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7/29/2019 E_Plaque http://slidepdf.com/reader/full/eplaque 1/10 AMERICAN ACADEMY OF PEDIATRIC DENTISTRY ENDORSEMENTS 317 Gingivitis and periodontitis are the 2 major orms o inamma- tory diseases aecting the periodontium. Teir primary etiology is bacterial plaque, which can initiate destruction o the gingi- val tissues and periodontal attachment apparatus. 1,2 Gingivitis is inammation o the gingiva that does not result in clinical attachment loss. Periodontitis is inammation o the gingiva and the adjacent attachment apparatus and is characterized by loss o connective tissue attachment and alveolar bone. Each o these diseases may be subclassied based upon etiology, cli- nical presentation, or associated complicating actors. 3 Gingivitis is a reversible disease. Terapy is aimed primarily at reduction o etiologic actors to reduce or eliminate inam- mation, thereby allowing gingival tissues to heal. Appropriate supportive periodontal maintenance that includes personal and proessional care is important in preventing re-initiation o inammation. Terapeutic approaches or periodontitis all into 2 major categories: 1) anti-inective treatment, which is designed to halt the progression o periodontal attachment loss by removing etiologic actors; and 2) regenerative therapy, which includes anti-inective treatment and is intended to restore structures destroyed by disease. Essential to both treatment approaches is the inclusion o periodontal maintenance procedures. 4 Inammation o the periodontium may result rom many causes (eg, bacteria, trauma). However, most orms o gingivitis and periodontitis result rom the accumulation o tooth- adherent microorganisms. 5-7 Prominent risk actors or devel- opment o chronic periodontitis include the presence o specic subgingival bacteria, 8-10 tobacco use, 9-13 diabetes, 9,10,14  age, 9,10 and male gender. 9,10 Furthermore, there is evidence that other actors can contribute to periodontal disease pathogenesis: environmental, genetic, and systemic (eg, diabetes). 14,15 Tis paper primarily reviews the treatment o plaque- induced gingivitis and chronic periodontitis, but there might be some situations where the described therapies will not resolve disease or arrest disease progression. Furthermore, the treatments discussed should not be deemed inclusive o all possible therapies, or exclusive o methods o care reasonably directed at obtaining good results. Te ultimate decision regard- ing the appropriateness o any specic procedure must be made by the practitioner in light o the circumstances presented by an individual patient. Plaque-induced Gingivitis Terapy or individuals with chronic gingivitis is initially directed at reduction o oral bacteria and associated calcied and noncalcied deposits. Patients with chronic gingivitis, but  without signicant calculus, alterations in gingival morphology, or systemic diseases that aect oral health, may respond to a therapeutic regimen consisting o improved personal plaque control alone. 16 Te periodontal literature documents the short- and long-term eects ollowing sel-treatment o gingivitis by personal plaque control. 16-20 However, while it may be possible under controlled conditions to remove most plaque with a variety o mechanical oral hygiene aids, many patients lack the motivation or skill to attain and maintain a plaque-ree state or signicant periods o time. 21-23 Clinical trials also indicate that sel-administered plaque control programs alone, without periodic proessional reinorcement, are inconsistent in provi- ding long-term inhibition o gingivitis. 19,24,25 Many patients with gingivitis have calculus or other associa- ted local actors (eg, deective dental restorations) that interere  with personal oral hygiene and the ability to remove bacterial plaque. An acceptable therapeutic result or these individuals is usually obtained when personal plaque control measures are perormed in conjunction with proessional removal o plaque, calculus, and other local contributing actors. 26,27 Removal o dental calculus is accomplished by scaling and root planing procedures using hand, sonic, or ultrasonic instru- ments. Te therapeutic objective o scaling and root planing is to remove plaque and calculus to reduce subgingival bacteria below a threshold level capable o initiating clinical inammation. Originating Group  American Academy of Periodontology - Research, Science, and Therapy Committee Endorsed by the American Academy of Pediatric Dentistry 2004 Copyright© 2004 by the American Academy o Periodontology; all rights reserved. Copyrighted and reproduced with permission rom the American Academy o Periodontology. No part o this publication may be reproduced, stored in a retrieval system, or transmitted in any orm or by any means, electronic, mechanical, photo- copying, or otherwise without written permission o the publisher. reatment o Plaque-induced Gingivitis, Chronic Periodontitis, and Other Clinical Conditions. J Periodontol 2001;72:1790-1800. Available through the American Academy o Periodontology, Department o Scientic, Clinical and Educational Aairs, 737 North Michigan Avenue, #800, Chicago, IL 60611-2690, Phone: (312) 787-5518, Fax: (312) 787-3670. Treatment of Plaque-induced Gingivitis, Chronic Periodontitis, and Other Clinical Conditions

