Proceedings From The

State of the Art Workshop

on

Surgical Therapy for Periodontitis

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:

Goals of WorkshopDr. Irwin Mandel,

Workshop Chairman

Report of Task ForceDr. William McHugh, Task Force Chairman

Dr.
Dr.
Dr.
Dr.
Dr.

Paul RobertsonIntroduction
Bruce PihlstromNo Therapy
Stanley HazenInitial Therapy; Alternative Therapies
Saul Schluger and Dr. Raul CaffessePeriodontal Surgery
Jack Caton, Jr.Maintenance Therapy

Research

Papers

Dr. Raul Caffesse for Dr. Sigurd RamfjordClinical Applications of Recent

Periodontal Research
Dr. Bengt RoslingThe Important Relationship Between Surgical Results and
Maintenance CareBased on a Six Year Study
Dr. William AmmonsLongitudinal Evaluation of Osseous Resective Surgery & Open

Flap Curettage

Dr. Timothy O'LearyTreatment of the

Periodontally Involved Root Surfaces

476

Volume 53

Surgical Therapy for Periodontitis

Number 8

Review & Critiques of Workshop

Dr. Robert Genco
Dr. Helmut Zander
Audience

Participation

This workshop report includes the Background Paper authored

the Summary Recommendations concluded by the Review Panel.

by the Task Force and

WORKSHOP BACKGROUND PAPER

Task Force
William D. McHugh, D.D.S., Chairman, Eastman Dental Center, Rochester
Raul G. Caffesse, D.D.S., University of Michigan, Ann Arbor
Jack G. Caton, Jr., D.D.S., Eastman Dental Center, Rochester
Stanley P. Hazen, D.D.S., University of Detroit, Detroit
James T. Mellonig, D.D.S., U.S. Navy, Great Lakes
Bruce L. Pihlstrom, D.D.S. University of Minnesota, Minneapolis
Richard R. Ranney, D.D.S., Virginia Commonwealth University, Richmond
Paul B. Robertson, D.D.S., University of Connecticut, Farmington
Saul Schluger, D.D.S., University of Washington, Seattle

PREFACE TO THE WORKSHOP BACKGROUND PAPER

Chronic Periodontitis, the most common cause of tooth loss, is a widely prevalent disease
of the tissues supporting the teeth. Caused principally by bacterial plaque, it is aggravated
by several conditions in the host. Treatment is aimed at removing the bacterial plaque and
restoring the tissues to a healthy condition which can be maintained throughout life.
Gingivitis and the earliest stages of Periodontitis usually can be treated effectively
without surgery, but more advanced Periodontitis is usually treated by some type of surgery
which will facilitate the removal of both soft and calcified bacterial deposits from tooth
surfaces. Only when these deposits are removed and the levels of bacterial plaque are
reduced to a minimum can the disease be controlled.
Surgical treatment also aims at restoring the supporting tissues to a healthy state and at
maintaining that state on a long-term basis. There are two categories of surgical therapy.
One accepts the tissue destruction that has already occurred and is designed only to restore
the supporting tissues to health at a "reduced" level. The other attempts to repair some of
the loss of attachment which has resulted from the Periodontitis.
Alternatives to surgical therapy are no treatment of any sort or treatment to remove or
control the etiologic agents without surgery.
The object of this paper is to report and evaluate the available data on the selection and
value of surgical therapy for Periodontitis and, where possible, to compare them with
alternative forms of nonsurgical therapy. The Task Force hopes thereby to determine the
relative value and appropriateness of different types of periodontal surgery.

477

478

J. Periodontol.
August, 1982

Proceedings From State of the Art Workshop

INTRODUCTION

Periodontitis is the major cause of tooth loss in adult

populations. Several clinical forms of Periodontitis have
been recognized and described. This review is directed
to chronic Periodontitis, a painless, slowly progressing
disease that is characterized by inflammation of the
gingiva caused by microbial colonization of adjacent
tooth surfaces, extending into deeper periodontal tissues,
and resulting in pocket formation, destruction of alveolar
bone, mobility of teeth, and their exfoliation.1 This process has been clinically subdivided into chronic gingivitis
and Periodontitis, depending on the probing depth relative to the cementoenamel junction. The transition from
chronic gingivitis to Periodontitis, however, is not well
understood. Historically, chronic gingival inflammation
has been considered an early phase of Periodontitis, often
termed the gingivitis-periodontitis continuum. Some evidence, however, suggests that whereas chronic gingivitis
may predispose to Periodontitis, it is a separate disease.
Both the initiation and progression of chronic gingivitis are caused by the accumulation of microorganisms
near the gingival margin. In addition, the incidence and
severity of periodontal diseasewhether it be gingivitis,
Periodontitis, or loss of alveolar bonehave been correlated with lack of oral hygiene. Except for microbial
plaque no specific causal organisms or related pathogenic
pathways have been clearly indicted. Since microorganisms are rarely found within periodontal tissues, the
destruction of supporting structures associated with Periodontitis is generally assumed to result from the pathologic products of the oral microflora. Such products may
originate from exogenous organisms not normally present in the oral flora or from increased numbers of certain
species in the indigenous flora. Distinct patterns of flora
associated with periodontal health, gingivitis, and Periodontitis have not been clearly demonstrated, but the
available evidence favors the role of indigenous microflora rather than a more classical infection by specific
exogenous organisms. Once established in sufficient
numbers, the products of the "disease-associated" flora
may cause destruction of periodontal tissues directly or
by activating host-response mechanisms. Both the constitution of the flora and the modulation of the host
response may be affected by several other mechanisms
including local oral environment, neutrophil function,
and general systemic alterations.
Before effective prevention and treatment can be formulated, the microflora and related pathogenic mechanisms responsible for periodontal disease must be identified. For example, targeted therapeutic approaches
would be feasible if gingivitis and Periodontitis are separate entities, each initiated by specific microbial species
or mediated by particular pathogenic pathways. The
presence of active disease could be determined by evaluating the periodontal microflora or other pathogenic
agents, and antimicrobial therapy could be directed
against particular causal organisms. Currently, we still

knowledge; as a result, the fundamental principle underlying all therapy of Periodontitis is broad
lack such

control of the oral microflora.

Natural

History and Epidemiology of Periodontitis

Diseases of the periodontium are among the most

common afflictions of mankind. Bone rsorption consistent with Periodontitis has been observed in the fossil
remains of Neanderthal man, and detailed descriptions
of periodontal disease in Chinese and Egyptian writings
predate this conference by over 4,000 years.2,3 Epidemiologica! surveys conducted during this century suggest
that essentially all the world's adult population have
experienced some form of periodontal disease.4,5
The natural history of periodontal disease over an age
range of 15 to 40 recently has been described in longitudinal studies of populations in Norway and Sri Lanka.6
The groups had major geographical, cultural, socioeconomic, and educational differences and represented extremes with respect to dental care. The predominant
periodontal diseases reported in both populations were
chronic gingivitis and Periodontitis. Indeed, in the Norwegian group, no cases of acute gingivitis or rapidly
progressing Periodontitis were noted. Destruction of supporting structures associated with chronic Periodontitis
was continuous and progressed at a relatively even rate
over time in both groups, although annual rates of
periodontal attachment loss were significantly different,
averaging 0.09 mm in the Norwegian population and
0.25 mm in Sri Lankans.
In general, interpretation of epidemiological studies is
complicated by deficiencies in indices used for the measurement of periodontal disease and the assumption,
made in most studies, that all pathosis affecting the
periodontium is a single entity. Nevertheless, despite a
variety of experimental approaches using populations
with divergent cultural, socioeconomic, and geographic
backgrounds, the results of epidemiological surveys have
been remarkably uniform with respect to the universality
of periodontal disease and the strong positive correlation
between periodontal disease and both age and the presence of microbial plaque.7"11 Gingivitis affects the majority of young children and, by 20 years of age, the
prevalence of gingivitis approaches 100%. While the
development of Periodontitis in children is relatively
uncommon, pocket formation and related bone loss in
the teenage population has been estimated at approximately 6%. The prevalence of Periodontitis increases
almost linearly with age and, in the adult population,
accounts for well over 50% of missing teeth. The strong
correlation between age and alveolar bone loss appears
to reflect the cumulative result of plaque-induced inflammation rather than diminished resistance in older individuals.
The relation between periodontal disease and other
social and demographic factors is less clear. In western
cultures, the disease is less severe in females than in

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

Plaque Factors. Dental plaque, a general term for

tooth-adherent material composed principally of microorganisms and microbial products, is the primary etiological agent in gingivitis and Periodontitis. Evidence
implicating oral microflora12"14 includes the epidemiologica! observations previously discussed, the induction of
the disease process solely by allowing the accumulation
of bacteria15"18 and the reversal of the periodontal lesion

by mechanical19"22

or

chemotherapeutic plaque

re-

moval.23"26 Individuals who initially demonstrated excel-

lent periodontal health consistently developed gingivitis

by 1 to 3 weeks after all methods of plaque control were
withdrawn; when oral hygiene measures were reinstituted, gingival health was restored within 10 days.
The microbiological contents of plaque appear to vary
widely among individuals and among sites within the
same individual. Moreover, in periodontally involved
sites, the supragingival microflora is different from that
found subgingivally. In addition, recent evidence suggests that different forms of periodontal disease, including chronic gingivitis and Periodontitis, have specific
microbial etiologies.
The subgingival microflora obtained immediately before experimental gingivitis is induced and associated
clinically with gingival health, where some supragingival
plaque is present, is composed mainly of Gram-positive
organisms, especially species of streptococcus.27'28 Both
chronic gingivitis and Periodontitis are characterized by
an increasing shift of the subgingival microflora to the
Gram-negative community. Gram-negative facultative
and anaerobic rods have been reported to comprise
approximately 40% of the cultivable subgingival microflora in chronic gingivitis29 and from 65 to 75% of the
subgingival flora in chronic Periodontitis.30'31 Species of
Bacteroides, Actinomyces, Haemophilus, Eubacterium, Selenomonas, Treponema, and Fusobacterium are reportedly prominent in chronic disease, but no specific organisms or groups of organisms have been indicted for the
initiation of gingivitis or its progression to Periodontitis.
Nonplaque Factors. Both epidemiological and experimental studies have failed to demonstrate any local or
systemic factors, aside from microorganisms, that cause
gingivitis or Periodontitis. Several of these factors, however, including anatomic oral abnormalities, mouthbreathing, dental appliances, and certain systemic conditions, may modify the progress of the disease once
established.32 In many cases, modifying local factors such
as defective restorations, prosthetic appliances,
ligatures
and calculus may interfere with the patient's ability to
remove plaque or may provide an environment that

Surgical Therapyfor Periodontitis 479

facilitates the establishment of a more pathogenic flora.
The latter may also account for the increased severity of
gingivitis and Periodontitis associated with hormonal

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

There is little evidence that nutritional deficiencies

either initiate or affect periodontal disease.42

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.

Proceedings From State of the Art Workshop

the host response to products of oral microorganisms
plays a major role in the destruction of collagenous and

480

connective tissue which characterizes established

lesions.45 Agents elaborated by microorganisms appear to traverse the junctional epithelium and
may interact with various host cells which in turn mediate the destruction of the periodontium. Immune and
nonimmune host mechanisms have been postulated for
virtually all events in the disease process on the basis
mainly of in vitro observations. No single substance or
mechanism has been indicted, however; their involvement probably varies according to time, site, and the
types of microorganisms colonizing the area.
osseous

and advanced

Conclusions

predominant periodontal diseases, chronic ginand

givitis
Periodontitis, are found in all populations and
are among the most common diseases of mankind. Gingivitis frequently appears during the first decade of life;
world-wide, Periodontitis is responsible for the majority
of tooth loss in adults.
2. Chronic gingivitis and Periodontitis are initiated
and perpetuated by oral microorganisms. Epidemiological studies have shown a strong correlation between lack
of oral cleanliness and these periodontal diseases. Differences in prevalence and severity, based on such demographic characteristics as sex, race, geographical area,
and socioeconomic class, virtually disappear when
groups are distributed according to levels of oral hygiene.
No single organism or specific group of organisms, however, has been clearly identified as responsible for periodontal disease.
3. A wide variety of both immune and nonimmune
inflammatory responses of the host to microbial products
can cause the clinical changes associated with periodontal disease. There are few direct data, however, that
strongly implicate any one substance or mechanism.
4. It is not clear which microbiological and host factors mediate the progression from gingivitis to Periodontitis or account for the different rates of periodontal
destruction. Current treatment of gingivitis and Periodontitis, therefore, must include control ofthe microbial
flora on a broad basis rather than a narrowly targeted
effort to control particular microbial species.

