaluation of craniofacial
growth and, 856 (V3)
concepts of craniofacial skeletal
growth and development and,
849f, 849t, 849-850, 850t
(V3)
cranio-orbital dysmorphology and,
856-858 (V3)
cranium and, 850-851, 852f (V3)
mandible and, 855-856, 856f, 857f
(V3)
mandibular hyperplasia and, 859-
860, 860f (V3)
mandibular hypoplasia and, 858-
859, 859f (V3)
maxilla and, 851, 854f, 855f (V3)
maxillary hypoplasia and, 860-861
(V3)
orbits and, 851, 853f (V3)
vertical maxillary excess and, 861f,
861-862 (V3)
zygoma and, 851, 853f (V3)
Le Fort III osteotomy for, 205-218
(V3)
for craniofacial dysostosis, 205-206
(V3)
indications for, 205 (V3)
for midface deficiency, 206, 207-
210f (V3)
modified, 211-218 (V3)
subcranial, 210-211, 212-217f (V3)
technique in, 206-210 (V3)
occlusal plane rotation for, 248-271
(V3)
clockwise rotation in, 252-256,
252-256f (V3)
counterclockwise rotation in, 256-
260, 257-263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-
249, 249f, 250f (V3)
geometry of treatment design using
constructed
maxillomandibular triangle in,
261f, 261-262 (V3)
linear dimensions between
maxillary length and vertical
facial height in, 250, 250f
(V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
stretching of soft tissues in, 267-
268 (V3)
Skeletal facial evaluation, 10-17 (V3)
cephalometric evaluation form for,
15b (V3)
changes with age and, 15-17, 17f
(V3)
dental relations in, 14-15,
16f (V3)
skeletal relations in, 12-14, 13-15f
(V3)
soft tissue relations in, 11-12, 12f
(V3)
Skeletal nasal width, 35 (V3)
Skelid; See Tiludronate
Skin
ABCDE and P method of evaluation,
750 (V2)
abnormal healing of, 22 (V2)
of eyelid, 582f, 582 (V3)
facial; See Facial skin
laser resurfacing of, 513-552 (V3)
anesthesia and, 521, 522f (V3)
Skin (Continued)
carbon dioxide laser in, 514f, 514-
516, 515f (V3)
contact dermatitis and, 539 (V3)
dyschromias and, 541-542, 542f,
543f (V3)
erbium:YAG laser in, 532-534,
536-538f (V3)
fractional photothermolysis in,
532, 536f (V3)
history of, 513-514 (V3)
infection and, 540-541, 541f (V3)
laser blepharoplasty with, 544-545,
545-547f (V3)
laser properties in, 514f, 514-516,
515f (V3)
laser settings for, 521-522, 522f
(V3)
milia and acne formation and,
539-540, 540f (V3)
ocular complications in, 543-544
(V3)
patient evaluation in, 516-519,
518b (V3)
postoperative care in, 524-529,
526-528f, 530-531f (V3)
preoperative considerations in, 519
(V3)
prolonged erythema and, 535-537,
539f (V3)
pruritus and, 537-538, 539f (V3)
resurfacing acne scars in, 529 (V3)
rhytidectomy with, 545-548, 547-
548f (V3)
scarring and, 542-543, 543f (V3)
sepsis and, 544 (V3)
single-pass resurfacing in, 529-532,
533-534f (V3)
skin preparation for, 519-521 (V3)
telangiectasias and, 538-539 (V3)
traditional technique in, 522-524,
523f, 525-526f (V3)
traumatic and surgical scars
improvement in, 529 (V3)
treatment of benign skin lesions
in, 529 (V3)
nasal, 270 (V2), 559-560 (V3)
Skin biopsy
in dermatofibrosarcoma protuberans,
728 (V2)
in malignant melanoma,
753 (V2)
in skin cancer, 731f, 731-732, 732f
(V2)
Skin cancer
melanoma, 749-757 (V2)
diagnosis of, 752t, 752-754, 753f,
753t (V2)
epidemiology of, 749, 750b (V2)
incidence and etiology of, 749-750,
750b, 750t, 750-752f, 751t
(V2)
management of regional disease in,
754 (V2)
staging of, 754-755, 755t (V2)
treatment of, 755-756 (V2)
non-melanoma, 724-748 (V2)
aggressive behavior of, 728-730,
729f (V2)
basal cell carcinoma in, 725, 725f
(V2)
cryotherapy for, 734 (V2)
curettage/electrodesiccation in,
734, 735f (V2)
dermatofibrosarcoma protuberans
in, 727-728, 728f (V2)
epidemiology and etiology of, 724-
725 (V2)
laser ablation and resurfacing in,
734-735 (V2)
laser-assisted procedures for, 248,
249t (V1)
of lip, 742-744, 743f (V2)
lymph node involvement in, 737-
739 (V2)
Merkel cell carcinoma in, 727
(V2)
microcystic adnexal carcinoma in,
726-727, 727f (V2)
Skin cancer (Continued)
Mohs’ micrographic surgery in,
735-736, 736b, 736f (V2)
photodynamic therapy for, 741
(V2)
physical examination in, 730t,
730-733, 731b, 731-733t (V2)
radiation therapy in, 741-742 (V2)
sebaceous gland carcinoma in, 727,
727f (V2)
squamous cell carcinoma in, 725-
726, 726f (V2)
staging of, 733-734 (V2)
systemic and topical medications
for, 739-741 (V2)
traditional surgical excision in,
736-737 (V2)
Skin conditioner, laser skin resurfacing
and, 250 (V1)
Skin creep, 738 (V2)
Skin graft
in internal derangement of
temporomandibular joint, 938-
939, 939f (V2)
for maxillectomy-related defect, 696,
697f (V2)
postauricular, 297f (V2)
in skin cancer, 739 (V2)
Skin lesions
laser skin resurfacing and
as complication of, 529 (V3)
preoperative evaluation in, 518
(V3)
laser therapy for, 251 (V1)
Skin preparation
for chemical peel, 663 (V3)
for laser skin resurfacing, 519-521
(V3)
Skin resurfacing, 513-552 (V3)
botulinum toxin in, 658-661 (V3)
contraindications and adverse
effects of, 661, 662f (V3)
history and pharmacology of, 658
(V3)
preparations of, 658-659, 659t
(V3)
treatment technique for, 660-661,
661f (V3)
uses in facial cosmetics, 659f, 659-
660, 660f (V3)
carbon dioxide laser in, 521-532
(V3)
anesthesia and, 521, 522f (V3)
fractional photothermolysis in,
532, 536f (V3)
laser properties in, 514f, 514-516,
515f (V3)
laser settings for, 521-522, 522f
(V3)
postoperative care in, 524-529,
526-528f, 530-531f (V3)
resurfacing acne scars in, 529 (V3)
single-pass resurfacing in, 529-532,
533-534f (V3)
traditional technique in, 522-524,
523f, 525-526f (V3)
traumatic and surgical scars
improvement in, 529 (V3)
treatment of benign skin lesions
in, 529 (V3)
complications of, 534-544 (V3)
contact dermatitis in, 539 (V3)
dyschromias in, 541-542, 542f,
543f (V3)
infection in, 540-541, 541f (V3)
milia and acne formation in, 539-
540, 540f (V3)
ocular, 543-544 (V3)
prolonged erythema in, 535-537,
539f (V3)
pruritus in, 537-538, 539f (V3)
scarring in, 542-543, 543f (V3)
sepsis in, 544 (V3)
telangiectasias in, 538-539 (V3)
erbium:YAG laser in, 532-534, 536-
538f (V3)
history of, 513-514 (V3)
intrinsic and extrinsic aging and, 513
(V3)
Skin resurfacing (Continued)
laser blepharoplasty with, 544-545,
545-547f (V3)
laser-assisted, 249-250 (V1)
patient evaluation in, 516-519, 518b
(V3)
preoperative considerations in, 519
(V3)
rhytidectomy with, 545-548, 547-
548f (V3)
skin preparation for, 519-521 (V3)
Skin slough in rhytidectomy, 507f, 508,
509f (V3)
Skip lesion, 730 (V2)
Skull
cloverleaf anomaly of, 909-914, 910-
914f (V3)
osteoma of, 605 (V2)
pediatric, 352, 353f (V2), 849f (V3)
Skull base ameloblastoma, 964f (V3)
Skull base osteotomy, 884 (V3)
Skull fracture
initial assessment of, 50 (V2)
management of, 59-60 (V2)
orbital fracture and, 212 (V2)
types of, 59 (V2)
Skull radiography in head injury, 57b
(V2)
Sleep apnea, 316-337 (V3)
in craniofacial dysostosis syndromes,
881 (V3)
Delaire cephalometric analysis in,
321-323, 325-327f (V3)
diagnosis and treatment planning in,
319-321, 322-324f (V3)
laser therapy in, 252-253 (V1)
mandibular lengthening by
distraction osteogenesis for, 342-
346, 342-346f (V3)
maxillary and mandibular
advancement for, 323-330, 327-
332f (V3)
pathophysiology of, 316-318, 318f
(V3)
patient outcomes in, 330-336, 333-
335f (V3)
treatment options for, 318-319, 320-
322f (V3)
Sleep dysfunction, chronic head and
neck pain and, 141 (V1)
Sleep study for sleep apnea, 252 (V1)
Sleeping after surgery, 412 (V3)
Slit-lamp examination
in eye surface injury, 78 (V2)
in orbital fracture, 209 (V2)
SLNB; See Sentinel lymph node biopsy
SLOB rule, 167, 168f, 196 (V1)
Slow dentoalveolar expansion in
transverse maxillary deficiency,
223-224 (V3)
Slow-flow vascular malformations, 581-
588 (V2)
capillary malformation in, 581, 581f
(V2)
lymphatic malformation in, 581-583,
582-585f (V2)
venous malformation in, 585-588,
586-588f (V2)
Small diameter implant, 567-574, 568f
(V1)
for orthodontic anchorage, 570-574,
572-574f (V1)
for pontic support of fixed partial
denture, 568 (V1)
for retention of obturators, 568-569
(V1)
for single-tooth implant restoration
in narrow space, 569, 570f, 571f
(V1)
for stabilization of complete dentures,
567-568, 569f (V1)
for stabilization of removable partial
dentures, 568 (V1)
Small-cell osteosarcoma, 682 (V2)
Smell, orthognathic surgery-related
changes in, 74 (V3)
Smile evaluation, 273f (V3)
Smokeless tobacco, oral cavity cancer
and, 706 (V2)

Smoking
anesthesia and, 70-71 (V1)
extrinsic aging of skin and, 513 (V3)
impaired healing and, 419 (V3)
interaction with estrogen, 398 (V1)
oral cavity cancer and, 706 (V2)
postoperative infection and, 443
(V3)
preoperative evaluation of, 4-5 (V1)
pulmonary complications in geriatric
patient and, 383 (V2)
squamous cell carcinoma and, 777
(V2)
Smoking cessation
in autogenous bone graft for implant,
422 (V1)
cardiopulmonary complications and,
384 (V3)
in guided tissue regeneration, 429
(V1)
in rhytidectomy, 499 (V3)
in sinus-lift subantral augmentation,
462 (V1)
in total maxillary segmental
osteotomy, 196-197 (V3)
Snake bite, 315-316 (V2)
Snap and distraction test, 588, 589f
(V3)
Snapping jaw, 790-791, 791f (V2)
Snellen chart, 74, 75 (V2)
SNODENT; See Systemized
Nomenclature of Dentistry
SNOMED; See Systemized
Nomenclature of Medicine
Snoring, laser therapy for, 252-253
(V1)
Soap bubble myxoma, 969f (V3)
SOAP charting, 380 (V1)
Social factors in perioperative patient
management, 391 (V3)
Social history
of geriatric patient, 379-380 (V2)
in rhytidectomy, 498 (V3)
Societal considerations in trauma, 408,
410-411 (V2)
Socket preservation in basic exodontia,
190-191 (V1)
Socket wall fracture, 115t, 126 (V2)
Sodium channels, central sensitization
and, 963 (V2)
Sodium hyaluronate, 914-915 (V2)
Sodium lauryl sulfate, 611 (V2)
Sodium thiopental, 30 (V2)
Soft diet after surgery, 408 (V3)
Soft Form lip implant, 693 (V3)
Soft palate
Beh[ced]cet’s syndrome and, 621
(V2)
embryology of, 701-705, 704t (V3)
herpangina of, 617t, 617-618 (V2)
Soft splint, 883, 884f (V2)
Soft tissue
assessment in implant surgery
autogenous bone graft and, 408,
408f, 409f (V1)
health considerations and, 479,
480f (V1)
carbon dioxide laser properties and,
514f, 514-516, 515f (V3)
changes in Le Fort I osteotomy, 184-
185, 185-188f (V3)
facial skeleton evaluation and, 11-12,
12f (V3)
interference in maxillary
repositioning in Le Fort I
osteotomy, 470-471, 471f (V3)
nasal, 270-273, 272f, 273f (V2)
readaptation in naso-orbital-
ethmoid fracture, 248,
249f (V2)
trauma to, 301, 302-305f (V2)
platelet-rich plasma for healing of,
501-510 (V1)
allograft and alloplastic
materials and, 504f, 504-506
(V1)
benefits of, 502-503 (V1)
case report of, 509, 509f (V1)
concept of, 501-502, 502f (V1)
Soft tissue (Continued)
processing of, 506-508, 507f, 508f
(V1)
positioning of injectable filler in,
631f, 631-632, 632f (V3)
prediction of changes in orthognathic
surgery and, 372-381 (V3)
cephalometric, 372-375, 373f (V3)
computerized-video imaging, 375-
377, 376f (V3)
photographic, 375 (V3)
three-dimensional computer-
assisted, 377-379, 378f (V3)
Treacher Collins syndrome and
deformities in, 938 (V3)
reconstruction and, 955, 955f (V3)
Soft tissue dissection
in bilateral sagittal split osteotomy,
102-106, 106f (V3)
in forehead and brow lift
endoscopic, 603-605 (V3)
trichophytic, 612-613 (V3)
in genioplasty, 141, 141f (V3)
in Le Fort I osteotomy, 65-66, 176,
176f (V3)
in Le Fort III osteotomy, 206-210
(V3)
in modified Le Fort III osteotomy,
211 (V3)
in subcranial Le Fort III osteotomy,
210-211 (V3)
Soft tissue injuries, 283-326 (V2)
abrasion in, 289 (V2)
after repair of zygomatic fracture, 195
(V2)
from air bag device blast, 313, 314f,
315f (V2)
anatomic considerations in, 283,
284t, 285f (V2)
anesthesia for, 284 (V2)
avulsive wounds in, 289-290, 290f,
291f (V2)
bite wounds in, 290-292, 292f, 313-
316, 314-317f (V2)
burn-related, 321-323, 321-323f, 322t
(V2)
of cheek, 320f, 320-321, 321f (V2)
closure of, 284, 285f, 288f (V2)
in condylar fracture, 166-168, 170
(V2)
of ear, 294, 297f, 310-313, 312f, 313f
(V2)
of eyelid and nasolacrimal apparatus,
292-294, 295f, 296f (V2)
initial evaluation and early
management of, 283, 284f (V2)
laceration in, 289, 290f (V2)
in Le Fort fracture, 253 (V2)
of lip, 294, 298f (V2)
nasal, 301, 302-305f (V2)
of neck, 94-95, 96f, 294, 316-318,
318f (V2)
of parotid gland, 294, 318-320, 320f
(V2)
pediatric, 292, 293f, 371f, 372 (V2)
periorbital, 301-310, 306-311f (V2)
of peripheral nerves, 318, 319f (V2)
reconstruction in avulsive facial
injury, 327-351 (V2)
Abbe flap in, 329, 330f (V2)
aesthetic and prosthetic
rehabilitation and, 346-350f
(V2)
airway management in, 327 (V2)
anterolateral thigh free flap in,
335, 335f (V2)
cervicofacial flap in, 329-330, 333f
(V2)
of cheek defects, 344, 345-348f
(V2)
clinical examination in, 327-328
(V2)
debridement in, 328 (V2)
facial artery musculomucosal flap
in, 329 (V2)
fibular free flap in, 333-335, 335f
(V2)
imaging in, 328 (V2)
of lip defects, 343f, 343-344 (V2)
Soft tissue injuries (Continued)
of lower face and mandible, 335-
340f, 336-337 (V2)
of nasal defects, 337, 343 (V2)
paramedian forehead flap in, 329,
331-332f (V2)
pectoralis major myocutaneous flap
in, 330-331 (V2)
radial forearm flap in, 332-333,
334f (V2)
rectus abdominis free flap in, 335
(V2)
of scalp defects, 346 (V2)
submental island flap in, 331-332,
334f (V2)
temporoparietal fascia flap in, 330
(V2)
wound assessment in, 317, 328f
(V2)
of scalp, 292, 293-294f, 323-324,
324f, 325f (V2)
suture materials for, 284-289, 286-
287t (V2)
wound care in, 294-299 (V2)
Soft tissue procedures
around implants, 479-490 (V1)
aesthetic considerations and, 479-
480, 480t, 481f (V1)
AlloDerm in, 486, 487f (V1)
connective tissue grafting in, 485,
485f, 486f (V1)
epithelialized free-gingival grafting
in, 483f, 484-485 (V1)
gingivectomy in, 481-484, 484f,
485f (V1)
modified roll tissue graft in, 486,
488f (V1)
papilla regeneration technique in,
487-489, 489f (V1)
pediculated connective tissue graft
in, 486 (V1)
soft tissue health considerations
and, 479, 480f (V1)
laser-assisted, 244-245, 254-255
(V1)
in pediatric dentoalveolar surgery,
173-174, 173-176f (V1)
Solar elastosis, 513 (V3)
Solar lentigines, 518 (V3)
Solar radiation exposure
extrinsic aging and, 513 (V3)
history in laser skin resurfacing, 517
(V3)
lip cancer and, 743 (V2)
malignant melanoma and, 749 (V2)
skin cancer and, 724, 726 (V2)
Sole proprietorship, 285-286, 286t (V1)
Solid ameloblastoma, 479-485, 494-
495f, 500-501 (V2)
Solo practice, 288 (V1)
Soma; See Carisoprodol
Somatic sensation evaluation in head
injury, 56 (V2)
Somatization, chronic head and neck
pain in, 141-142 (V1)
Sorafenib, 781t (V2)
Sore throat, laser-assisted
uvulopalatoplasty-related, 253
(V1)
Soy isoflavones, 400 (V1)
Space maintenance, guided bone
regeneration procedures and, 428-
429 (V1)
Space making, guided tissue
regeneration procedures and, 430-
431, 431f, 432f (V1)
Spatial relationships in nasal anatomy,
553, 554f (V3)
Special damages in malpractice lawsuit,
375 (V1)
Specialty board certification, 308 (V1)
SPECT; See Single photon emission
computed tomography
Speech
cleft lip and palate repair and, 719,
724-726, 791-805 (V3)
articulation and intelligibility and,
794-795 (V3)
articulation testing in, 797 (V3)
INDEX I-87
Speech (Continued)
dental and alveolar anomalies and,
791-792, 792t (V3)
intelligibility assessment and, 797
(V3)
lateral still cephalometry and, 797-
798 (V3)
multiview videofluoroscopy and,
798, 799f (V3)
nasal air emission and, 793-794
(V3)
nasal emission testing and, 796,
796f, 797b (V3)
nasometry and, 800-801, 801f (V3)
nostril pinch test and, 795-796
(V3)
perceptual rating scales and, 796-
797 (V3)
pressure-flow method of speech
assessment and, 798-800, 800f
(V3)
reduced intraoral air pressure and,
794 (V3)
resonance imbalance and, 793,
793f (V3)
velopharyngeal dysfunction and,
791, 792t, 801-803 (V3)
video nasoendoscopy and, 798
(V3)
vocal dysfunction and, 795 (V3)
cleft palate repair and, 761, 766-767,
767b, 774-775 (V3)
orthognathic surgery-related changes
in, 74-75 (V3)
Speech appliance, 802 (V3)
Speech therapy after cleft surgery, 802-
803 (V3)
Sphenoid bone, 469f (V3)
Sphenoid fontanel, 865f (V3)
Sphenoid process of zygoma, 182 (V2)
Sphenomandibular ligament, 162, 804-
805 (V2)
Sphenopalatine artery, 175f (V3)
maxilla and, 63, 63f, 66f (V3)
maxillary sinus and, 459 (V1)
nose and, 554, 555f (V3)
Sphenopalatine ganglion block
for cluster headache, 149 (V1)
for testing in chronic head and neck
pain, 141 (V1)
Sphincter pharyngoplasty, 802 (V3)
Sphygmomanometry, 24 (V1)
Spielberger State-Trait Anxiety
Inventory, 142 (V1)
Spiessl and Schroll classification of
condylar process fractures, 167,
168b (V2)
Spinal accessory nerve evaluation, 52
(V2)
Spinal radiography
in cervical spine injury, 63 (V2)
in initial assessment of trauma
patient, 41 (V2)
Spinal trigeminal nucleus caudalis, 961-
962 (V2)
Spinal trigeminal nucleus interpolaris,
961 (V2)
Spinal trigeminal nucleus oralis, 961
(V2)
Spindle cell ameloblastoma, 481f (V2)
Spindle cell carcinoma, 726 (V2)
Splenic marginal zone lymphoma, 760-
761 (V2)
Splint
in alveolar distraction, 349, 350f
(V3)
combined maxillary and mandibular
osteotomies and, 240f, 240-241,
241f (V3)
construction in model surgery, 368-
369, 369f, 370f (V3)
