Beruflich Dokumente
Kultur Dokumente
Sponsored by
National Institute of Dental Research
National Institutes of Health
May 13-14,
1981
Conference Coordinators:
Samuel Kakehashi,
Paul F. Prakkal,
National Institute of Dental Research
Bethesda, MD 20205
475
PREFACE
A state-of-the-art workshop titled: Surgical Therapy for Periodontitis, sponsored by the
National Institute of Dental Research, was held on May 13-14, 1981, at the National
Institutes of Health, Bethesda, Maryland. More than 380 general dentists, hygienists,
periodontists, researchers, academicians and health-consumers attended the 2 day meeting.
The objectives of the workshop were to review and evaluate the available scientific
evidence on the efficacy of surgical therapy for adult Periodontitis and to formulate
summary recommendations on this treatment modality. The scope of this workshop was
intentionally limited to address the technical question of whether the surgical treatment of
Periodontitis is scientifically sound, safe and efficacious. Thus, economic and societal issues
in reference to this treatment modality impacting on the individual patient as well as the
public-at-large were omitted from the agenda. To help focus on the pertinent issues relating
to the current status of surgical treatment, the following questions were addressed:
When is periodontal surgery necessary?
What are the morbidity factors?
Are there feasible alternatives to surgical treatment?
What are the risks in delaying surgery?
What are the research needs?
Prior to the meeting, a Task Force of ten recognized clinicians, academicians and clinical
researchers were assembled to write a background review paper on the surgical treatment
of adult Periodontitis including the etiology, pathogenesis and the spectrum of treatment
considerations including the various surgical approaches. In an attempt to develop a
balanced paper representing all views, the Task Force undertook a critical review and
objective assessment of the available scientific data on the treatment of Periodontitis. The
background paper was sent to all workshop attendees prior to the meeting.
A special review panel of experts from a variety of backgrounds participated in the
workshop. The Panel included general dentists, a statistician, epidemiologist, pathologist,
microbiologist, and periodontist clinicians, academicians and clinical scientists. This panel
was charged with the responsibility of reviewing and analyzing the existing information
including data presented during the workshop in an attempt to provide the most useful
current views on the efficacy of surgical therapy for Periodontitis. At the conclusion of the
workshop the Review Panel presented its summary recommendations based on the
information reviewed in the background paper, the workshop presentations and the
resultant audience participation.
The workshop program was as follows:
Workshop Chairman
Paul RobertsonIntroduction
Bruce PihlstromNo Therapy
Stanley HazenInitial Therapy; Alternative Therapies
Saul Schluger and Dr. Raul CaffessePeriodontal Surgery
Jack Caton, Jr.Maintenance Therapy
Research
Papers
Flap Curettage
476
Volume 53
Number 8
Participation
477
478
J. Periodontol.
August, 1982
knowledge; as a result, the fundamental principle underlying all therapy of Periodontitis is broad
lack such
Volume 53
Number 8
males. Increased levels of education, income, and socioeconomic status also have been associated with less
disease. The correlation for all these factors, however, is
quite weak and is often lost entirely when groups are
stratified by measures of oral hygiene.5'8
Etiology of Periodontitis
by mechanical19"22
or
chemotherapeutic plaque
re-
changes33 and with both local34 and systemic35"37 neutrophilic leukocyte dysfunction.
How much occlusal factors contribute to the progression of periodontal disease remains controversial. Studies
in man, primates, and beagle dogs have consistently
shown that excessive occlusal forces do not initiate either
gingivitis or Periodontitis or convert an established gingivitis or Periodontitis.38 When occlusal trauma was superimposed on experimentally-induced Periodontitis, the
rate of loss of periodontal attachment was accelerated in
dogs39 but not in monkeys,40 and bone regeneration was
retarded after the resolution of Periodontitis in mon-
keys.41
Pathogenesis of Periodontitis
The histopathological events that occur after the microbial colonization of tooth surfaces adjacent to healthy
gingiva and during the progression from gingivitis to
Periodontitis have been divided into four general, overlapping stages: initial, early, established, and advanced.43
The first stage consists of vasculitis below the junctional
epithelium and is concomitant with the increased migration of neutrophils. Alterations in the junctional epithelium and some loss of perivascular collagen are sometimes observed. The early stage, beginning about 4 to 7
days after plaque accumulation, is characterized by the
appearance of an inflammatory infiltrate consisting principally of lymphocytes, continuing collagen destruction,
and the proliferation of basal junctional epithelial cells.
During the ensuing weeks, plasma cells become more
numerous and, in the established stage, dominate the
inflammatory infiltrate. The infiltrated area continues to
enlarge; and proliferation, apical migration, and lateral
extension of junctional epithelium are apparent. This
established lesion is compatible with a clinical diagnosis
of chronic gingivitis and may persist without further
involving the deeper supporting structures. Under conditions not well understood, however, it may progress to
the advanced stage, Periodontitis, with the extension of
epithelium apically along the root surface, subsequent
pocket formation, destruction of alveolar bone and periodontal ligament, and eventual tooth loss.
Direct bacterial and indirect host-response mechanisms responsible for periodontal destruction recently
have been reviewed.44"46 The direct activity of microbial
enzymes, organic acids, and various cytotoxic materials
may contribute to changes in the epithelium and the
nearby connective tissue, particularly during the early
stages of pathogenesis. The absence of microorganisms
in tissues with obvious Periodontitis, the slowly progressing nature of the disease, the extent of involvement, and
typical lymphocyte and plasma cell infiltrate suggest that
J. Periodontol.
480
and advanced
Conclusions
August,
1982
Many clinical trials have proven the longitudinal effectiveness of periodontal therapy in controlling chronic
Periodontitis.19,50-61 In addition, retrospective studies
over many years have documented the effectiveness of
periodontal therapy.62"66 Abundant evidence also indicates that the amount of periodontal support is increased
after various surgical therapies.67"86
Conclusions
1. Untreated chronic Periodontitis leads to progressive
destruction of periodontal support and eventually causes
tooth loss.
2. Periodontal therapy does control the progressive
destruction associated with chronic Periodontitis and
restores some tooth support.