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 to Control Etiologic Factors

The purpose of initial therapy is to remove and control

the etiological agents responsible for Periodontitis and to
establish an oral environment that facilitates oral cleanliness.
Plaque Control. Microbial plaque is the principal etiagent of inflammatory periodontal disease,17'
ological
is, 27,87-90
fjjg routine daily prevention or removal of
the
tooth surface by the patient is a sine qua
on
plaque
non in
Achieving this
periodontal
the
is
a
of
self-care
major objective of
by patient
aspect
the presurgical phase of treatment.
The mechanical approaches for controlling dental
plaque formation are the most applicable methods available to the patient and the clinician. Such methods
include the use of devices that remove microbial plaque
from the tooth surface: tooth brushes, flosses, wooden
points, rubber tips, toothpicks, interproximal brushes,
yarn, and many others. These devices require different
levels of motor skills. The daily routines that must be
established require the patient to be diligent, motivated,
educated, and skillful.
The achievement of adequate mechanical plaque control requires an oral environment that enables the patient
to remove plaque. Calculus must be professionally removed and the plaque-retaining areas on the teeth, such

therapy.52'54,57'91'92

Volume 53
Number 8

inadequate margins and contours of restorations, must

be eliminated.93"99
The reduction of plaque levels will decrease gingival
inflammation. Frequent careful scaling, root planing and
polishing of teeth, and closely monitored patient plaque
control efforts have been shown to control gingival inflammation effectively19'22 49'100"104 and to retard or halt
attachment loss.49'103'104 Although such rigorous programs effectively control plaque and maintain periodontal health, they involve a heavy investment of dental
manpower and, therefore, are beyond the limits of practicability; hence the "search for a practical method of
maintaining optimum oral health remains a challenge."105 The cost-effectiveness of such programs for a
nation's population is not fully known106,107 except as an
arithmetic exercise based on the extension of the cost of
the methods applied in such a study to an entire population. Even so, such costs appear prohibitive.108
The monitoring of the effectiveness of plaque control
measures is important for both the patient and the
dentist. The patient's self-evaluation requires some type
of plaque disclosant.109"111 The dentist may select from a
variety of indices that assess the quantity of supragingival
plaque.111"114 A microscope may be used to provide
qualitative information on both supra- and subgingival
plaque. Certain classes of microorganisms31'115'116 appear
to be associated with defined severity levels of periodontal diseases. The Gram-positive flora of the "healthy"
state changes to a motile Gram-negative flora with spirochetes in the "diseased" state. It would be diagnostically beneficial if the therapist could have a simple
means of evaluating the quantity and quality of the
microbial deposits on the teeth with respect to their
pathogenic potential. A simple, objective method easily
usable in office or field is needed to determine whether
active disease is present, whether treatment is necessary,
and when treatment is completed.
Finally, it must be recognized that the application of
current plaque control methods
(especially of mechanical
involves a modification of human behavior.117"
methods)
125
A plaque control approach may be highly effective,
but if the patient will not or cannot apply it in his or her
own mouth, it is ineffective for that
person.
Scaling and Root Planing. Scaling and root planing are
procedures routinely used in periodontal therapy. Scaling is the removal of calculus, bacteria, and their products from the root surface; root planing is the smoothing
of roughened root surfaces.126 In practice, the procedures
are often combined as a single operation. Their
purpose
is to alter the local environment associated with periodontal inflammation and thereby control the destructive effects of the latter. Specifically, the environmental
factors associated with inflammation include bacterial
plaque,8'9'18'87'88 127"12998' its
products,130"134 and calcified
plaque or calculus.88' 128'135-138 Other factors, such as
defective restorations, are also associated with periodontal disease94'139-146 and are often corrected during scaling
and root planing.
as

Surgical Therapyfor Periodontitis 481

Dental plaque, its products, and calculus are closely
associated with the tooth surface adjacent to periodontal

inflammation. The adherence of dental plaque to tooth

surfaces is usually mediated by a salivary glycoprotein
pellicle and interbacterial matrix.147"156 The root surface
itself may adsorb bacterial products that appear to be
toxic.107"162 Bacterial endotoxin is a potential pathogenic
agent that can be identified on cementum adjacent to
periodontal pockets.108 Calculus can be attached to the
surface of teeth by several mechanisms including attachment by pellicle and penetration into intact, resorbed, or
separated areas of cementum.163"170 Moreover, calculus
is often closely related to the tooth structure in its organic
and crystalline components.167
Clinically, mechanical debridement is used to remove
or alter the local factors associated with
periodontal
inflammation. Scaling and root planing are meticulous
and time-consuming procedures that are limited by the
technical skill of the operator and the accessibility of
root surfaces adjacent to periodontal pockets. Even after
extensive scaling and root planing, calculus can be microscopically observed on root surfaces.171 Various mechanical means of scaling and root planing include hand
and ultrasonic instrumentation. Although the root
smoothness obtained by these methods differs,172"181 such
differences appear to have only slight biologic significance in supragingival plaque retention or periodontal
inflammation.182,183 Both techniques remove calculus,173, 179-181184 but hand instruments are more effective
in removing calculus185 and endotoxin.186
Scaling and root planing may affect the bacterial flora
associated with periodontal inflammation. When the root
surfaces adjacent to periodontal pockets are subjected to
these procedures, the subgingival bacterial flora is altered
significantly. This alteration includes a shift of the predominant flora from Gram-negative anaerobic and motile forms to Gram-positive aerobic and nonmotile
forms.187"190 More specifically, the number of bacteroides
and spirochetes is sometimes markedly reduced as a
result of regular instrumentation.190 This alteration of the
flora is accompanied by improved periodontal health,
namely, reduced inflammation and pocket depth.187"189
In addition, thorough scaling and root planing reduce
the endotoxin level of root surfaces.161,186 In other words,
the quality of the bacterial flora as well as the potentially
toxic material associated with root surfaces adjacent to
periodontal pockets is significantly altered by scaling
and root planing.
The clinical effectiveness of scaling and root planing
as a separate
therapeutic entity is somewhat difficult to
assess. This is because it is routinely used in conjunction
with oral hygiene measures that, when used alone, have
a significant effect in
reducing inflammation.21'101,191-196
However, oral hygiene measures alone are not as effective in reducing pockets and inflammation as when
accompanied by professional care.197'198 The reduction
in gingival inflammation by scaling and root planing
combined with oral hygiene is well-documented.48'102'

Proceedings From State of the Art Workshop

183,197-202 short-term studies have shown that
scaling and
root planing, combined with oral hygiene, also result in
decreased pocket depth183 197 198,201"203 and increased
levels of "clinical attachment."193,198,201,202,204 This gain
in attachment is associated with a long junctional epithelial adaptation to the root surface.205 When compared
with baseline data acquired before therapy, the available
data on longer term results of scaling and root planing
indicate that the procedure can at least maintain attach-

J. Periodontol.

August,

482

ment

level204 and prevent further increases in pocket

depth.19,55,206"209

Chemotherapy. The prospect of using a chemical agent

control dental microbial plaque is a pleasant one
because it would not require the high level of motivation

to

skills necessary for mechanical methods of

The search for such an agent has been
control.
plaque
for
pursued nearly a century.
Miller, in 1889,210 proposed the use of antibacterial
substances against the "parasites" associated with caries.
He believed that such agents would not only arrest decay
but prevent it. Effective "antiseptic" agents of that time,
such as bichloride of mercury, were too toxic; the search
for a substitute has persisted.
Numerous chemical agents have since been tested but
with mixed results. The most promising, Chlorhexidine,
has been the most consistently effective; however, it is
not available for patient care in the United States. Several studies have demonstrated significant reduction in
supragingival plaque and improved gingival health when
it was used as an oral rinse or applied topically at various
concentrations of 0.015%, 0.1%, 0.2%, 1%, and 2%.26,2U"
214
When it is used, bacteria do not colonize the teeth,215
and it has had a marked bactericidal effect on salivary
microorganisms.214 However, the daily application of a
2% Chlorhexidine solution did not inhibit subgingival
plaque formation in dogs.216 When incorporated into a
gel or dentifrice, Chlorhexidine was not as consistently
effective as the rinse.217,218
Because of the undesirable side effects of Chlorhexidine,20 compounds with a similar chemical structure but
without such effects have been sought to achieve the
same plaque prevention. Such a substance, alexidine,
219, 220
was used as an oral rinse in clinical studies.23,
When used in a concentration of 0.035% or 0.05%, it
reduced plaque levels significantly, but consistent results
in the reduction of gingival inflammation were not observed; alexidine was clearly less effective than Chlorhexidine.
Many other chemical agents have been tested for their
but the results have not
plaque-inhibiting properties,
been encouraging 20, 221-227 Antibiotics were also used
both topically and systemically to control the microbial
population of dental plaque. Oral rinses of 0.5% tetracycline, 0.5% vancomycin, or 0.25% polymyxin were
used three times a day for 5 days by human subjects.16
All three reduced plaque formation, tetracycline more
effectively than the others. Vancomycin depressed the
Gram-positive organisms and masses of Gram-negative
and

motor

1982

cocci, rods, and filaments, but fusobacterium-like organisms proliferated. Polymyxin

caused a proliferation
of the Gram-positive cocci and short rods and depressed
the growth of Gram-negative microorganisms. The microbial population of the controls was similar to that
described earlier in a study of experimental gingivitis in
man.

Other antibiotics tested222, 228-231 had no significant

plaque inhibition. Tetracycline appeared to be the most
promising, but when taken systemically, it had little
effect on the results of a study in which it was tested
against scaling procedures.201 Further studies187 that included microbial and histological observations noted a
significant effect on microbial composition during drug
ingestion. The proportions of coccoid cells were higher
and those of motile rods and spirochetes lower than
pretreatment levels. The flora reverted to baseline levels
after the tetracycline was discontinued. Many organisms
developed resistance to the antibiotic.232
Concern about the prolonged use of systemic antibiotics has led to attempts for their slow release in extremely
small quantities in the pocket area.233,234
Salt and hydrogen peroxide were used years ago to
control or modify the microorganisms involved in Periodontitis.235 Recently, Keyes236'237 has combined the use
of these classical medicaments with microscopic monitoring of the pocket flora to follow changes in the type
and number of these microorganisms and to help motivate the patient to maintain high levels of plaque control.
This approach is attractive in its simplicity, but its value
has not been demonstrated in controlled studies.
Occlusa! and Orthodontic Therapy. Occlusal forces of
sufficient magnitude can cause periodontal injury, which
is called occlusal trauma.238,239 Histologically, this lesion
in the periodontal ligament ranges from a slight derangement of the ligament to an area of necrosis.240,241 Occlusal
therapy to manage this lesion consists of several procedures designed principally to redistribute forces on the
teeth: occlusal adjustment, control of parafunctional
habits, orthodontics, splinting, and occlusal rehabilitation by restorative procedures.242
When the lesion of trauma occurs in a normal periodontium (primary occlusal trauma),126 morphologic alterations occur in the periodontal ligament and alveolar
bone.40, 60, 241,243-248 These are reversible when the force
is discontinued or the tooth moves away from the displacing force.41,249'250 Periodontal pockets are not formed
nor is connective tissue attachment lost as a result.40,245,
247,248,251,252 Tncrease(i t00th
mobility and the roentgenographic appearance of a widened periodontal ligament
space are the clinical manifestations of primary occlusal
trauma. They represent an adaptation by the periodontium to accommodate the excessive forces acting upon
the tooth. In this state of increased mobility, the lesions
of trauma are replaced by widened periodontal ligaments
and decreased bone density to accommodate the displac-

ing forces.40,60,249
Secondary occlusal trauma has been defined as normal

Volume 53

Surgical Therapy for Periodontitis

Number 8

occlusal forces traumatizing the attachment apparatus of

teeth weakened by the loss of support.126 When the lesion
of trauma is superimposed on a healthy but reduced
periodontium, the same morphologic alterations occur as
in primary occlusal trauma but with no changes in the
level of connective tissue attachment.253'254
When the lesion of trauma occurs in conjunction with
Periodontitis, 240, 255-259 the progress of existing chronic
Periodontitis may be accelerated and intrabony pockets
with angular bone loss may result. Studies with squirrel
monkeys39 and beagles258 have suggested that when
trauma is associated with marginal Periodontitis, the
amount of alveolar bone loss is increased; however, some
differences in the loss of connective tissue attachment
have been reported. Trauma superimposed on Periodontitis caused an increased loss of connective tissue attachbut not in the squirrel monkey.258
ment in the
in
animals
have indicated that in the
Investigations
of
management Periodontitis accompanied by tooth hyresolution of inflammation must be emphapermobihty,
259'260 these results
sized;41'
agree with studies relating to
the control of Periodontitis in human subjects.52' 54' 261
After therapeutic techniques designed to resolve marginal inflammation have been accomplished, bone regeneration accompanied by a significant decrease in tooth
hypermobihty can occur.52' 54' 57' 79' 92' 261"263 Osseous
repair was observed throughout the circumferential extent of intrabony pockets around hypermobile teeth, and
even though there was no occlusal therapy, the mobility
of each tooth decreased in proportion to the amount of
repair.79 Moreover, increased tooth mobility does not
seem to alter the level of connective tissue attachment
No eviduring healing after periodontal
dence to support temporary stabilization as a biologic
aid in periodontal healing after surgery is available.
Current knowledge of the management of Periodontitis alone or in combination with trauma indicates that
the control of inflammation should be the principal
objective. Such control may cause a significant decrease
in tooth mobility. Any residual tooth hypermobihty may
be due to the loss of periodontal support from periodontal disease. Since this mobility will not initiate further
periodontal pocket formation, there is no scientific basis
for reducing it to preserve periodontal health. The management of any remaining mobility can be justified only
on the basis of function and comfort, and to halt any
patterns of increasing mobility that may lead to tooth
avulsion.
There is no substantial evidence to indicate that orthodontic therapy improves periodontal health. On the contrary, several studies report loss of attachment, bone
recession, gingivitis, and root rsorption as a result of
orthodontic
Scientific information on the role of orthodontic therapy in the treatment of Periodontitis is scarce. Both
increased270 and decreased273 pocket depth have been
reported after tooth movement. Forced eruption has
been used to reduce or repair angular bony defects and

beagle,39

surgery.264"266

therapy.267"272

483

aid in the management of fractured teeth.2

Significant changes can occur in the configuration of bone
and gingival tissues as a result of orthodontic therapy.271,
274, 276
Therefor^ orthodontic therapy should precede
periodontal surgery in the management of certain types
of periodontal defects. Inflammation should be resolved
before orthodontic therapy to avoid the possibility of
attachment loss during tooth movement. The most recent
evidence from studies on beagles and squirrel monkeys
shows that traumatic lesions and their sequelae, superimposed upon severely reduced but healthy periodontal
tissues, do not lead to further loss of connective tissue
to

attachment.250'253'254
Conclusions

1. Because the principal etiologic agent of chronic

Periodontitis is microbial plaque, plaque control measures are necessary not only to treat it but also to
maintain periodontal health.
2. Current mechanical plaque control methods are
effective when used by strongly motivated individuals.
They require such diligence and dexterity, however, that
they probably would not be an effective public health
measure.

3.
oral

Scaling and root planing, combined with adequate

hygiene measures, reduce inflammation, pocket
depth, and loss of periodontal attachment. The effectiveness of scaling and root planing is greatly influenced by
the accessibility of the root surface and the skill of the

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.