in dentoalveolar injury, 128-130,
129f (V2)
in internal derangement of
temporomandibular joint, 931,
941 (V2)
lingual, 148 (V2)
in nasal fracture, 278, 302f (V2)
in rhinoplasty, 573, 573f (V3)
I-88 INDEX
Splint (Continued)
surgical stabilizing, 397-399, 397-399f
(V3)
in temporomandibular disorders, 881-
885, 882b, 883f, 884f, 984-985
(V2)
Split-finger technique to improve
aesthetics of soft tissue around
implant, 489, 489f (V1)
Split-thickness skin graft in skin cancer,
739 (V2)
Spreader graft, 560, 560f (V3)
Squamous cell carcinoma, 705-723
(V2)
anatomy in, 705-706 (V2)
chemotherapy in, 777-788 (V2)
background of, 777, 778f (V2)
epidemiology and, 777 (V2)
epidermal growth factor receptors
and, 782-783, 783t (V2)
induction, 777-778 (V2)
for metastatic carcinoma, 778-781,
779t, 781t, 782t (V2)
salivary gland cancers and, 783-
785, 785f (V2)
taxanes in, 781-782 (V2)
diagnostic adjuncts in, 708-709, 709f
(V2)
genetic abnormalities in, 707-708
(V2)
of lip, 742-744, 743f (V2)
non-surgical management of, 710-713
(V2)
pretreatment evaluation in, 710 (V2)
radiation therapy in, 767-776 (V2)
altered radiation fractionation
schemes and, 772 (V2)
complications of, 773-774 (V2)
definitive radiotherapy and, 771
(V2)
histologies and, 767-768 (V2)
preoperative and postoperative,
771-772 (V2)
sites of disease and, 768t, 768-771,
769f, 770f, 770t, 771t (V2)
systemic therapy with, 772, 772t
(V2)
techniques in, 772-773, 773f (V2)
risk factors for, 706-707 (V2)
of salivary gland, 549-550, 552f (V2)
screening for, 708 (V2)
of skin, 725-726, 726f (V2)
staging of, 710, 711t (V2)
surgical management of, 713-720
(V2)
buccal mucosa cancer and, 714-
715, 715f, 716f (V2)
floor of mouth cancer and, 714,
714f, 715f (V2)
follow-up in, 719-720 (V2)
primary tumor and, 713-714 (V2)
retromolar trigone, alveolar ridge,
and palate cancer and, 716-
719 (V2)
tongue cancer and, 716-717, 716-
718f (V2)
types of neck dissection in, 719,
719t, 720f (V2)
trismus and, 899 (V2)
Squamous odontogenic tumor, 472f,
472-473, 531 (V2)
SSRO; See Sagittal split ramus
osteotomy
Stab wound, 42 (V2)
Stabilization splint, 881-883, 883f (V2)
Stable dynamics, 276 (V3)
Staff office, 357-358, 358f (V1)
Staging
of arteriovenous malformations, 589
(V2)
of bisphosphonate-related
osteonecrosis, 560-561, 561t
(V2)
of lip cancer, 742-743 (V2)
of melanoma, 754-755, 755t (V2)
of oral cavity cancer, 710, 711t (V2)
of skin cancer, 733-734 (V2)
Stambaugh technique for determining
chin position, 683t (V3)
Standards of care, malpractice claim
and, 374 (V1)
Stanford protocol, 252 (V1)
Staphylococcal infection
in acute suppurative parotitis, 540-
541, 541f, 542f (V2)
in laser skin resurfacing, 540 (V3)
in otoplasty, 676 (V3)
in rhinoplasty, 573 (V3)
in septic arthritis, 864 (V2)
Stapling in rhytidectomy, 505, 505f
(V3)
State licensure
in dentistry, 307 (V1)
of surgicenter, 304-306, 305t (V1)
State practice acts, 375 (V1)
Static dynamics, 276 (V3)
Static evaluation of occlusion, 17-18,
18b (V3)
Static wrinkles, 518 (V3)
Statue of limitations, 375 (V1)
Steiner cephalometric analysis, 249f
(V3)
Stellate ganglion block
for complex regional pain syndrome,
158 (V1)
for postherpetic neuralgia, 152 (V1)
for testing in chronic head and neck
pain, 141 (V1)
Stem cell, 23, 23f (V2)
effects of antibiotics on, 389, 389t
(V1)
Stenting
nasal
in functional cleft lip repair, 755f,
755-756 (V3)
in nasoalveolar molding, 786 (V3)
in parotid gland trauma, 319-320
(V2)
Stereotactic radiosurgery
for chronic head and neck pain, 157
(V1)
for posttraumatic trigeminal
neuralgia, 157 (V1)
for trigeminal neuralgia, 151 (V1)
Sterilization and infection control area,
354, 354f (V1)
Sterilization room equipment,
360 (V1)
Sternoclavicular graft in hemifacial
microsomia, 299 (V3)
Sternocleidomastoid muscle, 503 (V3)
Steroid therapy
for facial paralysis, 292 (V3)
for ICU patient, 72 (V2)
for infantile hemangioma, 580 (V2)
for laryngeal edema, 442 (V3)
in laser skin resurfacing
preoperative use of, 520-521 (V3)
for prolonged erythema, 537 (V3)
for scarring, 543 (V3)
in modified Le Fort III osteotomy,
212 (V3)
for neuropathy secondary to neuritis,
1000 (V2)
perioperative patient management
and, 393 (V3)
for postoperative pain, 86 (V1)
in temporomandibular joint
arthrocentesis, 914 (V2)
Stickler’s syndrome, 715 (V3)
Stiffness
in ankylosing spondylitis, 860 (V2)
in osteoarthritis of
temporomandibular joint, 855
(V2)
Still’s disease, 859 (V2)
Stock abutment, 528 (V1)
Stomatitis
aphthous, 619f, 619-620 (V2)
primary herpetic gingivostomatitis,
612-613, 613f (V2)
Stomatodynia, 967-968, 995-996 (V2)
Stomatopyrosis, 967-968, 995-996 (V2)
Storage space in office, 358, 359f (V1)
Strabismus in craniofacial dysostosis
syndromes, 881 (V3)
Streeter human facial embryogenesis,
697-705, 698f, 700-704f (V3)
Streptococcal infection
in acute suppurative parotitis, 540-
541, 541f, 542f (V2)
following rhinoplasty, 573 (V3)
laser skin resurfacing-related, 540
(V3)
Stress ulcer, 48 (V2)
Stroke
central poststroke pain and, 994-995
(V2)
preoperative evaluation for, 18 (V1)
Stryker oscillating saw, 125f (V3)
Stryker Pain Pump, 974 (V2)
Sturge-Weber syndrome, 581, 581f
(V2)
Styloid process, 163f (V2)
Stylomandibular ligament, 162, 805
(V2)
Subantral bone augmentation
guided tissue regeneration in, 436-
438, 437f (V1)
sinus-lift subantral augmentation in,
458-470 (V1)
anesthesia for, 459 (V1)
biologic and anatomic
considerations in, 458-459
(V1)
bone marrow aspirate for, 468-469,
469f (V1)
complications of, 462-464, 463f,
464f (V1)
elevation of schneiderian
membrane in, 460-462f (V1)
graft materials for, 468 (V1)
grafting osseous cavity in, 460-462,
462f (V1)
historical perspective of, 458 (V1)
incision in, 459, 459f (V1)
postoperative instructions in, 462
(V1)
preoperative preparation for, 459
(V1)
quadrilateral buccal osteotomy in,
459-460, 460f (V1)
trephine core membrane elevation
in, 464-468, 464-468f (V1)
vascular supply, lymphatic
drainage, and innervation in,
459 (V1)
Subapical osteotomy, complete
mandibular, 155-171 (V3)
complications in, 158, 437f, 437-438
(V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
Subarachnoid hemorrhage
traumatic, 62 (V2)
vitreous hemorrhage with, 82, 82f
(V2)
Subciliary approach
to lower eyelid, 205f (V2)
in orbital fracture, 221 (V2)
in zygomatic fracture, 190-191, 191f
(V2)
Subcondylar fracture, 162-181 (V2)
closed treatment of, 171 (V2)
conservative management of, 171
(V2)
diagnostic imaging of, 100f, 100-101,
168-170, 169f (V2)
endoscopic-assisted repair of, 172-
176, 176-180f (V2)
facial nerve and, 164-165,
166f (V2)
open treatment of, 171 (V2)
physical examination of, 168 (V2)
retromandibular approach in, 171-
172, 172-175f (V2)
retromandibular vein and, 164 (V2)
skeletal injuries in, 167, 167f, 170-
171 (V2)
soft tissue injuries in, 166-167, 170
(V2)
Subcondylar fracture (Continued)
Spiessl and Schroll classification of,
167, 168b (V2)
superficial temporal artery and, 163-
164, 164f, 165f (V2)
temporomandibular joint anatomy
and, 162-163, 163f (V2)
treatment outcomes in, 177-179
(V2)
trigeminal nerve and, 165, 166f (V2)
Subconjunctival hemorrhage, 78, 83,
83f (V2)
Subcranial approach in pediatric
craniomaxillofacial tumor, 964
(V3)
Subcranial Le Fort III osteotomy, 210-
211, 212-217f (V3)
Subcutaneous emphysema, 214 (V1)
Subcutaneous tissue, 10, 10f (V3)
Subcuticular running suture, 289f (V2)
Subdural hematoma
acute, 60, 61f (V2)
chronic, 61, 62f (V2)
third nerve palsy and, 85-86 (V2)
Subgaleal fascia, 182-183 (V2)
Sublimaze; See Fentanyl
Sublingual artery
bleeding in genioplasty and, 439
(V3)
mandibular orthognathic surgery and,
68 (V3)
Sublingual gland
floor of mouth squamous cell
carcinoma and, 714 (V2)
nonsalivary tumor of, 552 (V2)
ranula of, 539, 540f (V2)
sialolithiasis of, 543 (V2)
Subluxation
of mandibular condyle, 820, 820f,
825, 827f (V2)
of temporomandibular joint, 905,
905b (V2)
of tooth, 114t, 118 (V2)
Submandibular approach for mandibular
internal distractor device, 1000f
(V3)
Submandibular gland
acute suppurative infection of, 541-
542, 542f (V2)
chronic obstructive sialoadenitis of,
545 (V2)
nonsalivary tumor of, 551-552, 553f
(V2)
sialolithiasis of, 543-544, 544-547f
(V2)
Submandibular intubation in
maxillectomy, 694, 694f, 695f (V2)
Submandibular lymph nodes, neck
dissection and, 711t (V2)
Submental artery, 439 (V3)
Submental fat, cervicofacial liposuction
and, 618-625 (V3)
complications of, 623-624 (V3)
history of, 618 (V3)
patient selection in, 618-620, 619f
(V3)
preoperative preparation in, 620 (V3)
surgical technique in, 620-623, 620-
625f (V3)
Submental intubation in maxillectomy,
694, 694f, 695f (V2)
Submental island flap, 331-332, 334f
(V2)
Submental lymph nodes, neck
dissection and, 711t (V2)
Submentovertex projection in
temporomandibular disorders, 837,
837f (V2)
Submucous cleft palate, 839-840 (V3)
in oculoauriculovertebral spectrum,
927 (V3)
in Treacher Collins syndrome, 939
(V3)
Subnasale perpendicular to chin, 12
(V3)
Subnasale perpendicular to lower lip, 12
(V3)
Subnasale perpendicular to upper lip,
12 (V3)

Subnasale-lower lip vermilion to lower
lip vermilion-menton, 11 (V3)
Subnasale-stomion to stomion-menton,
11 (V3)
Subperiosteal approach
in endoscopic forehead and brow lift,
600 (V3)
in genioplasty, 141, 141f (V3)
in total maxillary segmental
osteotomy, 193 (V3)
Subperiosteal dissection, 226f, 227f
(V2)
in Le Fort III osteotomy, 206-210
(V3)
limits of, 204, 204f (V2)
in modified Le Fort III osteotomy,
211 (V3)
in subcranial Le Fort III osteotomy,
210-211 (V3)
Subpoena duces tecum, 384 (V1)
Substance abuse
chronic head and neck pain in, 141
(V1)
pain management considerations in,
971 (V2)
Substance P, 962, 963, 963f (V2)
Subtarsal approach
to lower eyelid, 205f (V2)
in zygomatic fracture, 191 (V2)
Subtotal anterior maxillectomy, 698-
699, 699f (V2)
Subtotal inferior maxillectomy, 697f,
697-698, 698f (V2)
Subtraction radiography, 551 (V1)
Succinylcholine
for laryngospasm in anesthetized
child, 106 (V1)
in rapid-sequence intubation, 30 (V2)
Sulcular approach in bone graft harvest
from mandibular symphysis, 410
(V1)
Sulindac, 887t (V2)
Sumatriptan, 148, 149 (V1)
Summons and complaint, 376 (V1)
Sun exposure
extrinsic aging and, 513 (V3)
history in laser skin resurfacing, 517
(V3)
lip cancer and, 743 (V2)
malignant melanoma and, 749 (V2)
skin cancer and, 724, 726 (V2)
Sunderland classification of nerve
injury, 216, 260t, 260-261 (V1)
Superficial musculoaponeurotic system
cervicofacial liposuction and, 619
(V3)
forehead and brow lift and, 597 (V3)
nasal musculature and, 553, 554f
(V3)
rhytidectomy and, 504 (V3)
Superficial palmar arch, 334f (V2)
Superficial parotidectomy
for lymphoepithelial cyst, 539 (V2)
for pleomorphic adenoma, 547-549,
549f (V2)
Superficial peroneal artery, 335f (V2)
Superficial plane rhytidectomy, 497-512
(V3)
complications in, 506-510, 507-510f
(V3)
patient evaluation in, 497-500, 498t,
499f, 499t (V3)
surgical technique in, 500-506, 500-
506f (V3)
Superficial spreading malignant
melanoma, 751f, 751t, 752t (V2)
Superficial temporal artery, 69f (V3)
condylar fracture and, 163-164, 164f,
165f (V2)
ear and, 667, 668f (V3)
Superficial temporal vein, 433f (V3)
Superior and lateral approaches to
orbital rim, 222-225, 224-226f
(V2)
Superior auricular muscle, 668f (V3)
Superior compartment of
temporomandibular joint,
arthroscopy and, 918-920, 919f
(V2)
Superior constrictor muscle, 831t, 835f
(V3)
Superior crus of external ear, 667f (V3)
Superior division of oculomotor nerve,
584f (V3)
Superior labial artery, 555f (V3)
Superior line of cranial base,
genioplasty and, 139, 139f, 140f
(V3)
Superior mandibular transverse buttress,
91 (V2)
Superior oblique muscle, 196t (V2),
584f (V3)
Superior oblique tendon, 583 (V3)
Superior orbital fissure, 203f, 203t (V2)
Superior orbital fissure syndrome, 212f,
212 (V2)
Superior orbital fracture, 355 (V2)
Superior pterygoid, 807 (V2)
Superior rectus muscle, 196t (V2), 581f,
584f (V3)
Superior tarsal plate, 586f (V3)
Superior thyroid artery, 69f (V3)
Superior transverse facial buttress, 91
(V2)
Superior turbinate, 257f (V2)
Supernumerary teeth, impacted, 172-
173, 173f (V1)
Supplemental oxygen
in cranio-maxillofacial trauma, 2
(V2)
delivery system for, 360 (V1)
during laser therapy, 243 (V1)
Supraglottic airway device, 26-28, 27f,
28f (V2)
Suprahyoid muscles, genioplasty and,
142 (V3)
Supraomohyoid neck dissection, 720f
(V2)
Supraorbital artery, 69f, 555f (V3)
endoscopic forehead and brow lift
and, 601, 601f (V3)
Supraorbital nerve
forehead and brow lift and, 598, 598f
(V3)
nose and, 557f (V3)
Suprascapular artery, 69f (V3)
Supratarsal crease, 584f, 588 (V3)
Supratip break, 554b (V3)
Supratrochlear artery, 69f, 555f (V3)
Supratrochlear nerve
forehead and brow lift and, 598, 599
(V3)
nose and, 557f (V3)
Surface osteosarcoma, 683-684 (V2)
Surgeon employment agreement
outline, 300t (V1)
Surgeon-pathologist interaction, 413-
414 (V2)
Surgery practice; See Practice
management
Surgery-related mandibular
hypomobility, 901 (V2)
Surgery-related risks for pulmonary
complications, 6, 6t, 7t (V1)
Surgical airway, 3-4, 4-5f, 32f, 32-33
(V2)
Surgical assistant, 324 (V1)
Surgical chair, 360 (V1)
Surgical excision
in arteriovenous malformation, 590
(V2)
of branchial cleft cyst, 460 (V2)
of calcifying odontogenic cyst, 447
(V2)
in dermatofibrosarcoma protuberans,
728 (V2)
of dermoid and epidermoid cysts, 455
(V2)
in juvenile ossifying fibroma, 600,
600f (V2)
of median palatal cyst, 451 (V2)
in melanoma, 754 (V2)
of nasolabial cyst, 448, 450f (V2)
in neurofibroma, 602 (V2)
in odontoma, 519 (V2)
in ossifying fibroma, 598, 599f (V2)
in osteoma, 605 (V2)
in osteosarcoma, 683 (V2)
Surgical excision (Continued)
in sebaceous gland carcinoma, 727
(V2)
in skin cancer, 736-737 (V2)
in squamous odontogenic tumor, 473
(V2)
in submandibular sialolithiasis, 543,
546f (V2)
of thyroglossal duct cyst, 456 (V2)
Surgical gut suture, 286t (V2)
Surgical lesioning for posttraumatic
trigeminal neuralgia, 157 (V1)
Surgical pathology, 413-788 (V2)
aspiration biopsy techniques in, 414f,
414-415, 415f (V2)
benign nonodontogenic tumors and,
592-610 (V2)
aneurysmal bone cyst in, 596-597,
597-598f (V2)
central giant cell granuloma in,
592-594, 593f, 593t (V2)
cherubism in, 595-596, 596f (V2)
chondroma in, 605-606 (V2)
desmoplastic fibroma in, 606-608,
607-608f (V2)
fibrous dysplasia in, 600-601 (V2)
florid cemento-osseous dysplasia in,
601, 601f (V2)
focal cemento-osseous dysplasia in,
601 (V2)
giant cell tumor in, 594 (V2)
hyperparathyroidism lesion in,
594f, 594-595 (V2)
juvenile ossifying fibroma in,
599-600, 600f (V2)
neurofibroma in, 602, 604f (V2)
ossifying fibroma in, 598, 599f
(V2)
osteoblastoma in, 602-604, 605f
(V2)
osteochondroma in, 606 (V2)
osteoid osteoma in, 602 (V2)
osteoma in, 604-605, 606f (V2)
periapical cemental dysplasia in,
601 (V2)
schwannoma in, 601-602, 603f
(V2)
bisphosphonate-related
osteonecrosis of jaw and,
557-566 (V2)
clinical presentation of, 559-560,
560f, 561f (V2)
clinical use of bisphosphonates
and, 558-559 (V2)
future research in, 564 (V2)
mechanism of action of
bisphosphonates and, 557-
558, 558f, 558t (V2)
pathophysiology and risk factors
for, 559 (V2)
staging of, 560-561, 561t (V2)
treatment outlines for, 561-564,
563f, 563t, 564f (V2)
electron microscopy in, 416, 416f
(V2)
exfoliative cytology in, 415 (V2)
flow cytometry in, 416-417 (V2)
frozen section in, 414 (V2)
historical background of, 413 (V2)
immunohistochemistry in, 415f, 415-
416, 416f (V2)
jaw sarcomas and, 680-704 (V2)
chondrosarcoma in, 684f, 684-685
(V2)
Ewing’s sarcoma in, 687, 688f,
689f (V2)
mandibular approaches in, 699-
702, 701f, 702f (V2)
maxillectomy in, 692-699, 694f,
695f, 697-699f (V2)
metastatic tumors to jaw and, 687-
689 (V2)
multiple myeloma and, 685-687,
686f, 687f (V2)
osteosarcoma in, 680-684, 681f,
682f (V2)
patient evaluation in, 689-692,
690t, 691f (V2)
radiation-induced, 685 (V2)
INDEX I-89
Surgical pathology (Continued)
Langerhans cell histiocytosis and,
567-576, 568f (V2)
classification of, 569b, 569-570
(V2)
clonality of, 570 (V2)
diagnosis, treatment, and prognosis
of, 571-575, 571-575f (V2)
histopathology of, 570, 570f (V2)
Langerhans cell and, 568-569, 569f
(V2)
lymphoma and, 758-766, 759b (V2)
angiocentric, 761-762 (V2)
diagnosis of, 758-759, 759f, 760f
(V2)
Hodgkin’s, 759-760, 760f (V2)
non-Hodgkin’s, 760-761, 761f
(V2)
of parotid gland, 551, 556 (V2)
prognosis of, 763-764, 764b (V2)
radiographic evaluation of, 762f,
762-763 (V2)
treatment of, 763 (V2)
medical oncology in head and neck
cancer and, 777-788 (V2)
background of, 777, 778f (V2)
chemotherapy for metastatic
carcinoma and, 778-781, 779t,
781t, 782t (V2)
epidemiology and, 777 (V2)
epidermal growth factor receptors
and, 782-783, 783t (V2)
induction chemotherapy and, 777-
778 (V2)
salivary gland cancers and, 783-
785, 785f (V2)
taxanes in, 781-782 (V2)
melanoma and, 749-757 (V2)
diagnosis of, 752t, 752-754, 753f,
753t (V2)
epidemiology of, 749, 750b (V2)
incidence and etiology of, 749-750,
750b, 750t, 750-752f, 751t
(V2)
management of regional disease in,
754 (V2)
staging of, 754-755, 755t (V2)
treatment of, 755-756 (V2)
molecular biologic testing in, 417
(V2)
molecular biology of cancer and, 645-
