periodontal disease in the child and adolescent

8/9/2019 Periodontal Disease in the Child and Adolescent

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J Cl in Periodontol 2002; 29: 400410 C opy r i ght C B l ac k wel l M unk s gaar d 2002

Printed in Denmark . All rights reserved

ISSN 0303-6979

Tae-Ju Oh, Robert Eber and

Hom-Lay WangPeriodontal diseases inthechildDepartment of Periodontics/Prevention/Geriatrics, School of Dentistry, University ofMichigan, Ann Arbor, MI, USAandadolescent

Oh T -J, E ber R, W ang H -L : Periodontal diseases in the chil d and adolescent.J Cli n P eri odontol 2002; 29: 400410.C Blackwell M unksgaard, 2002.

Abstract

Background: Periodontal diseases are among the most frequent diseases affectingchildren and adolescents. Theseincludegingivitis, localized or generalized aggres-siveperiodontitis (a.k.a., early onset periodontitis which includes generalized orlocalized prepubertal periodontitis and juvenile periodontitis) and periodontal

diseases associated with systemic disorders. The best approach to managing peri-odontal diseases is prevention, followed by early detection and treatment.Methods:This paper reviews the current literatureconcerning the most commonperiodontal diseases affectingchildren: chronic gingivitis (or dental plaque-inducedgingival diseases) and early onset periodontitis (or aggressive periodontitis), in-cluding prepubertal and juvenile periodontitis. I n addition, systemic diseases Key words: periodontal disease; children;

pedodontics; early onset periodontitis;that affect the periodontium and oral lesions commonly found in young childrenaggressive periodontitis; localized juvenileare addressed. The prevalence, diagnostic characteristics, microbiology, host-periodontitis

related factors, and therapeutic management of each of these disease entities arethoroughly discussed. Accepted for publication 15 May 2001

Dental cliniciansmust beadept at diag-nosis and management of periodontaldisease in children and adolescents.Periodontal diseases are not limited toadults. On the contrary, periodontaldiseases are prevalent among childrenand adolescents. For example, gingivitisaffects morethan 70% of children olderthan seven years of age (Page & Schro-eder 1982, Stamm 1986). Bimstein(1991) stressed the importance of pre-vention, early diagnosis and early treat-ment of periodontal diseases in children

and adolescents because (1) the preva-lence of and severity of periodontal dis-eases are high; (2) incipient periodontaldiseases in children may develop intoadvanced periodontal diseases inadults; (3) there is association betweenperiodontal and systemic diseases; (4)patients, families, or populationsat riskmay be identified and included inspecial prevention or treatment pro-grams; and (5) prevention and treat-ment of most periodontal diseases arerelatively simple and very effective, pro-viding lifetimebenefits.

The nomenclature and classificationsystems we use to describe periodontaldisease have changed periodically overthepast few decades. Thisleadsto someconfusion when onereviews past litera-ture about disease prevalence, treat-ment, etc. The Consensus Reportof the1989 World Workshop in Clinical Peri-odonticsused the following criteria todistinguish various forms of peri-odontitis: (1) age of onset; (2) rate ofdisease progression; (3) distribution ofaffected sites; (4) presenceor absenceof

systemic medical conditions; (5) pres-ence or absence of specific microbial orhost factors; and (6) responseof thedis-ease to therapy (American A cademy ofPeriodontology: AAP 1989). Theclassi-fication (AAP 1989) was simplified bythe Consensus Report of the FirstEuropean Workshop on Periodonto-logy (Attstrm & van der Velden 1994),and more recently, a new classificationof periodontal diseases and conditionswas presented at the1999 InternationalWorkshop on Periodontics (Armitage1999). The 1999 International Work-

shop classification system includes agreater variety of diseasecategories thatbase the diagnosis on clinical historyand findings, relying less on age of on-set as a major criterion (Table1).

This paper primarily follows theclassification of periodontal diseasefromthe1989 World Workshop in Clin-ical Periodontics (AAP 1989) when de-scribing conditions because most clini-cians arefamiliar with it. For each con-dition, wealso includetheInternationalWorkshop in Periodontics classification

(Armitage 1999) parenthetically to in-troduce readers to the new system andto highlight the changes between thetwo.

Theaimof this paper is to review thecurrent literature concerning the mostcommon periodontal diseases affectingchildren: chronic gingivitis and earlyonset periodontitis, including prepuber-tal and juvenile periodontitis. In ad-dition, systemic diseases that affect theperiodontium and oral lesions com-monly found in young children will beaddressed.


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Periodontal diseases in children 401

Table 1. Classifications of periodontitis

The1989WorldWorkshopinClinical PeriodonticsI. Adult periodontitisII . Early-onset periodontitis

A. Prepubertal periodontitis (generalized, localized)B. Juvenile periodontitis (generalized, localized)C. Rapidly progressiveperiodontitis

III . Periodontitis associated with systemic disease

IV. Necrotizing ulcerative periodontitisV. Refractory periodontitis

The1994FirstEuropeanWorkshoponPeriodontologyI. Early onset periodontitisII . Adult periodontitisII I . Necrotizing periodontitis

The1999InternationalWorkshoponPeriodontologyI. Gingival diseasesII . Chronic periodontitisII I . Aggressive periodontitisIV. Periodontitis as a manifestation of systemic diseasesV. Necrotizing periodontal diseasesVI . Abscesses of the periodontiumVI I. Periodontitis associated with endodontic lesionsVI II. Developmental or acquired deformities and conditions

(I). Chronic Gingivitis (Dental Plaque-

induced Gingival Diseases)

Chronic gingivitis is the most commonperiodontal infection among children,and adolescents. These may includeplaque-induced chronic gingivitis (themost prevalent form), steroid hormonerelated gingivitis, drug-influenced gin-gival overgrowth, and others. It is char-

acterized by inflammation of the mar-ginal gingiva without detectable loss ofbone or connective tissue attachment.