6. There is no evidence that tooth stabilization is a

biologic aid to periodontal healing after surgery or that
mobility need be reduced to preserve periodontal health.
7. There is no evidence that othodontic therapy improves periodontal health, except in some cases of isolated defects.
Rvaluation

After the initial

phase of therapy, the need for further

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

Proceedings From State of the Art Workshop

oral hygiene measures. In evaluating the level of plaque

J. Periodontol.

484

control, many clinicians use various clinical indices to

monitor the quantity of supragingival plaque.192' 278-284
Such clinical indices are of great value, but they do not
determine the pathogenicity of plaque. In periodontal
disease, specific groups of organisms appear to be associated with various levels of severity.30,31' 115' 116' 285'286 It
would be beneficial if the therapist could effectively
monitor plaque control in terms of both the quantity and
the quality of the bacterial flora with respect to its
pathogenic potential. Assays for endotoxin287 and darkfield microscopy of subgingival plaque286 have been used,
but their clinical importance has not been clearly established.
Indicators of Periodontal Inflammation. It is important
to evaluate the periodontal response to hygienic measures used by the patient and the therapist.202 The classical signs and symptoms of periodontal inflammation
include changes in gingival color, contour, and consistency as well as edema, hemorrhage, exdate, tooth mobility, pathologically deepened pockets, and continued
loss of support.202'287-291 After the initial phase of therapy,
the periodontium should be studied for evidence of these
symptoms. Subjective clinical signs are difficult to assess
in terms of objective criteria, but the clinician should
apply objective criteria whenever possible. Pocket
depth,284'292 the level of clinical attachment,284'292 and
evidence of bleeding after probing293'294 or suppuration295 can be evaluated in a fairly objective manner. The
clinician should also be aware that the penetration depth
of the periodontal probe tip may vary with the degree of
gingival inflammation and amount of force used.296-300
Changes in pocket depth and attachment level should be
viewed with this in mind when the response to initial
periodontal therapy is being reevaluated. Furthermore,
as measured by routinely used clinical techniques, tooth
mobility is subjective because such techniques lack sensitivity when applied to a single tooth.301'302 However,
these measurements may be useful for diagnosing and
treatment planning by individual practitioners.303 The
use of gingival fluid or exdate as an indicator of periodontal disease is somewhat controversial. Crevicular
fluid increases with clinical signs of gingival inflamma304-313
however, the correlation between it and
tion, 275,
of inflammation varies in published
histologie evidence
308' 310-312'314'315 Several studies also indicate
reports.307'
that crevicular fluid is a product of clinically healthy
gingival crevices.304' 306'308'316-318 Gingival fluid may represent a preinflammatory osmotic exdate as well as a
clinical inflammatory exdate.319
It would be prudent therefore, for the clinician to use
multiple criteria for periodontal evaluation. By balancing
the signs of periodontal disease with a knowledge of the
limitations involved, the experienced clinician should be
able to clinically assess the effectiveness of therapeutic
procedures. Clearly, no single clinical parameter may be
used as the sole criterion for evaluating periodontal
response to therapy.320'321

August, 1982

Needfor Further Periodontal Therapy. Whether further

periodontal therapy is necessary is a critical decision
which should be based on objective criteria. To use
pocket depth as the sole criterion upon which to base a
decision for periodontal surgery is questionable.322'323
Other criteria, such as the degree of inflammation determined by bleeding on probing, exdate, and other
changes, also warrant consideration. Furthermore, any
decision for periodontal surgery must consider specific
teeth (such as maxillary molars) which may be more at
risk from periodontal disease.62 Complete elimination of
such etiologic factors as calcified plaque (calculus) from
root surfaces is time-consuming and extremely difficult
if not impossible by nonsurgical means.171' 179' 324'325'326
One of the main objectives of periodontal surgery is to
gain access for root preparation.322 In addition, the degree of periodontal support in terms of attachment level
and osseous support can be increased by various surgical
procedures.50' 55-59' 61' 67-82'84-86'327 Surgery also appears
to be more beneficial for advanced periodontal disease
than scaling and root planing alone.55'206 Surgical therapy is, therefore, indicated when nonsurgical root preparation is not possible, when additional support is a
likely outcome of such therapy, or when the disease
process cannot be adequately controlled by other means.
Alternatives to surgery include repeated scaling and
root planing and continued attempts to control plaque.
Such therapy may be the only alternative for those
patients at surgical risk such as elderly patients or those
with a debilitating systemic disease. For them, regular
maintenance therapy, combined perhaps with localized
surgical therapy when the disease is clearly out of control,
is indicated.
The clinician must closely monitor the disease to
ensure that the measures taken to arrest periodontal
destruction are appropriate. In addition, the therapist
should be able to use one or more of the various surgical
modalities that are effective in arresting periodontal
disease and even in regenerating lost support.
Conclusions
1. The clinical signs and symptoms available to the
clinician for evaluating the periodontal response to therapy are relatively subjective. They do provide important
and valuable means of assessing the activity of Periodontitis, but more accurate and reliable methods need to be

developed.

2. The aim of periodontal surgery is to provide access

for root preparation and removal of local irritants adjacent to periodontal pockets and to provide a means of
controlling disease when nonsurgical methods are ineffective.
3. Alternatives to surgical therapy include continued
scaling and root planing at regular intervals to further
control bacterial plaque. This method, however, does not
ensure that bacteria and their products will not remain
in inaccessible areas.

Volume 53
Number 8

Periodontal

Surgery

Procedures. Various periodontal surgical procedures

available. The distinctions between them are not
always clear, and procedures are often combined. For
purposes of analysis, the major procedures will be listed
separately; the order in which they are considered does
not necessarily reflect their relative effectiveness.
Gingivectomy. The major advantage of gingivectomy
is that it provides access to the root surface.288 This is
particularly important in view of our current knowledge
of the importance of root surface preparation.157' 158' 161
186, 328 Another
advantage is that it avoids denudation of
alveolar bone and minimizes postoperative bone rsorption.329 In 1956, Glickman330 justified its use in 200 cases.
Gingivectomy is a better method than curettage for
removing relatively shallow pockets even though the loss
of attachment reported with gingivectomy did not occur
with curettage.203'209'331-337
are

Subgingival Curettage. Subgingival curettage

consists

of scraping the inner surface of the gingival wall of the

periodontal pocket to clean out, separate, and remove
diseased soft tissue and granulation tissue.242' 288'291'338340
The technique is seldom used as a single procedure
but is usually combined with scaling and/or root planing.
Over the years, the indications and uses for subgingival
curettage have included pocket reduction and new at-

tachment,336, 338' 341-343 "~c,^,Vc1

presurgical
preparation, 338, 341, 344341
242,
338,
and maintenance of
compromised cases
treated cases.341'
Reportedly, pocket reduction by
subgingival
curettage can be achieved by gingival shrink347
nrn,tmn

age336'

and/or new attachment.325'347'348

Although histologie evidence of the formation of new

epithelial and connective tissue attachment after curet349
most recent studies205,
report only the formation of a long junctional epithelium

tage has been presented,325 the

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

Surgical Therapyfor Periodontitis 485

prevent discrepancies between levels and shapes of bone
and gingiva which predispose to recurrence of pocket
depth. This involved thinning bony ledges, leveling craters, and generally reshaping marginal bone to resemble
the alveolar process undamaged by periodontal disease.
Clinical reports of successfully treated cases have
caused

these

redefined over the

of
apically positioned
years.242'339'354-360
flaps with osseous recontouring in reducing overall
pocket depth and improving tissue contour has provided
a periodontal environment which can be maintained in
health. This approach, however, involves some loss of
tenets

The

to

be

success

attachment.50'59,92'203

There is some concern that osseous resection can lead

excessive and continued tooth mobility.361 However,
studies of mobility after osseous surgery show that while
the mobility increases in the first few weeks after surgery,
it returns to presurgical levels in about 6 months.59'362
Open-Flap Curettage. Open-flap curettage is the reflection of a flap with minimal removal of marginal
gingiva to expose and provide access for debridement of
root surfaces and adjacent periodontal defects. The indications for open-flap curettage have been summarized09' 363 and include patients with advanced periodontal disease in whom resective surgical procedures might
jeopardize the results of treatment; anatomic defects
capable of repair; and conditions where preservation of
tissue is important because of esthetics, particularly in
anterior areas.
From a practical standpoint, the modified Widman
flap is similar to open-flap curettage. Thus, results of
clinical studies of the modified Widman flap can be
to

regarded as applicable to open-flap curettage.

Modified Widman Flap. The chief objective of the
modified Widman flap operation is not pocket elimination per se but maximum healing of periodontal pockets
with minimal loss of periodontal tissues during and after
surgery.

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-

Proceedings From State of the Art Workshop

ulous oral hygiene is maintained, the interdental tissues
will repair over a few months with gain rather than loss
of clinical attachment.364'366 Despite its failure to improve tissue contour, the modified Widman procedure is
as successful as the apically positioned flap procedure
with respect to plaque control, gingivitis scores, and

J. Periodontol.
August, 1982

486

maintenance of attachment levels.347

The modified Widman flap has been evaluated
in longitudinal studies begun in 1961 by Ramfjord
366-369
and many co-workers.50'51-m- ** 261'291m' 342> 364'
Short-term clinical comparisons of different surgical modalities have indicated that pocket depth was reduced
more effectively by pocket elimination surgery than by
either the modified Widman flap or subgingival curettage.367 With regard to attachment level, these short-term
results were better with subgingival curettage than with
the modified Widman flap. Pocket elimination surgery
produced some initial loss of clinical attachment.367
Eight-year results on pocket reduction and level of
clinical attachment show that the effects from the modified Widman flap were similar to those from pocket
elimination surgery. Subgingival curettage was not as
effective as the other two procedures, especially in deep
pockets and molar regions.51
Histologie evaluation of the modified Widman flap in
nonhuman primates has demonstrated healing by means
of a long, thin junctional epithelium to the depth of the
surgical wound with no gain in connective tissue attachment and no increase in crestal bone height.200'370 Bone
repair varied within intrabony pockets, but a junctional
epithelium is always interposed between the new bone
and root surface.370 Longitudinal studies suggest that this
epithelial adherence can be maintained with little or no

change over time.50' 51'322'347

Excisional New Attachment Procedure. The excisional

attachment procedure (ENAP) is subgingival curettage performed with a knife.61' 322'347'371-374 The stated
objectives of the procedure are to allow proper soft-tissue
preparation, to gain better access to the root surface, and
to enable soft tissue to adapt intimately to the root
surface. ENAP is indicated for suprabony pockets which
do not extend beyond the mucogingival junction or
involve angular bony defects. Among its reported advantages are the definitive, clean excision of the epithelial
pocket lining, the epithelial attachment, and the subjacent granulation tissue; improved access to the root
surface; and increased predictability of new clinical atnew

tachment.347' 374

Initial studies showed the technique to be feasible for

reducing pocket depth and gaining clinical attachment
in suprabony
The clinical improvement evident after 1 year was maintained for 3 years, but probing
depths increased slightly, and the amount of previously
gained new attachment decreased slightly at each postoperative evaluation period from 1 to 5
According to histological evidence in monkeys, ENAP
healed with a long thin junctional epithelium and a
minimal amount of connective tissue reattachment.371

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

autografts,68,73 and frozen iliac

allografts.73 However, junctional epithelium may extend

apically to the new alveolar crest;73,74,397 what that implies is not yet known.
Osseous Grafts Compared With Nongraft Regenerative

Volume 53
Number 8

Procedures. In defects of a certain morphology, nongraft

regenerative procedures may stimulate the same amount
of bone repair as do osseous grafts.79'80'298
Two studies which compared osseous graft and nongraft regenerative procedures in human patients indicated that alveolar defects respond with similar or greater
levels of osseous repair if a bone graft is implanted.70'398
In another study, however, the results of intraoral cancellous bone and marrow autografts did not differ from
those of the nongraft approach.78 The increase in the
amount of new bone was greater with the iliac cancellous
bone and marrow autografts than with the nongraft
procedure.70'78 In a study which compared freeze-dried
bone allograft with a nongraft procedure, the levels of

repair were similar.67

Grafts. There are occasional
to
osseous
problems peculiar
grafts: sequestration, exotissue
reaction, external root rsorpphytic granulation
tion, and the immunologie implications of allografts.381' 399'400 Of special importance is external root
with fresh iliac cancellous bone
rsorption associated 327'401'402
marrow autografts.73'
The frequency of root
varied
from
20%
less
than 1% in reported
to
rsorption
69, 402
osseous

Problems With Osseous

cases

Other Grafts. In the past, several types of xenografts

(grafts between two different species) were tried in human subjects with less than satisfactory results. The use
of bioceramics, such as tricalcium phosphate, in human
periodontal osseous defects has been evaluated on a
limited scale with equivocal results.403"405 Therefore, they
should not be used in the routine treatment of Periodontitis. Likewise, further clinical and histologie data are
necessary before scierai allografts can be accepted for
routine clinical use.406"408
Soft Tissue Grafts. Reconstructive soft tissue grafts
have been designed to repair alterations in the normal
morphological arrangement between the attached gingiva and the alveolar mucosa at the level of the mucogingival line. The main goals of mucogingival surgery
are to create or increase the band of attached or keratinized gingiva, to increase vestibular depth, and to cover
localized gingival recessions.
Classical Techniques. All the classical techniques to
create or increase the amount of keratinized
gingiva,357'409-415 as well as some techniques specifically
designed to increase vestibular depth,416 were based on
the assumption that functional adaptation occurs after
surgery. If in an area where attached gingiva was insufficient or nonexistent, the tissue of the alveolar mucosa
was stripped off leaving the bone exposed, whether
covered by periosteum or not, the healing tissue would
develop into attached gingiva simply because function
would so indicate. This was the rationale for all the
periosteal retentions, bone denudations, and periosteal
fenestrations described in the literature.357,410-415417 Special surgical procedures to increase vestibular depth, like
the Edlan Mejchar operation and others,
were
based on the same principle. Although biometrie evalu-

Surgical Therapyfor Periodontitis 487

ation of some of these techniques has shown them to be
relatively effective in maintaining the clinical results,420
all of them, in different degrees, have been associated
with stormy postoperative complications, unpredictable
gain and loss of marginal alveolar bone. Furthermore,
although the tissues thus obtained functioned as attached
did not achieve its histologie characgingiva, they
330' 421"439
teristics.235'

adaptation does not follow heterotopic

transplantation of the soft tissues because the epithelial
tissues of the gingiva and alveolar mucosa maintain their
specificity even after changing their location and thus
Functional