679 (V2)
cancer cell evasion of apoptosis
and, 660-662, 661f (V2)
cancer cell insensitivity to growth
inhibitory signals and, 658-
660, 659f (V2)
cancer cell release from growth
signal requirement and, 655-
658, 657f (V2)
cancer cell versus normal cell and,
646-647, 647f (V2)
chromosomal abnormalities in
cancer cells and, 652-653,
653-655f (V2)
epigenetic alteration of gene
expression in cancer cells and,
655 (V2)
gene regulation of cell function
and, 648-652, 649-651f (V2)
immortalization of cancer cell and,
662-664, 663f (V2)
molecular diagnostics in oncology
and, 666-669, 667f (V2)
neovascularization and, 664, 665f
(V2)
nucleotide sequence abnormalities
in cancer cells and, 653-655,
656f (V2)
strategies of cancer-related
molecular therapeutics and,
669-671, 670f (V2)
stromal changes in cells and, 645,
646f (V2)
targeted therapy based on
tumor behavior and,
671-673 (V2)
tissue invasion and metastases and,
664-666, 666f (V2)
I-90 INDEX
Surgical pathology (Continued)
non-melanoma skin cancer and, 724-
748 (V2)
aggressive behavior of, 728-730,
729f (V2)
basal cell carcinoma in, 725, 725f
(V2)
cryotherapy for, 734 (V2)
curettage/electrodesiccation in,
734, 735f (V2)
dermatofibrosarcoma protuberans
in, 727-728, 728f (V2)
epidemiology and etiology of, 724-
725 (V2)
laser ablation and resurfacing in,
734-735 (V2)
of lip, 742-744, 743f (V2)
lymph node involvement in, 737-
739 (V2)
Merkel cell carcinoma in, 727
(V2)
microcystic adnexal carcinoma in,
726-727, 727f (V2)
Mohs’ micrographic surgery in,
735-736, 736b, 736f (V2)
photodynamic therapy for, 741
(V2)
physical examination in, 730t,
730-733, 731b, 731-733t (V2)
radiation therapy in, 741-742 (V2)
sebaceous gland carcinoma in, 727,
727f (V2)
squamous cell carcinoma in, 725-
726, 726f (V2)
staging of, 733-734 (V2)
systemic and topical medications
for, 739-741 (V2)
traditional surgical excision in,
736-737 (V2)
nonodontogenic cysts and, 447-460
(V2)
branchial cleft, 458-460, 458-460f
(V2)
dermoid and epidermoid, 451-455,
454f, 455f (V2)
globulomaxillary, 451 (V2)
median mandibular, 451 (V2)
median palatal, 451 (V2)
nasolabial, 447-448, 449f, 450f
(V2)
nasopalatine duct, 448-451, 451-
453f (V2)
thyroglossal duct, 455-458, 455-
458f (V2)
odontogenic cysts and, 418-447 (V2)
calcifying, 445-447, 447f (V2)
dentigerous, 424-426, 425-428f
(V2)
gingival, 442, 445f (V2)
glandular, 444-445 (V2)
lateral periodontal, 442-444 (V2)
in nevoid basal cell carcinoma
syndrome, 441b, 441-442,
442t, 443f, 444f (V2)
odontogenic keratocyst, 426-441
(V2); See also Odontogenic
keratocyst
paradental, 421-424 (V2)
radicular, 419-421, 420f, 422f (V2)
residual, 421, 423f (V2)
odontogenic tumors and, 466-538
(V2)
adenomatoid, 469-472, 470-472f
(V2)
ameloblastic fibrodentinoma in,
524-527, 527f (V2)
ameloblastic fibroma in, 522-524,
523f (V2)
ameloblastic fibro-odontoma in,
524, 525f, 526f (V2)
ameloblastoma in, 476-502 (V2);
See also Ameloblastoma
biopsy of, 467-468 (V2)
calcifying, 473-476, 474f, 475f
(V2)
cementoblastoma in, 510-512
(V2)
classification of, 466-467 (V2)
clear cell, 502-508, 503-507f (V2)
Surgical pathology (Continued)
clinical considerations in, 467
(V2)
fibroma in, 508-510, 509f, 511f
(V2)
imaging of, 467 (V2)
intraosseous odontogenic
carcinoma in, 527-532, 528-
530f (V2)
management objectives in, 468-
469 (V2)
myxoma in, 512-517f, 512-518
(V2)
odontoameloblastoma in, 519-522
(V2)
odontoma in, 518-519, 519-521f
(V2)
sarcoma in, 532-533 (V2)
squamous, 472f, 472-473 (V2)
oral and maxillofacial squamous
cell carcinoma and,
705-723 (V2)
anatomy in, 705-706 (V2)
buccal mucosa, 714-715, 715f, 716f
(V2)
diagnostic adjuncts in, 708-709,
709f (V2)
floor of mouth, 714, 714f, 715f
(V2)
follow-up in, 719-720 (V2)
genetic abnormalities in, 707-708
(V2)
non-surgical management of, 710-
713 (V2)
pretreatment evaluation in, 710
(V2)
primary tumor and, 713-714 (V2)
retromolar trigone, alveolar ridge,
and palate, 716-719 (V2)
risk factors for, 706-707 (V2)
screening for, 708 (V2)
staging of, 710, 711t (V2)
tongue, 716-717, 716-718f (V2)
types of neck dissection in, 719,
719t, 720f (V2)
osteomyelitis and, 633-639 (V2)
classifications of, 633, 634b (V2)
clinical and radiographic
presentation of, 633-635, 634-
636f (V2)
pathogenesis of, 633 (V2)
risk factors for, 634b (V2)
treatment of, 635-638, 636t, 637f
(V2)
unique complications in, 638b,
638f, 638-639 (V2)
osteoradionecrosis and, 639-642 (V2)
clinical and radiographic diagnosis
of, 639, 639f, 640f (V2)
hyperbaric oxygen therapy for,
639-641 (V2)
prevention and maintenance of,
641-642, 642f (V2)
treatment of, 639, 640f, 641b, 641t
(V2)
radiation therapy in head and neck
cancer and, 767-776 (V2)
altered radiation fractionation
schemes and, 772 (V2)
complications of, 773-774 (V2)
definitive radiotherapy and, 771
(V2)
histologies and, 767-768 (V2)
preoperative and postoperative,
771-772 (V2)
sites of disease and, 768t, 768-771,
769f, 770f, 770t, 771t (V2)
systemic therapy with, 772, 772t
(V2)
techniques in, 772-773, 773f (V2)
salivary gland disease and, 539-556
(V2)
cystic conditions in, 539, 540f
(V2)
inflammatory conditions in, 540-
543, 541f, 542f (V2)
obstructive disease in, 543-546,
544-547f (V2)
tumors in, 546-555, 548-555f (V2)
Surgical pathology (Continued)
surgeon-pathologist interaction and,
413-414 (V2)
vascular anomalies and, 577-591
(V2)
arteriovenous malformation in,
588-590, 589f (V2)
binary classification of, 578b (V2)
capillary malformation in, 581,
581f (V2)
congenital hemangioma in, 579f,
579-581, 580f (V2)
infantile hemangioma in, 577-579,
578f (V2)
lymphatic malformation in, 581-
583, 582-585f (V2)
venous malformation in, 585-588,
586-588f (V2)
vesiculobullous diseases and, 611-632
(V2)
aphthous stomatitis in, 619f, 619-
620 (V2)
Beh[ced]cet’s syndrome in, 620-
622 (V2)
epidermolysis bullosa in, 626-627
(V2)
erythema multiforme in, 627-628
(V2)
herpangina in, 617t, 617-618 (V2)
lichen planus in, 618f, 618-619
(V2)
linear IgA disease in, 625-626
(V2)
pediatric herpes simplex infection
in, 615-617 (V2)
pemphigoid in, 622-624, 623f (V2)
pemphigus in, 624-625, 625f (V2)
primary herpetic gingivostomatitis
in, 612-613, 613f (V2)
Reiter syndrome in, 622 (V2)
secondary herpes in, 613-614 (V2)
Surgical plan development, 401-404,
403-406f (V2)
Surgical practice management; See
Practice management
Surgical site influence on postoperative
pulmonary complications, 6t (V1)
Surgical stabilizing splints, 397-399,
397-399f (V3)
Surgical supplies, 360-361 (V1)
Surgical track lighting, 360 (V1)
Surgical treatment area, floor plan in
office design and, 352-353, 353f
(V1)
Surgical treatment objectives
in maxillomandibular complex
rotation, 260-265, 261-266f
(V3)
in transoral vertical ramus osteotomy,
123, 124f, 125f (V3)
Surgical ward, trauma patient on, 72-73
(V2)
Surgically assisted maxillary expansion,
67f, 67-68, 219-237 (V3)
clinical evaluation in, 219, 220-220f,
221f (V3)
complications of, 231-232, 233f (V3)
incidence and origin of transverse
maxillary deficiency and, 219,
220f (V3)
modification of, 232-233, 234f (V3)
orthopedic rapid maxillary expansion
and, 224-226, 224-226f (V3)
radiographic evaluation in, 220-223,
221-223f (V3)
segmental maxillary osteotomy
versus, 233-235 (V3)
technique in, 227-231, 228-232f
(V3)
in two-jaw surgery, 239 (V3)
Surgicel, trigeminal neurotoxicity of,
274 (V1)
Surgicenter accreditation, 304-306, 305t
(V1)
SurgiGuide, 560, 561f (V1)
Surround hyperalgesia, 140 (V1)
Suspensory system of eyelid, 585, 586f,
587f (V3)
Sutton’s disease, 620 (V2)
Suture materials, 284-289, 286-287t
(V2)
Suturing
in complete mandibular subapical
osteotomy, 156 (V3)
in endoscopic forehead and brow lift,
605-606 (V3)
in exodontia, 201 (V1)
in facial skin laxity with weight loss,
687, 687f (V3)
in functional cleft lip repair, 755-756,
755-757f (V3)
in genioplasty, 143, 145f (V3)
in immediate implant placement, 513
(V1)
in internal derangement of
temporomandibular joint, 934,
935f (V2)
laser therapy and, 245 (V1)
in Le Fort I osteotomy, 181, 183f
(V3)
in mandibular lengthening by
distraction osteogenesis, 344
(V3)
in nasal fracture, 280 (V2)
in otoplasty
Davis method and, 672f (V3)
Mustard[ac]e method and, 673,
674f (V3)
in primary unilateral cleft lip repair,
721f (V3)
removal of, 14 (V2)
in rhinoplasty
closed, 572-573 (V3)
open, 565f, 566 (V3)
in rhytidectomy, 504, 505 (V3)
in ridge preservation using guided
tissue regeneration, 442 (V1)
techniques of, 284, 285f, 288f (V2)
in Tennison-Randall triangular flap
technique in unilateral cleft lip
repair, 749, 759f (V3)
in trigeminal nerve repair, 268 (V1)
in zygomatic implant, 496 (V1)
Swallowing
difficulty after laser-assisted
uvulopalatoplasty, 253 (V1)
of tooth during exodontia, 215 (V1)
Sweat ducts, microcystic adnexal
carcinoma of, 726-727, 727f (V2)
Swelling, 403-404 (V3)
in acute traumatic arthritis of
temporomandibular joint, 855
(V2)
in bilateral sagittal split osteotomy,
111 (V3)
in chondrosarcoma, 872 (V2)
effects of laser on, 254b, 254 (V1)
exodontia-related, 217-218 (V1)
injectable facial filler and, 643, 643f
(V3)
in Langerhans cell histiocytosis, 571,
571f, 572f (V2)
in mandibular orthognathic surgery,
441-442, 442f (V3)
in osteomyelitis, 633 (V2)
in osteosarcoma, 680 (V2)
in rhytidectomy, 507 (V3)
in sinus-lift subantral augmentation,
463 (V1)
of temporomandibular joint, 413
(V3)
Swimming after surgery, 412 (V3)
Swinging flashlight test, 76 (V2)
Sympathetic nervous system of child,
94 (V1)
Sympathetically maintained pain, 997
(V2)
Symphyseal mandibular fracture, 141,
142f (V2)
diagnostic imaging of, 101,
102f (V2)
pediatric, 364, 365-367f (V2)
Symptomatic glossopharyngeal
neuralgia, 994 (V2)
Symptomatic trigeminal neuralgia, 991t
(V2)
Syncope, glossopharyngeal neuralgia
and, 994 (V2)

Syndactylism in craniofacial dysostosis
syndromes, 882 (V3)
Synechiae after nasal fracture repair,
282 (V2)
Synergy in marketing, 335-336, 336b
(V1)
Synovial chondromatosis, 817, 819f,
872 (V2)
Synovial chondrosarcoma, 872-873
(V2)
Synovial cyst, 869 (V2)
Synovial fluid, inflammatory mediators
in, 850 (V2)
Synovial fluid analysis
in osteoarthritis, 857 (V2)
in rheumatoid arthritis, 858 (V2)
in temporomandibular disorders, 930
(V2)
Synovial hemangioma, 869-870 (V2)
Synovial joint of temporomandibular
joint, 127-128, 128f (V1)
Synovial membrane of
temporomandibular joint, 128
(V1), 803 (V2)
Synovial sarcoma of temporomandibular
joint, 873 (V2)
Synovial surgery, laser-assisted, 247
(V1)
Synovitis, 831t (V2)
Synthetic bioresorbable membranes for
guided tissue regeneration, 435
(V1)
Syringe in facial fat transplantation,
626, 626f (V3)
Syringe-assisted cervicofacial
liposuction, 622, 622f (V3)
Systemic disease
chronic head and neck pain in, 141
(V1)
chronic orofacial pain in, 118 (V1)
influence on nerve injury responses,
261 (V1)
salivary gland disease associated with,
555-556 (V2)
Systemic inflammatory response, 44, 44t
(V2)
Systemic lupus erythematosus
facial asymmetry in, 309 (V3)
temporomandibular joint
involvement in, 865 (V2)
Systemized Nomenclature of Dentistry,
365 (V1)
Systemized Nomenclature of Medicine,
365 (V1)
T ankylosis in, 901-905, 952-953, 953f,
Tachycardia in cranio-maxillofacial
trauma, 6 (V2)
Tacrolimus, 624 (V2)
TACT; See Tuned aperture computed
tomography
Talwin; See Pentazocine
Tamponade, 38, 38f (V2)
Tannerella forsythia, 391 (V1)
Tapered locking plate, 155 (V2)
Target market, marketing and, 334
(V1)
Targeted therapy based on tumor
behavior, 671-673 (V2)
Tarsal plate, 582f, 585, 586f (V3)
Tarsus, 581f, 585, 586f, 587f (V3)
Tartaric acid for chemical peel, 663
(V3)
Tattoo removal, 251 (V1)
Taxanes, 778, 781-782 (V2)
Tear trough injection, 638-639, 639f
(V3)
Tears, 587 (V3)
Technical difficulties
in genioplasty, 439-441, 441f (V3)
in intraoral vertical ramus osteotomy,
436 (V3)
in LE Fort I osteotomy, 471-472,
472f (V3)
in sagittal split ramus osteotomy, 433
(V3)
in segmental mandibular surgery,
438-439 (V3)
Teeth; See Tooth
Teflon mantle leaf for guided bone
regeneration, 429 (V1)
Tegmen tympani, 802 (V2)
Tegretol; See Carbamazepine
Telangiectasia
laser skin resurfacing-related, 538-539
(V3)
laser therapy for, 251 (V1)
Telecanthus
direct fixation techniques for, 233
(V2)
in orbital fracture, 215-217, 218f
(V2)
Telemedicine, risk management and,
385 (V1)
Telephone call-on-hold device, 345
(V1)
Telephone ear deformity, 676 (V3)
Telephone system in office, 359 (V1)
Telogen affluvium, 607 (V3)
Telomerase, cancer and, 662, 663f (V2)
Temazepam, 889t (V2)
Temperature monitor, 29 (V1)
Temporal approach to zygomatic arch
fracture, 194, 194f (V2)
Temporal arteritis
chronic orofacial pain in, 116 (V1)
trismus and, 899 (V2)
Temporal artery, 668f (V3)
Temporal fusion line, 596-597 (V3)
Temporal nerve, 600-601 (V3)
Temporal process of zygoma, 182 (V2)
Temporalis fascia, 597-598 (V3)
Temporalis muscle, 806f, 806-807 (V2)
forehead and brow lift and, 597 (V3)
hypertrophy-related facial asymmetry
and, 292 (V3)
innervation and blood supply to, 809
(V2)
maxillomandibular rotation and, 270f
(V3)
Temporalis muscle flap
in internal derangement of
temporomandibular joint, 937,
937f (V2)
in temporomandibular joint
reconstruction, 945-946, 947f
(V2)
Wakely’s, 793, 793f (V2)
Temporary crown, prefabricated ceramic
abutment and, 536f, 536-537, 537f
(V1)
Temporofacial nerve, 668f (V3)
Temporomandibular disorders, 789-
1004 (V2)
953t (V2)
ankylosing spondylitis and, 901-
902 (V2)
facial asymmetry in, 294-298, 297f,
298f (V3)
history of therapy for, 791-792,
792t (V2)
pseudoankylosis and, 899-901 (V2)
arthrocentesis of temporomandibular
joint in, 912-917 (V2)
outcome assessment in, 915 (V2)
pathophysiology of
temporomandibular disorder
and, 912-913 (V2)
prognostic and predictive factors
in, 916 (V2)
technique in, 913-915, 914f (V2)
arthroscopy for, 918-928 (V2)
anatomic considerations in, 918-
920, 919f (V2)
arthroplasty and, 924 (V2)
capsular release in, 924, 925f (V2)
complications in, 926-927 (V2)
diagnostic uses of, 920 (V2)
disk repositioning in, 924-926,
925f, 926f (V2)
equipment for, 921-923, 922f (V2)
fluid analysis and, 921 (V2)
inferolateral technique in, 923,
923f (V2)
in internal derangement, 920-921,
921f (V2)
lysis and lavage in, 924, 924f (V2)
Temporomandibular disorders
(Continued)
postoperative care in, 927 (V2)
removal of adhesions in, 924 (V2)
assessment in, 815-834 (V2)
abnormal biomechanics and, 817-
818, 818f, 819f (V2)
adjunctive diagnostic testing in,
824 (V2)
anatomy and, 815f, 815-816, 816f
(V2)
auscultation in, 826-828 (V2)
diagnostic imaging in, 821-823,
821-823f (V2)
in intracapsular pathofunctional
disorders, 818-821, 819-821f
(V2)
mandibular gait and, 825-826, 825-
828f (V2)
mandibular range of motion and,
824-825 (V2)
muscle evaluation in, 829, 830-
831b, 831-832t, 833f (V2)
normal biomechanics and, 816-
817, 817f (V2)
in orofacial pain disorders, 824,
824b (V2)
palpation in, 828f, 828-829, 829f
(V2)
screening questionnaire in, 824,
824t (V2)
chronic facial pain in, 961-978 (V2)
antidepressants for, 973 (V2)
atypical facial pain and, 967-968
(V2)
barriers to management of,
970-971 (V2)
botulinum toxin injection for, 974-
975 (V2)
of cardiac origin, 969 (V2)
central mechanisms of, 963 (V2)
clinically based comprehensive
pain management program
for, 975 (V2)
complex regional pain syndrome
and, 966-967 (V2)
Eagle’s syndrome and, 969-970,
970f (V2)
evaluation of, 963-966, 965f, 966t
(V2)
future directions in management
of, 975-976 (V2)
muscle relaxants for, 974 (V2)
nerve injury from dental
procedures and, 968f, 968-969
(V2)
neuralgia-inducing cavitational
osteonecrosis and, 967 (V2)
neuropathic agents for, 973-974 (V2)
nonsteroidal antiinflammatory
drugs for, 972-973, 973t (V2)
opioid therapy for, 971-972, 972t
(V2)
osteonecrosis-related, 970 (V2)
peripheral mechanisms of, 962,
963f (V2)
physical therapy for, 971 (V2)
surgical intervention for, 975 (V2)
therapeutic injections for, 974 (V2)
topical capsaicin for, 975 (V2)
trigeminal anatomy and, 961-962,
962f (V2)
chronic head and neck pain in, 143,
145-146 (V1)
classification of, 930b (V2)
clinical presentation in, 980-982,
981f (V2)
current concepts in diagnosis and
management of, 126 (V1)
diagnostic tests in, 982b, 982 (V2)
etiology and epidemiology of, 979-
980 (V2)
facial asymmetry and, 272-315 (V3)
in adolescent internal condylar
resorption, 299-305, 303-304f,
306f (V3)
in autoimmune and connective
tissue diseases, 309-313, 310-
313f (V3)
INDEX I-91
Temporomandibular disorders
(Continued)
categories of, 278 (V3)
clinical evaluation in, 272-274,
273f (V3)
dentoalveolar and occlusal
assessment in, 274 (V3)
dentoalveolar asymmetry and, 282,
283-284f (V3)
developmental, 282 (V3)
diagnostic and treatment
considerations in, 275-277,
276f (V3)
in hemifacial microsomia, 298-299,
300-302f (V3)
iatrogenic, 294 (V3)
imaging in, 274-275 (V3)
in mandibular condylar
osteochondroma or osteoma,
285-291, 289-291f (V3)
in muscle hypertrophy, 291-292
(V3)
in neuromuscular disorders, 292,
292f (V3)
presurgical patient preparation
and, 277-278 (V3)
pseudoasymmetry and, 278-282,
279-281f (V3)
in reactive arthritis, 305-309, 307-
309f (V3)
in temporomandibular joint
ankylosis, 294-298, 297f, 298f
(V3)
trauma-related, 294, 295f, 296f (V3)
in tumor, 293, 293f (V3)