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AMERICAN ACADEMY OF PEDIATRIC DENTISTRY

ENDORSEMENTS 317

Gingivitis and periodontitis are the 2 major orms o inamma-tory diseases aecting the periodontium. Teir primary etiology is bacterial plaque, which can initiate destruction o the gingi-val tissues and periodontal attachment apparatus.1,2 Gingivitisis inammation o the gingiva that does not result in clinicalattachment loss. Periodontitis is inammation o the gingiva 

and the adjacent attachment apparatus and is characterized by loss o connective tissue attachment and alveolar bone. Eacho these diseases may be subclassied based upon etiology, cli-nical presentation, or associated complicating actors.3

Gingivitis is a reversible disease. Terapy is aimed primarily at reduction o etiologic actors to reduce or eliminate inam-mation, thereby allowing gingival tissues to heal. Appropriatesupportive periodontal maintenance that includes personal andproessional care is important in preventing re-initiation o inammation.

Terapeutic approaches or periodontitis all into 2 majorcategories: 1) anti-inective treatment, which is designed to halt

the progression o periodontal attachment loss by removing etiologic actors; and 2) regenerative therapy, which includesanti-inective treatment and is intended to restore structuresdestroyed by disease. Essential to both treatment approaches isthe inclusion o periodontal maintenance procedures.4

Inammation o the periodontium may result rom many causes (eg, bacteria, trauma). However, most orms o gingivitisand periodontitis result rom the accumulation o tooth-adherent microorganisms.5-7 Prominent risk actors or devel-opment o chronic periodontitis include the presence o specic subgingival bacteria,8-10 tobacco use,9-13 diabetes,9,10,14 age,9,10 and male gender.9,10 Furthermore, there is evidence thatother actors can contribute to periodontal disease pathogenesis:environmental, genetic, and systemic (eg, diabetes).14,15

Tis paper primarily reviews the treatment o plaque-induced gingivitis and chronic periodontitis, but there mightbe some situations where the described therapies will notresolve disease or arrest disease progression. Furthermore, the

treatments discussed should not be deemed inclusive o allpossible therapies, or exclusive o methods o care reasonably directed at obtaining good results. Te ultimate decision regard-ing the appropriateness o any specic procedure must be madeby the practitioner in light o the circumstances presentedby an individual patient.

Plaque-induced GingivitisTerapy or individuals with chronic gingivitis is initially directed at reduction o oral bacteria and associated calciedand noncalcied deposits. Patients with chronic gingivitis, but

 without signicant calculus, alterations in gingival morphology,or systemic diseases that aect oral health, may respond to a therapeutic regimen consisting o improved personal plaquecontrol alone.16 Te periodontal literature documents the short-and long-term eects ollowing sel-treatment o gingivitis by personal plaque control.16-20 However, while it may be possibleunder controlled conditions to remove most plaque with a 

variety o mechanical oral hygiene aids, many patients lack themotivation or skill to attain and maintain a plaque-ree stateor signicant periods o time.21-23 Clinical trials also indicatethat sel-administered plaque control programs alone, withoutperiodic proessional reinorcement, are inconsistent in provi-ding long-term inhibition o gingivitis.19,24,25

Many patients with gingivitis have calculus or other associa-ted local actors (eg, deective dental restorations) that interere

 with personal oral hygiene and the ability to remove bacterialplaque. An acceptable therapeutic result or these individualsis usually obtained when personal plaque control measures areperormed in conjunction with proessional removal o plaque,calculus, and other local contributing actors.26,27

Removal o dental calculus is accomplished by scaling androot planing procedures using hand, sonic, or ultrasonic instru-ments. Te therapeutic objective o scaling and root planing is toremove plaque and calculus to reduce subgingival bacteria below a threshold level capable o initiating clinical inammation.

