Institute Of Dental Sciences,

JOURNAL OF DENTAL SCIENCES

& ORAL REHABILITATION
An official publication of institute of dental sciences, Bareilly

INSTITUTE OF DENTAL SCIENCES,

Pilibhit Bypass Road, Bareilly 243006

Journal of Dental Sciences & Oral Rehabilitation

Assistant Editor
DR SATISH KUMARAN
DR ASHISH AGGARWAL

DR (MRS) S. S. BHARATI

Communication, articles for review are to be addressed to the chief editor, Editorial office,
Intitute of Dental Sciences, Pilibhit bypass road, Bareilly, 243006
Email: drpuneetanand@gmail.com

The statement and opinions expressed in this journal are the responsibility of the concerned
authors and do not necessarily reflect the opinions of the editorial board. The editorial board will
not be responsible for any inaccuracy or misleading data, opinion or statement published in the journal
Permission of the editorial board is mandatory for reproduction of the contents of the journal in full
or in part in any form.

Published by: Institute of Dental Sciences, Bareilly, 243006

 Journal
Institute of Dental Sciences
Information For Authors
Manuscripts must be prepared in accordance with “Uniform the references and abstract).
requirements for Manuscripts to Biomedical Journal” developed by 8. Source(s) of support in the form of grants, equipment, drugs, or
International Committee of Medical Journal Editors. all of these.
9. Acknowledgement, if any; and.
Types of Manuscripts and Limits 10. If the manuscript was presented as part at a meeting the
Original articles: Up to 300 words excluding references and abstract. organization, please, and exact date on which it was read.
Case reports: Up to 1000 words excluding reference and abstract and upto
10 references. Abstract Page
Online Submission of the Manuscripts The second page should carry the full title of the manuscript and an
Articles can also be submitted online from http://www.jdsor.in abstract (of no more than150 words for case reports, brief reports and 250
1) First page File Prepare the title page, covering letter, words for original articles).The Context (Background) Aims, Settings
acknowledgement, etc using a word processor program. All and Design, Methods and Material, Statistical analysis used, Result and
information which reveals your identity should be here. Use Conclusions. Below the abstract should provide 3 to 10 key word.
text/rtf/doc/PDF files. Do not zip the files.
2) Article file; the main text of the article, beginning form Introduction:
Abstract till references (including tables) should be in this file. State the purpose of the article and summaries the rational form the study
Do not including any information (such as acknowledgement, or observation.
your names in page headers, etc.) In this file. Use text / rtf
/doc/PDF files. Do not zip the files. Limit the size to 400 kb. Methods:
Do not incorporate image in the file. If file size is large, graphs The Methods section should include only information that was available
can be submitted as image separately without incorporating at the time the plan or protocol for the study was written; all information
them in the article file to reduce the size of the file. obtained during the conduct of the study belongs in the Results Section.
3) Image; Submit good quality color image. Each image should Reports of randomized clinical trials should based on CONSORT
be less than 100 kb in size. Size of the image can be reduce by Statement (http:// www.consort-statement.org.) when reporting
decreasing the actual height and width of the images (keep up experiments on human subjects, indicate whether the procedures
to 400 pixels or 3 inches). All images formats (jpeg, tiff, gif, followed were in accordance with the ethical standards of the responsible
bmp, png, eps ect) are acceptably; jpeg is most suitable. committee on human experimentation (institutional or regional) and
4) Legends; Legends for figures / images should include at the end with the Helsinki Declaration of 1975, as revised in 2000 (available at
of the article file. http://www.wna.net/e/policy/70-c_e.html).

If the manuscripts is submitted online, the contributors form and Results

copyright transfer form has to be submitted in original with the signatures Present your results in logical sequence in the text, tables, and
of all the contributors within two weeks from submission. Hard copies of illustrations, giving the main or most important finding first. Do not
the images (3 set), for articles submitted online, should send to the journal repeat in the text all the data in the tables or illustrations; emphasize or
office at the time of submission of a revised manuscript. Editorial office: summarize only important observations extra or supplementary
Dr. Puneet Anand Editor in Chief, JDSOR. materials and technical details can be placed in an appendix where it will
be accessibly but will not interrupt the flow of the text; alternatively it can
Preparation of the Manuscript be published only in the electronic version of the journal.
Text of observational and experimental articles should be divided into
sections with headings; Introduction. Methods, Result, Discussion, Discussion:
References, Tables, Figures, Figure legends, and Acknowledgement. Do Include Summary of key findings (primary outcome measures,
not make subheadings in these sections. secondary outcome measures, results as they relate to a prior hypothesis);
Strengths and limitations of the study (study question, study design, data
Title Page collection, analysis and interpretation); interpretation and implications
The title page should carry: in the context of the totality of evidence (is there a systematic) review to
1. Type of manuscript (e.g. Original article, Case Report) refer to, if not could one be reasonable done here and now ?, What this
2. The title of the article, which should be concise, but study adds to the available evidence, effects on patient care and health
informative. policy, possible mechanisms) ; Controversies raised by this study; and
3. Running title or short title not more than 50 characters, future research direction ( for this particular research collaboration,
4. The name by which each contributor is known (last name, First underlying mechanism, clinical research). Do not repeat in detail data or
name and initials of middle name), with his or her highest other material given in the introduction or result section.
academic degree (s) and institutional affiliation. References
5. The name of the department(s) and institution(s) to which the References should be numbered consecutively in the order in which they
work should be attributed. are first mentioned in the text (not in alphabetic order). Identity
6- The name, address, phone numbers, facsimile numbers and e- references in text, tables, and legends by Arabic numerals in square
mail address of the contributor responsible for correspondence bracket ( e.g. [10] ). P l e a s e r e f e r t o I C M J E G u I d e l I n e s
about the manuscript. (http:// www.nlm.nih.gov/bsd/uniform _requirements.html) for more
7. The total number of pages, total numbers of photograph and examples.
word counts separately for abstract and for the text (excluding 1. Standard journal article: Kulkarni SB, Chitri RG, Satoskar RS.

Journal of Dental Sciences & Oral Rehabilitation

 Serum proteins in tuberculosis. J. Postgrad Med 1960: 6113-20 List
first six contributors followed by et al.
2. Chapter in a book; Phillips SJ, Whisnant JP. Hypertension and
stroke. In; Laragh JH, Brenner BM, editors. Hypertension;
Pathophysiology, diagnosis and management. 2nd ed. New York;
Raven Press; 1995 pp. 465 78.
Tables
? Tables should be self explanatory and should not duplicate
textual material
? Tables with more than 10 columns and 25 rows not acceptable.
? Number tables, in Arabic numerals, consecutively in the order
of their first citation in the text and supply a brief title for each.
? Explain in footnotes all none standard abbreviation that are
used in each table
? For footnotes use the following symbols, in the sequence:
Illustrations (Figures)
? Send sharp, glossy, un-mount, color photographic prints, with height
of 4 inches and width of 6 inches.
? Figures should be numbered consecutively according to the order in
which they have been first cited in the text.
? Each figure should have a label pasted (avoid use of liquid gum for
pasting) on its back indicating the number of the figure, the running
title, top of the of the figure and legends of the figure. Do not write on
the back of figures, scratch, or mark them by using paper clips.
? Print outs of digital photographs are not acceptable. For digital
images send TIFF files of minimum 1200 x 1600 pixel size.
? Type of print out legends (maximum 40 words, excluding the credit
line) for illustrations using double spacing, with Arabic numerals
corresponding to the illustrations.
Sending a revised manuscript
While submitting a revised manuscript, contributors are requested to
include, along with single copy of the final revised manuscript, a
photocopy of the revised manuscript with the changes underlined in red
and copy of the comments with the point to point clarification to each
comment. The manuscript number should be written on each of these
documents. If the manuscript is submitted online, the contributors form
and copyright transfer form has to be submitted in original with the
signatures of all the contributors within two weeks of submission. Hard
copy of images should be sent to the office of the journal. There is no need
to send printed manuscript for articles submitted online.
Reprints
Journal provides no free printed reprints.
Copyrights
The whole of the literary matter in the IJDS is copyright and can not be
reproduced without the written permission.
Covering Letter
! Signed by all contributors
! Previous publication/presentations mentioned
! Source of funding mentioned
! Conflicts of interest disclosed
Authors
! Middle name initials provided
! Author for correspondence, with e-mail addresses provided
! Number of contributors restricted as per the instructions
! Identity not revealed in paper except title page (e.g. name of the
institute in Methods, citing previous study as, 'our study, names on figures
levels, name of institute in photographs, etc.)
Presentation and format
! Double spacing.
! Margins 2.5 cm from all four sides
! Title page contains all the desired information
! Running title provided (not more the 50 chapters)
! Abstract page contains the full title of the manuscript
! Abstract provided (about 150 words for case reports and 250 words
for original articles)
Journal of Dental Sciences & Oral Rehabilitation
! Structured abstract provided for an original article
! Key words provided (three or more)
! Introduction of 75-100 words
! Headings in title case (not ALL CAPITALS)
! References cited in square brackets.
! References according to the journal's instructions, punctuations
marks checked
Language and grammar
! Uniformly American English
! Abbreviations spent out in full for the first time
! Numerals from 1to10 spelt out
! Numerals at the beginning of the sentence spelt out
Tables and figures
! No repetition of data in tables and graphs and in text
! Actual numbers from which graphs drawn, provided
! Figures necessary and of good quality (color)
! Table and figure numbers in Arabic letters (not Roman)
! Labels pasted on back of the photographs (no name written)
! Figure legends provided (not more than 40 words)
! Patients' privacy maintained (if not permission taken)
! Credit note for borrowed figures/tables provided
! Manuscript provided on a floppy (with single spacing)
The Journal
Journal of Dental Sciences & Oral Rehabilitation (ISSN 2231-1491 ) is
published on behalf of IDS Bareilly. The journal publishes information
relating to Dental Research. The journal is published quarterly.
Registration, Abstracting and Indexing Information
The journal is in progress of getting Indexed with various indexing
societies.
Information for Authors
There are no page charges for submissions of the journal.
http://www.jdsor.in Please check http:// www.jdsor.in/ for details.
All manuscript must be submitted on line at http://www.jdsor.in/
online_submission.php
Subscription Information
Copies are sent to the members of JDSOR free of cost. A subscription to
journal of JDSOR comprises 4 issues. Prices include postage. Annual
Subscription Rate for none-members
Institutional; - INR 1600
Personal; - INR 1200
For mode of payment and other details, Please Send Demand Draft in
favor of 'Journal Of Dental Sciences & Oral Rehabilitation,' payable at
Bareilly.
Claims for missing issues will be serviced at no charge if received within
60 days of the cover date for domestic subscribers, and 3 months for
subscriber out side India. Duplicate copies can not be sent to replace
issues not delivered because of failure to notify publisher of change of
address.
The Journal is published and distributed by Institute Of Dental Sciences
Bareilly. Copies are sent to subscribers directory form the publisher's
address.
The copies of the journal of the members of JDSOR are sent by ordinary
post. The editorial board association or publisher will not be responsible
for none receipt of copies. If any member / subscriber wishes to receive
the copies by registered post or courier. Kindly contact the publisher's
office. If a copy returns due to incomplete, incorrect or change address
of a member/subscriber on two consecutive occasion, the names of such
members will be deleted from the mailing list of the journal. Providing
complete, correct and up-to-date address is the responsibility of the
member/subscriber.
Advertising Polices
The journal accepts display and classified advertising.Frequency
discounts and special positions are available.Inquiries about advertising
should be sent to Indian Journal of Dental Sciences Publications. The
journal receivers the right to reject any advertisement considered
unsuitable according to the set policies of journal.
The appearance of advertising or Product information in the various
sections in the journal does not constitute an endorsement or approval by
the journal and or its publisher of the quality of value of the said product
or of claim made for it by its manufacturer.
Copyright
The entire contents of the Journal of JDSOR are protected under Indian
and International Copyrights. The Journal, however, grants to all users a
free, irrevocable worldwide, perpetual right of access to and a license to
copy, use, distribute, perform and display the work publicly and to make
and distribute derivative works in any digital medium for any reasonable
noncommercial purpose, subject to proper attribution of authorship and
ownership or the rights. The journal also grants the right to make small
number of printed copies for their personal noncommercial use.
Permissions
For information on how to request permission to reproduce articles/
information from this journal, please visit http://www.jdsor.in .
Disclaimer
The information and opinions presented in the journal reflect the views
of the authors and not of the journal or its Editorial Board. Publications
do not constitute endorsement by the journal. Neither the journal of
JDSOR nor its publishers nor anyone else involved in creating,
producing or delivering the journal of JDSOR or the materials contained
therein, assumes any liability or responsibility for accuracy,
completeness, or usefulness of any information provided in the journal of
JDSOR, nor shall they be liable for any direct, indirect, incidental,
special, consequential or punitive damages arising out of the use of the
journal of JDSOR. The journal of JDSOR, nor is publishers, nor any
other party involved in the preparation of material contained in the
journal of JDSOR represents or warrants that the information contained
herein is in every respect accurate or complete, and they are not
responsible for any errors or omissions or for the results obtained from
the use of such material. Readers are encouraged to confirm the
information contained herein with other sources.
It is mandatory for the authors to enclosed the dully signed below
mentioned declaration and e-mail it along with the manuscript /
Available at the website-www.jdsor.in
(1) Declaration
Title of the article:
To,
The Editor,
Institute of Dental Sciences,
Bareilly, U.P.
Subject; Submission of Manuscript for publication
Dear Sir,
We intend to publish an article entitled
“_______________________________________________________
___________________________________________”
In your journal as a Case Report / review Article / Original Article. On
behalf all the contributors I will act as a guarantor and will correspond
with journal from this point onward.
Prior publication nil
Support nil
Conflicts of Interest nil
Permissions nil
We hereby transfer, assign, or otherwise convey all copyright ownership,
including any and all rights incidental thereto, exclusively to the journal,
in the event that such work is published by the journal.
Thanking your
Yours' sincerely,
Signature
Corresponding contributor: Dr._______________________________
Declaration
Journal of Dental Sciences & Oral Rehabilitation
E-mail address: ___________________________________________
Contributors' form (to be modified as applicable and one singed copy
attached with the manuscript)
Manuscript Title ___________________________________________
________________________________________________________
________________________________________________________
I/we certify that I/we have participated sufficiently in the intellectual
content, conception and design of this work or the analysis and
interpretation of the data (when applicable), as well as the writing of the
manuscript, to take public responsibility for it and have agreed to have
my/our name listed as a contributor. I/we believe the manuscript
represents valid work neither this manuscript nor one with substantially
similar content under my/our authorship has been published or is being
considered for publication elsewhere, except as described in the
covering letter. I/we certify that all the data collected during the study is
presented in this manuscript and no data from the study has been or will
be published separately. I/we attest that, if request by the editors, I/we
will provide the data / information or will cooperate fully in obtaining
and providing the data/information on which the manuscript is based,
for examination by the editors or their assignees. Financial interests,
direct or indirect, those exist or may be perceived to exist for individual
contributors in connection with the content of this paper has been
disclosed in the cover letter.
I/we hereby transfer(s), assign(s), or otherwise convey(s) all copyright
ownership, including any and all rights incidental thereto exclusively to
the journal, in the event that such work is published by the journal. The
journal shall own the work, including 1) copyright; 2) the right to grant
permission to republish the article in whole or in part, with or without
fee; 3) the right to produced preprints or reprints and translate into
languages other than English for sale or free distribution; and 4) the
right republish the work in a collection of articles in any other
mechanical or electronic format.
We give the rights to the corresponding author to make necessary
changes as per the request of journal, do the rest of the correspondence
on our behalf and he/she will act as the guarantor for the manuscript on
our behalf.
All persons to have made substantial contributions to the work reported
in the manuscript, but who are not contributors, are named in the
Acknowledgement and have given me/us their written permission to be
named, if I/we do not include an Acknowledgement that means I/we have
not received substantial contributions form non-contributors and no
contributor has been omitted.
Name/Names with Designations
1-__________________________________________
2-__________________________________________
3-__________________________________________
4-__________________________________________
5-__________________________________________
Acknowledgement: (If Any)
 Our journey with the college journal is continuing & we have published the second
issue of the current year. The enthusiasm with which all the staff & students have submitted
their articles needs to be acknowledged.

Yet again we have worked with a single aim i.e. to maintain the high standards of
the articles which are being published by having the peer review committee.

Talks our on with Rohilkhand university to make this journal a university journal, it
might still take some more time, but we are hopeful that the result shall be positive

The next thing which I would like to request is to get some advertisement for the
college journal, so that it becomes a financially independent body.

Prof Dr Puneet Anand

Editor in Chief

Journal of Dental Sciences & Oral Rehabilitation

 Contents
1. White Lesions Of Oral Mucosa - A Diagnostic Dilemma : Review ............................................................8
Dr. S. R Panat, Dr. Nidhi Yadav, Dr. Sangamesh N.C, Dr. Ashish Aggarwal, Deptt. of Oral Medicine & Radiology

2. Gingival Pigmentation And Its Treatment Modalities : Review ..............................................................11

Prof. (Dr.) Anirban Chatterjee, Dr. Nidhi Singh, Dr. Parvati Malhotra, Dr. Neha Ajmera, Daswani Dental College & Research Center, Kota

3. Osseointegration - The Key To Successful Implant Placement : Review ....................................................15

Dr. K.L. Gupta, Dr. Puneet Anand, Dr Neeraj Nagpal, Dr Dinker Goel, Dr Tamanna Chabra, Dr Alok Kumar, Deptt. of Prosthodontics

4. Dentigerous Cyst : Case Report ......................................................................................................18

Dr. Sudhapalli Chidanand Rao, Dr.Nikhil Pandit , Dr Hitesh Hans Baweja , Dr. Himanshu Pratap Singh, Deptt. of Oral and Maxillofacial Surgery

5. In Vitro Fracture Resistance Of Endodontically Treated Central Incisors With Varying Ferrule
Heights And Configurations. ..........................................................................................................20
Dr.Anurag Singhal, Dr.Chandrawati Guha, Dr.Anuraag Gurtu, Dr.Payal Singhal, Department Of Conservative Dentistry & Endodontics

6. Hypoplastic Amelogenesis Imperfecta : Case Report ............................................................................22

Dr. Sunil R Panat, Dr. Ashish Aggarwal, Dr. Prakash Chandra Jha, Deptt. of Oral Medicine & Radiology

7. Mesiodens: An Etiology of Severe Malocclusion : Case Report ..............................................................24

Dr. Preeti Bhattacharya, Dr. Abhishek Agarwal, Dr. D.K. Agarwal,Dr. P.S Raju, Dr. Ankur Gupta, Dr. Siddharth Kaushal, Dept of Orthodontics

8. Fixed Prosthodontics For A Missing Primary Tooth : Case Report ..........................................................26

Prof (Dr.) Puneet Anand, Dr. Anand's Dental Clinic and Implant Centre

9. Xerostomia- A Review And Update : Review .....................................................................................28

Dr.Gaurav Sapra, Department of Oral Pathology and Microbiology

10. Mandibular Prognathism: Sagittal Split Ramus Osteotomy : Case Report.................................................32

Dr. Dayanand Saraswathi, Dr. Anuradha V, Dr. Himanshu Sharma, Dr. Umang Agarwal, Deptt. of Oral & Maxillofacial Surgery

11. Peripheral Neurectomy In The Management Of Trigeminal Neuralgia : Case Report ..................................35
Dr. Ramakant Dandriyal, Dr. S.c.rao, Dr. Meenal Airan, Dr. Umang Agarwal, Deptt. of Oral & Maxillofacial Surgery

12. Periodontal Emergencies : Review ...................................................................................................37

Dr. Manvi Agarwal, Dr. H.S. Bhattacharya, Dr. Shalini Singhal, Dept Of Periodontics

13. Pregnancy Tumor : Case Report .....................................................................................................39

Dr. Sunil R Panat, Dr. Ashish Aggarwal, Dr. Rajan Rajput, Deptt. of Oral Medicine & Radiology

14. Management of Extra Oral Sinus Using Shoe Lace Technique : Case Report.............................................41
Dr. Chandra Vijay Singh, Dr. Anurag Singhal, Dr. Anuraag Gurtu, Dr. Chandrawati Guha , Department Of Conservative Dentistry & Endodontics

15. Multiple Myeloma Presenting As Periapical Pathology : Case Report ......................................................43

Dr Satish Kumaran, Dr.Anuradha.V, Dr. Lalitha Thambiah, Oral pathology

16. Lateral Periodontal Cyst : Case Report ............................................................................................46

Dr. Shalini Singhal, Dr. Hirak Bhattacharya, Dr Manvi Agarwal, Department of Periodontics

17. Surgical Management of Iatrogenic Perforation Using Mta : Case Report ................................................49
Dr. Anuraag Gurtu, Dr. Anurag Singhal, Dr. Payal Singhal, Dr. Sumit Mohan, Department Of Conservative Dentistry & Endodontics

18. Are Denture Adhesive Toxic? Yes!!! : Review.....................................................................................51

Prof. Dr. Puneet Anand, Dr. K.L. Gupta , Dr. Dinker Goel, Dr. Tamanna Chabra, Dr. Alok Kumar Department of Prosthodontics Crown & Bridge

Journal of Dental Sciences & Oral Rehabilitation

www.rmcbareilly.com REVIEW ARTICLE

WHITE LESIONS OF ORAL MUCOSA -

A DIAGNOSTIC DILEMMA

AUTHORS:
Dr. S. R Panat
ABSTRACT
Principal, Professor & Head White lesions of the oral cavity are commonly encountered in routine clinical dental practice. Some
CO-AUTHOR: common conditions like Fordyce's granules may cause diagnostic confusion. White lesions are usually
Dr. Nidhi Yadav
PG student painless but can be focal, multifocal, striated or diffuse. Detection and early identification of these
Dr. Sangamesh N.C lesions is extremely important, as some of these lesions may represent early stage of malignancy.
Reader
Dr. Ashish Aggarwal Clinical diagnostic skills and good judgment forms the key to successful diagnosis and management of
Senior Lecturer white lesions of the oral cavity. This review lists the white lesions affecting the oral mucosa ranging from
Deptt. of Oral Medicine & Radiology,
Institute of Dental Sciences, those that are genetically determined to those that are neoplastic and also highlights the specific
Bareilly (UP). features of each of these lesions.
Key words: White lesions of the oral cavity, leukoplakia, oral lichen planus.
INTRODUCTION: (a) Squamous cell carcinoma
White lesions of the oral cavity are commonly HEREDITARY/DEVELOPMENTAL:
encountered during clinical dental practice. Although Leukoedema:
some benign physiologic entities may present as white Leukoedema represents a variation of a normal
lesions, systemic conditions, infections, and condition. It is characterized by a diffuse, grayish white
malignancies may also present as white oral lesions. opalescent appearance, occurring bilaterally on the
This emphasizes the need for an efficient chair-side buccal mucosa (Picture 1). The surface appears folded,
work up to find out whether a particular white lesion resulting in wrinkling of the mucosa. It cannot be
can turn problematic in future. It is required to scrapped off and it disappears or fades upon stretching
categorize the lesion and determine whether it belongs the mucosa. Leukoedema is a benign condition and no
to the commonly seen reactive group or to the more treatment is required.2
dangerous precancerous group.1
White lesions of the oral mucosa obtain their
characteristic appearance because of a thickened layer
of keratin (hyperkeratosis), superficial debris on oral
mucosa, blanching caused by reduced vascularity and
loss of pigmentation due to acquired causes. The
treatment ranges from reassurance from the clinician
for lesions that are harmless to medicinal and surgery.
CLASSIFICATION OF WHITE LESIONS:
1. Hereditary/Developmental:
(a)Leukoedema (b) White spongy nevus
(c) Hereditary benign intraepithelial dyskeratosis
(d)Pachyonychia congenita (e)Dyskeratosis congenita
2. Reactive:
(a) Frictional keratosis ( b) Morsicatio buccarum
(c) Nicotine stomatitis (d) Tobacco pouch keratosis
(e) Chemical burn Leukoedema (Picture 1)
3. Immunologic:
White Spongy Nevus:
(a) Lichen planus (b) Lichenoid mucositis
White spongy nevus is inherited as an autosomal
(c) Discoid lupus erythematosus dominant trait. The lesions appears at birth or in early
(d) Graft-versus- host disease childhood and presents as asymptomatic, symmetrical,
4. Bacterial/Viral/Fungal: white corrugated or velvety diffuse plaques on the
(a) Candidiasis (b) Mucous patches in secondary buccal mucosa bilaterally (Picture 2). Other intra oral
syphilis (c) Oral hairy leukoplakia site like ventral tongue, labial mucosa, soft palate, floor
5. Systemic disease: of the mouth and extra oral sites like nasal, pharyngeal
(a) Uremic stomatitis and anogenital mucosa may also be involved.
6. Potentially malignant disorders:
(a) Leukoplakia (b) Actinic cheilitis
7. Neoplastic:

Journal of Dental Sciences & Oral Rehabilitation 08

 White sponge nevus (Picture 2)
Hereditary Benign Intraepithelial Dyskeratosis (HBID):
HBID is an autosomal dominant condition characterized by oral and
conjunctival lesions. The oral lesions show thick corrugated white
plaques on the buccal and labial mucosa. In bulbar conjunctiva, thick
plaques form early in life. No treatment is indicated for oral lesions. For
evaluation and treatment of conjunctival lesions, the patient is referred to
ophthalmologist.
Pachyonychia Congenita:
Pachyonychia congenita is an autosomal dominant condition where all
the patients have tubular configuration of the nails due to accumulation of
keratinaceous material in the nail beds. Thick, callous-like thickenings
and hyperhidrosis are noted in the palms and soles. Oral lesions are seen
only in type I pachyonychia congenita in the form of thickened white
plaques on the dorsum and lateral margins of the tongue. Oral lesions do
not require treatment, but the quality of life is affected due to nail loss and
continuous removal of excess keratin on the soles and palms.3
Dyskeratosis Congenita:
Dyskeratosis congenita is a rare condition inherited as X-linked trait,
resulting in a striking male predilection. The oral lesions start before the
age of 10 years as bullae on the tongue and buccal mucosa and are
followed by erosions and later turning to squamous cell carcinoma. The
oral changes are associated with dystrophic nails and hyper-pigmentation
of the skin of the face and neck. The oral lesions are managed
symptomatically and periodic recall to check for malignant
transformation.
REACTIVE:
Frictional Keratosis:
Frictional keratosis refers to a white lesion with a rough surface and is
related to an identifiable source of mechanical irritation and is reversible
on elimination of the irritant. This lesion is frequently associated with
rough dentures or sharp cusps. On removal of the offending agent, the
lesion should resolve within 2 weeks. Biopsies should be performed on
lesions that do not heal to rule out a dysplastic lesion.
Morsicatio Buccarum:
White lesions of buccal mucosa may arise from chronic irritation due to
sucking, nibbling or chewing. Cheek chewing is most commonly seen in
people who are under stress or who exhibit psychological conditions. The
lesions are found bilaterally on the anterior buccal mucosa along the
plane of occlusion. Patients often complain of small tags of tissue that
they tear free from the surface. The lesions are thickened, shredded white
area that may be intermixed with areas of erythema and ulceration. In
some cases an oral acrylic shield may be constructed for treatment.
Nicotine Stomatitis:
Nicotine stomatitis refers to a white lesion that develops on the palate in
heavy cigarette, pipe and cigar smokers in response to heat of tobacco
smoke. The palatal mucosa becomes diffusely gray or white. Numerous
elevated white papules with red centers representing inflamed ductal
orifices are noted (Picture 3). The condition is reversible, usually within
to 2 weeks of smoking cessation.
Journal of Dental Sciences & Oral Rehabilitation
Nicotina stomatitis (Picture 3)
Tobacco Pouch Keratosis:
The habitual chewing of tobacco results in the development of white
mucosal lesion in the area of contact called tobacco pouch keratosis. The
most common areas of involvement are the anterior mandibular
vestibule and buccal sulcus. The lesion is a thin grayish white translucent
plaque that is soft on palpation. On stretching of the mucosa there is a
distinct “pouch” caused by flaccidity in chronically stretched tissues in
the area of tobacco placement (Picture 4). Habit cessation results in
normal mucosal appearance within 2 weeks in most of the lesions.
Tobacco pouch keratosis (Picture 4)
Chemical Burn:
Chemical injuries due to caustic agents, such as aspirin, formocresol,
hydrogen peroxide and sodium hypochlorite can cause white lesion.
These are due to formation of a superficial pseudomembrane composed
of a necrotic surface and an inflammatory exudate. The lesions are
usually located on the mucobuccal fold area and gingiva. With short
exposure, the affected mucosa exhibits a white, wrinkled appearance.
Long term contact can cause necrosis and sloughing of mucosa. Most
superficial burns heal within 2 weeks, while deep burns required
debridement followed by antibiotic coverage. The best treatment of oral
chemical burns is prevention. Use of a rubber dam during endodontic
procedures reduces the risk of iatrogenic chemical burns.4
3. IMMUNOLOGIC:
Lichen Planus:
Lichen planus is an immunologically mediated mucocutaneous disease,
in which T lymphocytes
accumulate beneath the epithelium. Women are more commonly
affected. The most common reticular form consists of interlacing white
lines called Wickham's striae, seen usually on the posterior buccal
mucosa bilaterally (Picture 5). Other intraoral sites involved include
tongue, gingiva and palate. On the dorsum of the tongue the lesion appear
as keratotic white plaques with atrophy of the papillae. The erosive type
is symptomatic. Surrounding oral mucosa is erythematous with dusky
red discoloration. Lesions show remissions and exacerbations associated
with periods of stress.
09