The initial clinical findings in gingivitisinclude redness and swelling of mar-ginal gingiva, and bleeding upon prob-ing. As the condition persists, tissuesthat were initially edematous may be-come more fibrotic. Gingival margins,normally knife-edged in contour, maybecome rolled, and interdental papillaemay become bulbous and enlarged.Probing depths may increase if signifi-cant hypertrophy or hyperplasia of the

gingiva occurs.Histologically, ulceration of the sul-cular epithelium and inflammatory cellinfiltration of theunderlying connectivetissue characterize gingivitis. At themicroscopic level, T-lymphocytes pre-dominate in children (Seymour et al.1981) whereas B-cells predominate inadults (Page& Schroeder 1976).

M atsson & Goldberg (1985) sug-gested that there is no clear-cut age atwhich the gingival reaction to bacterialinsult in children becomes similar tothat in adults. However, thereis gradual

increase in gingival activity from earlychildhood to adult age. Previously,M atsson (1978) performed a 21-day ex-perimental gingivitis study comparing6children, aged 4 to 5 years, with 6 den-tal students, aged 23 to 29 years. Theyfound that the children developed gin-givitisless readily than theadults. After21 days without plaque removal, thechildren had less gingival exudate and

a lower percentage of bleeding sitesthan the adults. Also, the children hada smaller increase in gingival crevicularleukocytes than the adults in responseto plaque accumulation. The studyhypothesized that children may have adifferent vascular response than adults.

Gingivitis does not always progressto periodontitis, but periodontitis ispreceded by gingivitis. According toM arshall-Day et al. (1955), gingivitiswithout evidence of bone loss was con-fined to a younger age group, and boneloss without gingival alterations was

rarely found.Plaque-induced chronic gingivitis iscommonly found in young children andcan bemanaged by mechanical removalof plaque and high levels of oral hy-giene. Theetiologic natureof plaque ingingivitis was demonstrated by experi-mental gingivitis studies in humans(Le et al. 1965, Theilade et al. 1986).

Therefore, dentists and dental hygien-ists must educate parents and theirchildren about the importance of oralhygiene in the prevention of caries andperiodontal diseases. Electric tooth-

brushes and antibacterial mouthrinsesmay be useful adjuncts to standardtoothbrushing and flossing for childrenwho are physically challenged, such aschildren with Downssyndrome, and forchildren undergoing orthodontic care(Trombelli et al. 1995, Grossman &

Proskin 1997, Boyd 1989).Steroid hormone-related gingiviti s isassociated with elevated sex hormonelevels that amplify clinical inflamma-tory changes of gingivitis (Suzuki1988). Increased levels of estrogen andprogesterone during pregnancy (L e1965), during puberty, or in patientsmedicated with oral contraceptives(K alkwarf 1978) have been reported toresult in increased gingival vascularityand inflammation. Removal of localfactors is thekey to themanagement ofsteroid hormone-related gingivitis;

however, it is often necessary to surgic-ally excise unresolved gingival over-growth.

D rug-influenced gingi val enlar gementhas been observed in patients takingcyclosporin, phenytoin and calciumchannel blockers, with higher preva-lence in children (M ariotti 1999, Seym-our et al. 2000). Gingival enlargementwas reported in 30% of patients takingcyclosporin (Seymour & Heasman1992), 50% of patients taking phenytoin(Hassell 1981), and 15% of patientstak-ing calcium channel blockers such as

nifedipine(L ederman et al. 1984), vera-pamil (Pernu et al. 1989), and amlodipi-ne (Seymour et al. 1994). Gingival en-largement starts in the interdental pa-pilla region and spreads to involve themarginal gingiva. In severecasestheen-larged gingiva may cover theincisal andocclusal surfaces of the teeth (Chapple1996). Histologically, the overgrowth isfibroepithelial in nature, with epithelialacanthosis, increased numbers offibroblasts and increased collagen pro-duction. The severity of gingival en-largement is closely related to the level

of plaque control, and therefore reduc-tions in dental plaque can limit the se-verity of thelesion (M ariotti 1999).

Treatment of drug-influenced gingi-val enlargement should start with oralhygiene instructions, and scaling andpolishing of the teeth to remove bac-terial deposits. This may require severalvisits. 2 daily chlorhexidine rinses(Lang et al. 1982) should be prescribedwhen normal brushing and flossing donot achieve the desired level of plaquecontrol. Gingivectomy or gingivoplastymay be needed to correct gingival con-


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402 Oh et al.

tours for hygienic and esthetic reasons.The patient and parent should be toldthat gingival enlargement may recurafter surgery, and that immaculatehome plaque control and regular peri-odontal maintenance arethe key to de-creasing thelikelihood or severity of re-

currence. In addition, the patientsphysician should be consulted to deter-mineif the patient could beswitched toa medication that does not cause gingi-val enlargement. The dentist shouldnever recommend that a patient discon-tinue or change medications withoutmedical consultation.

(II). Early Onset Periodontitis (New

Classification: Aggressive

Periodontitis)

Characteristics of early onset peri-

odontitis include onset before age 35years, rapid disease progression, some-what different distribution of lesionsthan in adult periodontitis, and distinctetiologic characteristics.

