8. 1981 Samuel Kakehashi, Paul F. Parakkal. Proceedings From the State of the Art Workshop

8/19/2019 8. 1981 Samuel Kakehashi, Paul F. Parakkal. Proceedings From the State of the Art Workshop

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Proceedings From TheState of the Art Workshop

on

Surgical Therapy for Periodontitis

Sponsored by

National Institute of Dental ResearchNational Institutes of Health

May 13-14, 1981

Conference Coordinators:

Samuel Kakehashi,Paul F. Párakkal,

National Institute of Dental ResearchBethesda, MD 20205

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PREFACE

A state-of-the-art workshop titled: Surgical Therapy for Periodontitis, sponsored by theNational Institute of Dental Research, was held on May 13-14, 1981, at the NationalInstitutes 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 scientificevidence on the efficacy of surgical therapy for adult Periodontitis and to formulatesummary recommendations on this treatment modality. The scope of this workshop wasintentionally limited to address the technical question of whether the surgical treatment ofPeriodontitis is scientifically sound, safe and efficacious. Thus, economic and societal issuesin reference to this treatment modality impacting on the individual patient as well as thepublic-at-large were omitted from the agenda. To help focus on the pertinent issues relatingto 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 clinicalresearchers were assembled to write a background review paper on the surgical treatmentof adult Periodontitis including the etiology, pathogenesis and the spectrum of treatmentconsiderations including the various surgical approaches. In an attempt to develop abalanced paper representing all views, the Task Force undertook a critical review andobjective assessment of the available scientific data on the treatment of Periodontitis. Thebackground paper was sent to all workshop attendees prior to the meeting.

A special review panel of experts from a variety of backgrounds participated in theworkshop. The Panel included general dentists, a statistician, epidemiologist, pathologist,microbiologist, and periodontist clinicians, academicians and clinical scientists. This panelwas charged with the responsibility of reviewing and analyzing the existing informationincluding data presented during the workshop in an attempt to provide the most usefulcurrent views on the efficacy of surgical therapy for Periodontitis. At the conclusion of theworkshop the Review Panel presented its summary recommendations based on theinformation reviewed in the background paper, the workshop presentations and theresultant audience participation.

The workshop program was as follows:

Goals of Workshop—Dr. Irwin Mandel, Workshop Chairman

Report of Task Force—Dr. William McHugh, Task Force ChairmanDr. Paul Robertson—IntroductionDr. Bruce Pihlstrom—No

TherapyDr. Stanley Hazen—Initial Therapy; Alternative TherapiesDr. Saul Schluger and Dr. Raul Caffesse—Periodontal SurgeryDr. Jack Caton, Jr.—Maintenance Therapy

Research PapersDr. Raul Caffesse for Dr. Sigurd Ramfjord—Clinical Applications of Recent

Periodontal ResearchDr. Bengt Rosling—The Important Relationship Between Surgical Results and

Maintenance Care—Based on a Six Year StudyDr. William Ammons—Longitudinal Evaluation of Osseous Resective Surgery & Open

Flap CurettageDr. Timothy O'Leary—Treatment of the Periodontally Involved Root Surfaces

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Volume 53Number 8 Surgical Therapyfor Periodontitis 477

Review & Critiques of WorkshopDr. Robert GencoDr. Helmut Zander

Audience Participation

This workshop report includes the Background Paper authored by the Task Force andthe Summary Recommendations concluded by the Review Panel.

WORKSHOP BACKGROUND PAPER

Task Force

William D. McHugh, D.D.S., Chairman, Eastman Dental Center, RochesterRaul G. Caffesse, D.D.S., University of Michigan, Ann ArborJack G. Caton, Jr., D.D.S., Eastman Dental Center, RochesterStanley P. Hazen, D.D.S., University of Detroit, DetroitJames T. Mellonig, D.D.S., U.S. Navy, Great LakesBruce L. Pihlstrom, D.D.S. University of Minnesota, MinneapolisRichard R. Ranney, D.D.S., Virginia Commonwealth University, RichmondPaul B. Robertson, D.D.S.,

University of Connecticut,

FarmingtonSaul 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 diseaseof the tissues supporting the teeth. Caused principally by bacterial plaque, it is aggravatedby several conditions in the host. Treatment is aimed at removing the bacterial plaque andrestoring the tissues to a healthy condition which can be maintained throughout life.

Gingivitis and the earliest stages of Periodontitis usually can be treated effectivelywithout surgery, but more advanced Periodontitis is usually treated by some type of surgerywhich will facilitate the removal of both soft and calcified bacterial deposits from toothsurfaces. Only when these deposits are removed and the levels of bacterial plaque arereduced to a minimum can the disease be controlled.

Surgical treatment also aims at restoring the supporting tissues to a healthy state and atmaintaining 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 restorethe supporting tissues to health at a "reduced" level. The other attempts to repair some ofthe loss of attachment which has resulted from the Periodontitis.

Alternatives to surgical therapy are no treatment of any sort or treatment to remove orcontrol the etiologic agents without surgery.

The object of this paper is to report and evaluate the available data on the selection andvalue of surgical therapy for Periodontitis and, where possible, to compare them withalternative forms of nonsurgical therapy. The Task Force hopes thereby to determine therelative value and appropriateness of different types of periodontal surgery.


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478 Proceedings From State ofthe Art Workshop

INTRODUCTION

Periodontitis is the major cause of tooth loss in adultpopulations. Several clinical forms of Periodontitis havebeen recognized and described. This review is directedto chronic Periodontitis, a painless, slowly progressingdisease that is characterized by inflammation of thegingiva caused by microbial colonization of adjacenttooth surfaces, extending into deeper periodontal tissues,and resulting in pocket formation, destruction of alveolarbone, mobility of teeth, and their exfoliation.1 This proc-ess has been clinically subdivided into chronic gingivitisand Periodontitis, depending on the probing depth rela-tive to the cementoenamel junction. The transition fromchronic gingivitis to Periodontitis, however, is not wellunderstood. Historically, chronic gingival inflammationhas been considered an early phase ofPeriodontitis, oftentermed the gingivitis-periodontitis continuum. Some ev-idence, however, suggests that whereas chronic gingivitismay predispose to Periodontitis, it is a separate disease.

Both the initiation and progression of chronic gingi-vitis are caused by the accumulation of microorganismsnear the gingival margin. In addition, the incidence andseverity of periodontal disease—whether it be gingivitis,Periodontitis, or loss of alveolar bone—have been cor-related with lack of oral hygiene. Except for microbialplaque no specific causal organisms or related pathogenicpathways have been clearly indicted. Since microorga-nisms are rarely found within periodontal tissues, thedestruction of supporting structures associated with Peri-odontitis is generally assumed to result from the patho-logic products of the oral microflora. Such products mayoriginate from exogenous organisms not normally pres-ent in the oral flora or from increased numbers of certainspecies in the indigenous flora. Distinct patterns of floraassociated with periodontal health, gingivitis, and Peri-odontitis have not been clearly demonstrated, but theavailable evidence favors the role of indigenous micro-flora rather than a more classical infection by specificexogenous organisms. Once established in sufficientnumbers, the products of the "disease-associated" floramay cause destruction of periodontal tissues directly orby activating host-response mechanisms. Both the con-stitution 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 for-

mulated, the microflora and related pathogenic mecha-nisms responsible for periodontal disease must be iden-tified. For example, targeted therapeutic approacheswould be feasible if gingivitis and Periodontitis are sep-arate entities, each initiated by specific microbial speciesor mediated by particular pathogenic pathways. Thepresence of active disease could be determined by eval-uating the periodontal microflora or other pathogenicagents, and antimicrobial therapy could be directed

against particular causal organisms. Currently, we still

J. Periodontol.

August, 1982

lack such knowledge; as a result, the fundamental prin-ciple underlying all therapy of Periodontitis is broadcontrol of the oral microflora.