1. The
NO THERAPY
studies have highlighted the pathogenesis of untreated chronic Periodontitis and have established that it leads to continued loss of support,6'47
increased pocket depth,47 and eventual tooth loss.47 The
rate of loss of periodontal support is greater in individuals not receiving regular therapy than in those who do
receive such care.6,19'48'49 The risk of delaying periodontal therapy in the presence of persistent inflammation
may therefore include progressive destruction of supporting tissues and eventual tooth loss.
Longitudinal
PERIODONTAL THERAPY
The goal of periodontal therapy is to restore health
and function to the periodontium and to preserve the
teeth for a lifetime. The following discussion of treatment
methods designed to meet that goal is divided into four
general sectionsInitial Therapy to Control Etiologic
Factors, Rvaluation, Periodontal Surgery, and Maintenance Therapyand is based on the sequence of care
that should be delivered to a patient manifesting chronic
Periodontitis. The listing of these treatment phases and
of the procedures included within each phase serves
mainly for organizational purposes and does not imply
that all patients require all treatment modalities.
Initial
therapy.52'54,57'91'92
Volume 53
Number 8
J. Periodontol.
August,
482
ment
depth.19,55,206"209
to
motor
1982
ing forces.40,60,249
Secondary occlusal trauma has been defined as normal
Volume 53
Number 8
beagle,39
surgery.264"266
therapy.267"272
483
attachment.250'253'254
Conclusions
3.
oral
clinician.
4. Many chemotherapeutic agents can reduce or modify the levels of dental plaque, but at present, none
completely inhibit sub- and supragingival plaque.
5. Occlusal trauma will not initiate gingivitis or Periodontitis nor will it cause gingivitis to develop into
Periodontitis.
treatment must be determined. To make a rational decision about this, one must reevaluate the
considresponse to the reduction of local irritants.
erations enter into these decisions, several of which
appear to be more important than others. These include
periodontal
Many
the
cooperation and effectiveness of the patient in controlling plaque; the improvement in gingivitis, pocket
depth, and clinical attachment level; and the systemic
status of the
patient.
Evaluation ofPlaque Control. Plaque control is important to maintain the beneficial effect of periodontal
therapy.52, 54' 57' 58' 91, 277 Therefore, it is necessary that
the patient be evaluated in terms of the effectiveness of
J. Periodontol.
484
August, 1982
developed.
Volume 53
Number 8
Periodontal
Surgery
consists
age336'
without any evidence of new connective tissue attachment. The new attachment and gingival recession associated with subgingival curettage may be due entirely to
the concurrent plaque removal and root planing.205'350
effective in cases with minCurettage has been342'
reported
351'352
imal pockets.51,203'
However, curettage was not
as effective as other surgical techniques in reducing
deeper pockets.51
Apically Positioned Flap With and Without Osseous
Recontouring. The characteristic feature of the apically
positioned flap is placement of the flap margin at the
crest of the alveolar bone. This requires resection of
gingiva to the bone crest on the palatal aspect. In other
areas, this is accomplished by displacing the flap apically.
The objective of the procedure, in addition to providing
access for complete subgingival debridement, is to reduce
pocket or sulcular depth. Osseous recontouring is often
performed in combination with the apically positioned
flap.
In 1949, Schluger353 expressed concern about the behavior of soft tissue after gingivectomy and curettage.
He suggested that the topography of bone be altered to
these
The
to
be
success
attachment.50'59,92'203
Leonard Widman introduced the reverse beveled incision in 1916 to obtain access for root preparation.360
The modified Widman flap, described in detail in
1974,364,366 is basically a flap for reattachment and is
more conservative than that described by Widman.347
The reported advantages of the modified Widman flap
are that it optimizes access to the root surface, and the
close postsurgical adaptation of healthy connective tissue
to the root surface enhances the potential for new attachment.322' 347'366 In addition, it allows optimal soft tissue
coverage of root surfaces and thus provides a result that
is both esthetically desirable and amenable to oral hygiene procedures.322,347 Less exposure of root surfaces
also means potentially less root sensitivity and fewer
problems with root caries.322,364'366
The disadvantages of this technique include the fact
that it is technically exacting, especially interproximally.
The interproximal architecture of the tissue may be poor
immediately after removal of the dressing, especially in
areas of interproximal bony craters. However, if metic-
J. Periodontol.
August, 1982
486
tachment.347' 374
pockets.373
years.61,347,373
Osseous Grafts. Osseous grafts are used in the treatof Periodontitis to restore lost alveolar bone, to
regenerate a functional attachment apparatus, and to
reduce the periodontal pocket.375
Graft Materials. Bone grafts can be divided into autografts and allografts. An autografi is a tissue graft
transferred from one position into a new position in the
body of the same individual. Periodontal autografts have
been obtained from intraoral or extraoral sites. An allograft, formerly referred to as a homograft, is a tissue
graft between individuals of nonidentical genetic disposition.
Bone autografi materials used in periodontal therapy
include bone chips,77 mixtures of blood and ground
intraoral bone and marrow,
and iliac
bone,
crest bone and marrow.327,379
Allografts have been used because of the difficulty of
obtaining sufficient bone-graft material from within the
patient's mouth and because of problems in obtaining it
elsewhere. Materials used for allografts include frozen
iliac crest bone,375,380,381 decalcified382 and undecalcified
freeze-dried bone,76 and merthiolate-treated bone.383
With the exception of freeze-dried bone, the allograft
materials are still experimental.
Clinical EvaluationsAutografts. Most of the publications which evaluate osseous autografts are case reports, and most of these indicate that a significant
amount of osseous repair is possible in all types of
intraosseous defects, including furcations.69, 77, 82, m' 85,
384-387
pewer investigations include data which would
enable one to compare various autografts. Mean bone
repair reported in several studies of intraosseous defects
ranged from 2.1 to 4.4 mm.68,71,72,327 Of all the available
graft materials, iliac cancellous bone and marrow autografts probably offer the greatest potential for Osteogenment
esis.385-390
Clinical EvaluationsAllografts. Freeze-dried bone allograft is the only bone-graft material that has been field
tested. Reports indicated that more than 50% osseous
repair occurs in 60% of the defects treated.76,391,392 Pockets were reduced to a level proportional to the degree of
osseous repair. A principal concern with all allografts is
the problem of graft rejection. The results of animal
studies suggest that freeze drying reduces or abolishes
the antigenicity of a bone allograft.393,394 Various autograft and allograft materials can achieve significant levels
of osseous repair. However, the studies to date were
without adequate controls.