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

Biometrie examination has shown that after the 1st

months the grafted tissues remained stable after initial
shrinkage of the transplanted band of keratinized gingiva.461"463 Some reduction in the amount of root exposure has been shown by means of the "creeping reattachment" phenomenon.464,465 A free gingival graft is used
to treat a localized gingival recession, mainly to halt its
progression by creating a wider band of keratinized
gingiva, but this clinical result has never been proven.
However, when such grafts are placed over a denuded
root to cover an area of gingival recession, their predictability is reduced. Only a "narrow and shallow" defect
can be adequately covered by a free graft since only that
size lesion can provide adequate collateral circulation
during initial healing to assure the "take" of the

graft.446,466-469

Pedicle Gingival Flaps. Pedicle gingival flaps maintain

direct vascularization and thus assure the nutrition and
vitality of the tissue postoperatively. Many techniques
have been described since the classical lateral sliding flap
was first introduced in 1956.
All modifications since
then have been designed to protect the teeth adjacent to
the recession.368,417'444' ^471"489
The procedures that have been tested clinically showed
a 60 to 75% reduction in the amount of recession. These
include lateral sliding
coronally positioned
flap,472'492,495 split-thickness lateral sliding flap with a
free gingival graft,496 lateral sliding flap, and raised
technique.496 The results have remained stable over
time.478'497'498 When a lateral sliding flap is performed
as originally described, gingival recession may be produced on the donor tooth to an average of 1 mm.390'490'491
All the other techniques tested have overcome this undesirable
Histological examination has shown that all these procedures cover the tooth
reattachment and
by a combination of connective tissue
longjunctional epithelium. 494, 499, 500 Electron microscopy
has shown hemidesmosomes and a basement lamina at

flap,490"494

complication.492'495-497
'

Proceedings From State of the Art Workshop

the interphase between the junctional epithelium and the
connective tissue.501 None of these procedures has produced bone regeneration in the area of recession.
Other Techniques. Other techniques, mainly designed
to increase the amount of keratinized gingiva and deepen
the vestibule, include freeze-dried skin allografts,372 lyophilized dura,002 and scierai grafts.503 Since their use is
still experimental, they should not be used in the routine
treatment of Periodontitis.
Need for Mucogingival Surgery. The attached or keratinized gingiva follows a regular pattern of normal

J. Periodontol.

488

distribution.504"507 The anterior teeth have the widest

band, the cuspids and molars on the upper and lower
vestibular sides, the narrowest. The lower lingual gingiva

is narrower on the incisor area and widens distally. Areas

with 2 mm of keratinized gingiva have been reported to
be compatible with the absence of clinically detectable
inflammation! measured by the Gingival Index and the
amount of crevicular fluid flow.006 More recently, even
areas with no keratinized gingiva at all have been maintained free of inflammation.508 Furthermore, in an experimental model of gingivitis, no deleterious effects
were observed either in areas with no attached or keratinized gingiva or in those with an adequate band.507'508
No correlation has been found between vestibular depth
and gingival health.507
In a three-year longitudinal study that compared areas
with insufficient attached gingiva that had been treated
with a free gingival graft with those that had not received
any surgical treatment (controls), no difference was ob-

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

the modified Widman flap are indicated when access to

surfaces is required. They are equally effective in
restoring and maintaining periodontal health.
4. Osseous recontouring improves alveolar architecture, but its value in restoring and maintaining periodontal health has not been established.
5. The utility of the excisional new attachment procedure seems to be limited, the initial gain in attachment
appearing to be lost with time.
6. Subgingival curettage combined with scaling and
root planing is an effective treatment for Periodontitis.
Without scaling and root planing, however, it has no
demonstrable value.
7. Sufficient data have been published to justify the
inclusion of some types of osseous grafts in the armamentarium of accepted periodontal therapy. Although
there have been few longitudinal studies of osseous
grafting in human patients, the available evidence suggests that, in certain morphologic types of alveolar defects, osseous grafting resulted in more bone repair than
root

nongraft techniques.

8. There is no evidence of a detrimental effect from

lack of attached or keratinized gingiva in the maintenance of a healthy dentition. Prophylactic soft-tissue
grafting is not justified; but tooth hypersensitivity, esthetic problems associated with isolated gingival recession, and a gingival contour which precludes adequate
plaque control are appropriate indications.

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

Surgical Therapy for Periodontitis

scaling and root planing alter the composition of

subgingival microbial flora188 and thus cause a shift

489

SPECIFIC RESEARCH NEEDS

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.

the value and place of

surgical therapy in the treatment of Periodontitis reveals
gaps in our knowledge. Research is needed to:
1. Define the role of specific microorganisms and host
response factors in the etiology and pathogenesis of
periodontal disease.
2. Determine those factors that mediate the progression from gingivitis to Periodontitis.
3. Develop simple, reliable methods to establish the
relationships between disease activity and periodontal

Conclusions

Walker B. Moore, Jr., D.D.S., Private Practice, Atlanta

Roy C. Page, D.D.S., Ph.D., University of Washington,
Seattle
William Schwartz, D.D.S., Private Practice, Philadelphia (Representative, Academy of General Dentistry)
Nell Sedransk, Ph.D., State University of New York,

i~

1. Maintenance therapy is of critical importance after

surgery in preserving periodontal health and preventing
the recurrence of Periodontitis.
2. There is evidence that maintenance therapy every
3 months may prevent further attachment loss, but the
value of longer recall intervals and the importance of
variations for individual patients have not yet been
determined.

A review of the evidence

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)

Gerald M. Bowers, D.D.S., University of Maryland at

Baltimore
Marilyn J. Bradshaw, D.D.S., Private Practice, Honolulu
D. Walter Cohen, D.D.S., University of Pennsylvania,

Philadelphia

Robert Gottsegen, D.D.S., Columbia University, New

York
Genevive E. Matanoski, M.D., Johns Hopkins Uni-

versity, Baltimore

Albany

Sigmund S.
Boston

Socransky, D.D.S., Forsyth Dental Center,

490

J. Periodontol.

Proceedings From State of the Art Workshop

WORKSHOP SUMMARYRECOMMENDATIONS
INTRODUCTION

Periodontitis causes more tooth loss than dental caries

and costs the American public an estimated 4 billion
dollars a year to treat and repair its ravages. This major
oral health problem, one of the most ubiquitous of all
human diseases, is strongly correlated with age and oral
uncleanliness.
A major concern of the Panel is the inadequacy of
the present health care force using conventional methods
to cope with the staggering number of Periodontitis
patients needing treatment. The workshop participants
expressed concern that the trained dental manpower
currently available in the United States may not be
sufficient to meet this overwhelming demand. In order
to save millions of hours for the U.S. work force and
billions of dollars in reparative dental care cost, the
participants believe that periodontal disease must be
identified early when treatment can be simple and cost
effective.
In preparing for the workshop on "Surgical Therapy
for Periodontitis," a task force wrote a critical review of
the existing literature on the subject. Having analyzed
this paper as well as the data presented by the workshop
participants, the Review Panel developed a summary
statement to respond to five questions proposed by the
workshop planning committee.
1. When Is Periodontal

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

included and therefore the conclusions derived from

these results cannot be extrapolated to all teeth.
The data published so far on some types of osseous
grafts are sufficiently encouraging to consider including
them as acceptable periodontal therapy. This evidence
suggests that in certain morphologic types of alveolar
defects the bone repair effected by osseous grafting was
better than that effected by the nongraft technique.
Since advanced Periodontitis often requires extensive
restorative dentistry that can complicate plaque control
and professional maintenance, surgical reduction of deep
pockets was considered to have merit.
There was serious question about the need to perform
plastic and reconstructive surgery on the soft tissues to
improve the prognosis of individual teeth. However, in
some limited cases, such as a high frenum attachment
that inhibits plaque control or as a corrective of unfavorable esthetics or hypersensitivity, mucogingival surgery would be indicated. A conservative approach to
mucogingival surgery was suggested.
The workshop expressed a pressing need for more
sensitive and reliable diagnostic methods than those
provided by accepted clinical criteria to enable clinicians
to identify sites of active disease in the periodontium.
Workshop participants agreed that subgingival scaling
and root planing are fundamental treatments of Periodontitis but are also among the most demanding and
difficult clinical techniques in which to develop an acceptable level of proficiency. They therefore recommended that dental schools expand their curricula so
that dental students be given the necessary training not
only to recognize the early signs of gingival disease but
also to effectively treat periodontally diseased roots.
2. What Are the Risk Factors in Periodontal

Surgery?

periodontal therapeutic interventions involve inherently hazardous risks such as the use of local anesthesia, hemorrhaging, transient bacteremia, and stress as
All

well as risks related to the nature of the disease, the

anatomical variations of the involved tissues, the patient's age or complicating medical problems.
Further loss of periodontal attachment will follow
periodontal surgery if the dentition is reinfected by
plaque. This is preventable in highly motivated patients
who become efficient in maintaining high levels of oral
hygiene after thorough professional removal of deposits
in the presurgical phase of treatment. Sometimes brief
postoperative discomfort is experienced. Depending
upon the presurgical extent of disease-caused tissue defects and also upon the specific procedures used, root
exposure, with the related risk of root sensitivity and
root caries, may increase. Periodontal surgery for advanced lesions in the anterior part of the mouth is
occasionally followed by gingival recession and the opening of spaces between the teeth. This cosmetically undesirable result sometimes alters certain speech sounds.

Volume 53
Number 8

Surgical Therapy for Periodontitis

3. Are There Feasible Alternatives to

Surgical

Treatment?
The panel

agreed that surgery is the only feasible

obtain
the maximum access necessary for
procedure
debridement, especially when periodontal pockets are
deep, tortuous, irregular, or involve root surfaces such as
furcas. However, when and where root surfaces are
accessible to instrumentation and plaque control is thorough, disease can be arrested without surgery. Recent
clinical studies suggest that when such conditions exist,
pocket depth alone cannot justify the use of surgery.
They also indicate that surgery can be avoided by frequent professional tooth cleaning, including root planing, and by effective plaque control by the patient.
Subgingival scaling and root planing, along with scrupulous oral hygiene, not only reduce probing depth to a
variable degree but also permit a limited gain in attachment levels. However, for maximum pocket reduction or
elimination and for maximum clinical attachment gain
and bone regeneration, surgical intervention is indicated.
When pocket depth is related to a tilted tooth, orthodontic correction may result in pocket reduction.
If the desired goal is to repair a gingival cleft, to cover
root surfaces denuded by recession, or to increase the
zone of keratinized gingiva, there is no alternative to
mucogingival surgery. However, even when there is
recession but no attached gingiva, inflammation and
further recession can be prevented for up to 4 years by
meticulous plaque control alone. If restorations must
extend subgingivally, neither gingival health nor recession is affected by the absence of a zone of attached
to

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

4. What Are the

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.

5. What Are the Research Needs?

Both the preceding sections of this report and the Task

Force background paper indicate that clinical periodontal research has progressed considerably since the world
workshops of 1966 and 1977. The increased knowledge
has intensified our conviction of the continuing need for
clinical research. Most of the progress has resulted from
the parallel advances in basic and clinical understanding;
this parallel development should be encouraged.
Chief among the factors that have inhibited progress
in clinical periodontal research, however, are the scarcity
of trained clinical investigators and the difficulties in
obtaining adequate research support for sufficient periods of time.
The workshop participants have identified the following urgent research needs:
1.

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

learn the role of the response mechanisms in the

host.
4. More detailed information about the natural history
of Periodontitis.

In any longitudinal human study, all surgical methods

used should be explicitly described, including the personnel (hygienist, periodontal co-therapist, specialist, resident, generalist) performing all procedures. Reports on
the results of clinical research should include the predictability of the therapeutic effect, the range of the
observed results, and the average observed effect. The
statistical methods for design and analysis of studies
should be sufficiently sophisticated to accommodate the
heterogenicity of the disease and of the patients.
In surgical therapy, the following studies are urgently
needed:

492

1.

Proceedings From State of the Art Workshop

Basic and clinical studies aimed at determining the
healing process of the periodontal tissues and the
regeneration of destroyed components. The development and testing of appropriate graft materials

and the management of the root surface should be

included.
2. Studies to evaluate the role of chemotherapeutic
agents in the control of pathogenic species of mi-

croorganisms.

3. Studies to determine the effects of various surgical

procedures on the subgingival flora and the defense
mechanisms of the host.
4. Continued evaluation of the efficacy of various
therapeutic modalities.

investigation should include:

Studies of the role trauma from occlusion plays in

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.

F., Kramer, G., Stahl, S., Stallard, R., and Swenson,

H.: Glossary of terms. J Periodontol (Suppl.) 1977.

2. Ruffer, . .: Studies in the Paleopathology of Egypt. Chicago,
University of Chicago Press, 1921.
3. Weinberger, B. W.: An Introduction to the History of Dentistry.
St. Louis, C. V. Mosby Co., 1949.
4. Chilton, N. W., and Miller, M. I.: Epidemiology of Periodontal
Disease. International Conference on Research in the Biology of Periodontal Disease. Chicago, The College of Dentistry, University of
Illinois, 1977.
5. Waerhaug, J.: Epidemiology of periodontal diseasea review of
the literature. World Workshop in Periodontics. University of Michigan,

1966.

6. Loe, ., Anerud, ., Boysen, ., and Smith, M.: The natural

history of periodontal disease in man. The rate of periodontal destruction before 40 years of age. J Periodontol 49: 607, 1978.

7. Marshall-Day, C. D.: The epidemiology of periodontal disease.

J Periodontol 22: 13, 1951.
8. Ramfjord, S. P., Emslie, R. D., Greene, J. C, Held, A. J., and
Waerhaug, J.: Epidemiologie studies of periodontal disease. Am J
Public Health 58: 1713, 1968.
9. Russell, A. L.: Epidemiologie research, 1960-63. J. Am. Dent.
Assoc. 68: 820, 1964.
10. Russell, A. L.: International nutrition surveys: A summary of
preliminary findings. J Dent Res 42: 232, 1963.
11. Schei, O., Waerhaug, J., Lovdal, ., and Arno, .: Alveolar
bone loss related to oral hygiene and age. J Periodontol 30: 7, 1959.
12. Ellison, S. .: Oral bacteria and periodontal disease. J Dent Res
49: 198, 1970.
13. Kelstrup, J., and Theilade, E.: Microbes and periodontal disease.
J Clin Periodontol 1: 15, 1974.
14. Socransky, S. S.: Microbiology of periodontal diseasePresent
status and future considerations. J Periodontol 48: 497, 1977.

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.

Nisengard, R. J.: The role of immunology in periodontal disease.

JPeriodontol 48: 505, 1977.