Natural History and Epidemiology of Periodontitis

Diseases of the periodontium are among the mostcommon afflictions of mankind. Bone résorption con-sistent with Periodontitis has been observed in the fossilremains of Neanderthal man, and detailed descriptionsof periodontal disease in Chinese and Egyptian writingspredate this conference by over 4,000 years.2,3 Epide-miologica! surveys conducted during this century suggestthat essentially all the world's adult population haveexperienced some form of periodontal disease.4,5

The natural history of periodontal disease over an agerange of 15 to 40 recently has been described in longi-tudinal studies ofpopulations in Norway and Sri Lanka.6The groups had major geographical, cultural, socioeco-nomic, and educational differences and represented ex-tremes with respect to dental care. The predominant

periodontal diseases reported in both populations werechronic gingivitis and Periodontitis. Indeed, in the Nor-wegian group, no cases of acute gingivitis or rapidlyprogressing Periodontitis were noted. Destruction of sup-porting structures associated with chronic Periodontitiswas continuous and progressed at a relatively even rateover time in both groups, although annual rates ofperiodontal attachment loss were significantly different,averaging 0.09 mm in the Norwegian population and0.25 mm in Sri Lankans.

In general, interpretation of epidemiological studies iscomplicated by deficiencies in indices used for the mea-

surement of periodontal disease and the assumption,made in most studies, that all pathosis affecting theperiodontium is a single entity. Nevertheless, despite avariety of experimental approaches using populationswith divergent cultural, socioeconomic, and geographicbackgrounds, the results ofepidemiological surveys havebeen remarkably uniform with respect to the universalityof periodontal disease and the strong positive correlationbetween periodontal disease and both age and the pres-ence of microbial plaque.7"11 Gingivitis affects the ma-

jority of young children and, by 20 years of age, theprevalence of gingivitis approaches 100%. While the

development of

Periodontitis in children is

relativelyuncommon, pocket formation and related bone loss inthe teenage population has been estimated at approxi-mately 6%. The prevalence of Periodontitis increasesalmost linearly with age and, in the adult population,accounts for well over 50% of missing teeth. The strongcorrelation between age and alveolar bone loss appearsto reflect the cumulative result of plaque-induced inflam-mation rather than diminished resistance in older indi-viduals.

The relation between periodontal disease and othersocial and demographic factors is less clear. In westerncultures, the disease is less severe in females than in


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Volume 53Number 8

males. Increased levels of education, income, and socio-economic status also have been associated with lessdisease. The correlation for all these factors, however, is

quite weak and is often lost entirely when groups arestratified by measures of oral hygiene.5'8

Etiology of Periodontitis

Plaque Factors. Dental plaque, a general term fortooth-adherent material composed principally of micro-organisms and microbial products, is the primary etio-logical agent in gingivitis and Periodontitis. Evidenceimplicating oral microflora12"14 includes the epidemiolog-ica! observations previously discussed, the induction ofthe disease process solely by allowing the accumulationof bacteria15"18 and the reversal of the periodontal lesionby mechanical19"22 or chemotherapeutic plaque re-moval.23"26 Individuals who initially demonstrated excel-lent periodontal health consistently developed gingivitisby 1 to 3 weeks after all methods of plaque control werewithdrawn; when oral hygiene measures were reinsti-

tuted, gingival health was restored within 10 days.The microbiological contents of plaque appear to varywidely among individuals and among sites within thesame individual. Moreover, in periodontally involvedsites, the supragingival microflora is different from thatfound subgingivally. In addition, recent evidence sug-gests that different forms of periodontal disease, includ-ing chronic gingivitis and Periodontitis, have specificmicrobial etiologies.

The subgingival microflora obtained immediately be-fore experimental gingivitis is induced and associatedclinically with gingival health, where some supragingival

plaque is

present, is

composed mainly of

Gram-positiveorganisms, especially species of streptococcus.27'28 Bothchronic gingivitis and Periodontitis are characterized byan increasing shift of the subgingival microflora to theGram-negative community. Gram-negative facultativeand anaerobic rods have been reported to compriseapproximately 40% of the cultivable subgingival micro-flora in chronic gingivitis29 and from 65 to 75% of thesubgingival flora in chronic Periodontitis.30'31 Species ofBacteroides, Actinomyces, Haemophilus, Eubacterium, Se-lenomonas, Treponema, and Fusobacterium are report-edly prominent in chronic disease, but no specific orga-nisms or groups of organisms have been indicted for theinitiation of gingivitis or its progression to Periodontitis.

Nonplaque Factors. Both epidemiological and experi-mental studies have failed to demonstrate any local or

systemic factors, aside from microorganisms, that causegingivitis or Periodontitis. Several of these factors, how-ever, including anatomic oral abnormalities, mouth-breathing, dental appliances, and certain systemic con-ditions, may modify the progress of the disease onceestablished.32 In many cases, modifying local factors suchas defective restorations, prosthetic appliances, ligaturesand calculus may interfere with the patient's ability toremove 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 ofgingivitis and Periodontitis associated with hormonalchanges33 and with both local34 and systemic35"37 neutro-philic leukocyte dysfunction.

How much occlusal factors contribute to the progres-sion of periodontal disease remains controversial. Studiesin man, primates, and beagle dogs have consistentlyshown that excessive occlusal forces do not initiate eithergingivitis or Periodontitis or convert an established gin-givitis or Periodontitis.38 When occlusal trauma was su-perimposed on experimentally-induced Periodontitis, therate of loss of periodontal attachment was accelerated indogs39 but not in monkeys,40 and bone regeneration wasretarded after the resolution of Periodontitis in mon-keys.41

There is little evidence that nutritional deficiencieseither initiate or affect periodontal disease.42

Pathogenesis of Periodontitis

The histopathological events that occur after the mi-crobial colonization of tooth surfaces adjacent to healthygingiva and during the progression from gingivitis toPeriodontitis have been divided into four general, over-lapping stages: initial, early, established, and advanced.43The first stage consists of vasculitis below the junctionalepithelium and is concomitant with the increased migra-tion of neutrophils. Alterations in the junctional epithe-lium and some loss of perivascular collagen are some-times observed. The early stage, beginning about 4 to 7days after plaque accumulation, is characterized by theappearance of an inflammatory infiltrate consisting prin-

cipally of

lymphocytes, continuing collagen destruction,and the proliferation of basal junctional epithelial cells.During the ensuing weeks, plasma cells become morenumerous and, in the established stage, dominate theinflammatory infiltrate. The infiltrated area continues toenlarge; and proliferation, apical migration, and lateralextension of junctional epithelium are apparent. Thisestablished lesion is compatible with a clinical diagnosisof chronic gingivitis and may persist without furtherinvolving the deeper supporting structures. Under con-ditions not well understood, however, it may progress tothe advanced stage, Periodontitis, with the extension ofepithelium apically along the root surface,

subsequentpocket formation, destruction of alveolar bone and peri-odontal ligament, and eventual tooth loss.