1. Prepubertal periodontitis (PP) (new

classification: aggressive periodontitis)

The prevalence of PP ranges from0.84% to 26.9%, based on a limitednumber of case reports (J amison 1963,Sweeney et al. 1987, Bimstein et al.1988). Variation in the reported preva-

lences of PP may depend on genetic fac-tors, methodological factors, and theselection of non-random sample popu-lations (Watanabe 1990). Prepubertalperiodontitis may be generalized or lo-

Table 2. Diagnostic characteristicsof prepubertal periodontitis

Localizedprepubertal periodontitis (LPP)O Onset: around 4 years of age or olderO Affected teeth: either few or many teethO Gingival manifestation: minor inflammation, if anyO M icrobial plaque: minimalO Alveolar bone destruction: faster than adult periodontitis but much slower than

generalized form of PPO Functional defects: either neutrophils or monocytes but not bothO Otitis media and upper respiratory infections in some casesO Amenable to mechanical and antibiotic therapy

Generalizedprepubertal periodontitis (GPP)O Onset: at thetime of tooth eruptionO Affected teeth: all primary teeth; thepermanent dentition may or may not beaffectedO Gingival manifestation: fiery red gingiva with acuteinflammation around all teeth;

gingival proliferation, cleft formation, and recessionO Alveolar bone destruction: rapidO Functional defects: both neutrophils and monocytesO Absence of PM Ns in the gingival tissueand marked increase in peripheral blood white

cell countO Otitis media and upper respiratory infections in most casesO Refractory to mechanical and antibiotic therapy

calized and can affect both primary andmixed dentition. Onset occurs betweenthe eruption of the primary dentitionand puberty. PP is characterized by se-vere gingival inflammation, rapid boneloss, tooth mobility, and tooth loss. Su-zuki (1988) reported that PP patients

are usually between ages 5 and 8, theyhave low caries rates, and there is nosex predilection. Page et al. (1983) firstdescribed prepubertal periodontitisas a disease entity and further subdi-vided it into a localized form of PP(LPP) and a generalized form of PP(GPP). This was based on the clinicaldescription of only three and two cases,respectively. Diagnostic characteristicsfor prepubertal periodontitis are listedin Table 2.

Pathogenic bacteria that have beenassociated with PP include Actino-

bacill us actinomycetemcomitans (A.a.),Pr evotella intermedia ( P.i .), Capnocyto-phaga species (Delaney & K ornman1987, Sweeney et al. 1987), Porphyro-monas gi ngivali s ( P.g.) (Mishkin et al.1986), and Eik enella corrodens ( E.corrodens)(Delaney & K ornman 1987).Delaney & K ornman (1987) found anincreased proportion of black-pig-mented anaerobic rods, E. corrodens,Capnocytophaga species, A.a., and F u-sobacterium nucleatum ( F. nucleatum)in the cultivable flora in L PP patientscompared to controls. Studies have

tried to determine whether PP ulti-mately progresses to juvenile peri-odontitis (J P). According to Watanabe(1990), if pathogenic bacteria aroundthe deciduous dentition in PP patients

remain to infect thearea or neighboringarea during eruption of the permanentteeth, subsequent infection of newlyerupted permanent teeth may occur.

The coexistence of A.a. in lesions ofboth PP and localized juvenile peri-odontitis (LJ P) (Zambon et al. 1983)

may explain the possibility. However,the possible mechanism of disease pro-gression needs to be re-evaluated sincenot all PP develops into J P.

Although the primary etiology re-mains bacterial plaque, other factorsmay predispose otherwise healthy pa-tients to PP. These may include ce-mentum defects (Page & Baab 1985),functional defects in leukocyte chemo-taxis (Page et al. 1983), and/or presenceof bacteriophage (Watanabe 1990). Ithas been generally recognized that GPPand leukocyte adhesion deficiency

(LA D) are related. Waldrop et al.(1987) demonstrated that the molecularbasis of GPP was leukocyte adhesiondeficiency by using monoclonal anti-bodies against M ac-1, L FA-1, andp150,95surfaceadhesion molecules. Onthe other hand, immunological dataabout L PP have shown that a neutro-phil or monocyte chemotaxis defect,but not both, exists in LPP patients.

Systemic diseases associated with pre-pubertal periodontit is ( new classifi-cation: periodontit is as a manifestationof systemic diseases) may include insu-

lin dependent diabetes mellitus(IDDM ), Papillon-Lefevre syndrome,hypophosphatasia, neutropenia, Ched-iak-Higashi syndrome, leukemias,histiocytosis X, acrodynia, acquired im-munodeficiency syndrome (AIDS),Down syndrome, and leukocyte ad-hesion deficiency.

I nsulin dependent diabetes mellit us( I DD M , Juvenile D M ) is a relative orabsolute decrease in insulin secretion oravailability, caused by a genetic defectin pancreatic beta cell productivity, de-fective insulin release mechanisms

(J ohnes & M ason 1980) or by destruc-tion of beta cells (Jackson & Guthrie1986). Bernick et al. (1975), Gislen etal. (1980), and Cianciola et al. (1982)studied theassociation between juvenilediabetes and periodontal diseases inyoung children. Bernick et al. (1975)examined 50 diabetic children and 36healthy control children who werematched for age and oral hygiene sta-tus. They found that gingival inflam-mation was more prevalent in the dia-betic group. Furthermore, Gislen et al.(1980) showed that diabetic children


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with poor metabolic control appearedto have greater gingival index scoresthan children without diabetes. Cianci-ola et al. (1982) investigated prevalenceof periodontal disease in IDD M in 263IDD M patients and 208 control sub-

jects. For children between 11 and 18

years old, 9.8 % of the IDD M patientsshowed signs of periodontitis versusonly 1.7% of the controls. T hey foundno periodontitis in children 10 yearsoldor younger in either group. T he articleargues that probing alone is not suf-ficient to assess periodontitis, particu-larly when applied to the mixed den-tition. Adjunctive use of radiographswas recommended for theassessment ofperiodontitis in children. IDD M pa-tients have also been shown to have areduced PM N response to chemotacticstimuli (M iller 1972).

Papillon-L efe`vre syndrome ( PL S) isa genetic condition inherited as anautosomal recessive trait, characterizedby hyperkeratosis of the palms of thehands and soles of the feet and earlyonset periodontitis (Johnes & M ason1980). Severe periodontitis can affectboth the primary and permanent den-titions(Smith & Rosenzweig 1967, Gor-lin et al. 1964). Theprevalenceof PM Nchemotactic defects in thePL S patientsremains controversial.