45. Ranney, R.: Pathogenesis of Periodontal Disease. International

Conference on Research in the Biology of Periodontal Disease. Chicago. The College of Dentistry, University of Illinois, 1977.
46. Rizzo, . ., and Mergenhagen, S. E.: Host Responses in
Periodontal Disease. International Conference on Research in the
Biology of Periodontal Disease. Chicago. The College of Dentistry,
University of Illinois, 1977.
47. Becker, W., Berg, L., and Becker, . E.: Untreated periodontal
disease: A longitudinal study. J Periodontol 50: 234, 1979.
48. Chawla, . N., Nanea, R., and Kappoor, . K.: Dental prophylaxis procedures in control of periodontal diseases in Lucknow (rural)
India. / Periodontol 46: 498, 1975.
49. Suomi, J. D., Greene, J. C, Vermillion, J. R., Doyle, J., Chang,
J. J., and Leatherwood, E. C: The effect of controlled oral hygiene
procedures on the progression of periodontal disease in adults. Results
after third and final year. / Periodontol 42: 152, 1971.
50. Knowles, J. W., Brge, F. G., Morrison, E. C, Nissle, R. R.,
and Ramfjord, S. P.: Comparison of results following three modalities
of periodontal therapy related to tooth type and initial pocket depth.
J Clin Periodontol 7: 32, 1980.
51. Knowles, J. W., Burgett, F. G., Nissle, R. R., Shick, R. .,
Morrison, E. C, and Ramfjord, S. P.: Results of periodontal treatment
related to pocket depth and attachment level: Eight years. J Periodontol
50: 225, 1979.
52. Lindhe, J., and Nyman, S.: The effect of plaque control and
surgical pocket elimination on the establishment and maintenance of
periodontal health. A longitudinal study of periodontal therapy in
cases of advanced disease. J Clin Periodontol 2: 67, 1975.
53. Nyman, S., and Lindhe, J.: A longitudinal study of combined
periodontal and prosthetic treatment of patients with advanced periodontal disease. J Periodontol 50: 163, 1979.
54. Nyman, S., Rosling, B., and Lindhe, J.: Effect of professional
tooth cleaning on healing after periodontal surgery. / Clin Periodontol
2: 80, 1975.
55. Pihlstrom, B. L., Ortiz-Campos, C, and McHugh, R. B.: A
randomized four year study of periodontal therapy. J Periodontol 52:

227,1981.

56. Ramfjord, S. P., Knowles, J. W., Morrison, E. C, Burgett, F.

G., and Nissle, R. R.: Results of periodontal therapy related to tooth
type. J Periodontol 51: 270, 1980.
57. Rosling, B., Nyman, S., and Lindhe, J.: The effect of systematic

control on bone regeneration in infrabony pockets. J Clin

Periodontol 3: 38, 1976.
58. Rosling, B., Nyman, S., Lindhe, J., and Jern, B.: The healing
potential of periodontal tissues following different techniques of periodontal surgery in plaque free dentitions. J Clin Periodontol 3: 233,
1976.
59. Smith, D. H., Ammons, W. F., Jr., and Van Belle, G.: A
longitudinal study of periodontal status comparing osseous recontouring with flap curettage. 1. Results after 6 months. J Periodontol 51:
367, 1980.
60. Svanberg, G., and Lindhe, J.: Experimental tooth hypermobility
in the dog. Odontol Revy 24: 269, 1973.
61. Yukna, R. ., and Williams, R. .: Five year evaluation of the
excisional new attachment procedure. J Periodontol 51: 382, 1980.
62. Hirschfeld, L., and Wasserman, B.: A long term survey of tooth
loss in 600 treated periodontal patients. J Periodontol 49: 225, 1978.
63. Oliver, R. C: Tooth loss with and without periodontal therapy.

plaque

Surgical Therapy for Periodontitis

493

Periodont Abstr 17: 8, 1969.

64. Ross, I. F., and Thompson, R. H., Jr.: Furcation involvement in
maxillary and mandibular molars. J Periodontol 51: 450, 1980.
65. Ross, I. F., and Thompson, R. H., Jr.: A long term study of root
retention in the treatment of maxillary molars with furcation involvement. J Periodontol 49: 238, 1978.
66. Ross, I. F., Thompson, R. H., and Galdi, M.: The results of
treatment. A long term study of one hundred and eighty patients.
Parodontologie 25: 125, 1971.
67. Altiere, E. T., Reeve, C. M., and Sheridan, P. J.: Lyophilized
bone allografts in periodontal osseous defects. J Periodontol 50: 510,
1979.
68. Dragoo, M. R., and Sullivan, H. C: A clinical and histologie
evaluation of autogenous iliac bone grafts in humans. Part I. Wound
healing 2 to 8 months. J Periodontol 44: 614, 1973.
69. Ellegaard, B., and Le, H.: New attachment of periodontal
tissues after treatment of infrabony lesions. J Periodontol 42: 648, 1971.
70. Froum, S. J., Ortiz, M., Witkin, R. T., Thaler, R., Scopp, I. W.,
and Stahl, S. S.: Osseous autografie. III. Comparison of osseous
coagulum-bone blend implants with open curettage. / Periodontol 47:
287, 1976.
71. Froum, S. J., Thaler, R., Scopp, I. W., and Stahl, S. S.: Osseous
autografts. I. Clinical responses of bone blend or hip marrow grafts. J
Periodontol 46: 515, 1975.
72. Hiatt, W. H., and Schallhorn, R. G.: Intraoral transplants of
cancellous bone and marrow in periodontal lesions. / Periodontol 44:
194, 1973.
73. Hiatt, W. H., Schallhorn, R. G., and Aaronian, A. J.: The
induction of new bone and cementum formation. IV. Microscopic
examination of the periodontium following human bone and marrow
autografi, allograft, and nongraft periodontal regenerative procedures.
J Periodontol 49: 495, 1978.
74. Listgarten, . ., and Rosenberg, M. M.: Histological study of
repair following new attachment procedures in human periodontal
lesions. J Periodontol 50: 333, 1979.
75. Mann, W. V.: Autogenous transplant in the treatment of infrabony pockets. Periodontics 2: 205, 1964.
76. Mellonig, J. T., Bowers, G. M., Bright, R. W., and Lawrence, J.
J.: Clinical evaluation of freeze-dried bone allografts in periodontal
osseous defects. J Periodontol 47: 125, 1976.
77. Nabers, C. L., and O'Leary, T. J.: Autogenous bone transplants
in the treatment of osseous defects. J Periodontol 36: 5, 1965.
78. Patur, B.: Osseous defects: Evaluation of diagnostic and treatment methods. J Periodontol 45: 523, 1974.
79. Poison, A. M., and Heijl, L. C: Osseous repair in infrabony
periodontal defects. J Clin Periodontol 5: 13, 1978.
80. Prichard, J.: The infrabony technique as a predictable procedure. J Periodontol 28: 202, 1957.
81. Prichard, J.: Regeneration of bone following periodontal therapy. Oral Surg 10: 247, 1957.
82. Rosenberg, M. M.: Free osseous tissue autografi as a predictable
procedure. J Periodontol 42: 195, 1971.
83. Ross, S. E., and Cohen, D. W.: The fate of free osseous tissue
autografi: Clinical and histologie case report. Periodontics 6: 145, 1968.
84. Schallhorn, R. G.: The use of autogenous hip marrow biopsy
implants for bony crater defects. J Periodontol 39: 145, 1968.
85. Seibert, J. S.: Reconstructive periodontal surgery: Case report.
J Periodontol 4\: 113, 1970.
86. Shaffer, E. M.: The new attachment operation in subcrestal
pockets. Oral Surg 11: 253, 1958.
87. Ash, M. M., Gitlin, B. N., and Smith, W. .: Correlation
between plaque and gingivitis. J Periodontol 35: 424, 1964.
88. Greene, J. C: Oral hygiene and periodontal disease. Am J
Public Health 53: 913, 1963.
89. MacDonald, J. B., and Gibbon, R. J.: The relationship of
indigenous bacteria to periodontal disease. J Dent Res 41: 320, 1962.
90. Socransky, S. S.: Relationship of bacteria to the etiology of
periodontal disease. J Dent Res 49: 203, 1970.

494

Proceedings From State of the Art Workshop

and Rosling, B.: Periodontal surgery in

plaque infected dentitions. J Clin Periodontol 4: 240, 1977.
92. Rosling, B., Nyman, S., and Lindhe, J.: The healing potential of
the periodontal tissues in plaque-free dentitions: A two year clinical
study. J Clin Periodontol 3: 233, 1976.
93. Carranza, F. ., and Romanelli, J. .: The effects of fillings
and prosthetic appliances on the marginal gingiva. Int Dent J 23: 64,
1973.
94. Gilmore, N., and Sheiham, .: Overhanging dental restorations
and periodontal disease. J Periodontol 42: 8, 1971.
95. Highfield, J. E., and Powell, R. N.: Effects of removal of
posterior overhanging metallic margins of restorations upon the periodontal tissues. J Clin Periodontol 5: 169, 1978.
96. Waerhaug, J.: Effect of rough surfaces on gingival tissues. /
Dent Res 35: 323, 1956.
97. Waerhaug, J.: Healing of the dento-epithelial junction following
subgingival plaque control. J Periodontol 49: 119, 1978.
98. Waerhaug, J.: Microscopic demonstration of tissue reaction to
removal of subgingival calculus. J Periodontol 26: 26, 1955.
99. Youdelis, R. ., Weaver, S. D., and Sapkos, S.: Facial and
lingual crown contours of artificial crown restorations and their effects
on the periodontium. J Prosthet Dent 29: 61, 1973.
100. Baderston, ., Egelberg, J., and Koch, G.: Effect of monthly
prophylaxis on caries and gingivitis in school children. Community
Dent Oral Epidemiol 3: 1, 1975.
101. Lightner, L. M., O'Leary, T. J., Drake, R. B., Crump, P. P.,
and Allen, M. F.: Preventive periodontic treatment procedures: Results
over 46 months. J Periodontol 42: 555, 1971.
102. Lovdal, ., Arno, ., Schei, O., and Waerhaug, J.: Combined
effect of subgingival scaling and controlled oral hygiene on the incidence of gingivitis. Acta Odontol Scand 19: 557, 1961.
103. Suomi, J., Greene, J. C, Vermillion, J. R., Chang, J. J., and
Leatherwood, E. C: The effect of controlled oral hygiene procedures
on the progression of periodontal disease in adults: Results after two
years. J Periodont-Periodontics 40: 416, 1969.
104. Suomi, J. D., West, T. D., Chang, J. J., and McClendon, B. J.:
The effect of controlled oral hygiene procedures on the progression of
periodontal disease in adults: Radiographic findings. J Periodontol 42:
562, 1971.
105. Greene, J. C, and Vermillion, J. R.: The effects of controlled
oral hygiene on the human adult population. Int Dent J 21: 8, 1971.
106. Burt, . .: Some areas requiring economic analysis in the
prevention of dental caries. Int Dent J 29: 131, 1979.
107. Henry, J. L., and Sinkford, J. C: The economic and social
impact of periodontal disease. Public Health Rep 94: 172, 1979.
108. Ingle, J. I.: The Health, Economic and Cultural Impact of
Periodontal Disease on an Aging Population. NIH Conference on Aging,
Louisville, KY., 1975.
109. Arnim, S. S.: The use of disclosing agents for measuring tooth
cleanliness. J Periodontol 34: 227, 1963.
110. Cohen, D. W., Stoller, N., Chace, R and Laster, L.: A
comparison of bacterial plaque disclosants in periodontal disease. /
Periodontol 43: 333, 1972.
111. Podshadley, A. G., and Haley, J. V.: A method for evaluating
oral hygiene performance. Public Health Rep 83: 259, 1968.
112. Greene, J. C: Oral hygiene index (OHI)Development and
uses. J Periodontol 38: 625, 1967.
113. Greene, J. C, and Vermillion, J. R.: The simplified oral
hygiene index. J Am Dent Assoc 68: 7, 1964.
114. Silness, J., and Le, H.: Periodontal disease in pregnancy. II.
Correlation between oral hygiene and periodontal condition. Acta
Odontol Scand 72: 112, 1964.
115. Lindhe, J., Liljenberg, B., and Listgarten, . .: Some microbiological and histopatholgical features of periodontal disease in man.
J Periodontol 51: 264, 1980.
116. Slots, J.: Subgingival microflora and periodontal disease. J
Clin Periodontol 6: 351, 1979.
117. Becker, M. H., and Maiman, L. .: Sociobehavioral determinations of compliance with health and medical care recommendations.
91.

Nyman, S., Lindhe, J.,

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

plaque accumulation by well adapted subgingival and supragingival

proximal restorations. Heh Odontol Acta 15: 99, 1972.
146. Sackett, . P., and Gildenhuys, R. R.: The effect of axial crown
adolescents. J Periodontol 47: 320, 1976.
147. Gibbone, R. J., and Fitzgerald, R. J.: Dextran-induced agglutination of Streptococcus mutans, and its potential role in the formation
of microbial dental plaques. J Bacteriol 98: 341, 1969.
148. Gibbons, R. J., and Nygaard, M.: Interbacterial aggregation
of plaque bacteria. Arch Oral Bio! 15: 1397, 1970.
149. Gibbons, R. J., and Van Houte, J.: On the formation of dental
plaque. /. Periodontol. 44: 347, 1973.
150. Hay, D. I., Gibbons, R. J., and Spinnel, D. M.: Characteristics
of some high molecular weight constituents with bacterial aggregating
activity from whole saliva and dental plaque. Caries Res 5: 111, 1971.
151. Jenkins, G. N.: The mode of formation of dental plaque.
Caries Res 2: 130, 1968.
152. Kashket, S., and Donaldson, C. G.: Saliva induced aggregation
of oral streptococci. J Bacteriol 112: 1127, 1972.
153. Lie, T.: Growth of dental plaque on hydroxyapatite splints. A
method of studying early plaque morphology. J Periodont Res 9: 135,
1974.
154. Lie, T.: Ultrastructural study of early dental plaque formation.
J Periodont Res 13: 391, 1978.
155. Ostavik, D., Kraus, F. W., and Henshaw, C: In vitro attachment of streptococci to the tooth surface. Infect Immun 9: 794, 1974.
156. Van Houte, J., Gibbons, R. J., and Banghart, S. .: Adherence
as a determinant of the presence of Streptococcus salivarious and
Streptococcus sanguis on the tooth surface. Arch Oral Biol 15: 1025,
1970.
157. Aleo, J. J., De Renzis, F. ., and Frber, P. .: In vitro
attachment of human gingival fibroblasts to root surfaces. J Periodontol
46: 639, 1975.
158. Aleo, J. J., De Renzis, F. ., Farber, P. ., and Varboncoeur,
A. P.: The presence and biologic activity of cementum bound endotoxin. / Periodontol 45: 672, 1974.
159. Fine, D. H., Morris, M. L., Tabak, L., and Cole, J. D.:
Preliminary characterization of material elected from the roots of
periodontally diseased teeth. J Periodont Res 15: 10, 1980.
160. Hatfield, C. G., and Baumhammers, .: Cytotoxic effects of
periodontally involved surfaces of human teeth. Arch Oral Biol 16:465,
1971.
161. Jones, W. ., and O'Leary, T. J.: The effectiveness of in vivo
root planing in removing bacterial endotoxin from the roots of periodontally involved teeth. / Periodontol 49: 337, 1978.
162. Lopez, N. J., Belvederessi, M., and deLaSotta, R.: Inflammatory effects of periodontally diseased cementum studied by autogenous
root implants of humans. J Periodontol 51: 582, 1980.
163. Canis, M. F., Kramer, G. M., and Pameijer, C. M.: Calculus
attachment. Review of the literature and findings. / Periodontol 50:
406, 1979.
164. Jones, S.: Morphology of calculus formation on the human
tooth surface. Proc R Soc Med 65: 903, 1972.
165. Kopcyk, R., and Conroy, C. W.: The attachment of calculus to
root planed surfaces. Periodontics 6: 78, 1968.
166. Moskow, B. S.: Calculus attachment in cementai separations.
J Periodontol 40: 125, 1969.
167. Selvig, . .: Attachment of plaque and calculus to tooth
surfaces. J Periodont Res 5: 8, 1970.
168. Theilade, J.: Electron microscopic study of calculus attachment
to smooth surfaces. Acta Odont Scand 21: 571, 1963.
169. Vordreas, E. G., and Zander, . .: Cuticular calculus attachment. Oral Surg 11: 1170, 1958.
170. Zander, . .: The attachment of calculus to root surfaces. J
Periodontol 24: 16, 1953.
171. Walker, S. L., and Ash, . M., Jr.: A study of root planing by
scanning electron microscopy. Dent Hyg 50: 109, 1976.
172. Allen, E. F., and Rhoades, R. H.: Effect of high speed periodontal instruments on tooth surfaces. / Periodontol 34: 352, 1963.
173. Jones, S. J., Lozdan, J., and Boyde, .: Tooth surfaces treated
overcontour on