Direct bacterial and indirect host-response mecha-nisms responsible for periodontal destruction recentlyhave been reviewed.44"46 The direct activity of microbialenzymes, organic acids, and various cytotoxic materialsmay contribute to changes in the epithelium and thenearby connective tissue, particularly during the earlystages of pathogenesis. The absence of microorganismsin tissues with obvious Periodontitis, the slowly progres-sing nature of the disease, the extent of involvement, andtypical lymphocyte and plasma cell infiltrate suggest that


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480 Proceedings From State of the Art Workshop

the host response to products of oral microorganismsplays a major role in the destruction of collagenous andosseous connective tissue which characterizes establishedand advanced lesions.45 Agents elaborated by microor-ganisms appear to traverse the junctional epithelium andmay interact with various host cells which in turn me-

diate the destruction of the periodontium. Immune andnonimmune host mechanisms have been postulated for

virtually all events in the disease process on the basismainly of in vitro observations. No single substance ormechanism has been indicted, however; their involve-ment probably varies according to time, site, and thetypes of microorganisms colonizing the area.

Conclusions

1. The predominant periodontal diseases, chronic gin-givitis and Periodontitis, are found in all populations andare among the most common diseases of mankind. Gin-

givitis 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. Epidemiolog-ical studies have shown a strong correlation between lackof oral cleanliness and these periodontal diseases. Dif-ferences in prevalence and severity, based on such dem-ographic characteristics as sex, race, geographical area,and socioeconomic class, virtually disappear whengroups are distributed according to levels oforal hygiene.No single organism or specific group of organisms, how-ever, has been clearly identified as responsible for peri-odontal disease.

3. A wide variety of both

immune and nonimmune

inflammatory responses of the host to microbial productscan cause the clinical changes associated with periodon-tal disease. There are few direct data, however, that

strongly implicate any one substance or mechanism.4. It is not clear which microbiological and host fac-

tors mediate the progression from gingivitis to Periodon-titis or account for the different rates of periodontaldestruction. Current treatment of gingivitis and Peri-odontitis, therefore, must include control of the microbialflora on a broad basis rather than a narrowly targetedeffort to control particular microbial species.

NO THERAPY

Longitudinal studies have highlighted the pathogen-esis of untreated chronic Periodontitis and have estab-lished that it leads to continued loss of support,6'47increased pocket depth,47 and eventual tooth loss.47 Therate of loss of periodontal support is greater in individ-uals not receiving regular therapy than in those who doreceive such care.6,19'48'49 The risk ofdelaying periodon-tal therapy in the presence of persistent inflammationmay therefore include progressive destruction of sup-

porting tissues and eventual tooth loss.

J. Periodontol.

August, 1982

Many clinical trials have proven the longitudinal ef-fectiveness of periodontal therapy in controlling chronicPeriodontitis.19,50-61 In addition, retrospective studiesover many years have documented the effectiveness of

periodontal therapy.62"66 Abundant evidence also indi-cates that the amount of periodontal support is increasedafter various surgical therapies.67"86

Conclusions1. Untreated chronic Periodontitis leads to progressive

destruction of periodontal support and eventually causestooth loss.

2. Periodontal therapy does control the progressivedestruction associated with chronic Periodontitis andrestores some tooth support.

PERIODONTAL THERAPY

The goal of periodontal therapy is to restore health

and function to the periodontium and to

preserve theteeth for a lifetime. The following discussion of treatmentmethods designed to meet that goal is divided into fourgeneral sections—Initial Therapy to Control EtiologicFactors, Réévaluation, Periodontal Surgery, and Main-tenance Therapy—and is based on the sequence of carethat should be delivered to a patient manifesting chronicPeriodontitis. The listing of these treatment phases andof the procedures included within each phase servesmainly for organizational purposes and does not implythat all patients require all treatment modalities.

Initial Therapy to Control Etiologic Factors

The purpose of initial therapy is to remove and controlthe etiological agents responsible for Periodontitis and toestablish an oral environment that facilitates oral clean-

liness.

Plaque Control. Microbial plaque is the principal eti-ological agent of inflammatory periodontal disease,17'is, 27,87-90 fjjg routine daily prevention or removal ofplaque on the tooth surface by the patient is a sine quanon in periodontal therapy.52'54,57'91'92 Achieving thisaspect of self-care by the patient is a major objective ofthe presurgical phase of treatment.

The mechanical approaches for controlling dental

plaque formation are the most applicable methods avail-able to the patient and the clinician. Such methodsinclude the use of devices that remove microbial plaquefrom the tooth surface: tooth brushes, flosses, wooden

points, rubber tips, toothpicks, interproximal brushes,yarn, and many others. These devices require differentlevels of motor skills. The daily routines that must beestablished require the patient to be diligent, motivated,educated, and skillful.

The achievement of adequate mechanical plaque con-trol requires an oral environment that enables the patientto remove plaque. Calculus must be professionally re-

moved and the plaque-retaining areas on the teeth, such


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as inadequate margins and contours of restorations, mustbe eliminated.93"99

The reduction of plaque levels will decrease gingivalinflammation. Frequent careful scaling, root planing andpolishing of teeth, and closely monitored patient plaquecontrol efforts have been shown to control gingival in-flammation effectively19'22 49'100"104 and to retard or haltattachment loss.49'103'104 Although such rigorous pro-grams effectively control plaque and maintain periodon-tal health, they involve a heavy investment of dentalmanpower and, therefore, are beyond the limits of prac-ticability; hence the "search for a practical method ofmaintaining optimum oral health remains a chal-lenge."105 The cost-effectiveness of such programs for anation's population is not fully known106,107 except as anarithmetic exercise based on the extension of the cost ofthe methods applied in such a study to an entire popu-lation. Even so, such costs appear prohibitive.108

The monitoring of the effectiveness of plaque controlmeasures is important for both the patient and the

dentist. The patient's self-evaluation requires some typeof plaque disclosant.109"111 The dentist may select from avariety of indices that assess the quantity ofsupragingivalplaque.111"114 A microscope may be used to providequalitative information on both supra- and subgingivalplaque. Certain classes ofmicroorganisms31'115'116 appearto be associated with defined severity levels of periodon-tal diseases. The Gram-positive flora of the "healthy"state changes to a motile Gram-negative flora with spi-rochetes in the "diseased" state. It would be diagnosti-cally beneficial if the therapist could have a simplemeans of evaluating the quantity and quality of themicrobial

deposits on the

teeth with respect to theirpathogenic potential. A simple, objective method easilyusable in office or field is needed to determine whetheractive disease is present, whether treatment is necessary,and when treatment is completed.

Finally, it must be recognized that the application ofcurrent plaque control methods (especially ofmechanicalmethods) involves a modification of human behavior.117"125 A plaque control approach may be highly effective,but if the patient will not or cannot apply it in his or herown mouth, it is ineffective for that person.

Scaling and Root Planing. Scaling and root planing areprocedures routinely used in periodontal

therapy. Scal-

ing is the removal of calculus, bacteria, and their prod-ucts from the root surface; root planing is the smoothingof roughened root surfaces.126 In practice, the proceduresare often combined as a single operation. Their purposeis to alter the local environment associated with peri-odontal inflammation and thereby control the destruc-tive effects of the latter. Specifically, the environmentalfactors associated with inflammation include bacterial

plaque,8'9'18'87'88 127"129 its products,130"134 and calcifiedplaque or calculus.88' 98' 128'135-138 Other factors, such asdefective restorations, are also associated with periodon-tal disease94'139-146 and are often corrected during scalingand root planing.

