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REFERENCE MANUAL V 34 / NO 6 12 / 13

Epidemiologic studies indicate that gingivitis o varying se-verity is nearly universal in children and adolescents.1-19 Tesestudies also indicate that the prevalence o destructive ormso periodontal disease is lower in young individuals than inadults. Epidemiologic surveys in young individuals have beenperormed in many parts o the world and among individualswith a widely varied background. For the most part, these sur-veys indicated that loss o periodontal attachment and sup-

porting bone is relatively uncommon in the young but thatthe incidence increases in adolescents aged 12 to 17 whencompared to children aged 5 to 11.15-22 In general, in the UnitedStates, epidemiologic studies indicate that the prevalence osevere attachment loss on multiple teeth among children andyoung adults is approximately 0.2% to 0.5%.23 Despite thislow prevalence, children and adolescents should receive pe-riodic periodontal evaluation as a component o routinedental visits.

On October 30-November 2, 1999, the American Aca-demy o Periodontology assembled an International Workshopor a Classication o Periodontal Diseases and Conditions,which resulted in a new classication.24 Periodontal diseasesdiscussed here will reect the new classication system. Cli-nically distinct periodontal inections that can aect youngindividuals include: 1) dental plaque-induced gingival diseases;2) chronic periodontitis; 3) aggressive periodontitis; 4) perio-dontitis as a maniestation o systemic diseases; and 5) necro-tizing periodontal diseases.

Dental plaque-induced gingival diseasesGingivitis associated with dental plaque only and gingivaldiseases modifed by systemic actors associated with theendocrine systemGingivitis characterized by the presence o gingival inammation

without detectable loss o bone or clinical attachment is com-monin children.1-19,25 Although the microbiology o this disease hasnot been completely characterized, increased subgingival le-vels oActinomycessp., Capnocytophagasp., Leptotrichiasp., andSelenomonassp. have been ound in experimental gingivitis in

children when compared to gingivitis in adults. Tese speciesmay thereore be important in its etiology and pathogenesis.26,27

Normal and abnormal uctuation in hormone levels,including changes in gonadotrophic hormone levels duringthe onset o puberty, can modiy the gingival inammatoryresponse to dental plaque.28,29 Similarly, alterations in insulinlevels in patients with diabetes can aect gingival health.28,29 Inboth situations, there is an increased inammatory response to

plaque.28,29

However, the gingival condition usually respondsto thorough removal o bacterial deposits and improved dailyoral hygiene.28,29

PeriodontitisAggressive periodontitis, chronic periodontitis, and periodon-titis as a maniestation o systemic diseasesChildren and adolescents can have any o the several ormso periodontitis as described in the proceedings o the 1999International Workshop or a Classication o PeriodontalDiseases and Conditions (aggressive periodontitis, chronicperiodontitis, and periodontitis as a maniestation o systemicdiseases). However, chronic periodontitis is more common inadults, while aggressive periodontitis may be more commonin children and adolescents.24

Te primary eatures o aggressive periodontitis include ahistory o rapid attachment and bone loss with amilial aggrega-tion. Secondary eatures include phagocyte abnormalities anda hyperresponsive macrophage phenotype.24Aggressive perio-dontitis can be localized or generalized. Localized aggressiveperiodontitis (LAgP) patients have interproximal attachmentloss on at least two permanent rst molars and incisors, withattachment loss on no more than two teeth other than rstmolars and incisors. Generalized aggressive periodontitis(GAgP) patients exhibit generalized interproximal attachment

loss including at least three teeth that are not rst molars andincisors. In young individuals, the onset o these diseases isoten circumpubertal. Some investigators have ound that thelocalized orm appears to be sel-limiting,30 while others sug-gest that it is not.20 Some patients initially diagnosed as having

Originating GroupAmerican Academy of Periodontology Research, Science and Therapy Committee

Endorsed/ Reafrmed by the American Academy o Pediatric Dentistry1992, 1995, 2004

Copyright 2004 by the American Academy o Periodontology; all rights reserved. No part o this publication may be reproduced, stored in a retrieval system,or transmitted in any orm or by any means, electronic, mechanical, photocopying, or otherwise without written permission o the publisher. Periodontal diseaseso children and adolescents. J Periodontol 2003;74:1696-704. Available through the American Academy o Periodontology, Department o Scientic, Clinicaland Educational Aairs, 737 North Michigan Avenue, #800, Chicago, IL 60611-2690, Phone: 312-787-5518, Fax: 312-787-3670. Approved by the AmericanAcademy o Periodontology Board o rustees, April 1991.