Lichen planus (Picture 5)
Lichenoid Reaction:
Lichenoid reaction has lesions clinically and histologically similar to
lichen planus, but is associated with administration of a drug or contact
with metal (Picture 6). The lesions resolve when the drug or other factors
are eliminated.5
Lichenoid reaction (Picture 6)
Discoid Lupus Erythematosus:
Discoid lupus erythematosus (DLE) is a chronic autoimmune disease
affecting the skin and oral mucosa. The oral lesions are characterized by
erythematous central zone, surrounded by white radiating striae or
hyperkeratotic plaques on the buccal mucosa, palate and tongue. Unlike
lichen planus, the distribution of DLE lesions is usually asymmetric,
peripheral striae are subtle and the oral lesions seldom occur in the
absence of skin lesions. The diagnosis is based on the coexistence of skin
lesions, histopathology and immunofluroscent studies. Topical steroids
are used in treating the skin and oral lesions of DLE.
Graft-Versus-Host Disease (GVHD):
GVHD is an immunologically mediated disease occurring in recipients
of allogenic bone marrow transplantation, where the grafted cells of
donor destroy the normal cells of the host. The intra oral lesions are
extensive and involve the cheeks, tongue, lips and gingiva. In most
patients, there is a fine reticular network of white striae resembling
lichen planus, although a diffuse pattern of white papules has also been
described. Topical steroids or tacrolimus are effective in the
management of oral lesions.
4. BACTERIAL/VIRAL/FUNGAL:
(A) Candidiasis:
Candidiasis is the most common oral fungal infection caused by candida
albicans. The pseudomembranous and hyperplastic type of candidiasis
present as white lesions of the oral cavity. Pseudomembranous
candidiasis has white plaques resembling curdled milk (Picture 7).
Scraping the white lesion can remove the plaques. The hyperplastic
candidiasis or candidal leukoplakia presents as non-scrapable white
patch usually located on the anterior buccal mucosa. The diagnosis is
confirmed by the presence of candidal hyphae in the lesions. There is
resolution of the lesion after antifungal therapy.
(B) Mucous Patches in Secondary Syphilis:
The lesions of secondary syphilis in oral cavity are characterized by
Candidiasis (Picture 7)
multiple painless grayish-white plaques overlying an ulcerated necrotic
surface. The lesions occur on the tongue, gingiva, palate and buccal
mucosa. The associated systemic features include fever, sore throat,
malaise and headache. The lesions are highly infective, but resolve within
few weeks.
Oral Hairy Leukoplakia (OHL):
OHL is a white lesion seen commonly in severe immunodeficient patient
Journal of Dental Sciences & Oral Rehabilitation
and is caused by Epstein Barr virus (EBV). OHL clinically presents as
white vertical streaks or thickened, furrowed white areas on the lateral
borders of the tongue. The definitive diagnosis is made by demonstration
of EBV within the lesion using in situ hybridization, PCR, Southern blot
or electron microscopy.
5. SYSTEMIC DISEASE:
Uremic Stomatitis: Uremic stomatitis is a complication of renal failure.
The onset is abrupt, with white plaques present predominantly on the
buccal mucosa, tongue and floor of the mouth. The clinician may detect
an odor of ammonia or urine on the patient's breath.
6. POTENTIALLY MALIGNANT DISORDERS:
Leukoplakia: Leukoplakia is defined as “white patch or plaque that
cannot be characterized clinically or pathologically as any other
disease”. The tem is strictly clinical. The habit of tobacco is closely
associated with leukoplakia development. Leukoplakia is divided into
two clinical types, homogeneous and non-homogeneous types.
Homogeneous lesions are slightly elevated grayish white non-scrapable
plaques, which may appear fissured or wrinkled. Non-homogeneous
varieties include
a) Speckled: mixed white and red lesions, but retaining predominantly
white color (Picture 8)
b) Nodular: small polypoid outgrowths
c) Verrucous: corrugated surface appearance
d) Proliferative verrucous leukoplakia (PVL): multiple keratotic plaques
with roughened surface projections.
Leukoplakia is a potentially malignant disorder with a malignant
transformation rate ranging from 4% to 47%. Habit cessation is
recommended along with clinical evaluation for every 6 months.
Actinic Cheilitis: Actinic cheilitis is a potentially malignant disorder
found on the vermillion border of the lower lip and is directly related to
long-term sun exposure. It appears as a white plaque, oval or linear in
shape, usually measuring less than 1 cm in size.
7. NEOPLASTIC:
Oral Squamous Cell Carcinoma (OSCC): OSCC can present clinically as
a white patch resembling leukoplakia. In such cases biopsy is mandatory
to know if the dysplastic features are limited to the epithelium or if true
invasion into the underlying connective tissue has occurred.
CONCLUSION:
White lesions of the oral cavity can range from genetic disorders like
white spongy nevus to neoplastic lesions like Oral squamous cell
carcinoma. Proper diagnosis is important because the corresponding
treatment varies. A careful observant eye and sensible judgement can add
to the diagnostic skills of the clinician and are considered important for
proper patient care.
REFERENCES:
1) Joshy V.R, Hari.S, White lesions of the oral cavity - diagnostic
appraisal & management strategies, Journal of Clinical Dentistry
2005;1(1):27-30
2) Burket L W, Oral Medicine Diagnosis and Treatment, 9th edition,
J.B Lippincott Company.
Oral leukoplakia (Picture 8)
3) Wood N.K, Goaz P W, Differential Diagnosis of Oral and
Maxillofacial Lesions, 5th edition, Elsevier.
4) Neville B W, Damm D D, Allen C M, Oral and Maxillofacial
Pathology 2nd Edition, 2005, Elsevier.
5) Isaac van der Waal, Oral lichen planus and oral lichenoid lesions; a
critical appraisal with emphasis on the diagnostic aspects, Med
Oral Patol Oral Cir Bucal. 2009 Jul 1;14 (7):E310-4.
10
www.rmcbareilly.com REVIEW ARTICLE

GINGIVAL PIGMENTATION AND ITS TREATMENT

MODALITIES

AUTHORS:
Prof. (Dr.) Anirban Chatterjee
ABSTRACT
HOD and Professor The pigments are not only the most beautiful but some of the most vital substances in the body .
Dr. Nidhi Singh Pigmentation is both the normal and abnormal discoloration of oral mucous membrane. Etiology of
PG Student
Dr. Parvati Malhotra pigment is multifoctorial etiology. Most of the pigmentation is physiologic but sometimes it can be a
Professor Lecturer precursor of severe diseases. Melanin pigment irregularities and color changes of the oral tissues could
Dr. Neha Ajmera
Senior Lecturer provide significant diagnostic evidence of both local and systemic disease. Gingival melanin
Daswani Dental College pigmentation occurs in all races of man. The differential diagnosis, clinical, etiology, and treatment of
& Research Center, Kota
pigmentation are discussed
KEYWORDS: Oral pigmentation, melanin , oral lesions, depigmentation ,aesthetic.
INTRODUCTION within different areas of the same mouth[8].
Oral pigmentation may be physiological or Physiologic pigmentation is probably genetically
pathological in nature[1]. It may represent a localized determined, but as Dummett suggested, the degree of
anomaly of limited significance or the presentation of pigmentation is partially related to mechanical,
potentially life-threatening multisystem disease[2]. chemical and physical stimulation[9]. In darker skinned
Pigmented lesions arecommonly found in the mouth. people oral pigmentation increase, but there is no
Such lesions represent a variety of clinical difference in the number of melanocytes between fair
entities, ranging from physiologic changes (e.g., racial skinned and dark skinned individuals. There is some
pigmentation) to manifestations of systemic illness controversy about the relationship between age and oral
(e.g., Addison's disease) and malignant pigmentation. Steigmann and Amir et al stated all kinds
neoplasms (e.g., melanoma and Kaposi's sarcoma). of oral pigmentation appear in young children. Prinz, on
“The colour of healthy gingiva is variable ranging the other hand, claimed physiologic pigmentation did
from a pale pink to a deep bluish purple hue. [3]. not appear in children and was clinically visible only
Between these limits of normalcy are a large number of after puberty.[10]
pigmentation mosaics which depend primarily upon CLINICAL CHARACTERISTICS :
the intensity of melanogenesis, deapth of epithelial The gingiva are the most frequently pigmented
cornification and arrangement of gingival vascularity. intraoral tissues.[8]
More over colour variation may not be uniform and Microscopically, melanoblasts are normally present in
may exists as unilateral, bilateral mottled, macular or the basal layers of the lamina propria[11,12]. The most
blotched and may involve gingival papillae alone or common location was the attached gingiva(27.5%)
extend throughout the gingival on to other soft followed in decreasing order by the papillary gingiva,
tissues”.[4] the marginal gingiva, and the alveolar mucosa.[13]
Although clinically melanin pigmentation of the The total number of melanophores in the attached
gingiva does not present any medical problems it can gingival was approximately 16 times greater than in the
be an esthetic concern for the patient. Demand for free gingiva[14]. The prevalence of gingival
cosmetic therapy is made, especially by fair skinned pigmentation was higher on the labial part of the
people with moderate or severe gingival pigmentation. gingiva than on the palatal / lingual parts of the arches.
Gingival depigmentation is a periodontal plastic The shade of pigment was classified as very dark brown
surgical procedure whereby the gingival to black, brown, light brown yellow. Melanin
hyperpigmentation is removed or reduced by various pigmentation of the oral tissues usually does not present
techniques. The first indication for depigmentation is a medical problem, but patients complain of black
patient demand for improved esthetics. gums.
Various depigmentation techniques have been Melanin has been intensively studied, because it is
employed with similar results. Selection of technique the most important pigment of the skin. Chemical,
should be based on clinical experiences and individual melanin is a high molecular weight which is insoluble
preferences. in water and most organic solvents. Melanin is formed
EPIDEMIOLOGY : only in the cytoplasm of melanin forming cells, or the
Oral pigmentation occurs in all races of man.[5,6] melanocyte. These are dendritic or branched cells
There were no significant difference in oral found at the epidermal dermal junction of the skin and
pigmentation between males and females[7]. The the mucous membrane, in the leptomeninges of the
intensity and distribution of racial pigmentation of the central nervous system, in the uveal tract and in the
oral mucosa is variable, not only between races, but retina of the eye. The melanocytes are located in the
also between different individuals of the same race and intercellular epidermal spaces and form intricate
patterns by their long processes. The degree of
Journal of Dental Sciences & Oral Rehabilitation 11
pigmentation depends on a variety of factors, especially the activity of area.
melanocytes. A No.11 or 15 BP blade is held parallel to the gingival surface, the
It also appears that the degree of gingival pigmentation of the epithelium and a portion of the C.T. is gently dissected out from one end
gingiva and skin is reciprocally related. Fair skinned individuals are very of the vertical incision.
likely to have non pigmented gingiva, but, in darker skinned persons, the Care is taken not to tear the tissue or leave any pigmented posts behind
chance of having pigmented gingiva is extremely high. The highest rate or expose the bone.
of gingival pigmentation has been observed in the area of the incisors. Periodontal dressing applied for 1 week.
The rate decreases considerably in the posterior areas.
Etiological factors[15,16]
1. Endogenous 2. Exogenous
Most pigmentation is caused by 5 primary pigments.[7]
a. Melanin b. Melanoid c. Oxyhemoglobin d. Reduced hemoglobin
e. Carotene
Others include :
1. Bilirubin 2. Iron
Color of the gingiva is determined by several factors ;
1. Number and size of blood vessels 2. Epithelial thickness 3. Quality of
keratinization 4. Pigments within the epithelium
Mechanism of Melanin [7]
Melanocytic Stimulating Hormone (MSH) increases the skin
pigmentation by stimulating the dispersion of melanin granules in
melanocytes, thus causing darkening of the skin. Secretion of this
hormone is stimulated by MSH stimulating factor. Glucocorticoids have
an inhibiting effect on MSH, when there is adrenal insufficiency, there is
reduced glucocorticoids secretion increase in MSH increase melanin
pigmentation
Classification and Differential Diagnosis of Oral Pigmentation :[17,18]
A. Localized pigmentation - Amalgam tattoo - Graphite or other tattoos Pre operative view two vertical and one
- Nevus - Melanotic macules - Melanoacanthoma - Malignant melanoma
- Kaposi's sarcoma - Epitheloid oligamatosis - Verruciform xanthoma horizontal incision given
B. Multiple or generalized pigmentations
1. Genetics Idiopathic melanin pigmentation (racial or physiologic)
- Peutz-Jegher's syndrome - Complex of Myxomas - Carney syndrome -
Leopard syndrome etc
2. Drugs – Smoking, betal - Anti-malarial - Anti microbial (minocycline)
- Cloropromazine - ACTH - Zidovudine - Ketoconazole
- Methyldopa - Heavy metals (Gold, Silver, Bismuth, Mercury, Lead,
Copper) - Balulphan - Menthol
3. Endocrine - Addison's disease - Albright's syndrome - Acanthosis
Nigrecans - Pregnancy - Hyperthyroidism
4. Post-inflammator - Periodontal disease - Postsurgical gingival
repigmentation partial thickness flap Immediately after
5. Others - Hemochromatosis - Generalized neurofibromatosis raised in max.arch
- Goucher's disease - HIV - Thalassaemia - Nutritional deficiencies surgery in maxillary arch
Gingival Depigmentation :
Melanin hyperpigmentation usually does not present as a medical
problem, but patients may complain their black gums are unaesthetic.
This problem is aggravated in patients with a gummy smile or excessive
gingival display depigmentation is a periodontal plastic surgical
procedure whereby the gingival hyperpigmentation is removed or
reduced by various techniques. Various techniques have been employed
with similar results. The selection of a technique should be based on
clinical experience and individual preference.
Different Technique Employed :-
I. Methods aimed at removing the pigment layer
A. Surgical methods of depigmentation
1. Scalpel surgical technique a. Slicing, or partial thickness flap
technique b. Bone denudation c. Abrasion d. Scraping e. Gingivectomy
2. Cryosurgery
3. Electrosurgery
4. Lasers
1. Nd:YAG 2. Er : YAG 3. CO2 lasers Recall after 1 month
B. Chemical method of depigmentation using caustic chemicals.
Eg. 90% phenol 2) Scrapping Technique [19]
II. Methods aimed at masking the pigmented gingiva with grafts from less After infiltrating the area with local anesthesia No.15 or 11 B.P. blade
pigmented areas. with handle is used to scrape the epithelium with underlying pigmented
1. Free gingival grafts (FGG) layer carefully.
2. Acellular dermal matrix allografts The raw surface is irrigated, cleaned and dressing is given for 1 week.
1) Slicing Technique :[19]
Under Local anesthetic infiltration, two incisions are placed extending
from the gingival margin to the vestibular area, a little beyond the limits
of the pigmented band. These vertical incisions demarcate the surgical
Journal of Dental Sciences & Oral Rehabilitation 12

Pre operative view
Immediately after surgery
of Maxillary region Recall after one month
3) Abrasion Technique : [20]
It involves removing the epithelium of the pigmented areas with a
high speed hand piece. After adequate local anesthesia a high speed
handpiece with a diamond bur (straight No.8) with copious water lavage
is selected.
It is recommended to use larger size diamond bur because smaller
burs do not smoothen the surface easily and has a tendency to make small
pits in the area to be corrected.
Feather, light brushing strokes should be used to remove the
pigmented areas without holding the bur in one place.
Pre- operative view carbide bur
Immediately after surgery of the Recall after 1 month
mandibular anterior region
4) Chemical Cauterization [21] - Using 90% phenol
Disadvantages : Harmful to oral tissues Heavy bands of pigmented
gingiva are difficult to remove. Depth of action not controlled.
5) Gingivectomy Technique [2]
This procedure is associated with loss of alveolar bone, prolonged
healing by secondary intention and excessive post-operative pain.
It also results in non-permanent depigmentation.
6) Bone denudation Technique [22]
Under local anesthesia, two vertical incisions are placed, each extending
from the gingival margin to the vestibular area, a little beyond the limits
Journal of Dental Sciences & Oral Rehabilitation
of the pigmented band.
The papillae were splint into labial and lingual halves with B.P. blades.
A horizontal incision was then made into the vestibule, apical to the
pigmented band, connecting the two vertical incisions.
With a periosteal elevator, the tissue along with the periosteum was
gently separated from the underlying alveolar bone and was removed en-
mass entirely exposing the subjacent alveolar bone. Periodontal pack
was placed at weekly intervals.
7) Cryosurgical treatment of melanin-pigmented gingiva [23]
The method used for treatment was direct application of liquid nitrogen
(-196°C) with a cotton swab on the pigmented gingiva.
Topical anesthesia with 45 xylocaine spray was used to minimize
discomfort for 1 to 2 minutes before treatment.
The swab, 5 mm in diameter, was gently rolled forward and backward
across 1 cm of the affected area.
Freezing was continuously maintained for 20 to 30 seconds in each area.
All pigmented gingiva in both jaws were treated during a single
appointment.
A second course of cryosurgical treatment was usually needed after 1
week to remove any residual pigmentation.
Patients were examined at 2 and 7 days and 2 and 4 weeks and again at the
3rd and 6th months after treatment. They were subsequently recalled
once every year.
Slight erythema of gingiva developed immediately after the cryosurgery.
During the next 2 to 3 days, superficial necrosis became apparent and a
whitish slough could be separated from the underlying tissue, leaving a
clean pink surface.
The gingiva appeared normal within 1 to 2 weeks, and keratinization was
completed in 3 to 4 weeks after the treatment.
No post operative pain, hemorrhage, infection, or scarring occurred in
any of the patients.
Healing was uneventful, patient acceptance of the procedure was good,
and the results were excellent. A follow-up period that spanned 3 months
to 2 years showed no repigmentation
8)Treatment of gingival hyperpigmentation for esthetic purposes
by Nd:YAGLASER [23]
The Nd:YAG laser produces invisible, near infrared light with a
wavelength of 1064 nm. This type of laser is used to eliminate various
types of hyperpigmented lesion in dermatological surgery, as well as to
produce depigmentation in skin.
Because the Nd:YAG laser has a particular affinity for melanin or other
dark pigments, it works more efficiently when the entry is applied in the
presence of pigment.
With its range of power and fiber-optic delivery, it has been extensively
used in minor oral and periodontal surgery. Therefore, it may be another
optional treatment for melanin.
A carpule of anesthesia was infiltrated in the operating area.
The patient and staff were protected from the laser by wearing the
manufacturer's spectacles.
The Nd:YAG laser was set at 6 watts, 60 millijoules, and 100 pulses per
second. The ablation was operated using a handpiece with a fiber optic
filament 320 ìm in diameter. he procedure was performed in a contact
mode with cervico-apical direction in all pigmented areas. The laser was
cautiously used to avoid injury to the tooth surface & adjacent tissues
during the ablation. This procedure was completed in 15 minutes. After
ablating the epithelium with the Nd:YAG laser, the wound was covered
with some dried and charred epidermis.
The wound was almost healed completely within 3 weeks. The color of
ablated gingiva was dark pink in some areas. The patient did not have any
pain or bleeding complications.
Four weeks after the operation, the gingiva was generalized pink in color
and healthy in appearance.
The patient was routinely checked every 2 months. After the 11 month
follow up, there was no recurrence of gingival hyperpigmentation.
Melanin's absorption spectrum ranges from 351 to 1064 nm and
therefore lends itself to treatment with a wide variety of lasers. Many
laser systems such as Q-switched ruby laser, flash lamp pumped-dye
laser, Argon laser, CO2 laser,
13
 The post surgical problems after using the argon and CO2 laser for
skin depigmentation have been reported as scarring, textural changes,
and hypopigmentation. The Q-switched ruby laser, flash lamp pumped
dye laser, and pulsed Nd:YAG laser were reported as successful devices
for pigmented skin depigmentation. Using 6 watts, 60 millijoules, and
100 pulses per second, the Nd:YAG laser demonstrated good result in
gingival depigmentation. The procedure were minimally invasive,
convenient, fast, and safe. No severe pain was reported during and/or
after the procedure. The Nd:YAG laser does not require local anesthesia
because it generates pulse energy in a short duration that allows for a long
resting time. The Nd:YAG laser could produce effects at tissue depths of
4 to 6 mm into the dermis resulting in a large volume of coagulated issue.
If the Nd:YAG laser is used repeatedly, profound thermal damage could
be produced unknowingly and tissue damage would occur. II. Treatment
of severe physiologic gingival pigmentation with 1.Free Gingival
Autograft [6]
Preparation of the Recipient Site : The surgical procedure was
performed after application of local anesthesia in the area of gingival
melanin pigmentation.
In each patient, at least two areas were grafted. In one area, the
recipient bed was prepared in such a way that the bony surface would
remain covered with periosteum and thin connective tissue (partial
thickness dissection).
In the second surgical area, the periosteum, connective tissue, and
epithelium were completely removed (full-thickness bed preparation).
To control bleeding in the surgical area, pressure was applied to the
recipient site with wet gauze after injection of lidocaine with
epinephrine. Donor Site : The autogenous gingival graft was obtained
from the unpigmented area of the palate. A No.15 scalpel was used to
elevate a split thickness section of a 1 to 2 mm thick graft. The graft was
placed in close contact with the recipient site and held in place by simple
sutures of 4-0 silk. Sutures were removed after 1week.
The pigmented gingival tissue was histologically examined by a
pathologist. All histologic reports indicated that there was no evidence
of malignancy and corroborated the clinical diagnosis of physiologic
melanin pigmentation. Patients were examined upto 4.5 years following
surgery. Clinical healing of free gingival autograft used to replace areas
of gingival pigmentation proceeded uneventfully. All 10 patients were
followed for 4.5 years postsurgically.In all 10 areas in which the recipient
bed was prepared by full-thickness dissection, no evidence of
repigmentation was seen. During the follow up period, only one of 10
grafted areas in which the recipient bed was prepared by partial thickness
dissection exhibited repigmentation, after 1 year.
Healing : A clearly incised wound produces an initial inflammatory
reaction followed by relatively quick epithelization that takes place over
a smooth bed of connective tissue.
The initial response will be hemorrhage followed by the formation
of a serofibrinous exudates and blood clot covering the wound area.
Conclusion: The depigmentation procedure was successful and the
patient was satisfied with the result of the depigmentation tecnique.
REFERENCES :-
1. Cicek Y, Ertas U. The normal and pathological pigmentation of oral
mucous membrane: a review. J Contemp Dent Pract.
2003:15;4(3):76-86.
2. Dummett, C.O: Oral pigmentation. First symposium of oral
pigmentation. J Periodontol 1960;31:356
3. Shafer WG, Hine MK, Levy BM. Text book of oral Pathology.
Philadelphia: WB Saunders co; 1984; pp. 89-136
4. Dummet CO, Barens G. Oromucosal pigmentation: an updated
literary review. J Periodontol. 1971;42(11):726-36.
5. Perlmutter S, Tal H. Repigmentation of the gingiva following
surgical injury. J Periodontol. 1986 Jan;57(1):48-50.
6. Tamizi M, Taheri M. Treatment of severe physiologic gingival
Journal of Dental Sciences & Oral Rehabilitation
pigmentation with free gingival autograft. Quintessence Int. 1996
Aug;27(8):555-8.
7. Steigmann S. Treatment of melanin-pigmented gingiva and oral
mucosa by CO2 laser. Oral Surg Oral Med Oral Pathol Oral
RadiolEndod. 2000 Jul;90(1):14-5.
8. Özbayrak S, Dumlu A, Ercalik-Yalcinkaya S. Treatment of
melanin-pigmented gingiva and oral mucosa by CO2 laser. Oral
Surg Oral Med Oral Pathol Oral Radiol Endod 2000; 90: 14-15
9. Dummett CO. Clinical observation on pigment variations in healthy
oral tissues in the Negro. J Dent Res. 1945;24:7-13.
10. Prinz H. Pigmentation of the oral mucous membrane. Dental
Cosmos. 1932;72:554-561.
11. Dummett CO. Oral tissue color changes (I). Quintessence Int. 1979
Nov;10(11):39-45. No abstract available.
12. Brown FH, Housten GD. Smoker's melanosis. A case report. J
Periodontol. 1991 Aug;62(8):524-7. Review.
13 Gorsky M, Buchner A, Fundoianu-Dayan D, et. al. Physiologic
pigmentation of the gingiva in Israeli Jews of different ethnic origin.
Oral Surg Oral Med Oral Pathol. 1984 Oct;58(4):506-9.
14. Patsakas A, Demetriou N, Angelopoulos A. Melanin pigmentation
and inflammation in human gingiva. J Periodontol. 1981 Nov;52
(11):701-4.
15. Meyerson MA, Cohen PR, Hymes SR. Lingual hyperpigmentation
associated with minocycline therapy. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. 1995 Feb;79(2):180-4.
16. Amir E, Gorsky M, Buchner A, et. al. Physiologic pigmentation of
the oral mucosa in Israeli children. Oral Surg Oral Med Oral Pathol.
1991 Mar;71(3):396-8.
17. Porter SR, Flint SR, Scully C. Oral Diseases. Martin Dunitz, second
edition, London1996,1-371.
18. Laskaris G. Color atlas of oral diseases in children and adolescents.
Thieme Stuttgart, New York 1999,1-337.
19. Hirschfeld I and Hirschfeld L. Oral pigmentation andmethod of
removing it. Oral Surg Oral Med Oral Path.1951;4:1012
20. Mokeem SA: Management of Gingival Hyperpigmentation by
Surgical Abrasion: Report of Three Cases. mSaudi Dental Journal,
2006 ; 18( 3) , 162-166.
21. Bishop K : Treatment of unslightly oral pigmentation: A case report.
Dental Update, 1994; 21(6):236-237.
22. Yeh CJ: Cryosurgical management of melanin pigmented gingival.
Oral Surgery Oral Medicin, Oral Pathology Oral Radiology
Endodontolgy, 1998; 86(6):660-663
23. Stabholz A, Zeltser R, Sela M, Peretz B, Moshonov J, Ziskind D,
Stabholz A.:The use of lasers in dentistry: principles of operation
and clinical applications. Compendium of Continuing Education in
Dentistry 2003; 24(12): 935-948.
14
www.rmc_bareilly.com REVIEW ARTICLE