Dental plaque, its products, and calculus are closelyassociated with the tooth surface adjacent to periodontalinflammation. The adherence of dental plaque to toothsurfaces is usually mediated by a salivary glycoproteinpellicle and interbacterial matrix.147"156 The root surfaceitself may adsorb bacterial products that appear to betoxic.107"162 Bacterial endotoxin is a potential pathogenicagent that can be identified on cementum adjacent toperiodontal pockets.108 Calculus can be attached to thesurface of teeth by several mechanisms including attach-ment by pellicle and penetration into intact, resorbed, orseparated areas of cementum.163"170 Moreover, calculusis often closely related to the tooth structure in its organicand crystalline components.167

Clinically, mechanical debridement is used to removeor alter the local factors associated with periodontalinflammation. Scaling and root planing are meticulousand time-consuming procedures that are limited by thetechnical skill of the operator and the accessibility ofroot surfaces adjacent to periodontal pockets. Even afterextensive scaling and root planing, calculus can be mi-croscopically observed on root surfaces.171 Various me-chanical means of scaling and root planing include handand ultrasonic instrumentation. Although the rootsmoothness obtained by these methods differs,172"181 suchdifferences appear to have only slight biologic signifi-cance in supragingival plaque retention or periodontalinflammation.182,183 Both techniques remove calcu-lus,173, 179-181·184 but hand instruments are more effectivein removing calculus185 and endotoxin.186

Scaling and root planing may affect the bacterial floraassociated with periodontal inflammation. When the root

surfaces adjacent to periodontal pockets are subjected tothese procedures, the subgingival bacterial flora is alteredsignificantly. This alteration includes a shift of the pre-dominant flora from Gram-negative anaerobic and mo-tile forms to Gram-positive aerobic and nonmotileforms.187"190 More specifically, the number of bacteroidesand spirochetes is sometimes markedly reduced as aresult of regular instrumentation.190 This alteration of theflora is accompanied by improved periodontal health,namely, reduced inflammation and pocket depth.187"189In addition, thorough scaling and root planing reducethe endotoxin level of root surfaces.161,186 In other words,the

quality of the bacterial flora as well as the

potentiallytoxic material associated with root surfaces adjacent toperiodontal pockets is significantly altered by scalingand root planing.

The clinical effectiveness of scaling and root planingas a separate therapeutic entity is somewhat difficult toassess. This is because it is routinely used in conjunctionwith oral hygiene measures that, when used alone, havea significant effect in reducing inflammation.21'101,191-196However, oral hygiene measures alone are not as effec-tive in reducing pockets and inflammation as whenaccompanied by professional care.197'198 The reductionin gingival inflammation by scaling and root

planingcombined with oral hygiene is well-documented.48'102'


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482 Proceedings From State of the Art WorkshopJ. Periodontol.

August, 1982

183,197-202 short-term studies have shown that scaling androot planing, combined with oral hygiene, also result indecreased pocket depth183 197 198,201"203 and increasedlevels of "clinical attachment."193,198,201,202,204 This gainin attachment is associated with a long junctional epithe-lial adaptation to the root surface.205 When comparedwith baseline data acquired before therapy, the availabledata on longer term results of scaling and root planingindicate that the procedure can at least maintain attach-ment level204 and prevent further increases in pocketdepth.19,55,206"209

Chemotherapy. The prospect of using a chemical agentto control dental microbial plaque is a pleasant onebecause it would not require the high level of motivationand motor skills necessary for mechanical methods of

plaque control. The search for such an agent has beenpursued for nearly a century.

Miller, in 1889,210 proposed the use of antibacterialsubstances against the "parasites" associated with caries.He believed that such agents would not only arrest decaybut prevent it. Effective "antiseptic" agents of that time,such as bichloride of mercury, were too toxic; the searchfor a substitute has persisted.

Numerous chemical agents have since been tested butwith mixed results. The most promising, Chlorhexidine,has been the most consistently effective; however, it isnot available for patient care in the United States. Sev-eral studies have demonstrated significant reduction insupragingival plaque and improved gingival health whenit was used as an oral rinse or applied topically at variousconcentrations 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

salivarymicroorganisms.214 However, the daily application of a2% Chlorhexidine solution did not inhibit subgingivalplaque formation in dogs.216 When incorporated into agel or dentifrice, Chlorhexidine was not as consistentlyeffective as the rinse.217,218

Because of the undesirable side effects of Chlorhexi-

dine,20 compounds with a similar chemical structure butwithout such effects have been sought to achieve thesame plaque prevention. Such a substance, alexidine,was used as an oral rinse in clinical studies.23, 219, 220

When used in a concentration of 0.035% or 0.05%, itreduced

plaque levels

significantly, but consistent results

in the reduction of gingival inflammation were not ob-served; alexidine was clearly less effective than Chlorhex-idine.

Many other chemical agents have been tested for theirplaque-inhibiting properties, but the results have notbeen encouraging 20,

221-227 Antibiotics were also used

both topically and systemically to control the microbialpopulation of dental plaque. Oral rinses of 0.5% tetra-cycline, 0.5% vancomycin, or 0.25% polymyxin wereused three times a day for 5 days by human subjects.16All three reduced plaque formation, tetracycline moreeffectively than the others. Vancomycin depressed the

Gram-positive organisms and masses of Gram-negative

cocci, rods, and filaments, but fusobacterium-like orga-nisms proliferated. Polymyxin caused a proliferationof the Gram-positive cocci and short rods and depressedthe growth of Gram-negative microorganisms. The mi-crobial population of the controls was similar to thatdescribed earlier in a study of experimental gingivitis inman.

Other antibiotics tested222, 228-231 had no significantplaque inhibition. Tetracycline appeared to be the mostpromising, but when taken systemically, it had littleeffect on the results of a study in which it was testedagainst scaling procedures.201 Further studies187 that in-cluded microbial and histological observations noted asignificant effect on microbial composition during drugingestion. The proportions of coccoid cells were higherand those of motile rods and spirochetes lower thanpretreatment levels. The flora reverted to baseline levelsafter the tetracycline was discontinued. Many organismsdeveloped resistance to the antibiotic.232

Concern about the prolonged use of systemic antibiot-

ics has led to attempts for their slow release in extremelysmall quantities in the pocket area.233,234Salt and hydrogen peroxide were used years ago to

control or modify the microorganisms involved in Peri-odontitis.235 Recently, Keyes236'237 has combined the useof these classical medicaments with microscopic moni-toring of the pocket flora to follow changes in the typeand number of these microorganisms and to help moti-vate the patient to maintain high levels ofplaque control.This approach is attractive in its simplicity, but its valuehas 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 lesionin the periodontal ligament ranges from a slight derange-ment of the ligament to an area ofnecrosis.240,241 Occlusaltherapy to manage this lesion consists of several proce-dures designed principally to redistribute forces on theteeth: occlusal adjustment, control of parafunctionalhabits, orthodontics, splinting, and occlusal rehabilita-tion by restorative procedures.242