in unilateral condylar hyperplasia,
284-285, 286-288f (V3)
unilateral facial underdevelopment
or degeneration and, 294-313
(V3)
functional, 898-911 (V2)
hypermobility in, 905b, 905-908f,
905-909 (V2)
hypomobility in, 898-905 (V2)
history of therapy for, 789-800 (V2)
after World War II, 794-796, 796f
(V2)
dental occlusion and, 792-793,
793b (V2)
early arthroplasty and, 790-792,
791f, 792f (V2)
mid-twentieth century and, 793f,
793-794 (V2)
minimally invasive treatment and,
798 (V2)
non-surgical treatment and, 796
(V2)
open joint surgery and, 796-797,
797f (V2)
pioneers in, 789-790, 790f (V2)
total joint replacement and, 797-
798, 798f (V2)
imaging in, 835-848 (V2)
advanced modalities in, 839 (V2)
computed tomography in, 839-840,
840f, 841f (V2)
cone beam computed tomography
in, 843, 845f, 846f (V2)
conventional, 835-836 (V2)
functional, 843-845 (V2)
fusion, 845 (V2)
lateral oblique views in, 837, 837f
(V2)
linear tomography in, 838 (V2)
magnetic resonance imaging in,
840-841, 842-843f (V2)
multidirectional tomography in,
838-839 (V2)
panoramic radiography in,
837-838, 838f (V2)
reverse Towne’s projection in, 836,
837f (V2)
submentovertex projection in, 837,
837f (V2)
transcranial radiography in, 836,
836f (V2)
transmaxillary or transorbital
radiography in, 836, 836f
(V2)
I-92 INDEX
Temporomandibular disorders
(Continued)
tuned aperture computed
tomography in, 841-843, 844f
(V2)
ultrasonography in, 846 (V2)
internal derangement in, 929-944,
930b (V2)
capsular incisions in, 934, 934f (V2)
condylotomy in, 939-940 (V2)
diagnostic imaging in, 931, 932f
(V2)
disk repair in, 936, 936f (V2)
disk repositioning in, 935f, 935-
936 (V2)
diskectomy in, 936 (V2)
diskectomy with replacement in,
936-939, 937-939f (V2)
endaural incision in, 933f, 933-
934, 934f (V2)
goals and criteria for surgery in,
931 (V2)
history and physical examination
in, 929-930 (V2)
pathogenesis of, 930-931 (V2)
postoperative care in, 940-941
(V2)
preauricular incision in, 932-933,
933f (V2)
preoperative therapies for, 931
(V2)
surgical complications in, 940 (V2)
wound closure in, 934, 935f (V2)
internal derangement theory of, 126-
127, 128f (V1)
maximization of joint mobility in,
130 (V1)
motor function of trigeminal nerve
in, 118 (V1)
neoplasia in, 832t (V2)
neuropathic orofacial pain in, 989-
1004 (V2)
burning mouth syndrome in, 995-
996 (V2)
central poststroke pain in, 994-995
(V2)
diagnosis of, 989-990 (V2)
glossopharyngeal neuralgia in, 993-
994 (V2)
herpes zoster and, 994 (V2)
secondary to neuritis, 1000 (V2)
traumatic orofacial neuropathies
in, 996-999, 998t, 999t (V2)
trigeminal neuralgia in, 990-992t,
990-993 (V2)
nonsurgical management of, 881-897
(V2)
occlusal management in, 889-890
(V2)
pharmacotherapy in, 885b, 885-
889 (V2)
philosophies of treatment and, 881
(V2)
physical therapy in, 890-892, 891t
(V2)
splint therapy in, 881-885, 882b,
883f, 884f (V2)
pathology of, 849-880 (V2)
aneurysmal bone cyst and, 868 (V2)
ankylosing spondylitis and, 860-
861 (V2)
arteriovenous malformation and,
870 (V2)
benign osteoblastoma and, 871
(V2)
central giant cell granuloma in,
869 (V2)
chondroblastoma and, 868 (V2)
chondrosarcoma and, 872 (V2)
condylar hyperplasia and, 868 (V2)
degenerative osteoarthritis and,
855-857 (V2)
fibrous dysplasia and, 870 (V2)
ganglion and synovial cysts and,
869 (V2)
Garr[ac]e’s osteomyelitis and, 874
(V2)
gout and pseudogout and, 865
(V2)
Temporomandibular disorders
(Continued)
hemangioma and, 869-870 (V2)
heterotopic bone formation and,
874-875 (V2)
idiopathic bone cavity cyst and,
869 (V2)
infectious arthritis and, 861-864,
862-863f (V2)
joint physiology and
pathophysiology in, 849-852,
850-854f (V2)
juvenile rheumatoid arthritis and,
859 (V2)
Langerhans cell histiocytosis and,
874 (V2)
Lyme disease-associated arthritis
and, 864 (V2)
metastatic carcinoma and, 874 (V2)
mixed connective tissue disease
and, 866 (V2)
multiple myeloma and, 873-874
(V2)
nonossifying fibroma and, 870
(V2)
osteochondroma and, 871 (V2)
osteoid osteoma and, 871 (V2)
osteoma and, 871 (V2)
osteosarcoma and, 873 (V2)
phantom bone disease and, 875
(V2)
pigmented villonodular synovitis
and, 871-872 (V2)
pseudocyst and, 868-869 (V2)
psoriatic arthritis and, 859-860
(V2)
Reiter syndrome and, 861 (V2)
rheumatoid arthritis and, 857b,
857-858 (V2)
scleroderma and, 865-866 (V2)
Sj[um]ogren’s syndrome and, 866
(V2)
synovial chondromatosis and, 872
(V2)
synovial chondrosarcoma and, 872-
873 (V2)
synovial sarcoma and, 873 (V2)
systemic lupus erythematosus and,
865 (V2)
traumatic arthritis and, 854-855
(V2)
pathophysiology and mechanisms in,
980 (V2)
postoperative, 72-73, 396, 406, 407f,
414 (V3)
in bilateral sagittal split osteotomy,
113-114 (V3)
psychologic evaluation in, 123-124
(V1)
reduction of inflammation and pain
in, 130-131 (V1)
reduction of joint loading in, 129-
130 (V1)
subluxation in, 905, 905b (V2)
surgical management of
laser-assisted, 246-248 (V1)
principles of, 131-134 (V1)
synovial joint maladaptive changes
in, 128-129, 129f (V1)
synovial joint structure and function
in, 127-128, 128f (V1)
temporomandibular joint
reconstruction in, 945-960
(V2)
distraction osteogenesis and, 955
(V2)
in failed alloplastic joint
reconstruction, 954, 954f
(V2)
in failed tissue grafts, 953-954,
954f (V2)
historic perspective of, 945-950,
946-950f (V2)
in inflammatory arthritis, 950-952,
952f (V2)
in loss of vertical mandibular
height and occlusal
relationship, 954-955, 955f
(V2)
Temporomandibular disorders
(Continued)
in recurrent fibrosis and bony
ankylosis, 952-953, 953f, 953t
(V2)
tissue engineering and, 955 (V2)
transoral vertical ramus osteotomy
for, 119, 121t (V3)
treatment of, 982-987, 983t (V2)
cognitive-behavioral therapy in,
985 (V2)
control of contributing factors in,
984 (V2)
criteria for complex cases in, 983b
(V2)
goals of, 983t (V2), 983-984
muscle exercises in, 985f, 985-986
(V2)
muscle therapy in, 986 (V2)
pain clinic team management in,
987 (V2)
pharmacotherapy in, 885b, 885-
889, 985, 986-987 (V2)
self-care and, 984, 984b (V2)
splint therapy in, 881-885, 882b,
883f, 884f, 984-985 (V2)
Temporomandibular joint
abnormal biomechanics of, 817-818,
818f, 819f (V2)
aging of, 377 (V2)
arthrocentesis of, 912-917 (V2)
outcome assessment in, 915 (V2)
pathophysiology of
temporomandibular disorder
and, 912-913 (V2)
prognostic and predictive factors
in, 916 (V2)
technique in, 913-915, 914f (V2)
condylar fracture and, 141-142, 142f,
162-181 (V2)
anatomy in, 162-163, 163f (V2)
closed treatment of, 171 (V2)
conservative management of, 171
(V2)
diagnostic imaging of, 100f, 100-
101, 168-170, 169f (V2)
endoscopic-assisted repair of, 172-
176, 176-180f (V2)
facial nerve and, 164-165, 166f
(V2)
open treatment of, 171 (V2)
physical examination of, 168 (V2)
retromandibular approach in, 171-
172, 172-175f (V2)
retromandibular vein and, 164 (V2)
skeletal injuries in, 167, 167f, 170-
171 (V2)
soft tissue injuries in, 166-167, 170
(V2)
Spiessl and Schroll classification
of, 167, 168b (V2)
superficial temporal artery and,
163-164, 164f, 165f (V2)
treatment outcomes in, 177-179
(V2)
trigeminal nerve and, 165, 166f
(V2)
dislocation of, 905, 905b (V2)
hypermobility of, 905b, 905-908f,
905-909 (V2)
hypomobility of, 898-905 (V2)
ankylosis and, 901-905 (V2)
complications of, 905 (V2)
imaging in, 898 (V2)
pseudoankylosis and, 899-901 (V2)
treatment of, 905 (V2)
trismus and, 898-899 (V2)
imaging of, 835-848 (V2)
advanced modalities in, 839 (V2)
computed tomography in, 839-840,
840f, 841f (V2)
cone beam computed tomography
in, 843, 845f, 846f (V2)
conventional, 835-836 (V2)
functional, 843-845 (V2)
fusion, 845 (V2)
lateral oblique views in, 837, 837f
(V2)
linear tomography in, 838 (V2)
Temporomandibular joint (Continued)
magnetic resonance imaging in,
840-841, 842-843f (V2)
multidirectional tomography in,
838-839 (V2)
panoramic radiography in, 837-
838, 838f (V2)
reverse Towne’s projection in, 836,
837f (V2)
submentovertex projection in, 837,
837f (V2)
transcranial radiography in, 836,
836f (V2)
transmaxillary or transorbital
radiography in, 836, 836f
(V2)
tuned aperture computed
tomography in, 841-843, 844f
(V2)
ultrasonography in, 846 (V2)
internal derangement of, 929-944,
930b (V2)
capsular incisions in, 934, 934f
(V2)
condylotomy in, 939-940 (V2)
diagnostic imaging in, 931, 932f
(V2)
disk repair in, 936, 936f (V2)
disk repositioning in, 935f, 935-
936 (V2)
diskectomy in, 936 (V2)
diskectomy with replacement in,
936-939, 937-939f (V2)
endaural incision in, 933f, 933-
934, 934f (V2)
goals and criteria for surgery in,
931 (V2)
history and physical examination
in, 929-930 (V2)
pathogenesis of, 930-931 (V2)
postoperative care in, 940-941
(V2)
preauricular incision in, 932-933,
933f (V2)
preoperative therapies for, 931
(V2)
surgical complications in, 940 (V2)
wound closure in, 934, 935f (V2)
mandibular lengthening by
distraction osteogenesis and,
344-345 (V3)
normal biomechanics of, 816-817,
817f (V2)
physiology and pathophysiology of,
849-852, 850-854f (V2)
postsurgical complications of, 414,
445, 453 (V3)
protection during surgical procedures,
125 (V1)
structure and function of, 801-814,
810b (V2)
articular disc and, 802-803, 803f
(V2)
capsule and extracapsular
ligaments and, 803-804, 804f
(V2)
condyle and, 803, 804f (V2)
developmental perspective in, 801
(V2)
digastric muscle and, 808 (V2)
free movements of mandible and,
810-811 (V2)
geniohyoid muscle and, 808, 809f
(V2)
glenoid fossa and, 802, 802f (V2)
innervation and blood supply in,
809, 809f (V2)
lateral pterygoid muscle and, 807-
808, 808f (V2)
masseter muscle and, 805f, 805-
806 (V2)
masticatory movements of
mandible and, 811-812 (V2)
medial pterygoid muscle and, 807,
807f (V2)
mylohyoid muscle and, 808, 808f
(V2)
sphenomandibular ligament and,
804-805 (V2)

Temporomandibular joint (Continued)
stylomandibular ligament and, 805
(V2)
synovial membrane and, 803 (V2)
temporalis muscle and, 806f, 806-
807 (V2)
translation of, 817, 817f (V2)
Treacher Collins syndrome and, 936-
960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956 (V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
zygomatic deformity in, 851 (V3)
Temporomandibular joint muscles, 162-
163, 805-808 (V2)
digastric muscle in, 808 (V2)
evaluation of, 829, 830-831b, 831-
832t, 833f (V2)
geniohyoid muscle in, 808, 809f (V2)
lateral pterygoid muscle in, 807-808,
808f (V2)
main actions of, 810b (V2)
masseter muscle in, 805f, 805-806
(V2)
medial pterygoid muscle in, 807, 807f
(V2)
mylohyoid muscle in, 808, 808f (V2)
temporalis muscle in, 806f, 806-807
(V2)
Temporomandibular joint prosthesis,
904 (V2)
Temporomandibular joint
reconstruction, 945-960 (V2)
distraction osteogenesis and, 955 (V2)
in failed alloplastic joint
reconstruction, 954, 954f (V2)
in failed tissue grafts, 953-954, 954f
(V2)
historic perspective of, 945-950, 946-
950f (V2)
in inflammatory arthritis, 950-952,
952f (V2)
in loss of vertical mandibular height
and occlusal relationship, 954-
955, 955f (V2)
in oculoauriculovertebral spectrum,
927-928, 928f (V3)
in recurrent fibrosis and bony
ankylosis, 952-953, 953f, 953t
(V2)
tissue engineering and, 955 (V2)
Temporomandibular ligament, 804,
804f (V2)
Temporoparietal fascia flap, 330 (V2)
Tennison-Randall triangular flap
technique in unilateral cleft lip
repair, 722, 723f, 743-751, 744f,
745f (V3)
comparison of cleft surgery
techniques, 736 (V3)
Millard rotation and advancement
flap versus, 745 (V3)
surgical planning and markings in,
745-746, 746f, 746t, 747f (V3)
surgical procedure in, 746-749, 747-
751f (V3)
Tenon’s capsule, 581f (V3)
TENS; See Transcutaneous electrical
nerve stimulation
Tensile strain of high magnitude, 850
(V2)
Tensile strain of low magnitude, 850
(V2)
Tensile strength of wound healing, 61-
62, 62f (V3)
Tension pneumothorax, 36, 37f, 42
(V2)
Tension-type headache, 148 (V1)
Tensor veli palatini muscle, 831t, 835f
(V3)
Teratoid cyst, 451 (V2)
Termination of employee, 328-329
(V1)
Terson’s syndrome, 82, 82f (V2)
Tertiary examination of trauma patient,
72 (V2)
Tessier classification scheme for
craniofacial clefting, 705-712,
710f, 711f, 716, 717f (V3)
Tetanic stimulation, 30 (V1)
Tetanus prophylaxis, 284f (V2)
Tetracaine
chemical structure of, 37f (V1)
topical, 49 (V1)
Tetracycline
effect on osteoblast, 389t, 389-390
(V1)
for periimplantitis, 392 (V1)
trigeminal neurotoxicity of, 274 (V1)
Thalamus, 962, 962f (V2)
Therapeutic clenching, 407 (V3)
Therapeutic injections
for chronic facial pain, 974 (V2)
for temporomandibular disorders, 986
(V2)
Thermal injury
during exodontia, 214 (V1)
facial soft tissue injury in, 321-323,
321-323f, 322t (V2)
in laser skin resurfacing, 521-522 (V3)
Thermal methods of topical anesthesia,
50 (V1)
Thermal relaxation time of tissue, 514,
515f (V3)
Thermal therapy for temporomandibular
disorders, 891-892 (V2)
Thermistor, 29 (V1)
Thermocouple, 29 (V1)
Thermoregulation, pediatric anesthesia
and sedation and, 96 (V1)
Third intention healing, 62 (V3)
Third molar surgery
chart documentation in, 368 (V1)
chronic orofacial pain and,
125 (V1)
before complete mandibular subapical
osteotomy, 156, 162f (V3)
for impaction, 201-210 (V1)
bone removal and tooth
sectioning in, 205-206,
207-210f (V1)
classification of, 203, 204f (V1)
indications and contraindications
for, 202-203 (V1)
instrumentation for, 203, 203t
(V1)
mandibular, 203-205, 205b, 206f
(V1)
maxillary, 207, 208-210f (V1)
postoperative instructions in, 208-
210, 209b (V1)
preoperative management in, 207t,
207-208, 208b (V1)
third molar displacement into
infratemporal fossa and,
213-214 (V1)
trigeminal nerve injury and, 276-
278 (V1)
wound closure in, 206-207 (V1)
mandibular ramus for bone harvest
in, 413 (V1)
outpatient, 494 (V3)
Third nerve palsy, 50, 85-86 (V2)
Third-degree burn, 322t (V2)
Third-party payer, 369-370 (V1)
Thomas principle, 141f (V2)
Thoracoabdominal wound, 42 (V2)
Thorax, penetrating injury of, 42 (V2)
Thread lift, 695, 696t (V3)
Threaded locking plate, 155 (V2)
3dMDface System software, 378f, 379
(V3)
Three-dimensional computer-assisted
prediction, 377-379, 378f (V3)
Three-dimensional imaging
of facial injury, 92-93 (V2)
in orbital fracture, 210-211, 211f
(V2)
Three-dimensional modeling in
computed tomography, 554-556,
554-556f (V1)
Three-dimensional radiation
treatment planning, 772-773,
773f (V2)
Three-wall extraction socket defect,
541, 543f (V1)
Throat examination, 9, 10f (V2)
Thrombin
platelet-rich plasma and, 501, 502f,
508 (V1)
wound repair and, 17 (V2)
Thrombocytopenia, 16, 16t (V1)
Thromboembolism, 383 (V2)
Thrombus formation in wound repair,
17 (V2)
Thyrocervical trunk, 69f (V3)
Thyroglossal duct cyst, 455-458, 455-
458f (V2)
Thyroid, preoperative evaluation of,
12-13, 13t (V1)
Thyroid cancer
radiation therapy for, 767-768 (V2)
thyroglossal duct cyst and, 456-458,
457f (V2)
Thyroid disease
in geriatric patient, 384 (V2)
salivary disease in, 556 (V2)
use of vasoconstrictors with local
anesthetics and, 44, 44b (V1)
Thyroid storm, 384 (V2)
Thyromental distance, 69 (V1)
in child, 97-98 (V1)
Tibia for bone graft harvest, 414f, 414-
415, 415f (V1)
Tic convulsif, 991 (V2)
Tic douloureux, 149-151 (V1), 991
(V2)
Tidal volume, pediatric versus adult, 96t
(V1)
Tiludronate, 558t (V2)
Time-oriented anesthesia record, 22
(V1)
Tip defining point, 554b, 556 (V3)
Tip onlay graft, 563 (V3)
Tip plasty in rhinoplasty, 562, 563f, 571
(V3)
Tip projection in rhinoplasty, 562-564,
563-565f (V3)
Tip rotation in rhinoplasty, 564, 565f
(V3)
Tip shape, rhinoplasty and, 565-566,
566f (V3)
Tissue
carbon dioxide laser properties and,
514f, 514-516, 515f (V3)
healing of, 17-24 (V2)
aberrant bone healing in, 22-23
(V2)
abnormal wound healing in, 22
(V2)
bone regeneration in, 22 (V2)
coagulation and, 17, 18f (V2)
formation of granulation tissue
and, 19-21, 20f (V2)
future directions in, 23, 23f (V2)
inflammation and, 17-19,
19f (V2)
neural control of, 21 (V2)
phases of, 17, 18f (V2)
prevention of infection in, 21-22
(V2)
remodeling phase of, 21f, 21 (V2)
laser therapy interactions with, 238,
239t, 239-241f, 239-241 (V1)
INDEX I-93
Tissue (Continued)
positioning of injectable filler in,
631f, 631-632, 632f (V3)
Tissue emphysema, 215 (V1)
Tissue engineering in
temporomandibular joint
reconstruction, 955 (V2)
Titanium-reinforced membrane, 430-
431, 431f, 432f (V1)
in alveolar ridge augmentation, 450f,
450-451, 451f (V1)
for fenestration defects, 436 (V1)
in flapless buccal wall reconstruction,
430-431, 431f, 432f (V1)
Tizanidine, 974 (V2)
T-lymphocyte, wound repair and, 21
(V2)
TMD; See Temporomandibular
disorders
TMJ; See Temporomandibular joint
TMJ Concepts custom-made prosthesis,
904 (V2)
TNM staging
in lip cancer, 742-743 (V2)
in melanoma, 754-755, 755t (V2)
in skin cancer, 733-734 (V2)
Tobacco, oral cavity cancer and, 706
(V2)
Tofranil; See Imipramine
Tolerance to opioid analgesics, 81 (V1),
970-971 (V2)
Toluidine blue, 708-709, 709f (V2)
Tongue, 706 (V2)
lymphatic malformation of, 582-583,
583-585f (V2)
orthognathic surgery-related changes
in, 75 (V3)
squamous cell carcinoma of, 716-717,
716-718f, 769f (V2)
radiation therapy in, 768, 768t,
769f (V2)
Tongue flap in residual palatal fistula
closure, 830, 831, V3)
Tongue reduction for obstructive sleep
apnea syndrome, 316 (V3)
Tonometry in orbital fracture, 209 (V2)