OSSEOINTEGRATION-THE KEY TO SUCCESSFUL

IMPLANT PLACEMENT: A REVIEW

AUTHORS:
Dr. K.L. Gupta (M.D.S.) ABSTRACT
READER
Co author Osseointegration is a defined as : "the formation of a direct interface between an implant and bone,
Dr. Puneet Anand without intervening soft tissue".[1] Osseointegrated implant is a type of implant defined as "an
Professor
Deptt. Of Prosthodontics endosteal implant containing pores into which osteoblasts and supporting connective tissue can
Dr. Neeraj Nagpal migrate".[2] Applied to oral implantology, this thus refers to bone grown right up to the implant surface
Professor
Deptt. Of Prosthodontics without interposed soft tissue layer. No scar tissue, cartilage or ligament fibers are present between the
Dr. Dinker goel bone and implant surface. The direct contact of bone and implant surface can be verified
Dr. Tamanna Chabra
Dr. Alok kumar microscopically.
Department of Prosthodontics Dental implants are by far the main field of application, Retention of a craniofacial prosthesis such
Institute of Dental Sciences, Bareilly
as an artificial ear (ear prosthesis), eye (orbital prosthesis), or nose (nose prosthesis), Bone anchored
hearing conduction amplification (Bone Anchored Hearing Aid).
This article reviews how Osseointegration has enhanced the science of medical bone and joint
replacement techniques.
INTRODUCTION encompasses many fields of research and clinical
Per-Ingvar Brånemark introduced the concept of endeavor.
osseointegrated dental implants and raised the bar for Definition of Osseointegration
management of dental and orofacial deficits. As a Osseointegration was originally defined as a
result, long-termclinical outcomes from the direct structural and functional connection between
technique's scrupulously applied surgical and ordered living bone and the surface of a load-carrying
prosthodontic protocols ushered in a new and exciting implant. It is now said that an implant is regarded as
dental treatment era, particularly for partially and osseointegrated when there is no progressive relative
completely edentulous patients. movement between the implant and the bone with
Subsequent routine dental use of osseointegration which it has direct contact. In practice, this means that
resulted from a long research voyage in a vessel made in osseointegration there is an anchorage mechanism
seaworthy by the synergistic efforts of numerous whereby nonvital components can be reliably and
clinical scientists. predictably incorporated into living bone and that this
The loosening of implants from bone tissues has anchorage can persist under all normal conditions of
been a cause of problems in reconstructive surgery and loading.
joint replacement. The thought for decades has been Experimental Studies
that the layer of fibrous tissue that develops around the The initial observations of osseointegration were
implant diminishes the integrity and mechanical made in the 1950s during the study of the circulation in
stability of the implant/bone interface. bone marrow. In a modification of the rabbit ear
In this brief review article we will attempt to chamber, a titanium implant with a central canal and a
highlight key developments in the research and transverse opening at one level was threaded into bone
application of osseointegration. Over the years, the to allow bone and vessels to grow into the chamber. It
concept of osseointegration has developed into as occurred to this investigator that such integration of
much of a philosophy as it is a technique for titanium screws and bone might be useful for
rehabilitation supporting dental prostheses on a long-term basis. Thus
DISCUSSION began a continuing program of research and clinical use
The patient has always been the focus of advances of titanium implants.
in the technique of osseointegration, and these Study of the biomechanics of osseointegration
advances have been the result of unprecedented levels was a key early research activity, which was overseen
of collaboration between health care providers, the by Professor Richard Skalak . Detailed biomechanical
research community, and the medical industry. The tests were performed by R. Brånemark and coworkers
proceedings of the recent research conference in this to evaluate implants during healing, after irradiation, in
area, Osseointegration, From Molecule to Man, experimental arthritis, in osteoarthritis and rheumatoid
documents the strength of the key components of arthritis, and in vivo in rat, rabbit, dog, and man. This
science and health that have contributed to the success series of studies provided evidence that the
and growth of osseointegration. It also documents the biomechanics of bone-anchored implants are complex.
value of an interdisciplinary and multidisciplinary There was a plastic deformation of the bone-implant
approach to rehabilitation patient care that interface subjected to shear, and no elastic deformation
was observed. In pullout and lateral load tests the load-
Journal of Dental Sciences & Oral Rehabilitation 15
deformation curve showed an elastic behavior, indicating that these tests
mainly reflect the mechanics of the surrounding bone. In dental
applications, the clinical experience is now sufficient in length of time
and in total patient numbers to say that neither stress shielding nor fatigue
appear to be limiting factors in the long-term successful function of
titanium dental fixtures (1).
Titanium Properties
A thin oxide layer covers the surface of pure titanium after being
spontaneously formed at atmospheric conditions. More extensive oxide
growth occurs on titanium implants subjected to biological tissues (2).
Inflammatory cells, especially macrophages, may contribute to
development of the oxide layer by excreting proteolytic enzymes,
cytokines, superoxide, and hydrogen peroxide (3). It is hypothesized that
the actual interface of the titanium implant to the living tissue is a
hydrated titanium peroxy matrix. The formation of such a matrix is
unique to titanium, as the other possible transition metals either have too
low solubility of their peroxy complex or too low stability of the complex.
Osseoperception
Osseoperception is the term used to describe the ability by patients
with osseointegrated fixtures to identify tactile thresholds transmitted
through their prostheses.
The oxide of titanium is covered with a very thin layer of titanium
peroxy compounds, which are in contact with the living bone. It is a
phenomenon of importance in both dental and orthopaedic applications
of osseointegration. The identification of osseoperception as a
phenomenon of osseointegration was the result of work carried out in the
dental sciences by Torgny Haraldson . In 1979 he characterized the
sensory feedback in patients with osseointegrated bridges and concluded,
“Patients with osseointegrated bridges have been restored to a level of
functional capacity of the masticatory system equal to that in individuals
with a natural but reduced dentition of the same extension as in the
osseointegration group.” Osseoperception has also been studied in
orthopaedic applications. Experimentally, vibratory perception around
implants in the femoral, tibial, ulnar, radial, and (meta)carpal bones has
been assessed by means of the psychophysical threshold determination of
passive stimuli applied to the implants, whereby the subject has to answer
whether he/she detects the stimulus or not (figure 1).
Experiments were carried out on two groups of patients who had
suffered limb amputation.. This method was also applied for threshold
determination of the stump of amputees in Group 2 to compare these
values to implant stimulation threshold. The measured perception of
vibration with an osseointegrated amputation prosthesis in place was
generally comparable to that of the normal contralateral hand or foot.
This was different from the corresponding measurements obtained with a
conventional amputation prosthesis. This finding has recently been
repeated in a series of 32 patients, and it was further documented that
boneanchored prostheses yielded better perception than socket
prostheses . These tests suggest that direct stable and permanent
anchorage of amputation prostheses to the skeleton via osseointegrated
fixtures and skin-penetrating abutments will be a useful clinical
technique that improves an amputee's perception of the environment.
osseoperception is its use in providing for hearing prostheses.
ESTABLISHED CLINICAL APPLICATIONS OF
OSSEOINTEGRATION
Osseointegration provides an attachment mechanism for the
incorporation into living bone of non-vital components made of titanium.
As a biological phenomenon it has been amply demonstrated and
clinically tested, and is now widely accepted. The present range of
clinical applications is as follows:
Dental
In the field of oral surgery, the most common application of
osseointegration has been the dental and oral reconstruction of patients
who have lost teeth. The anatomical and functional rehabilitation after
the loss of teeth implies replacement of the teeth and part of the
surrounding tissues because the loss of teeth results in involution of
periodontal tissues. Osseointegration has been used for the replacement
of missing single teeth, for the restoration of the partially edentulous
segment of the mouth, and for the reconstruction of the completely
edentulous patient by means of implant-supported fixed bridges or
removable overdentures that attach to an implant-supported framework.
The superior performance of osseointegration in dental applications
by comparison with other techniques has been confirmed in a number of
multicenter studies. Worldwide, more than 800,000 patients have been
treated since 1965 until now with osseointegration dental
reconstructions, according to Brånemark. The results indicate a clear
superiority over conventional prosthodontics with respect to long-term
Journal of Dental Sciences & Oral Rehabilitation
success rates (4,5). It should be pointed out that osseointegration in
dental sciences has been the subject of more than 2,000 scientific articles,
thus creating a solid research and clinical basis for this treatment
modality. Continued development and adaptation of surgical and
prosthetic procedures has allowed rehabilitation even of patients with
extensive loss of alveolar jawbone, including discontinuities of the jaw
skeleton, whether congenital, posttraumatic, or after tumor surgery.
Autologous bone grafts have proven beneficial in many of these
situations in combination with bone-anchored devices. Requirements on
precise fitting of prosthetic superstructures exceed those for devices
anchored to teeth, since the osseointegrated fixtures do not adapt to a
misaligned prosthetic framework by changing their position in the
jawbone. This, on the other hand, means that fixtures can be used in
orthodontic procedures.
There has been a rapid development in orthodontic applications of
dental implants to provide anchorage for orthodontic, orthopaedic, and
orthognathic movements. One recent young patient with extensive
oligodontia has undertaken a program of several steps (6). The initial step
was the replacement of the missing mandibular dentition anterior to the
molar teeth by implant-anchored bridgework. Subsequently, implants
were placed in the missing maxillary cuspid areas to initially provide
anchorage for orthodontic realignment of the premolar teeth and to
thereafter provide support for freestanding single-tooth implant
restorations. Pterygoid plate maxillary fixtures were used to provide
distal support for the bridgework.
Facial Prostheses
Complex problems of facial tissue loss are often amenable to
management by means of implant-supported maxillofacial prostheses.
Many previously irradiated patients have been treated successfully with
implant reconstructions. One such patient had a hemimandibulectomy
performed as part of her ablation and the surgery was followed by
radiation. After reconstruction of the mandible with a bone graft and
prophylactic hyperbaric oxygen, implants were used to stabilize a full
fixed lower partial denture. Extraoral applications of osseointegration
include anchorage for craniofacial prostheses including ear, eye, and
nose (figure 2). When the external ear has been removed due to tumor or
trauma, a satisfactory replacement can be made by the maxillofacial
prosthodontist and the artificial pinna is anchored to the temporal bone
by means of special implants. In a similar manner, implants placed
around the orbital rim can be used to anchor an orbital prosthesis. These
facial prostheses are more hygienic, comfortable, and satisfactory than
earlier models retained with adhesives.
CONCLUSION
Dental implants are truly a revolution, solving an age old problem safely
and predictably by successful osseointegration (figure 3). Implant
dentistry can change the smiles and lives of millions for years to
come.Dental implants are an effective, safe and predictable solution to
the problems resulting from missing teeth. Many patients report exciting
benefits from dental implants, such as:
Replacement teeth look, feel and function like natural teeth
Improved taste and appetite
Improved cosmetic appearance
The ability to chew without pain or gum irritation
Improved quality of life
One additional and very important benefit can be the reduction or
elimination of bone atrophy or shrinkage, commonly associated with
loss of teeth.
16
REFERENCES
1. Skalak R. Biomechanics of osseointegration. In: Brånemark P-I,
Rydevik BL, Skalak R, editors. Osseointegration in skeletal
reconstruction and joint replacement. Carol Stream, IL:
Quintessence Publishing Co; 1997. p. 45–56.
2. Sundgren JE, Bodö P, Lundström I. Auger electronspectroscopic
studies of the interface between human tissue and implants of
titanium and stainless steel. J Coll Int Sci 1986;110:9–20.
3. Bjursten L-M. The bone-implant interface in osseointegration. In:
Rydevik B, Brånemark P-I, Skalak R, editors. International
Workshop on Osseointegration in Skeletal Reconstruction and Joint
Replacement. The Institute for Applied Biotechnology, Göteborg,
Sweden, 1991; p. 25–31.
4. Adell R, Ericksson B, Kekholm U, Brånemark P-I, Jemt T.
Longterm follow-up study of osseointegrated implants in the
treatment of totally endentulous jaws. Int J Oral Maxillofac Implants
1990;5:347–59.
5.. Esposito M, Hirsch JM, Lekholm U, Thornsen P. Biological factors
contributing to failures of osseointegrated oral implants. (I). Success
criteria and epidemiology. Eur J Oral Sci 1998;106:527–51. FIGURE 3
6. Henry PJ. Osseointegration in dentistry. In: Williams E, Rydevik B,
Brånemark P-I, editors. Osseointegration from molecule to man.
Institute for Applied Biotechnology, Proceedings of
Interdisciplinary Conference, 1999 May 2; Göteborg, Sweden:
Artisten; p. 2–12.

FIGURE 1

FIGURE 2
Journal of Dental Sciences & Oral Rehabilitation 17
www.rmcbareilly.com CASE REPORT

DENTIGEROUS CYST : A CASE REPORT

AUTHORS:
Dr. Sudhapalli Chidanand Rao INTRODUCTION lower third molars were unerupted. A routine
Professor The dentigerous cyst is the second most common cyst panoramic radiograph (Fig 1) revealed horizontally
Dr. Nikhil Pandit of the jaws comprising 14–20 per cent of all jaw cysts, impacted lower third molar.
Dr. Hitesh Hans Baweja
Dr. Himanshu Pratap Singh and they are more frequent in males and more common Teeth was associated with a well defined unilocular
PG Students in the mandible.1, 2, 3, 4 By definition, this lesion is radiolucency, approximately 1.5 cms in diameter,
Dept.t of Oral and Maxillofacial Surgery,
Institute of dental Science, Bareilly
attached to the cervix of an impacted tooth and results encompassing the crowns and attached to the
from proliferation of reduced enamel epithelium after amelocemental junction. On both sides the
the enamel formation. Dentigerous cysts are usually radiolucencies extended to the mesial aspect of the
discovered on routine radiographic examination or lower second molars, inferiorly to within 2 mm of the
when films are taken to determine the reason for failure lower border of the mandible and superiorly to just
of a tooth to erupt. They are always radiolucent and below the alveolar crest. There was no displacement of
usually unilocular, although large lesions occasionally the teeth and there was no apparent resorption of the
show a scalloping multilocular pattern.3, 4, 5, 6 roots of the lower second molar, as there were no
Third molars followed by maxillary canines (the most symptoms arising from these third molar.
commonly impacted teeth) and occasionally
supernumerary teeth or odontomas are involved in cyst
formation. Their pathogenesis remains unknown.
Proliferation of the epithelium in a fluid-filled sac may
be induced by osmotic pressure during the extended
period of time the tooth is impacted. Were the tooth to
erupt, the dentigerous cyst would burst and cease to be
a pathologic entity, as is usually the case in small
eruption cysts.1, 2, 3, 4 Small cysts are also easy to treat
surgically.
However, dentigerous cysts occasionally become
extensive since lesions are asymptomatic even when
reaching considerable size and then treatment is more
difficult as associated teeth are often impacted and
displaced a considerable distance due to cyst pressure;
surgery may require removal of several teeth or tooth
buds or endanger vitality of adjacent teeth. FIGURE NO-1
Nevertheless, because of the many damaging sequelae,
dentigerous cysts must be surgically eliminated. MANAGEMENT
Methods employed for elimination have included Cyst size and site, patient age, the dentition involved,
decompression, marsupialisation, and enucleation.1, 2, 3, and involvement of vital structures, were criteria which
4
However, the criteria for selecting these treatment were considered and used to dictate the treatment
modalities (indications and contraindications) are not modality .
Cyst enucleation and extraction of third molar was
clearly defined. Moreover, large study series and long- treatment of choice in our case.(fig. no. 2)
term follow-up to assess various treatment results,
recurrence, and to compare demographic data, are
lacking in the literature.
CASE REPORT
A 48 year old male patient was referred to our
department with the complain of heaviness on left side
of lower face since 6 month. There was no history of
trauma and he had no symptoms from the third molars.
Patient was the known case of COPD.
Clinical examination revealed a click from both
temporomandibular joints on opening but with no
limitation or deviation of the mandible. Intraorally, the
Journal of Dental Sciences & Oral Rehabilitation 18
DISCUSSION Philadelphia: WB Saunders, 2000, pp88.
Radiographic findings are not diagnostic for dentigerous cysts because 4. Martínez-Pérez D, Varela-Morales M. Conservative treatment of
odontogenic keratocysts, unilocular ameloblastomas, and many other dentigerous cysts in children: report of four cases. J Oral Maxillofac
odontogenic and non-odontogenic tumours have radiographic features Surg 2001; 59: 331–334.
essentially identical to those of a dentigerous cyst. These are ruled out 5. Dammer R, Niederdellmann H, Dammer P, et al. Conservative or
after negative biopsy and histologic examination.2,4 Thus, in large radical treatment of keratocysts: A retrospective view. Br J Oral
dentigerous cysts an incisional biopsy from an accessible site is done to Maxillofac Surg 1997; 35: 46.
rule out other lesions which mandate separate, more aggressive, 6. Aguiló L, Gandía JL. Dentigerous cyst of mandibular second
treatment protocols. premolar in a five-year-old girl, related to a non vital primary molar
Microscopic examination removed one year earlier: A case report. J Clin Pediatr Dent 1998;
Microscopic examination of dentigerous cysts reveals a thin, 22: 155.
nondistinctive, nonkeratinised, fluid filled, epithelium lined, sac.2 The 7. Motamedi MHK, Khodayari A. Cystic ameloblastomas of the
epithelial lining consists of two to four layers of cuboidal epithelial cells, mandible. Med J Islamic Rep Iran 1992; 6: 75–79.
and the epithelium-connective tissue interface is flat.1, 2, 3, 4 It is possible 8. Motamedi MHK:Periapical ameloblastoma: a case report. Br Dent J
for the lining of a dentigerous cyst to undergo neoplastic transformation 2002; 193: 443–447.
to an ameloblastoma and this has been reported.1, 2, 3, 4 Squamous cell 9. Sain DR, Hollis WA, Togrye AR. Correction of a superiorly
carcinoma may also arise in the lining of a dentigerous cyst.2 The displaced canine due to a large dentigerous cyst. Am J Dentofac
frequency of such neoplastic transformation is very low. Orthop 1992; 102: 270.
Surgery 10. Clauser C, Zuccati G, Barone R et al. Simplified surgical
Surgery is commonly recommended for dentigerous cysts because they orthodontic treatment of a dentigerous cyst. J Clin Orthod 1994; 28:
often block eruption of teeth, become large, displace teeth, destroy bone, 103.
encroach on vital structures (ie encompass or displace the alveolar nerve, 11. Ziccardi VB, Eggleston TI, Schneider RE. Using a fenestration
shrink the maxillary sinus) and occasionally even lead to pathologic technique to treat a large dentigerous cyst. J Am Dent Assoc 1997;
128: 201.
fracture.1, 2, 3, 4 This treatment has however, classically consisted of cyst
12. Takagi S, Koyama S. Guided eruption of an impacted second
enucleation and extraction of the tooth or teeth embedded in it, or
premolar associated with a dentigerous cyst in the maxillary sinus
impacted by it.1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12 This treatment option although
of a 6 year-old child. J Oral Maxillofac Surg 1998; 56: 237.
favourable in cases involving a single impaction such as a useless
13. Motamedi MHK. Application of the osteoplastic flap in oral and
wisdom tooth in an adult, will however in extensive cysts, lead to a loss of
maxillofacial surgery. J Oral Med Oral Surg Oral Pathol 1999; 87:
several teeth. When the teeth involved with the cyst are extracted
647–648.
(especially in children), functional, cosmetic, and psychological
consequences may follow. In addition, the problems of how to replace
such teeth in a growing child are also of concern. Thus, based on the fact
that dentigerous cysts are benign, we feel that several factors or
evaluation criteria may help dictate which treatment option is indicated:
Cyst size. Cyst size is an important factor when formulating a treatment
plan. Small cysts may easily be enucleated and submitted for pathologic
examination (excisional biopsy), while preserving the strategic tooth or
teeth involved.
Patient age and proximity of vital structures. Patient age and the
proximity of vital structures are other factors requiring consideration. In
children with extensive cysts, tooth germs may be damaged and teeth
devitalised by enucleation, thus, an initial phase of decompression of the
lesion to diminish the size of the osseous defect followed by surgical
enucleation at a later date may be indicated.
Significance of the impacted tooth. The significance of the associated
impacted tooth should also be considered prior to surgery. For instance an
upper or lower canine tooth has enough merits with regard to aesthetics
and occlusion to warrant its retention, thus, cyst removal with tooth
preservation is indicated. The other extreme is an impacted third molar
tooth which often warrants extraction with cyst enucleation.
Several recent articles mention the acceptance of cyst decompression in
children with dentigerous cysts, describing case reports where the cysts
were opened to the oral cavity and stents (either a rubber tube, removable
devices, or gauze packing) were used to keep the opening patent to permit
shrinkage of the cyst enucleated at a later date with a less extensive and
safer surgical procedure.9, 10, 11, 12 However, reports regarding treatment of
extensive dentigerous cysts via enucleation while salvaging the involved
tooth or teeth, using orthodontic treatment to assist eruption and align the
dentition are sparse. This was done effectively in our recent case.
REFERENCES
1. Assael LA. Surgical management of odontogenic cysts and tumors.
In Peterson L J, Indresano T A, Marciani R D, Roser S M. Principles
of Oral and Maxillofacial Surgery. Philadelphia: JB Lippincott,
1992, Vol 2, pp685–688.
2. Neville BW. Odontogenic cysts and tumors. In Neville B W, Damm
D D, Allen C M, Bouquot J E. Oral and Maxillofacial Pathology.
Philadelphia: WB Saunders, 1995, pp493–496.
3. Regezi JA. Cyst and cystlike lesions. In Regezi J A, Sciubba J,
Pogrel M A. Atlas of Oral and Maxillofacial Pahtology.

Journal of Dental Sciences & Oral Rehabilitation 19

www.rmcbareilly.com CASE REPORT

IN VITRO FRACTURE RESISTANCE OF

ENDODONTICALLY TREATED CENTRAL
INCISORS WITH VARYING FERRULE HEIGHTS
AND CONFIGURATIONS.

AUTHORS: ABSTRACT
Dr. Anurag Singhal
(MDS) Restoration of endodontically treated teeth is a unique and complex procedure. Several criteria have
Prof.& Head been put forward for the evaluation and treatment planning of final restoration for endodontically
Dr. Chandrawati Guha
(MDS)
treated teeth. The clinician must consider the advantages and disadvantages of saving teeth according
Reader to their eventual role in restoring occlusion, function and esthetics. Root fracture of endodontically
Dr. Anuraag Gurtu treated teeth restored with post and core is a common problem. So this study was conducted to
(MDS)
Reader evaluate the efficacy and comparison of uniform and non uniform ferrule designs in preventing the root
Dr. Payal Singhal fracture.This in vitro study investigated the resistance to static loading of endodontically treated teeth
BDS (MDS)
PG Student with uniform and non uniform ferrule configurations.
Department of Conservative KEYWORDS
Dentistry & Endodontics
Institute of Dental Sciences Bareilly.
Post & core; Dowel; Ferrrule; Crown
INTRODUCTION the respective teeth and subsequently cemented with a
The restoration of the endodontically treated tooth Type- I glass ionomer cement. Crown wax patterns
is an important aspect of successful endodontic were then made for the specimens with the aid of the
therapy. There are wide ranges of treatment options of reduction guide to recreate the original crown contour.
varying complexity. The clinician must be able to A lingual ledge was added to create a standard loading
predict the probability of restoring such teeth point. Wax pattern from each group was invested and
successfully. (1) Generally, endodontically treated cast using the same protocol used with the dowels and
teeth experience significant coronal destruction as well cores.Crowns were cemented with a Type- I glass
as loss of radicular dentin, due to the removal of tooth ionomer cement and stored for 3 days in an
structure during endodontic access opening and post- environment with 100% humidity
space preparation. Clinical longevity of post- and- core Teeth were divided into one control and five groups
restoration can be influenced by many factors, with 8 teeth in each group
including the magnitude and direction of the occlusal (0) teeth restored with crowns (CRN).
load, design of the dowel, thickness of the remaining (1) Endodontically treated teeth restored with crowns
dentin, quality of the cement layer and creation of (RCT/CRN).
ferrule effect to enhance the structural durability of the (2) Endodontically treated teeth restored with cast
final restoration.(1,2) dowels and cores and crowns incorporating a 1-mm
MATERIALS AND METHODS ferrule (1 FRL).
48 intact maxillary central incisor teeth were selected (3) Endodontically treated teeth restored with cast
from the Department Of Oral Surgery (Institute Of dowels and cores and crowns incorporating a 2-mm
Dental Sciences, Bareilly, U.P.) Working length was ferrule (2 FRL).
set at 1 mm short of the apical foramen.Canal (4) Endodontically treated teeth restored with cast
preparation was completed by using a step back dowels and cores and crowns incorporating a ferrule of
technique with K- files. Obturation was accomplished nonuniform height (0.5/2 FRL).
by cold lateral condensation with gutta percha and AH- (5) Endodontically treated teeth restored with cast
26 sealer. Reduction guides were made from vinyl dowels and cores and crowns without a ferrule (0 FRL).
polysiloxane putty.
Specimens were tested with a universal testing
Dowel space preparation began with the removal of machine set to deliver an increasing load until failure.
gutta percha using a heated plugger. Final gutta percha Failure was defined as a 25% drop in the applied load.
removal was performed with peezoreamers, taking The crosshead speed was 2.5 mm per minute, and the
care to preserve 4 mm of apical gutta percha. The apical load was applied to the lingual ledge at a 45-degree
region of the dowel space was prepared with a drill. angle to the long axis of the tooth. The specimens were
Dowel-and-core patterns were made from blue inlay tested in random order (samples were pooled, mixed,
wax to replace the coronal dentin that had been and chosen without visualization), and the operator of
removed. Pattern from each of the groups was invested the machine was not informed of the group designation
in a gypsum bonded investment material. Thirty of the specimen being tested.
minutes after the start of the mix, the investment was
placed in a preheated burnout oven at a temperature of
1100°C and left for 45 minutes. The patterns were cast RESULTS
in Nickel Chromium alloy with the aid of a centrifugal • Figure summarizes the findings of the
casting machine. The dowels and cores were fitted to investigation. Significant differences were detected by

Journal of Dental Sciences & Oral Rehabilitation 20

1-way ANOVA (P<.0001).

FIG I: MAXILLARY FIG II: COMPLETE PORCELAIN

CENTRAL INCISORS FUSED TO SAMPLES

FIG III: GP 0 &I- CEMENTED CROWN

DISCUSSION
Post endodontic restoration is very important for the clinical success
of the endodontically treated tooth. Endodontically treated teeth have
significantly different physical and mechanical properties when
compared to vital teeth. It has been assumed that endodontically treated
teeth are brittle and more prone to fracture because of loss of water. But
the exact phenomena occurs due to the disorganization and change in the
collagen structure of the dentin and incorporation of tensile stresses.(3)
So the successful restoration of root filled teeth requires an adequate
coronal seal, protection of the remaining tooth, while restoring function
and acceptable aesthetics. A crown, a cast indirect post and core may be
required to replace missing tooth structure and provide retention for the
restoration.
The magnitude of the difference in failure load between the teeth
with a uniform 2-mm ferrule and teeth with a nonuniform ferrule was
surprising. This difference in failure load is attributed to the difference in
remaining coronal tooth structure. (4) The ferrule is a band that encircles
the external dimensions of the residual tooth. It is formed by the walls and
margins of the crown or by cast telescopic coping encasing at least 2 to 3
mm of sound tooth structure.
The crown and crown preparation must have 5 requirements: (5)
1) The dentin axial wall height must be at least 2 to 3 mm.
2) Axial wall must be parallel.
3) The restoration must completely encircle the tooth.
4) The margins must be on sound tooth structure.
5) The crown and crown preparation must not invade the attachment 3.
apparatus.
CONCLUSION 4.
The following conclusions were drawn:
1. The mean fracture strengths of endodontically treated maxillary
central incisors restored with a crown without a dowel and 5.
endodontically treated maxillary central incisors restored with a
cast dowel and core and crown with a uniform 2-mm ferrule were
not significantly different. 6.
2. Endodontically treated maxillary central incisors with a uniform 2-
mm ferrule were more fracture resistant than those with a ferrule
varying between 0.5 mm and 2 mm (P=.0001).
3. Endodontically treated maxillary central incisors with a ferrule
length varying between 0.5 mm and 2 mm were more fracture
resistant than those without a ferrule (P=.001).
REFRENCES
1. Naumann M, Preuss A, Rosentritt M. Effect of incomplete crown
GP II ,III,IV,V- CEMENTATION
WITH POST & CORE
FIG IV: UNIVERSAL TESTING MACHINE
FIG V: SAMPLES MOUNTED ON
UNIVERSAL TESTING MACHIENE
ferrules on load capacity of endodontically treated maxillary
incisors restored with fiber posts, composite build-ups, all-ceramic
crowns: an invitro evaluation after chewing simulation. Acta
Odontol Scand. 2006 Feb; 64(1): 31-6.
2. Tan PL, Aquilino SA, Gratton DG, Stanford CM, Tan SC, Johnson
WT, Dawson D. In vitro fracture resistance of endodontically
treated central incisors with varying ferrule heights and
configurations. J Prosthet Dent 2005 Apr; 93(4): 331-6.
Pereira JR, De Ornelas F, Conti PC, Do Valle AL. Effect of a crown
ferrule on the fracture resistance of endodontically treated teeth
restored with prefabricated posts. J Prosthet Dent 2006; 95(1): 50-
4.
Libman WJ, Nicholls JI. Load fatique of teeth restored with cast
posts and cores and complete crowns. Int J Prosthodont 1995 Mar-
Apr;8(2): 155-61.
Barkhordar RA, Radke R, Abbasi J. Effect of metal collars on
resistance of endodontically treated teeth to root fracture. J Prosthet
Dent 1989; 61:676- 8.
Tan PL, Aquilino SA, Gratton DG, Stanford CM, Tan SC, Johnson
WT, Dawson D. In vitro fracture resistance of endodontically
treated central incisors with varying ferrule heights and
configurations. J Prosthet Dent 2005 Apr; 93(4): 331-6.