When the lesion of trauma occurs in a normal perio-dontium (primary occlusal trauma),126 morphologic al-terations occur in the periodontal ligament and alveolarbone.40, 60, 241,243-248 These are reversible when the forceis discontinued or the tooth moves away from the dis-

placing force.41,249'250 Periodontal pockets are not formednor is connective tissue attachment lost as a result.40,245,247,248,251,252 Tncrease(i t00th mobility and the roentgen-ographic appearance of a widened periodontal ligamentspace are the clinical manifestations of primary occlusaltrauma. They represent an adaptation by the periodon-tium to accommodate the excessive forces acting uponthe tooth. In this state of increased mobility, the lesionsof trauma are replaced by widened periodontal ligamentsand decreased bone density to accommodate the displac-ing forces.40,60,249

Secondary occlusal trauma has been defined as normal


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Number 8 Surgical Therapyfor Periodontitis 483

occlusal forces traumatizing the attachment apparatus ofteeth weakened by the loss of support.126 When the lesionof trauma is superimposed on a healthy but reducedperiodontium, the same morphologic alterations occur asin primary occlusal trauma but with no changes in thelevel of connective tissue attachment.253'254

When the lesion of trauma occurs in conjunction with

to aid in the management of fractured teeth.2 Sig-

Periodontitis, 240, 255-259 the progress of existing chronic

Periodontitis may be accelerated and intrabony pocketswith angular bone loss may result. Studies with squirrelmonkeys39 and beagles258 have suggested that whentrauma is associated with marginal Periodontitis, theamount of alveolar bone loss is increased; however, somedifferences in the loss of connective tissue attachmenthave been reported. Trauma superimposed on Periodon-titis caused an increased loss of connective tissue attach-ment in the beagle,39 but not in the squirrel monkey.258

Investigations in animals have indicated that in themanagement of Periodontitis accompanied by tooth hy-permobihty, resolution of inflammation must be empha-sized;41' 259'260 these results agree with studies relating tothe control of Periodontitis in human subjects.52' 54' 261After therapeutic techniques designed to resolve mar-ginal inflammation have been accomplished, bone regen-eration accompanied by a significant decrease in toothhypermobihty can occur.52' 54' 57' 79' 92' 261"263 Osseousrepair was observed throughout the circumferential ex-tent of intrabony pockets around hypermobile teeth, andeven though there was no occlusal therapy, the mobilityof each tooth decreased in proportion to the amount ofrepair.79 Moreover, increased tooth mobility does notseem to alter the level of connective tissue attachment

during healing after periodontal surgery.264"266 No evi-dence to support temporary stabilization as a biologicaid in periodontal healing after surgery is available.

Current knowledge of the management of Periodon-titis alone or in combination with trauma indicates thatthe control of inflammation should be the principalobjective. Such control may cause a significant decreasein tooth mobility. Any residual tooth hypermobihty maybe due to the loss of periodontal support from periodon-tal disease. Since this mobility will not initiate furtherperiodontal pocket formation, there is no scientific basisfor reducing it to preserve periodontal health. The man-

agement of

any remaining mobility can be

justified onlyon the basis of function and comfort, and to halt anypatterns of increasing mobility that may lead to toothavulsion.

There is no substantial evidence to indicate that ortho-dontic therapy improves periodontal health. On the con-trary, several studies report loss of attachment, bonerecession, gingivitis, and root résorption as a result oforthodontic therapy.267"272

Scientific information on the role of orthodontic ther-

apy in the treatment of Periodontitis is scarce. Bothincreased270 and decreased273 pocket depth have beenreported after tooth movement. Forced eruption hasbeen used to reduce or repair angular bony defects and

nificant changes can occur in the configuration of boneand gingival tissues as a result of orthodontic therapy.271,274, 276 Therefor^ orthodontic therapy should precedeperiodontal surgery in the management of certain typesof periodontal defects. Inflammation should be resolvedbefore orthodontic therapy to avoid the possibility ofattachment loss during tooth movement. The most recentevidence from studies on beagles and squirrel monkeysshows that traumatic lesions and their sequelae, super-imposed upon severely reduced but healthy periodontaltissues, do not lead to further loss of connective tissueattachment.250'253'254

Conclusions

1. Because the principal etiologic agent of chronicPeriodontitis is microbial plaque, plaque control mea-sures are necessary not only to treat it but also tomaintain periodontal health.

2. Current mechanical plaque control methods are

effective when used by strongly motivated individuals.They require such diligence and dexterity, however, thatthey probably would not be an effective public healthmeasure.

3. Scaling and root planing, combined with adequateoral hygiene measures, reduce inflammation, pocketdepth, and loss of periodontal attachment. The effective-ness of scaling and root planing is greatly influenced bythe accessibility of the root surface and the skill of theclinician.

4. Many chemotherapeutic agents can reduce or mod-ify the levels of dental plaque, but at present, none

completely inhibit sub- and supragingival plaque.5. Occlusal trauma will not initiate gingivitis or Peri-odontitis nor will it cause gingivitis to develop intoPeriodontitis.

6. There is no evidence that tooth stabilization is a

biologic aid to periodontal healing after surgery or thatmobility need be reduced to preserve periodontal health.

7. There is no evidence that othodontic therapy im-proves periodontal health, except in some cases of iso-lated defects.

Réévaluation

After the initial

phase of

therapy, the need for further

treatment must be determined. To make a rational de-cision about this, one must reevaluate the periodontalresponse to the reduction of local irritants. Many consid-erations enter into these decisions, several of whichappear to be more important than others. These includethe cooperation and effectiveness of the patient in con-trolling plaque; the improvement in gingivitis, pocketdepth, and clinical attachment level; and the systemicstatus of the patient.

Evaluation ofPlaque Control. Plaque control is impor-tant to maintain the beneficial effect of periodontaltherapy.52, 54' 57' 58' 91, 277 Therefore, it is necessary thatthe patient be evaluated in terms of the effectiveness of


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August, 1982

oral hygiene measures. In evaluating the level of plaquecontrol, many clinicians use various clinical indices tomonitor the quantity of supragingival plaque.192' 278-284Such clinical indices are of great value, but they do notdetermine the pathogenicity of plaque. In periodontaldisease, specific groups of organisms appear to be asso-ciated with various levels of severity.30,31' 115' 116' 285'286 Itwould be beneficial if the therapist could effectivelymonitor plaque control in terms of both the quantity andthe quality of the bacterial flora with respect to itspathogenic potential. Assays for endotoxin287 and dark-field microscopy of subgingival plaque286 have been used,but their clinical importance has not been clearly estab-lished.