Tonsil
Beh[ced]cet’s syndrome and, 621
(V2)
herpangina and, 617t, 617-618 (V2)
lymphoma of, 758 (V2)
Tooth
dentoalveolar injury and, 104-138,
105f, 106f (V2)
alveolar process fracture in, 126-
128, 127f, 128f (V2)
calcium hydroxide root canal fill
for, 119, 119f (V2)
classification of, 110-112, 111f,
112b, 113-115t (V2)
comminution of alveolar socket in,
125 (V2)
complete tooth avulsion in, 120-
122, 121f, 122b (V2)
concussed tooth in, 118 (V2)
crown infraction in, 112-113
(V2)
crown-root fracture in, 116 (V2)
displacement of tooth in, 118,
118b (V2)
enamel, dentin, and pulp exposure
in, 113-114 (V2)
enamel fracture in, 113 (V2)
extrusive luxation in, 118f (V2)
general considerations in, 112
(V2)
gingival injury in, 130 (V2)
history in, 105-107 (V2)
intrusive luxation in, 118, 119f
(V2)
lateral luxation of tooth in, 119-
120 (V2)
pediatric, 364 (V2)
physical examination in, 107-109,
107-109f (V2)
primary tooth injury in, 122-125,
123b, 123-126f (V2)
prognosis in, 132f, 132-135, 134f,
135f (V2)
I-94 INDEX
Tooth (Continued)
pulp exposure with non-vital pulp
in, 115-116, 116f (V2)
pulp exposure with vital pulp in,
114-115 (V2)
reactions of teeth to trauma and,
130b, 130-131, 131f, 132f
(V2)
root fracture in, 116-117, 117f,
118f (V2)
socket wall fracture in, 126 (V2)
splinting techniques for, 128-130,
129f (V2)
subluxation of tooth in, 118 (V2)
displacement during exodontia, 213-
214 (V1)
fracture of
basic exodontia for, 186 (V1)
crown-root, 116 (V2)
enamel, 113 (V2)
during extraction, 194f, 212 (V1)
root, 116-117, 117f, 118f (V2)
socket wall, 126 (V2)
injury of
during extraction, 191, 212, 213f
(V1)
during laser therapy, 243 (V1)
mandibular asymmetry and, 99t (V3)
mandibular fracture and, 156 (V2)
postoperative movement of, 401 (V3)
postsurgical discoloration of, 412
(V3)
tooth size discrepancy
mandibular surgery complications
and, 422-423, 423f (V3)
maxillary surgery complications
and, 458 (V3)
Tooth ankylosis, 412-413 (V3)
Tooth bleaching, laser-assisted, 256
(V1)
Tooth bud, 165 (V1)
Tooth decay, 185 (V1)
Tooth extraction, 185-211 (V1)
alveolar ridge preservation after, 438-
440 (V1)
autotransplantation of impacted
tooth versus, 171-172 (V1)
basic, 185-192 (V1)
complications in, 191-192 (V1)
diagnosis and treatment planning
in, 187 (V1)
indications for, 186-187 (V1)
pain management in, 192 (V1)
principles of, 187-190, 188-190f
(V1)
socket preservation and wound
closure in, 190-191 (V1)
complicated, 192-201 (V1)
bone removal in, 193-194, 194f
(V1)
of canines, 196-197, 197-199f (V1)
flap design in, 192-193, 193f, 194f
(V1)
general principles of, 192 (V1)
of impacted teeth other than third
molars, 195-196 (V1)
indications for, 192b (V1)
of premolars, 197-199, 200f (V1)
sectioning of teeth and removal in,
194-195, 195f, 196f (V1)
of teeth located in uncommon
anatomic positions, 200-201,
201f (V1)
wound closure in, 201 (V1)
complications of, 212-222 (V1)
alveolar osteitis in, 216 (V1)
bisphosphonate-related
osteonecrosis in, 217, 218t
(V1)
displacement of teeth and root tips
in, 213-214 (V1)
hemorrhage in, 219 (V1)
infection in, 216-217 (V1)
injuries to teeth or adjacent
structures in, 212, 213f (V1)
oroantral communication in, 214f,
214-215 (V1)
osseous injuries in, 219f, 219i-220,
220f (V1)
Tooth extraction (Continued)
osteoradionecrosis in, 217 (V1)
removal of wrong tooth in, 212
(V1)
residual root remnants in, 213
(V1)
sensory nerve injuries in, 215f,
215-216, 216f (V1)
soft tissue injuries in, 214 (V1)
swallowing or aspiration of teeth,
crowns, or restorations in, 215
(V1)
temporomandibular joint problems
in, 218 (V1)
tissue emphysema in, 215 (V1)
trismus, pain, and swelling in,
217-218 (V1)
immediate implant loading following,
534f, 534-535, 535f, 540-546
(V1)
adaptive morphology of maxillary
alveolar process and, 541
(V1)
atraumatic extraction techniques
and, 541, 542f (V1)
bone loss following extraction and,
541, 541f (V1)
classification of extraction
socket defects and, 541,
543f (V1)
clinical situations for, 542-544,
544f, 545f (V1)
healing of extraction socket and,
540-541 (V1)
of impacted third molar tooth, 201-
210 (V1)
bone removal and tooth sectioning
in, 205-206, 207-210f (V1)
classification of, 203, 204f (V1)
indications and contraindications
for, 202-203 (V1)
instrumentation for, 203, 203t
(V1)
mandibular, 203-205, 205b, 206f
(V1)
maxillary, 207, 208-210f (V1)
postoperative instructions in, 208-
210, 209b (V1)
preoperative management in, 207t,
207-208, 208b (V1)
wound closure in, 206-207 (V1)
informed consent for, 212, 213b (V1)
open technique in guided bone
regeneration in, 454f, 454-455,
455f (V1)
Tooth mass relation in occlusion
evaluation, 18, 18b (V3)
Tooth sectioning
of impacted third molar, 205-206,
207-210f (V1)
in simple extraction, 194-195, 195f,
196f (V1)
Tooth-borne appliance
in mandibular widening, 338, 340f
(V3)
in maxillary distraction by intraoral
device, 347 (V3)
Tooth-tooth contact, mandible and,
812 (V2)
Topical anesthesia, 48-50 (V1)
in laser skin resurfacing, 521 (V3)
Topical ascorbic acid, 537 (V3)
Topical capsaicin for chronic facial
pain, 973t, 975 (V2)
Topical corticosteroids
for aphthous stomatitis, 620 (V2)
for oral lichen planus, 619 (V2)
for pemphigoid, 624 (V2)
for pemphigus, 625 (V2)
for prolonged erythema, 537 (V3)
for scarring in laser skin resurfacing,
543 (V3)
Topical hydroquinone, 520 (V3)
Topical lidocaine
for acute trigeminal nerve injury, 266
(V1)
for postherpetic neuralgia, 152 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)
Topical lidocaine testing
in chronic head and neck pain, 140-
141 (V1)
in trigeminal nerve injury, 264 (V1)
Topical medications for skin cancer,
739-741 (V2)
Toradol; See Ketorolac
Toronto-Melbourne approach in
cleidocranial dysplasia, 177 (V1)
Torticollis, facial asymmetry and, 853f
(V3)
Total body surface area, 321 (V2)
Total joint replacement, 797-798, 798f
(V2)
Total mandibular subapical osteotomy,
155-171 (V3)
complications in, 158, 437f, 437-438
(V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
Total maxillary intrusion
cephalometric analysis and, 373-375
(V3)
videocephalometric prediction and,
376 (V3)
Total maxillary segmental osteotomy
complications in, 198, 198f, 199f
(V3)
historical background of, 192 (V3)
indications for, 192-193 (V3)
for maxillary deficiency, 199-203f
(V3)
osteotomy design in, 196 (V3)
postoperative care in, 196-197, 197f
(V3)
surgical planning in, 197-198 (V3)
technique in, 193-196, 194-196f (V3)
Total midface deficiency
in Apert syndrome, 902 (V3)
in craniofacial dysostosis syndromes,
881, 884-886 (V3)
in Crouzon syndrome, 889-900, 892-
900f (V3)
Total parenteral nutrition, 15, 15t (V2)
Touch-evoked pain, 140 (V1)
TOVRO; See Transoral vertical ramus
osteotomy
Towne’s projection of mandible, 97,
101, 144, 145f (V2)
TPN; See Total parenteral nutrition
Trabecular ameloblastoma, 480f (V2)
Trachea of child, 94, 95f (V1)
Tracheal tube introducer, 31 (V2)
Tracheostomy
in maxillectomy, 694 (V2)
in trauma, 33, 71 (V2)
Tracheotomy
in cranio-maxillofacial trauma, 12-14,
12-14f (V2)
postoperative care of, 14 (V2)
Traction test in naso-orbital-ethmoid
fracture, 245-246 (V2)
Traditional surgical excision in skin
cancer, 736-737 (V2)
Tragus, 667f (V3)
Train-of-four pattern of stimulation, 30
(V1)
Trajectory pattern of gunshot to face,
328f (V2)
Tramadol
for acute postoperative pain, 81t, 82
(V1)
in complicated exodontia, 207t (V1)
for neuropathic orofacial pain, 999
(V2)
for temporomandibular disorders,
888t, 987 (V2)
Transbuccal approach in mandibular
fracture, 148-150, 149f, 150f (V2)
Transcaruncular approach, 226f (V2)
Transcervical-retromandibular approach
in mandibular fracture, 152, 152f,
153f (V2)
Transcervical-submandibular approach
in mandibular fracture, 150-152,
150-152f (V2)
Transcolumellar incision, 561, 561f,
567 (V3)
Transconjunctival approach
in Le Fort III osteotomy, 206 (V3)
in orbital fracture, 221-222, 222f,
223f, 224-225 (V2)
in primary reconstruction of orbit,
235f (V2)
in zygomatic fracture, 188-190, 188-
190f (V2)
Transconjunctival blepharoplasty, 544-
545, 545-547f (V3)
Transconjunctival lower lid
blepharoplasty, 590-591, 592f (V3)
Transcranial radiography in
temporomandibular disorders, 821-
822, 822f, 836, 836f (V2)
Transcutaneous capnometry, 100 (V1)
Transcutaneous electrical nerve
stimulation, 88-89 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)
for temporomandibular disorders,
892, 986 (V2)
Transcutaneous lower lid
blepharoplasty, 591, 592f (V3)
Transdermal fentanyl patch, 972, 972t
(V2)
Transfacial swing procedure, 967 (V3)
[beta]2-Transferrin test, 256 (V2)
Transfixion incision in rhinoplasty, 561,
562f (V3)
Transforming growth factors
in platelet-rich plasma, 501, 503
(V1)
temporomandibular disorders and,
849, 850f (V2)
Transfusion therapy, 15t (V1)
Transglabellar fixator in mandibular
resection, 701, 702f (V2)
Transient ischemic attack, 382 (V2)
Transient receptor potential family of
channels, 963, 976 (V2)
Transitional implant, 567-574, 568f
(V1)
for orthodontic anchorage, 570-574,
572-574f (V1)
for pontic support of fixed partial
denture, 568 (V1)
for retention of obturators, 568-569
(V1)
for single-tooth implant restoration
in narrow space, 569, 570f, 571f
(V1)
for stabilization of complete dentures,
567-568, 569f (V1)
for stabilization of removable partial
dentures, 568 (V1)
Translation of temporomandibular
joint, 817, 817f (V2)
reduction of, 905-908 (V2)
Translocation, 652, 654f (V2)
Transmaxillary radiography, 836, 836f
(V2)
Transmission, laser property, 514 (V3)
Transmission electron microscope, 416,
416f (V2)
Transnasal canthopexy, 247-248 (V2)
Transnasal wire fixation in naso-orbital-
ethmoid fracture, 247, 249f (V2)
Transoral approach
in lymphatic malformation of tongue,
582 (V2)
in mandibular fracture, 148-150,
149f, 150f (V2)
in total inferior maxillectomy, 697
(V2)
Transoral vertical ramus osteotomy,
119-136 (V3)
advantages and disadvantages of,
120-121, 121t, 122f (V3)
historical background of, 119 (V3)
indications and contraindications for,
121-122 (V3)
intraoperative procedure in, 123-128,
125-127f (V3)

Transoral vertical ramus osteotomy
(Continued)
for mandibular prognathism and
maxillary retrognathism, 130-
135 (V3)
with severe facial asymmetry, 130f,
130-131, 131f (V3)
with severe open bite, 132-135,
132-135f (V3)
postoperative physiotherapy in, 128f,
128-129 (V3)
sagittal split ramus osteotomy versus,
119, 120f, 120t (V3)
surgical treatment objectives in, 123,
124f, 125f (V3)
in two-jaw surgery, 240 (V3)
Transorbital radiography, 836, 836f (V2)
Transosseous wiring in mandibular
fracture, 156, 158f (V2)
Transpalatal arch for anchorage, 224
(V1)
Transplant recipient, cutaneous
squamous cell carcinoma in, 726,
730 (V2)
Transplantation
facial fat, 625-627, 626-628f (V3)
hair, 651-657 (V3)
complications of, 655-656 (V3)
current medical treatment for
alopecia and, 651 (V3)
micrograft and minigraft technique
in, 651-653, 652-655f (V3)
pathophysiology of alopecia and,
651 (V3)
rotational flaps in, 655, 655f, 656f
(V3)
scalp reduction in, 655, 656f (V3)
Transverse buttresses of face, 91 (V2)
Transverse cervical artery, 69f (V3)
Transverse dental arch discrepancy
clinical evaluation in, 219, 220-220f,
221f (V3)
combined maxillary and mandibular
osteotomies for, 238-247 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
complete mandibular subapical
osteotomy for, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
incidence and origin of, 219, 220f
(V3)
mandibular surgery complications
and, 421-422 (V3)
maxillary surgery complications and,
456-458 (V3)
orthopedic rapid maxillary expansion
for, 224-226, 224-226f (V3)
surgically assisted maxillary
expansion for, 219-237 (V3),
227-231, 228-232f (V3)
clinical evaluation in, 219, 220-
220f, 221f (V3)
complications of, 231-232, 233f
(V3)
modification of, 232-233, 234f (V3)
orthopedic rapid maxillary
expansion and, 224-226, 224-
226f (V3)
radiographic evaluation in, 220-
223, 221-223f (V3)
segmental maxillary osteotomy
versus, 233-235 (V3)
Transverse dental arch discrepancy
(Continued)
total maxillary segmental osteotomy
for, 192-204 (V3)
complications in, 198, 198f, 199f
(V3)
historical background of, 192 (V3)
indications for, 192-193 (V3)
for maxillary deficiency, 199-203f
(V3)
osteotomy design in, 196 (V3)
postoperative care in, 196-197,
197f (V3)
surgical planning in, 197-198 (V3)
technique in, 193-196, 194-196f
(V3)
Transverse facial artery, 69f, 668f (V3)
Transverse mandibular deficiency,
mandibular widening for, 338-342,
339-342f (V3)
Transverse nasalis muscle, 554f (V3)
Tranylcypromine, 2t (V1)
Trauma, 1-411 (V2)
airway management in, 25-34 (V2)
airway assessment and, 25, 26b
(V2)
airway maneuvers and adjuncts in,
26, 26b (V2)
complications in, 33 (V2)
cricothyroidotomy in, 32f, 32-33
(V2)
endotracheal intubation in, 28-31,
31f (V2)
supraglottic airway devices for, 26-
28, 27f, 28f (V2)
systematic approach to, 25 (V2)
tracheostomy in, 33 (V2)
complex regional pain syndrome and,
157 (V1)
comprehensive patient care in, 395-
411 (V2)
accident circumstances and, 395-
396, 396f, 397f (V2)
algorithm for decision making in,
399f (V2)
final discharge planning and, 405-
409 (V2)
identification of psychosocial issues
and, 400 (V2)
long-term rehabilitation and, 408-
411, 409-410f (V2)
pre-injury health and, 398-400 (V2)
preparation for postoperative
events and, 404-405, 407f
(V2)
primary survey and, 396, 397b,
398f (V2)
prioritization and integration of
surgery and, 400b, 400-401,
402f (V2)
secondary survey and, 396-397
(V2)
surgical plan and, 401-404, 403-
406f (V2)
treatment goals in, 396b, 396t
(V2)
condylar fracture and, 141-142, 142f,
162-181 (V2)
closed treatment of, 171 (V2)
conservative management of, 171
(V2)
diagnostic imaging of, 100f, 100-
101, 168-170, 169f (V2)
endoscopic-assisted repair of, 172-
176, 176-180f (V2)
facial nerve and, 164-165, 166f
(V2)
geriatric, 389-391f, 390-393 (V2)
open treatment of, 171 (V2)
pediatric, 364-369, 369f (V2)
physical examination of, 168 (V2)
retromandibular approach in, 171-
172, 172-175f (V2)
retromandibular vein and, 164
(V2)
skeletal injuries in, 167, 167f, 170-
171 (V2)
soft tissue injuries in, 166-167, 170
(V2)
Trauma (Continued)
Spiessl and Schroll classification
of, 167, 168b (V2)
superficial temporal artery and,
163-164, 164f, 165f (V2)
temporomandibular joint anatomy
and, 162-163, 163f (V2)
treatment outcomes in, 177-179
(V2)
trigeminal nerve and, 165, 166f
(V2)
dentoalveolar, 104-138, 105f, 106f
(V2)
alveolar process fracture in, 126-
128, 127f, 128f (V2)
classification of, 110-112, 111f,
112b, 113-115t (V2)
comminution of alveolar socket in,
125 (V2)
complete tooth avulsion in, 120-
122, 121f, 122b (V2)
concussed tooth in, 118 (V2)
crown fracture in, 113-118, 116-
118f (V2)
crown infraction in, 112-113 (V2)
displacement of tooth in, 118,
118b (V2)
extrusive luxation in, 118f (V2)
general considerations in, 112
(V2)
gingival injury in, 130 (V2)
history in, 105-107 (V2)
intrusive luxation in, 118, 119f
(V2)
lateral luxation of tooth in, 119-
120 (V2)
pediatric, 364 (V2)
physical examination in, 107-109,
107-109f (V2)
primary tooth injury in, 122-125,
123b, 123-126f (V2)
prognosis in, 132f, 132-135, 134f,
135f (V2)
radiographic examination in, 102,
102f, 109-110, 110f (V2)
reactions of teeth to, 130b, 130-
131, 131f, 132f (V2)
socket wall fracture in, 126 (V2)
splinting techniques for, 128-130,
129f (V2)
subluxation of tooth in, 118 (V2)
facial; See Facial trauma
frontal sinus fracture and, 256-269
(V2)
classification of, 257-259, 261f
(V2)
clinical evaluation in, 256, 258f,
259f (V2)
pediatric, 355, 356-357f (V2)
postoperative care in, 266-268,
268f (V2)
radiologic evaluation in, 256-257,
260f, 261f (V2)
surgical anatomy and, 256, 257f,
258f (V2)
surgical management of, 259-266,
262-269f (V2)
head; See Head injury
imaging in, 91-103 (V2)
in angle of mandible fracture, 101,
101f (V2)
in avulsive facial injury, 328 (V2)
in comminuted, complicated, and
impacted fractures, 99, 99f
(V2)
in complications of treatment of
mandibular fracture, 102-103
(V2)
computed tomography in, 98-99
(V2)
in condylar fracture, 100f, 100-101,
168-170, 169f (V2)
in coronoid process and ramus
fractures, 101 (V2)
in dentoalveolar injuries, 102,
102f, 109-110, 110f (V2)
in greenstick and pathologic
fractures, 99, 100f (V2)
mandibular anatomy and, 96 (V2)
INDEX I-95
Trauma (Continued)
in mandibular body fracture, 101,
102f (V2)
mandibular series in, 96-98, 97f
(V2)
in mandibular symphysis and
parasymphysis fractures, 101,
102f (V2)
midfacial anatomy and, 91, 92f
(V2)
in orbital fracture, 209-211, 210f,
211f (V2)
panoramic radiography in, 98, 99f
(V2)
rendering techniques in, 92-94, 93-
95f (V2)
in simple and compound fractures,
99, 99f (V2)
in soft tissue trauma to neck, 94-
95, 96f (V2)
supplemental radiographs in, 98
(V2)
techniques in, 91-92, 92f, 92t (V2)
in zygomatic fracture, 184-185,
185f (V2)
initial assessment in, 35-42, 36t (V2)
adjuncts to primary survey and, 39-
40 (V2)
adjuncts to secondary survey and,
40-41 (V2)
airway evaluation in, 35-36 (V2)
breathing evaluation in, 36, 36f,
37f (V2)
circulation evaluation in, 37-38,
38f, 38t (V2)
definitive care and, 41 (V2)