Histologie Observations. Regeneration of new attachment composed of bone, cementum, and periodontal
ligament has been reported in human patients with
osseous coagulum-bone blend,395 cancellous bone and
marrow from intraoral donor sites,72,83,396 iliac cancellous bone and
marrow
Volume 53
Number 8
cases
their environment.440"443
Free Gingival Grafts. Free gingival grafts obtained
from masticatory mucosa have been used successfully444
to increase the band of keratinized gingiva and to cover
localized gingival recessions. Grafts are predictable procedures if they are placed on a bed capable of inducing
revascularization,445'446 such as periosteum or bare
bone.447"460
graft.446,466-469
flap,490"494
complication.492'495-497
'
J. Periodontol.
488
served.509
Some have claimed that mucogingival problems associated with tooth malposition in children should be
treated surgically before orthodontic treatment.510 However, the band of attached gingiva has been shown to
increase after a tooth has been moved back orthodontically into the basal bone.511'012 Obviously then, a conservative approach to mucogingival surgery is indicated.513 Rvaluation of tissue response 1 to 2 months
after completion of the hygienic phase of therapy may
show that the preplanned surgery is not needed. On the
other hand, additional complications to areas of recessionroot hypersensitivity, demineralization, lack of
marginal epithelial seal associated with a frenum or
muscle pull, unfavorable esthetic appearancemay indicate the need for surgery.
Conclusions
1. Effective plaque control is necessary to the success
of all methods.
2. Gingivectomy is still a valuable procedure despite
its limited applicability. It should not be used to treat
osseous deformities or in areas where it will remove all
gingiva.
Apically positioned flaps, open-flap curettage, and
keratinized
3.
August, 1982
nongraft techniques.
Maintenance Therapy
Periodontal maintenance therapy is the term applied
the measures taken by both patient and therapist to
preserve periodontal health and thereby to prevent further destruction of the periodontium by recurrent Periodontitis. Maintenance therapy consists of plaque removal from the teeth by the patient; periodic examination of periodontal status by the therapist; professional
removal of tooth deposits by scaling, root planing, and
polishing; and motivation and instruction of the patient
in personal plaque removal.
Rationale. The basis for maintenance therapy is the
removal of bacterial deposits located at or apical to the
gingival margin. Such deposits are the principal cause of
gingivitis and Periodontitis.17'514,515 Periodontal health
can be maintained after surgery, even in patients with
advanced destruction of the periodontium, by periodic
recall of the patient for scaling, root planing, polishing
of the teeth, and instruction in oral hygiene.52' 54' 57' 58' 206'
261, 369
gy jjjg same token, periodontal health rapidly
deteriorates when there is no maintenance therapy91 or
when such therapy cannot keep the levels of plaque and
gingival inflammation at a minimum.277 Patient participation in a maintenance program motivates personal
oral hygiene, which probably accounts, in large measure,
for the preservation of periodontal health.516 Furtherto
Volume 53
Number 8
489
more,
the
away from the flora associated with Periodontitis to one
commonly found with gingivitis or normal gingiva.187'188
Frequency. Several longitudinal studies have determined the frequency of maintenance therapy necessary
to preserve periodontal health after surgery. Professional
tooth cleaning and oral hygiene instruction, at intervals
2 weeks and 6 months, were valuvarying 54,between
206,
261, 368, 369 Maintenance
57,
58,
ai*
tnerapy per.
formed at 2-week intervals for 2 years after various
surgical procedures resulted in low levels of plaque and
and
gingival inflammation, a gain in clinical attachment,
57'58'206 Mainlesions.54'
significant repair of infrabony
tenance performed at 3- to 6-month intervals was adeand bone levels for 5 or
quate to stabilize attachment
'S! 52 977
after
more years
surgery.
The effect of periodic scaling and root planing, with
and without oral hygiene instruction, has also been
evaluated in subjects who have not undergone periodontal surgery.19' 48' 49'101'207 Professional cleaning without
oral hygiene instruction was significantly less effective
than a combination of the two.48 When performed at
intervals varying from 2 months to 1 year, maintenance
therapy was effective in retarding or preventing loss of
clinical attachment and decreasing gingival inflam207
In general, better periodontal
mation 19, 48, 49, 101,
health was maintained with increasing frequency of recall appointments.101
Periodic examination after periodontal surgery is necessary to determine both the patient's cooperation in
personal plaque removal and the status of the periodontium. Continuing destruction of the periodontium would
indicate the need for increasing frequency of maintenance therapy, improving the patient's oral hygiene and,
where necessary, further periodontal surgery. The examination consists of an evaluation of plaque and gingival status, iatrogenic factors, pocket depth, and attachment levels. Radiographic and occlusal status is also
often examined. Measurements of gingival crevicular
fluid flow and microbiological techniques are seldom
used. The clinical judgment of the therapist must be
exercised to evaluate the findings of the examination and
to determine the need for further therapy. So far, no
objective clinical method for ascertaining whether active
destruction of the periodontium is occurring is available.
Conclusions
i~
on
destruction.
4. Determine the relative long-term effects of periodontal surgical procedures, scaling and root planing,
and other therapy for chronic Periodontitis.
5. Develop chemo therapeutic agents that will inhibit
dental microbial plaque without significant deleterious
side effects.
6. Define those situations in which trauma from occlusion will or will not accelerate the loss of connective
tissue attachment associated with Periodontitis.
7. Evaluate the long-term effect of orthodontic therapy on the periodontium.
8. Determine the relative effects of subgingival curettage, plaque control, and scaling and root planing.
9. Develop optimum graft materials and improve
upon those factors which will enhance a favorable response and strengthen predictability.