H ypophosphatasia is a genetic dis-order. Diagnostic findings include low

levels of serum alkaline phosphataseand excretion of phosphoethanolamine,the substrate for alkaline phosphatase,in theurine. The disorder can beclassi-fied into 3 types: (1) infantile, an auto-somal recessive condition occurring be-fore 6 months of age (the most severeform); (2) childhood, an autosomal re-cessive or autosomal dominant con-dition occurring after 6 months of age;and (3) adult hypophosphatasia, anautosomal dominant condition that isthe least severe form (Watanabe 1990).

The most consistent clinical sign is

prematureloss of deciduous teeth (Fal-lon et al. 1984). The teeth may havelarge pulp chambers, and skeletal de-formities may occur. Baer & Benjamin(1974) claimed that only deciduousteeth are generally affected. Baab et al.(1986) reported normal polymorpho-nuclear leukocyte (PM N) chemotaxisand abnormal monocyte chemotaxis in3 children with hypophosphatasia; how-ever, age range was not designated inthe study.

Neutropenia is a disorder in whichthe number of PM Ns in the peripheral

blood is below 1000/mm3 in infants, be-low 1000/mm3or 1500/mm3 in children,and below 1800/mm3 in adults. Neutro-penias associated with oral manifes-tations in children include agranulo-cytosis (malignant neutropenia, rare inchildren), cyclic neutropenia, chronic

benign neutropenia of childhood,chronic idiopathic neutropenia, andfamilial benignneutropenia. Prichard etal. (1984) and Cohen & M orris (1961)reported that cyclic neutropenia was as-sociated with severe gingivitis with ul-ceration and frequent history of recur-rent infections such as otitis media andupper respiratory infection.

Chediak-H igashi syndrome is a rareautosomal recessive disease associatedwith impaired function of cytoplasmicmicrotubules or microtubule assemblyin PM Ns. Diagnostic features include

characteristic, abnormally large gran-ules in granulocytes. According toClawson et al. (1978), PM N chemo-tactic defects in Chediak-Higashi syn-drome may be dueto mechanical inter-ference in deformability by the giantcytoplasmic granules. M oreover, im-paired microtubule assembling function(Oliver 1976) and hyperadhesiveness(K eller et al. 1984) were suggested asthe mechanism for PM N chemotacticdefects.

L eukemiasare characterized by pro-gressive uncontrolled proliferation of

white blood cells and classified intoacute and chronic lymphocytic leukem-ia, acute and chronic granulocytic leu-kemia, acute and chronic monocyticleukemia, and other rare forms such asplasma cell leukemia. Oral manifes-tationsof leukemias in children aregin-gival hemorrhage, petechiae, lymph-adenopathy, gingival hyperplasia orhypertrophy, and gingival pallor.Bender (1944) and Deasy et al. (1976)reported association between peri-odontal disease and leukemia inchildren.

H istiocytosis X represents a disturb-ance of the reticulo-endothelial system.It resultsfromtheproliferation and dis-semination of pathological L angerhanscells and includes three disorders: Let-terer-Siwedisease(themost severeformand usually occurs in infants or beforeage 3); Hand-Schuller-Christian disease(usually occurs beforeage5, but can oc-cur in adolescents and even in youngadults); and eosinophilic granuloma(occurs primarily in older children andyoung adults) (Hartman & Colonel1980). Increased susceptibility to bac-

terial infections in histiocytosis X pa-tients may result from PM N defects(Tomooka et al. 1986) or decreasedmonocyte function (K ragballe et al.1981).

Acrodyniais a raredisease character-ized by a wide variety of clinical signs

including gingival and mucosal hyper-plasia, alveolar bonelosswith early lossof primary teeth, lossof hair, abnormalcramps, profuse sweating and sali-vation, and gastrointestinal upsets.Etiology of acrodynia is known to be amercurial toxicity reaction, either actualmercury poisoning or, more likely, anidiosyncracy to mercury (Warkany &Hubbard 1948).

A cquired immunodeficiency syndrome( AI DS)developsasa result of infectionwith the human immunodeficiency vi-rus(HIV). Children withAIDS may de-

velop an atypical form of acutenecrot-izing ulcerative gingivitis (AN UG)(L eggott 1987); however, no reports ofprepubertal pediatric AIDS patientspresenting with alveolar boneloss exist.

Downs syndrome ( Tr isomy 21 syn-drome; M ongolism) is a common andeasily recognizable chromosomal aber-ration. Thedentition exhibits a numberof characteristic anomalies includingmalformation of the teeth, enamel hy-poplasia, and microdontia. Other com-mon oral manifestationsincludemacro-glossia, fissured or pebbly tongue, and

a high arched palate. Due to a defectiveimmune system, rampant and pre-cocious periodontal diseaseis prevalent.Barr-A gholme et al. (1998) compared20 Downs syndromepatients, aged 9 to21 years, with 19 healthy controls andreported that gingival inflammation,probing depth, calculus, and marginalbone loss were significantly greater inthe Downs syndrome group. No sig-nificant differences were found betweenthe two groups, regarding levels ofserum IgA, IgG2, IgG3, IgG4, IgM, oralbumin. However, the proportion of

IgG1 in total IgG was significantlyhigher in the Downs syndrome groupcompared to the control group.

L eukocyte adhesion deficiency( LA D ) is a genetic disease inherited asan autosomal recessive condition inwhich the expression of M ac-1, L FA -1,and p150,95 glycoprotein adhesionmolecules on leukocytes is severely re-duced. Springer et al. (1984) suggestedthat LA D occurs as a result of a defectin the gene that codes for the commonbeta subunit of cell surface integrinswhich are required for leukocyte diap-


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404 Oh et al.