Originating Group American Academy of Periodontology - Research, Science, and Therapy Committee

Endorsed by the American Academy of Pediatric Dentistry2004

Copyright© 2004 by the American Academy o Periodontology; all rights reserved. Copyrighted and reproduced with permission rom the American Academy o 

Periodontology. No part o this publication may be reproduced, stored in a retrieval system, or transmitted in any orm or by any means, electronic, mechanical, photo-

copying, or otherwise without written permission o the publisher. reatment o Plaque-induced Gingivitis, Chronic Periodontitis, and Other Clinical Conditions. J

Periodontol 2001;72:1790-1800. Available through the American Academy o Periodontology, Department o Scientic, Clinical and Educational Aairs, 737 North

Michigan Avenue, #800, Chicago, IL 60611-2690, Phone: (312) 787-5518, Fax: (312) 787-3670.

Treatment of Plaque-induced Gingivitis, ChronicPeriodontitis, and Other Clinical Conditions

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318 ENDORSEMENTS

REFERENCE MANUAL V 34 / NO 6 12 / 13

Te success o instrumentation is determined by evaluating the periodontal tissues ollowing treatment and during themaintenance phase o therapy.

Te use o topical antibacterial agents to help reduce bac-terial plaque may be benecial or the prevention and treat-ment o gingivitis in some patients.28-30

A number o these agents in oral rinses and dentirices

have been tested in clinical trials.28 However, to be accepted by the American Dental Association ( ADA ) Council on DentalTerapeutics as an eective agent or the treatment o gingivitis,a product must reduce plaque and demonstrate eective reduc-tion o gingival inammation over a period o at least 6 months.Te agent must also be sae and not induce adverse side eects.

Tree medicaments have been given the ADA Seal o  Acceptance or the control o gingivitis. Te active ingredientso one product are thymol, menthol, eucalyptol, and methylsalicylate.29 Active ingredients in the other two are chlorhexidinedigluconate and triclosan.29 I properly used, the addition o a topical anti-plaque agent to a gingivitis treatment regimen or

patients with decient plaque control will likely result in reduc-tion o gingivitis.30 However, experimental evidence indicatesthat penetration o topically applied agents into the gingivalcrevice is minimal.31 Tereore, these agents are useul or thecontrol o supragingival, but not subgingival plaque. Among individuals who do not perorm excellent oral hygiene, supra-gingival irrigation with and without medicaments is capable o reducing gingival inammation beyond that normally achievedby toothbrushing alone. Tis eect is likely due to the ushing out o subgingival bacteria.32

I gingivitis remains ollowing the removal o plaque andother contributing local actors, thorough evaluation should beundertaken o systemic actors (eg, diabetes, pregnancy, etc.). I 

such conditions are present, gingival health may be attained oncethe systemic problem is resolved and plaque control is maintained.

 Acute Periodontal DiseasesNecrotizing ulcerative gingivitis (NUG) is associated withspecic bacterial accumulations occurring in individuals withlowered host resistance.1 NUG usually responds rapidly to thereduction o oral bacteria by a combination o personal plaquecontrol and proessional debridement. I lymphadenopathy orever accompanies oral symptoms, administration o systemicantibiotics may be indicated. Te use o chemotherapeuticrinses by the patient may be benecial during the initial treat-

ment stages. Ater the acute inammation o the NUG lesionis resolved, additional intervention may be indicated to preventdisease recurrence or to correct resultant sot tissue deormities.