WORKSHOP SUMMARY RECOMMENDATIONS
Review Panel
Irwin Mandel, D.D.S., Chairman, Columbia University, New York
Sheldon D. Benjamin, D.M.D., Private Practice, Los
Angeles (Representative, American Academy of Per-
iodontology)
Philadelphia
versity, Baltimore
Albany
Sigmund S.
Boston
490
J. Periodontol.
WORKSHOP SUMMARYRECOMMENDATIONS
INTRODUCTION
Surgery Necessary?
Periodontal surgery is an appropriate therapeutic procedure to gain visibility, and to provide access for root
preparation and for the removal of subgingival microorganisms and other local irritants adjacent to deep or
tortuous periodontal pockets or in furcation involvements. It is also used to control the disease when nonsurgical methods prove ineffective. Periodontal surgery
is also indicated to create optimal conditions for regeneration, replacement, or reconstruction of lost periodontal structures. Longitudinal studies have demonstrated
that loss of attachment can be arrested by periodontal
surgery and plaque control. Without meticulous plaque
control, however, further loss of attachment may occur.
Since moderately advanced and advanced periodontal
disease (Case Patterns Classes III and IV, American
Dental Association, Uniform Code, Procedures & Nomenclature) frequently is treated by surgical treatment,
the dental profession must be able to recognize and to
treat incipient disease before it reaches those stages.
The benefits of osseous recontouring remain uncertain.
Studies on this form of surgery should provide precise
definition of the techniques utilized.
In some of the published studies, the evaluation of
various surgical techniques has been hampered because
only single rooted teeth were involved. Workshop participants believe that the results of these studies might have
been different had molar teeth with multiple roots been
August, 1982
Surgery?
periodontal therapeutic interventions involve inherently hazardous risks such as the use of local anesthesia, hemorrhaging, transient bacteremia, and stress as
All
Volume 53
Number 8
Surgical
Treatment?
The panel
gingiva.
A recently revived therapy, proposed as an alternative
to periodontal surgery, uses subgingival scaling and root
planing as its basis but adds to conventional oral hygiene
the application of various salt pastes in hydrogen peroxide and the irrigation subgingivally with salt solutions.
This technique also involves the monitoring of subgingival plaque samples in wet preparations under the
phase-contrast microscope. Proponents claim that disease activity can be determined by the cellular and
bacterial composition of these samples and that the
efficacy of control can also be monitored in this way.
The panel observes that in its dependence on scaling and
plaque control as the basis of its methodology, this
technique does what conventional therapy has been
doing for years. Moreover, there is no evidence that the
other features of this technique seem to have any therapeutic value. The claims by some dentists and patients
that this technique offers a simple therapeutic alternative
to periodontal surgery have not been substantiated in
controlled studies.
Current data suggest that antibiotics may be an effective adjunct to other periodontal therapeutic modalities
in the treatment of refractory Periodontitis or when
systemic diseases impair the host response to infections.
However, the evidence does not support the use of these
drugs alone for the treatment of Periodontitis.
491
Disadvantages in Delaying
Surgery? (Rephrased by the review panel from
"What are the risks in delaying surgery?")
Clinical studies indicate that untreated periodontal
disease leads to continued loss of attachment. If the
disease remains active after initial or alternative treatment procedures and a surgical approach is necessary
for access, delaying surgical intervention may result in
further loss of attachment. This, in turn, may make the
surgery itself more complicated. Disease initially localized at one site, one root, or one tooth may soon involve
adjacent structures.
2.
3.
Development of methods to measure disease activity by means of both clinical and laboratory techniques. Such methods are needed to compare the
efficacy of various treatment modalities and to
develop and test new therapeutic methods.
Studies to differentiate the various forms of Periodontitis, especially those refractory to treatment.
Such differentiation is important for designing clinical trials and for diagnosis and treatment planning.
Studies to determine which microorganisms cause
each of the various periodontal diseases and to
492
1.
croorganisms.
Additional
1.
areas
for
human Periodontitis.
2. Studies on the long-term effects of orthodontic
therapy on the periodontium.
3. Studies on whether inadequate nutrition increases
4.
5.
susceptibility to Periodontitis.
Studies on the role of professional and patient
behavior in maintaining periodontal health and in
treating of Periodontitis.
Investigation of other factors which are related to
the etiology or progression of the disease.
REFERENCES
1.
Prichard,
J.
1966.
J. Periodontol.
August, 1982
15. Le, .: Human research model for the production and prevention of gingivitis. J Dent Res 50: 256, 1971.
16. Le, ., Theilade, E., Jensen, S. ., and Schiott, C. R.: Experimental gingivitis in man. II. The influence of antibiotics on gingival
plaque development. J Periodont Res 2: 282, 1967.
17. Le, H., Theilade, E., and Jensen, S. B.: Experimental gingivitis
in man. J Periodontol 36: 177, 1965.
18. Theilade, E., Wright, W. E., Jensen, S. B., and Le, H.: Experimental gingivitis in man. II. A longitudinal clinical and bactriologie
investigation. J Periodont Res 1: I, 1966.
19. Axelsson, P., and Lindhe, J.: Effect of controlled oral hygiene
procedures on caries and periodontal disease in adults. J Clin Periodontol 5: 133, 1978.
20. Axelsson, P., and Lindhe, J.: Effect of fluoride on gingivitis and
dental caries in a preventive program based on plaque control. Community Dent Oral Epidemiol 3: 156, 1975.
21. Axelsson, P., and Lindhe, J.: The effect of a preventive programme on dental plaque, gingivitis and caries. Results after one and
two years. J Clin Periodontol 1: 126, 1976.
22. Axelsson, P., Lindhe, J., and Waseby, J.: The effect of various
plaque control measures on gingivitis and caries in school children.
Community Dent Oral Epidemiol 4: 232, 1976.
23. Lobene, R. R., and Soparkar, P. M.: The effect of an alexidine
mouthwash on human plaque and gingivitis. J Am Dent Assoc 87: 848,
1973.
24. Le, H.: Chlorhexidine in the prophylaxis of dental diseases. J
Periodont Res (suppl. 8) 12: 5, 1973.
25. Le, H.: Does Chlorhexidine have a place in the prophylaxis of
dental disease? J Periodont Res 8: (suppl. 12) 93, 1973.