Indicators ofPeriodontal Inflammation. It is importantto evaluate the periodontal response to hygienic mea-sures used by the patient and the therapist.202 The class-ical signs and symptoms of periodontal inflammationinclude changes in gingival color, contour, and consist-ency as well as edema, hemorrhage, exúdate, tooth mo-

bility, pathologically deepened pockets, and continuedloss of support.202'287-291 After the initial phase of therapy,the periodontium should be studied for evidence of thesesymptoms. Subjective clinical signs are difficult to assessin terms of objective criteria, but the clinician shouldapply objective criteria whenever possible. Pocketdepth,284'292 the level of clinical attachment,284'292 andevidence of bleeding after probing293'294 or suppura-tion295 can be evaluated in a fairly objective manner. Theclinician should also be aware that the penetration depthof the periodontal probe tip may vary with the degree ofgingival inflammation and amount of force used.296-300

Changes in pocket depth and attachment level should beviewed with this in mind when the response to initialperiodontal therapy is being reevaluated. Furthermore,as measured by routinely used clinical techniques, toothmobility is subjective because such techniques lack sen-sitivity when applied to a single tooth.301'302 However,these measurements may be useful for diagnosing andtreatment planning by individual practitioners.303 Theuse of gingival fluid or exúdate as an indicator of peri-odontal disease is somewhat controversial. Crevicularfluid increases with clinical signs of gingival inflamma-tion,275,

304-313 however, the correlation between it and

histologie evidence of inflammation varies in

publishedreports.307' 308' 310-312'314'315 Several studies also indicatethat crevicular fluid is a product of clinically healthygingival crevices.304' 306'308'316-318 Gingival fluid may rep-resent a preinflammatory osmotic exúdate as well as aclinical inflammatory exúdate.319

It would be prudent therefore, for the clinician to usemultiple criteria for periodontal evaluation. By balancingthe signs of periodontal disease with a knowledge of thelimitations involved, the experienced clinician should beable to clinically assess the effectiveness of therapeuticprocedures. Clearly, no single clinical parameter may beused as the sole criterion for evaluating periodontalresponse to therapy.320'321

Needfor Further Periodontal Therapy. Whether furtherperiodontal therapy is necessary is a critical decisionwhich should be based on objective criteria. To usepocket depth as the sole criterion upon which to base adecision for periodontal surgery is questionable.322'323Other criteria, such as the degree of inflammation deter-mined by bleeding on probing, exúdate, and otherchanges, also warrant consideration. Furthermore, anydecision for periodontal surgery must consider specificteeth (such as maxillary molars) which may be more atrisk from periodontal disease.62 Complete elimination ofsuch etiologic factors as calcified plaque (calculus) fromroot surfaces is time-consuming and extremely difficultif not impossible by nonsurgical means.171' 179' 324'325'326One of the main objectives of periodontal surgery is togain access for root preparation.322 In addition, the de-gree of periodontal support in terms of attachment leveland osseous support can be increased by various surgicalprocedures.50' « 55-59' 61' 67-82'84-86'327 Surgery also appearsto be more beneficial for advanced periodontal disease

than scaling and root planing alone.55'206 Surgical ther-apy is, therefore, indicated when nonsurgical root prep-aration is not possible, when additional support is alikely outcome of such therapy, or when the diseaseprocess cannot be adequately controlled by other means.

Alternatives to surgery include repeated scaling androot planing and continued attempts to control plaque.Such therapy may be the only alternative for thosepatients at surgical risk such as elderly patients or thosewith a debilitating systemic disease. For them, regularmaintenance therapy, combined perhaps with localizedsurgical therapy when the disease is clearly out of control,

is indicated.The clinician must closely monitor the disease toensure that the measures taken to arrest periodontaldestruction are appropriate. In addition, the therapistshould be able to use one or more of the various surgicalmodalities that are effective in arresting periodontaldisease and even in regenerating lost support.

Conclusions

1. The clinical signs and symptoms available to theclinician for evaluating the periodontal response to ther-apy are

relatively subjective. They do

provide importantand valuable means of assessing the activity of Periodon-titis, 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 adja-cent to periodontal pockets and to provide a means ofcontrolling disease when nonsurgical methods are inef-fective.

3. Alternatives to surgical therapy include continuedscaling and root planing at regular intervals to furthercontrol bacterial plaque. This method, however, does notensure that bacteria and their products will not remainin inaccessible areas.


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Periodontal Surgery

Procedures. Various periodontal surgical proceduresare available. The distinctions between them are not

always clear, and procedures are often combined. Forpurposes of analysis, the major procedures will be listedseparately; the order in which they are considered doesnot necessarily reflect their relative effectiveness.

Gingivectomy. The major advantage of gingivectomyis that it provides access to the root surface.288 This isparticularly important in view of our current knowledgeof the importance of root surface preparation.157' 158' 161·186, 328 Another advantage is that it avoids denudation ofalveolar bone and minimizes postoperative bone résorp-tion.329 In 1956, Glickman330 justified its use in 200 cases.Gingivectomy is a better method than curettage forremoving relatively shallow pockets even though the lossof attachment reported with gingivectomy did not occurwith curettage.203'209'331-337

Subgingival Curettage. Subgingival curettage consists

of scraping the inner surface of the gingival wall of theperiodontal pocket to clean out, separate, and removediseased soft tissue and granulation tissue.242' 288'291'338-340 The technique is seldom used as a single procedurebut is usually combined with scaling and/or root planing.

Over the years, the indications and uses for subgingivalcurettage have included pocket reduction and new at-tachment,336, 338' 341-343 "~cì,^„,Vc1 nr»n,„tmn 338, 341, 344-presurgical preparation,

compromised casestreated cases.341'

242, 338, 341 and maintenance of

Reportedly, pocket reduction bysubgingival curettage can be achieved by gingival shrink-age336' 347 and/or new attachment.325'347'348

Although histologie evidence of the formation of new

epithelial and connective tissue attachment after curet-tage has been presented,325 the most recent studies205, 349report only the formation ofa long junctional epitheliumwithout any evidence of new connective tissue attach-ment. The new attachment and gingival recession asso-ciated with subgingival curettage may be due entirely tothe concurrent plaque removal and root planing.205'350Curettage has been reported effective in cases with min-imal pockets.51,203' 342' 351'352 However, curettage was notas effective as other surgical techniques in reducingdeeper pockets.51

Apically Positioned Flap With and Without OsseousRecontouring. The characteristic feature of the apicallypositioned flap is placement of the flap margin at thecrest of the alveolar bone. This requires resection ofgingiva to the bone crest on the palatal aspect. In otherareas, this is accomplished by displacing the flap apically.The objective of the procedure, in addition to providingaccess for complete subgingival debridement, is to reducepocket or sulcular depth. Osseous recontouring is oftenperformed in combination with the apically positionedflap.

In 1949, Schluger353 expressed concern about the be-havior of soft tissue after gingivectomy and curettage.He suggested that the topography of bone be altered to

prevent discrepancies between levels and shapes of boneand gingiva which predispose to recurrence of pocketdepth. This involved thinning bony ledges, leveling cra-ters, and generally reshaping marginal bone to resemblethe alveolar process undamaged by periodontal disease.

Clinical reports of successfully treated cases havecaused these tenets to be redefined over the

years.242'339'354-360 The success of apically positionedflaps with osseous recontouring in reducing overallpocket depth and improving tissue contour has provideda periodontal environment which can be maintained inhealth. This approach, however, involves some loss ofattachment.50'59,92'203

There is some concern that osseous resection can leadto excessive and continued tooth mobility.361 However,studies of mobility after osseous surgery show that whilethe 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 re-flection of a flap with minimal removal of marginal

gingiva to expose and provide access for debridement ofroot surfaces and adjacent periodontal defects. The in-dications for open-flap curettage have been summa-rized09' 363 and include patients with advanced periodon-tal disease in whom resective surgical procedures might

jeopardize the results of treatment; anatomic defectscapable of repair; and conditions where preservation oftissue is important because of esthetics, particularly inanterior areas.

From a practical standpoint, the modified Widmanflap is similar to open-flap curettage. Thus, results ofclinical studies of the modified Widman flap can be

regarded as

applicable to

open-flap curettage.Modified Widman Flap. The chief objective of themodified Widman flap operation is not pocket elimina-tion per se but maximum healing of periodontal pocketswith minimal loss of periodontal tissues during and aftersurgery.