Journal of Dental Sciences & Oral Rehabilitation 21

 www.rmcbareilly.com CASE REPORT

HYPOPLASTIC AMELOGENESIS IMPERFECTA

AUTHORS:
Dr. Sunil R Panat ABSTRACT
Principal, Professor & Head Amelogenesis Imperfecta (AI) is a collective term for a number of conditions with abnormal enamel
CO-AUTHOR:
Dr. Ashish Aggarwal formation. Many cases are inherited, either as an X-linked, autosomal dominant or autosomal
Senior Lecturer recessive trait. Several classifications have evolved since 1945, based primarily on phenotype with the
Dr. Prakash Chandra Jha mode of inheritance being used in some systems as a secondary factor in allocating a case into a
PG student
Deptt. of Oral Medicine & Radiology, particular category. The prevalence of this condition has been estimated to range from(1 in 718) to (1 in
Institute of Dental Sciences, Bareilly (UP). 14,000). Hypoplastic AI represents 60-73 percent of all cases, hypomaturation AI represents 20-40
percent, and hypocalcification AI represents 7 percent. Here we report a case of Hypoplastic type of
Amelogenesis Imperfecta in a 23 year old male patient with positive family history.

KEY WORDS: Amelogenesis Imperfecta (AI), Enamel, Dental, Genetic, Hypoplastic Enamel.
INTRODUCTION
Amelogenesis imperfecta (AI) is a heterogeneous
group of genetic disorders characterized by defects in
tooth enamel formation in the absence of any
generalized or systemic diseases. The prevalence of AI
is reported at 1/700 in northern Sweden and 1/14,000
in the US. AI is currently classified into 14 distinct
subtypes based on the clinical phenotype and mode of
inheritance (Witkop, 1988); however, the gene
responsible for every subtype has not yet been defined.
Major enamel matrix proteins (amelogenin, enamelin,
and ameloblastin) are suggested to contribute to the
enamel formation of teeth .During the secretory stage
of enamel formation, these proteins are secreted by
ameloblasts and play key roles in the growth of enamel
crystal.Several reports have shown that mutations in
the amelogenin gene located at Xp22.1-p22.3 cause X-
linked AI .However, the X-linked AI presents in less
than 5% of all reported cases. The most common type
of AI is the autosomal-dominant form it is possible
that heterogeneous mutations within the enamelin
gene might also be responsible for the autosomal-
dominant hypoplastic forms of AI.1
CASE REPORT
A 23 year old male patient reported to the Department
of Oral Medicine & Radiology with the chief
complaint of missing teeth and discolored teeth on both
upper and lower jaw region. History of presenting
illness revealed that teeth were not normal since
childhood. Initially teeth were loosened and gradually
he lost most of his teeth for last 10-12 years and some
teeth were removed by a local practitioner.
Family history was revealed that his sister also
had similar type of discolored teeth since her childhood
with multiple missing teeth.
Intra oral examination revealed that discoloration was
present all over the teeth which were yellowish white
in color with conical shaped crown. There were
multiple missing teeth in relation to 32,33,34,35,41,
Journal of Dental Sciences & Oral Rehabilitation
42,43, and 44, and root stumps were present i.r.t-15, 25,
37, and 47. Dental caries was seen in relation to 16, 46
and 31 was mobile.
Considering the history and clinical examination, the
provisional diagnosis of Amelogenesis Imperfecta was
given. Differential diagnosis considered the
dentinogenesis imperfect..
Full mouth Intra-oral peri-apical radiograph and OPG
was advised to the patient. Radiographs revealed that
enamel density was not appreciable and open contact
between the teeth was seen. Cemento-enamel junction
was completely absent. Radiolucency on the coronal
portion cofirmed generalized attrition of the tooth.
Radiopacity in the pulp chambers of the tooth was
suggestive of generalised pulp stone. Multiple
impacted teeth were present without enamel capping.
Extraction of teeth with poor prognosis i.e. 31, 25 and
37 was done and sent for the ground sectioning and
histological examination, which came out to be
Hypoplastic Amelogenesis Imperfecta.
DISCUSSION
Amelogenesis imperfecta encompasses a complicated
group of conditions that demonstrate developmental
alterations in the structure of the enamel in the absence
of a systemic disorder. It is a developmental disturbance
that interferes with normal enamel formation. It is an
inherited disorder related to the alteration of the gene
involved in the formation and maturation of the enamel.
Different inherited patterns are present like Autosomal
dominant, Autosomal recessive and X-linked. Most
common type is autosomal dominant type.2
The first contribution on the subject was a paper by Finn
in 1938, who differentiated two groups of tooth
anomalies based on clinical characteristics, namely
defects of dentine – hereditary brown opalescent
dentine – and enamel – brown hypoplasia of enamel.
The first definition of AI – as a disease caused by a
primary defect in enamel – has been attributed to
22
Weinmann et al (1945) who classified AI into two types, namely CONCLUSION
hypoplastic and hypocalcified. This definition was subsequently adopted Amelogenesis Imperfecta is an uncommon disorder; however, its clinical
by both Darling (1956) and Witkop (1957). Darling (1956) stated that AI and radiological manifestations are characteristic. Management of
implied a generalized fault of enamel structure affecting all the teeth of patient with amelogenesis Imperfecta is important because it provides
one or both dentitions, unrelated to any specific time or period of good aesthetics and maintains healthy supporting tissues. It helps the
amelogenesis, or to any intermittent dietary abnormality or disease. He patient to develop a good psychologic self image. New alternatives for
also remarked on the inherited pattern of the disease and added that there rehabilitation for such patient must be carefully considered, taking into
was a possibility that the condition could occur spontaneously in one or account the presence of exposed dentin.
more members of the same family Subsequently, According To Witkop References:
(1989) 3
Type I Hypoplastic
I A– Hypoplastic, Pitted Autosomal Dominant.
I B - Hypoplastic,local Autosomal Dominant.
I C - Hypoplastic,local Autosomal Recessive.
I D - Hypoplastic,smooth Autosomal Dominant.
I E - Hypoplastic,smooth X-linked Dominant.
I F - Hypoplastic,rough Autosomal Dominant.
I G - Enamel Agenesis, Autosomal Recessive.
Type II Hypomaturation
II A – Hypomaturation ,Pigmented Autosomal Recessive.
II B - Hypomaturation , X-linked Recessive.
II C – Snow Caped Teeth,autosomal Dominant.
Type III Hypocalcified
III A - Autosomal Dominant.
III B - Autosomal Recessive.
Type IV Hypoplastic-Hypomaturation
IVA –Hypomaturation-Hypoplastic with taurodontism,autosomal
dominant.
IVB -Hypoplastic-Hypomaturation with taurodontism,autosomal
dominant.
In Hypoplastic amelogenesis imperfecta, the basic alteration
centers are on inadequate depostion of enamel matrix. In the generalized
pattern, there are pinpoint-to-pinhead sized pits scattered across the
surface of the teeth. The buccal surface of the teeth is affected more
frequently. Pits may be arranged in rows or columns. In the localized
pattern, the altered area is located in the middle third of the buccal
surfaces of the teeth. The Incisal edge or occlusal surface usually is not
affected. Both dentition (and only the primary teeth) may be affected.
In the autosomal dominant smooth patteren, enamel of all the teeth
exhibits a smooth surface and is thin, hard and glossy. Color of the teeth
varies from opaque white to translucent brown. The absence of
appropriate enamel thickness results in teeth that are shaped like crown
preparations.
X-linked smooth pattern exhibit diffuse thin, smooth and shiny
enamel in both dentitions. Color varies from brown to yellow brown. In
females, vertical furrows of thin hypoplastic enamel are seen. An open
bite is present in almost all males and in a minority of females. 1. MJ Aldred, R Savarirayan, PJM Crawford, Oral Diseases (2003) 9,
In rough pattern, enamel is thin, hard and rough-surfaced. Teeth taper 19–23
toward the incisal/ occlusal surface and demonstrate open contact points. 2. M. Kida, T. Ariga, T. Shirakawa,H. Oguchi, and Y. Sakiyama,
Anterior open bite is common. Journal of Dental Research 81(11):738-742, 2002
In condition of enamel agenesis there is total lack of enamel formation. 3. Shafer's Text Book Of Oral Pathology Shafer,Hine 6th Edition.
Teeth have the shape and color that of the dentin, with a yellow brown hue 4. Oral And Maxillofacial Pathology Neville ,Dam,Allen 3rd Edition.
and open contact points. Crowns taper toward the incisal-occlusal 5. Witkop CJ Jr (1988). Amelogenesis imperfecta, dentinogenesis
surface.4 imperfecta and dentin dysplasia revisited: problems in
Diagnosis of amelogenesis imperfecta is based on-5 classification. J Oral Pathol 17:547-553.
A. Clinical examination-visual & flaking of enamel and/or piercing
enamel with an explorer.
B. Family history.
C. Radiographic assessment.
D. Scanning electron microscope.
Primary treatment includes cosmetic improvement of the patient
with the help of placement of crown or facial veneer on the teeth.
Desensitizing agents are advised to treat the hypersensitivity in the
patients due to dentine exposure of the teeth. Over dentures are also
advised in case of patient who doesn't have sufficient crown length for the
restoration.

Journal of Dental Sciences & Oral Rehabilitation 23

www.rmcbareilly.com CASE REPORT

MESIODENS: AN ETIOLOGY OF
SEVERE MALOCCLUSION

AUTHORS:
Dr. Preeti Bhattacharya ABSTRACT
M.D.S Supernumerary tooth (ST) is a developmental anomaly and has been argued to arise from multiple
Reader
Dr. Abhishek Agarwal etiologies. These teeth may remain embedded in the alveolar bone or can erupt into the oral cavity.
M.D.S When it remains embedded, it may cause disturbance to the developing teeth. The erupted
Senior lecturer
Dr. D.K. Agarwal supernumerary tooth might cause aesthetic and/or functional problems especially if it is situated in the
M.D.S maxillary anterior region. A case of supernumerary teeth is presented where the teeth have been left in
Professor
Dr. P.S Raju
place and which later gave rise to some problems. The patient had requested orthodontic treatment for
M.D.S the misalignment of his anterior teeth. The treatment options are further discussed.
Professor & Head KEY WORDS
Dr. Ankur Gupta
M.D.S Supernumerary teeth, Mesiodens, Class II malocclusion, Esthetics, Severe rotations
Senior lecturer
Dr. Siddharth Kaushal INTRODUCTION opposite direction. Maxillary and mandibular arches
BDS were U-shaped with mild crowding in mandible arch.
Lecturer Nance1 described dental crowding as the difference He had Angle's class II molar relationship, an overjet of
Dept of Orthodontics between spaces needed in the dental arch and space 3 mm and over bite of 4 mm.
Institute of Dental Sciences, Bareilly available in that arch that is the space discrepancy.
Thus crowding or spacing can be described as an The cephalometric analysis showed mild proclination
expansion of an altered tooth/tissue ratio or as of upper & lower incisors with mild skeletal class II
dentoalveolar disproportion. relationship because of mandibular retrusion (SNA-
84O, SNB-78O,ANB-6O). The mandibular plane angle
The causes of crowding are however, still not fully (GoGn-SN – 25O, FMA-20O) indicates hypo divergent
understood. Hootan2 suggested that crowding was growth.
probably the result of an evolutionary trend toward a
reduced facial skeletal size without a corresponding Arch perimeter and Carey's analysis showed tooth
decrease in tooth size. Brash3 said that crowding was material excess in maxillary arch by 8mm and in
hereditary. The result of interbreeding in ethnic groups mandibular by 2 mm.
who are physically dissimilar. Other investigators such The patient was diagnosed as Angle's class II Division I
as Barber4 and Moore, Larelle and Spence5 suggested malocclusion on class II skeletal bases due to mild
that environmental factors were more important then mandibular retrusion having hypodivergent growth
genetic factors. pattern with severe crowding in maxillary anterior
Supernumerary teeth are one of the common region due to mesiodense.
etiological factor in dental crowding. A supernumerary . The goal of orthodontic treatment was to correct
tooth is a term used to describe more than the normal crowding in the maxillary arch while maintaining the
number of a full complement of teeth in either the molar. It was decided to extract mesiodense and both
primary or permanent dentitions. Most common first premolar in maxillary arch.
supernumerary teeth is mesiodens. Prevalence of TREATMENT PROGRESS
mesiodens in children varies from 0.15-3.8%.6 Orthodontic treatment was started with 0.018” slot
Mesiodens may cause a wide range of associated Preadjusted Edgewise MBT system. Banding was done
problem ranging from median diastema, a delay of for 11 and 12 instead of bonding to derotate the teeth so
eruption of permanent central incisors, alteration of the that the bonding will be facilitated in the later stages.
position of permanent incisors, root resorption, An initial 0.016” round NiTi arch wire was placed.
Canines were retracted initially to gain space and open
dentigerous cyst formation and severe rotations and coil spring was placed between 11 and 12 for rotation
crowding of incisors.7 correction. It was followed by 016 x 022” NiTi wire ,
CASE SUMMARY used for alignment & levelling of both arches for
A male patient of age 24 years came to the Department 5months. Space consolidation was started with 0.016 x
0.022” S-S wire using friction mechanics and
of orthodontics with the chief complaint of rotated continued for a period of further 5 months. Finishing
teeth in the upper front region. He had mesoprosopic and detailing was done by 0.017” x 0.025” NiTi
face type & mesocephalic head with no facial followed by 0.017” x 0.025” S-S wire for 2 months.
asymmetry. A convex profile with straight divergence, Active treatment was around 12 months. At the end of
acute nasiolabial angle and deep mentolabial sulcus the treatment molar relation was maintained, normal
with competent lips were noted. overjet and overbite were achieved. Retention was
Intra oral examination revealed that he had permanent given for a period of 9 months using removable
Hawley's retention appliance.
dentition with mesiodense and severe crowding in the
maxillary region 11 and 12 showed 900 rotation in DISCUSSION
Development of the tooth is a continuous process with

Journal of Dental Sciences & Oral Rehabilitation 24

a number of physiologic growth processes and various morphologic 289-294.
stages interplay to achieve the tooth's final form and structure.
Interference with the stage of initiation, a momentary event, may result in
single or multiple missing teeth (hypodontia or oligodontia respectively)
or supernumerary teeth8. A supernumerary tooth is one that is additional
to the normal series and can be found in almost any region of the dental
arch9. The term mesiodens denotes10 a supernumerary tooth located
between the maxillary central incisors .
The aetiology of the ST however remains unclear. Several theories have
been suggested for their occurrence such as the 'phylogenetic theory'11,
the 'dichotomy theory'12, a hyperactive dental lamina7 and a combination
of genetic and environmental factors-unified etiologic explanation13.
The 'phylogenetic theory' relates to the phylogenetic process of atavism
(evolutionary throwback) has been suggested. Hyperdontia is the result
of the reversional phenomenon or atavism. Atavism is the return to or the
reappearance of an ancestral condition or type.
The 'dichotomy theory' is where a supernumerary tooth is created as a
result of dichotomy of the tooth bud. The supernumerary tooth may
develop form the complete splitting of tooth bud12. The tooth bud splits
into two equal or different-sized parts resulting in two teeth of equal size
or one normal and one dysmorphic tooth, respectively.
A hyperactive dental lamina where the localized and independent
hyperactivity of dental lamina is the most accepted cause for the
development of the supernumerary teeth; it is suggested that
supernumerary teeth are formed as a result of local, independent,
conditioned hyperactivity of the dental lamina7, 12. According to this
theory, the lingual extension of an additional tooth bud leads to a
eumorphic tooth, while the rudimentary form arises from proliferation of
epithelial remnants of the dental lamina induced by pressure of the
complete dentition10. Hattab and co-workers8 tend to believe that
hyperdontia is a disorder with pattern of multifactorial inheritance
originating from hyperactivity of dental lamina. Remnants of the dental
lamina can persist as epithelial pearls or islands, “rests of Serres” within
the jaw. If the epithelial remnants are subjected to initiation by induction
factors, an extra tooth bud is formed resulting in the development of either
a supernumerary tooth or odontome.
It is essential not only to enumerate but also to identify the supernumerary
teeth (ST) present clinically and radiographically before a definitive
diagnosis and treatment plan can be formulated14. Mesiodens may often
cause retardation or obstruction of eruption of permanent incisors. Early Fig. 1 Pre treatment Photographs
diagnosis and extraction of a mesiodens may prevent malocclusion and
dental abnormalities such as delayed eruption of permanent incisors,
rotation of the permanent incisors and diastema15.
In this case we observed that mesiodens caused severe rotations which
hampered the esthetics severely. After treatment the results showed
properly aligned arches with pleasing esthetics for which patient was
completely satisfied.
REFRENCES
1. Nance HN: The Limitations of orthodontic treatment, AM J
ORTHOD ORAL SURGERY 1947,33,177-223.
2. Hooton EA: Up from the ape. New York: The Macmillan Company,
1947.
3. Brash JC: The aetiology of irregularity and malocclusion of the Fig. 2 With wire photographs
teeth, 2nd ed. London, Dental board of United Kingdom, 1956.
4. Barber TK. The crowded arch. J.S Calif Dent Hyg Assoc, 1967, 35,
232-40.
5. Moore WJ, Lavelle CLB, Spence TF: Changes in the size and shape
of the human mandible in Britain. British Dental Journal, 1968,
125,163-9.
6. Ray D, Bhattacharya B, Sarkar S, Das G: Erupted maxillary conical
mesiodens in deciduous dentition in a begali girl – a case report, J.
Indian Soc Pedod Dent, 2005,23,153-5.
7. Primosch RE: Anterior supernumerary teeth- assessment and
surgical intervention in children. Pediatric Dent, 1981, 3, 205-15.
8. Hattab FN, Yassin OM and Rawashdeh MA (1994).Supernumerary
teeth: Report of three cases and review of the literature. ASDC J
Dent Child, 61: 382- 393.
9. Garvey MT, Barry HJ and Blake M (1999). Supernumerary teeth –
an overview of classification, diagnosis and management. J Can
Dent Assoc, 65: 612-616.
10. Sykaras SN (1975). Mesiodens in primary and permanent
dentitions. Oral Surg, 39: 870-874.
11. Smith JD (1969). Hyperdontia: report of a case. J Am Dent Assoc,
79: 1191-1192.
12. Liu JF (1995). Characteristics of premaxillary supernumerary teeth:
A survey of 112 cases. ASDC J Dent for Child, 62: 262-265.
13. Brook AH (1984). A unifying etiological explanation for anomalies
of human tooth number and size. Archs Oral Biol, 29: 373-378.
14. Scheiner MA and Sampson WJ (1997). Supernumerray teeth: a Fig. 3 Post Treatment Photographs
review of the literature and four case reports. Aust Dent J, 42: 160-
165.
15. Tay F, Pang A and Yuen S (1984). Unerupted maxillary anterior
supernumerary teeth: report of 204 cases. ASDC J Dent Child, 51:

Journal of Dental Sciences & Oral Rehabilitation 25

www.rmc_bareilly.com CASE REPORT
FIXED PROSTHODONTICS FOR A MISSING
PRIMARY TOOTH (CASE REPORT)
AUTHOR:
Prof Dr. Puneet Anand ABSTRACT
Dr. Anand's Dental Clinic A THREE AND A HALF-YEAR-OLD BOY lost his two maxillary primary incisors when he was playing
and Implant Centre
with his friends at school. The teeth could not be found. Two weeks later, the child was brought to
the, and his parents asked for fixed replacement of the lost teeth. A fixed partial denture was
constructed and delivered to the child, and the aesthetic and functional demands were restored. This
lead to a successful result for both the child and the parents.
Oral and dental trauma are common in infants and
preschool children. Treatment is however often
delayed because parents cannot ascertain the
seriousness of the injury or are unsure where to seek
treatment for their children(1). Injuries to the primary
dentition are common: it has been estimated that up to
30% of preschool children are affected. Dentists who
treat a significant number of children under 4 years of
age are likely to encounter a child with an avulsed
maxillary incisor.(1, 2, 6)
Dental trauma often occurs in this population because
young children tend to be unstable on their feet as they
first start to walk, which results in accidents and
damaged teeth. The age group in which primary tooth
injury occurs most is 1.5 - 2.5 years, at this age the child
has started to walk and to discover the new world
around him.(2) Traumatic injuries of the oral tissues
could be variable and may affect the hard as well as the
soft tissues, anterior teeth could be affected and the
final result could be one of the following damages:
1. Crown fracture.
2. Luxation.
3. Intrusion.
4. Extrusion.
5. Root fracture.
6. Avulsion.
AVULSION
Tooth avulsion is the complete displacement of the
tooth out of its socket. It may affect primary as well as
permanent anterior teeth.(4, 7)
The incidence of tooth avulsion from traumatic
injury of primary dentition is 7-13 % while in
permanent dentition it is 1-16 %. The high incidence of
primary tooth avulsion has been related to the nature
of the jaw bone in children, which is so
resilient and spongy that it could absorb the force of the
trauma. The backdraw in this case is that the tooth
completely comes out of its socket. This bony nature
will change to a rigid one with the permanent dentition,
in which tooth fracture constitutes the major type of
dental trauma, because there is no time for the bone to
absorb the traumatic force completely. And as an
adverse effect, the permanent tooth shows some
Journal of Dental Sciences & Oral Rehabilitation
damages. (3, 4)
CASE HISTORY
A THREE AND A HALF-YEAR-OLD BOY was
referred to our dental clinic and implant center on May
15, 2010. A dental record was opened for the child, in
order to register his medical as well as his dental history
with a proper extra and intra oral examination.
His mother told us her son lost his anterior primary
incisors at school while playing with his friends. The
teeth could not be found and the child was taken to the
school clinic to take the necessary measures for
controlling the bleeding and sterilize the area. Two
weeks later, his mother brought him to our clinic
asking for teeth replacement because she was very
anxious about the appearance of her son, and she
insisted on having a fixed appliance as a teeth
replacement. (Fig. 1)
Intra oral examination revealed a healthy gingival
tissue with sound remaining primary teeth and the
sockets of the lost teeth were about to heal. An
appointment was given to the patient to construct the
fixed appliance. (Fig. 2)
One week later, the child was brought to our clinic and
selection of the orthodontic bands on his maxillary
second molars was done. An alginate impression was
taken and poured into a dental cast. A laboratory work
was done by wires attached to the bilateral orthodontic
bands posteriorly and with two front teeth anteriorly on
which these teeth have an acrylic base. The wire would
not be particularly visible because it is located on the
lingual side. (Fig. 3)
After one week, the appliance was fitted in the child's
mouth by bonding the orthodontic bands with zinc
oxide cement.(Fig. 4)
Both the child and the parents were pleased with the
new look of the child, which gave him a normal
appearance. Some instructions were given to his
mother to maintain a good oral hygiene for the child and
recall visits to make any necessary adjustments for the
appliance if needed. (Fig. 5)
DISCUSSION
Loosing a tooth can be physically and emotionally
trying, as the resulting empty site is functionally
26
damaged and the aesthetic appearance bothers the parents as well as the
child, in addition to psychological problems affecting the child in
relation with his teeth loss. (3, 5)
The treatment options in these cases are removable maintainers of space
or fixed partial dentures. Choosing a treatment depends on factors
associated with each case regarding the child age, oral hygiene, child
cooperation as well as parents' desire of having fixed or removable
replacement. This appliance is recommended especially if the
removable space maintainers are considered to provoke discomfort or

Fig. 4

Fig. 1

Fig. 5

if the child cannot tolerate such an appliance because of its early age.(5)
REFERENCES
1 Arthur J. Nowak, DMD, and Rebbeca L.Slayton, DDS, PhD. Trauma
to primary teeth: setting a steady management course for the office
contemporary pediatrics. J. November 2002
Fig. 2 2 Jionus F. Tahmassebi and Elizabeth A.O Sullivan. Diagnosis and
management of trauma to primary dentition. Dental update J 1999;
26:138-142
3 Lynnus Peng, MD and Amin Antoine Kazzi, MD. Dental, Avulsed
tooth. E medecine Continuing Education, June 28, 2001
4 Ronald Johnson, DDS, D.Walter Cohen, DDS. Continuing dental
education, the treatment of traumatized incisor in the child patient.
Quintessence Publishing Co, 1981
5 Iara Augusta Oris, DDS, MS Jose Francisco Rodrigues Faris, DDS
Ivana Bolsoni DDS, Aldevina Campos Freitas DDS, MS Paula
Gatti, DT. The use of a resinbonded denture to replace primary
incisors: case report. AAPD 1999 V.21 I.1
6 Erica L. Zamon, B.SC., David J. Kenny, DDS, PhD. Replantation
of Avulsed Primary Incisors: A Risk Benefit Assessment. J of Can
Dent Assoc 2001; 67:386
7 Grahams Roberts and Peter Longhurst. Oral and Dental Trauma in
Children and Adolescents. Oxford University Press 1996

Fig. 3

Journal of Dental Sciences & Oral Rehabilitation 27

 www.rmc_bareilly.com REVIEW ARTICLE

“XEROSTOMIA- A REVIEW AND UPDATE”

AUTHORS:
Dr. Gaurav Sapra ABSTRACT
Senior Lecturer
Department of Oral Pathology
Xerostomia is a condition of dry mouth that is experienced by many patients and is frequently
and Microbiology, encountered in medical practice. It often develops when the amount of saliva that moistens the oral
Institute of Dental Sciences, Bareilly (U.P.) mucous membrane is reduced. A number of commonly prescribed drugs with a variety of
Dr. P.K.Singh
Assistant Professor
pharmacological activities have been found to cause xerostomia as a side effect. Additionally,
Department of Anatomy xerostomia often is associated with Sjögren's syndrome and complication of radiation therapy.
R.M.C.H., Bareilly (U.P.) Xerostomia is related with difficulties in chewing, swallowing, tasting or speaking. Xerostomia can
Dr. Rahul Agarwal
Assistant Professor predispose to an increased risk of developing dental caries. It can also cause oral discomfort for
Faculty of Dental Sciences denture wearers. Management strategy for this condition should include caries prevention and
IMS, BHU, Varanasi (U.P.)-INDIA elimination of drugs having anticholinergic effects. Treatment is based primarily on replacement
Dr. K. T. Chandrashekar
Professor & Head, therapies and gustatory, masticatory, and pharmacological stimulants. Healthcare professionals can
Deptt. of Periodontology & Implantology play a vital role in identifying patients at risk for developing xerostomia, and should provide appropriate
Hitakarini Dental College & Hospital,
Jabalpur (MP)- INDIA.
preventative and therapeutic measures that will help to preserve a person's health, function, and quality
of life. The purpose of this review is to discuss the common causes, clinical manifestations,
complications and treatment modalities available, which will assist the clinicians to manage the
xerostomic patients.
KEY WORDS: Xerostomia; Sjögren's syndrome; Oral mucous membrane.