Necrotizing ulcerative periodontitis (NUP) maniests asrapid necrosis and destruction o the gingiva and periodontalattachment apparatus. It may initiate gingival bleeding and pain,and it usually represents an extension o necrotizing ulcerativegingivitis in individuals with lowered host resistance. NUP hasbeen reported among both HIV-positive and negative individu-als, but its true prevalence is unknown.33-38 Management o 

NUP involves debridement which may be combined withirrigation with antiseptics (eg, povidone iodine), antimicrobialmouth rinses (eg, chlorhexidine), and administration o sys-temic antibiotics.39 Tere is also evidence that HIV-immunedeciency may be associated with severe loss o periodontalattachment that does not necessarily present clinically as anulcerative lesion.40 Although not an acute disease, linear gin-

gival erythema (LGE) occurs in some HIV-inected individualsand does not appear to respond to conventional scaling, rootplaning, and plaque control.39 Antibiotic therapy should beused in HIV-positive patients with caution due to the possi-bility o inducing opportunistic inections.39,40

Te oral maniestations o a primary herpes simplex virustype I inection oten include gingivitis. By the time gingivitisis present, patients are usually ebrile, in pain, and have lymph-adenopathy. Diagnosis is generally made rom the clinicalappearance o the oral sot tissues. Although not perormedroutinely, a viral culture may provide denitive identicationo the inective agent. In otherwise healthy patients, treatment

or herpetic gingivitis consists o palliative therapy. Te in-ection is sel-limiting and usually resolves in 7 to 10 days.Systemic antiviral therapy with acyclovir is appropriate orimmunocompromised patients with herpetic gingivitis.41

Gingival Enlargement Chronic gingival inammation may result in gingival enlarge-ment. Tis overgrowth o gingiva may be exaggerated in patients

 with genetic or drug-related systemic actors (eg, anticonvul-sants, cyclosporine and calcium channel blocking drugs).42-46 

 Among individuals taking phenytoin, gingival overgrowth may be minimized with appropriate personal oral hygiene and proes-sional maintenance.47,48 However, root debridement in patients

 with gingival overgrowth oten does not return the periodontiumto normal contour. Te residual overgrowth may not only com-plicate the patient’s ability to adequately clean the dentition,but it may also present esthetic and unctional problems.49

For patients with gingival overgrowth, the modicationo tissue topography by surgical recontouring may be under-taken to create a maintainable oral environment.47,50 Postoper-ative management ollowing tissue resection is important.Te benets o surgical reduction may be lost due to rapidprolieration o the tissues during the post-therapy phase.51 Recurrence is common in many patients with drug-inducedgingival overgrowth.51 For these patients, consultation with the

patient’s physician is advisable to determine i it is possible touse an alternative drug therapy that does not induce gingivalovergrowth. I not, then repeated surgical and/or non-surgicalintervention may be required.

Chronic Periodontitis Appropriate therapy or patients with periodontitis variesconsiderably with the extent and pattern o attachment loss,local anatomical variations, type o periodontal disease, andtherapeutic objectives. Periodontitis destroys the attachment

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apparatus o teeth resulting in periodontal pocket ormationand alteration o normal osseous anatomy. Te primary objec-tives o therapy or patients with chronic periodontitis are tohalt disease progression and to resolve inammation. Terapy at a diseased site is aimed at reducing etiologic actors below the threshold capable o producing breakdown, thereby allow-ing repair o the aected region. Regeneration o lost peri-

odontal structures can be enhanced by specic procedures.However, many variables responsible or complete regenerationo the periodontium are unknown and research is ongoing inthis area.