26. Le, H., Schiott, C. R., Glavind, L., and Karring, T.: Two years
oral use of Chlorhexidine in man. 1. General design and clinical effects.
J Periodont Res 11: 135, 1976.
27. Loesche, W. J., and Syed, S. .: Bacteriology of human experimental gingivitis: Effect of plaque and gingivitis score. Infect Immun
21: 830, 1978.
28. Slots, J.: Microflora in the healthy gingival sulcus in man. Scand
J Dent Res 85: 247, 1977.
29. Slots, J., Moenbo, D., Langeback, J., and Frandsen, .: Microbiota of gingivitis in man. Scand J Dent Res 86: 174, 1978.
30. Slots, J.: The predominant cultivable microflora of advanced
Periodontitis. Scand J Dent Res 85: 1141, 1977.
31. Tanner, A. C. R., Haffner, C, Bratthall, G. T., Visconti, R. .,
and Socransky, S. S.: A study of the bacteria associated with advancing
Periodontitis in man. J Clin Periodontol 6: 278, 1979.
32. Pennel, . M., and Keagle, J. C: Predisposing factors in the
etiology of chronic inflammatory periodontal disease. / Periodontol 48:
517, 1977.
33. Kornman, K. S., and Loesche, W. J.: The subgingival microflora
during pregnancy. J Periodont Res 15: 111, 1980.
34. Murray, P. ., and Patters, M. R.: Gingival crevice neutrophil
function in periodontal lesions. J Periodont Res 15: 463, 1980.
35. Cianciola, L. J., Genco, R. J., Patters, M. P., McKenna, J., and
VanOss, C. J.: Defective polymorphonuclear leukocyte function in
human periodontal disease. Nature 265: 445, 1977.
36. Clark, R. ., and Kimball, H. R.: Defective Chemotaxis in
Chediak-Higashi syndrome. J Clin Invest 50: 2645, 1971.
37. Cohen, D. W., and Morris, A. L.: Periodontal manifestations of
cyclic neutropenia. J Periodontol 32: 159, 1961.
38. Zander, . ., and Poison, A. M. Present status of occlusion
and occlusal therapy in periodontics. J Periodontol 48: 540, 1977.
39. Lindhe, J., and Svanberg, G.: Influence of trauma from occlusion on progression of experimental Periodontitis in the beagle dog. J
Clin Periodontol 1: 3, 1974.
40. Poison, A. M., Mehner, S. W., and Zander, . .: Trauma and
progression of marginal Periodontitis in squirrel monkeys. III. Adaptation of interproximal alveolar bone to repetitive injury. J Periodont
Res 11: 279, 1976.
41. Poison, A. M., Mehner, S. W., and Zander, . .: Trauma and
Volume 53
Number 8
progression of marginal Periodontitis in squirrel monkeys. IV. Reversibility of bone loss due to trauma alone and trauma superimposed
upon Periodontitis. J Periodont Res 11: 290, 1976.
42. Epidemiology, Etiology and Prevention of Periodontal DiseasesReport of WHO Scientific Group. Moscow, 1977.
43. Page, R. C, and Schroeder, H. E.: Pathogenesis of inflammatory
periodontal disease. A summary of current work. Lab Invest 33: 235,
1976.
44.
227,1981.
plaque
493
494
J. Periodontol.
August, 1982
Med Care 13: 10, 1975.
118. Cohen, L. K: Comments during International Conference on
Research in the Biology of Periodontal Disease, p. 482, 1977.
119. Cohen, L. K., O'Shea, R. M., and Putnam, W. J.: Toothbrushing: Public opinion and dental research. J Oral Ther Pharmacol 4: 229,
1967.
120. Corah, N. L.: The dental practitioner and preventive health
behavior. Health Ed Monogr 2: 226, 1974.
121. Emier, B. F., Windchy, A. M., Zaino, S. W., Feldman, S. M.,
and Scheetz, J. P.: The value of repetition and reinforcement in
improving oral hygiene performance. J Periodontol 51: 228, 1980.
122. Kegeles, S. S.: Current status of preventive dental health
behavior in the population. Health Ed Monogr 2: 197, 1974.
123. Levy, R. L., Weinstein, P., and Milgrom, P.: Behavioral guidelines for plaque control programs. Dent Hyg 51: 13, 1977.
124. Putnam, W. J., O'Shea, R. M., and Cohen, L. K.: Communication and patient motivation in preventive periodontics. Public Health
Rep 82: 779, 1967.
125. Ratcliff, P. .: World Workshop in Periodontics. Ramfjord, S.
P. (ed), pp. 291-298, Ann Arbor, Mich., 1966.
126. Glossary of Terms: J Periodontol 48: 1, (suppl.) 1977.
127. Greene, J. C: Periodontal disease in India: Report of an
epidemiologie study. J Dent Res 39: 302, 1960.
128. Lovdal, ., Arno, ., and Waerhaug, J.: Incidence of clinical
manifestations of periodontal disease in light of oral hygiene and
calculus formation. J Am Dent Assoc 56: 21, 1958.
129. Scherp, H. W.: Current concepts in periodontal disease research. Epidemiologie contributions. J Am Dent Assoc 68: 667, 1964.
130. Courant, P. R., and Baeder, H.: Bacteroides melaninogenicus
and its products in the gingiva of man. Periodontics 4: 131, 1966.
131. Maryon, L. W., and Loiselle, R. J.: Bacterial antigens and
antibodies in human periodontal tissue. J Periodontol 44: 164, 1973.
132. Mergenhagen, S. E., Hamp, E. G., and Scherp, H. W.: Preparation and biological activities of endotoxin from oral bacteria. J Infect
Dis 108: 304, 1961.
133. Shapiro, L., Lodato, F. M., Courant, P. R., and Stallard, R. E.:
Endotoxin determination in gingival inflammation. J Periodontol 43:
591, 1972.
134. Simon, B. L, Goldman, H. M., Ruben, M. P., and Baker, E.:
The role of endotoxin in periodontal disease. I. A reproducible quantitative method for determining the amount of endotoxin in human
gingival exdate. J Periodontol 40: 695, 1969.