INTRODUCTION: impairing chewing ability. Furthermore, it may alter

Saliva is a complex fluid produced by the
salivary glands. It forms a film of fluid coating the
teeth and mucosa thereby creating and regulating a
healthy environment in the oral cavity.[1]
Saliva is derived predominantly from three
paired major salivary glands, i.e. the parotid,
submandibular and sublingual glands (together
accounting for about 90% of the fluid production) as
well as from the minor salivary glands in the oral
mucosa. Whole saliva also contains gingival
crevicular fluid, microorganisms from dental plaque
and food debris. In healthy individuals the daily
production and swallowing of saliva normally ranges
from 0.5 to 1.5 Liters and it is composed of more than
99% water and less than 1% solids, mostly proteins
and salts.[2] Saliva is thought to be secreted by a two-
stage mechanism. Acinar cells produce an osmotic
gradient that is mediated by a co-transporter loop in
the basolateral membrane. This osmotic gradient
results in the production of salivary fluid.[3, 4]
Reduced saliva, either qualitatively or
quantitatively, may negatively impact on oral health.
Research indicates that there is a loss of salivary
parenchymal acinar cells which occurs in ageing.[5]
These effects are often unrecognized as the parotid
gland is capable of maintaining function without
obvious changes in amount, composition or
variability.[6]
Xerostomia is a condition associated with both a
decrease in the amount of saliva produced and an
alteration in its chemical composition, therefore
causing feeling of dry mouth. This can have a
deleterious effect on many aspects of oral function and
general well being. It can cause a significant decline in
quality of life by decreasing taste sensation and
Journal of Dental Sciences & Oral Rehabilitation
regular eating patterns, reducing the pleasure of eating
due to impaired or diminished taste sensation. Patients
with xerostomia often report an avoidance of some
foods, such as dry foods (bread) and sticky foods, due
to the inability to chew or swallow effectively. Also,
xerostomia may impair a patient's ability to speak,
cause cracks and fissures in the oral mucosa and
halitosis. It can cause denture wearing to be very
uncomfortable, exacerbating chewing difficulties.
Xerostomia can affect numerous aspects of oral
function, contributing to pain, caries and oral
infections.[7]
EPIDEMIOLOGY
Xerostomia may develop in any person of any
age, But it is frequently described as a symptom of
middle-aged and elderly individuals.
In a questionnaire based study on 710 American adults
ranging in age from 19 to 88 years, it was observed that
24% of females and 18% of males suffered from
xerostomia. It was also found that xerostomia was
associated with the use of medications and in males,
cigarette smoking was the main cause associated. The
hyposalivatory side-effects like difficulty in
consuming dry foods, cracked lips, dry eyes, difficulty
in swallowing were also reported.[8] It has also been
reported that the prevalence of dry mouth symptoms
increased with age, was more common in women than
men and was greater in whites than blacks.[9]
The prevalence of perceived dry mouth among a
group of elderly people in Japan was also investigated.
It was found that 37.8% reported oral dryness on
waking, yet only 9.1% of individuals noticed a
subjective feeling of dry mouth during eating.[10] The
relationship between complaints of xerostomia and
food avoidance in geriatric patients was analysed in a
28
veteran affairs clinic and retirement home. Among 529 subjects older
than 56 years, 72% reported that they experience xerostomia sometime
during the day and 55% of these said they use one or more medications
for it.[11]
The oral problems of 147 elderly patients in long term care hospital
wards were investigated and 35% complained of dry mouth.[12] It was
reported that subjects with Type 1 diabetes reported symptoms of dry
mouth more frequently. Salivary flow rates were also found impaired in
Type 1 diabetics.[13] The literature also suggests that xerostomia is more
commonly associated with HIV positive patients.[14]
Recent literature suggests that symptoms of xerostomia start when there
is a decrease of 45% in normal salivary flow.[15] Cross-sectional and
longitudinal studies report that parotid salivary gland function in healthy
individuals is predominantly age-independent.[16,17] Salivary flow
changes are associated with medical conditions and medications that
tend to be more common in middle-aged and older individuals.
Xerostomia in the geriatric population is generally due to medications,
systemic diseases and head and neck radiotherapy. Not only is there a
relationship between number of drugs and subjective dryness of the
mouth, there is also an important relationship between subjective dryness
and number of identified diseases in an individual. Overall, the
prevalence of xerostomia increases with age and accounts for
approximately 30% of the population aged 65 and older.[18]
CAUSES
Salivary gland dysfunction, resulting in inadequate saliva
composition and/or reduced salivary flow (hyposalivation), may be
temporary or permanent. Hyposalivation is a term based on objective
measures of the saliva secretion, where the flow rates are significantly
lower than the generally accepted 'normal values'. Flow rates of
unstimulated whole saliva, ≤0.1 ml min -1, and those of chewing
stimulated whole saliva, ≤0.5–0.7 ml min-1, fulfill the criteria for
hyposalivation.[19,20]
Sensation of dry mouth (xerostomia) may also occur without signs of
hyposalivation (for example, in mouth breathing, xerostomia is related to
mucosal dehydration).[21,22] A variety of causes have been suggested
for xerostomia.
Drugs
Xerostomia is a common and significant side effect of many
commonly prescribed drugs/medications. Establishing relative
incidence rates for xerostomia for a particular drug, however, is difficult.
As with other side effects, reported rates depend on how the information
is accessed (direct vs. open-ended questions), the severity of concomitant
adverse reactions, over-reporting for new drug entities, the disorder
being treated and the dose of the medication. Nevertheless, the risk for
xerostomia increases with the number of drugs being taken.[23] Older
people, therefore, are more likely to be affected. In the geriatric
population, drug-induced xerostomia has been reported to contribute to
difficulty with chewing and swallowing; this may result in avoidance of
certain foods.
A variety of drugs that have a wide range of therapeutic activities have
been reported to cause xerostomia. The main mechanism of these drugs is
by inhibiting signaling pathways within salivary tissue and reducing
fluid output of the gland.[24] The most common drugs causing
xerostomia are presented in Table 1. Drug-induced hyposalivation also
can be an extension of the drug's intended action, as seen with the
parasympatholytic agents (such as atropine), or as an anticholinergic side
effect with drugs such as tricyclic antidepressants.[24]
Radiation
Xerostomia is one of the major side effects of radical radiation
therapy for head and neck malignancies. It may be related to the disease,
or as a result of the irradiation volume to the salivary glands.[25] As
radiation treatment progresses, the destruction of the parenchyma of the
salivary glands and their vascular supply produces xerostomia.[26]
Journal of Dental Sciences & Oral Rehabilitation
The degree of destruction of glandular tissue depends largely on the dose
of radiation administered and is most often permanent. The level of
radiation necessary to destroy malignant cells ranges from 40-70 Gy. The
salivary tissue is extremely sensitive to radiation and dosages greater
than 30 Gy are sufficient to change salivary function permanently.[27]
Unless the whole gland has undergone high doses of radiation, partial
recovery of the gland is likely to occur, taking 6-12 months. Xerostomia
may be prevented by shielding the salivary glands during radiotherapy or
modulation of the intensity of radiation when possible.[28]
Sjögren's Syndrome
Sjögren's syndrome is a chronic autoimmune and rheumatic
disorder. The salivary and lacrimal glands are the principal targets of a
supposedly T cell mediated chronic inflammation, giving rise to
deficient function and leading to dry eyes (keratoconjunctivitis sicca)
and mouth (xerostomia). Other exocrine glands including those of the
pancreas, sweat glands and mucous secreting glands of the bowel,
bronchial tree and vagina, can be involved. Sjögren's syndrome is a
world-wide disease and may occur in all ages. How ever, the peak
incidence is in the fourth and fifth decades of life with a female/male ratio
of 9:1.[29]
Primary Sjögren's syndrome occurs when xerostomia and
keratoconjunctivitis sicca develop as isolated clinical entities, whereas
secondary Sjögren's syndrome is when there is a complication of pre-
existing connective tissue disease.[30] The pathognomic histological
finding in biopsies is a focal infiltration of mononuclear lymphoid cells
in the salivary glands, replacing glandular epithelium (lymphoepithelial
lesion), and which is progressive. Another pattern of inflammation in
labial salivary gland biopsy is chronic sialadenitis characterized by
scattered mononuclear cell infiltration without focal aggregates and
accompanied by degenerative changes (acinar atrophy, ductal
hyperplasia, fibrosis and/or fatty infiltration).[31]
Sarcoidosis
Sarcoidosis is another chronic inflammatory disease that alters salivary
gland function causing xerostomia. In this disease, non-caseating
granulomas are formed, contributing to the destruction of the glands.[32]
Miscellaneous
Other factors that may contribute to xerostomia include poorly
controlled diabetes mellitus.[13,33],chronic graft versus host disease,
hepatitis C infection [30], Milkulicz's disease[24], surgical removal of
the salivary glands, dehydration and psychogenic conditions such as
fear, anxiety, depression, mouth breathing and nasal obstruction. Also,
patients that have had an injury to the head and neck can damage the
nerves that innervate the salivary glands and thus produce
xerostomia.[34]
DIAGNOSIS
Treatment of xerostomia begins with appropriate diagnosis. Once a
diagnosis has been established, treatment is based upon the
etiopathogenesis of the disorder. For example, if the etiology is
medication-induced xerostomia, then drug substitution or modification
can ameliorate some symptoms of dry mouth.
Diagnosis involves careful evaluation of signs and symptoms.
Clinical techniques of assessment that can be used include extra-oral and
intra-oral examinations, proper investigation of salivary gland function
by calculating resting and stimulated flow rates, and a biopsy of salivary
glands. In addition to a clinical investigation, a detailed inquiry about
medications and systemic conditions is critical.
During the intra-oral examination, the practitioner should first
visually examine the opening of the duct in the parotid and
submandibular glands. Following this, gentle extraoral pressure should
be applied to palpate each gland. Normally parotid and submandibular
glands are not palpable because they are softer than their surrounding
tissues.
Upon clinical examination, depending on the cause of dry mouth, a
variety of signs and complications are visible that can vary in severity. It
is important to first determine a differential diagnosis and to ensure that
other conditions are not present simultaneously. It is possible for
example, that a patient suffering from burning mouth syndrome may
have no obvious etiology accompanying the dry mouth and hence this
may mask the true diagnosis.[27]
An affirmative response to at least one of the five following
questions about symptoms has been shown to correlate with a decrease in
saliva: "Does your mouth usually feel dry?, Does your mouth feel dry
when eating a meal?, Do you have difficulty swallowing dry foods?, Do
you sip liquids to aid in swallowing dry foods?, Is the amount of saliva in
your mouth too little most of the time, or don't you notice it?[23]
Measuring salivary flow under resting or stimulated secretions is a
critical step in evaluating dry mouth and helping to make an accurate
diagnosis. It was reported that unstimulated whole salivary flow rate
below 0.12 to 0.16 ml min-1 shows a higher incidence of abnormalities of
29
the soft and hard tissues.[35]
It may be difficult to measure salivary flow rates in common
practice. Therefore, following four methods as the clinical measures of
salivary flow rates have been suggested. They are dryness of the buccal
mucosa, absence of saliva expressible from the ducts, the total number of
decayed, missing and filled teeth, and dryness of the lips.[35]
CLINICAL MANIFESTATIONS
Patient with xerostomia usually complaints of a dry mouth, burning
sensation of oral mucosa and a sensation of a loss of or altered taste.
Another manifestation may be an increased need to sip or drink water
when swallowing, difficulty with swallowing dry foods or an increasing
aversion to dry foods.[11] Patients who develop Sjögren's syndrome
secondary to a connective tissue disease also may complain of having dry
eyes, and progressive parotid gland enlargement may become evident.
These initial manifestations may precede clinically apparent alterations
of the oral mucosa or any measurable reduction in salivary gland
function.
As the xerostomia progresses, inspection of the oral cavity may
disclose an erythematous pebbled, cobblestoned or fissured tongue and
atrophy of the filiform papillae. The oral tissues may be erythematous
and appear parched. Palpation of the oral mucosa may result in the
finger's adhering to the mucosal surfaces instead of readily sliding over
the tissues. Application of a dry cotton swab at the parotid and sub-
mandibular duct orifices followed by external palpation of the glands
may reveal delayed or inapparent salivary flow from the ducts. Halitosis
is a common problem and the dryness of the mouth and lips can cause
discomfort ranging from mild irritation to a severe burning sensation.
.[36]
Desiccated oral mucosal tissues are more susceptible to ulcerations
and traumatic lesions. Soft tissue management includes maintaining
mucosal integrity to avoid local or systemic infections from oral
microflora. Dry mouth induced oral lesions are susceptible to developing
secondary infections by microbial flora that normally inhabit the oral
cavity as well as by exogenous organisms. Patients with significantly
decreased salivary output due to prolonged xerostomia have an increased
risk of developing dental caries. .[37] This is a result of the decrease in pH
of saliva and the colonization of cariogenic bacteria, namely
Streptococcus mutans and Lactobacillus species. Reduction of saliva
increases the risk of developing candidiasis also.[38]
MANAGEMENT
The general approach to treat patients with xerostomia is primarily
palliative for the relief of symptoms and prevention of oral complications.
Dental Caries Prevention
With reduction in saliva, the patients are more prone to dental caries and
therefore diligent oral hygiene and regular dental care is essential. A
number of therapeutic interventions are available for the control and
prevention of dental caries. These primarily consist of rigorous attention
to personal oral hygiene, strict adherence to a non-cariogenic diet,
placement of sealants and the application of topical fluorides. The latter
may be useful if an increased incidence of coronal caries, root caries or
both becomes apparent, even when fluoridated community water is
available. This strategy may be effective for both prevention of caries and
possible reversal of decalcification. Supplements that contain sodium
fluoride, acidulated phosphate fluoride or sodium mono-
fluorophosphate are available for professional application as well as for
home use.[39] Use of fluoride varnishes can provide prolonged exposure
to fluoride.[40]
Saliva Substitutes
Artificial saliva substitutes have been shown to give relief by rehydrating
the oral mucosa.[41] Since saliva is a complex secretion with a variety of
functions, it is difficult to mimic through artificial methods.
Milk also contains many chemical and physical properties suitable
as a saliva substitute. It acts by moisturizing and lubricating dehydrated
tissues, buffering oral acids, decreasing the risk of enamel
demineralisation, and it also contributes to remineralization due to its
calcium and phosphate content.[42]
Artificial saliva preparations can be categorized based on their
contents: glycerine and lemon or carboxy-methyl-cellulose and mucin.
They include remineralising contents such as calcium, phosphate,
fluoride and sugar alcohols (e.g. sorbitol), which have a low cariogenic
potential.[43]They are important for lubrication of the mucosa and throat
and help to clean teeth from bacteria and debris. Saliva substitutes are
available as lozenges, rinses, sprays, swab sticks and as reservoirs in
dentures.[44]
Treatment with Optimoist (liquid spray saliva substitute), Saliva
Orthana (mucin-based artifcial saliva), Freedent (low-tack, sugar-free
chewing gum) and Xialine (xanthan gum-based saliva substitute) have
also been suggested.[45]
Journal of Dental Sciences & Oral Rehabilitation
Cholinergic Agonists- Salivary Secretion Stimulants
Treating xerostomia with medications that enhance salivation is another
therapeutic option, particularly in the relatively healthy person.
Secretogogues such as pilocarpine can increase secretions and diminish
xerostomic complaints in patients with sufficiently remaining exocrine
tissue. Pilocarpine is typically given in a dosage of 5 mg orally three
times a day and before bedtime. When taken 30 min before mealtime,
patients may benefit from the increased salivation in eating their meal.
The total daily dose should not exceed 30 mg. Adverse effects include
increased perspiration, greater bowel and bladder motility, and feeling
hot and flushed. Patients with a history of bronchospasm, severe chronic
obstructive pulmonary disease, congestive heart disease, and angle
closure glaucoma should not take pilocarpine.[45]
A new secretogogue, cevimeline, has recently been approved by the
United States Food and Drug Administration for the treatment of dry
mouth in Sjögren's syndrome in a dosage of 30 mg orally three times
daily. Like pilocarpine, it is a muscarinic agonist that increases
production of saliva. Pilocarpine is a non-selective muscarinic agonist,
whereas cevimeline reportedly has a higher affinity for M1 and M3
muscarinic receptor subtypes. Bethanechol, another cholinergic agonist,
has been used (25 mg tid) to stimulate saliva in post head and neck
radiotherapy patients, with few reported significant side-effects.[45]
Regenerative Medicine And Tissue Engineering
Muscarinic agonist medications such as pilocarpine and cevimeline
induced salivary secretion from the residual functional tissue. However,
they only provided temporary relief of symptoms and had a limited
effect on the recovery of damaged tissue. Accordingly, the development
of a novel treatment to restore or regenerate damaged salivary gland
tissue is eagerly awaited. Recently, the occurrence of proliferative,
multipotent salivary gland stem/progenitor cells has been reported in
neonatal mice. A similar cell type was also reported in adult mice,
although their pluripotency was limited.[46,47] More recently, the
potential of mesenchymal stem cells to regenerate salivary glands was
reported using a radiation-damage model.[47,48]
CONCLUSION
Without adequate salivary output, oral and pharyngeal health declines
along with a person's quality of life. Diagnosis of salivary disorders
begins with a careful medical history and examination of head and neck.
While complaints of xerostomia may be indicative of a salivary gland
disorder, salivary diseases can present without symptoms. Therefore,
routine examination of salivary function must be a part of any head,
neck, and oral examination. Therapies are designed to prevent the
development of oral and pharyngeal sequelae of salivary hypofunction.
Current xerostomia-based treatments include replacement therapies and
gustatory, masticatory, and pharmacological stimulants. Regenerative
medicine and tissue engineering may provide new treatment modalities
for atrophic salivary gland. However, such efforts are still in a very early
stage, and a more basic understanding of salivary gland tissue
regeneration and stem cells is required. Healthcare professionals can
play a vital role in identifying patients at risk for developing salivary
dysfunction, and should provide appropriate preventative and
therapeutic techniques that will help to preserve a person's health,
function, and quality of life.
REFERENCES
1. Nieuw Amerongen AV, Veerman ECI. Saliva- the defender of the
oral cavity. Oral Diseases 2002;8:12-22.
2. Pedersen AM, Bardow A, Beier Jensen S, Nauntofte B. Saliva and
gastrointestinal functions of taste, mastication, swallowing and
digestion. Oral Diseases 2002;8:117-29.
3. Thaysen J H, Thorn N A, Schwartz I L. Excretion of sodium,
potassium, chloride and carbon dioxide in human parotid saliva.
Am J Physiol 1954;178:155-59.
4. Turner R J. Mechanisms of fluid secretion by salivary glands. Ann
NY Acad Sci 1993;694:24-35.
5. Drummond J R, Newton J P, Abel R W. Tomographic
measurements of age changes in the human parotid gland.
Gerodontology 1995;12:26-30.
6. Wu A J, Atkinson J C, Fox P C, et al. Crosssectional and
longitudinal analyses of stimulated parotid salivary constituents in
healthy different aged subjects. J Gerontol Med Sci
1993;48:M219-24.
7. Rhodus N L, Brown J. The association of xerostomia and
inadequate intake in older adults. J Am Diet Assoc 1990;90:1688-
92.
8. Billings R J, Proskin H M, Moss M E. Xerostomia and associated
factors in a community dwelling adult population. Community
Dent Oral Epidemiol 1996;24:312-16.
9. Hochberg M C, Tielsch J, Munoz B, et al. Prevalence of symptoms
30
 of dry mouth and their relationship to saliva production in therapy. J Am Dent Assoc 1997;128:1128-33.
community dwelling elderly: the SEE project. Salisbury Eye 37. Mersel A. Oral health status and dental needs in a geriatric
Evaluation. J Rheumatol 1998;25:486-91. institutionalized population in Paris. Gerodontology 1989;8:47-
10. Ikebe K, Nokubi T, Sajima H, et al. Perception of dry mouth in a
sample of community-dwelling older adults in Japan. Spec Care 51.
Dent 2001;21:52-59. 38. Samaranayake LP. Host factors and oral candidosis. In:
11. Loesche W J, Bromberg J, Terpenning M S, et al. Xerostomia, Samaranayake LP, MacFarlane TW, eds. Oral candidosis. London,
xerogenic medications and food avoidances in selected geriatric Wright;1990:66–103.
groups. J Am Geriatr Soc 1995;43:401-07. 39. Fox P C. Management of dry mouth. Dent Clin North Am
12. Samaranayake L P, Wilkieson C A, Lamey P J, et al. Oral disease in 1997;41:863-875.
the elderly in long-term hospital care. Oral Diseases 1995;1:147-
151. 40. Beltrán-Aguilar ED, Goldstein JW, Lockwood SA. Fluoride
13. Moore PA, Guggenheimer J, Etzel KR, Weyant RJ, Orchard T. Type varnishes: a review of their clinical use, cariostatic mechanism,
1 diabetes mellitus, xerostomia, and salivary flow rates. Oral Surg efficacy and safety. J Am Dent Assoc 2000;131:589–96.
Oral Med Oral Pathol Oral Radiol Endod. 2001;92:281–91. 41. Smith G, Smith A J, Shaw L, et al. Artificial saliva substitutes and
14. Schiodt M. Less common oral lesions associated with HIV mineral dissolution. J Oral Rehabil 2001; 28:728-731.
infection: prevalence and classification. Oral Diseases
1997;3(1):208-13. 42. Herod G I. The use of milk as a saliva substitute.J Public Health
15. Ghezzi E M, Lange L A, Ship J A. Determination of variation of Dent 1994;54:184-189.
stimulated salivary flow rates. J Dent Res 2000;79:1874-78. 43. Kielbassa A M, Parichereh Shohadai A, Schulte-Monting J. Effect
16. Baum B J. Evaluation of stimulated parotid saliva flow rate in of saliva substitutes on mineral content of demineralized and sound
different age groups. J Dent Res 1981;60:1292-96. dental enamel. Support Care Cancer 2000;9:40-47.
17. Ship J A, Nolan N, Puckett S. Longitudinal analysis of parotid and
submandibular salivary flow rates in healthy, different aged adults. 44. Sinclair C F, Frost P M, Walter J D. New design for an artificial
J Gerontol Med Sci 1995;50A:M285-89. saliva reservoir for the mandibular complete denture. J Pros Dent
18. Ship J A, Pillemer S R, Baum B J. Xerostomia and the geriatric 1996;75:276-280.
patient. J Am Geriatr Soc 2003;50:535-43. 45. Ship JA. Diagnosing, managing, and preventing salivary gland
19. Heintze U, Birkhed D, Bjørn H. Secretion rate and buffer effect of Disorders. Oral Diseases 2002;8:77–89.
resting and stimulated whole saliva as a function of age and sex.
Swed Dent J 1983;7:227–38. 46. Kishi T, Takao T, Fujita K. Clonal proliferation of multipotent
20. Sreebny LM. Saliva in health and disease: an appraisal and update. stem/progenitor cells in the neonatal and adult salivary gland.
Int Dent J 2000;50:140–61. Biochem Biophys Res Commun 2006;340:544-52.
21. Fox PC, Busch KA, Baum BJ. Subjective reports of xerostomia and 47. H Kagami1, Wang S, Hai B. Restoring the function of salivary
objective measures of salivary gland performance. J Am Dent glands. Oral Diseases 2008;14:15–24.
Assoc 1987;115:581–84. 48. Lombaert IM, Wierenga PK, Kok T et al. Mobilization of bone
22. Ship JA, Fox PC, Baum BJ. How much saliva is enough? 'Normal'
function defined. J Am Dent Assoc 1991;122:63–69. marrow stem cells by granulocyte colony-stimulating factor
23. Guggenheimer J, Moore PA. Xerostomia: Etiology, recognition and ameliorates radiation-induced damage to salivary gland. Clin
treatment. J Am Dent Assoc 2003;134(1):61-69. Cancer Res 2006;12:1804–12.
24. Carranza F A, Newman M G, Takei T T., 9th Ed. Carranza's Clinical
Periodontology. Philadelphia, W.B. Saunders, 2002.
25. Warde P, Kroll B, O'Sullivan B, et al. A phase II study of Biotene in
the treatment of postradiation xerostomia in patients with head and
neck cancer. Support Care Cancer 2000;8:203-208.
26. Baum BJ. Salivary gland fluid secretion during ageing. J Am
Geriatr Soc 1989;37:453.
27. Wynn R L, Meiller T F. Artificial saliva products and drugs to treat
xerostomia. Gen Dent 2000;48:630-636
28. Atkinson J C, Baum B J. Salivary Enhancement: Current Status and
Future Therapies. J Dent Educ 2001;65:1096-1101.
29. Jonsson R, Moen K, Vestrheim D, Szodoray P. Current issues in
Sjögren's syndrome. Oral Diseases 2002;8:130-140
30. Al-Hashimi I. The management of Sjögren's syndrome in dental
practice. J Am Dent Assoc 2001;132:1409-1417.
31. Jonsson R, Kroneld U, Bäckman K et al. Progression of
sialoadenitis in Sjögren's syndrome. Br J Rheum
1993;32:578–581.
32. Nagler R, Marmary Y, Krausz Y, et al. Major salivary gland
dysfunction in human acute and chronic graft-versus-host disease
(GVHD). Bone Marrow Transplant 1996;17:219-224.
33. Chavez EM, Taylor GW, Borrell LN, Ship JA. Salivary function and
glycemic control in older persons with diabetes. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod 2000;89: 305-311.
34. Navazesh M, Brightman V J, Pogoda J M. Relationship of medical
status, medications, and salivary flow rates in adults of different
ages. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
1996;81:172-176.
35. Navazesh M, Christensen C, Brightman V. Clinical criteria for the
diagnosis of salivary gland hypofunction. J Dent Res
1992;71:1363-69.
36. Garg A K, Malo M. Manifestations and treatment of xerostomia and
associated oral effects secondary to head and neck radiation
Journal of Dental Sciences & Oral Rehabilitation 31
www.rmcbareilly.com CASE REPORT
MANDIBULAR PROGNATHISM:
SAGITTAL SPLIT RAMUS OSTEOTOMY
AUTHORS: INTRODUCTION:
DR. DAYANAND SARASWATHI. M.C
Reader Dentofacial deformities affect approx. 20% of the
DR. ANURADHA V population. Patients with dentofacial deformities may
Prof & HOD
DR. HIMANSHU SHARMA demonstrate various degrees of functional and esthetic
SR. Lectuter compromise. Such malformation may be isolated to
DR. UMANG AGARWAL
Deptt. of Oral & Maxillofacial Surgery one jaw or they may extend to multiple craniofacial
Institute of Dental Sciences, Bareilly structures. They may occur unilaterally or bilaterally
and may be expressed to varying degrees in the
vertical, horizontal and transverse facial planes. Many
patients with dentofacial deformities can benefit from
corrective orthognathic treatment.
“Orthognathic surgery is the art and science of
diagnosis, treatment planning and execution of
treatment by consisting orthodontics and oral and
maxillofacial surgery to correct musculoskeletal,
dento-osseous and soft tissues deformities of the jaws
and associated structures”.
Successful orthognathic surgery demands the
understanding and co-operation of the team members-
oral and maxillofacial surgery, orthodontics and
general dentist. Sometimes support from other dental
and medical professional may be necessary to provide
the optimal functional and esthetic outcome that
results in-patient satisfaction.
HISTORY;
The development of mandibular osteotomies for
correction of dentofacial deformities closely parallels
the advancement of oral and maxillofacial surgery as a
specialty more than in 1849 when Obwegessor first
described a modalities osteotomy, in a original paper in
German.
Hullihen corrected a patient with anterior open bite and
mandibular dentoalveolar protrusion with an intra-oral
osteotomy. His efforts were then simulated 50 years
later by Angle, who described body osteotomy done by
V. P. Blair for mandibular horizontal excess. Since then
only efforts were done to preserve vital structures and
using an intra-oral approach.
Blair populated horizontal osteotomy of vertical ramus
done via extra-oral route. The intra-oral approach for
same was then described by Ernst.
The subcondylar osteotomy, a form of which was first
described by Limberg as an extra-oral approach. Then
the subcondylar osteotomy was used to describe the
condylar neck osteotomies of Kostecka and of Moose.
Letterman and Caldwell described a vertical
osteotomy of mandibular ramus. The terms vertical
Journal of Dental Sciences & Oral Rehabilitation
subsigmoid osteotomy (VSO) and vertical ramus
osteotomy (VRO) are used interchanging, but
primarily this osteotomy type was designed for
correction of mandibular horizontal excess of
asymmetries.
The modification of inverted-L osteotomy by Caldwell
and colleagues, describing horizontal cut above the
inferior border created a new design – 'C' osteotomy,
which avoided use of graft since it had more bony
contact.
The greater developments in ramus osteotomy were
done by Obwegessor and Trauner.
The refinement of osteotomy cuts were given by
DalPont, which was further modified by Hunsuck, to
decrease trauma to overlying soft tissues.
DIAGNOSIS:
In order for patients to receive state-of-the-art care
when correcting their deformities, the orthognathic
team must be able to -
1. Correctly diagnose existing deformities.
2. Establish an appropriate treatment plan.
3. Execute the recommended treatment.
! Quantitative assessment of the antero-posterior
position of the mandible and the degree of mandibular
horizontal dysplasia is useful in planning:
! Anterior mandibular horizontal advancement or
reduction.
! Total mandibular horizontal advancement or
reduction.
Radiographic Evaluation :
The lateral and PA cephalometric radiographs are
among the most important tools in the diagnosis of jaw
deformities. They are used to analyze skeletal,
dentoalveolar, and soft tissue relationships in the
anteroposterior (AP), transveres, and vertical
dimensions
There are numerous cephalometric analyses available
to evaluate lateral cephalometric radigoraphs. When a
significant difference occurs, the clinical evaluation is
far more important for treatment planning.
Cephalometric analysis is only and aid to clinical
assessment and should not be used as the sole
diagnostic tool.
32
UNDERSTANDING THE RELATIONSHIP OF HARD & SOFT
TISSUE CHANGES WILL LEAD TO BETTER
PREDICTABLITY

SOFT TISSUE ANALYSIS (LINEAR PARAMETERS)

G-Pg’(mm), G-Sn & Sn-Me(mm), Li -(Sn-Pg’)(mm)
HARD TISSUE ANALYSIS (ANGULAR PARAMETERS)
SNB, N-A-Pg, MP-HP, Ar-Go-Gn Si (Li -Pg’)(mm), Sn-Gn & Gn-C(mm), Pg-Pg’(Chin Thickness) (mm)

Dental model analysis :

Dental model analysis is important in establishing proper diagnosis
and treatment goals, particularly in reference to orthodontics. Proper
dental model analysis improves the understanding and development of
the presurgical orthodontic goals
The sagittal split ramus osteotomy : (SSRO)
Devised by Hugo Obwegessor. is one of the most common orthognathic
procedure used.
Access : Intra oral approach along anterior border of ramus
Technique :
Trauner and Obwegessor - 1955, Horizontal cut on medial side of
mandibular ramus through med cortex above mandibular foramen. A
vertical cut taken down the anterior border of ramus.