disability evaluation in, 38-39, 39t
(V2)
exposure and environment control
in, 39, 39f (V2)
penetrating injuries and, 41-42
(V2)
secondary survey and, 40 (V2)
intensive care in, 42-48, 43t (V2)
abdominal compartment syndrome
and, 45-46, 46f (V2)
acalculous cholecystitis and, 45
(V2)
acute adrenal insufficiency and, 46-
47 (V2)
acute renal failure and, 46 (V2)
acute respiratory distress syndrome
and, 43-44, 44t (V2)
adynamic ileus and, 45 (V2)
atrial fibrillation and, 44-45 (V2)
blood loss and, 46 (V2)
blunt myocardial injury and, 44
(V2)
fluids, electrolytes, and nutrition
and, 45 (V2)
infectious disease and, 47 (V2)
intensive insulin therapy and, 46-
47 (V2)
intubation and mechanical
ventilation and, 43 (V2)
pain control and sedation and, 47
(V2)
prophylaxis and, 48 (V2)
rehabilitation and, 48 (V2)
shock and, 44 (V2)
systemic inflammatory
response and multiple
organ failure syndrome and,
44, 44t (V2)
tubes and lines and, 47-48 (V2)
mandibular fracture and; See
Mandibular fracture
maxillofacial fracture in geriatric
patient and, 374-394 (V2)
aging of face and neck in, 377
(V2)
anesthetic management in, 385,
385b (V2)
closed versus open reduction of
fractures in, 386t (V2)
cognitive evaluation and informed
consent in, 380 (V2)
considerations in management of,
392t (V2)
I-96 INDEX
Trauma (Continued)
epidemiology of, 374-377, 375t,
376-377f (V2)
mandibular fractures in, 389-392f,
390-393 (V2)
maxilla and midface fractures in,
386-390, 387-389f (V2)
medications and over-the-counter
drug history and, 380 (V2)
nutrition and fluid and electrolyte
management in, 379 (V2)
perioperative risk assessment of co-
morbid systemic disease in,
380t, 380-385 (V2)
social history and, 379-380 (V2)
wound healing and, 377-378, 378f
(V2)
midface fracture and, 239-255 (V2)
anatomy in, 239, 240f (V2)
classification of, 239-240, 240f,
241f (V2)
complications in, 253-254 (V2)
geriatric, 386-390, 387-390f, 392t
(V2)
imaging of, 241f, 241-242, 242f
(V2)
Le Fort fractures in, 248-253, 250-
252f (V2)
naso-orbital-ethmoid fracture in,
243-248, 243-249f (V2)
neurologic injury in, 242-243 (V2)
pediatric, 253, 363 (V2)
multi-system, 65-73 (V2)
abdominal evaluation and, 65-67,
66f, 67f (V2)
antibiotics and, 73 (V2)
complex pelvic fractures and, 68f,
68-69, 69f (V2)
deep venous thrombosis
prophylaxis and, 72-73 (V2)
ICU considerations and, 70-72
(V2)
occult pneumothorax and, 68, 68f
(V2)
occult vascular injuries and, 69-70,
70f (V2)
preparation for rehabilitation and,
73 (V2)
steroids and, 72 (V2)
tertiary examination and, 72 (V2)
myofascial pain syndromes and, 143
(V1)
nasal fracture and, 270-283, 271f
(V2)
anatomy and pathogenesis of, 270-
273, 272f, 273f (V2)
classification of, 275, 275t (V2)
closed reduction in, 276-278, 278f,
279f (V2)
complications of, 281-282 (V2)
diagnosis and evaluation of, 273-
275, 274f (V2)
medical management of, 275 (V2)
open reduction in, 278-281, 280f
(V2)
pediatric, 281, 362-363 (V2)
neurologic assessment in, 11, 49-56
(V2)
detailed evaluation in, 51-52 (V2)
grading severity of injury and, 52-
56, 54f, 54t (V2)
initial evaluation and, 49-51 (V2)
ocular, 74-90 (V2)
carotid cavernous fistula and, 89
(V2)
cranial nerve injury in, 85-86 (V2)
eyelid injuries in, 88 (V2)
globe dystopia in, 88 (V2)
nasolacrimal injuries in, 88-89, 89f
(V2)
nonperforating, 78-82, 78-82f (V2)
ophthalmic assessment in, 74-78,
75-78f (V2)
orbital fractures in, 86f, 86-88, 87f
(V2)
orbital injury and, 83-85, 84f (V2)
penetrating, 83, 83f (V2)
orbital, 83-86 (V2)
cranial nerve injury in, 85-86 (V2)
Trauma (Continued)
displacement of globe in, 88 (V2)
intraorbital foreign body in, 83-84,
84f (V2)
optic disc avulsion in, 83, 84f (V2)
orbital fracture in, 86f, 86-88, 87f
(V2); See also Orbital fracture
traumatic optic neuropathy in, 84-
85 (V2)
traumatic retrobulbar hemorrhage
in, 84f, 84 (V2)
perioperative management of, 1-16
(V2)
abdominal assessment in, 11 (V2)
airway assessment in, 2-4, 3f, 4f
(V2)
breathing assessment in, 4-6 (V2)
chest imaging studies in, 11 (V2)
circulation problems and, 6-7, 7t
(V2)
disability status in, 7-8, 8t (V2)
ear examination in, 9 (V2)
exposure and environmental
control in, 8 (V2)
eye examination in, 9 (V2)
head injury and, 8-9 (V2)
historic perspective in, 1, 2f (V2)
history in, 8 (V2)
musculoskeletal assessment in, 11-
12 (V2)
neck examination in, 10f, 10-11
(V2)
neurologic examination in, 11
(V2)
nose and neurologic evaluation in,
9 (V2)
perineal, rectal, and vaginal
assessment in, 11 (V2)
primary survey in, 1 (V2)
secondary survey in, 8 (V2)
throat examination in, 9, 10f (V2)
postoperative management of, 14-15,
15f, 15t (V2)
reactions of teeth to, 130b, 130-131,
131f, 132f (V2)
soft tissue, 283-326 (V2)
abrasion in, 289 (V2)
from air bag device blast, 313,
314f, 315f (V2)
anatomic considerations in, 283,
284t, 285f (V2)
anesthesia for, 284 (V2)
avulsive wounds in, 289-290, 290f,
291f (V2)
bite wounds in, 290-292, 292f,
313-316, 314-317f (V2)
burn-related, 321-323, 321-323f,
322t (V2)
of cheek, 320f, 320-321, 321f (V2)
closure of, 284, 285f, 288f (V2)
of ear, 294, 297f, 310-313, 312f,
313f (V2)
of eyelid and nasolacrimal
apparatus, 292-294, 295f, 296f
(V2)
initial evaluation and early
management of, 283, 284f
(V2)
laceration in, 289, 290f (V2)
of lip, 294, 298f (V2)
nasal, 301, 302-305f (V2)
of neck, 294, 316-318, 318f (V2)
of parotid gland, 294, 318-320,
320f (V2)
pediatric, 292, 293f, 371f, 372
(V2)
periorbital, 301-310, 306-311f
(V2)
of peripheral nerves, 318, 319f
(V2)
of scalp, 292, 293-294f, 323-324,
324f, 325f (V2)
suture materials for, 284-289, 286-
287t (V2)
wound care in, 294-299 (V2)
temporomandibular disorders and,
979 (V2)
of temporomandibular joint, 218
(V1), 820-821 (V2)
Trauma (Continued)
wound repair in, 17-24 (V2)
aberrant bone healing in, 22-23
(V2)
abnormal wound healing in, 22
(V2)
bone regeneration in, 22 (V2)
coagulation and, 17, 18f (V2)
formation of granulation tissue
and, 19-21, 20f (V2)
future directions in, 23, 23f (V2)
inflammation and, 17-19, 19f (V2)
neural control of, 21 (V2)
phases of, 17, 18f (V2)
prevention of infection in, 21-22
(V2)
remodeling phase of, 21f, 21 (V2)
zygomatic fracture and, 182-201 (V2)
anatomy in, 182-183, 183f (V2)
Carroll-Girard screw for, 186, 186f
(V2)
coronal approach in, 191-192 (V2)
eyebrow approach in, 187, 188f
(V2)
fixation in, 192, 193f (V2)
fracture patterns in, 206-207, 206-
208f (V2)
history and physical examination
in, 183b, 183-184, 184f (V2)
indications for radiographs and
surgery in, 184-185, 185f (V2)
infraorbital paresthesia and, 194-
195 (V2)
late-onset post-traumatic
enophthalmos and, 198 (V2)
lateral canthotomy in, 186-187
(V2)
lower eyelid approaches in, 187-
188, 188f (V2)
malunion of, 197f, 197-198 (V2)
persistent diplopia following, 195-
197, 196f, 196t (V2)
primary reconstruction in, 231f,
231-233, 232f (V2)
radiography in, 184-185, 185f (V2)
retrobulbar hemorrhage and, 198-
199 (V2)
soft tissue complications of, 195
(V2)
subciliary approach in, 190-191,
191f (V2)
subtarsal approach in, 191 (V2)
transconjunctival approach in,
188-190, 188-190f (V2)
traumatic optic neuropathy and,
197 (V2)
upper eyelid approach in, 187, 187f
(V2)
vestibular approach in, 186 (V2)
zygomatic arch fracture and, 192-
194, 194f (V2)
Traumatic arthritis of
temporomandibular joint, 854-855
(V2)
Traumatic bone cyst, 869 (V2)
Traumatic intracerebral hematoma/
cerebral contusion, 61-62 (V2)
Traumatic intraventricular hemorrhage,
63 (V2)
Traumatic iritis, 80f, 80-81 (V2)
Traumatic neuroma, trigeminal, 154-
155 (V1)
Traumatic neuropathic pain assessment,
264-265, 265f (V1)
Traumatic optic neuropathy, 84-85
(V2)
after zygomatic fracture repair, 197
(V2)
in orbital fracture, 213-214 (V2)
Traumatic orofacial neuropathies, 996-
999, 998t, 999t (V2)
Traumatic pupil, 50 (V2)
Traumatic retrobulbar hemorrhage, 84,
84f (V2)
Traumatic subarachnoid hemorrhage,
62 (V2)
Traumatic telecanthus, 243, 243f (V2)
Tray setup, 360-361 (V1)
Trazodone, 889t (V2)
Treacher Collins syndrome, 936-960,
937f (V3)
classification of temporomandibular
joint-mandibular malformation
in, 939-943, 943-944f (V3)
considerations during infancy and
early childhood, 939, 943f (V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956 (V3)
external ear reconstruction in, 955-
956 (V3)
facial growth potential in, 939, 940-
942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855 (V3)
mandibular distraction osteogenesis
in, 998-1001f, 998-1002 (V3)
maxillomandibular reconstruction in,
948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital reconstruction
in, 943-948, 944-948f (V3)
zygomatic deformity in, 851 (V3)
Trephine bone core sinus elevation
technique, 464-468, 464-468f (V1)
Treponema denticola, 391 (V1)
Tretinoin, 519-520 (V3)
Triamcinolone acetonide, 543 (V3)
Triangular fossa of external ear, 667f
(V3)
Triazolam, 58, 58t (V1), 889f (V2)
Trichloroacetic acid for chemical peel,
663 (V3)
Trichophytic forehead and brow lift,
610-617 (V3)
comparison of lift techniques and,
611t (V3)
complications in, 614-616, 616f, 617f
(V3)
fixation techniques in, 610-611 (V3)
patient selection for, 613-614, 615f,
616f (V3)
surgical technique in, 611-614f, 612-
613 (V3)
Tricyclic antidepressants
for chronic facial pain, 973, 973t (V2)
for complex regional pain syndrome,
158 (V1)
interaction with local anesthetics
with vasoconstrictors, 42t, 42-43
(V1)
for migraine, 148 (V1)
for myofascial pain, 144 (V1)
for neuropathic orofacial pain, 999,
999t (V2)
for postherpetic neuralgia, 152 (V1)
for posttraumatic headache, 153 (V1)
for posttraumatic trigeminal
neuralgia, 156 (V1)
for temporomandibular disorders,
888, 889t, 986 (V2)
Trigeminal brainstem sensory nuclear
complex, 79-80, 80f (V1)
Trigeminal nerve
burning mouth syndrome and, 995
(V2)
chronic facial pain and, 117 (V1),
961-962, 962f (V2)
condylar fracture and, 165, 166f (V2)
eyelid and, 585 (V3)
forehead and brow lift and, 598 (V3)
head injury and, 52 (V2)
maxillary sinus and, 459 (V1)
nose and, 556 (V3)
pain sensation and, 79 (V1)
temporomandibular joint and, 809
(V2)
Trigeminal nerve block for trigeminal
neuralgia, 150 (V1)
Trigeminal nerve injury, 259-284 (V1)
acute, 265-266, 266f, 267f (V1)
classification of, 259-261, 260t (V1)
clinical neurosensory testing in, 262f,
262-264, 263f (V1)

Trigeminal nerve injury (Continued)
decompression in, 268 (V1)
determinants of nerve injury
responses, 261 (V1)
in facial trauma, 272-273 (V1)
function impairment assessment in,
261, 261t (V1)
impacted third molar removal-
related, 276-278 (V1)
implant-related, 275-276 (V1)
inferior alveolar nerve repairs in,
266f, 270 (V1)
infraorbital nerve repairs in, 270
(V1)
internal neurolysis in, 268-269 (V1)
lingual nerve repairs in, 269f, 269-
270 (V1)
local anesthetic injection-related,
273-274 (V1)
medicolegal issues in, 278-279 (V1)
nerve grafting in, 269 (V1)
neuroma resection in, 268 (V1)
neurorrhaphy in, 269 (V1)
orthognathic, 275 (V1)
outcomes of repair in, 271-272 (V1)
pain and discomfort assessment in,
261t, 261-262 (V1)
patient selection for nerve repair in,
265 (V1)
pharmacologic testing in, 264 (V1)
postoperative management of, 270-
271 (V1), 405 (V3)
sensory reeducation and patient
follow-up in, 271 (V1)
in skin cancer, 729 (V2)
surgical and endodontic medicament-
related, 274-275 (V1)
surgical instrumentation for, 267-268
(V1)
timing of surgery for, 266-267 (V1)
traumatic neuropathic pain
assessment in, 264-265, 265f
(V1)
Trigeminal nerve repair
decompression in, 268 (V1)
inferior alveolar nerve repairs and,
266f, 270 (V1)
infraorbital nerve repairs and, 270
(V1)
internal neurolysis in, 268-269 (V1)
lingual nerve repairs and, 269f, 269-
270 (V1)
nerve grafting in, 269 (V1)
neuroma resection in, 268 (V1)
neurorrhaphy in, 269 (V1)
outcomes of, 271-272 (V1)
postoperative management in, 270-
271 (V1)
for posttraumatic trigeminal
neuralgia, 156-157 (V1)
sensory reeducation and patient
follow-up in, 271 (V1)
surgical instrumentation for, 267-268
(V1)
timing of, 266-267 (V1)
Trigeminal neuralgia, 990-992t, 990-
993 (V2)
chronic head and neck pain in, 149-
151 (V1)
chronic orofacial pain in, 118 (V1)
postherpetic, 994 (V2)
posttraumatic, 154-156 (V1)
Trigeminal root and brainstem
procedures, 151 (V1)
Trigeminoautonomic variants, 148-149
(V1)
Trigemino-cardiac reflex, bradycardia
during Le Fort I osteotomy and,
470 (V3)
Trigeminoreticular tract, 962, 962f
(V2)
Trigeminothalamic tract, 962, 962f
(V2)
Trigger point, 979, 980, 981f (V2)
Trigger point injection, 986 (V2)
Trigonocephaly, 852f, 871-874, 874-
876f (V3)
Tripod concept in tip plasty, 562, 563f
(V3)
Tripod fracture, 93f, 93-94 (V2)
Trismus, 898-899 (V2)
exodontia-related, 217-218 (V1)
local anesthetic-related, 47 (V1)
Trochlear nerve
chronic orofacial pain and, 117 (V1)
eyelid and, 584f (V3)
head injury and, 51-52 (V2)
True cementoma, 511 (V2)
Tuberculosis, 541 (V2)
Tube-shift technique, 167, 168f (V1)
Tumescent solution
in cervicofacial liposuction, 622 (V3)
in hair transplantation, 653 (V3)
in rhytidectomy, 500 (V3)
Tumor(s)
benign nonodontogenic, 592-610
(V2)
aneurysmal bone cyst in, 596-597,
597-598f (V2)
central giant cell granuloma in,
592-594, 593f, 593t (V2)
cherubism in, 595-596, 596f (V2)
chondroma in, 605-606 (V2)
desmoplastic fibroma in, 606-608,
607-608f (V2)
fibrous dysplasia in, 600-601 (V2)
florid cemento-osseous dysplasia in,
601, 601f (V2)
focal cemento-osseous dysplasia in,
601 (V2)
giant cell tumor in, 594 (V2)
hyperparathyroidism lesion in,
594f, 594-595 (V2)
juvenile ossifying fibroma in, 599-
600, 600f (V2)
neurofibroma in, 602, 604f (V2)
ossifying fibroma in, 598, 599f
(V2)
osteoblastoma in, 602-604, 605f
(V2)
osteochondroma in, 606 (V2)
osteoid osteoma in, 602 (V2)
osteoma in, 604-605, 606f (V2)
periapical cemental dysplasia in,
601 (V2)
schwannoma in, 601-602, 603f
(V2)
chronic facial pain in, 964 (V2)
facial asymmetry and, 293, 293f, 853f
(V3)
infantile hemangioma in, 577-579,
578f (V2)
lymphoma, 758-766, 759b (V2)
angiocentric, 761-762 (V2)
diagnosis of, 758-759, 759f, 760f
(V2)
Hodgkin’s, 759-760, 760f (V2)
non-Hodgkin’s, 760-761, 761f
(V2)
of parotid gland, 551, 556 (V2)
prognosis of, 763-764, 764b (V2)
radiographic evaluation of, 762f,
762-763 (V2)
treatment of, 763 (V2)
medical oncology in, 777-788 (V2)
background of, 777, 778f (V2)
chemotherapy for metastatic
carcinoma and, 778-781, 779t,
781t, 782t (V2)
epidemiology and, 777 (V2)
epidermal growth factor receptors
and, 782-783, 783t (V2)
induction chemotherapy and, 777-
778 (V2)
salivary gland cancers and, 783-
785, 785f (V2)
taxanes in, 781-782 (V2)
molecular biology of, 645-679 (V2)
cancer cell evasion of apoptosis
and, 660-662, 661f (V2)
cancer cell insensitivity to growth
inhibitory signals and, 658-
660, 659f (V2)
cancer cell release from growth
signal requirement and, 655-
658, 657f (V2)
cancer cell versus normal cell and,
646-647, 647f (V2)
Tumor(s) (Continued)
chromosomal abnormalities in
cancer cells and, 652-653,
653-655f (V2)
epigenetic alteration of gene
expression in cancer cells and,
655 (V2)
gene regulation of cell function
and, 648-652, 649-651f (V2)
immortalization of cancer cell and,
662-664, 663f (V2)
molecular diagnostics in oncology
and, 666-669, 667f (V2)
neovascularization and, 664, 665f
(V2)
nucleotide sequence abnormalities
in cancer cells and, 653-655,
656f (V2)
strategies of cancer-related
molecular therapeutics and,
669-671, 670f (V2)
stromal changes in cells and, 645,
646f (V2)
targeted therapy based on tumor
behavior and, 671-673 (V2)
tissue invasion and metastases and,
664-666, 666f (V2)
odontogenic, 466-538 (V2)
adenomatoid, 181 (V1) 469-472,
470-472f (V2)
ameloblastic fibrodentinoma in,
524-527, 527f (V2)
ameloblastic fibroma in, 522-524,
523f (V2)
ameloblastic fibro-odontoma in,
524, 525f, 526f (V2)
ameloblastoma in, 476-502 (V2);
See also Ameloblastoma
biopsy of, 467-468 (V2)
calcifying, 445-447, 447f, 473-476,
474f, 475f (V2)
cementoblastoma in, 510-512 (V2)
classification of, 466-467 (V2)
clear cell, 502-508, 503-507f (V2)
clinical considerations in, 467
(V2)
fibroma in, 508-510, 509f, 511f
(V2)
imaging of, 467 (V2)
intraosseous odontogenic
carcinoma in, 527-532, 528-
530f (V2)
management objectives in, 468-
469 (V2)
myxoma in, 512-517f, 512-518
(V2)
odontoameloblastoma in, 519-522
(V2)
odontoma in, 518-519, 519-521f
(V2)
sarcoma in, 532-533 (V2)
squamous, 472f, 472-473 (V2)
pediatric, 961-995 (V3)
adenomatoid odontogenic tumor
in, 968, 968f (V3)
ameloblastic fibroma in, 968-970,
970f (V3)
ameloblastic fibro-odontoma in,
970, 970f (V3)
ameloblastoma in, 967f, 967-968
(V3)
anatomic classification in, 962
(V3)
aneurysmal bone cyst in, 972, 974-
975 (V3)
central giant cell lesions in, 970-
972, 973f (V3)
craniofacial fibrous dysplasia in,
977-980, 980-985f (V3)
craniomaxillofacial access and,
962-967, 963-965f (V3)
endoscopic approaches in, 967
(V3)
imaging of, 961-962 (V3)
juvenile aggressive fibromatosis in,
970, 972f (V3)
juvenile nasopharyngeal
angiofibroma in, 972-974,
976-977f (V3)
INDEX I-97
Tumor(s) (Continued)
juvenile ossifying fibroma in, 974-
977, 978-979f (V3)
neurofibromatosis in, 980-984, 986f
(V3)
odontogenic myxoma in, 968, 969f
(V3)
odontoma in, 970, 971f (V3)
reconstruction in, 988-993, 991f,
992f (V3)