Periodontal Diseases of Children and Adolescents


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LAgP were ound to have GAgP or to be periodontally healthyat a 6-year ollow-up exam.31,32

LAgP occurs in children and adolescents without clinicalevidence o systemic disease and is characterized by the severeloss o alveolar bone around permanent teeth.31 Frequently, thedisease is localized to the permanent rst molars and incisors.However, some retrospective data obtained rom LAgP patients

suggest that bone loss around the primary teeth can be an earlynding in the disease.33 Linkage studies o the Brandywinepopulation (a segregated group o people in Maryland that repre-sents a relatively closed gene pool) have ound a gene conerringincreased risk or LAgP on chromosome 4.34 Subsequent linkagestudies o Arican American and Caucasian amilies did notconrm linkage to this locus, suggesting that there may be genet-ic and/or etiologic heterogeneity or aggressive periodontitis.35-37

Reported estimates o the prevalence o LAgP in geographicallydiverse adolescent populations range rom 0.1% to 15%.23,33-35,37-42 Most reports suggest a low prevalence (0.2%), which ismarkedly greater in Arican American populations (2.5%).

Many reports suggest that patients with LAgP generallyorm very little supragingival dental plaque or calculus.31,43

In contrast, other investigators nd plaque and calculus atlevels similar to other periodontal diseases.44,45 Bacteria oprobable etiologic importance include highly virulent strainsoActinobacillus actinomycetemcomitans in combination withBacteroides-like species.46-49 In some populations,Eubacteriumsp. have been associated with the presence o LAgP.50,51 odate, however, no single species is ound in all cases o LAgP.52

A variety o unctional deects have been reported inneutrophils rom patients with LAgP.53-55 Tese include anoma-lies o chemotaxis,56-58 phagocytosis,59,60 bactericidal activity,61

superoxide production,62-66 FcgIIIB (CD16) expression,67

leukotriene B4 generation,68,69 and Ca2+channel and secondmessenger activation.70-75 Te deect in chemotaxis is thought tobe an intrinsic deect by some investigators56-58 and an induceddeect by others.76 Te inuence o these unctional deects onthe susceptibility o individuals to LAgP is unknown, but it ispossible that they play a role in the clinical course o diseasein some patients. Indeed, in some cases exhibiting phagocyteabnormalities, neutrophil deects may still be present ater treat-ment.77 Molecular markers o LAgP can include an abnormallylow number o chemoattractant receptors78-81 and an abnormallylow amount o another cell surace glycoprotein designatedGP-110.82,83 Adherence receptors on neutrophils and monocytes,

such as LFA-1 and Mac-1, are normal in LAgP patients.82,83GAgP, oten considered to be a disease o adolescentsand young adults, can begin at any age and oten aects theentire dentition.84,85 Individuals with GAgP exhibit markedperiodontal inammation and have heavy accumulations oplaque and calculus.84 In the United States, the reported preva-lence o GAgP in adolescents (14 to 17 years o age) is 0.13%.23Subgingival sites rom aected teeth harbor high percentages onon-motile, acultatively anaerobic, Gram-negative rods includ-ingPorphyromonas gingivalis.86,87 In one report, the levels oP.

gingivalis and Treponema denticolawere signicantly higher in

GAgP and LAgP patients compared to matched controls, withGAgP patients having the highest levels.88 Neutrophils rompatients with GAgP requently exhibit suppressed chemotaxisas observed in LAgP77,87 with a concomitant reduction in GP-110. Tis suggests a relationship between the two variants oaggressive periodontitis.82,83

Alterations in immunologic actors such as immuno-

globulins are known to be present in aggressive periodontitis.Immunoglobulins appear to be inuenced by both genetic andenvironmental actors and have important protective disease-limiting eects in aggressive periodontitis patients.89-93 HumanIgG antibody molecules (immunoglobulin G) are categorizedinto our subclasses designated as IgG1-4. Most o the antibodyreactive withA. actinomycetemcomitans is specic or highmolecular weight lipopolysaccharide and is o the IgG2 sub-class. Tis antibody response appears to be protective, as early-onset periodontitis patients having high concentrations oantibody reactive withA. actinomycetemcomitans lipopolysac-charide have signicantly less attachment loss (a measure o

disease severity) than patients who lack this antibody.89,90

Overall levels o IgG2 in serum are under genetic control.91Tese levels have also been shown to be aected by periodontaldiagnosis (LAgP patients have very high levels), race (AricanAmericans have higher levels than Caucasians), and smoking(smokers have lower levels o IgG2, with notable exceptionsin some patient groups).91,92,94,95 Tese actors also inuencespecic antibody responses toA. actinomycetemcomitans.91-93,95Tus, the protective antibody response aorded by IgG2, aswell as the clinical maniestations o aggressive periodontitis,is modied by patients genetic background as well as environ-mental actors such as smoking and bacterial inection.89,91-93,95,96