Table 3. Diagnostic characteristicsof juvenile periodontitis

Localizedjuvenileperiodontitis(LJP)O Onset: around pubertyO Affected teeth: permanent incisors and/or first molarsO Associated microorganism:Act inobacill us acti nomycetemcomit ansO Greater prevalence in blacksO Neutrophil dysfunction and high IgG2 responseO Familial distribution

Generalizedjuvenileperiodontitis(GJ P)O Onset: during lateteen yearsO Affected teeth: generalized involvement of permanent teethO Associated microorganism: not clear (P. gingivalismay be involved)O Greater prevalence in blacksO Neutrophil dysfunctionO Familial distribution

edesis. Because emigration of PM Nsfrom blood vessels is dependent uponadhesion of PM Ns to endothelial cellsurfaces, patients with LAD have a

poor response to bacterial infections.Therefore, these children are plaguedwith recurrent bacterial infections andimpaired wound healing. Patients withthis rare disease present with extremelyacuteinflammation, proliferation of thegingival tissues, and rapid bone loss.An association between generalized pre-pubertal periodontitis and L AD wasdemonstrated by Waldrop et al. (1987)and Page et al. (1987).

Treatment for PP has ranged fromscaling and root planing or curettage,with or without systemic antibiotics, to

theextraction of involved teeth (Watan-abe1990). Thegeneralized form, unfor-tunately, does not respond as favorablyto treatment as thelocalized form. T hemajority of cases have been treated byextraction of involved deciduous teethand permanent teeth. Since these pa-tients may have associated L AD andmay be undergoing antibiotic therapyfor recurrent serious infections, it isnecessary to have a consultation withthetreating physician.

2. Juvenile periodontitis (JP) (new

classification: aggressive periodontitis)

J uvenile periodontitis, formerly calledperiodontosis, occurs in children andteenagers who are otherwise healthyand is characterized by a rapid alveolarbone loss in one or more teeth of thepermanent dentition (Baer 1971). Ter-minology for this disease entity has re-peatedly changed. Gottlieb et al. (1923)first described this condition diffuseatrophy of thealveolar bone. His find-ings in this case included widened peri-odontal ligament (PDL), cementopa-

thia and alveolar bone resorption, butno pathology in gingival tissues. L ater,the degenerative process was termedperiodontosis (Orban & Weinmann

1942), who described threestages of thedisease: degeneration of PDL fibers;proliferation of the junctional epithel-ium; and the development of deepinfrabony pockets. The term peri-odontosis was favored by Baer (1971).In his article, the disease entity was di-vided into two categories, a localizedform affecting the first molars and in-cisors, and more generalized form af-fecting most of dentition. The termjuvenile periodontitis, introduced byButler (1969), accurately describes thedisease as an inflammatory process.

Waerhaug (1977) described that thepri-mary etiology of thediseaseis subgingi-val bacterial plaque. Theplaquefront isconsistently located within 0.2 mm to1.5 mm from the border of loss ofattachment. The plaque grows with afaster speed of 3 to 5 microns a day inthis disease compared to 0.2 to 1.0mma day in ordinary cases. Diagnosticcharacteristics of juvenile periodontitisare illustrated in Table3.

Estimates of the prevalence of J Pvary from 0.1% to 15% (Sjdin et al.1993, Hart et al. 1993, Saxen 1980,

L e & Brown 1991, Neely 1992), withdifferences attributed to varying cri-teria, geographics, and a diverse database. Reports show greater prevalencein African-Americans than in Caucasi-ans (Burmeister et al. 1984, Le &Brown 1991, M elvin et al. 1991). Al-bandar et al. (1997a) estimated preva-lence of EOP (JP) in a group of school-children, aged 13 to 17 years, based onthedata of a national survey conductedduring the19861987 school year. Theyshowed that approximately 10.0% ofAfrican-American, 5.5% of Hispanic,

and 1.3% of whiteadolescentshad EOP.Hrmand & F randsen (1979) explainedthat the higher incidence of L J P in fe-males could result from an earlier oc-currenceof thediseasein females. Stab-holz et al. (1998) reported a high preva-lence of LJ P in an Israel population

consisting of 86 individuals from 30families, aged 12to 20 years. Out of 86subjects, 33 individuals from15 familiesshowed L J P (38.4%), but none of thesubjects showed signs of generalized

juvenile periodontitis. Except for twopairs of families with genetic ties, nofamilial connectionscould betraced be-tween the different nuclear familiesaffected by L J P, and there were no dif-ferences in oral hygiene status betweenL J P and non-L J P groups. The studysuggests that environmental factorsmay influence theoccurrence of L J P.

The microflora associated with J P ismainly composed of Gram-negative,capnophilic, and anaerobic rods (Slots1979, Newman & Socransky 1977).A ctinobacill us actinomycetemcomitans(A.a.), a Gram-negative, non-motile,coccobacillus hasbeen well documentedin relation to L J P (Newman & Socran-sky 1977, Slots et al. 1980, 1982, K orn-man & Robertson 1985). Asikainen etal. (1991) examined A .a. isolates fromsubgingival sites in 136 subjects in Fin-land and found that among five sero-types ofA.a., serotype b was predomi-

nant in L J P and adult periodontitis,whereas serotype c predominated inhealthy individuals. Wilson & Hamilton(1992) also demonstrated that blacksubjects with L J P responded to A.a.serotype b serospecific antigens by theproduction of IgG antibodies of theIgG2 subclass. Lu et al. (1993, 1994)confirmed this by demonstrating thatIgG2 was markedly elevated over allother Ig classes reactive withA.a. sero-type b. Albandar et al. (1997b) foundthat EOP patients had higher preva-lence and levels ofP.g.,P.i.,F. nucleat-

um., C. rectus, and T. denticola com-pared to healthy controls. P.g., T .denticola, andP.i., in descending orderof importance, weresignificantly associ-ated with thegeneralized and/or rapidlyprogressing disease.