Leonard Widman introduced the reverse beveled in-cision in 1916 to obtain access for root preparation.360The modified Widman flap, described in detail in1974,364,366 is basically a flap for reattachment and ismore conservative than that described by Widman.347

The reported advantages of the modified Widman flapare that it optimizes access to the root surface, and theclose postsurgical adaptation ofhealthy connective tissueto the root surface enhances the potential for new attach-ment.322' 347'366 In addition, it allows optimal soft tissuecoverage of root surfaces and thus provides a result thatis both esthetically desirable and amenable to oral hy-giene procedures.322,347 Less exposure of root surfacesalso means potentially less root sensitivity and fewerproblems with root caries.322,364'366

The disadvantages of this technique include the factthat it is technically exacting, especially interproximally.The interproximal architecture of the tissue may be poorimmediately after removal of the dressing, especially inareas of interproximal bony craters. However, if metic-


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August, 1982

ulous oral hygiene is maintained, the interdental tissueswill repair over a few months with gain rather than lossof clinical attachment.364'366 Despite its failure to im-prove tissue contour, the modified Widman procedure isas successful as the apically positioned flap procedurewith respect to plaque control, gingivitis scores, andmaintenance of attachment levels.347

The modified Widman flap has been evaluated

in longitudinal studies begun in 1961 by Ramfjordand many co-workers.50'51-m- ** 261'291·m' 342> 364'

366-369

Short-term clinical comparisons of different surgical mo-dalities have indicated that pocket depth was reducedmore effectively by pocket elimination surgery than byeither the modified Widman flap or subgingival curet-tage.367 With regard to attachment level, these short-termresults were better with subgingival curettage than withthe modified Widman flap. Pocket elimination surgeryproduced some initial loss of clinical attachment.367

Eight-year results on pocket reduction and level ofclinical attachment show that the effects from the mod-

ified Widman flap were similar to those from pocketelimination surgery. Subgingival curettage was not aseffective as the other two procedures, especially in deeppockets and molar regions.51

Histologie evaluation of the modified Widman flap innonhuman primates has demonstrated healing by meansof a long, thin junctional epithelium to the depth of thesurgical wound with no gain in connective tissue attach-ment and no increase in crestal bone height.200'370 Bonerepair varied within intrabony pockets, but a junctionalepithelium is always interposed between the new boneand root surface.370 Longitudinal studies suggest that this

epithelial adherence can be maintained with little or no

change over time.50' 51'322'347Excisional New Attachment Procedure. The excisional

new attachment procedure (ENAP) is subgingival curet-tage performed with a knife.61' 322'347'371-374 The statedobjectives of the procedure are to allow proper soft-tissuepreparation, to gain better access to the root surface, andto enable soft tissue to adapt intimately to the rootsurface. ENAP is indicated for suprabony pockets whichdo not extend beyond the mucogingival junction orinvolve angular bony defects. Among its reported advan-tages are the definitive, clean excision of the epithelialpocket lining, the epithelial attachment, and the subja-cent granulation tissue; improved access to the rootsurface; and increased predictability of new clinical at-tachment.347' 374

Initial studies showed the technique to be feasible forreducing pocket depth and gaining clinical attachmentin suprabony pockets.373 The clinical improvement evi-dent after 1 year was maintained for 3 years, but probingdepths increased slightly, and the amount of previouslygained new attachment decreased slightly at each post-operative evaluation period from 1 to 5 years.61,347,373According to histological evidence in monkeys, ENAPhealed with a long thin junctional epithelium and aminimal amount of connective tissue reattachment.371

Osseous Grafts. Osseous grafts are used in the treat-ment of Periodontitis to restore lost alveolar bone, toregenerate a functional attachment apparatus, and toreduce the periodontal pocket.375

Graft Materials. Bone grafts can be divided into au-tografts and allografts. An autografi is a tissue grafttransferred from one position into a new position in thebody of the same individual. Periodontal autografts havebeen obtained from intraoral or extraoral sites. An allo-graft, formerly referred to as a homograft, is a tissuegraft between individuals of nonidentical genetic dispo-sition.

Bone autografi materials used in periodontal therapyinclude bone chips,77 mixtures of blood and groundbone, intraoral bone and marrow, and iliaccrest bone and marrow.327,379

Allografts have been used because of the difficulty ofobtaining sufficient bone-graft material from within thepatient's mouth and because of problems in obtaining itelsewhere. Materials used for allografts include frozen

iliac crest bone,375,380,381 decalcified382 and undecalcifiedfreeze-dried bone,76 and merthiolate-treated bone.383With the exception of freeze-dried bone, the allograftmaterials are still experimental.

Clinical Evaluations—Autografts. Most of the publi-cations which evaluate osseous autografts are case re-ports, and most of these indicate that a significantamount of osseous repair is possible in all types ofintraosseous defects, including furcations.69, 77, 82, m' 85,384-387 pewer investigations include data which wouldenable one to compare various autografts. Mean bonerepair reported in several studies of intraosseous defects

ranged from 2.1 to 4.4

mm.68,71,72,327 Of all the availablegraft materials, iliac cancellous bone and marrow auto-grafts probably offer the greatest potential for Osteogen-esis.385-390

Clinical Evaluations—Allografts. Freeze-dried bone al-lograft is the only bone-graft material that has been fieldtested. Reports indicated that more than 50% osseousrepair occurs in 60% of the defects treated.76,391,392 Pock-ets were reduced to a level proportional to the degree ofosseous repair. A principal concern with all allografts isthe problem of graft rejection. The results of animalstudies suggest that freeze drying reduces or abolishesthe antigenicity of a bone

allograft.393,394 Various auto-

graft and allograft materials can achieve significant levelsof osseous repair. However, the studies to date werewithout adequate controls.

Histologie Observations. Regeneration of new attach-ment composed of bone, cementum, and periodontalligament has been reported in human patients withosseous coagulum-bone blend,395 cancellous bone andmarrow from intraoral donor sites,72,83,396 iliac cancel-lous bone and marrow autografts,68,73 and frozen iliacallografts.73 However, junctional epithelium may extendapically to the new alveolar crest;73,74,397 what that im-plies is not yet known.

Osseous Grafts Compared With Nongraft Regenerative


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Volume 53

Number 8 Surgical Therapyfor Periodontitis 487

Procedures. In defects of a certain morphology, nongraftregenerative procedures may stimulate the same amountof bone repair as do osseous grafts.79'80'298

Two studies which compared osseous graft and non-graft regenerative procedures in human patients indi-cated that alveolar defects respond with similar or greaterlevels of osseous repair if a bone graft is implanted.70'398In another study, however, the results of intraoral can-cellous bone and marrow autografts did not differ fromthose of the nongraft approach.78 The increase in theamount of new bone was greater with the iliac cancellousbone and marrow autografts than with the nongraftprocedure.70'78 In a study which compared freeze-driedbone allograft with a nongraft procedure, the levels ofosseous repair were similar.67

Problems With Osseous Grafts. There are occasionalproblems peculiar to osseous grafts: sequestration, exo-phytic granulation tissue reaction, external root résorp-tion, and the immunologie implications of allo-grafts.381' 399'400 Of special importance is external root

résorption associated with fresh iliac cancellous bonemarrow autografts.73' 327'401'402 The frequency of rootrésorption varied from 20% to less than 1% in reportedcases 69,

402

Other Grafts. In the past, several types of xenografts(grafts between two different species) were tried in hu-man subjects with less than satisfactory results. The useof bioceramics, such as tricalcium phosphate, in humanperiodontal osseous defects has been evaluated on alimited scale with equivocal results.403"405 Therefore, theyshould not be used in the routine treatment of Periodon-titis. Likewise, further clinical and histologie data are

necessary before scierai allografts can

be accepted forroutine clinical use.406"408Soft Tissue Grafts. Reconstructive soft tissue grafts

have been designed to repair alterations in the normalmorphological arrangement between the attached gin-giva and the alveolar mucosa at the level of the muco-gingival line. The main goals of mucogingival surgeryare to create or increase the band of attached or keratin-ized gingiva, to increase vestibular depth, and to coverlocalized gingival recessions.