Successul treatment o aggressive periodontitis depends on

early diagnosis, directing therapy against the inecting micro-organisms and providing an environment or healing that is ree oinection.97 While there is some disagreement among individualstudies regarding treatment o LAgP, most authors recommenda combination o surgical or non-surgical root debridement inconjunction with antimicrobial (antibiotic) therapy.47,98 Tesendings are supported by other work in which meticulousand repeated mechanical therapy with antibiotics proved to besu-cient to arrest most cases o LAgP.99 However, surgical treatment may be eective in eliminatingA. actinomycetemcomitanswithout the use o antibiotics.100 In a study o 25 deep perio-dontal lesions (probing depths 5 to 11 mm) in young LAgP

patients, scaling and root planing alone were ineective or theelimination oA. actinomycetemcomitans, while surgical therapywas eective.100 It is not known, however, iA. actinomycetem-comitansis the only organism involved in disease pathogenesis. Te majority o reports suggest that the use o antibio-tics is usually benecial in the treatment o LAgP. wo reportsdescribed using antibiotics exclusively.97,101 In both reports,LAgP patients attained signicant clinical attachment gainwhen assessed ater 12 months with tetracycline therapy alone.Most reports in the past 10 years, however, have recommend-ed combination therapy using antibiotics and surgical or


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non-surgical root debridement as the optimal treatment orLAgP.98,102-116 Te most successul antibiotics reported are thetetracyclines, sometimes prescribed sequentially with metroni-dazole.103,117,118 Metronidazole in combination with amoxicillinhas also been utilized, especially where tetracyline-resistant A.actinomycetemcomitansare present.111 A single randomized con-trol study in which oral penicillin was used reported that

therapy was successul with or without the antibiotic.119While the use o antibiotics in conjunction with surgical

or non-surgical root debridement appears to be quite eectiveor the treatment o LAgP, GAgP does not always respond wellto conventional mechanical therapy or to antibiotics common-ly used to treat periodontitis.30,118,120 Alternative antibiotics maybe required, based upon the character o the pathogenic ora.In GAgP patients who have ailed to respond to standardperiodontal therapy, laboratory tests o plaque samples mayidentiy periodontal pathogens that are resistant to antibioticstypically used to treat periodontitis.103 It has been suggestedthat ollow-up tests ater additional antibiotic or other therapy

is provided may be helpul in conrming elimination o tar-geted pathogenic organisms.103

Chronic periodontitis is most prevalent in adults, but canoccur in children and adolescents. It can be localized (less than30% o the dentition aected) or generalized (greater than30% o the dentition aected) and is characterized by a slowto moderate rate o progression that may include periods orapid destruction. Furthermore, the severity o disease can bemild (1 to 2 mm clinical attachment loss), moderate (3 to 4mm clinical attachment loss), or severe (5 mm clinical attach-ment loss). Children and young adults with this orm o diseasewere previously studied along with patients having LAgP andGAgP. Tereore, published data are lacking or this group. Inpatients with one o several systemic diseases that predisposeto highly destructive disease o the primary teeth, the diagnosisis periodontitis as a maniestation o systemic disease. As withadults, periodontitis associated with systemic diseases occursin children and adolescents. Such diseases include Papillon-Levre syndrome,121-125 cyclic neutropenia,126-130 agranulocy-tosis,131,132 Down syndrome,133-135 hypophosphatasia,136 andleukocyte adherence deciency.137,138 It is probable that deectsin neutrophil and immune cell unction associated with thesediseases play an important role in increased susceptibility toperiodontitis and other inections. In Down syndrome, or ex-ample, the amount o periodontal destruction has been shown

to be positively correlated with the severity o the neutrophilchemotaxis deect.135 In some cases, specic genes have beenassociated with these diseases. Examples include the cathepsinC gene and Papillon-Levre syndrome139-141 and the tissue non-specic alkaline phosphatase gene and hypophosphatasia.136