Various osteotomy procedures for correction of

HARD TISSUE ANALYSIS (LINEAR PARAMETERS)
N-B(II HP)(mm), N-Pg(II HP)(mm), N-Pog(mm)
mandibular deformities that can be performed
Ar-Go & Go-Pg(mm), ANS-Gn( HP)(mm)
1) Ramus Osteotomies:

• Condylotomy
• Subcondylar osteotomy
• Vertical sub-sigmoid osteotomy E/o and
I/o approaches

• The sagittal split and its modification

• Inverted “L” and “C” osteotomies

2) Osteotomies of body of mandible including
symphysis.
3) Segmental procedures
4) Genioplasty.
SOFT TISSUE ANALYSIS (ANGULAR PARAMETERS)
G-Sn-Pg (Angle of Facial Convexity)
Sn-Gn-C (Lower Face Throat Angle)
Cm-Sn-Ls (Naso-labial Angle)

Journal of Dental Sciences & Oral Rehabilitation 33

 Table 1
N-Pg : Indicates prominence of Chin.
• Any large or small value obtained.
• Compare with N-B or B-PG.
• Indications if the discrepancy is in;
§ Alveolar process
§ The chin
§ Mandible proper.
These measurements help in deciding;
• Genioplasty procedure.
• Anterior mandibular horizontal advancement or reduction.
• Total mandibular advancement or reduction.
ANS-GN : Indicates the lower facial height.
MP-HP : Shows the divergence of mandible posteriorly.
• This angle relates the posterior facial Case of mandibular prognathism: showing pre operative profile
divergence w.r.t. to anterior facial height.
Requires: view and intraoral view with anterior openbite
• Mandibular ramus rotation
• Ramus height reduction.
Ar-Go : Quantitates the length of mandibular ramus.
Go-PG - Length of mandibular body.
• Assessing variation in ramus height that
effect open bite or deep bite problems.
• Length of body - skeletal open or deep bite.
Ar-Go-Gn - Acute / Obtuse - Closed / Open bite.
B-Pg - Prominence of chin related to mandibular denture base.

Indications : SSRO
Mandibular advancement
Mandibular setback
Control the occlusion
Correction of mandibular asymmetry.
An oblique cut through lateral cortex towards angle of jaw.
Satisfactory for prognathism but very little bone contact in mandibular
retrusion.
Dalpont (1961) modified :
Advanced the oblique cut towards molar region and made it vertical
through the lateral cortex.
Hunsuck (1968) :
Shortened the cut through the medial cortex taking is only as far as the
mandibular foramen.
Bell schendel (1977) and Epker (1978) :
Hunsuck technique is adopted but on the lateral aspect the vertical cut is
taken downwards from an oblique line through outer cortex to lower
border where the lower border is sectioned.
Advantages :
! Healing is good because of good bony interface.
! Mandible can be advanced or set back
! Rigid fixation can be used.
! Maintain the angle of mandible in original position even in large
advancements
! Major muscles of mastication remain in original spatial position.
! Contraindications : SSRO
! Severe decreased posterior mandibular body height.
! Thin medial - lateral width of ramus.
! Severe ramus hypoplasia
! Severe asymmetries.
DISCUSSION:
The sagittal split mandibular ramus osteotomy (SSRO) was
developed to avoid complications associated with the vertical oblique
ramus osteotomy in the correction of mandibular deformities.
Obwegessor believed that the broader areas of bony contact would
maximize bony union and prevent some skeletal relapse, although he
believed that relapse had multiple causes. The tongue was believed to be
the most likely cause of relapse after a mandibular setback.
Although skeletal fixation did not prevent sagittal relapse, it did
minimize vertical changes during IMF. Amount of setback to be
correlated significantly with the amount of proximal segment rotation,
which was found to contribute to the amount of skeletal relapse. if the
proximal segment is inadvertently rotated in a clock-wise direction intra-
operatively, this violates the physiologic harmony of the
pterygomaxillary sling and results in the muscles of mastication
becoming loaded. In the post-operative period, the muscles tend to shift
the mandible anteriorly to regain the original proximal segment
orientation and lead to relapse.
Vertical growers showed no horizontal relapse in ANB in the 5 years
after mandibular setback surgery, whereas there was an 18% sagittal
relapse 4 years postoperatively in the horizontal growers. Significant
correlations were found between the amount of setback and the amount
of relapse and between intra-operative lateral movement and
Journal of Dental Sciences & Oral Rehabilitation
Case of mandibular prognathism: showing six months post operative profile view
following SSRO and intraoperative view with correction of anterior openbite
Case of mandibular prognathism: surgical picture showing saggital split
of ramus on right side, fixation with titanium miniplates on left side
postoperative relapse.
A consistent and significant skeletal relapse in non-growing
patients after SSROs with rigid fixation, but this was judged to be
clinically insignificant because the occlusion was not jeopardized. No
relationship was found between the amount of setback and the amount of
relapse. Most pre-operative dental decompensation is stable and that
postoperative skeletal relapse, although limited, is highly variable and
multifactorial in nature.
SUMMARY :
Skeletal relapse after mandibular setbacks using sagittal
osteotomies thus appears to be quite variable, with relapse figures
ranging from 2.3% to 43.7%. Although clockwise proximal segment
rotation appears to be the only universally accepted causative factor,
other factors postulated included the age of the patient, condylar growth,
lateral movement of the mandible during surgery, amount of setback, and
facial morphology.
orthognathic surgery is still the treatment of choice for patients in whom
growth is complete or for those who have a severe skeletal discrepancy.
It should be noted, however, that the results of surgery with regard to
stability and skeletal and occlusal relapse are highly variable. Relapse is
acknowledged to be multifactorial, and much more work must be done to
understand this phenomenon as a physiologic adaptation to orthognathic
surgery.
REFERENCES:
1. Principles of Oral and Maxillofacial Surgery. L. J. Peterson vol-2
2. Maxillofacial Surgery- Peter Ward Booth.
3. Bruce N. Epker - Craniofacial deformity - Surgical and Orthodontic
correction.
4. Dolwick - Orthognathic surgery.
5. Fumndamentals of Orthognathic surgery. Malcom Harris.
6. O.M.S.C North Amercia, May 1997.
34
www.rmcbareilly.com CASE REPORT

PERIPHERAL NEURECTOMY IN
THE MANAGEMENT OF TRIGEMINAL NEURALGIA

AUTHORS:
Dr. RAMAKANT DANDRIYAL ABSTARCT
Reader
Dr. S.C.RAO
One of the worst types of pain usually encountered by a dental patient is neuralgic pain. The pain is so
Professor severe that it may drive the patients to the brink of suicide (Harris, 1926). We report a case of trigeminal
Corresponding Author neuralgia treated with peripheral neurectomy of the involved branch of trigeminal nerve.
Dr. MEENAL AIRAN
Post Graduate Student
Dr. UMANG AGARWAL
Post Graduate Student MANUSCRIPT
Deptt. of Oral & Maxillofacial Surgery Trigeminal neuralgia is defined as a sudden,
Institute of Dental Sciences, Bareilly
usually unilateral, severe, brief, stabbing, lancinating,
recurring pain in the distribution of one or more
branches of V cranial nerve. The pain usually
manifests at 5th or 6th decade of life (except for in
patients with multiple sclerosis)1 and is more common
in females. It occurs more commonly on the right side
(Zakrzewska and Hamlyn, 1999) and V3 is the most
affected branch. The pain emanates from a specific
trigger zone which may be stimulated by talking,
shaving, eating, etc. Attacks of pain do not occur
during sleep and is confined to the distribution of
trigeminal nerve. A well taken history is essential to
make a correct diagnosis. Figure 1: Pre-operative Figure 2: Exposed Infra
CASE REPORT photograph orbital nerve
A 75 years old male patient was referred to the
department of oral & maxillofacial surgery with a
complaint of episodes of sudden, electric shock like
pain on the right side of face which lasts for about 2
minutes since last 6 years. The pain aggravated on
touching cheek, ala nasi, upper lips and upper gums on
the right side and during eating food. A complete
medical history was taken taken which was non-
contributory. The intraoral examination revealed
presence of only four teeth in the oral cavity 24 32 33
34 (FDI Notation System). No radiographic findings
contributing to severe pain on right side were evident Figure 3: Infra-orbital Figure 4: Infra-orbital
in the radiographs. A diagnostic nerve block test was foramen after foramen after applying
carried out to confirm the involvement of right
infraorbital nerve. After being explained all the neurectomy bone wax
different treatment modalities, the patient gave his
consent for peripheral neurectomy as he had DISCUSSION
undergone conservative treatment for about 4 years Trigeminal Neuralgia, often called as “tic douloureux”
with episodes of recurrence. is one of the most painful and debilitating craniofacial
Under local anaesthesia, a U-shaped Caldwell- pain disorders.2 It is either idiopathic (primary), or
Luc incision was made in the upper vestibule in the secondary due to a structural lesion involving the
canine fossa region. The infraorbital foramen was trigeminal system, or associated with some other
located and the nerve exposed. The nerve trunk was neurological process.3
held with a haemostat at the exit point of the foramen Peripheral neurectomy is one of the most effective
and removed by winding it around the haemostat and peripheral nerve destructive technique. A single
pulling it out. The foramen was plugged with bone wax neurectomy yields 26.5 months free of pain (Quinn,
and wound was closed with interrupted sutures. 1965). Even those whose pain was not completely
The patient was kept on a regular follow-up with controlled by peripheral neurectomy proved more
no episodes of recurrence in one year follow up period. responsive to carbamazepine subsequently.
Infraorbital neurectomy can be performed through
Caldwell-Luc incision approach or Braun's transantral
approach. Inferior alveolar neurectomy can be
performed through Risdon's incision approach or via
Dr. Ginwalla's incision approach.
Peripheral neurectomy generally produces less severe

Journal of Dental Sciences & Oral Rehabilitation 35

 Management Algorithm for Trigeminal
Neuralgia6

FACIAL PAIN
Further Evaluation by Inter-
Diagnostic disciplinary Oral, Facial and
Criteria by Head Pain Center

White & No
1. Paroxysmal
Sweet4
2. Trigger Zones

3. Unilateral Neurology
Neurosurgery
4. Restricted to areas of Consult
trigeminal nerve Lesions
Yes
No Neurology
Trigger Zones: 5 MRI normal Demyelinating
Plaques Consult
V1: Supraorbital ridge of the affected
side
Gabapentin Vascular
V2: Skin of upper lip, ala nasi, cheek, Carbamazepine Imaging
Abnormality
infra-orbital margin Lamotrigine No Neurosurgery
Consult
V3: Lower lip, gums of lower jaw, skin Baclofen
Not Tolerated
over the mandible, tongue(rare) Topiramate

Pain Relief Not Effective

Management:
PHARMACOLOGIC SURGICAL Yes
Strong evidence Moderate Preliminary Operative Radiosurgical Percutaneous
evidence evidence Decrease dose
Radifrequency
Carbamazepine Gabapentin Lamotrigine Peripheral Stereotactic slowly
(400-1000mg/day) (900-2400/day) (200-600mg/day) Neurectomy gamma knife
Baclofen Phenytoin Oxcarbazepine Microvascular Thermal Rhizotomy
(50-60mg/day) (300mg/day) Decompression Yes
Pregabalin Percutaneous
Rhizotomy Recurrence of pain No
Botulinum toxin Balloon
Compression Decrease Dose Slowly
Subcutaneous
local alcohol
block

post-operative effects when compared with alcohol injection and 2337-2344

cryotherapy. It is known that nerve tissues at levels prior to the gasserian 4. Scrivani, Matthews : Trigeminal Neuralgia; Oral Surgery, Oral
ganglion have the ability to regenerate. To prevent them from doing so, Medicine, Oral Pathology, Oral Radiolology, and Endodontology
several materials, such as rubber, sterile wood points, silastic plugs, Volume 100, Issue 5 , Pages 527- 538, November 2005
amalgam and bone wax have been used by surgeons worldwide to
obturate the foramen of the nerves that were avulsed. With the recent use 5. Zakrzewska JM. Assessment and management of orofacial pain.
Elsevier; 2002: 267-370
of titanium screws , a more secure and thorough coverage of the foramen
can be established. 6. Bennetto L, Patel NK: Trigeminal neuralgia and its management;
British Medical Journal 334:201
CONCLUSION
Peripheral neurectomy is a simple surgical procedure for the trigeminal
neuralgia involving its terminal branches. It is beneficial for patients who
are refractory to carbamazepine therapy or who suffer from its side-
effects. In case of recurrence, a repeat neurectomy can be performed
without untoward complications and distress. However, a constant
patient follow-up is mandatory. The clinician should familiarize himself
with the various modes of treatment so that the most appropriate therapy
may be offered to his patient.
REFERENCES
1. Katusic S, Beard CM, Bergstralh E, Kurland LT. Incidence and
clinical features of trigeminal neuralgia, Rochester, Minnesota,
1945-1984. Ann Neurol 1990; 27:89-95
2. Burchiel KJ, Slavin KV: On the natural history of trigeminal
neuralgia, Neurosurgery. Jan 2006:46(1); 152-4
3. Wilkins R: Trigeminal neuralgia- introduction. Neurosurgery: 1985;
Journal of Dental Sciences & Oral Rehabilitation 36
www.rmcbareilly.com A REVIEW
PERIODONTAL EMERGENCIES : A REVIEW
AUTHORS:
Dr. Manvi Agarwal ABSTRACT:
Senior Lecturer
Co-authors: Periodontal emergencies are a part of the everyday practice of dentistry. The clinician must be able to
Dr. H.S. Bhattacharya assess the emergent conditions rapidly and accurately in order to provide relief for the patient. Effective
Reader
Dr. Shalini Singhal management of periodontal emergencies aids in both the patient's physical and psychological well-
Senior Lecturer being. The present article details the most commonly encountered periodontal emergencies, their
Dept of Periodontics
Institute of Dental Sciences, Bareilly.
clinical manifestations and general treatment regimens.
INTRODUCTION:
A periodontal emergency is any circumstance that
adversely affects the periodontium and requires
immediate attention. This definition encompasses a
wide variety of conditions that involve the
periodontium. However, this article is limited to the
emergencies most often encountered including:
1. Pericoronitis
2. Periodontal and gingival abscess
3. Chemical and physical injuries
4. Acute herpetic gingivostomatitis
5. Necrotizing ulcerative gingivitis
6. Cracked tooth syndrome
7. Periodontic and endodontic problems
8. Dentine hypersensitivity
DISCUSSION:
One of the most difficult yet awarding challenges in
dentistry is arriving at an accurate diagnosis and
rendering appropriate treatment for the emergency
patient. A diagnosis may be determined by first
obtaining a complete history of the problem from the
patient and compiling a targeted clinical and
radiographic examination.
PERICORONITIS:
Pericoronitis is probably the most common periodontal
emergency, and the partially erupted and impacted
mandibular third molar is the site most frequently
involved. The overlying gingival flap is an excellent
harbour for the accumulation of the debris and an ideal
breeding ground for bacteria. Additional insult to the
pericoronal flap is often produced by trauma from an
opposing tooth1.
Signs and symptoms: The clinical picture is a red,
swollen, possibly suppurative lesion that is extremely
painful to touch. Swelling of the cheek at the angle of
jaw, partial trismus, and radiating pain to ear and
systemic complications such as fever, leukocytosis and
general malaise are common findings.
Treatment:
Ø After anaesthesia, the underside of the operculum
flap may be irrigated to remove any debris.
Ø It may be necessary to perform some occlusal
adjustment on the opposing tooth to eliminate
that source of trauma.
Ø Antibiotics usually penicillins and appropriate
Journal of Dental Sciences & Oral Rehabilitation
analgesics are indicated if there are systemic signs
and symptoms.
Ø Once the acute phase of2 the infection has subsided,
tooth may be extracted .
Gingival and periodontal abscess:
A gingival abscess is a superficial, painful, rapidly
expanding purulent inflammatory lesion found in the
superficial gingival tisssues.
A periodontal abscess is localized purulent
inflammation deeper in the periodontal tissues.
A gingival abscess may occur in a patient who has
chronic periodontal disease. The most likely cause is
the lodging of a foreign object or other irritant usually
food in the gingival tissues. A periodontal abscess may
be caused by the entrapment of a foreign object, loose
calculus after scaling and root planing, or by superficial
healing of the gingival tissues with active infection
deeper in the pocket3.
Signs and symptoms:
The clinical signs of an acute abscess are: Severe pain,
Swelling of soft tissues, tenderness to percussion,
Extrusion of the involved tooth, Mobility of the
involved tooth.
Treatment:
Ø Primary treatment for an abscess is to establish
drainage to relieve pressure. Drainage may be
achieved through the pocket itself using a
periodontal curette or may require an external
incision to establish drainage. Once the drainage
has been established and any foreign material
removed from the area, the abscess is rinsed
thoroughly to remove any remaining debris.
Ø Occlusal adjustment may be necessary if the tooth
in question has extruded in the socket.
Ø Flap surgery may be accomplished to remove
granulomatous tissue and stimulate regeneration
of lost periodontal tissues.
Ø If the abscess is an acute exacerbation of a chronic
condition and there has been extensive attachment
loss, removal of the tooth may be the best
treatment option. Antibiotics are generally not
indicated unless there is some systemic
involvement such as fever or lymphadenopathy.
Chemical and physical injuries:
Injuries caused by toothbrush trauma, chemical burns,
cheek and tongue biting, factitious habits are
occasionally observed2. Emergencies of this type are
37
painful but of little consequence. Healing usually occurs uneventfully in
10 days- 2 weeks. Treatment is chiefly symptomatic and patient
discomfort is controlled through the use of topical anaesthetics or warm
saline rinses.
Acute herpetic gingivostomatitis:
Acute herpetic gingivostomatitis is caused by herpes simplex virus type-
I. It is characterised by small ulcers with elevated margins that may be
dispersed throughout the mouth on both attached and unattached
mucosa4. Systemic signs and symptoms such as fever and malaise are
also present. The course of the disease generally lasts from 7-10 days.
Treatment:
Antiviral agents, such as acyclovir may be used topically and/or
systemically to control the infection. In addition palliative therapy to
relieve pain must be initiated to allow the patient to eat and drink.
Necrotizing ulcerative gingivitis:
The patient with NUG presents for treatment because of pain. This
disease is characterised by pain that may be severe, fetid oris (bad
breath), necrosis of the gingival papillae that appears to be punched out,
pseudomembrane formation at the tips of the papillae and spontaneous
gingival bleeding. Systemic sign and symptoms include fever,
lymphadenopathy on the affected side, loss of appetite and malaise.
Stress, fatigue, smoking, poor oral hygiene and an impaired immune
system may all contribute to the development of NUG.
TREATMENT:
Ø At the first visit, as much debris, plaque and calculus should be
removed as gently as possible either with hand or powered
instrumentation.
Ø The patient should be instructed in plaque control using a new
toothbrush. Chemotherapeutic mouthrinses may be helpful
although could be uncomfortable at first due to their alcohol
content4.
Ø Antibiotics such as penicillins are indicated if there is systemic
involvement. Patient should refrain from smoking until the acute
phase subsides.
Ø A bland diet should be recommended along with drinking plenty of
water. The patient should return 24 hours after the first appointment
to continue the debridement of the area and to polish the teeth.
Ø The patient should return for a third visit 1-2 days later. By this time
the acute phase should have subsided. If signs and symptoms
persist, other systemic diseases must be ruled out.
Cracked tooth syndrome:
The diagnosis of fractured teeth can be very difficult. It is unusual for the
condition to be undiagnosed for months or years. The most common
fractures are incomplete crown root fractures and fractures of the root
associated with prior endodontic therapy.
DIAGNOSIS:
Pain is a characteristic of fractured teeth. They are particularly sensitive
to mastication and chewing. If the pulp is involved, the tooth will exhibit
the signs and symptoms of acute or chronic pulpitis. A piece of wooden
tongue blade enables the clinician to determine whether a particular cusp
is sensitive to chewing forces and therefore possible fracture.
Radiographs provide inconsistent results. Fiberoptic transillumination is
also a useful diagnostic aid. Light will not cross the fracture line if a
fiberoptic light is shined over a tooth, a sharp distinction in illumination
may indicate a fracture. In many cases, periodontal probing is very
helpful for the diagnosis of root fractures. A deep, narrow pocket is often
a sign of a root fracture. In such a case, a deep narrow pocket is almost
always indicative of a fractured root or a periodontal and endodontic
lesion. If there is no restoration in a tooth and no history of trauma
diagnosis is almost certainly a fractured tooth.
Periodontal and endodontic problems:
Diagnosis and treatment:
It is sometimes necessary to differentiate between a periodontal and
periapical abscess. A non-vital pulp is usually indicative of a periapical
abscess, and the tooth should be either treated endodontically or
extracted. A clinically responsive vital pulp is not always assurance that
the problem is still not pulpal5. Radiography is of some assistance in
differential diagnosis but clinical findings such as extensive caries, tooth
vitality testing, pocket formation and continuity between the abscess and
the gingival margin are of greater practical significance. the probability
exists that periodontitis can result in the death of the pulp and due to
pulpal disease tissue destruction may proceed from the apical region
towards the gingival margin.
This process is termed retrograde periodontitis to differentiate it from
periodontitis in which the disease spreads from the gingival margin to the
apex of the tooth. Whether the periodontal pocket is a result of a
retrograde or marginal periodontitis or a combination of both is
Journal of Dental Sciences & Oral Rehabilitation
academic. In all cases treatment should consists of either combined
endodontic periodontal therapy or extraction of the tooth. In cases in
which the tooth is retained, endodontic therapy must be completed first.
Dentine hypersensitivity:
It is often a management problem for both the patient and the dentist.
Etiology:
Hypersensitivity of exposed dentine can occur when dentinal tubules are
exposed either by caries, fractures, periodontal disease or periodontal
instrumentation. Under such circumstances, thermal stimuli (hot or cold
foods ) and tactile stimuli (toothbrushes and dental instruments) can
excite a painful response1.
Treatment:
Ø Hypersensitivity can be controlled by eliminating the etiologic
factors and by using desensitizing agents (patient applied and dentist
applied).
Ø One of the first treatments to be considered, especially after surgical
procedures, should be occlusal adjustment. Even a slightly heavy
occlusal contact can make a teeth in a recently treated area very
sensitive.
Ø Strontium chloride and potassium nitrate containing toothpastes
may be used as medicaments, applied for 1-2 min after regular
plaque control procedures. Relief should be achieved within 1 week.
Dentist applied medicaments include suspensions of prednisolone
acetate, sodium fluoride solution, stannous fluoride gels, fluoride
varnish, sodium fluoride- glycerine- kaolin paste, and dibasic
calcium phosphate4. Each of these is applied after the sensitive area
is polished with a suitable polishing agent. The medicament is then
applied with a cotton pledget. Several applications may be needed to
achieve complete relief. Dentine bonding agents can be used in areas
that are accessible.
Ø Refractory cases may require root canal therapy if the tooth is to be
retained. Recently, lasers have been used with some success.
Conclusion:
In periodontal emergent conditions, patient presents with an acute
problem and seeks immediate relief. Proper treatment of the emergency
may provide the practitioner with a life-long patient and may contribute
to personal satisfaction for the treating clinician.
REFERENCES:
1. Corbet EF. Diagnosis of acute periodontal lesions. Periodontol
2000 2004; 34: 204-216.
2. Gilbert GN et al. The Stanford Guide to antimicrobial Therapy,
35 ed: Antimicrobial Therapy, Inc, 2005: 30.
3. Herrera D et al. The periodontal abscess. Clinical and
microbiological findings. J Clin Periodontol 2000; 27: 387-
394.
4. Walker CB, Baehni P et al. Chemotherapeutics: antibiotics and
other antimicrobials. Periodontol 2000. 2004; 36: 146-165.
5. Nabers JM. Treatment of the symptomatic periodontal lesions.
Dent Clin North Am 1969; 13: 169-180.
38
 www.rmcbareilly.com CASE REPORT

PREGNANCY TUMOR

AUTHORS:
Dr. Sunil R Panat ABSTRACT
Principal, Professor & Head Pregnancy tumor is a benign tumor like growth that occurs in pregnant women. It usually appears on
CO-AUTHOR:
Dr. Ashish Aggarwal the Anterior maxillary gingiva as a single pedunculated mass with a smooth surface and red color. The
Senior Lecturer pregnancy tumor is histologically similar to a pyogenic granuloma but it is a distinct lesion on the basis
Dr. Rajan Rajput of etiology, biologic behavior, and treatment protocol. In this report, a rapidly growing pregnancy tumor
PG student
Deptt. of Oral Medicine & Radiology, in a 27-year-old female in the third trimester of pregnancy is described.
Institute of Dental Sciences, Bareilly (UP).