Surgical Therapyfor Periodontitis

495

in situ with periodontal instruments. Br Dent J132: 57, 1972.

174. Kerry, G. J.: New method for viewing root surfaces. J Periodontol 46: 673, 197'5.
175. Kerry, G. J.: Roughness of root surfaces after use of ultrasonic
and hand scaling. J Periodontol 38: 340, 1967.
176. Meyer, K., and Lie, T.: Root surface roughness in response to
periodontal instrumentation studied by combined use of microhardness
measurements and scanning electron microscopy. J Clin Periodontol 4:
77, 1977.
177. Moskow, B. S., and Bressman, E.: Cementai response to ultrasonic and hand instrumentation. J Am Dent Assoc 68: 698, 1964.
178. Pameijer, C. H., Stallard, R. E., and Heip, N.: Surface characteristics of teeth following periodontal instrumentation: A scanning
electron microscope study. J Periodontol 43: 628, 1972.
179. Stende, G. W. and Schaffer, E. M.: A comparison of ultrasonic
and hand scaling. / Periodontol 32: 312, 1961.
180. Wilkinson, R. F., and Maybury, J. E.: Scanning electron
microscopy of the root surface following instrumentation. J Periodontol
44: 559, 1973.
181. Woodruff, H. C, Levin, M. P., and Brady, J. M.: The effects
of two ultrasonic instruments on root surfaces. / Periodontol 46: 119,
1975.
182. Rosenberg, R. M., and Ash, M. M.: The effect of root roughness on plaque accumulation and gingival inflammation. J Periodontol
45: 146, 1974.
183. Torfason, T., Kiger, R., Silvig, . ., and Egelberg, J.: Clinical
improvement of gingival conditions following ultrasonic versus hand
instrumentation of periodontal pockets. J Clin Periodontol 6: 165, 1979.
184. Stewart, J. L., Drisco, R. R., and Herlach, A. D.: Comparison
of ultrasonic and hand instruments for the removal of calculus. J Am
Dent Assoc 75: 153, 1967.
185. Lie, T., and Meyer, K.: Calculus removal and loss of tooth
substance in response to different periodontal instruments. A scanning
electron microscopy study. J Clin Periodontol 4: 250, 1977.
186. Nishimine, D., and O'Leary, T. J.: Hand instrumentation
versus ultrasonics in the removal of endotoxin for root surfaces. J
Periodontol 50: 345, 1979.
187. Listgarten, . ., Lindhe, J., and Hellden, L.: Effect of tetracycline and/or scaling on human periodontal disease. Clinical, microbiological and histological observations. / Clin Periodontol 5:246, 1978.
188. Mousques, T., Listgarten, M., and Phillips, R. .: Effect of
scaling and root planing on the composition of human subgingival
microbial flora. J Periodont Res 15: 144, 1980.
189. Slots, J., Mashimo, P., Levine, M. J., and Genco, R. J.:
Periodontal therapy in humans. I. Microbiological and clinical effects
of a single course of periodontal scaling and root planing, and of
adjunctive tetracycline therapy. J Periodontol 50: 495, 1979.
190. Syed, S. ., Morrison, E. C, Loesch, W. J., and Ramfjord, S.
P.: The bacterial flora of treated periodontal pockets. J Dent Res 59:
Abstr. No. 76, Special Issue B, 1980.
191. Curtis, C. H., McCall, C. M., and Overaa, . I.: A clinical
study of the effectiveness of the roll and Charters' methods of brushing
teeth. / Periodontol 28: 277, 1957.
192. Elliot, J. R., Bowers, G. M., Clemmer, . ., and Rovelstad,
G. H.: Evaluation of an oral physiotherapy center in the reduction of
bacterial plaque and periodontal disease. J Periodontol 43: 221, 1972.
193. Kilner, R. M., Wohl, B. R., Deasy, M. J., and Formicola, D.
J.: Gingival inflammation as related to frequency of plaque removal.
J Periodontol 45: 303, 1974.
194. Koch, G., and Lindhe, J.: The effect of oral hygiene on the
gingiva of children. The effect of toothbrushing. Odontol Revy 16: 327,
1965.
195. Lang, N. P., Cumming, B. R., and Le, H.: Toothbrushing
frequency as it relates to plaque development and gingival health. J
Peridontol 44: 396, 1973.
196. Soumi, J. D.: Periodontal disease and oral hygiene in an
institutionalized population. Report of an epidemiologie study. J Periodontol 40: 5, 1969.
197. Hughes, T. P., and Caffesse, R. G.: Gingival changes following

496

Proceedings From State of the Art Workshop

scaling, root planing and oral hygiene. A biometrie evaluation. J

Periodontol 49: 245, 1978.
198. Tagge, D. L., O'Leary, T. J., and Kafrawy, A. H.: The clinical
and histological response of periodontal pockets to root planing and
oral hygiene. J Periodontol 46: 527, 1975.
199. Alexander, A. G.: The effect of subgingival scaling on gingival
inflammation. J Periodontol 40: 717, 1969.
200. Ambrose, J. ., and Detamore, R. J.: Correlation of histologie
and clinical findings in periodontal treatment: Effect of scaling in
reduction of inflammation prior to surgery. J Periodontol 31: 238, 1960.
201. Helldin, L., Listgarten, M., and Lindhe, J.: The effect of
tetracyclines and/or scaling on human periodontal diseases. J Clin
Periodontol 6: 222, 1979.
202. Morrison, E. C, Ramfjord, S. P., and Hill, R. W.: Short-term
effects of initial, nonsurgical periodontal treatment (Hygienic phase).
J Clin Periodontol 1: 199, 1980.
203. Zamet, J. S.: A comparative clinical study of three periodontal
surgical techniques. J Clin Periodontol 2: 87, 1975.
204. Ramfjord, S. P., Morrison, E. C, Hill, R. W., Appleberry, E.,
Caffesse, R. G., Kerry, G. J., and Nissle, R. R.: Four types of
periodontal treatment. Two year follow-up. / Dent Res 59: Abstr. No.
374, Special Issue B, 1980.
205. Caton, J., and Zander, H: The attachment between tooth and
gingival tissues after periodic root planing and soft tissue curettage. J
Periodontol 50: 462, 1979.
206. Lang, N. P., Morrison, E. C, Le, H., and Ramfjord, S. P.:
Longitudinal therapeutic effects on the periodontal attachment level
and pocket depth in beagle dogs. I. Clinical findings. J Periodont Res
14:418, 1979.
207. Morrison, E. C, Lang, N. P., Le, J., and Ramfjord, S. P.:
Effects of repeated scaling and root planing and/or controlled oral
hygiene on the periodontal attachment level and pocket depth in beagle
dogs. I. Clinical findings. J Periodont Res 14: 428, 1979.
208. Pihlstrom, B. L., and Ortiz, C: Four year longitudinal study of
two methods of periodontal therapy. J Dent Res 59: Abstr. No. 122,
Special Issue A, 1980.
209. Waite, I. M.: A comparison between conventional gingivectomy and a nonsurgical regime in the treatment of Periodontitis. J Clin
Periodontol 3: 173, 1976.
210. Miller, W. D.: The Microorganism of the Human Mouth. Philadelphia, PA., S. S. White, 1889.
211. Bay, L. M. and Russell, B. G.: Effect of Chlorhexidine on
dental plaque and gingivitis in mentally retarded children. Community
Dent Oral Epidemiol 3: 267, 1975.
212. Flotra, L., Gjermo, P., Rolla, G., and Waerhaug, J.: A 4 month
study on the effect of Chlorhexidine mouthwashes on 50 soldiers. Scand
J Dent Res 80: 10, 1972.
213. Luoma, H., Murtomaa, H, Nuuja, T., Nyman, ., Nummikoski, P., Abinamo, J., and Luoma, A. R.: A simultaneous reduction
of caries and gingivitis in a group of school children receiving chlorhexidine-fluoride applications. Caries Res 12: 290, 1978.
214. Schiott, C. R., Le, ., Jensen, S. ., Kilian, M., Davies, R.
M., and Glavind, .: The effect of Chlorhexidine mouthrinses on the
human oral flora. J Periodont Res 5: 84, 1970.
215. Davies, R. M., Jensen, S. B., Schiott, C. R., and Le, .: The
effect of topical application of Chlorhexidine on the bacterial colonization of the teeth and gingiva. J Periodont Res 5: 96, 1970.
216. Oliver, R. C, and Egelberg, J.: The effect of topical application
of Chlorhexidine on subgingival microbial colonization. J Periodont
Res Suppl 10: 8, 1972.
217. Dolles, O. K., and Gjermo, P.: Caries increment and gingival
status during 2 years' use of Chlorhexidine and fluoride containing
dentifrices. Scand J Dent Res 88: 22, 1980.
218. Johansen, J. R., Gjermo, P., and Eriksen, H. B.: Effect of 2years' use of chlorhexidine-containing dentifrices on plaque, gingivitis,
and caries. Scand J Dent Res 83: 288, 1975.
219. Duany, L. F., and Zinner, D. D.: Longitudinal effects of an
antibacterial oral rinse on gingivitis and dental plaque. Pharmacol Ther
Dent 2: 229, 1975.

J. Periodontol.
August, 1982

220. Spolsky, V. W., Bhatia, H. L., Forsythe, ., and Levin, D.:

The effect of an antimicrobial mouthwash on dental plaque and
gingivitis in young adults. J Periodontol 46: 685, 1975.
221. Barnes, G. P., Roberts, D. W., Katz, R. V., and Woolridge, E.
D., Jr.: Effects of two cetylpyridium chloride containing mouthwashes
on bacterial plaque. J Peridontol 47: 419, 1976.
222. Lobene, R. R.: A clinical study of the effect of dextranase on
human dental plaque. J Am Dent Assoc 82: 132, 1971.
223. Lobene, R. R., Kashket, S., Soparkar, P. M., et al.: The effect
of cetylpyridium chloride on human plaque bacteria and gingivitis.
Pharmacol Ther Dent 4: 33, 1979.
224. Shapiro, W. B., Kaslick, R. S., Chasens, A. L, et al.: The
influence of urea peroxide gel on plaque, calculus and chronic gingival
inflammation. J Periodontol 44: 636, 1973.
225. Skjorland, K, Gjermo, P., and Rolla, G.: Effect of some
polyvalent cations on plaque formation in vivo. Scand J Dent Res 86:

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

Surgical Therapy for Periodontitis

497

245. Svanberg, G.: Influence of trauma from occlusion of the

periodontium of dogs with normal or inflamed gingivae. Odontol Revy

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,

dontically treated and untreated

Angle Orthod 43: 412, 1973.

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

Proceedings From State of the Art Workshop

299. Spray, J. R., Garnick, J. J., Doles, L. R., and Klawitten, J. J.:
Microscopic demonstration of the position of periodontal probes. J

Periodontol 49: 148, 1978.