rhabdomyosarcoma in, 984-986,
987f (V3)
salivary gland tumor in, 987-988
(V3)
sarcomas in, 986-987, 988-990f
(V3)
salivary gland, 546-555 (V2)
benign, 547-549, 549-551f (V2)
high-grade malignant, 549-550,
552f (V2)
low-grade malignant, 549 (V2)
nonsalivary, 550-555, 553-556f
(V2)
parotid gland, 546-547, 548f (V2)
pediatric, 987-988 (V3)
sarcomas of jaws, 680-704 (V2)
chondrosarcoma in, 684f, 684-685
(V2)
Ewing’s sarcoma in, 687, 688f, 689f
(V2)
mandibular approaches in, 699-
702, 701f, 702f (V2)
maxillectomy in, 692-699, 694f,
695f, 697-699f (V2)
metastatic tumors to jaw and, 687-
689 (V2)
multiple myeloma and, 685-687,
686f, 687f (V2)
osteosarcoma in, 680-684, 681f,
682f (V2)
patient evaluation in, 689-692,
690t, 691f (V2)
radiation-induced, 685 (V2)
temporomandibular joint, 866-875,
867b (V2)
aneurysmal bone cyst in,
868 (V2)
arteriovenous malformation in, 870
(V2)
benign osteoblastoma in, 871 (V2)
central giant cell granuloma in,
869 (V2)
chondroblastoma in, 868 (V2)
chondrosarcoma in, 872 (V2)
condylar hyperplasia in, 868 (V2)
fibrous dysplasia in, 870 (V2)
ganglion and synovial cysts in, 869
(V2)
Garr[ac]e’s osteomyelitis and, 874
(V2)
hemangioma in, 869-870 (V2)
heterotopic bone formation in,
874-875 (V2)
idiopathic bone cavity cyst in, 869
(V2)
Langerhans cell histiocytosis and,
874 (V2)
metastatic carcinoma and, 874
(V2)
multiple myeloma in, 873-874
(V2)
nonossifying fibroma in,
870 (V2)
osteochondroma in, 871 (V2)
osteoid osteoma in, 871 (V2)
osteoma in, 871 (V2)
osteosarcoma in, 873 (V2)
phantom bone disease and, 875
(V2)
pigmented villonodular synovitis
and, 871-872 (V2)
pseudoankylosis and, 900 (V2)
pseudocyst in, 868-869 (V2)
synovial chondromatosis and, 872
(V2)
synovial chondrosarcoma in, 872-
873 (V2)
synovial sarcoma in, 873 (V2)
trigeminal neuralgia and, 992 (V2)
I-98 INDEX
Tumor, node, and metastases staging
in lip cancer, 742-743 (V2)
in melanoma, 754-755, 755t (V2)
in skin cancer, 733-734 (V2)
Tumor biomarkers, 668 (V2)
Tumor dormancy therapy, 672 (V2)
Tumor necrosis factor-alpha,
temporomandibular disorders and,
849, 850f (V2)
Tumor suppressor gene, 647 (V2)
Tumor suppressor proteins, 655 (V2)
Tuned aperture computed tomography
in temporomandibular disorders,
841-843, 844f (V2)
Turbinate modification in rhinoplasty,
571 (V3)
Two-dimensional radiation treatment
planning, 772 (V2)
Two-flap palatoplasty, 763-771 (V3)
for closure of palatal fistula, 829-830,
830f (V3)
controversies in, 762 (V3)
fistula rates in, 765-766, 766t (V3)
growth outcomes in, 769-770 (V3)
history of, 764 (V3)
muscular reconstruction in, 768 (V3)
outcomes based on cleft type or
severity and, 768-769 (V3)
principle techniques in, 764, 764f,
765f (V3)
speech outcomes in, 766-767, 767b
(V3)
surgical procedure in, 770f, 770-771,
771f (V3)
syndromic associations and outcomes
in, 769 (V3)
technique comparisons in, 768 (V3)
timing of, 767-768 (V3)
Two-hit hypothesis of cancer, 647-648,
655 (V2)
Two-jaw surgery, 238-247 (V3)
cephalometric analysis and, 375 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
model surgery and, 364-371 (V3)
construction of intermediate splint
in, 368-369, 369f, 370f (V3)
marking cast in, 366-367 (V3)
measurements in, 367f, 367-368
(V3)
mounting case in, 364-366, 365f,
366f (V3)
positioning of maxilla in, 368, 368f
(V3)
for segmental surgery, 369-370,
370f (V3)
for special situations, 370-371 (V3)
occlusal plane rotation in, 248-271
(V3)
clockwise rotation in, 252-256,
252-256f (V3)
counterclockwise rotation in, 256-
260, 257-263f (V3)
development of surgical
cephalometric treatment
objective and, 260-265, 264-
266f (V3)
geometry and planning of, 248-
249, 249f, 250f (V3)
geometry of treatment design using
constructed
maxillomandibular triangle in,
261f, 261-262 (V3)
linear dimensions between
maxillary length and vertical
facial height in, 250, 250f
(V3)
muscle orientation and, 268-271,
270f (V3)
neuromuscular adaptation in, 268,
268f, 269f (V3)
orthodontic considerations in, 266-
267 (V3)
reconciliation of cephalometric
rotation point with surgical
rotation point in, 266, 267f
(V3)
Two-jaw surgery (Continued)
stretching of soft tissues in, 267-
268 (V3)
postsurgical complications in, 396
(V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
in unilateral adolescent internal
condylar resorption, 305 (V3)
for vertical maxillary excess,
transverse discrepancy, and
mandibular excess, 242f, 242-
243, 243f (V3)
videocephalometric prediction and,
376 (V3)
Two-stage palate repair for cleft palate,
776-778 (V3)
Two-wall extraction socket defect, 541,
543f (V1)
Tylenol; See Acetaminophen
Tympanosquamosal fissure, 802 (V2)
Type 1 bovine collagen membrane, 429
(V1)
in alveolar ridge augmentation, 448f,
448-449, 449f (V1)
selection rationale for, 433-435, 434f
(V1)
Type 1 collagen cross-linked N-
telopeptide, 396-397, 397f (V1)
Type 1 diabetes mellitus, 12 (V1)
Type 2 diabetes mellitus, 12 (V1)
Type II histiocytosis, 567 (V2)
Tyrosine kinase B, 963 (V2)
U nasal dissection in, 754-755 (V3)
Ulceration
in angiocentric lymphoma, 761-762
(V2)
in basal cell carcinoma, 725 (V2)
in cutaneous hemangioma,
580 (V2)
in melanoma, 754 (V2)
in vesiculobullous diseases, 611-632
(V2)
aphthous stomatitis in, 619f, 619-
620 (V2)
Beh[ced]cet’s syndrome in, 620-
622 (V2)
epidermolysis bullosa in, 626-627
(V2)
erythema multiforme in, 627-628
(V2)
herpangina in, 617t, 617-618 (V2)
lichen planus in, 618f, 618-619
(V2)
linear IgA disease in, 625-626
(V2)
pediatric herpes simplex infection
in, 615-617 (V2)
pemphigoid in, 622-624, 623f (V2)
pemphigus in, 624-625, 625f (V2)
primary herpetic gingivostomatitis
in, 612-613, 613f (V2)
Reiter syndrome in, 622 (V2)
secondary herpes in, 613-614 (V2)
Ulcerative colitis
perioperative management of, 386-
387, 387t (V3)
preoperative evaluation of, 9 (V1)
Ulnar artery, 334f (V2)
Ulnar nerve, 334f (V2)
Ultracet; See Tramadol
Ultradol; See Etodolac
Ultram; See Tramadol
Ultrapulsation of laser, 238 (V1)
UltraPulse encore, 522 (V3)
Ultrasonography
in midface fracture, 242 (V2)
in temporomandibular disorders, 846,
892 (V2)
Ultraviolet radiation exposure
extrinsic aging and, 513 (V3)
history in laser skin resurfacing, 517
(V3)
lip cancer and, 743 (V2)
malignant melanoma and, 749 (V2)
skin cancer and, 724, 726 (V2)
Umbrella graft, 563, 564f (V3)
Underdevelopment of face, 294-313
(V3)
in adolescent internal condylar
resorption, 299-305, 303-304f,
306f (V3)
in autoimmune and connective tissue
diseases, 309-313, 310-313f (V3)
in hemifacial microsomia, 298-299,
300-302f (V3)
iatrogenic, 294 (V3)
in reactive arthritis, 305-309, 307-
309f (V3)
in temporomandibular joint
ankylosis, 294-298, 297f, 298f
(V3)
trauma-related, 294, 295f, 296f (V3)
Undifferentiated ameloblastoma, 481f
(V2)
Unicoronal craniosynostosis, 851 (V3)
Unicystic ameloblastoma, 478-479, 482-
484f, 486f, 501-502 (V2), 967f,
967-968 (V3)
Uniformity in marketing, 331b (V1)
Unilateral adolescent internal condylar
resorption, 299-305, 303-304f, 306f
(V3)
Unilateral cleft lip repair, 735-758 (V3)
comparison of surgical techniques for,
735-737 (V3)
functional approach to, 752-757 (V3)
cleft model and repair in, 752f,
752-753, 753f (V3)
closure in, 755-756, 755-757f (V3)
lip incisions in, 753-754, 754f
(V3)
review of studies in, 756 (V3)
Millard rotation and advancement
flap technique in, 737-741 (V3)
Asensio technique and, 740f, 740-
741, 741f (V3)
nasal reshaping in, 741 (V3)
postoperative care in, 741 (V3)
preoperative management in, 738
(V3)
surgical technique in, 738-739,
739f, 740f (V3)
wide cleft defect and, 742f, 743f
(V3)
presurgical dentofacial orthopedics
in, 783-790 (V3)
complications of, 786 (V3)
goals of, 784-786, 788f, 789f (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t
(V3)
presurgical nasoalveolar molding
and, 783 (V3)
Tennison triangular flap technique
in, 743-751, 744f, 745f (V3)
Millard rotation versus, 745 (V3)
surgical planning and markings in,
745-746, 746f, 746t, 747f
(V3)
surgical technique in, 746-749,
747-751f (V3)
Unilateral condylar hyperplasia, 284-
285, 286-288f, 370-371 (V3)
Unilateral dentoalveolar asymmetry,
282, 283-284f (V3)
Unilateral facial underdevelopment or
degeneration, 294-313 (V3)
in adolescent internal condylar
resorption, 299-305, 303-304f,
306f (V3)
in autoimmune and connective tissue
diseases, 309-313, 310-313f (V3)
in hemifacial microsomia, 298-299,
300-302f (V3)
iatrogenic, 294 (V3)
in reactive arthritis, 305-309, 307-
309f (V3)
in temporomandibular joint
ankylosis, 294-298, 297f, 298f
(V3)
trauma-related, 294, 295f, 296f (V3)
Unilateral lateral gaze palsy, 50-51 (V2)
Unilateral oronasal cleft deformity, 783-
790 (V3)
Unilateral oronasal cleft deformity
(Continued)
complications of, 786 (V3)
history of, 783-784, 785t (V3)
nasal deformity and, 783, 784t (V3)
presurgical nasoalveolar molding and,
783 (V3)
surgical goals in, 784-786, 788f, 789f
(V3)
Unilateral overdevelopment of face,
282-293 (V3)
in mandibular condylar
osteochondroma or osteoma,
285-291, 289-291f (V3)
in muscle hypertrophy, 291-292 (V3)
in neuromuscular disorders, 292, 292f
(V3)
in tumor, 293, 293f (V3)
in unilateral condylar hyperplasia,
284-285, 286-288f (V3)
Unilateral reactive arthritis, 305-309,
307-309f (V3)
Unincorporated entities, 285-286, 286t
(V1)
Unknown primary tumor, 771, 771t
(V2)
Unsworn statement, lawsuit and, 377
(V1)
Upper airway
of child, 94-95, 95f (V1)
obstructive sleep apnea syndrome
and, 316-337 (V3)
Delaire cephalometric analysis in,
321-323, 325-327f (V3)
diagnosis and treatment planning
in, 319-321, 322-324f (V3)
maxillary and mandibular
advancement for, 323-330,
327-332f (V3)
pathophysiology of, 316-318, 318f
(V3)
patient outcomes in, 330-336, 333-
335f (V3)
treatment options for, 318-319,
320-322f (V3)
Upper blepharoplasty incision in orbital
fracture, 223, 224f (V2)
Upper compartment of
temporomandibular joint,
arthroscopy and, 918-920, 919f
(V2)
Upper eyelid
anatomy of, 581f (V3)
blepharoplasty of, 544-545, 546-548f,
589-590, 590f, 591f (V3)
physical examination of, 587-588
(V3)
ptosis of, 579, 580f, 588 (V3)
in craniofacial dysostosis
syndromes, 881 (V3)
following Botox injection, 661 (V3)
sebaceous gland carcinoma of, 727,
727f (V2)
Upper eyelid approach in zygomatic
fracture, 187, 187f (V2)
Upper lid height, 4, 5f (V3)
Upper lip, Botox injection in, 660 (V3)
Upper lip length, 11 (V3)
Upper molar position, 14, 16f (V3)
Upper respiratory tract infection
pediatric preanesthetic assessment
and, 98 (V1)
preoperative evaluation of, 5 (V1)
Upper third of face
endoscopic forehead and brow lift
and, 595-609, 596f (V3)
bone anatomy and, 595-597 (V3)
complications in, 606-607 (V3)
endoscopic anatomy and, 600-602,
601f (V3)
muscle and fascial anatomy and,
597-598, 598f (V3)
postoperative care in, 606 (V3)
preoperative evaluation in, 602t,
602-603 (V3)
technique in, 603f, 603-606, 605f
(V3)
vessel and nerve anatomy and,
598-600, 598-600f (V3)

Upper third of face (Continued)
profile evaluation and, 3 (V3)
trichophytic forehead and brow lift
and, 610-617 (V3)
comparison of lift techniques and,
611t (V3)
complications in, 614-616, 616f,
617f (V3)
fixation techniques in, 610-611
(V3)
patient selection for, 613-614,
615f, 616f (V3)
surgical technique in, 611-614f,
612-613 (V3)
Uprighting tooth, skeletal anchorage
for, 232 (V1)
Urethritis, 861 (V2)
Uric acid arthritis, 865 (V2)
Urie flap, 324 (V2)
Urinalysis, 19t (V1), 387 (V3)
Urinary catheter
as adjunct to primary survey, 39 (V2)
for monitoring urine output in
hemorrhagic shock, 7 (V2)
Urine output
in hemorrhagic shock, 7 (V2)
in pediatric craniomaxillofacial
trauma, 354-355 (V2)
preoperative, 387 (V3)
Urine urea nitrogen, 15 (V2)
Uvulopalatopharyngoplasty, 316, 319,
320f (V3)
laser-assisted, 252, 253 (V1)
Uvulopalatoplasty, 252-253 (V1)
V outcomes based on cleft type or
Vacuum-assisted closure device, 739
(V2)
Vaginal assessment
in cranio-maxillofacial trauma, 11
(V2)
in secondary survey, 40 (V2)
Vagus nerve evaluation
in chronic orofacial pain, 118 (V1)
in head injury, 52 (V2)
Valacyclovir
for herpes simplex virus infection,
614-615, 616-617 (V2)
for herpetic lesions, 520 (V3)
for laser skin resurfacing-related viral
infection, 541 (V3)
Valdecoxib, 393-394 (V1)
Valium; See Diazepam
Valve of Hasner, 206 (V2)
van der Woude’s syndrome, 715 (V3)
Vanishing bone disease, 875 (V2)
VAP; See Ventilator-associated
pneumonia
Vapo-coolants, 50 (V1)
Variable costs, 298 (V1)
Varicella zoster virus, 785 (V2)
Vascular ameloblastoma, 480f (V2)
Vascular anomalies, 577-591 (V2)
binary classification of, 578b (V2)
congenital hemangioma in, 579f,
579-581, 580f (V2)
infantile hemangioma in, 577-579,
578f (V2)
vascular malformations in, 581-590
(V2)
arteriovenous malformation in,
588-590, 589f (V2)
capillary malformation in, 581,
581f (V2)
lymphatic malformation in, 581-
583, 582-585f (V2)
venous malformation in, 585-588,
586-588f (V2)
Vascular endothelial growth factor in
platelet-rich plasma, 501 (V1)
Vascular head and neck pain, 146-149
(V1)
clinical examination in, 140 (V1)
cluster headache and
trigeminoautonomic variants
and, 148-149 (V1)
migraine and, 146-148, 147f (V1)
orofacial migraine variants and, 149
(V1)
Vascular infarction in Le Fort I
osteotomy, 475 (V3)
Vascular lesions of face, laser therapy
for, 251 (V1)
Vascular malformations, 581-590 (V2)
arteriovenous malformation in, 588-
590, 589f (V2)
capillary malformation in, 581, 581f
(V2)
lymphatic malformation in, 581-583,
582-585f (V2)
venous malformation in, 585-588,
586-588f (V2)
Vascular orofacial pain syndromes, 149
(V1)
Vascular trauma
arthroscopic-related, 926 (V2)
computed tomography angiography
in, 92, 93f (V2)
occult, 69-70, 70f (V2)
Vasoconstriction, inflammatory phase of
healing and, 60 (V3)
Vasoconstrictors use with local
anesthetics, 39-45, 40t, 43-45t, 44b
(V1)
Vastus lateralis muscle, anterolateral
thigh flap and, 335f (V2)
Veau score, 765, 766t (V3)
Veau-Wardill-Kilner two-flap
palatoplasty, 763-771 (V3)
controversies in, 762 (V3)
fistula rates in, 765-766, 766t (V3)
growth outcomes in, 769-770 (V3)
history of, 764 (V3)
muscular reconstruction in, 768 (V3)
severity and, 768-769 (V3)
principle techniques in, 764, 764f,
765f (V3)
speech outcomes in, 766-767, 767b
(V3)
surgical procedure in, 770f, 770-771,
771f (V3)
syndromic associations and outcomes
in, 769 (V3)
technique comparisons in, 768 (V3)
timing of, 767-768 (V3)
Velocardiofacial syndrome, 769 (V3)
Velopharyngeal dysfunction
after cleft lip and palate repair, 719,
791, 792t, 795 (V3)
after cleft palate repair, 761, 766-767,
767b (V3)
cleft orthognathic surgery and, 819-
826 (V3)
complications related to surgical
procedures for, 839 (V3)
management of, 801-803 (V3)
maxillary bone transport and, 360,
361-362, 362f (V3)
in oculoauriculovertebral spectrum,
927 (V3)
orthognathic surgery-related, 73 (V3)
secondary cleft palate surgery for,
831t, 831-835, 835f, 836-839,
837f, 838f (V3)
Velopharyngeal mechanism, 831, 835f
(V3)
Venlafaxine
for chronic facial pain, 973f, 973-974
(V2)
for neuropathic orofacial pain, 999t
(V2)
Venous access device, 47-48 (V2)
Venous drainage
of ear, 668 (V3)
of eyelid, 585 (V3)
of forehead and brow, 598 (V3)
of maxillary sinus, 459 (V1)
of nose, 273 (V2), 555 (V3)
Venous malformation, 585-588, 586-
588f (V2)
Ventilator-associated pneumonia, 47,
71 (V2)
Ventricular septal defect, 382-383
(V3)
Verapamil, 149 (V1)
VereFil lip implant, 693 (V3)
Verstan; See Prazepam
Vertebral artery, blunt trauma to, 69-70
(V2)
Vertical buttresses of face, 91, 92f (V2)
Vertical dental arch discrepancy
combined maxillary and mandibular
osteotomies for, 238-247 (V3)
for horizontal maxillary deficiency
and mandibular excess, 244f,
244-245, 245f (V3)
indications for, 238-239 (V3)
stability in, 239-240 (V3)
techniques in, 240f, 240-241, 241f
(V3)
transverse discrepancy and
mandibular excess with, 242f,
242-243, 243f (V3)
complete mandibular subapical
osteotomy for, 155-171 (V3)
complications in, 158 (V3)
indications for, 155, 156f (V3)
for mandibular alveolar deficiency,
166-170f (V3)
for midface deficiency and
mandibular dentoalveolar
protrusion, 161-165f (V3)
technique in, 156-158, 157-160f
(V3)
total maxillary segmental osteotomy
for, 192-204 (V3)
complications in, 198, 198f, 199f
(V3)
historical background of, 192 (V3)
indications for, 192-193 (V3)
for maxillary deficiency, 199-203f
(V3)
osteotomy design in, 196 (V3)
postoperative care in, 196-197,
197f (V3)
surgical planning in, 197-198 (V3)
technique in, 193-196, 194-196f
(V3)
Vertical elastics, 400 (V3)
Vertical facial height, 250, 250f (V3)
Vertical mattress suture, 288f (V2)
Vertical maxillary deficiency, 257f, 257-
258, 258f (V3)
Vertical maxillary excess, 861f, 861-862
(V3)
Vertical proportions of face
ear, 8f (V3)
nose, 7f (V3)
perioral, 8f (V3)
periorbital, 5f (V3)
Vertical ramus osteotomy, 70-71, 119-
136 (V3)
advantages and disadvantages of,
120-121, 121t, 122f (V3)
complications in, 433-436, 434f, 435f
(V3)
historical background of, 68 (V3),
119 (V3)
indications and contraindications for,
121-122 (V3)
intraoperative procedure in, 123-128,
125-127f (V3)
Le Fort I segmental osteotomy with,
199-203f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe facial asymmetry, 130f,
130-131, 131f (V3)
for mandibular prognathism and
