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Epidemiologic studies indicate that gingivitis ofvarying severity is nearly universal in childrenand adolescents.1-19 These studies also indicatethat the prevalence of destructive forms of periodon-tal disease is lower in young individuals than in adults.

Epidemiologic surveys in young individuals have beenperformed in many parts of the world and amongindividuals with a widely varied background. For themost part, these surveys indicated that loss of peri-odontal attachment and supporting bone is relativelyuncommon in the young but that the incidenceincreases in adolescents aged 12 to 17 when com-pared to children aged 5 to 11.15-22 In general, in theUnited States, epidemiologic studies indicate that theprevalence of severe attachment loss on multiple teethamong children and young adults is approximately0.2% to 0.5%.23 Despite this low prevalence, childrenand adolescents should receive periodic periodontal

evaluation as a component of routine dental visits.On October 30-November 2, 1999, the AmericanAcademy of Periodontology assembled an InternationalWorkshop for a Classification of Periodontal Diseasesand Conditions, which resulted in a new classification.24Periodontal diseases discussed here will reflect the newclassification system. Clinically distinct periodontalinfections that can affect young individuals include: 1)dental plaque-induced gingival diseases; 2) chronicperiodontitis; 3) aggressive periodontitis; 4) periodon-titis as a manifestation of systemic diseases; and 5)necrotizing periodontal diseases.

DENTAL PLAQUE-INDUCED GINGIVAL

DISEASES

Gingivitis Associated with Dental Plaque Onlyand Gingival Diseases Modified by SystemicFactors Associated with the Endocrine SystemGingivitis characterized by the presence of gingivalinflammation without detectable loss of bone or clini-cal attachment is common in children.1-19,25 Although

the microbiology of this disease has not been com-pletely characterized, increased subgingival levels ofActinomycessp., Capnocytophagasp., Leptotrichiasp.,and Selenomonassp. have been found in experimen-tal gingivitis in children when compared to gingivitis in

adults. These species may therefore be important in itsetiology and pathogenesis.26,27

Normal and abnormal fluctuation in hormone lev-els, including changes in gonadotrophic hormone lev-els during the onset of puberty, can modify thegingival inflammatory response to dental plaque.28,29

Similarly, alterations in insulin levels in patients withdiabetes can affect gingival health.28,29 In both situ-ations, there is an increased inflammatory responseto plaque.28,29 However, the gingival condition usuallyresponds to thorough removal of bacterial depositsand improved daily oral hygiene.28,29

PERIODONTITIS

Aggressive Periodontitis, Chronic Periodontitis,and Periodontitis as a Manifestation of SystemicDiseasesChildren and adolescents can have any of the severalforms of periodontitis as described in the proceedingsof the 1999 International Workshop for a Classifica-tion of Periodontal Diseases and Conditions (aggres-sive periodontitis, chronic periodontitis, andperiodontitis as a manifestation of systemic diseases).However, chronic periodontitis is more common inadults, while aggressive periodontitis may be more

common in children and adolescents.24The primary features of aggressive periodontitisinclude a history of rapid attachment and bone losswith familial aggregation. Secondary features includephagocyte abnormalities and a hyperresponsivemacrophage phenotype.24 Aggressive periodontitiscan be localized or generalized. Localized aggressiveperiodontitis (LAgP) patients have interproximalattachment loss on at least two permanent first molarsand incisors, with attachment loss on no more thantwo teeth other than first molars and incisors. Gener-

Position Paper

Periodontal Diseases of Children and Adolescents*

This paper was prepared by the Research, Science and Therapy Committee of the American Academy ofPeriodontology and is intended for the information of the dental profession and the public. It represents a briefsummary of the current state of knowledge about periodontal diseases in children and adolescents. J Peri-odontol 2003;74:1696-1704.

* This paper was developed under the direction of the Research, Scienceand Therapy Committee and approved by the Board of Trustees of theAmerican Academy of Periodontology in August 2003.