Reports indicate that J P patientshave defects in neutrophil chemotaxisor phagocytosis (Cianciola et al. 1977,Clark et al. 1977, Van Dykeet al. 1987,Suzuki et al. 1984, K imura et al.1992,etc.). Neutrophils in L J P patients havefewer receptors on their plasma mem-brane for certain chemotaxis-inducing


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factors, such as FM L P, C5a, andGP110 (Van Dyke et al. 1981, 1983,1987). Agarwal et al. (1994) further sug-gested that cytokines, such astumor ne-crosis factor (TN F) and interleukin-1(IL-1), present in the serum of L J P pa-tients are responsible for priming and

inducing altered response in neutro-phils. In the study, it was found thattreatment of neutrophils in healthy sub-

jects with L J P-sera resulted in a de-creased neutrophil chemotactic re-sponse and down regulation of FM L Preceptors on the cell surface. On theother hand, pretreatment of L J P-serawith anti-TNF and anti-I L -1 antibodieseffectively neutralized the ability ofL J P-sera to modulate chemotaxis andFM L P receptor levels in healthy sub-

jects. Sigusch et al. (1998) found thatEOP patients showed reduced expres-

sion of monocyte HL A-DR , IFN -g,and IL -2 mRNA , and reduced prolifer-ation of peripheral blood monocytes,which are known to be positively ex-pressed by activated TH1 cells. This in-dicates an impaired TH1 cell responsein EOP patients. Ozmeric et al. (1998)further suggested that the IL -8, achemoattractant, produced by L J P pa-tientsmay beless activethan in healthyindividuals.

Theetiology of J P can be broadly di-vided into two categories, bacterialplaque and impaired host defense

mechanism; therefore, the treatmentshould aim to control pathogenic mi-croflora and compensate for impairedimmune function. Systemic approachessuch as antibiotic therapy are often in-dicated in the management of J P. Infact, several studies (Slots & Rosling1983, Christersson et al. 1985, K orn-man & Robertson 1985) showed thatscaling and root planing alonefailed tosuppressor eliminate A.a. fromthe dis-eased site and failed to improve clinicalconditions. Treatment modalities in themanagement of J P include mechanical

therapy, such as scaling and root plan-ing and periodontal surgery, local deliv-ery of antimicrobials, and systemicantibioticssuch as tetracycline, doxycy-cline, metronidazone, combination ofmetronidazole and amoxicillin, or com-bination of metronidazole and Aug-mentin (amoxicillin clavulanic acid).

Gunsolley et al. (1994) comparednonsurgical and surgical periodontaltreatment in 23 young patients with se-vere generalized periodontitis. Theyfound that P.g. wasvirtually eliminatedby scaling and root planing while levels

ofA.a.werenot significantly reduced byscaling and root planing alone. How-ever, after flap surgery, thelevels ofA.a.were significantly reduced, suggestingthat surgery and/or antibiotics arenecessary to reduce levels of A.a. inyoung patients with severe generalized

periodontitis. This result was in agree-ment with other studies (Slots & Ro-sling 1983, L indhe & L iljenberg 1984,K ornman & R obertson 1985).

Young individuals generally have ex-cellent healing potential. Therefore, in

J P patientsthecombination of systemicantibiotics and regenerative surgery isoften successful in treating intrabonydefectsand early furcation involvement.M attout and Roche(1984) found com-plete fill of furcations and significantsupracrestal repair in an 18-year-old J Ppatient after treatment with iliac crest

autografts. M abry et al. (1985) treatedintrabony defects in 16 L J P patientswith a combination of freeze-driedbone allograft (FD BA) and tetracy-cline. The group that received systemictetracyclinetherapy and local treatmentwith a mixture of tetracycline powderand F DBA had significantly better res-

Table 4. T herapeutic management of common pediatric oral lesions

Primaryherpetic gingivostomatitisO Topical anesthetics/coating agents:

1 to 1 mixture of diphenhydramine (Benadryl) elixir & M aalox [OTC]

diphenhydramine (Benadryl)/lidocaine/M aalox mouth rinse Acyclovir elixir

O Systemic acyclovir antiviral therapy

RecurrentherpessimplexO Avoidance of perpetuating factorsO Acyclovir (Zovirax) 5% ointment or elixirO Systemic acyclovir as active treatment or prophylaxis for immunosuppressed patients

RecurrentaphthousstomatitisO Topical anesthetics/coating agents: Zilactin-B [OTC], Orabase-B [OTC], or Oraloe[OTC]O Antimicrobial mouthrinses: 0.12% chlorhexidine gluconateO Topical steroids: triamcinolone (Kenalog) in orabase 0.1%, betamethasone valerate 0.1%

ointment, dexamethasone (Decadron) elixir 0.5 mg/5ml, or fluocinonide (L idex) gel 0.05%

CandidiasisO Topical antifungal agents:

Nysatin (M ycostatin) oral suspension 100,000units/ml or popsicles Clotrimazole (Mycelex) troches or swabs

O Antimicrobial mouthrinses: 0.12% chlorhexidine gluconate

Angular cheilitisO Topical antifungal agents: nystatin or clotrimazoleointmentO Topical antifungal/steroid agent: nystatin/triamcinoloneacetonide(Mucolog II ) ointmentO Topical antifungal/antibacterial/steroid agent: hydrocortisone/iodoquinol (Vytone) cream

1%

Geographic tongueO Topical anesthetic/analgesic mouth rinse: U lcer-Ease [OTC]O Topical antifungal/steroid agent: triamcinoloneacetonide 0.1% in nystatin suspensionO Alkaline saline mouth rinseO Topical anesthetics/coating agents: 1 to 1 mixture of diphenhydramine (Benadryl) elixir &

M aalox [OTC]

olution of intrabony defects than thegroups that received FDBA alone ordebridement alone with/without sys-temic tetracycline. Contrary to thesefindings, DiBattista et al. (1995) foundno statistically significant differencesbetween flap debridement alone and

various regenerative procedures in 7LJ P patients. A ll patients in this studyreceived systemic doxycycline. The re-generative procedures utilized wereePTFE membranes, ePTFE plus rootconditioning with doxycycline solution(pH: 2.5), and ePTF E root con-ditioningcomposite graft.