INTRODUCTION swelling involved the marginal and interdental gingiva

Pregnancy tumor is a benign tumor like growth on facial surface of maxillary left molars. It extends
that occurs in pregnant women. It usually appears as a superior-inferioly from vestibular fornix to palatal
red or reddish purple lesion on the anterior maxillary surface of 26 and 27and anterioly posteriorly from 26
gingiva that bleeds easily 7 .It is typically single but region to mesial surface of 28 .There were indentations
may be multiple, and may grow rapidly.7 presents on the lobulated mass.
The pregnancy tumor usually occurs during the second On palpation the inspector findings were
or third month of pregnancy2, but might also appear confirmed. The swelling is firm to resilent in
later in the pregnancy 3. constinsency ,pedunclated and non tender there was
The pregnancy tumor is clinically and slight bleeding on provocation.
histopathologically identical to pyogenic granuloma. It After the history and clinical examination the
is usually located on the gingiva in pregnant women provisional diagnosis of Pregnancy tumor was given.
related to increased hormone levels and an exaggerated INVESTIGATION :
inflammatory response of the gingiva to local 1The IOPAR in relation to 26, 27 , and 28.
pregnancy tumor can resolve spontaneously after Differentional diagnosis of pyogenic granuloma ,
parturition. Surgical excision preferably postpartum if peripheral giant cell granuoloma and peripheral
the granuloma persists. During pregnancy, it can be ossifying fibroma were considered.
removed under local anesthesia if it causes discomfort. The patient was advised excision of lesion.
CASE REPORT The patient was referred to department of periodontia
A 27 year old female patient reported to Department of where the lesions was excised.
Oral Medicine and Radiology ,Institute of Dental
Sciences, Bareilly, with the chief complain of painless
swelling in the left upper back tooth region region
since 1 month.
History of presenting illness revealed that the
swelling initially started one month back which was
smaller in size and gradually reached to present size.
Bleeding on brushing the teeth was present since last
25 days. It was associated with discomfort during
eating food. On extra-oral examination left sub-
mandibular lymph nodes were tender and palpable,
two in number, mobile and firm in consistency.
The medical history revealed that the patient was 8
month pregnant
A solitary swelling present in the left upper back
tooth region i.r.t 26, 27. The swelling was oval in
shape, nodular, circumscribed and measured about
4cm x 3cm. The colour of overlying mucosa varies
from pink to reddish in color that bleed easily . This
Journal of Dental Sciences & Oral Rehabilitation 39

DISCUSSION
The term pregnancy tumor was first coined by Blum in 1912. In 1946
Ziskin and Ness compiled a clinical classification of pregnancy
gingivitis as follows:
Class I – Characterized by bleeding gingivae with more or less, no other
manifestations.
Class II- Characterized by changes in the interdental papilla-edema and
swelling with subsequent blunting of interdental papilla.
Class III- Characterized by involvement of the free gum margin, which
takes on the color and general appearance of a raspberry.
Class IV– Generalized hypertrophic gingivitis of pregnancy
Class V – The pregnancy tumor
The physical and emotional changes that occur during pregnancy affect
the oral health of pregnant women to a greater extent. The hormonal
changes that occur during this time are linked to an increase in pregnancy
gingivitis and pregnancy tumor.
In addition to it, the recent researches have showed that periodontal
health may alter the systemic health of the patient and adversely affect the
well being of the fetus by elevating the risk for preterm, low-birth-weight
baby. In spite all this, by having well knowledge and being prepared,
these risks can be managed and prevented and can stay on the path of
health and well being. Other names of pregnancy tumor are Pyogenic
granuloma, Exuberant Granulation tissue, Granuloma Gravidarium,
Angiogranuloma, Pregnancy Epulis.6
In this article history, etiology, clinical, histopathological features,
treatment and preventive measures of pyogenic granulation tissue /
pregnancy are discussed.
Pregnancy itself cannot cause gingivitis; gingivitis in pregnancy is
caused by bacterial plaque. Clinically, the pregnancy tumor appears as a
single pedunculated mass with a smooth surface and red color9. The
incidence of occurrence is more common in maxilla than mandible and
anterior region than posterior that is in accordance with the present case
report
Clinically lesion appears as a discrete, mushroom like, flattened spherical
mass that protrudes from the gingival margin or more often from the
interproximal space and is attached by a sessile or pedunculated base. It is
purplish or dark red in color, with a bright red border. It is usually
semifirm and is a superficial lesion and usually does not invade the
underlying bone 2.
Histologically Florid\granulation tissue / pregnancy tumor exhibits
ulceration of the surface epithelium and characterized by a fibro
endothelial proliferation of the stroma amidst acute and chronic
inflammatory cells 5. It is histologically similar to a pyogenic granuloma
but it is a distinct lesion on the basis of etiology, biologic behavior, and
treatment protocol 8
During pregnancy estrogen and progesterone levels rise, which
create an enhanced tissue response to chronic low-grade irritation
(plaque, calculus, irregular dental restorations) in the oral cavity13.
The patient if given thorough dental prophylaxis and oral hygiene
instructions and then chances of resolution of tumor are there for
parturtion . Therefore, maintenance of oral hygiene and regular follow-up
appointments should be recommended for pregnant women.10
In all forms of gingival enlargements, good oral hygiene is necessary to
minimize the effects of systemic factors.
Although spontaneous reduction in the size of gingival enlargement
commonly occurs following childbirth, complete elimination of residual
inflammatory lesions requires the removal of all forms of local irritants.
Journal of Dental Sciences & Oral Rehabilitation
In the present case, size of the hyperplastic tissue was reduced but the
mass was still interfering with the patient's ability to chew, speak and
was causing serious esthetic problems so it was excised completely one
month after delivery.
How to Prevent Pregnancy Gingivitis and Pregnancy Tumors
Eat balanced diet
Brush twice daily for at least 5 minutes with fluoride containing tooth
paste
Use a soft bristled brush because it will prevent the irritation to gums
Use floss once a day
Avoid eating junk food between the meals
If a pregnant women has morning sickness, rinse mouth with plain water
to get rid of the acids in mouth caused by vomiting
Visit dentist regularly
CONCLUSION
Thus it is must for every pregnant woman to maintain fastidious oral
hygiene. Pregnancy itself cannot cause gingivitis; gingivitis in
pregnancy is caused by bacterial plaque, hormonal alteration and local
trauma. Hence if we take at most care with regular dental checkups it is
possible to avoid the pregnancy tumor.
REFERENCES:
1. Zarka FJ, Stark MM, gingival tumors of pregnancy review of
pregnancy tumors and a report of two cases, Obstetrics And
Gynecology 1956;8(5):595-600
2. Newman MG, Takie HH, klokkevold PR, carranza's clinical
periodontology10th ed Saunders 2007, pg 536
3. National organization for Rare Diseases (online) 1999 Aug69(cited
1999 Aug 21st)
4. Sousa S, Coelho, Bretegant,Vieira, Olivera, Clinical and
Histological evaluation of Granuloma Gravidarium case report.
Braz Dent J. 2000; 11(2): 135-139.
5. Rose LF, Mealey BL, Genco RJ, Cohen DW, Periodontics
Medicine, Surgery, Oral Implants selected soft and hard tissue
lesions with periodontal relevance 1st ed Mosby 2004 pg- 882.
6. Regezi JA, Sciubba J (eds): Oral Pathology, Clinical-Pahological
Correlations, 2nd edition. Philadelphia; WB Saunders. 1993;
pp196-202.
7. Daley TD, Nartey NO, Wysocki GP. Pregnancy tumor: an
analysis.Oral Surg Oral Med Oral Pathol 1991;72:196-199.
8. Maier AW, Orban B. Gingivitis in Pregnancy. Oral Surg
1949;2:234.
9. Cohen DW, Shapiro J, Friedman L, et al. A longitudinal
investigation of the periodontal changes during pregnancy and
fifteen monthspost partum. J periodontal 1971;42:653.
10. Kornman KS, Loesch WJ. The subgingival microbial flora during
pregnancy. J Perio dont Res 1980;15:111.
11. O'Neil TCA. Maternal T-lymphocyte response and gingivitis in
pregnancy. J Periodontal 1979;50:178.
12. Formicola AJ, Weatherford T, Grape H Jr. The uptake of H3-
estradiol by oral tissues in rats. J Periodontal Res 1970;5:269.
13. Gracia RI, Henshaw MM, Krall EA. Relationship between
periodontal disease and systemic health. J Periodontol 2000;25:21-
36.
40
www.rmcbareilly.com CASE REPORT
MANAGEMENT OF EXTRA ORAL SINUS
USING SHOE LACE TECHNIQUE
AUTHORS:
Dr. Chandra Vijay Singh
INTRODUCTION
(MDS) The term sinus tract "refers to a tract leading from
Senior Lecturer an enclosed area of inflammation to an epithelial
Dr. Anurag Singhal
surface" (An Annotated Glossary of Terms in
(MDS)
Prof.& Head Endodontics). It also states that the term dental fistula
Dr. Anuraag Gurtu "should be discouraged, and the more proper term sinus
(MDS) tract should be used." In 1961, Bender and Seltzer
Reader
reported that they found sinus tracts to be lined with
Dr. Chandrawati Guha
(MDS) granulation tissue not epithelium. (1)
Reader When an acute periapical abscess forms, it will
Department of Conservative drain along a path of least resistance. The odontogenic
Dentistry & Endodontics
abscess may spread to deeper tissues causing fascial
Institute of Dental Sciences, Bareilly
space infection or it may establish an intraoral or
extraoral drainage in the form of a sinus tract. Intraoral
or extraoral sinus-tract opening depends on the location
of the perforation in the cortical plate by the
inflammatory process and its relationship to facial-
muscle attachments. After formation of a sinus tract, the
inflammation at the apex of the root may persist for a
long period of time because of the drainage through the
sinus tract, a chronic abscess can remain asymptomatic
for extended periods of time. If there is a closure of the
sinus tract, then the chronic abscess may become
symptomatic. (2)
Sinus tracts on the oral mucosa adjacent to teeth
usually disappear spontaneously with elimination of the
causative factor. Although sinus tracts of pulpal origin
are common, they are seldom of periodontal origin.(3)
Cutaneous sinus tracts of dental origin have been
well documented in the medical literature (Lewin-
Epstein et al. 1978; Kaban 1980; Spear et al. 1983; Cioffi
et al. 1986; Held et al. 1989; Hodges et al. 1989; Cohen
& Eliezri 1990) and the dental literature (Bernick &
Jensen 1969; Strader & Seda 1971; Sakimoto &
Stratigos 1973; Braun & Lehman 1981; Sharma &
Chauchan 1985; McWalter et al. 1988; Maple & Eichel
1993; Caliskan et al. 1995).(4,5,6,7,8)
However, these lesions continue to be a diagnostic
dilemma. A review of several reported cases reveals that
patients have had multiple surgical excisions,
radiotherapy, multiple biopsies, and multiple antibiotic
regimens, all of which have failed, with recurrence of the
cutaneous sinus tract, as the primary etiology was dental
that was never correctly diagnosed or addressed.(10)
The present case report discusses an extraoral sinus
tract which was cutaneous in nature whose early and
prompt diagnosis led to its timely treatment by
endodontic therapy.
CASE REPORT:
A 30 year old male patient reported to the Department
Of Conservative Dentistry and Endodontics with chief
complaint of pus discharge around the submental
region associated with mild pain since last 2 weeks.
Detailed clinical examination revealed patient had
Journal of Dental Sciences & Oral Rehabilitation
grossly carious lower anterior teeth (31, 32, 41, 42). He
also presented with deep bite. Extra oral examination
revealed a cutaneous sinus tract near the chin.
Radiographic examination revealed that tooth 41 was
the cause.Vitality of the teeth were checked using
electric pulp tester and mandibular right central and
lateral incisors were found to be non vital.
Root canal treatment of the involved teeth and
management of the extraoral sinus tract was planned
using “Shoe Lace Technique”. Shoe Lace Technique
involved managing the sinus where a gauge piece
soaked in betadiene was inserted extraorally to disrupt
the epithelium of sinus tract to make a patency for pus
drainage.
Under local anesthesia flap reflection was performed
and the root was exposed. The granulation tissue was
removed using curettes (API). Shoe Lace Technique
was performed to disrupt the epithelium of sinus tract
The flap was repositioned and sutured using sling
suture technique. Patient reported back asymptomatic
after 3 months.
DISCUSSION
Cutaneous sinus tracts typically present as fixed,
nontender, erythematous, nodulocystic lesions on the
skin of the lower face. The patient is usually unable to
recall an acute or painful onset and the lesion is seldom
accompanied by symptoms in the oral cavity (4). Once
the infection from the offending tooth has perforated
the periosteum, the tooth may become asymptomatic.
Digital palpation of the involved area frequently
reveals a "cord" of tissue connecting the painless skin
lesion to the involved maxilla or mandible. During
palpation, an attempt should be made to 'milk' the sinus
tract; production of a purulent discharge confirms the
presence of a tract (Cohen & Eliezri 1990). (9) Often,
both the nodule and perilesional skin are slightly
retracted below the level of the surrounding skin
surface (7). The majority of dental sinus tracts develop
intraorally. When an extraoral dental sinus tract occurs,
it most often develops in close proximity to the
offending tooth (8).
Approximately 80% of reported cases of cutaneous
sinus tracts of odontogenic origin are associated with
mandibular teeth. Therefore, the most common areas of
involvement are the chin and submental regions (2).
Tracts in the mandibular and submandibular regions
are most often associated with mandibular molars (8).
Laskin has described the propagation of odontogenic
infection as being influenced by the relationship of the
root apices to the alveolar process and by the
arrangement of the muscles and fascia of the face and
neck. He also emphasized that these structures
represent only relative barriers and that systemic
reaction of the patient still governs the extent of spread
(9).
Evaluation of a cutaneous sinus tract must begin
41
with a thorough history and awareness that any cutaneous lesion of the
face and neck could be of dental origin (Lewin-Epstein et al. 1978; Cioffi
et al. 1986; Cohen & Eliezri 1990).(8)
If the sinus tract is patent, a lacrimal probe or a gutta-percha cone can
be used to trace its track from the cutaneous orifice to the point of origin,
which is usually a nonvital tooth (Sakimoto & Stratigos 1973; Mitchell
1994). (3, 9)
A radiograph is then exposed with the probe in situ, pointing to the
origin of the primary pathosis. Oral examination may reveal one or more
severely decayed teeth or a healthy looking tooth with an intact crown.
Pulpal and periradicular diagnostic testing should be performed on the
suspect tooth and adjacent teeth. More than one tooth may be pulpally
involved and associated with the cutaneous odontogenic sinus tract.
Cutaneous sinuses have a wide range of incidence. The youngest
individual reported to have a cutaneous odontogenic sinus tract was a boy
aged 10 months (Cohen & Eliezri 1990) and the oldest was 110 years of FIG I: PREOPERATIVE PICTURE
age (Cioffi et al. 1986). The cutaneous lesion may develop as early as a
few weeks (Spear et al. 1983) or as late as 30 years (Cohen & Eliezri
1990). Most patients are unaware of an associated dental problem (Cioffi
et al. 1986; Hodges et al. 1989; Caliskan et al. 1995), thus delaying the
correct diagnosis of the cutaneous lesion with its primary odontogenic
origin.(10) These patients are usually healthy. The sinus tract prevents
swelling or pain from pressure build-up because it provides drainage of
the odontogenic primary site (McWalter et al. 1988). Thus, the draining
sinus tract maintains a localized condition and prevents systemic
involvement.
Treatment involves making a patent pathway for the pus to drain. Many
methods have been propagated which range from periapically perforating
the root of tooth during root canal treatment thus draining the pus through
orthograde approach to creating an extraoral pathway for providing rapid
relief to the patient in case of large sinuses. Shoe Lace Technique is one FIG II: PRESENCE OF AN EXTRA ORAL SINUS ON RIGHT SIDE
such method where the sinus is managed extraorally by inserting a gauge
piece soaked in betadiene to make a patency for pus drainage.
REFERENCES
1. N Cohenca, S Karni, I Rotstein. Extraoral Sinus Tract Misdiagnosed
as an Endodontic Lesion. J Endod 2003; 29 (12):841-843.
2. Am Association of Endodontists. Glossary of contemporary
terminology for endodontics, 5th edn. Chicago: Am Asso of
Endodo, 1994;22.
3. Heling I, Rotstein I. A persistant oronasal sinus tract of endodontic
origin. J Endod 1989; 15:132–4.
4. E .Tidwell, JD. Jenkins, CD. Ellis, B. Hutson, RA. Cederberg.
Cutaneous odontogenic sinus tract to the chin: a case report. Int
Endod J. 1997; 30,:352–355.
5. Braun RJ, Lehman JA. A dermatologic lesion resulting from a
mandibular molar with periapical pathosis. Oral Surg.1981; 52: FIG III: USING SHOE LACE TECHNIQUE TO MAINTAIN PATENCY
210–12.
6. Bernick SM, Jensen JR. Chronic draining extraoral fistula of 32
years duration. Oral Surg. 1969:27: 790–4.
7. Caliskan MK, Sen BH, Ozinel MA. Treatment of extraoral sinus
tracts from traumatized teeth with apical periodontitis. Endod
DentTraumatol. 1995; 11: 115–20.
8. CioffI GA, Terezhalmy GT, Parlette HL. Cutaneous draining sinus
tract: an odontogenic etiology. Journal of the Academy of
Dermatology. 1986;14:94–100.
9. Valderhaug J. A histologic study of experimentally produced intra-
oral odontogenic fistulae in monkeys. Int J Oral Surg 1973;2:54–61.
10. Johnson BR, Remeikis NA, Van Cura JE. Diagnosis and treatment
of cutaneous facial sinus tracts of dental origin. J Am Dent Assoc
1999;130:832–6. FIG IV; REFLECTION OF FLAP AND REMOVAL
11. McWalter GM, Alexander JB, del Rio CE, Knott JW. Cutaneous OF GRANULATION TISSUE
sinus tracts of dental etiology. Oral Surg Oral Med Oral Pathol
1988;66:608–14.

FIG V : REPOSITIONING AND APPLYING INR

AORAL & EXTRAORAL SUTURES

Journal of Dental Sciences & Oral Rehabilitation 42

www.rmcbareilly.com CASE REPORT

MULTIPLE MYELOMA PRESENTING AS

PERIAPICAL PATHOLOGY

AUTHORS:
Dr. Satish Kumaran. ABSTRACT
P, Reader Multiple myeloma is a relatively rare malignant haematological disease; characteristic of it are
Dr. Anuradha.V
Professor and H.O.D multicentric proliferation of plasma cells in the bone marrow, osteolytic bone lesions and detectable
Dr. Lalitha Thambiah presence of monoclonal immunoglobulins in serum and/or urine. Diagnosis of multiple myeloma can
Professor, Oral pathology
Deptt. of Oral and Maxillofacial Surgery
sometimes be challenging because of the abundance of its clinical signs and symptoms and
Institute of Dental Sciences, Bareilly because of the different types of unusual clinical manifestations of the malignant plasma cells.
The first sign of the disease in the case of a 55 years old female was periapical swelling in the anterior
maxilla in relation to 11.
KEY WORDS
Multiple myeloma, osteolytic lesion in maxilla, periapical radiolucencies, plasmacytoma.

INTRODUCTION Intra oral periapical radiograph revealed ill defined

Multiple myeloma is a relatively rare neoplastic
proliferation of monoclonal plasma cells. The disease
was first described in 1844 as a disease characterised
by proliferation of malignant plasma cells and
subsequent overabundant production of monoclonal
paraprotein.1 An intriguing feature of multiple
myeloma is that the plasma cells are neoplastic and,
therefore, may cause unusual manifestations.
Jaw lesions are rarely the first sign of the disease and
their incidence varies from 8-15%.2 In the
given case the initial and first sign of it presentation
was as a periapical lesion in the anterior maxilla of a 55
year old female. Multiple myeloma represents 1% of
all cancers and 10% of all haematological neoplasms.3
Case Report
A 55 year old female patient reported to the
craniofacial surgery unit of Annasawmy Mudaliar
General Hospital, Bangalore with a complaint of
swelling in the right side of the face near the nostril
lasting for a period of six months which was slow
growing and not painful. Earlier she consulted an
endodontist with a complaint of pain and tenderness in
relation to 11. She was diagnosed as having a non
vital 11 with periapical radiolucency. Endodontic
therapy in 11, along with an attempted incision and
drainage was performed by the attending Endodontist.
Later she was referred for apicoectomy in relation to11.
On examination the patient was well built; had no
history of any systemic disease. Extraorally, the patient
had a diffuse swelling in the right ala region measuring
1.0 cm x 1.5 cm. The colour of the skin was normal and
there was no pain on palpation. Intraorally, the patient
had a restored 11 tooth and periapical swelling in
relation to it. The lesion measured 2.5x3.0 cm, firm in
consistency; the overlying mucosa was reddish in
colour with break in the continuity of the mucosa (Fig.
1).
periapical radiolucency in relation to 11( Fig. 2). The
orthopantomograph was non contributory.
Routine blood examination was carried out and all
values were within normal limits. Under local
anaesthesia the lesion was surgically enucleated in toto
with intravenous sedation. The enucleated mass was
soft and fleshy in consistency, creamish brown in
colour and had an irregular surface. The specimen was
sent for histological examination with a clinical
provisional diagnosis of periapical granuloma.
HISTOLOGICAL FINDINGS
The haematoxylin and eosin stained sections of the
lesion showed an extremely cellular lesional tissue
showing diffuse sheets of neoplastic variably
differentiated plasmacytoid cells in the connective
tissue stroma. The nucleus of these cells appeared
round and eccentric with fine granular chromatin and
evident nucleolus. Mitotic activity was evident. These
features are characteristic of solid malignant
hemopoietic neoplasm and hence the lesional tissue in
the stained section was suggestive of plasmacytoma
(Fig.3).
The patient was advised to have, her urine analysed
for the presence of Bence Jones protein, serum
electrophoresis, a computerised axial tomograph (CT)
of the head and neck and a full body positron emission
tomograph (PET) scan.
Blood examination revealed increase of free kappa
light chains (392 mg/L). In the urine sample free kappa
light chain was seen (146mg/L) and urine kappa
lambda ratio was elevated (130.4). CT Scan
(paranasal with Axial and Coronal) was performed
which showed a small destructive lesion in the
maxillary alveolar process in the right paramedian
region extending to the hard palate; associated small
soft tissue mass was also seen. Small destructive
lesions were seen in the frontal bone (Fig 5), left frontal

Journal of Dental Sciences & Oral Rehabilitation 43

sinus in midline and left paramedian extending to the left ethmoidal sinus
(Fig.6). Associated mild enhancing soft tissue mass was seen extending
intracranially in the epidural plane. Small soft tissue mass was seen in the
right frontal sinus. A PET CT revealed bone defects in the anterior hard
palate and multiple lytic expansile lesions in the sternum and calvaria.
Detailed immunohistochemistry (IHC) work up was done for the
following markers; and the following were observed on the lesional
tissue.
1. CD138 - strongly positive (+++)
2. Kappa light chain- strongly positive (+++)
3. Lambda light chain- negative
4. Ki67- 70% proliferation ( Fig 4)
The patient was referred to the regional oncology unit and was treated
with chemotherapy and is awaiting a bone marrow transplant
DISCUSSION
Multiple myeloma is a debilitating malignancy and it is part of a
spectrum of diseases ranging from monoclonal gammopathy of unknown
significance to plasma cell leukaemia. Plasma cell tumours are
lymphoid neoplastic proliferations grouped among B-cell peripheral
lymphomas, according to the classification of the European-American
International Lymphoma Study Group.4 They may affect a single bone, Figure 3- Photomicrograph showing positivity (+++) for CD138 x 200.

Figure 4- Photomicrograph showing 70% positivity for Ki-67 x 200.

Figure 1- Intraoral periapical radiograph showing ill defined periapical

radiolucency in relation to 11.

Figure 5- Photomicrograph showing positivity (+++) for

kappa light chain.xss 200.
Figure 2- Photomicrograph showing plasmacytoid appearance of the
tumor cells.H&E x 200.

Journal of Dental Sciences & Oral Rehabilitation 44

which is a condition called solitary plasmacytoma or may involve only
soft tissues - an extramedullary plasmacytoma. However, in
approximately 95% of the cases, it involves several bones, and hence is
called multiple myeloma . The signs and symptoms of the disease were
first documented by Samuel Solley in 1844, though the name multiple
myeloma was given only in 1873 by Jvon Rustizky. 1 It is also known as
Kahlers disease, myelomatosis and medullary plasmacytoma.5 The
disease occurs frequently in individuals of 50-80 years of age with a
mean age of 60 years.6 The lesion is rarely seen in patients younger than
40 years of age1. It is more frequently seen in men, of all races, but more
commonly in African-Americans and less commonly in the Asian
population.1 Bone iinvolvement secondary to bone marrow infiltration is
most common.7 Frequently affected sites are vertebra, ribs, skull, femur,
clavicle, pelvis and scapula.8 Jaw lesions in multiple myeloma may vary
from 5-39% of cases and are the first sign of disease in approximately
17% of patients. Though its occurrence in the maxilla and mandible is
very common oral lesions rarely appear as primary manifestation of the
disease.9 More than 30% of patients with multiple myeloma develop
osteolytic lesions in the posterior mandible.2 Oral manifestations such as
gingival haemorrhage, odontalgia, paraesthesia, dental mobility,
ulcerations may be the first or early presenting symptom2.
Multiple myeloma lesions are more common in the mandibular
posterior region but in this case it presented itself as anterior maxillary
swelling.10 Hence when single or widespread involvement is seen in jaw
bones it is prudent to include multiple myeloma in the differential
diagnosis.
A plain radiograph remains the golden standard for imaging procedure
for diagnosis and staging of multiple myeloma.2 Soap bubble appearance
of the osteolytic lesion can be frequently seen. PET scanning and MRI
can add great value in diagnosis/prognosis and prediction. MRI has
higher sensitivity and specificity in diagnosis and treatment.2
Fine needle aspiration of jaw swellings can yield useful results.
Aspiration of bone/bone marrow can also be resorted to. Microscopic
appearance of the biopsy of the lesion and the bone marrow of multiple
myeloma, characteristically show a monoclonal population of
proliferating plasma cells with variable maturity. 7,11
Differential diagnosis of jaw swellings can be exhaustive clinically but
main histopathological differential diagnositic features are lymphomas
(lymphoplasmacytic), Granulomatosis (Langerhans cell) and metastatic
tumours.11
Immunohistochemistry proves a useful tool to differentiate
lymphomas and multiple myelomas and gives an insight into the
molecular basis of the disease. Myeloma cells express Syndecan–1 (CD
138) surface antigen that is limited to terminally differentiated plasma
cells of B cell lineage.12
Light chain restriction for Kappa or Lambda is usually observed, and
nearly 70% of plasma cell neoplasms are Kappa positive. AE1/AE3,
HMB45 and S100 immunoreactivity in plasmacytomas is generally
considered rare but are done to exclude other pathologies.13
Monoclonal precursors of myeloma cells in bone marrow originate in
lymph nodes. Not very well understood are the mechanisms that enable
these precursor cells to selectively lodge in the bone marrow where the
microenvironment is conducive to their differentiation, proliferation and
survival. However, it is probable that bone marrow microenvironment
provides specific chemotactic signals, and monoclonal myeloma
precursor cells express necessary cell surface receptors for bone marrow
lodgement. There is adhesion to and transmigration of the endothelium
that lines the bone marrow sinuses by monoclonal precursors, which
contribute to preferential trafficking of these cells in the bone marrow.
The interaction between tumour cells and bone marrow stromal cells
promotes neoangiogenesis essential for the growth of myeloma and
facilitates lodging of new tumour cells in the bone marrow and their
subsequent uncontrolled proliferation. This leads to osteolytic activity
responsible for the development of bone lesions characteristic of
myeloma.14
What clinched the diagnosis in the case presented was the histological
picture followed by subsequent immunohistochemical diagnosis and
diagnostic workup.
Conclusion
Multiple myeloma is a disseminated plasma cell neoplasm. It is a
systemic B cell lymphoproliferative disease with varied head and neck
Journal of Dental Sciences & Oral Rehabilitation
and systemic manifestations. Diagnosis of multiple myeloma can be
established by haematologic and biochemical findings, urine analysis
and skeletal radiographic survey. Cystic and radiolytic lesions of the jaw
bones reinforce the fundamental role of the dentist in the recognition and
early diagnosis of many a systemic condition including multiple
myeloma. It should be noted the disease has an unfavourable or poor
prognosis. Ongoing research in the field of molecular biology and
phenotyping can improve diagnosis, classification, management and
prognostic protocols of multiple myeloma.
REFERENCES
1 Kyle RA, Gertz MA, Witzig TE, Lust JA, Lacy MQ, Dispenzieri A
et al. Review of 1027 patients with newly diagnosed multiple
myeloma. Mayo Clin Proc 2003; 78:21-33.
2 Epstein JB, Voss NJ, Stevenson-Moore P. Maxillofacial
manifestations of multiple myeloma. An unusual case and review of
the literature. Oral Surg Oral Med Oral Pathol. 1984
Mar;57(3):267-71.
3 Katzel JA, Hari P, Vesole DH. Multiple myeloma: changing towards a
bright future. CA Cancer J Clin. 2007;57(5):301-318.
4 Seoane J, Aguirre-Urizar JM, Esparza-Gomez G, Suarez-
Cunqueiro M, Campos- Trapero J, Pomareda M. The spectrum of
plasma cell neoplasia in oral pathology. Med Oral 2003;8:269-80.
5 Grogan TM, VanCamp B, Kyle RA, Müller-Hermelink HK, Harris
NL. Plasma cell neoplasms. In: Jaffe ES, Harris NL, Stein H,
Vardiman JW, editors. World Health Organization Classification of
Tumors. Pathology and Genetics of tumors of the Haematopoietic
and Lymphoid Tissues. IARC Press: Lyon; 2001. p. 142-56.
6 Pisano JJ, Coupland R, Chen SY, Miller AS. Plasmacytoma of the oral
cavity and jaws: a clinicopathologic study of 13 cases. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod. 1997 Feb;83(2):265-71.
7 Mehdi G, Ansari HA, Haider N. Cytological diagnosis of multiple
myeloma presenting as a jaw swelling. J Cytol [serial online] 2009
[cited 2010 Feb 8];26:80-2.
8 Salmon SE, Cassady JR. Plasma cell neoplasms. In: DeVita VT,
Hellman S, Rosenberg S,editors. Cancer, Principles and practice of
oncology. JB Lippincott: Philadelphia; 1988. p. 1854
9 Bruce KW, Royer RQ. Multiple myeloma occurring in the jaws: A
study of 17 cases.Oral surg Oral Med Oral Pathol 1953;6:729-44.
10 Zachriades N, Papanicolaou S, Papavassiliou D, Vairaktaris E,
Triantafyllou D, Mezitis M. Plasma cell myeloma of the jaws. Int J
Oral Maxillofac Surg1987;16:510-5.
11 Daneshbod Y, Arabi MA, Ramzi M, Daneshbod K. Jaw lesion as the
first presentation of multiple myeloma diagnosed by fine needle
aspiration. Acta Cytol 2008;52:268-9.
12 Matsui W, Huff CA, Wang Q, Malehorn MT, Barner J, Tanhehco Y,
Smith BD, Civin CI, Jones RJ: Characterization of clonogenic
multiple myeloma cells. Blood 2004, 103:2332-6.
13 Bayer-Garner IB, Prieto VG, Smoller BR. Detection of clonality
with kappa and lambda immunohistochemical analysis in
cutaneous plasmacytomas. Arch Pathol Lab Med 2004;128:645-8.
14 Von Riet I: Homing mechanisms of myeloma cells. Pathol Biol
(Paris) 1999, 47:98-108.
45
www.rmcbareilly.com CASE REPORT