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alized aggressive periodontitis (GAgP) patients exhibitgeneralized interproximal attachment loss includingat least three teeth that are not first molars andincisors. In young individuals, the onset of these dis-eases is often circumpubertal. Some investigatorshave found that the localized form appears to be self-limiting,30 while others suggest that it is not.20 Somepatients initially diagnosed as having LAgP were foundto have GAgP or to be periodontally healthy at a 6-year follow-up exam.31,32

LAgP occurs in children and adolescents withoutclinical evidence of systemic disease and is charac-terized by the severe loss of alveolar bone aroundpermanent teeth.31 Frequently, the disease is local-ized to the permanent first molars and incisors. How-ever, some retrospective data obtained from LAgP

patients suggest that bone loss around the primaryteeth can be an early finding in the disease.33 Link-age studies of the Brandywine population (a segre-gated group of people in Maryland that represents arelatively closed gene pool) have found a gene con-ferring increased risk for LAgP on chromosome 4.34

Subsequent linkage studies of African American andCaucasian families did not confirm linkage to thislocus, suggesting that there may be genetic and/oretiologic heterogeneity for aggressive periodontitis.35-37 Reported estimates of the prevalence of LAgP ingeographically diverse adolescent populations rangefrom 0.1% to 15%.23,33-35,37-42 Most reports suggesta low prevalence (0.2%), which is markedly greaterin African American populations (2.5%).

Many reports suggest that patients with LAgP gen-erally form very little supragingival dental plaque orcalculus.31,43 In contrast, other investigators find plaqueand calculus at levels similar to other periodontal dis-eases.44,45 Bacteria of probable etiologic importanceinclude highly virulent strains ofActinobacillus actino-mycetemcomitansin combination with Bacteroides-like species.46-49 In some populations, Eubacteriumsp. have been associated with the presence ofLAgP.50,51 To date, however, no single species is found

in all cases of LAgP.52A variety of functional defects have been reportedin neutrophils from patients with LAgP.53-55 Theseinclude anomalies of chemotaxis,56-58 phagocyto-sis,59,60 bactericidal activity,61 superoxide produc-tion,62-66 FcRIIIB (CD16) expression,67 leukotrieneB4 generation,68,69 and Ca2

+-channel and secondmessenger activation.70-75 The defect in chemotaxisis thought to be an intrinsic defect by some investi-gators56-58 and an induced defect by others.76 Theinfluence of these functional defects on the suscep-

tibility of individuals to LAgP is unknown, but it ispossible that they play a role in the clinical course ofdisease in some patients. Indeed, in some casesexhibiting phagocyte abnormalities, neutrophil defectsmay still be present after treatment.77 Molecularmarkers of LAgP can include an abnormally low num-ber of chemoattractant receptors78-81 and an abnor-mally low amount of another cell surface glycoproteindesignated GP-110.82,83 Adherence receptors on neu-trophils and monocytes, such as LFA-1 and Mac-1,are normal in LAgP patients.82,83

GAgP, often considered to be a disease of adoles-cents and young adults, can begin at any age andoften affects the entire dentition.84,85 Individuals withGAgP exhibit marked periodontal inflammation andhave heavy accumulations of plaque and calculus.84

In the United States, the reported prevalence of GAgPin adolescents (14 to 17 years of age) is 0.13%.23

Subgingival sites from affected teeth harbor high per-centages of non-motile, facultatively anaerobic,Gram-negative rods including Porphyromonas gingi-valis.86,87 In one report, the levels ofP. gingivalisandTreponema denticolawere significantly higher in GAgPand LAgP patients compared to matched controls,with GAgP patients having the highest levels.88 Neu-trophils from patients with GAgP frequently exhibitsuppressed chemotaxis as observed in LAgP77,87 witha concomitant reduction in GP-110. This suggests arelationship between the two variants of aggressiveperiodontitis.82,83

Alterations in immunologic factors such as immuno-globulins are known to be present in aggressive peri-odontitis. Immunoglobulins appear to be influencedby both genetic and environmental factors and haveimportant protective disease-limiting effects in aggres-sive periodontitis patients.89-93 Human IgG antibodymolecules (immunoglobulin G) are categorized intofour subclasses designated as IgG1-4. Most of the anti-body reactive with A. actinomycetemcomitansis spe-cific for high molecular weight lipopolysaccharide andis of the IgG2 subclass. This antibody response appears

to be protective, as early-onset periodontitis patientshaving high concentrations of antibody reactive withA. actinomycetemcomitans lipopolysaccharide havesignificantly less attachment loss (a measure of dis-ease severity) than patients who lack this antibody.89,90

Overall levels of IgG2 in serum are under geneticcontrol.91 These levels have also been shown to beaffected by periodontal diagnosis (LAgP patients havevery high levels), race (African Americans have higherlevels than Caucasians), and smoking (smokers havelower levels of IgG2, with notable exceptions in some

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patient groups).91,92,94,95 These factors also influencespecific antibody responses to A. actinomycetem-comitans.91-93,95 Thus, the protective antibody responseafforded by IgG2, as well as the clinical manifestationsof aggressive periodontitis, is modified by patientsgenetic background as well as environmental factorssuch as smoking and bacterial infection.89,91-93,95,96