Based upon thecontradictory results,it is apparent that the results achievedwith regenerative procedures will varydepending on case selection, the pro-cedureutilized and operator experience.

Therefore, regenerative procedures

should be selected based on the appro-priate selection criteria.

(III). Common Intraoral Lesions

Dental care providers must be familiarwith oral lesions that are commonlyfound in pediatric patients. The 6 most


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406 Oh et al.

commonly found pediatric oral lesionsare: primary herpetic gingivostomatitis,recurrent herpes simplex infection, re-current aphthous stomatitis, diffusein-traoral candidiasis, angular cheilitis,and geographic tongue. Table 4 sum-marizes the therapeutic management of

each of these conditions.

Primary herpetic gingivostomatitis (PHG)

The primary etiology of this disease isherpes simplex virus (HSV) type 1.Viral transmission may occur via oral-genital or oral-oral direct mucocutane-ous contact of infected secretions. Theinitial infection of PHG primarily af-fects children under 10 yearsof agewitha peak incidence at 24 years of age,and secondarily young adults, aged 15to 25 years (M ain 1989). The incuba-

tion period of HSV infection ranges ap-proximately 3to 10 days. Clinical mani-festations include fever, malaise, irrita-bility, lymphadenopathy, widespreadinflammation in the marginal and at-tached gingiva, and small clusters ofvesiclesthroughout themouth. Theves-icles often coalescence and burst, form-ing large ulcers. It often causes severepain and debilitation. Consequently,mastication and swallowing may betoopainful, resulting in dehydration. Thiscan be managed by supportive treat-ment with high oral fluid intake or in-

travenous fluid infusion (Dohvoma1994). PHG is a contagious diseasethatusually regresses spontaneously within12 to 20 days. Amir et al. (1997) re-ported that acyclovir oral suspensiontreatment (15 mg/kg 5 times a day) forherpetic gingivostomatitis, startedwithin 3 days of onset, significantly re-duced the duration of clinical manifes-tations and infectivity of affectedchildren.

Recurrent herpes simplex (RHS)

Following primary infection by herpessimplexvirus, thevirus ascendsthroughsensory or autonomic nerves and per-sists in neuronal ganglia. It becomesdominantwithin thenucleusand is pres-ent as a latent HSV (Corey & Spear1986). In about30to 40%of population,secondary manifestations may occur asa result of precipitating factors such assunlight, trauma, fever, immunosup-pression, or stress. These secondarymanifestations are recurrent herpes la-bialis, herpes genitalis, ocular herpes,and herpes encephalitis (Park 1988).

Vesicles often develop at the same siteand areusually present in small clustersfollowingthedistributionof theinfectednerve. In healthy individuals, thediseaseis limitedto periosteal-bound, keratiniz-ed mucosa whereas recurrences in thebuccal mucosa and tongue may develop

in immunocomprimised patients. Thelesions aremost frequently seen as her-pes labialis, where lesions occur at thevermillion border of thelip.

Recurrent aphthous stomatitis (RAS)

RAS is the most common oral mucosaldisease in North America (Murray &Amedee 2000). Approximately 20% ofpopulation experiences minor apthae,which is the most common form ofchildhood RAS (Field et al. 1992).

These ulcerative lesions are often re-

ferred as canker sores by the patient.RAS lesions range from occasionalsmall (0.5 to 1.0 cm in diameter), well-defined round or ovoid shallow ulcerswith a gray-yellowish central area sur-rounded by an erythematous halo tolarger (1 to 3 cm in diameter) oval orirregular ulcers. Small lesions heal in 7to 10 days without scarring whereaslarger lesionspersist for weeks and healwith scarring (Eversole 1989). Theetiology is unknown, yet suggestedetiologiesincludetheL-formof strepto-coccus and/or an immunopathic pro-

cess involving cell-mediated cytolyticactivity in response to H LA or foreignantigens. Precipitating factors may in-clude trauma, stress, menstruation, nu-tritional deficiencies, food allergies, andendocrinopathies. In children withBehcets disease and HIV infection,RAS lesions are frequently found(K rause et al. 1999, Ramos-Gomez etal. 1999). Clinical management of RASmay includemouthrinses such aschlor-hexidine gluconate, topical cortico-steroids, topical tetracyclines, immuno-modulators, and others (Porter et al.

1998).

Candidiasis

Candidiasis is the most prevalent my-cotic infection in the oral mucosa. It iscaused byan overgrowth of a superficialfungus,Candida albicans, opportunisticfungus found in the oral cavity, gastro-intestinal tract, and vagina. Clinically,it appears as diffuse, curdy, or velvetywhite mucosal plaques that can bewip-ed off. Infants whose mothers displayvaginal thrush at the time of birth and

adults on long-term antibiotics or ster-oid therapy are frequently affected. Inaddition, individuals with diabetes, hy-poparathyroidism, immunodeficiency,or those undergoing chemotherapy arealso often affected. Particularly,children and adolescents with HIV-in-

fection are predisposed to the develop-ment of oral candidiasis (Flaitz& Hicks1999). L ike other forms of Candida in-fection, such as angular cheilitis andgeographic tongue, the lesions can bemanaged by both topical and systemictreatment with antifungal medications,such asNystatin ointment.