Scaling and Root Planing Te benecial eects o scaling and root planing combined

 with personal plaque control in the treatment o chronic peri-odontitis have been validated.52-65 Tese include reductiono clinical inammation, microbial shits to a less pathogenicsubgingival ora, decreased probing depth, gain o clinicalattachment, and less disease progression.52-65

Scaling and root planing procedures are technically de-manding and time-consuming. Studies show that clinicalconditions generally improve ollowing root planing; nonethe-less, some sites still do not respond to this therapy.62,63,66,67 Teaddition o gingival curettage to root planing in the treatmento generalized chronic periodontitis with shallow suprabony pockets does not signicantly reduce probing depth or gainclinical attachment beyond that attained by scaling and rootplaning alone.68,69 Te ollowing actors may limit the successo treatment by root planing: root anatomy (eg, concavities,urrows etc.), urcations,66 and deep probing depths.70-72

Several weeks ollowing the completion o root planing andeorts to improve personal plaque control, re-evaluation should

be conducted to determine the treatment response. Severalactors must be considered at sites that continue to exhibit signso disease. I the patient’s daily personal plaque control is notadequate to maintain gingival health, then additional instruc-tion and motivation in personal plaque control and/or the use o topical chemotherapeutics (eg, mouthrinses, local drug delivery devices) may be indicated. Anatomical actors that can limitthe eectiveness o root instrumentation or limit the patient’sability to perorm personal plaque control (eg, deep probing depths, root concavities, urcations) may require additionaltherapy including surgery. Host response may also have aneect on treatment outcome and patients with systemic con-

ditions (eg, diabetes, pregnancy, stress, AIDS, immunodecien-cies, and blood dyscrasias) may not respond well to therapy that is directed solely at controlling local actors. In suchpatients, it is important that attempts be made to control thecontributing systemic actors.

Pharmacological Terapy Pharmacotherapeutics may have an adjunctive role in themanagement o periodontitis in certain patients.73 Tese ad-

 junctive therapies are categorized by their route o administra-tion to diseased sites: systemic or local drug delivery.

Systemic Drug AdministrationNumerous investigations73 have assessed the use o systemicantibiotics to halt or slow the progression o periodontitis or toimprove periodontal status. Te adjunctive use o systemically delivered antibiotics may be indicated in the ollowing situa-tions: patients with multiple sites unresponsive to mechanicaldebridement, acute inections, medically compromised pa-

tients, presence o tissue-invasive organisms and ongoing dis-ease progression.74-77 Te administration o antibiotics orthe treatment o chronic periodontitis should ollow acceptedpharmacological principles including, when appropriate, iden-tication o pathogenic organisms and antibiotic sensitivity testing.

Considerable research eorts have ocused on systemicapplication o host modulating agents such as non-steroidalanti-inammatory drugs (NSAIDS)78-80 and subantimicrobialdose doxycycline.81-84 Investigators have reported some benet

 when these medications are incorporated into treatment proto-cols.78,81-84 Recently [year 2000], the United States Food and

Drug Administration (FDA 

) approved the use o a systemically delivered collagenase inhibitor consisting o a 20-mg capsule o doxycycline hyclate as an adjunct to scaling and root planing or the treatment o periodontitis. Benets included a statisti-cally signicant reduction in probing depths, a gain in clinicalattachment levels and a reduction in the incidence o diseaseprogression.82-84 Overall, the data suggest that use o subantimi-crobial dose doxycycline as an adjunct to scaling and root planing provides dened but limited improvement in periodontal status.

It is important to consider the potential benets andside eects o systemic pharmacological therapy. Benets may include the ability to treat patients unresponsive to conven-tional therapy or an individual with multiple sites experiencing 

recurrent periodonitits. In contrast, potential risks associated with systemically administered antibiotics include developmento resistant bacterial strains,85 emergence o opportunistic in-ections, and possible allergic sensitization o patients.73 Withregard to the prolonged administration o NSAIDS, harmuleects may include gastrointestinal upset and hemorrhage, renaland hepatic impairment, central nervous system disturbances, in-hibition o platelet aggregation, prolonged bleeding time, bonemarrow damage, and hypersensitivity reactions.73 At present,the incidence o negative side eects reported ater root planing 

 with or without administration o subantimicrobial dose doxy-cycline has been similar. In general, since patients with chronic

periodontitis respond to conventional therapy, it is unnecessary to routinely administer systemic medications such as anti-biotics, NSAIDS, or subantimicrobial dosing with doxycycline.