300. Van der Veiden, U.: Probing force and the relationship of the
probe tip to the periodontal tissues. J Clin Periodontol 6: 106, 1979.
301. Laster, L., Laudenbach, . W., and Stoller, . .: An evaluation of clinical tooth mobility measurements J Periodontol 46: 603,
1975.
302. Stoller, N. FL, and Laudenbach, . W.: Clinical standardization of horizontal tooth mobility. J Clin Periodontol 7: 242, 1980.
303. O'Leary, T. J.: Indices for measurement of tooth mobility in
clinical studies. J Periodont Res 9: (suppl. 14) 94, 1974.
304. Bjorn, A. L., Koch, G., and Lindhe, J.: Evaluation of gingival
fluid measurements. Odontol Revy 16: 300, 1965.
305. Borden, S. M., Golub, L. M., and Kleinberg, I.: The effect of
age and sex on the relationship between crevicular fluid flow and
gingival inflammation in human. / Periodont Res 12: 160, 1977.
306. Brill, N., and Bjorn, FL: Passage of tissue fluid into human
gingival pockets. Acta Odontol Scand 17: 11, 1959.
307. Daneshmand, H., and Wade, A. B.: Correlation between gingival fluid measurements and macroscopic as well as microscopic
characteristcs of gingival tissues. J Periodont Res 11: 35, 1976.
308. Egelberg, J.: Gingival exdate measurements for evaluation of
inflammatory changes in the gingivae. Odontol Revy 15: 281, 1964.
309. Mann, W. V.: The correlation of gingivitis, pocket depth and
exdate from the gingival crevice. J Periodontol 34: 379, 1963.
310. Oliver, R. C, Holm-Pederson, P., and Loe, H.: The correlation
between clinical scoring, exdate measurements and microscopic evaluation of inflammation in the gingiva. J Periodontol 40: 201, 1969.
311. Rudin, H. J., Overdiek, H. F., and Rateitschak, K. H.: Correlation between sulcus fluid rate and clinical histological inflammation
of the marginal gingiva. Helv Odontol Acta 14: 21, 1970.
312. Shapiro, L., Goldman, H., and Bloom, .: Sulcular exdate
flow in gingival inflammation. / Periodontol 50: 301, 1979.
313. Son, S., Hotz, P., and Muhlemann, .: The effect of marginal
gingivitis on tooth mobility. Helv Odontol Acta 15: 103, 1971.
314. Brill, N.: Gingival conditions related to flow of tissue fluid into
human gingival pockets. Acta Odontol Scand 18: 421, 1960.
315. Orban, J. E., and Stallard, R. E.: Gingival crevicular fluid: a
reliable predictor of gingival health? J Periodontol 40: 231, 1969.
316. Brill, N., and Krasse, .: The passage of tissue fluid into the
clinically healthy gingival pocket. Acta Odontol Scand 16: 233, 1958.
317. Egelberg, J.: Cellular elements in gingival pocket fluid. Acta
Odontol Scand 21: 283, 1963.
318. Weinstein, E., Mandel, I. D., Salkind, ., Oshrain, . E., and
Pappas, G.: Studies of gingival fluid. Periodontics 5: 161, 1967.
319. Alfano, M. C: The origin of gingival fluid. J Theor Biol 47:
127, 1974.
320. Garnick, J. J.: Methods of measuring and recording periodontal disease. Dent Clin North Am 24: 613, 1980.
321. Oliver, R. C: Patient evaluation. Int Dent J 27: 103, 1977.
322. Caffesse, R. G.: Longitudinal evaluation of periodontal surgery. Dent Clin North Am 24: 751, 1980.
323. Listgarten, . .: Periodontal probing: What does it mean? J
Clin Periodontol!: 165, 1980.
324. Orban, B., and Manella, V. B.: A macroscopic and microscopic
study of instruments designed for root planing. J Periodontol 21: 120,

1956.
325. Schaffer, . M.: Histological results of root curettage of human
teeth. / Periodontol 21: 296, 1956.
326. Schaffer, . M.: Periodontal instrumentation: scaling and root

planing. Int Dent 117: 297,

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.

330. Glickman, I.: The results obtained with the unembellished

in a clinical study in humans. J Periodontol
27: 247, 1956.
331. Barletta, ., Caffesse, R., Paladine, G, and Plot, C: Comparative biometrie evaluation of results obtained after gingivectomy and
reverse bevel periodontal flap surgery. J Dent Res 51: 1227, 1972.
332. Benjamin, E.: The quantitative comparison of subgingival
curettage and gingivectomy in the treatment of Periodontitis simplex.
J Periodontol 27: 144, 1956.
333. Grant, D.: Experimental periodontal surgery: Gingivectomy
excision to the alveolar crest. J Dent Res 43: 791, 1964.
334. Kambiz, ., and Stahl, S.: The remodeling of human gingival
tissue following gingivectomy. J Periodontol 48: 136, 1977.
335. Korn, N., Schaffere, and McHugh, R.: An experimental assessment of gingivectomy and soft tissue curettage in dogs. / Periodontol 36: 96, 1965.
336. Ramfjord, S. P., Nissle, R. R., Shick, R. ., and Cooper, H.:
Subgingival curettage versus surgical elimination of periodontal pockets. J Periodontol 39: 167, 1968.
337. Zamet, J. S.: A comparison of an embellished gingivectomy
with the inverse bevel flap procedure incorporating osseous recontouring. Dent Pract 17: 387, 1967.
338. Deasy, M. J., Vogel R., and Formicola, .: The relevance of
curettage in periodontal therapy. Ann Dent 37: 70, 1978.
339. Goldman, . M., and Cohen, D. W.: Periodontal Therapy, ed
6, St. Louis, C. V. Mosby, 1980.
340. World Workshop in Periodontics, Ramfjord, S. (ed), Ann Arbor, Michigan, 1966.
341. Chace, R.: Subgingival curettage in periodontal therapy. J
Periodontol 45: 107, 1974.
342. Ramfjord, S. P.: Surgical pocket therapy. Int Dent J 21: 263,
1977.
343. Raust, G.: What is the value of gingival curettage in periodontal therapy? Periodont Abst 17: 142, 1969.
344. Glickman, I.: The effect of pre-scaling upon gingival healing
following periodontal surgery. J Dent Med 16: 19, 1961.
345. Gottsegen, R.: Should teeth be scaled prior to surgery? J
Periodontol 32: 301, 1961.
346. Zamet, J. S.: Initial preparation of gingival tissues prior to
surgery. Dent Pract 17: 115, 1966.
347. Yukna, R. ., and Lawrence, J. J.: Gingival surgery for soft
tissue new attachment. Dent Clin North Am 24: 705, 1980.
348. Schaffer, . M., and Zander, H.: Histologie evidence of reattachment of periodontal pockets. Parodontologie 1: 101, 1953.
349. Catn, J., Nyman, S., and Zancer, H.: Histometric evaluation
of periodontal surgery II. Connective tissue attachment levels after
four regenerative procedures. J Clin Periodontol 1: 224, 1980.
350. Hill, R. W., Ramfjord, S. P., Morrison, E. C, Appleberry, E.,
Caffesse, R. G., Kerry, G. J., and Nissle, R. R.: Four types of
periodontal treatment compared over two years. J Periodontol 52: 655,
1981.
351. Hirschfeld, L.: Subgingival curettage in periodontal treatment.
J Am Dent Assoc 44: 59, 1952.
352. International Conference on Research in the Biology of Periodontal Disease, Klavan, B. (ed). Chicago, 111., 1977.
353. Schluger, S.: Osseous resection: A basic principle in periodontal surgery. Oral Surg 2: 316, 1949.
354. Flores-de-Jacoby, L., and Fesseler, .: The efficacy of osseous
surgery. Efficacy of Treatment Procedures in Periodontics (Workshop),
Shanley, D. B.; ed. Chicago, Quintessence Pubi, 1980.
355. Friedman, N.: Periodontal osseous surgery: Osteoplasty and
ostectomy. J Periodontol 26: 257, 1955.
356. Ochsenbein, C.: Current status of osseous surgery. J Periodontol 48: 577', 1977'.
357. Ochsenbein, C: The double flap procedure. Periodontics 1: 17,
1963.
358. Ochsenbein, G: Osseous resection in periodontal surgery. J
Periodontol 29: 15, 1958.
359. Ochsenbein, C, and Bohannon, H.: The palatal approach to

gingivectomy technique

Volume 53
Number 8

surgery. J Periodontol 35: 37, 1964.

360. Ochsenbein, C, and Ross, S.: A re-evaluation of osseous
surgery. Dent Clin North Am 13: 87, 1969.
361. Knoell, A. C, and Vogan, W. I.: A mathematical investigation
of the biochemical effects of simulated periodontal surgery. J Periodont
Res 12: 290, 1977.
362. Selipsky, H.: Osseous surgery how much need we compromise? Dent Clin North Am 20: 79, 1976.
363. Ammons, W. and Smith, D.: Flap curettage: Rationale, technique and expectations. Dent Clin North Am 20: 215, 1976.
364. Ramfjord, S. P., and Nissle, R. R.: The modified Widman
flap. J Periodontol 45: 601, 1974.
365. Everett, F., Waerhaug, J., and Widman, .: "Leonard Widman" surgical treatment of pyorrhea alveolaris. J Periodontol 42: 571,
1971.
366. Ramfjord, S. P.: Present status of the modified Widman flap
procedure. / Periodontol 48: 558, 1977.
367. Burgett, F. G., Knowles, J. W., Nissle, R. R., Shick, R. ., and
Ramfjord, S. P.: Short term results of three modalities of periodontal
treatment. J Periodontol 48: 131, 1977.
368. Knowles, J. W., and Ramfjord, S. P.: The lateral sliding flap
with a free gingival graft. The University of Michigan Dental School,
Video Cassettes, 1971.
369. Ramfjord, S. P., Knowles, J. W., Nissle, R. R., Burgett, F. G.,
and Shick, R. .: Results following three modalities of periodontal
therapy. / Periodontol 46: 522, 1975.
370. Catn, J., and Nyman, S.: Histometric evaluation of periodontal surgery. I. The modified Widman flap procedure. / Clin Periodontol
7: 212, 1980.
371. Yukna, R. .: A clinical and histologie study of healing
following the excisional new attachment procedure in Rhesus monkeys.
J Periodontol 47: 701, 1976.
372. Yukna, R. .: Comparative clinical evaluation of freeze dried
allograft and autogenous gingival graft in human. J Clin Periodontol 4:
191, 1977.
373. Yukna, R. .: Longitudinal evaluation of the excisional new
attachment procedure in humans. J Periodontol AS: 142, 1978.
374. Yukna, R. ., Bowers, G. M., Lawrence, J. L, and Fedi, P. F.:
A clinical study of healing in humans following the excisional new
attachment procedure. J Periodontol 47: 696, 1976.
375. Schallhorn, R. G.: Present status of osseous grafting procedures. J Periodontol 48: 570, 1977.
376. Diem, C. R., Bowers, G. M., and Moffitt, W. C: Bone bending:
A technique for osseous implants. J Periodontol 43: 295, 1972.
377. Robinson, R. E.: Osseous coagulum for bone induction. J
Periodontol 40: 503, 1969.
378. Soehren, S. E., and Van Swol, R. L.: The healing extraction
site: A donor area for periodontal grafting material. J Periodontol 50:
128, 1979.
379. Dragoo, M. R., and Urwin, R. K.: A method of procuring
cancellous iliac bone utilizing a trephine needle. J Periodontol 43: 82,
1972.
380. Hiatt, W. H., and Schallhorn, R. G.: Human allografts of iliac
cancellous bone and marrow m periodontal osseous defects. I. Rationale and methodology. JPeriodontol 42: 642, 1971.
381. Schallhorn, R. G., and Hiatt, W. H.: Human allografts of iliac
cancellous bone and marrow in periodontal osseous defects. II. Clinical
observations. J Periodontol 43: 67, 1972.
382. Libin, B. M., Ward, H. L., and Fishman, L.: Decalcified,
lyophilized bone allografts for use in human periodontal defects. J
Periodontol 46: 51, 1975.
383. Haggerty, P. C: Human allograftsthe efficient approach to
the infrabony defect. J Periodontol 48: 743, 1977.
384. Haggerty, P. C, and Maeda, I.: Autogenous bone grafts: A
revolution in the treatment of vertical bone defects. / Periodontol 42:
626, 1971.
385. Rosenberg, E. S., Graber, D. ., and Abrams, B.: Repair of
bony defect using an intraoral exostosis as the donor site. A case report.
J Periodontol 50: 476, 1979.
osseous

Surgical Therapyfor Periodontitis

499

386. Rosenberg, M. M.: Re-entry of an osseous defect treated by a

bone implant after a long duration. J Periodontol 42: 360, 1971.
387. Schallhorn, R. G.: Eradication of bifurcation defects utilizing
frozen autogenous hip marrow implants. Periodontal Abstr 15: 101,
1967.
388. Bierly, J. ., Sottosanti, J. S., Costly, J. M., and Cherrick, H.
H.: An evaluation of the osteogenic potential of marrow. J Periodontol
46: 277, 1975.
389. Cushing, M.: Autogenous red marrow grafts: Potential for
induction of Osteogenesis. J Periodontol 40: 492, 1969.
390. Schallhorn, R. G.: The role of iliac transplants in the practice
of periodontics. Ward, H. L., (ed), A Periodontal Point of View, pp 233275. Thomas, Springfield, 1973.
391. Sanders, J. J., Sepe, W. W., Koch, R. W., Bowers, G. M.,
Starkweather, R., and Pelleu, G. B.: A clinical evaluation of freezedried bone allografts and in combination with autogenous bone in
periodontal osseous defects. J Dent Res (Special Issue B) 56: 169, 1977.
392. Sepe, W. W., Bowers, G. M., Lawrence, J. J., Friedlaender, G.
E., and Koch, R. W.: Clinical evaluation of freeze-dried bone allografts
in periodontal osseous defectsPart II. J Periodontol 49: 9, 1978.
393. Friedlaender, G. E., Strong, D. M., and Sell, K. W.: Studies
on the antigenicity of bone, I. Freese-dried and deep frozen bone
allografts in rabbits. J Bone Joint Surg 58A: 854, 1976.
394. Turner, D. W., and Mellonig, J. T.: Antigenicity of freezedried bone allograft in periodontal osseous defects. J Periodont Res 16:
89, 1981.
395. Froum, S. J., Thaler, R., Scopp, I. W and Stahl, S. S.: Osseous
autografts. II. Histologie responses to osseous coagulum-bone blend
grafts. J Periodontol 46: 656, 1975.
396. Hawley, C. E., and Miller, J.: A histologie examination of a
free osseous autografi. J Periodontol 46: 289, 1975.
397. Moskow, B. S., Karsh, F., and Stein, S. D.: Histological
assessment of autogenous bone graft: A case report and critical evaluation. J Periodontol 50: 291, 1979.
398. Carraro, J. J., Sznajder, N., and Alonso, C. .: Intraoral
cancellous bone autografts in treatment of intrabony pockets. J Clin
Periodontol 3: 104, 1976.
399. Hoffman, I. D., and Flanagan, P.: Exophytic granulation
reactions associated with autogenous iliac marrow transplants into
periodontal defects. J Periodontol 45: 586, 1974.
400. Schallhorn, R. G.: Postoperative problems associated with iliac
transplants. J Periodontol 43: 3, 1972.
401. Burnette, E. W.: Fate of the iliac crest graft. J Periodontol 43:
88, 1972.
402. Dragoo, M. R., and Sullivan, H. C: A clinical and histologie
evaluation of autogenous iliac bone grafts in humans. Part II. External
root rsorption. J Periodontol 44: 614, 1973.
403. Nery, . B., and Lynch, K. L.: Preliminary clinical studies of
bioceramic in periodontal osseous defects. J Periodontol 49: 523, 1978.
404. Radell, B. L., and Cassingham, R. L: A clinical evaluation of
Proplast as a periodontal implant material. J Periodontol 51: 110, 1980.
405. Strub, J. R., Gaberthuel, T. W., and Firstone, A. R.: Comparison of tricalcium phosphate and frozen allogenic bone implants in
man. J Periodontol 50: 624, 1979.
406. Feingold, J. P., Chasen, A. I., Doyle, J., and Alfano, M. C:
Preserved scierai allografts in periodontal defects in man. II. Histologie
evaluation. J Periodontol 48: 4, 1977.
407. Iacono, V. J., Gomes, B. C, Sciubba, J. L, Davis, R. K.,
Klingsberg, J., and Baer, P. N.: Clinical and laboratory studies on
human sclera allografts. J Periodontol 51: 211, 1980.
408. Klingsberg, J.: Periodontal sclera grafts and combined grafts
of sclera and bone: Two year appraisal. J Periodontol 45: 262, 1974.
409. Corn, H: Periosteal fenestrationits clinical significance. J
Periodontol 33: 140, 1962.
410. Goldman, H. M., Schluger, S., and Fox, L.: Periodontal Therapy, ed 2, 342, St. Louis, C. V. Mosby, 1960.
411. Gottsegen, R.: Frenum position and vestibular depth in relation to gingival health. Oral Surg 7: 1069, 1954.
412. Hileman, A. C: Surgical repositioning of vestibule and fren-

500

Proceedings From State of the Art Workshop

urns in periodontal disease. J Am Dent Assoc 55: 676, 1957.