Successful treatment of aggressive periodontitisdepends on early diagnosis, directing therapy againstthe infecting microorganisms and providing an envi-ronment for healing that is free of infection.97 Whilethere is some disagreement among individual studiesregarding treatment of LAgP, most authors recommenda combination of surgical or non-surgical root debride-ment in conjunction with antimicrobial (antibiotic) ther-apy.47,98 These findings are supported by other work

in which meticulous and repeated mechanical therapywith antibiotics proved to be sufficient to arrest mostcases of LAgP.99 However, surgical treatment may beeffective in eliminating A. actinomycetemcomitanswith-out the use of antibiotics.100 In a study of 25 deep peri-odontal lesions (probing depths 5 to 11 mm) in youngLAgP patients, scaling and root planing alone wereineffective for the elimination of A. actinomycetem-comitans, while surgical therapy was effective.100 It isnot known, however, if A. actinomycetemcomitans isthe only organism involved in disease pathogenesis.

The majority of reports suggest that the use ofantibiotics is usually beneficial in the treatment ofLAgP. Two reports described using antibiotics exclu-sively.97,101 In both reports, LAgP patients attainedsignificant clinical attachment gain when assessedafter 12 months with tetracycline therapy alone. Mostreports in the past 10 years, however, have recom-mended combination therapy using antibiotics andsurgical or non-surgical root debridement as the opti-mal treatment for LAgP.98,102-116 The most successfulantibiotics reported are the tetracyclines, sometimesprescribed sequentially with metronidazole.103,117,118

Metronidazole in combination with amoxicillin hasalso been utilized, especially where tetracyline-resis-

tant A. actinomycetemcomitansare present.111 A sin-gle randomized control study in which oral penicillinwas used reported that therapy was successful withor without the antibiotic.119

While the use of antibiotics in conjunction with sur-gical or non-surgical root debridement appears to bequite effective for the treatment of LAgP, GAgP doesnot always respond well to conventional mechanicaltherapy or to antibiotics commonly used to treat peri-odontitis.30,118,120 Alternative antibiotics may berequired, based upon the character of the pathogenic

flora. In GAgP patients who have failed to respond tostandard periodontal therapy, laboratory tests of plaquesamples may identify periodontal pathogens that areresistant to antibiotics typically used to treat periodon-titis.103 It has been suggested that follow-up testsafter additional antibiotic or other therapy is providedmay be helpful in confirming elimination of targetedpathogenic organisms.103

Chronic periodontitis is most prevalent in adults,but can occur in children and adolescents. It can belocalized (less than 30% of the dentition affected) orgeneralized (greater than 30% of the dentitionaffected) and is characterized by a slow to moderaterate of progression that may include periods of rapiddestruction. Furthermore, the severity of disease canbe mild (1 to 2 mm clinical attachment loss), mod-

erate (3 to 4 mm clinical attachment loss), or severe(5 mm clinical attachment loss). Children and youngadults with this form of disease were previously stud-ied along with patients having LAgP and GAgP. There-fore, published data are lacking for this group.

In patients with one of several systemic diseases thatpredispose to highly destructive disease of the primaryteeth, the diagnosis is periodontitis as a manifestationof systemic disease. As with adults, periodontitis asso-ciated with systemic diseases occurs in children andadolescents. Such diseases include Papillon-Lefvresyndrome,121-125 cyclic neutropenia,126-130 agranulo-cytosis,131,132 Downs syndrome,133-135 hypophos-phatasia,136 and leukocyte adherence deficiency.137,138It is probable that defects in neutrophil and immunecell function associated with these diseases play animportant role in increased susceptibility to periodon-titis and other infections. In Downs syndrome, for exam-ple, the amount of periodontal destruction has beenshown to be positively correlated with the severity of theneutrophil chemotaxis defect.135 In some cases, specificgenes have been associated with these diseases. Exam-ples include the cathepsin C gene and Papillon-Lefvresyndrome139-141 and the tissue non-specific alkalinephosphatase gene and hypophosphatasia.136

The consensus report of the 1999 Workshop specif-ically excluded diabetes-associated periodontitis as aspecific form of periodontitis associated with systemicdisease. Participants concluded that diabetes is a sig-nificant modifier of all forms of periodontitis. In a sur-vey of 263 type 1 diabetics, 11 to 18 years of age,10% were found to have overt periodontitis oftenlocalized to first molars and incisors, although peri-odontitis was also found in a generalized pattern.142

Affected subgingival sites harbored A. actinomycetem-comitansand Capnocytophagasp.143

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hygiene among children. United States. Vital HealthStat 1 1972;11(117):1-28.

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