135. Alexander, A. G.: A study of the distribution of supra and
subgingival calculus, bacterial plaque and gingival inflammation in the
mouths of 400 individuals. J Periodontol 42: 21, 1971.
136. Brandtzaeg, P., and Jamison, H. C: A study of periodontal
health and oral hygiene in Norwegian army recruits. J Periodontol 35:
302, 1964.
137. Lilienthal, B., Amerena, V., and Gregory, G.: An epidemiological study of chronic periodontal disease. Arch Oral Biol 10: 553,
1965.
138. Ramfjord, S. P.: The periodontal status of boys 11 to 17 years
old in Bombay, India. J Periodontol 32: 237, 1961.
139. Bjorn, A. L., Bjrn, H., and Grkovic, B.: Marginal fit of
restorations and its relationship to periodontal bone lavel. Odontol
Revy (Malmo) 20: 311, 1969.
140. Gorzo, I., Newman, . N., and Strahan, J. D.: Amalgam
restorations, plaque removal and periodontal health. J Clin Periodontol
6: 98, 1979.
141. Jeffcoat, M. K., and Howell, T. H.: Alveolar bone destruction
due to overhanging amalgam in periodontal disease. J Periodontol 51:
599, 1980.
142. Leon, A. R.: Amalgam restorations and periodontal disease.
Br Dent J 140: 377, 1976.
143. Mormann, W., Regolati, ., and Renggli, H. H.: Gingival
reaction to well fitted subgingival proximal gold inlays. J Clin Periodontol 1: 120, 1974.
144. Perel, M.: Axial crown contour. J Prosthet Dent 28: 642, 1971.
145. Renggli, H., and Regolati, B.: Gingival inflammation and
Volume 53
Number 8
495
496
J. Periodontol.
August, 1982
103, 1978.
226. Weenstrom, J., and Lindhe, J.: Effects of hydrogen peroxide
on developing plaque and gingivitis in man. J Clin Periodontol 6: 115,
1979.
227. White, S. T., and Taylor, P. P.: The effect of stannous fluoride
on plaque scores. J Dent Res 58: 1850, 1979.
228. Counsell, L. .: Studies in dental health education: I. Effect of
antibiotic prophylaxis on the oral hygiene and periodontal health of
young men. J Dent Res 51: 1619, 1972.
229. Johnson, R. H, Rozanis, J., Schofield, I. D. F., and Haq, M.
J.: The effect of spiramycin on plaque accumulation and gingivitis. J
Can Dent Assoc 10: 456, 1978.
230. Loesche, W. J., Greene, R., Kenney, . ., and Nafe, D.: Effect
of topical kanamycin sulfate on plaque. J Am Dent Assoc 83: 1063,
1971.
231. Rozanis, J., Johnson, R. H, Haq, M. J., and Schofield, I. D.
F.: Spiramycin as a selective plaque control agent. J Periodont Res 14:
55, 1979.
232. Williams, B. L., Osterberg, S. K., and Jorgensen, J.: Subgingival microflora of periodontal patients on tetracycline therapy. J Clin
Periodontol 6: 210, 1979.
233. Goodson, J. M., Haffajee, ., and Socransky, S. S.: Periodontal
therapy by local delivery of tetracycline. J Clin Periodontol 6: 83, 1979.
234. Lindhe, J., Heijl, L., Goodson, J. M., and Scoransky, S. S.:
Local tetracycline delivery using hollow fiber devices in periodontal
therapy. J Clin Periodontol 6: 141, 1979.
235. Box, . K.: Twelve Periodontal Studies, 185, Toronto, Canada, U. of Toronto Press, 1940.
236. Keyes, P. H., Wright, W. E., and Howard, S. .: The use of
phase-contrast microscopy and chemotherapy in the diagnosis and
treatment of periodontal lesionsan initial report (I). Quintessence
Internat 1: 1, 1978.
237. Keyes, P. H., Wright, W. E., and Howard, S. .: The use of
phase-contrast microscopy and chemotherapy in the diagnosis and
treatment of periodontal lesionsan initial report (II). Quintessence
Internat 2: 7, 1978.
238. Glickman, I., and Zander, . .: Discussion of role of occlusion in the etiology and treatment of periodontal disease. J Dent Res
(suppl. to No. 2) 50: 199, 1971.
239. Ramfjord, S. P., Kerr, D. ., and Ash, . M.: World Workshop
in Periodontics, 271, Ann Arbor, Mich., University of Michigan, 1966.
240. Glickman, I.: Inflammation and trauma from occlusion: Codestructive factors in chronic periodontal disease. J Periodontol 34: 5,
1963.
241. Zander, . ., and Muhlemann, .: The effect of stress on the
periodontal structures. Oral Surg9: 380, 1956.
242. Schluger, S., Yuodelis, R., and Page, R.: Periodontal Disease.
Philadelphia, Lea and Febiger, 1977.
243. Bhaskar, S. N., and Orban, B.: Experimental occlusal trauma.
J Periodontol 26: 270, 1955.
244. Glickman, I., and Smulow, J.: Adaptive alterations in the
periodontium of the rhesus monkey in chronic trauma from occlusion.
/ Periodontol 29: 101, 1968.
Volume 53
Number 8
497
gingival pocket depth and clinical crown height. Angle Orthod 43: 402,
246. Svanberg, G., and Lindhe, J.: Vascular reactions in the periodontal ligament incident to trauma from occlusion. J Clin Periodontol
1: 58, 1974.
247. Waerhaug, J.: Pathogenesis of pocket formation in traumatic
occlusion. J Periodontol 26: 107, 1955.
248. Wentz, F., Jarabak, L, and Orban, B.: Experimental occlusal
trauma imitating cuspal interferences. J Periodontol 29: 117, 1956.
249. Muhlemann, H., and Herzog, H.: Tooth mobility and microscopic tissue changes produced by experimental occlusal trauma. Helv
Odontol Acta 5: 33, 1961.
250. Poison, A. M., and Zander, . .: Occlusal traumatism. Jundeen, H. and Gibbs, C. (eds), Vistas in Occlusion. Publishing Sciences
group. In press, 1982.