413. Robinson, R. E.: Mucogingival junction surgery. / Calif State
Dent Assoc and Nev State Dent Soc 33: 379, 1957.
414. Robinson, R. E.: Periodontal fenestration in mucogingival
surgery. J West Soc Periodontol 9: 107, 1961.
415. Stewart, J.: Reattachment of vestibular mucosa as an aid in
periodontal therapy. J Am Dent Assoc 49: 283, 1954.
416. Edlan, ., and Mejchar, B.: Plastic surgery of the vestibulum
in periodontal therapy. Int Dent J 13: 593, 1963.
417. Corn, H.: Edentulous area pedicle grafts in mucogingival
surgery. Periodontics 2: 229, 1964.
418. Kon, S., et al.: Split thickness flap, apically replaced, with
protected linear periosteal fenestration: A clinical and histological
study in dogs. J Periodontol 49: 174, 1978.
419. Schmid, M. O., et al.: Mucogingival surgery. The subperiosteal
vestibule extension. J Clin Periodontol 6: 22, 1979.
420. Redondo, V., Bustamonte, ., and Carranza, F.: Evaluacin
biometrica de la tecnica de extension gingival case fenestracion periostica. Rev Asoc Odontol Argentina 56: 346, 1968.
421. Arnold, N. R., and Hatchett, C. M.: A comparative investigation of two mucogingival surgical methods. J Periodontol 33: 129, 1962.
422. Bergenholtz, ., and Huguson, .: Vestibular sulcus extension
surgery in cases with periodontal disease. / Periodont Res 2: 221, 1967.
423. Bergenholtz, ., and Huguson, .: Vestibular sulcus extension
surgery in the mandibular front region. The Edlan-Mejchar method.
A five year follow-up study. J Periodontol 44: 309, 1973.
424. Bergenholtz, ., Persson, G., and Thilander, H.: Vestibular
sulcus extension surgery in the mandibular front region. Odontol Tidskr
73: 579, 1965.
425. Bohannan, . M.: Studies in the alteration of vestibular depth.
I. Complete denudation. J Periodontol 33: 120, 1962.
426. Bohannan, . M.: Studies in the alteration of vestibular depth.
II. Periosteum retention. J Periodontol 33: 354, 1962.
427. Carranza, F. ., and Carraro, J. J.: Effect of removal of
periosteum on postoperative results of mucogingival surgery. J Periodontol 34: 223, 1963.
428. Carraro, J. J., et al.: Effect of bone denudation in mucogingival
surgery in humans. / Periodontol 35: 463, 1964.
429. Costich, E. R., and Ramfjord, S. P.: Healing after partial
denudation of the alveolar process. J Periodontol 39: 127, 1968.
430. Glickman, I., et al.: Healing of the periodontium following
mucogingival surgery. Oral Surg 16: 530, 1963.
431. Grant, J.: A histological study of repositioning the attached
gingiva in periodontal therapy. Iowa Dent J 44: 62, 1958.
432. Ivancie, G. P.: Experimental and histological investigation of
gingival regeneration in vestibular surgery. J Periodontol 28: 259, 1957.
433. Pennel, B. M., et al.: Retention of periosteum in mucogingival
surgery. J Periodontol 36: 39, 1965.
434. Pfeifer, J. S.: The growth of gingival tissue over denuded bone.
J Periodontol 34: 10, 1963.
435. Ramfjord, S. P., and Costich, E. R.: Healing after exposure of
periosteum on the alveolar process. J Periodontol 39: 199, 1968.
436. Simann, G.: Histology study of the so-called attached gingiva
following the deepening of the vesticulum by the mucosal flap technique. Periodont Abstr 17: 116, 1969.
437. Wade, . .: Vestibular deepening by the technique of Edlan
and Mejchar. / Periodont Res 4: 300, 1969.
438. Wilderman, . M.: Repair after a periosteal retention procedure. J Periodontol 34: 487, 1963.
439. Wilderman, M. N., Wentz, F. M., and Orban, B. J.: Histogenesis of repair after mucogingival surgery. J Periodontol 31: 283, 1961.
440. Karring, T., Lang, N. P., and Le, H.: Role of connective
tissue in determining epithelial specificity. J Dent Res 51: 1303, 1972.
441. Karring, T., Ostergaard, E., and Le, H.: Conservation of
tissue specificity after heterotopic transplantation of gingiva and alveolar mucosa. J Periodont Res 6: 283, 1971.
442. Smith, R. M.: A study of the intertransplantation of alveolar
mucosa. Oral Surg 29: 328, 1970.
443. Smith, R. M.: A study on the intertransplantation of gingiva.

J. Periodontol.

August,

1982

Oral Surg 29: 169, 1970.

444. Bjorn, H.: Coverage of denuded root surfaces with a lateral
sliding flap. Use of free gingival grafts. Odontol Revy 22: 37, 1971.
445. Sullivan, H. C, and Atkins, J. H.: Free autogenous gingival
grafts. I. Principles of successful grafting. Periodontics 6: 5, 1968.
446. Sullivan, H. C, and Atkins, J. H.: The role of free gingival
grafts in periodontal therapy. Dent Clin North Am 133: 148, 1969.
447. Bissada, N., and Sears, S.: Quantitative assessment of free
gingival grafts with and without periosteum and osseous perforation.
J Periodontol 49: 17, 1978.
448. Brackett, R. C, and Gargiulo, A. W.: Free gingival grafts in
humans. J Periodontol 41: 581, 1970.
449. Brustein, D.: Cosmetic periodontics. Coronally repositioned
pedicle graft. Dental Survey, vol. 46, July 22, 1970.
450. Caffesse, R. G., Carraro, J. J., and Carranza, F. ., Jr.: Injertos
gingivales libres en perros. Estudio clinico-histologico. Rev Asoc Odontol Argentina 60: 465, 1972.
451. Caffesse, R. G., Nasjleti, C. E., Burgett, F. G., Kowalski, C. J.,
and Castelli, W. .: Healing of free gingival grafts with and without
periosteum. Part II. Radioautographic evaluation. J Periodontol 50:
595, 1979.
452. Dordick, B., et al.: Clinical evaluation of free autogenous
gingival grafts placed on alveolar bone. Part II. Coverage of nonpathologic dehiscences and fenestrations. J Periodontol 47: 568, 1976.
453. Dordick, B., Coslet, J. G., and Seibert, J. S.: Clinical evaluation
of free autogenous grafts placed on alveolar bone. I. Clinical predictability. J Periodontol 47: 559, 1976.
454. Gargiulo, A. W., and Arrocha, R.: Histo-clinical evaluation of
free gingival grafts. Periodontics 5: 285, 1967.
455. Gordon, H. P., Sullivan, H. C, and Atkins, J. C: Free autogenous gingival grafts. II. Supplemental findings. Histology of the graft
site. Periodontics 6: 130, 1968.
456. James, W. C. and McFall, W. T.: Placement of free gingival
grafts on denuded alveolar bone. Part I. Clinical evaluation. J Periodontol 49: 283, 1978.
457. James, W. C, McFall, W. T., and Burkes, E. J.: Placement of
free gingival grafts on denuded alveolar bone. Part II. Microscopic
observation. / Periodontol 49: 291, 1978.
458. Janson, W. ., et al.: Development of the blood supply to
splitthickness free gingival autografts. J Peridontol 40: 707, 1969.
459. Mormann, W., Bernimoulin, J. P., and Schmid, . O.: Fluorescein angiography of free gingival autografts. J Clin Periodontol 2:
177, 1975.
460. Oliver, R. C, Le, H., and Karring, T.: Microscopic evaluation
of the healing and revascularization of free gingival grafts. J Periodont
Res 3: 84, 1968.
461. Caffesse, R. G., Plot, C, and Albano, . .: Injertos gingivales
libres en perros. Estudio biometrico. Rev Asoc Odontol Argentina 60:
517, 1972.
462. Rateitschak, . H: Recession: A four year longitudinal study
after free gingival grafts. / Clin Periodontol 6: 158, 1979.
463. Van Hourse, R. L., Gillette, W. B., and O'Leary, T. J.: Dimensional changes of free gingival grafts in humans. I. A. D. R. Abstr. No.
Ill, 1978.
464. Bell, L., et al.: The presence of "creeping attachment" in
human gingiva. J Periodontol 49: 513, 1978.
465. Matter, J. and Cimasoni, G.: Creeping attachment after free
gingival grafts. J Periodontol 47: 574, 1976.
466. Livingston, H. L.: Total coverage of multiple and adjacent
denuded root surfaces with a free gingival autografi. J Periodontol 46:
209, 1975.
467. Mylinek, ., Smukler, H., and Bchner, .: The use of free
gingival grafts for the coverage of denuded root. J Periodontol 44: 248,
1973.
468. Vandersall, D. C: Management of gingival recession and a
surgical dehiscence with a soft tissue autografi: Four year observation.
J Periodontol 45: 274, 1974.
469. Ward, V. J.: A clinical assessment of the use of the free gingival
graft for correcting localized recession associated with frenai pull. J

Volume 53
Number 8

Periodontol 45: 78, 1974.

470. Grupe, . E., and Warren, R. F.: Repair of gingival defects by
sliding flap operation. J Periodontol 27: 92, 1956.
471. Ariaudo, . .: Problems in treating a denuded labial root
surface of a lower incisor. J Periodontol 37: 274, 1966.
472. Bernimoulin, J.: Deckung gingivaler rezessionen mit koronaler
Verschiebungsplastik. Dtsch Zahnaerztl 28: 1222, 1973.
473. Cohen, D., and Ross, S.: The double papillae flap in periodontal therapy. J Periodontol 39: 65, 1968.
474. Friedman, N., and Levine, H. L.: Mucogingival surgery: Current status. J Periodontol 35: 5, 1964.
475. Grupe, H. E.: Modified technique for the sliding flap operation. J Periodontol 37: 491, 1966.
476. Harvey, P.: Management of advanced Periodontitis. Part I.
Preliminary report of a method of surgical reconstruction. New Zealand
Dent J 61: 180, 1965.
477. Hauler, .: Mucogingival surgery. Utilization of interdental
gingiva as attached gingiva by surgical displacement. Periodontics 5:
126, 1967.
478. Maynard, L: Coronal positioning of a previously placed autogenous gingival graft. J Periodontol 48: 151, 1977.
479. McFall, W. T.: The laterally repositioned flapcriteria for
success. Periodontics 5: 89, 1967.
480. Nordenram, .: Parodontalkirurgisk rekonstruktion av gingivalranden efter partiell gingivectomi i samma seans. Sven Tandlak
Tisdkr 42: 373, 1959.
481. Nordenram, ., and Landt, H.: Evaluation of a surgical technique in the periodontal treatment of maxillary anterior teeth. Acta
Odontol Scand 27: 283, 1969.
482. Pennel, . M., et al.: Oblique rotated flap. J Periodontol 36:
305, 1965.
483. Restrepo, O.: Coronally repositioned flap: Report of four cases.
J Periodontol 44: 564, 1973.
484. Robinson, R. E.: Utilizing an edentulous area as a donor site
in the lateral repositioned flap. Periodontics 2: 79, 1964.
485. Ruben, M. P., Goldman, H. M., and Janson, W.: Biologic
considerations fundamental to successful employment of laterally repositioned pedicle flaps and free autogenous gingival grafts in periodontal therapy. S. Stahl (ed), Periodontal Surgery: Biologic Basis and
Technique. C. C. Thomas, 1976.
486. Smukler, H., and Goldman, H.: Laterally repositioned
"stimulated" osteoperiosteal pedicle grafts in the treatment of denuded
roots. Preliminary report. J Periodontol 50: 379, 1979.
487. Staffelino, H.: Management of gingival recession and root
exposure problems with periodontal disease. Dent Clin North Am
March, 1964.
488. Sumner, C: Surgical repair of recession on the maxillary
cuspid: Incisally repositioning the gingival tissues. J Periodontol 40:
119, 1969.
489. Ter-Manveliancova, M.: Metoda rozsireneho mustkoveho laloku chirurgii paradontu. Cesk Stomatol 14: 14, 1974.
490. Albano, E., et al.: Estudio biometrico de colgajos desplazados
laterelmente. Rev Asoc Odontol Argentina 61: 12, 1973.
491. Guinard, . ., and Caffesse, R. G.: Treatment of localized
gingival recessions. Part I. Lateral sliding flap. J Periodontol 49: 351,
1978.
492. Guinard, . ., and Caffesse, R. G.: Treatment of localized
gingival recessions. Part III. Comparison of results obtained with
lateral sliding and coronally repositioned flaps. J Periodontol 49: 457,
1978.
493. Sugarman, E.: A clinical and histological study of the attachment of grafted tissue to bone and teeth. J Peridontol 40: 381, 1969.

Surgical Therapyfor Periodontitis

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.

Send reprint requests to: Dr. Samuel Kakehashi, National Institute

of Dental Research, Bethesda, MD 20205.