LATERAL PERIODONTAL CYST

AUTHORS:
Dr. Shalini Singhal ABSTRACT
Senior lecturer LATERAL PERIODONTAL CYST is a rare odontogenic cyst of developmental origin. It occurs on the
Dr. Hirak Bhattacharya
Reader lateral periodontal region of a vital tooth and has specific histologic features. In this paper a case of a
Dr. Manvi Agarwal lateral periodontal cyst is presented.
Senior Lecturer
Department of Periodontics A variety of cysts, odontogenic or not, may develop in a lateral periodontal area of a tooth. Such cysts
Institute of Dental Sciences, Bareilly are mainly the odontogenic keratocyst, the inflammatory periodontal cyst which has developed from an
infected lateral accessory root canal or from infection through the gingival crevice, the nonodontogenic
globulomaxillary cyst, and the incisive canal cyst.
The lateral periodontal cyst is an uncommon but well recognized type of developmental odontogenic
cyst. It occurs in the lateral periodontal region of a vital tooth and has specific histologic features. It is
usually asymptomatic and is discovered on routine radiological examination of the teeth, although an
obvious swelling may be seen occasionally on the labial surface of the gingiva.
KEYWORDS:Odontogenic, Periodontal cyst, Globumaxillary cyst.
INTRODUCTION associated with the periodontal space discontinuing the
The Lateral Periodontal Cyst is a non- lamina dura with well demarcated radio-opaque
keratinized, non-inflammatory developmental cyst borders. Provided that the lesion is unilocular on
occurring adjacent to or lateral to a tooth root. It is a radiographic presentation
slow-growing radiolucent lesion occurring most
frequently in males during 5th to 7th decade. As part of
the differential diagnosis, it must be distinguished
from the collateral keratocyst and the gingival cyst of
adult. .
Diagnosing the lateral periodontal cyst from
the gingival cyst of adults is difficult since the two
cysts may have a common parentage. Also to be
considered in the differential diagnosis is the lateral
radicular cyst, inflammatory lateral periodontal cyst,
radiolucent odontogenic tumors, and benign
mesenchymal tumors1.
CASE REPORT
A 44 yrs male patient reported in the outdoor
patient department in Institute of Dental Sciences,
Bareilly with the chief complaint of pain in lower right
back tooth region since last 1 month.
History of present illness-Patient got trauma
to the lower right back tooth during an accident1 year
back. Temporarily he was on medication and became
all right but since last 1 month he again noticed pain
which was dull and continuous in nature. Radiograph showing discontinuation of lamina
Clinical Examination of 44 & 45-On clinical dura associated with second premolar
examination it was seen that vestibule in relation to 44 Treatment Provided-Access opening, Scaling and Root
and 45 was completely obliterated. 45 was tender on planing.,Root canal treatment done.
lateral percussion. There was expansion of buccal After elevation of mucoperiosteal flap a soft
cortical plate. Swelling was soft, fluctuant giving an granulomatous bluish grey mass 3'3'4'mm in
appearance of no buccal cortical plate. dimension, completely perforating the buccal cortical
Provisional Diagnosis-Lateral periodontal cyst in plate filling the cyst space was present which was
relation to 45. attached to the cyst lining. Cyst was completely
Electric Pulp Testing- tooth was vital Radiographic enucleated with the proper curettage of cyst cavity to
Investigation-An unilocular radiolucent area remove all the lining epithelium.

Journal of Dental Sciences & Oral Rehabilitation 46

 Preoperative view of cystic elevation on the buccal
surface of 1st and 2nd premolar area
Fragmented pieces of the lesion were freed from the bone with
curettes and submitted for histopathological evaluation, which
confirmed the diagnosis of a lateral periodontal cyst.
Potograph showing perforation of buccal cortical plate by cyst along with
visible lateral surface of root in the perforation area.
Photograph showing enucleated cystic mass
Journal of Dental Sciences & Oral Rehabilitation
After 2 weeks sutures removed.
Revaluation after 1 month shows that there was no recurrence of the cyst.
Histological Examination-Histologically the lateral periodontal cyst is
characterized by a thin lining of non-keratinized epithelium usually 1 to
5 cell layers thick which resembles the reduced enamel epithelium. The
thin lining is interspersed with conspicuous, sometimes numerous,
glycogen-rich clear cells. Presence of dense fibrocellular connective
tissue stroma. consist of numerous fibroblasts, collagen fibre bundles
and dense chronic inflammatory cells mainly comprising of
lymphocytes and plasma cells. Numerous proliferating, dilated blood
capillaries lined by plump endothelial lining filled with and extravasated
RBC's are seen.
47
DISCUSSION: advised to follow these cases over a number of years. Because the
Since pain or other clinical symptoms have seldom been reported, lateral lesions are benign and slow growing, left untreated they can enlarge 0.7
periodontal cysts are discovered on routine radiographic examination. mm per year and cause gingival expansion4.
The radiographic appearance is usually a round or teardrop-shaped, well REFERENCES:-
circumscribed radiolucency margin located between the apex and the 1- Nina B. Lehrhaupt, Carol N. Brownstein, and Michael J. Deasy
cervix of the tooth. 1997 Jun. Osseous Repair of a Lateral Periodontal Cyst. Journal of
The lateral periodontal cyst is not a common lesion. It's a non- Periodontology 608 – 611.
inflammatory type of periodontal cyst that could be a result of idiopathic
2- Willium G . Shafer et al. A text book of Oral Pathology; 4th edition ,
stimulation of cell rests.
265
The lateral periodontal cyst is an intraosseous (central) cyst, associated
3- Eleni Angelopoulou and Angelos P. Angelopoulos et al. 1990 Feb .
with the root of a vital tooth. It occurs mainly in adults in the mandibular
Lateral Periodontal Cyst Review of the Literature and Report of a
bicuspid-cuspid-incisor area. Clinically it presents no signs or symptoms
Case. Journal of Periodontology 126 – 131.
but occasionally a small swelling of the gingiva or alveolar mucosa may
4- George E. Tolson et al. 1996 May.: Report of a Lateral Periodontal
be seen2. Cyst and Gingival Cyst Occurring in the Same Patient. Journal of
The cyst is comprised of a cystic cavity with a connective tissue sac lined Periodontology 541 - 544
on the inner surface by a thin non-keratinized epithelium. The epithelial
lining varies from a single flat layer of squamous cells to a thin lining of
two to three cells interspersed with conspicuous clear cells while a thin
lining of cuboidal or short columnar cells may be seen. A thin, irregular
layer of cells with abundant, deeply eosinophilic cytoplasm projecting
into the lumen has also been described.
Other histologic features of the lateral periodontal cyst include the
absence of inflammation in the connective tissue, the artifactual
separation of the lining epithelium from the underlying connective tissue,
the hyalinization of connective tissue immediately beneath the
epithelium, and the presence of glycogen-rich clear cell rests of dental
lamina (The process seems to be similar to early stages of tooth
development, when there is a thickening of stomatodeal ectoderm to form
the dental lamina),with or without central cystic degeneration. typical
epithelial lining with characteristic focal thickenings. The presence of
mild chronic inflammation observed in the connective tissue is probably
a result of secondary involvement from the neighboring inflamed
gingiva.
Three possible sources of the epithelial lining:
1. Reduced enamel epithelium of an erupting tooth. There is a
morphologic similarity between the cyst lining and reduced enamel
epithelium. Also, the focal epithelial thickenings may be seen in the
lining of dentigerous cysts.
2. Rests of the dental lamina. The glycogen rich epithelial islands in the
wall of cysts are similar to these in dental lamina rests.
3. Rests of Malassez. These structures are characteristically present in the
periodontal ligament.
DIFFERENTIAL DIAGNOSIS-
There are differences of opinion regarding the differentiation of the
lateral periodontal cyst from gingival cyst of adults, which have similar
histologic features. It is believed that these two lesions are distinct
entities originating from similar epithelial sources (odontogenic
epithelium) and developing within the alveolar bone (the lateral
periodontal cyst) or within the gingiva (the gingival cyst).
The lateral periodontal cyst originates centrally in the alveolar bone or in
the periodontal ligament and as it enlarges may perforate the cortical
plate from the inside out, resulting in gingival swelling. It presents at the
time of surgical removal as a bone cavity with sharp borders, because the
surface of the alveolar bone forms an acute angle with the cyst cavity. The
gingival cyst on the other hand, originates in the connective tissue of the
gingiva and as it becomes larger finally erodes the surface of the alveolar
bone from the outside in, leaving a bone cavity with "blunt" borders in
which the surface of alveolar bone forms an obtuse angle with the cyst
cavity. Therefore careful evaluation of the borders of the bone cavity as
well as the angle which is formed between the labial surface of the
alveolar bone and the cyst cavity is extremely helpful in differentiating
between the lateral periodontal cyst and the gingival cyst in those cases of
cysts with both radiolucency and gingival swelling3.
Provided that the lesion is unilocular on radiographic presentation, the
lateral periodontal cyst is treated by surgical enucleation. Greer and
Johnson reported that 8 of 10 recurrent cases were unilocular
radiologically, but multilocular histologically. Therefore, clinicians are
Journal of Dental Sciences & Oral Rehabilitation 48
www.rmcbareilly.com CASE REPORT

SURGICAL MANAGEMENT OF IATROGENIC

PERFORATION USING MTA

AUTHORS:
Dr. Anuraag Gurtu ABSTRACT
(MDS) Perforations can have a negative impact on the prognosis of the affected tooth by compromising the
Reader
Dr. Anurag Singhal
attachment apparatus. Factors that influence the outcome of perforated teeth include size, time of
(MDS) repair, and level and location of the perforation. This case report describes the management of a large
Prof.& Head perforation in a maxillary central incisor. Despite of a poor prognosis, an attempt was made to repair the
Dr. Payal Singhal
BDS (MDS)
defect and restore the tooth. An absorbable GTR membrane was placed, and the defect was repaired
PG Student with white ProRoot mineral trioxide aggregate. Subsequently the endodontic treatment was completed;
Dr. Sumit Mohan the tooth was restored. 6-month recalls showed no evidence of periodontal breakdown, no symptoms
BDS (MDS)
PG Student
and complete healing of all periradicular lesions.
Department of Conservative KEYWORDS
Dentistry & Endodontics Perforation; MTA; Biomaterial; GTR.
Institute Of Dental Sciences, Bareilly.
INTRODUCTION #21 & #22 were discolored Periodontal pocket and
It is estimated that over 24 million endodontic iatrogenic perforation was clinically noticed irt #11
procedures are performed on an annual basis, with up to (maxillary right central incisor).
5.5% of those procedures involving endodontic apical Patient was informed of the problem and treatment
surgery, perforation repair, and apexification was planned. It consisted of root canal therapy irt #11,
treatment.(1) Endodontic surgery is performed to #21 & #22 followed by surgical repair of the perforation
resolve inflammatory processes that cannot be #11 (maxillary right central incisor).
successfully treated by conventional techniques, which After completing with the root canal treatment of
may be due to complex canal and/or apical anatomy and the teeth, surgical phase was initiated to repair the
external inflammatory processes.(2). Perforations are perforation where a full thickness flap was reflected
one of the clinical situations encountered by an from #13 to #23. The perforation was located and
endodontist. explored. Obturation of #11 was done and it was
Perforations can be defined as mechanical or followed by perforation repair using ProRoot WMTA.
pathologic communications between the root canal Root end resection was performed in all the offending
system and the external tooth surface. Seltzer et al. in teeth and retro filling was done using MTA..Guided
their in vivo histologic study on monkeys found that the Tissue Regeneration membrane (GTR) was placed to
repair of perforations was dependent on the location of enhance healing. The flap was repositioned and sutured
perforation and the time elapsed before sealing the with resorbable sutures.
defect. Sinai stated that middle third and apically Follow up after 6 months revealed complete
situated perforations were less serious than those that healing and an asymptomatic patient.
occurred in the coronal third of the canal, including DISCUSSION
furcal perforations. (3) Several materials have been used
to repair furcation perforations, including zinc oxide- The incidence of iatrogenic root perforation has
eugenol cements (IRM and Super-EBA), glass ionomer greatly increased in recent years as dentists with limited
cement, composite resins, resin-glass ionomer hybrids, experience and skills have attempt to provide
and mineral trioxide aggregate (MTA).(4) endodontic treatment. This has been at least partially
Mineral trioxide aggregate (MTA) is a biomaterial attributed to the advent of flared preparation techniques
that has been investigated for endodontic applications which are conducive to obturation with gutta-percha.
since the early 1990s. MTA was first described in the Iatrogenic root perforation is associated with a
dental scientific literature in 1993 and was given significant increase in the failure of endodontically
approval for endodontic use by the U.S. Food and Drug treated teeth, especially if sealing of the perforation is
Administration in 1998. It has become the material of delayed. It has also been reported that the incidence of
choice in majority of endodontic surgical cases including failure is dramatically increased when repair materials
perforation repair.(5) have been extruded beyond the root surface. (6).
The present case report discusses surgical Pitt Ford et al. (7) evaluated the histologic tissue
management of iatrogenic perforation using MTA. response to experimentally induced furcation
perforations in dog teeth repaired by either MTA or
CASE REPORT amalgam. They found that most MTA samples showed
A 27 year old male patient reported to the no inflammation and cementum deposition, whereas
Department of Conservative Dentistry and Endodontics Amalgam samples showed moderate to severe
with pain in upper front tooth region since 15 days. Pain inflammation with no cementum deposition. The
was severe in nature and radiated to the adjacent region. chemical composition of MTA was determined by
Pain got relieved on taking medication. Past dental history Torabinejad et al. (8). The material consisted of fine
revealed root canal therapy being performed irt #11, #21 hydrophilic particles, and the main components were
& #22 6 years back. After thorough clinical and tricalcium silicate, tricalcium aluminate, tricalcium
radiographic examination, it was observed that teeth #11, oxide, and silicate oxide. Bismuth oxide acted as a
Journal of Dental Sciences & Oral Rehabilitation 49
radioopacifier. They declared that calcium and phosphorus were the main
ions in MTA. Arens and Torabinejad (9) reported two cases of large
furcation perforation that were repaired by MTA. They stated that MTA
was an ideal material for such cases. It did not need a barrier. The extruded
material showed no adverse side effects, indicating its biocompatibility.
Cemental deposition had been noted also. Sluyk et al. (10) evaluated the
effect of time and moisture on setting, retention, and adaptability of MTA
when used to repair furcation perforations. The authors noted that the
presence of moisture in perforations during the placement of MTA
increased its adaptation to perforation walls. They concluded that a
moistened matrix can be used under MTA to prevent over- or underfilling
of the material. Bryan et al. (11) reviewed the etiology, diagnosis,
prognosis, and material selection of nonsurgical repair of furcation
perforation. They stated that furcal perforations had a bad prognosis. To
improve it, they should be sealed immediately with a biocompatible and FIG III: RADIOGRAPH FIG IV: RADIOGRAPH FIG V: RADIOGRAPH
sealable material. MTA showed promise in this respect and could enhance AFTER SHOWING SHOWING OBTURATED
the treatment modality for furcation perforation repair. GUTTAPERCHA REMOVAL PERFORATION IRT # 11 #21 #22
CONCLUSION
Although perforation cases present a poor prognosis, timely
detection, intervention and management can save the tooth and restore its
periodontal integrity. Use of Mineral Trioxide Aggregate (MTA) as a
perforation repair material has added a new dimension in its management
and prognosis.
BIBLIOGRAPHY
1. Roberts HW, Toth JM, Berzins DW, Charlton DG. Mineral Trioxide
Aggregate material use in endodontic treatment: A review of
literature, Dental Mater (2007). FIG VI: FLAP RAISED FOR FIG VII: IATROGENIC
2. Chong BS. Managing endodontic failure in practice. Chicago: REPAIR OF DEFECT PERFORATION irt # 11
Quintessence Publishing co., Ltd.;2004. 123-47.
3. Hashem AAR, Hassanien EE. ProRoot MTA, MTA-Angelus and
IRM Used to Repair Large Furcation Perforations: Sealability
Study. J Endod 2008; 34(1): 59-61.
4. Ruddle JC. Nonsurgical endodontic retreatment. In: Cohen S,
Burns RC, eds. Pathways of the pulp, 8th ed. St Louis: Mosby Inc,
2002:919.
5. Schmitt D, Bogen G. Multifaceted use of ProRoot MTA root canal
repair material. Pediatr Dent 2001;23:326–30.
6. Biggs JT, Benenati FW, Sabala CL. Treatment of latrogenic Root
Perforations withAssociated Osseous Lesions. J Endod 1988; FIG VIII: CANAL FIG X: PERFORATION REPAIR irt #11,
14(12):420-24. EXPLORED FOR #11 ROOT END RESECTION irt #11,#21,#22
7. Pitt Ford TR, Torabinejad M, McKendry DJ, Hong CU,
Kariyawasam SP. Use of mineraltrioxide aggregate for repair of
furcal perforations. Oral Surg Oral Med Oral PatholOral Radiol
Endod 1995;79:756–63.
8. Torabinejad M, Hong CU, McDonald F, Pitt Ford TR. Physical and
chemical propertiesof a new root-end filling material. J Endod
1995; 21:349 –53.
9. Arens DE, Torabinejad M. Repair of furcal perforations with
mineral trioxide aggregate: two case reports. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod 1996;82:84–8.
FIG XII: GTR PLACEMENT
10. Sluyk SR, Moon PC, Hartwell GR. Evaluation of the setting FIG IX: FIG XI: RADIOGRAPH
properties and retention characteristics of mineral trioxide OBTURATED #11 SHOWING PERFORATION
aggregate when used as a furcation perforation repair material. J REPAIR & ROOT END
Endod 1998;24: 768 –71. RESECTION
11. Bryan EB, Woollard G, Mitchell WC. Nonsurgical repair of furcal
perforations: a literature review. Gen Dent 1999;47:274–8.

FIG XIII: FLAP REPOSITIONED

FIG XIV: POST
& SUTURED
OPERATIVE RADIOGRAPH

FIG I: PREOPERATIVE PHOTOGRAPH FIG II: PREOPERATIVE

SHOWING PERFORATION irt #11 RADIOGRAPH SHOWING
IMPROPER OBTURATION FIG XV: FOLLOW UP AFTER 6 MONTHS

Journal of Dental Sciences & Oral Rehabilitation 50

www.rmc_bareilly.com Review Article

ARE DENTURE ADHESIVE TOXIC? YES!!!

AUTHORS:
Prof. Dr. Puneet Anand Abstract
Reader Dentures adhesive are products that are used to keep dentures in place during normal daily
Dr. K.L. Gupta
Sr. Leactcrer activity. They work by creating a bond between the dentures and the gums so that they do not fall out or
Dr. Dinker Goel shift during regular use. Denture Adhesive is applied in an even layer to the part of the dentures that is
Dr. Tamanna Chabra
Dr. Alok Kumar intended to fit against the gums. Once this layer has been applied, the dentures can be fitted into the
Department of Prosthodontics mouth so that they are fully connected to the gums.
Institute of Dental Sciences, Bareilly
Certain denture adhesive brands contain approx 17 to 34 milligrams/gram of zinc per dose.
Excessive use of Denture adhesives can lead to hyperzincemia and hypocupremia. Hyperzincemia
refers to high blood levels of zinc while hypocupremia is a condition where there is a low concentration
of copper blood levels.
Patients who use denture adhesives daily are exposed to at least 330 milligram of zinc per dose,
about 30 times more than the recommended daily intake of 8-11 milligrams.
Studies have shown that denture adhesives may lead to zinc toxicity and copper deficiency,
thereby manifesting into neurological issues.

Introduction: Sadly, many patients worldwide suffer with the

If experiencing numbness, tingling or muscle
weakness, one would least likely postulate that a
benign product such as a denture adhesive might be the
culprit. Denture adhesives are applied to the denture
before seating them onto the gums. Denture adhesives
promote denture retention and comfort and are most
often used by those who have ill-fitting dentures.
Research conducted by physicians from the University
of Texas, Southwestern Medical Center discovered
that denture adhesives, specifically the Fixodent and
Poligrip brands contain 17 to 34 milligrams/gram of
zinc per dose. In their study, four patients suffering
from hyperzincemia and hypocupremia were
examined. Hyperzincemia refers to high blood levels
of zinc while hypocupremia is a condition where there
is a low concentration of copper blood levels. All
subjects in the study used denture adhesives daily.
Subsequently, the subjects were exposed to at least 330
milligram of zinc per dose, about 30 times more than
the recommended daily intake of 8-11 milligrams.
Other possible sources of zinc were ruled out in all
subjects. Upon cessation of use of the products, the
zinc levels of three subjects' improved and mild
neurologic improvement resulted for two subjects who
received copper supplementation. The results led to the
conclusion that the use of denture adhesives may lead
to zinc toxicity and copper deficiency, thereby
manifesting into neurological issues.
condition for years that can be easily detected via a
simple blood test.
Denture adhesive creams come without a warning
label. They are classified by the U.S. Food and Drug
Administration (FDA) as a Class 1 medical device.
Under this class, manufacturers are not required to list
certain ingredients that are considered as bearing low
risk for toxicity or injury. There are more then 35
million people worldwide who wear dentures, most of
which are the elderly. The majority of users are
unaware of the relationship between denture adhesive
creams and the potential ill effects thereof.
Zinc is an essential trace mineral that is required
for normal body function. Zinc promotes growth,
digestion of protein, maintenance of serum vitamin A
concentration, burn and wound healing, acid-base
balance and is required for the maintenance of taste and
smell. Zinc works with key enzymes in the body that
synthesize other vitamins, phytonutrients and
minerals. Zinc also has antioxidant properties and
plays a role in the body's immune system. Antioxidants
neutralize free radicals which damage the cells.
Consequently, zinc plays a role in helping to prevent
heart disease, cancer and other medical maladies.
These are just some of the wonderful qualities of the
natural plant based essential mineral called zinc.
It is important to differentiate between 2 types of
zinc. There exists a metallic chemical element of zinc
ssified as a transition metal by chemists. This is an
inorganic form of zinc. This form of zinc is used in
industrial applications such as the zinc plating of steel
and a conductor in batteries. Zinc compounds are used

Journal of Dental Sciences & Oral Rehabilitation 51

which is classified as a transition metal by chemists. This is an inorganic not absorbed through the delicate tissues found in the mouth. They added
form of zinc. This form of zinc is used in industrial applications such as that it is unlikely that adverse effects will occur despite ingestion of small
the zinc plating of steel and a conductor in batteries. Zinc compounds are amounts of adhesive. Additionally, Procter & Gamble stated that
used in deodorants, shampoos and paints. Zinc compounds are also used Fixodent is within the standards of the FDA's manufacturing process and
in denture adhesives and are hardly the harmless nutritional form of zinc they monitor the safety of their product.
essential to human health and wellness. The FDA maintains that although these products are classified as low risk
An excessive amount of inorganic zinc in the body causes toxicity. Its products, the manufacturers should comply with the agency's standards.
signs and symptoms include diminished deep tendon reflexes, decreased It is the manufacturer's responsibility to report incidences of adverse
level of consciousness, malaise, nausea and vomiting, metallic taste in events related to product use, utilize manufacturing controls and label the
the mouth, leukopenia and diarrhea. Prolonged and excessive intake of product in a way that is neither false nor misleading. The FDA monitors
inorganic zinc can reduce copper absorption, cause impaired immune adverse events and has the authority to take action in order to protect
system function and anemia. The normal blood level of zinc in the body is public health. Or so it is believed.
1.10 micrograms/milliliter. In the aforementioned study, patients had Summary:
levels between less than 1.36 to 4.28 micrograms/milliliter. Dentures are pricey and it is likely that patients with ill-fitting sets will
Copper is a component of various enzymes in the body and is important in not consult their dentists for realignment services. The majorities tend to
the production of energy, formation of epinephrine, red blood cells, bones fix it themselves given that denture adhesives do not require a
and connective tissues. When there is an excessive amount of inorganic prescription and are inexpensive. This increases the possibility of
zinc in the body, the absorption of copper decreases. In cases of identifiable inorganic zinc toxicity cases. When in doubt, use organic
hypocupremia, anemia, weakness, altered respiratory status and skin products. Organic products are those that are derived from nature and are
lesions can be noted. Some people experience mild depression, designed to compliment and sometimes enhance the delicate balance of
irritability and confusion. Osteoporosis and nerve damage may also the human body. Organic products are preservative, metal, inorganic
result. Patients with nerve damage may feel tingling and loss of sensation compound and chemical free. If you are a denture wearer and are
in the hands and feet. Coordination may be affected. Normal copper experiencing unexplained numbness, tingling or muscle weakness, seek
blood levels are between 0.75 to 1.45 micrograms/milliliter. The subjects' the help of a medical professional immediately and have your blood zinc
copper levels in the study ranged between 0.1 to 0.23 levels tested.
micrograms/milliliter. REFERENCES:-
Several diseases may occur with the excess of inorganic zinc and 1- Vashon Organics, Natural and organic for Healthy Life Style.
associated depletion of copper in the body. The primary condition found
in most documented cases of hyperzincemia due to the use of denture
adhesives has been peripheral neuropathy. It is a disorder of the nervous
system characterized by pain, diminished reflexes, and muscle wasting in
the hands and feet. Patients typically experience weakness, numbness
and tingling in the extremities. Consequently, balance and coordination
are affected. Because the majority of denture adhesive users are the
elderly, peripheral neuropathy in this age group is an often overlooked
cause of falls as physicians tend to attribute a loss of balance as normal
sign of aging.
Anemia may result from hypocupremia. This is a condition where there
are below normal levels of red blood cells circulating in the body. Red
blood cells contain hemoglobin which is a carrier of oxygen. Diminished
oxygen levels are manifested by fatigue, dizziness and labored breathing.
The bone marrow attempts to compensate by increasing the production of
red blood cells. Osteoporosis may develop as serum copper diminishes.
Bones are de-mineralized and become porous and weak. Fractures are
more common and the development of curvature of the spine and
shoulders can be noted.
The serious adverse effect of denture adhesives has prompted action.
Currently, two lawsuits have been filed against GlaxoSmithKline, the
manufacturer of Poligrip. Manufacturers have the responsibility to warn
consumers about the inorganic zinc contents in their products and the
associated risks. However, they have failed to do this. The public is
unaware and unprotected against potential inorganic zinc toxicity and the
consequences thereof. Users suffering from the effects of inorganic zinc
toxicity and associated complications may seek compensation for the
damages related to denture adhesive use. It is expected that with the
advent of the campaign for awareness in the link between the use of these
products and associated serious side effects, lawsuits filed against the
manufacturers will increase.
Manufacturers of the identified denture adhesives have released a
statement regarding the issue. GlaxoSmithKline assures that Poligrip is
safe and effective when used according to directions. They defend that
the inorganic zinc found in their adhesive remains in the product and is
the standards of the FDA's manufacturing process and they monitor the
safety of their product.

Journal of Dental Sciences & Oral Rehabilitation 52