Local Delivery Controlled delivery o chemotherapeutic agents within peri-odontal pockets can alter the pathogenic ora and improveclinical signs o periodontitis.86-94 Local drug delivery systemsprovide several benets; the drug can be delivered to the siteo disease activity at a bactericidal concentration and it canacilitate prolonged drug delivery. Te FDA has approved the

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use o an ethylene vinyl acetate ber that contains tetracy-cline,86-91 a gelatin chip that contains chlorhexidine93 and a minocycline polymer ormulation92 as adjuncts to scaling androot planing. Te FDA has also approved doxycycline hyclatein a bioabsorbable polymer gel as a stand-alone therapy or thereduction o probing depths, bleeding upon probing, and gaino clinical attachment.94

Local delivery systems have potential limitations andbenets. I used as a monotherapy, problems associated withlocal delivery can include allergic reaction, possible inability todisrupt biolms, and ailure to remove calculus.95 Te benetsinclude the ease o application, selectively targeting a limitednumber o diseased sites that were unresponsive to conventionaltherapy, and possibly enhanced treatment results at speciclocations. Local delivery modalities have shown benecial clini-cal improvements with regard to probing depth reduction andgain in clinical attachment.91-94 Furthermore, there are limiteddata to suggest that local delivery o antibiotics may also bebenecial in preventing recurrent attachment loss in the ab-

sence o maintenance therapy.90

Utilization o antibiotics at an individual site will dependon the discretion o the treating therapist ater consultation

 with the patient. Te greatest potential o local delivery devicesmay be to enhance therapy at sites that do not respond toconventional treatment. Ultimately, the results o local drug delivery must be evaluated with regard to the magnitude o improvement that can be attained relative to disease severity. A more complete review o local drug delivery can be ound inthe American Academy o Periodontology position paper “TeRole o Controlled Drug Delivery or Periodontitis”.87

Surgical Terapy 

Surgical access to acilitate mechanical instrumentation o theroots has been utilized to treat chronic periodontitis or dec-ades. A surgical approach to the treatment o periodontitis isutilized in an attempt to: 1) provide better access or removalo etiologic actors; 2) reduce deep probing depths; and 3) re-generate or reconstruct lost periodontal tissues.96-98

Clinical trials indicate that both surgical and nonsurgicalapproaches can be eective in achieving stability o clinicalattachment levels.60-65,99-103 Flap reection is capable, however,o increasing the ecacy o root debridement, especially atsites with deep probing depths or urcations.60-65,70,72,99-104 Nevertheless, complete calculus removal, even with surgi-

cal access, may not always be achieved.70,72,104 Te addition o osseous resection during surgical procedures appears to producegreater reduction o probing depth due to gingival reces-sion,62,64,65 particularly in urcations.66 Regardless o the type o therapy, urcated teeth are problematic since they are still morelikely to lose clinical attachment than nonurcated teeth.66,67,105 

 While these overall ndings are helpul, the practitionershould base specic decisions or therapy on ndings or eachindividual patient.

Regenerative Surgical Terapy Te optimal goal o therapy or individuals who have lost a signicant amount o periodontal attachment is regenerationo lost tissues. While root debridement in combination withplaque control has demonstrated ecacy in resolving inam-mation and arresting periodontitis,26,27,60-65 healing typically results in the ormation o a long junctional epithelium106-108 

 with remodeling o the alveolus.109 Similarly, surgical debride-ment alone does not induce signicant amounts o new connective tissue attachment.110,111 However, some bone llmay occur in selected sites.107,112

Clinical trials suggest that obtaining new periodontalattachment or regenerating lost tissues is enhanced by theuse o adjunctive surgical technique devices and materials.Chemical agents that modiy the root surace, while promoting new attachment, have shown variable results when used inhumans.113-118 Bone grating 119-125 and guided tissue regeneration(GR) techniques, with or without bone replacement grats,126-133

may be successul when used at selected sites with advanced

attachment loss. Te use o biologically engineered tissue induc-tive proteins (eg, growth actors, extracellular matrix proteins,and bone morphogenic proteins) to stimulate periodontal orosseous regeneration has also shown promise.134-142 Literaturereviews on periodontal regeneration143,144 and mucogingivaltherapy 145 provide additional inormation regarding thesetherapies.