Classical Techniques. All the classical techniques tocreate or increase the amount of keratinized

gingiva,357'409-415 as well as some

techniques specificallydesigned to increase vestibular depth,416 were based onthe assumption that functional adaptation occurs aftersurgery. If in an area where attached gingiva was insuf-ficient or nonexistent, the tissue of the alveolar mucosawas stripped off leaving the bone exposed, whethercovered by periosteum or not, the healing tissue woulddevelop into attached gingiva simply because functionwould so indicate. This was the rationale for all the

periosteal retentions, bone denudations, and periostealfenestrations described in the literature.357,410-415·417 Spe-cial surgical procedures to increase vestibular depth, like

ation of some of these techniques has shown them to berelatively effective in maintaining the clinical results,420all of them, in different degrees, have been associatedwith stormy postoperative complications, unpredictablegain and loss of marginal alveolar bone. Furthermore,although the tissues thus obtained functioned as attachedgingiva, they did not achieve its histologie charac-teristics.235' 330' 421"439

Functional adaptation does not follow heterotopictransplantation of the soft tissues because the epithelialtissues of the gingiva and alveolar mucosa maintain theirspecificity even after changing their location and thustheir environment.440"443

Free Gingival Grafts. Free gingival grafts obtainedfrom masticatory mucosa have been used successfully444to increase the band of keratinized gingiva and to coverlocalized gingival recessions. Grafts are predictable pro-cedures if they are placed on a bed capable of inducingrevascularization,445'446 such as periosteum or barebone.447"460

Biometrie examination has shown that after the 1stmonths the grafted tissues remained stable after initialshrinkage of the transplanted band of keratinized gin-giva.461"463 Some reduction in the amount of root expo-sure has been shown by means of the "creeping reattach-ment" phenomenon.464,465 A free gingival graft is usedto treat a localized gingival recession, mainly to halt itsprogression by creating a wider band of keratinizedgingiva, but this clinical result has never been proven.However, when such grafts are placed over a denudedroot to cover an area of gingival recession, their predict-ability is reduced. Only a "narrow and shallow" defect

can be adequately covered by a free graft since only thatsize lesion can provide adequate collateral circulationduring initial healing to assure the "take" of thegraft.446,466-469

Pedicle Gingival Flaps. Pedicle gingival flaps maintaindirect vascularization and thus assure the nutrition and

vitality of the tissue postoperatively. Many techniqueshave been described since the classical lateral sliding flapwas first introduced in 1956. All modifications sincethen have been designed to protect the teeth adjacent tothe recession.368,417'444' ^471"489

The procedures that have been tested clinically showeda 60 to 75% reduction in the amount of recession. Theseinclude lateral sliding flap,490"494 coronally positionedflap,472'492,495 split-thickness lateral sliding flap with afree gingival graft,496 lateral sliding flap, and raisedtechnique.496 The results have remained stable overtime.478'497'498 When a lateral sliding flap is performedas originally described, gingival recession may be pro-duced on the donor tooth to an average of 1 mm.390'490'491All the other techniques tested have overcome this un-desirable complication.492'495-497 Histological examina-tion has shown that all these procedures cover the toothby a combination of connective tissue reattachment and

the Edlan Mejchar operation and others, were long junctional epithelium. '494, 499, 500 Electron microscopybased on the same principle. Although biometrie evalu- has shown hemidesmosomes and a basement lamina at


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the interphase between the junctional epithelium and theconnective tissue.501 None of these procedures has pro-duced bone regeneration in the area of recession.

Other Techniques. Other techniques, mainly designedto increase the amount of keratinized gingiva and deepenthe vestibule, include freeze-dried skin allografts,372 ly-ophilized dura,002 and scierai grafts.503 Since their use isstill experimental, they should not be used in the routinetreatment of Periodontitis.

Needfor Mucogingival Surgery. The attached or ker-atinized gingiva follows a regular pattern of normaldistribution.504"507 The anterior teeth have the widestband, the cuspids and molars on the upper and lowervestibular sides, the narrowest. The lower lingual gingivais narrower on the incisor area and widens distally. Areaswith 2 mm of keratinized gingiva have been reported tobe compatible with the absence of clinically detectableinflammation! measured by the Gingival Index and theamount of crevicular fluid flow.006 More recently, evenareas with no keratinized gingiva at all have been main-

tained free of inflammation.508 Furthermore, in an ex-perimental model of gingivitis, no deleterious effectswere observed either in areas with no attached or kera-tinized gingiva or in those with an adequate band.507'508No correlation has been found between vestibular depthand gingival health.507

In a three-year longitudinal study that compared areaswith insufficient attached gingiva that had been treatedwith a free gingival graft with those that had not receivedany surgical treatment (controls), no difference was ob-served.509

Some have claimed that mucogingival problems as-

sociated with tooth malposition in children

should betreated surgically before orthodontic treatment.510 How-ever, the band of attached gingiva has been shown toincrease after a tooth has been moved back orthodonti-

cally into the basal bone.511'012 Obviously then, a con-servative approach to mucogingival surgery is indi-cated.513 Réévaluation of tissue response 1 to 2 monthsafter completion of the hygienic phase of therapy mayshow that the preplanned surgery is not needed. On theother hand, additional complications to areas of reces-sion—root hypersensitivity, demineralization, lack ofmarginal epithelial seal associated with a frenum ormuscle pull, unfavorable esthetic appearance—may in-dicate the need for surgery.

Conclusions

1. Effective plaque control is necessary to the successof all methods.

2. Gingivectomy is still a valuable procedure despiteits limited applicability. It should not be used to treatosseous deformities or in areas where it will remove allkeratinized gingiva.

3. Apically positioned flaps, open-flap curettage, and

the modified Widman flap are indicated when access toroot surfaces is required. They are equally effective inrestoring and maintaining periodontal health.

4. Osseous recontouring improves alveolar architec-ture, but its value in restoring and maintaining periodon-tal health has not been established.

5. The utility of the excisional new attachment pro-cedure 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 nodemonstrable value.

7. Sufficient data have been published to justify theinclusion of some types of osseous grafts in the arma-mentarium of accepted periodontal therapy. Althoughthere have been few longitudinal studies of osseousgrafting in human patients, the available evidence sug-gests that, in certain morphologic types of alveolar de-fects, osseous grafting resulted in more bone repair than

nongraft techniques.8. There is no evidence of a detrimental effect fromlack of attached or keratinized gingiva in the mainte-nance of a healthy dentit

8. 1981 Samuel Kakehashi, Paul F. Parakkal. Proceedings From the State of the Art Workshop

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Transcript of 8. 1981 Samuel Kakehashi, Paul F. Parakkal. Proceedings From the State of the Art Workshop