251. Glickman, I. and Weiss, L.: Role of trauma from occlusion in
initiation of periodontal pocket formation in experimental animals. J
Periodontol 26: 14, 1955.
252. Orban, B.: Traumatic occlusion and gum inflammation. J
Periodontol 10: 39, 1939.
253. Ericsson, I, and Lindhe, J.: Lack of effect of trauma from
occlusion on the recurrence of experimental Periodontitis. J Clin Periodontol 4: 115, 1977.
254. Perrier, M., and Poison, A. M.: The effect of progressive and
increasing tooth hypermobility on reduced but healthy periodontal
supporting tissues. J Periodontol 53: 152, 1982.
255. Glickman, I.: Occlusion and the periodontium. J Dent Res 46:
53, 1967.
256. Glickman, I., and Smulow, L: Alterations in the pathway of
gingival inflammation into the underlying tissues induced by excessive
occlusal forces. J Periodontol 33: 7, 1962.
257. Glickman, L, and Smulow, J. B.: The combined effects of
inflammation and trauma from occlusion in Periodontitis. Int Dent J
19: 393, 1969.
258. Mehner, S. W.: Co-destructive factors of marginal Periodontitis
and repetitive mechanical injury. J Dent Res 54: Special Issue C: C78C85, 1975.
259. Kantor, M., Poison, A. M., and Zander, . .: Alveolar bone
regeneration after removal of inflammatory and traumatic factors. J
Periodontol 47: 687, 1976.
260. Poison, A. M., Adams, R. ., and Zander, . .: Osseous
repair in the presence of active tooth hypermobility. J Dent Res 58:
Special Issue A: Abst. No. 125, 1979.
261. Ramfjord, S. P., Knowles, J. W., Nissle, R. R., Shick, R. .,
and Burgett, F. G.: Longitudinal study of periodontal therapy. J
Periodontol 44: 66, 1973.
262. Poison, A. M., Kantor, . E., and Zander, . .: Periodontal
repair after reduction of inflammation. J Periodont Res 14: 520, 1979.
263. Waerhaug, J.: The infrabony pocket and its relationship to
trauma from occlusion and subgingival plaque. / Periodontol 50: 355,
1979.
264. Glickman, I., Smulow, J., Vogel, G., and Passamonti, G.: The
effect of occlusal forces on healing following mucogingival surgery. J
Periodontol 37: 319, 1966.
265. Kohler, C, and Ramfjord, S.: Healing of gingival mucoperiosteal flaps. Oral Surg 13: 89, 1960.
266. Lindhe, L, and Ericsson, L: The influence of trauma from
occlusion on reduced but healthy periodontal tissues in dogs. J Clin
Periodontol 3: 110, 1976.
267. Deshields, R.: A study of root rsorption in treated Class II,
Div. I malocclusions. Angle Orthod 39: 231, 1969.
268. Sjolien, T. and Zachrisson, B.: Periodontal bone support and
tooth length in orthodontically treated and untreated persons. Am J
Orthod 64: 28, 1973.
269. Trosello, U., and Gianelly, .: Orthodontic treatment and
periodontal status. J Periodontol 50: 665, 1979.
270. Zachrisson, B., and Alnaes, L.: Periodontal conditions in orthodontically treated and untreated individuals. I. Loss of attachment,
25:
165, 1974.
1973.
271.
Zachrisson, B., and Alnaes, L.: Periodontal condition in orthoindividuals. II. Alveolar bone loss.
272. Zachrisson, S., and Zachrisson, B.: Gingival condition associated with orthodontic treatment. Angle Orthod 42: 26, 1972.
273. Brown, I.: The effect of orthodontic therapy on certain types
of periodontal defects. I. Clinical findings. J Periodontol 44: 12, 1973.
274. Ingber, J.: Forced eruption: Part I. A method of treating
isolated one- and two-wall intrabony osseous defectsrationale and
case report. J Periodontol 45: 199, 1974.
275. Ingber, J.: Forced eruption: Part II. A method of treating nonrestorable teethperiodontal and restorative considerations. J Periodontol 47: 203, 1976.
276. Atherton, J. D. The gingival response to orthodontic tooth
movement. Am J Orthod 58: 199, 1970.
277. Knowles, J. W.: Oral hygiene related to long-term effects of
periodontal therapy. J Mich Dent Assoc 55: 147, 1973.
278. Garnick, J. J.: Use of indexes for plaque control. J Am Dent
Assoc 86: 1325, 1973.
279. Hazen, S. P.: Indices for the measurement of gingival inflammation in clinical studies. J Periodont Res (9, suppl.) 14: 61, 1974.
280. Lenox, J. ., and Kopczyk, R. .: A clinical system for scoring
a patient's oral hygiene performance. J Am Dent Assoc 86: 849, 1973.
281. Loe, .: The gingival index, the plaque index and the retention
index system. J Periodontol 38: 610, 1967.
282. Mandel, I. D.: Indices for the measurement of soft accumulations. J Periodont Res (9, Suppl.) 14: 9, 1974.
283. O'Leary, T. L, Drake, R. B., and Naylor, J. E.: The plaque
control record. J Periodontol 43: 38, 1972.
284. Ramfjord, S. P.: The periodontal disease index (PDI). J Periodontol 38: 602, 1967.
285. Listgarten, . .: Structure of the microbial flora associated
with periodontal health and disease in man. J Periodontol 47: 1, 1976.
286. Listgarten, . ., and Hellden, L.: Relative distribution of
bacteria at clinically healthy and periodontally diseased sites in humans. J Clin Periodontol 5: 115, 1978.
287. Fine, D. H., Tabak, L., Oshrain, H., Salkind, ., and Siegel,
.: Studies in plaque pathogenicity. I. Plaque collection and limulus
lysate screening of loosely adherent plaque. J Periodont Res 13: 17,
1978.
288. Carranza, F. ., Jr.: Glickman's Clinical Periodontology, ed 5.
Philadelphia, London, Toronto, W. B. Saunders Co., 1979.
289. Goldman, . M., and Cohen, D. W.: Periodontal Therapy. St.
Louis, Toronto, London, C. V. Mosby Co., 1980.