maxillary retrognathism with
severe open bite, 132-135, 132-
135f (V3)
postoperative physiotherapy in, 128f,
128-129 (V3)
sagittal split ramus osteotomy versus,
119, 120f, 120t (V3)
surgical treatment objectives in, 123,
124f, 125f (V3)
Vertical shear pelvic fracture, 68f, 68-
69 (V2)
Vesiculobullous diseases, 611-632
(V2)
aphthous stomatitis in, 619f, 619-620
(V2)
Beh[ced]cet’s syndrome in, 620-622
(V2)
INDEX I-99
Vesiculobullous diseases (Continued)
epidermolysis bullosa in, 626-627
(V2)
erythema multiforme in, 627-628
(V2)
herpangina in, 617t, 617-618 (V2)
herpes simplex virus infections in,
612-617, 613f (V2)
pediatric, 615-617 (V2)
primary herpetic gingivostomatitis
in, 612-613, 613f (V2)
secondary herpes in, 613-614 (V2)
systemic agents for, 614-615 (V2)
lichen planus in, 618f, 618-619 (V2)
linear IgA disease in, 625-626 (V2)
pemphigoid in, 622-624, 623f (V2)
pemphigus in, 624-625, 625f (V2)
Reiter syndrome in, 622 (V2)
Vestibular approach
in bone graft harvest
from mandibular ramus, 413, 413f
(V1)
from mandibular symphysis, 410
(V1)
in interpositional bone graft, 471
(V1)
to zygomatic arch fracture, 194 (V2)
in zygomatic fracture, 186 (V2)
Vestibular ecchymosis in zygomatic
fracture, 184f (V2)
Vestibular incision
in alveolar distraction, 350-351, 351f
(V3)
in genioplasty, 141, 142 (V3)
in pediatric craniomaxillofacial
tumor, 962 (V3)
in total maxillary segmental
osteotomy, 193 (V3)
Vestibulocochlear nerve evaluation
in chronic orofacial pain, 118 (V1)
in head injury, 52 (V2)
Viaspan, 120 (V2)
Vicodin; See Hydrocodone
Video nasoendoscopy, 798 (V3)
Videocephalometric prediction, 375-
377, 376f (V3)
Vidian artery, 63, 63f, 66f, 175f (V3)
View boxes, 360 (V1)
Vigilon, 526-528 (V3)
Vinblastine, 781t (V2)
Vincristine
for lymphoma, 763 (V2)
for metastatic tumors, 779, 779t (V2)
Vinorelbine, 781t, 782t (V2)
Viral infection
facial asymmetry after, 281-282 (V3)
herpes simplex, 612-617, 613f (V2)
oral cavity cancer and, 706 (V2)
oral mucositis and, 785 (V2)
pediatric, 615-617 (V2)
primary herpetic gingivostomatitis
in, 612-613, 613f (V2)
secondary herpes in, 613-614 (V2)
systemic agents for, 614-615 (V2)
herpes zoster
neuropathic orofacial pain in, 994
(V2)
postherpetic neuralgia and, 151-
152 (V1)
laser skin resurfacing-related, 541
(V3)
oral cavity cancer and,
706-707 (V2)
of parotid gland, 542-543 (V2)
Virchow’s law, 864, 880 (V3)
Vision in marketing, 321-322 (V1)
Vistaril; See Hydroxyzine
Visual acuity
in cranio-maxillofacial trauma, 9
(V2)
in ocular injury, 74-75, 75f (V2)
in orbital fracture, 208 (V2)
in periorbital soft tissue injury, 301-
306 (V2)
Visual fields
in ocular trauma, 75-76 (V2)
in orbital fracture, 209, 215, 216f
(V2)
traumatic disorders of, 85-86 (V2)
I-100 INDEX
Visual impairment
in craniofacial dysostosis syndromes,
881 (V3)
in craniosynostosis, 865 (V3)
in midface fracture, 254 (V2)
orbital fracture-related, 212f, 212-
214, 213f (V2)
potential sites of, 204f (V2)
Vital capacity, 96t (V1)
Vital signs
age-related values, 94t (V1)
in head-injured patient, 50 (V2)
Vitamin(s), 398-399, 399t (V1)
Vitamin B12, 398 (V1)
Vitamin C, 399t (V1)
Vitamin D, 398, 399t (V1)
Vitamin K, 398, 399t (V1)
Vitreous hemorrhage, 82, 82f, 213 (V2)
Vocal dysfunction after cleft surgery,
795 (V3)
Voltaren; See Diclofenac
Volume rendering in facial injury, 92-
93 (V2)
Vomer, 173f (V2), 272
Vomiting, postoperative, 393 (V3)
child and, 108 (V1)
in mandibular surgery, 443 (V3)
Von Langenback two-flap palatoplasty,
726, 763-771 (V3)
for closure of palatal fistula, 829-830
(V3)
controversies in, 762 (V3)
fistula rates in, 765-766, 766t (V3)
growth outcomes in, 769-770 (V3)
history of, 764 (V3)
muscular reconstruction in, 768 (V3)
outcomes based on cleft type or
severity and, 768-769 (V3)
principle techniques in, 764, 764f,
765f (V3)
speech outcomes in, 766-767, 767b
(V3)
surgical procedure in, 770f, 770-771,
771f (V3)
syndromic associations and outcomes
in, 769 (V3)
technique comparisons in, 768 (V3)
timing of, 767-768 (V3)
von Willebrand disease
perioperative management of, 384-
385 (V3)
preoperative evaluation of, 16-17
(V1)
V-Y closure in lingual frenectomy, 174,
176f (V1)
W indications and contraindications for,
W. Lorenz TMJ Replacement System,
904 (V2)
Waiting area of office, 355, 355f (V1)
Waiting patient, marketing and, 333
(V1)
Wakely, Cecil, 793f (V2), 793-794
Waldeyer’s ring, lymphoma and, 758,
762 (V2)
Walsham forceps for nasal fracture
reduction, 277-278 (V2)
Ward, Terence, 795 (V2)
Wardill-Kilner two-flap palatoplasty,
763-771 (V3)
controversies in, 762 (V3)
fistula rates in, 765-766, 766t (V3)
growth outcomes in, 769-770 (V3)
history of, 764 (V3)
muscular reconstruction in,
768 (V3)
outcomes based on cleft type or
severity and, 768-769 (V3)
principle techniques in, 764, 764f,
765f (V3)
speech outcomes in, 766-767, 767b
(V3)
surgical procedure in, 770f, 770-771,
771f (V3)
syndromic associations and outcomes
in, 769 (V3)
technique comparisons in,
768 (V3)
timing of, 767-768 (V3)
Warfarin
contraindication for vitamin K, 398
(V1)
preoperative evaluation of, 2t, 17, 17t
(V1)
prophylactic, 383 (V2)
Wassmund midface fracture system, 241
(V2)
Water, photothermolysis and, 514, 514f
(V3)
Waters’ view in orbital fracture, 209,
210f (V2)
Weaning from mechanical ventilation,
43 (V2)
Web-based office system, 303 (V1)
Weber-Ferguson incision, 695, 695f
(V2), 963f, 965f (V3)
Webster’s triangle, 569 (V3)
Weight gain in child with cleft lip and
palate, 718 (V3)
Weight loss, facial skin laxity with,
686-688, 686-688f (V3)
Weir procedure, 571 (V3)
Westergren erythrocyte sedimentation
rate, 858 (V2)
Wharton’s duct cannulation, 539, 540f
(V2)
White blood cell count, 19t (V1)
Whitnall’s inferior suspensory ligament,
205, 205f (V2), 585, 586f (V3)
Whitnall’s tubercle, 204, 205 (V2),
586f, 587f (V3)
Wickham’s striae, 618 (V2)
Wide dynamic range neurons, 138 (V1)
Wire fixation
in bilateral sagittal split osteotomy,
109 (V3)
in genioplasty, 143, 149f (V3)
in mandibular fracture, 391, 391f,
391f (V2)
in mandibular lengthening by
distraction osteogenesis, 343f
(V3)
in mandibular widening, 341, 341f
(V3)
in maxillary/midface fracture, 386-
388 (V2)
in naso-orbital-ethmoid fracture, 247
(V2)
of palatal splint, 397t, 398,
398f (V3)
Wisdom tooth removal, 201-210 (V1)
bone removal and tooth sectioning
in, 205-206, 207-210f (V1)
classification of impaction and, 203,
204f (V1)
202-203 (V1)
instrumentation for, 203, 203t
(V1)
mandibular, 203-205, 205b, 206f
(V1)
maxillary, 207, 208-210f (V1)
postoperative instructions in, 208-
210, 209b (V1)
preoperative management in, 207t,
207-208, 208b (V1)
trigeminal nerve injury and, 276-278
(V1)
wound closure in, 206-207 (V1)
Withdrawing from patient’s care, 383
(V1)
Wits analysis in rotation of
maxillomandibular complex, 249f
(V3)
Wolff’s law, 144-145 (V2)
Work attendance after surgery, 411
(V3)
Worker’s compensation insurance, 303
(V1)
Working-side condyle, 811 (V2)
World Health Organization
classification of cysts of jaw, 418-419,
419b, 419t (V2)
classification of lymphoma, 758, 759b
(V2)
on melanoma excision, 754 (V2)
World Wide Web for marketing, 342
(V1)
Wound care, 294-299 (V2)
in Millard rotation and advancement
flap technique for unilateral cleft
lip, 741 (V3)
in rhytidectomy, 505-506 (V3)
Wound closure
in alveolar split graft, 471 (V1)
in bone graft for implant, 420-422,
422f (V1)
in complete mandibular subapical
osteotomy, 158 (V3)
in double-opposing Z-plasty, 773-774,
774f (V3)
in endoscopic forehead and brow lift,
606 (V3)
in exodontia
basic, 190-191 (V1)
complicated, 201 (V1)
third molar, 206-207 (V1)
in functional cleft lip repair, 755-756,
755-757f (V3)
in graft harvest from mandibular
symphysis, 410-411 (V1)
in guided tissue regeneration, 431-
435, 433f, 434f (V1)
in internal derangement of
temporomandibular joint, 934,
935f (V2)
in interpositional bone graft, 472f
(V1)
in Le Fort I osteotomy, 181, 184f
(V3)
in mandibular resection, 701, 701f
(V2)
in maxillectomy, 696, 697f (V2)
in rhytidectomy, 505, 505f (V3)
in sagittal split ramus osteotomy, 433
(V3)
in Tennison-Randall triangular flap
technique in unilateral cleft lip
repair, 749, 759f (V3)
in zygomatic implant, 496 (V1)
Wound dehiscence
after repair of zygomatic fracture, 195
(V2)
in bilateral sagittal split osteotomy,
115-116, 116b (V3)
guided tissue regeneration for, 435-
436, 447, 447f (V1)
in sinus-lift subantral augmentation,
462 (V1)
Wound healing, 17-24 (V2)
aberrant bone healing in, 22-23 (V2)
abnormal wound healing in, 22 (V2)
after laser skin resurfacing, 250 (V1)
bone regeneration in, 22 (V2)
coagulation and, 17, 18f (V2)
effects of aging on, 377-378, 378f
(V2)
effects of smoking on, 71 (V1)
of extraction socket, 540-541 (V1)
formation of granulation tissue in,
19-21, 20f (V2)
future directions in, 23, 23f (V2)
inflammation and, 17-19, 19f (V2)
laser therapy and, 253 (V1)
in mandibular orthognathic surgery,
68-70, 70f (V3)
neural control of, 21 (V2)
in orthognathic surgery, 60-71, 403f,
403-408 (V3)
airway obstruction and, 404 (V3)
bone healing and, 62 (V3)
categorization of, 62 (V3)
genioplasty and, 71 (V3)
Le Fort 1 osteotomy and, 63-68,
64-67f (V3)
mandibular osteotomy and, 68-70f,
68-71 (V3)
maxillary surgery and, 62-63, 63f
(V3)
phases of, 60-62, 61f, 62f (V3)
psychological factors in, 404
(V3)
swelling and ecchymosis and, 403-
404 (V3)
phases of, 17, 18f (V2)
platelet-rich plasma for, 501-510
(V1)
Wound healing (Continued)
allograft and alloplastic materials
and, 504f, 504-506 (V1)
benefits of, 502-503 (V1)
case report of, 509, 509f (V1)
concept of, 501-502, 502f (V1)
processing of, 506-508, 507f, 508f
(V1)
prevention of infection in, 21-22
(V2)
remodeling phase of, 21f, 21 (V2)
by secondary intention in skin
cancer, 735, 735f, 738 (V2)
Wound infection, 412 (V3)
in bilateral sagittal split osteotomy,
115, 116b (V3)
chemical peel and, 664 (V3)
exodontia-related, 216-217 (V1)
in facial fat transplantation, 627
(V3)
in frontal sinus fracture, 267 (V2)
intensive care of trauma patient and,
47 (V2)
in laser skin resurfacing, 540-541,
541f (V3)
in mandibular surgery, 443 (V3)
in otoplasty, 676 (V3)
prophylactic antibiotics and, 392-393
(V3)
in rhinoplasty, 573 (V3)
in rhytidectomy, 508-509 (V3)
sinus-lift subantral augmentation-
related, 464 (V1)
Woven bone, 22 (V2)
Wrinkling
injectable facial filler for, 637-639,
638f, 639f (V3)
intrinsic and extrinsic aging and, 513
(V3)
laser skin resurfacing for, 513-552
(V3)
anesthesia and, 521, 522f (V3)
carbon dioxide laser in, 514f, 514-
516, 515f (V3)
contact dermatitis and, 539 (V3)
dyschromias and, 541-542, 542f,
543f (V3)
erbium:YAG laser in, 532-534,
536-538f (V3)
fractional photothermolysis in,
532, 536f (V3)
history of, 513-514 (V3)
infection and, 540-541, 541f (V3)
laser blepharoplasty with, 544-545,
545-547f (V3)
laser properties in, 514f, 514-516,
515f (V3)
laser settings for, 521-522, 522f
(V3)
milia and acne formation and,
539-540, 540f (V3)
ocular complications in, 543-544
(V3)
patient evaluation in, 516-519,
518b (V3)
postoperative care in, 524-529,
526-528f, 530-531f (V3)
preoperative considerations in, 519
(V3)
prolonged erythema and, 535-537,
539f (V3)
pruritus and, 537-538, 539f (V3)
resurfacing acne scars in, 529 (V3)
rhytidectomy with, 545-548, 547-
548f (V3)
scarring and, 542-543, 543f (V3)
sepsis and, 544 (V3)
single-pass resurfacing in, 529-532,
533-534f (V3)
skin preparation for, 519-521 (V3)
telangiectasias and, 538-539 (V3)
traditional technique in, 522-524,
523f, 525-526f (V3)
traumatic and surgical scars
improvement in, 529 (V3)
treatment of benign skin lesions
in, 529 (V3)
Written request for compensation, 375
(V1)

Zygoma (Continued)
X maxilla and, 172 (V3)
Xanax; See Alprazolam
Xenograft
in alveolar ridge augmentation, 450f,
450-451, 451f (V1)
guided tissue regeneration procedures
and, 430-431, 431f, 432f (V1)
in sinus-lift subantral surgery, 458
(V1)
Xeroderma pigmentosum, 725 (V2)
Xerophthalmia after Le Fort I
osteotomy, 475 (V3)
Xerostomia, 556 (V2)
salivary pellicle and, 611 (V2)
in Sj[um]ogren’s syndrome, 866 (V2)
X-linked hypohidrotic hereditary
ectodermal dysplasia, 177 (V1)
Y 926t (V3)
Yaw, term, 365f (V3)
Yeast infection, postoperative, 410 (V3)
Yellow pages advertising, 342 (V1)
Z in, 928-929 (V3)
Zanaflex; See Tizanidine
Zero meridian of Gonzales-Ulba, 682t
(V3)
Zoledronate, 395, 396t (V1)
Zoledronic acid, 558t (V2)
Zoloft; See Sertraline
Zolpidem, 146 (V1)
Zometa; See Zoledronate
Zone of adherence in forehead and
brow lift, 597, 598f, 601, 601f
(V3)
Zostrix; See Topical capsaicin
Z-plasty technique
Furlow double-opposing, 726, 730f,
772-775, 773-775f (V3)
in lingual frenectomy, 174, 175f (V1)
in primary unilateral cleft lip repair,
722, 723f (V3)
Zyderm, 629 (V3)
Zygoma
anatomy of, 182-183, 183f (V2)
average growth completion of, 850t
(V3)
forehead and brow lift and, 595
(V3)
growth and development of, 851,
853f (V3)
malformation in craniofacial
dysostosis syndromes,
882 (V3)
oculoauriculovertebral spectrum and,
922-935 (V3)
airway management in, 926 (V3)
classification of, 925, 925b (V3)
cleft lip and palate and
velopharyngeal insufficiency
in, 927 (V3)
dysmorphology in, 922-925, 925b
(V3)
ear reconstruction in, 930 (V3)
historical perspective of, 922 (V3)
mandibular lengthening with
distraction osteogenesis in,
928, 929-930f (V3)
orthognathic surgery in, 930-934,
931-933f (V3)
staged reconstruction in, 925-926,
temporomandibular joint
reconstruction in, 927-928,
928f (V3)
zygoma and orbit reconstruction
Treacher Collins syndrome and, 851,
936-960, 937f (V3)
classification of temporomandibular
joint-mandibular
malformation in, 939-943,
943-944f (V3)
considerations during infancy and
early childhood, 939, 943f
(V3)
dysmorphology in, 936-939 (V3)
external auditory canal and middle
ear reconstruction in, 956
(V3)
external ear reconstruction in,
955-956 (V3)
facial growth potential in, 939,
940-942f (V3)
inheritance, genetic markers, and
testing in, 936 (V3)
mandibular deformity in, 855
(V3)
maxillomandibular reconstruction
in, 948-954, 950-953f (V3)
nasal reconstruction in, 954-955
(V3)
soft tissue reconstruction in, 955,
955f (V3)
zygomatic and orbital
reconstruction in, 943-948,
944-948f (V3)
Zygomatic arch
condylar head and, 163f (V2)
coronal approach to, 191-192 (V2)
fracture of, 192-194, 194f (V2)
malar augmentation with injectable
fillers and, 639, 640f (V3)
osteotomy to limit condylar
translation, 909 (V2)
Zygomatic buttress, 91, 92f (V2)
counterclockwise rotation of
maxillomandibular complex at,
256, 259f, 259t (V3)
Zygomatic deficiency, 219 (V3)
Zygomatic fracture, 182-201 (V2)
anatomy in, 182-183, 183f (V2)
Carroll-Girard screw for, 186, 186f
(V2)
coronal approach in, 191-192 (V2)
eyebrow approach in, 187, 188f (V2)
fixation in, 192, 193f (V2)
fracture patterns in, 206-207, 206-
208f (V2)
history and physical examination in,
183b, 183-184, 184f (V2)
indications for radiographs and
surgery in, 184-185, 185f (V2)
infraorbital paresthesia and, 194-195
(V2)
late-onset post-traumatic
enophthalmos and, 198 (V2)
lateral canthotomy in, 186-187
(V2)
lower eyelid approaches in, 187-188,
188f (V2)
malunion of, 197f, 197-198 (V2)
neuropathic pain after, 996 (V2)
persistent diplopia following, 195-
197, 196f, 196t (V2)
primary reconstruction in, 231f, 231-
233, 232f (V2)
radiography in, 184-185, 185f (V2)
retrobulbar hemorrhage and, 198-199
(V2)
soft tissue complications of, 195 (V2)
subciliary approach in, 190-191, 191f
(V2)
subtarsal approach in, 191 (V2)
temporomandibular joint
pseudoankylosis and, 900 (V2)
transconjunctival approach in, 188-
190, 188-190f (V2)
traumatic optic neuropathy and, 197
(V2)
upper eyelid approach in, 187, 187f
(V2)
INDEX I-101
Zygomatic fracture (Continued)
vestibular approach in, 186 (V2)
zygomatic arch fracture and, 192-194,
194f (V2)
Zygomatic implant, 491-500 (V1)
in bone transport by distraction
osteogenesis, 361f (V3)
complications in, 498f, 498-499 (V1)
final prosthesis fabrication and, 499
(V1)
historical perspective in, 491 (V1)
patient selection for, 491-492, 492f
(V1)
postoperative care in, 498 (V1)
preoperative considerations in, 493,
493f (V1)
prosthetic conversion technique in,
496-497, 497f, 498f (V1)
radiographic evaluation in, 492, 492f
(V1)
regional anatomy in, 492-493 (V1)
surgical options in, 493-494, 494f (V1)
surgical protocol in, 494-496, 494-
497f (V1)
Zygomatic nerve, 585 (V3)
Zygomatic osteotomy, 211 (V3)
Zygomaticofacial artery, 69f (V3)
Zygomatico-facial nerve, 585 (V3)
Zygomaticofacial nerve injury, 498-499
(V1)
Zygomatico-frontal nerve, 599 (V3)
Zygomaticofrontal region, surgical
approaches to, 186-187, 187f, 188f
(V2)
Zygomaticofrontal suture, 93f (V2)
eyebrow incision in orbital fracture
and, 223, 224f (V2)
Zygomaticomaxillary buttress, 227, 227f
(V3)
Zygomaticomaxillary fracture
diagnostic imaging of, 93f, 93-94 (V2)
pediatric, 361-362, 362-363f (V2)
Zygomaticomaxillary suture, 93f (V2)
Zygomaticoorbitale artery, 69f (V3)
Zygomaticosphenoid suture, 93f (V2)
Zygomatico-temporal nerve, 585, 599
(V3)
Zygomaticotemporal suture, 93f (V2)
coronal approach to, 191-192 (V2)
Zygomaticus major muscle, 174, 174f
(V3)
Botox injection in, 659, 660f (V3)
Zygomaticus minor muscle, 174, 174f
(V3)
Zyplast, 629 (V3)