Regenerative therapy and other treatment modalities canbe aected by several risk actors (eg, diabetes and tobaccouse) which can diminish periodontal treatment outcomes.146 Inthis regard, cigarette smoking is associated with a high risk orprogressive periodontitis9-13,147 and treatment or periodontitismay be less eective in smokers than non-smokers.148-150 Tese

actors are reviewed in more depth in the Academy’s positionpaper obacco Use and the Periodontal Patient.151 o maximizeeective prevention and treatment o periodontitis, patientsshould be encouraged to stop smoking and to stop using smokeless tobacco.

Occlusal ManagementSeveral studies indicated that excessive occlusal orces do notinitiate plaque-induced periodontal disease or connective tissueattachment loss (periodontitis).152-155 However, other investiga-tions suggest that tooth mobility may be associated with adverseeects on the periodontium and aect the response to therapy 

 with respect to gaining clinical attachment.156,157 With regards totreatment, occlusal therapy may aid in reducing tooth mobility and gaining some bone lost due to traumatic occlusal orces.158 Occlusal equilibration also may be used to ameliorate a variety o clinical problems related to occlusal instability and restorativeneeds.159 Clinicians should use their judgment as to whetheror not to perorm an occlusal adjustment as a component o periodontal therapy based upon an evaluation o clinical ac-tors related to patient comort, health and unction.160

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Periodontal Maintenance ProceduresPeriodic monitoring o periodontal status and appropriatemaintenance procedures should be part o the long-termtreatment plan or managing chronic periodontitis.28 Althoughexperimental studies have demonstrated very successul treat-ment outcomes when patients are proessionally maintainedat 2-week intervals,161 such a program is impractical or most

chronic periodontitis patients. Tereore, to maximize success-ul therapeutic outcomes, patients must maintain eectivedaily plaque control. It also appears that in-oce periodontalmaintenance at 3 to 4 month intervals can be eective inmaintaining most patients.4 A more comprehensive review onthis subject can be ound in the American Academy o Periodontology’s position paper entitled Supportive Periodontal Terapy (SPT).162

SummaryTe inammatory components o plaque induced gingivitisand chronic periodontitis can be managed eectively or the

majority o patients with a plaque control program and non-surgical and/or surgical root debridement coupled with con-tinued periodontal maintenance procedures. Some patientsmay need additional therapeutic procedures. All o the thera-peutic modalities reviewed in this position paper may be utilizedby the clinician at various times over the long-term manage-ment o the patient’s periodontal condition.

References1. American Academy o Periodontology. he pathogen-

esis o periodontal diseases (position paper). J Periodontol1999;70:457-70.

2. American Academy o Periodontology. Diagnosis o Periodontal Diseases (position paper). Chicago, Ill: Te

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4. Ramjord SP. Maintenance care and supportive perio-dontal therapy. Quintessence Int 1993;24:465-71.

5. Page RC. Gingivitis. J Clin Periodontol 1986;13:345-59.6. Ranney RR, Debski BF, ew JG. Pathogenesis o gingi-

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7. Socransky SS, Haajee AD. Microbial mechanisms in the

pathogenesis o destructive periodontal diseases: A criticalassessment. J Periodont Res 1991;26:195-212.

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9. Grossi SG, Zambon JJ, Ho AW, et al. Assessment o risk or periodontal disease. I. Risk indicators or attachmentloss. J Periodontol 1994;65:260-7.

10. Grossi SG, Genco RJ, Machtei EE, et al. Assessment o risk or periodontal disease. II. Risk indicators or alveolarbone loss. J Periodontol 1995;66:23-9.