290. Grant, D. ., Stein, I. B., and Everett, F. G.: Periodontics, ed
5. St. Louis, Toronto, London, C. V. Mosby Co., 1979.
291. Ramfjord, S. P., and Ash, . M., Jr.: Periodontology and
Periodontics. Philadelphia, London, Toronto, W. B. Saunders Co.,
1979.
292. Glavind, L., and Loe, .: Errors in the clinical assessment of
periodontal destruction. J Periodont Res 2: 180, 1967.
293. Carter, H. G., and Barnes, G. P.: The gingival bleeding index.
J Periodontol 45: 801, 1974.
294. Muhlemann, H. R. and Sons, S.: Gingival sulcus bleedinga
leading symptom in initial gingivitis. Helv Odontol Acta 15: 107, 1971.
295. Singh, S., Cianciola, L., and Genco, R.: The Suppurative
index: An indicator of active disease. J Dent Res 53: (Special Issue B)
200, 1977.
296. Armitage, G. C, Svanber, G., and Le, H.: Microscopie evaluation of clinical measurement of connective tissue attachment levels.
J Clin Periodontol 4: 173, 1977.
297. Magnusson, I., and Listgarten, . .: Histological evaluation
of probing depth following periodontal treatment. J Clin Periodontol
7: 26, 1980.
298. Robinson, P. J., and Vitek, R. M.: The relationship between
gingival inflammation and resistance to probe penetration. J Periodont
Res 14: 239, 1979.
498
J. Periodontol.
August, 1982
299. Spray, J. R., Garnick, J. J., Doles, L. R., and Klawitten, J. J.:
Microscopic demonstration of the position of periodontal probes. J
1956.
325. Schaffer, . M.: Histological results of root curettage of human
teeth. / Periodontol 21: 296, 1956.
326. Schaffer, . M.: Periodontal instrumentation: scaling and root
1967.
327. Schallhorn, R. G., Hiatt, W. H., and Boyce, W.: Iliac transplants in periodontal therapy. J Periodontol 41: 566-580, 1970.
328. Aleo, J. J., and Vandersall, D. C: Cementum: Recent concepts
related to periodontal disease therapy. Dent Clin North Am 24: 627,
1980.
329. Bjorn, H.: Surgical handling of marginal Periodontitis (trans).
Tandlak Tidn 59: 996, 1967.
gingivectomy technique
Volume 53
Number 8
499
500
J. Periodontol.
August,
1982
Volume 53
Number 8
501
494. Sullivan, H., Dinner, D., and Carman, D.: Clinical evaluation
of the laterally positioned flap. IADR Abstr. No. 466, 1971.
495. Caffesse, R. G., and Guinard, . .: Treatment of localized
gingival recessions. Part II. Coronally repositioned flap with a free
gingival graft. J Peridontol 49: 357, 1978.
496. Espinel, M. C: Lateral Sliding Flaps With and Without Free
Gingival Grafts. M. S. Thesis, The University of Michigan, Ann Arbor,
1979.
497. Caffesse, R. G., and Guinard, . .: Treatment of localized
gingival recessions. Part IV. Results after three years. J Periodontol 51:
167, 1980.
498. Matter, J.: Free gingival graft and coronally repositioned flap.
A two year follow-up result. / Clin Periodontol 6: 437, 1979.
499. Pfeifer, J. S., and Heller, R.: Histologie evaluation of full and
partial thickness lateral repositioned flaps: A pilot study. J Periodontol
42: 331, 1971.
500. Wilderman, M. N, and Wentz, F. M.: Repair of a dentogingival defect with a pedicle flap. J Periodontol 36: 218, 1965.
501. Listgarten, M.: Electron microscopic study of the junction
between surgically denuded root surfaces and regenerated periodontal
tissue. J Periodont Res 1: 68, 1972.
502. Mrtis, C, et al.: Free transplantation of lyophilized dura for
vestibuloplasty: A clinical and histological study. J Oral Surg 37: 646,
1979.
503. Baer, P., et al.: Histologie healing of a human sclera graft
against a root surface. J Dent Res 58: Special Issue A, 346, 1979, Abstr.
504. Ainamo, J., and Le, H.: Anatomical characteristics of gingiva.
A clinical and microscopic study of the free and attached gingiva. J
Periodontol 37: 5, 1966.
505. Bowers, G. M.: A study of the width of attached gingiva. J
Periodontol 34: 210, 1963.
506. Lang, N. P., and Le, P.: The relationship between the width
of keratinized gingiva and gingival health. J Periodontol 43: 623, 1972.
507. Grevers, .: Width of Attached Gingiva and Vestibular Depth in
Relation to Gingival Health. Thesis, University of Amsterdam, 1977.
508. Miyasato, M., Crigger, M., and Egelberg, J.: Gingival condition
in areas of minimal and appreciable width of keratinized gingiva. J
Clin Periodontol 4: 200, 1977.
509. Dorfman, H., Kennedy, J., and Bird, W.: Longitudinal evaluation of free gingival autografts. J Clin Periodontol 1: 316, 1980.
510. Maynard, J. G., and Ochsenbein, C: Mucogingival problems,
prevalence and therapy in children. J Periodontol 46: 543, 1975.
511. Boyd, R.: Mucogingival considerations and their relationship
to orthodontics. J Periodontol 49: 67, 1978.
512. Dorfman, H: Mucogingival changes resulting from mandibular incisor tooth movements. Am J Orthod 14: 286, 1978.
513. Caffesse, R. G.: Fundamentos actuales de la ciruga mucogingival. Rev Asoc Odontol Argentina 64: 180, 1976.
514. Lindhe, J., Hamp, S. E., and Le, .: Plaque-induced periodontal disease in beagle dogs. A 4-year clinical, roentgenographical
and histometrical study. J Periodont Res 10: 243, 1975.
515. Saxe, S. R., Greene, J. C, Bohannan, H. M., and Vermillion,
J. R.: Oral debris, calculus and periodontal disease in the beagle dog.
Periodontics 5: 127, 1967.
516. Glavind, L.: Effect of monthly professional mechanical tooth
cleaning of periodontal health in adults. J Clin Periodontol 4: 100,
1977.