Angular cheilitis

Angular cheilitis, perleche, is a painfulcondition beginningasan inflammation

of the commissure of the lips, followedby erosion, ulceration, and fissuring. Itis known to beassociated with Candidaalbicans and St aphylococcus aureus.

The possible predisposing factors mayinclude immunodeficiency, riboflavin(vitamin B2) deficiency, trauma, andlossof vertical dimension. AccordingtoFlaitz & Hicks (1999), oral candidiasis,including angular cheilitis, is the mostcommon oral manifestation in HIV-in-fected children. Treatment may includeremoval, if possible, of predisposingfactors and application of antifungal

medications.

Geographic tongue (benign migratory

glossitis)

Geographic tongue is a benign in-flammatory condition that is character-ized by desquamation of superficialkeratin and the filiform papillae. It af-fects approximately 1 to 2% of popula-tion. K leinman et al. (1994) reported0.6% prevalence of geographic tonguein 39,206 U.S. schoolchildren, aged 5

17 years. The etiology is unknown, butcorrelation with nutritional deficienciesand/or emotional stress has been sug-gested. Thecondition is often restrictedto thedorsumand lateral borders of thetongue. Sometimes theseusually benignlesions can become symptomatic ex-hibiting a burning sensation. Palliativetreatment, includingavoidanceof acidicand spicy foodsand drinks is advisablefor those cases exhibiting symptoms.

Topical and systemic antihistaminemaybe used to manage the lesions of geo-graphic tongue(Sigal & M ock 1992).


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Summary

Periodontal diseases are among themost frequent diseases affectingchildren and adolescents. Dental clini-cians must be aware of the prevalence,diagnostic characteristics, micro-

biology, host-related factors, and thera-peutic management of each of thesedis-ease entities. It is well known that theprimary etiology of periodontal dis-eases is bacterial plaque. However, pa-tients affected by early onset peri-odontitis (or aggressive periodontitis)often present with impaired immunefunction, mainly neutrophil dysfunc-tion. Therefore, it is important whenmanaging periodontal diseases inyoung individuals, the dentist shouldrule out systemic diseases that can af-fect host defense mechanisms. In ad-

dition, commonly found oral lesionssuch asprimary herpetic gingivostoma-titis, recurrent herpes simplex, recurrentaphthous stomatitis, diffuse intraoralcandidiasis, angular cheilitis, and geo-graphic tongue should be promptlyidentified and treated if necessary. It isbelieved that thebest approach to man-age periodontal diseases is prevention,followed by early detection and treat-ment. To achievethis, profound knowl-edge about periodonticsand pedodont-ics as well as intimate periodontal-pe-dodontics interactions areessential.

Acknowledgements

This article was partially supported bytheU niversity of M ichigan, PeriodontalGraduateStudent Research Fund.

Zusammenfassung

Parodontale Er krankungen bei Ki ndern undH eranwachsendenHintergrund:Parodontale Erkrankungen ge-horen zu den haufigsten Erkrankungen, dieK inder und Heranwachsende betreffen. Diesbezieht die Gingivitis, die lokalisierte oder

generalisierte aggressive Parodontitis (fruheinsetzendeParodontitis, die die generalisier-teoder lokalisierte prapubertale Parodontitisund die juvenile Parodontitis einbezieht) undparodontale Erkrankungen verbunden mitsystemischen Storungen ein. Der beste Wegfur die Beschaftigung mit parodontalen Er-krankungen ist die Pravention, gefolgt vonder fruhen Entdeckungund der Behandlung.Methoden: Diese Arbeit bewertet die gegen-wartige Literatur diesich mit den haufigstenparodontalen Erkrankungen bei K indern be-schaftigt: chronische Gingivitis (oder Plaqueinduzierte gingivale Erkrankungen) undfruheinsetzende Parodontitis (oder aggressive Pa-

rodontitis), einschlielich prapubertale undjuvenile Parodontitis. Zusatzlich werden sy-stemische Erkrankungen, die das Parodonti-um und die orale Schleimhaut betreffen undbei jungen K indern gewohnlich gefundenwerden, behandelt. Die Pravalenz, die dia-gnostischen Merkmale, die M ikrobiologie,die Wirtsfaktoren und das therapeutische

M anagement von jeder dieser Erkrankungenwerden grundlich diskutiert.

Resume

M aladies parodontales chez lenfant et lado-lescentOrigine:Les maladiesparodontalessont par-mi les maladies les plus frequentes affectantles enfants et les adolescents. Ellescompren-nent la gingivite, la parodontite agressivelo-calisee ou generalisee (parodontite precocequi inclut les formes generalisees ou locali-sees de parodontite prepubertaire et la paro-dontite juvenile) et lesmaladies parodontales

associees aux problemes systemiques. Lameilleure approche pour traiter les maladiesparodontales est la prevention suiviepar unedetection precoceet un traitement.Methodes:Ce manuscrit revoit la litteratureactuelle concernant les maladies parodonta-les les plus communes affectant les enfants:gingivite chronique (ou maladie gingivale in-duite par la plaque dentair) et parodontiteprecoce (ou parodontite agressive) incluantles parodontitesprepubertaire et juvenile. Deplus, lesmaladiessystemiquesqui affectent leparodonteet leslesions oralescommunementtrouvees chez lesjeunes enfantssont reprises.La frequence globale, les caracteristiques dudiagnostic, la microbiologie, les facteurs de

lhote et lapproche therapeutique de chacu-nede ces entites de maladie sont discutes enprofondeur.

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Address:

H om-Lay W angDepartment of Periodontics/Prevention/

GeriatricsUniversity of M ichigan School of Dentistry1011 North University AvenueAnn Arbor, M ichigan 48109-1078U SA

Fax:17349360374e-mail: homlay/umich.edu

periodontal disease in the child and adolescent

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