11. Ismail A, Morrison E, Burt B, Caesse R, Kavanaugh M.Natural history o periodontal disease in adults: Findingsrom the ecumseh Periodontal Disease Study, 1959-1987. J Dent Res 1990;69:430-5.

12. Haber J, Wattles J, Crowley M, Mandell R, Joshipurak K,Kent RL. Evidence or cigarette smoking as a major risk actor or periodontitis. J Periodontol 1993;64:16-23.

13. Bergstrom J, Preber H. obacco use as a risk actor. JPeriodontol 1994;65:545-50.

14. Oliver RC, ervonen . Diabetes: A risk actor or perio-dontitis in adults? J Periodontol 1994;65:530-8.

15. Michalowicz BS. Genetic and heritable risk actors inperiodontal disease. J Periodontol 1994;65:479-88.

16. Löe H, Teilade E, Jensen SB. Experimental gingivitis inman. J Periodontol 1965;36:177-87.

17. Teilade E, Wright WH, Jensen SB, Löe H. Experimentalgingivitis in man. II. A longitudinal clinical and bacterio-logical investigation. J Periodont Res 1966;1:1-13.

18. Lindhe J, Axelsson P. Te eect o a preventive program-

me on dental plaque, gingivitis, and caries in school chil-dren. Results ater one and two years. J Clin Periodontol1974;1:126-38.

19. Suomi JD, Greene JC, Vermillion JR, Doyle J, Chang JJ,Leatherwood EC. he eect o controlled oral hygieneprocedures on the progression o periodontal disease inadults: Results ater third and inal year. J Periodontol1971;42:152-60.

20. Axelsson P, Lindhe J. Eect o controlled oral hygieneprocedures on caries and periodontal disease in adults.Results ater 6 years. J Clin Periodontol 1981;8:239-48.

21. De la Rosa M, Guerra JZ, Johnston DA, Radike AW.Plaque growth and removal with daily toothbrushing. J

Periodontol 1979;50:661-4.22. MacGregor IDM, Rugg-Gunn AJ, Gordon PH. Plaque

levels in relation to the number o toothbrushing strokesin uninstructed English schoolchildren. J Periodont Res1986;21:577-82.

23. Lang NP, Cumming BR, Löe H. oothbrushing re-quency as it relates to plaque development and gingivalhealth. J Periodontol 1973;44:396-405.

24. Listgarten MA, Schiter CC, Laster L. 3-year longitudinalstudy o the periodontal status o an adult population

 with gingivitis. J Clin Periodontol 1985;12:225-38.25. Agerbaek N, Melsen B, Lind OP, Glavind L, Kristiansen

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AcknowledgmentsTis paper was revised by Dr. Paul S. Rosen. It replaces thepaper entitled reatment of Gingivitis and Periodontitis  which

 was authored by Drs. William F. Ammons, Kenneth L.Kalkwar, and Stephen . Sonis in May 1993 and revised by Dr. Bruce L. Pihlstrom and William F. Ammons in September1997. Members o the 2000-2001 Research, Science and

Terapy Committee include: Drs. David Cochran, Chair;imothy Blieden; Otis J. Bouwsma; Robert E. Cohen; PetrosDamoulis; Connie H. Drisko; Joseph P. Fiorellini; Gary Greenstein; Vincent J. Iacono; Martha J. Somerman; erry D.Rees; Angelo Mariotti, Consultant; Robert J. Genco, Consul-tant; and Brian L. Mealey, Board Liaison. 

Individual copies o this position paper may be obtainedby accessing: “http://www.perio.org”. Members o the Amer-ican Academy o Periodontology have permission o the Aca-demy, as copyright holder, to reproduce up to 150 copies o 

this document or not-orprot, educational purposes only. Forinormation on reproduction o the document or any otheruse or distribution, please contact Rita Shaer at the Academy Central Oce; voice: (312) 573-3221; ax: (312) 573-3225; ore-mail: [email protected] .