Te consensus report o the 1999 Workshop specicallyexcluded diabetes-associated periodontitis as a specic ormo periodontitis associated with systemic disease. Participantsconcluded that diabetes is a signicant modier o all ormso periodontitis. In a survey o 263 type 1 diabetics, 11 to 18years o age, 10% were ound to have overt periodontitis oten

localized to rst molars and incisors, although periodontitiswas also ound in a generalized pattern.142 Aected subgin-gival sites harboredA. actinomycetemcomitans and Capnocyto-

phagasp.143

Periodontitis as a maniestation o systemic disease in chil-dren is a rare disease that oten begins between the time oeruption o the primary teeth up to the age o 4 or 5.144,145 Te

disease occurs in localized and generalized orms. In the local-ized orm, aected sites exhibit rapid bone loss and minimalgingival inammation.144 In the generalized orm, there is rapidbone loss around nearly all teeth and marked gingival inam-mation. Neutrophils rom some children with a clinical diagno-sis o periodontitis as a maniestation o systemic disease haveabnormalities in a cell surace glycoprotein (LFA-1, leukocyteunctional antigen1, also known as CD11, and Mac-1). Teneutrophils in these patients having LAD (leukocyte adhesiondeciency) are likely to have a decreased ability to move romthe circulation to sites o inammation and inection.137 Aectedsites harbor elevated percentages o putative periodontal path-

ogens such asA. actinomycetemcomitans, Prevotella intermedia,Eikenella corrodens,andCapnocytophaga sputigena.146,147

reatment o periodontitis as a maniestation o systemicdisease in children is similar to the treatment o localized andgeneralized aggressive periodontitis in the permanent denti-tion and has been reported to include surgical or non-surgicalmechanical debridement and antimicrobial therapy.124,127-130,132,134,142,144 Localized lesions have been treated successully with thisapproach,144,145 but the degree o predictable success in man-aging generalized periodontitis is low when systemic diseasesare contributing actors.144,145 In many cases, the aected teethhad to be extracted.138,144,145

Necrotizing periodontal diseasesNecrotizing periodontal diseases (NPD) occur with varying butlow requency (less than 1%) in North American and Euro-pean children. It is seen with greater requency (2% to 5%) incertain populations o children and adolescents rom develop-ing areas o Arica, Asia, and South America.148-150 Te twomost signicant ndings used in the diagnosis o NPD arethe presence o interproximal necrosis and ulceration and therapid onset o gingival pain. Patients with NPD can oten beebrile. Necrotizing ulcerative gingivitis/periodontitis sites har-bor high levels o spirochetes andP. intermedia,151 and invasiono the tissues by spirochetes has been shown to occur.152

Factors that predispose children to NPD include viral inec-tions (including HIV), malnutrition, emotional stress, lacko sleep, and a variety o systemic diseases.148-150,153 reatmentinvolves mechanical debridement, oral hygiene instruction,and careul ollow-up.154-156 Debridement with ultrasonics hasbeen shown to be particularly eective and results in a rapiddecrease in symptoms.157 I the patient is ebrile, antibioticsmay be an important adjunct to therapy. Metronidazole andpenicillin have been suggested as drugs o choice.151,158


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SummaryChildren and adolescents are subject to several periodontaldiseases. Although there is a much lower prevalence o destruc-tive periodontal diseases in children than in adults, childrencan develop severe orms o periodontitis.23 In some cases, thisdestructive disease is a maniestation o a known underlyingsystemic disease. In other young patients, the underlying cause

or increased susceptibility and early onset o disease is unknown.Tese diseases are oten amilial, suggesting a genetic predispo-sition or aggressive disease. Current modalities or managingperiodontal diseases o children and adolescents may includeantibiotic therapy in combination with non-surgical and/orsurgical therapy. Since early diagnosis ensures the greatest chanceor successul treatment,97 it is important that children receivea periodontal examination as part o their routine dental visits.

AcknowlegmentsTe primary author or this paper is Dr. Joseph V. Caliano.Members o the 2002-2003 Research, Science and Terapy

Committee include: Drs. erry D. Rees, Chair; ChristopherCutler; Petros Damoulis; Joseph Fiorellini; William Giannobile;Henry Greenwell; Angelo Mariotti; Steven Oenbacher;Leslie Salkin; Brian Nicoll, Board Liaison; Robert J. Genco,Consultant.

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