J ClinPeriodontol 2002; 29: 400410 Copyright C Blackwell Munksgaard 2002
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I SSN 0303-6979 Tae-Ju Oh, Robert Eber and Hom-Lay Wang Periodontal diseases inthechild Department of Periodontics/Prevention/ Geriatrics, School of Dentistry, University of Michigan, Ann Arbor, MI, USA andadolescent OhT-J , Eber R, WangH-L: Periodontal diseases inthechildandadolescent. J ClinPeriodontol 2002; 29: 400410. C Blackwell Munksgaard, 2002. Abstract Background: Periodontal diseases areamongthemost frequent diseases affecting children and adolescents. Theseincludegingivitis, localized or generalized aggres- siveperiodontitis (a.k.a., early onset periodontitis which includes generalized or localized prepubertal periodontitis and juvenileperiodontitis) and periodontal diseases associated with systemic disorders. Thebest approach to managingperi- odontal diseases is prevention, followed by early detection and treatment. Methods: This paper reviews thecurrent literatureconcerningthemost common periodontal diseasesaffectingchildren: chronicgingivitis(or dental plaque-induced gingival diseases) and early onset periodontitis (or aggressiveperiodontitis), in- cludingprepubertal and juvenileperiodontitis. I n addition, systemic diseases Key words: periodontal disease; children; pedodontics; early onset periodontitis; that affect theperiodontiumand oral lesions commonly found in youngchildren aggressive periodontitis; localized juvenile areaddressed. Theprevalence, diagnostic characteristics, microbiology, host- periodontitis related factors, and therapeutic management of each of thesediseaseentities are thoroughly discussed. Accepted for publication 15 May 2001 Dental cliniciansmust beadept at diag- nosis and management of periodontal disease in children and adolescents. Periodontal diseases are not limited to adults. On the contrary, periodontal diseases are prevalent among children andadolescents. For example, gingivitis affectsmorethan 70%of children older than seven years of age(Page& Schro- eder 1982, Stamm 1986). Bimstein (1991) stressed the importance of pre- vention, early diagnosisand early treat- ment of periodontal diseasesinchildren and adolescents because (1) the preva- lenceof and severity of periodontal dis- eases arehigh; (2) incipient periodontal diseases in children may develop into advanced periodontal diseases in adults; (3) there is association between periodontal and systemic diseases; (4) patients, families, or populationsat risk may be identied and included in special prevention or treatment pro- grams; and (5) prevention and treat- ment of most periodontal diseases are relatively simpleand very effective, pro- vidinglifetimebenets. The nomenclature and classication systems we use to describe periodontal disease have changed periodically over thepast fewdecades. Thisleadstosome confusion when onereviews past litera- ture about disease prevalence, treat- ment, etc. TheConsensus Report of the 1989 World Workshop in Clinical Peri- odontics used the following criteria to distinguish various forms of peri- odontitis: (1) age of onset; (2) rate of disease progression; (3) distribution of affectedsites; (4) presenceor absenceof systemic medical conditions; (5) pres- enceor absenceof specic microbial or host factors; and(6) responseof thedis- easeto therapy (American Academy of Periodontology: AAP 1989). Theclassi- cation (AAP 1989) was simplied by the Consensus Report of the First European Workshop on Periodonto- logy (Attstrm& van der Velden 1994), and more recently, a new classication of periodontal diseases and conditions was presented at the1999I nternational Workshop on Periodontics (Armitage 1999). The 1999 I nternational Work- shop classication system includes a greater varietyof diseasecategoriesthat base the diagnosis on clinical history and ndings, relying less on ageof on- set as a major criterion (Table1). This paper primarily follows the classication of periodontal disease fromthe1989WorldWorkshopinClin- ical Periodontics (AAP 1989) when de- scribing conditions because most clini- cians arefamiliar with it. For each con- dition, wealso includetheI nternational Workshop in Periodontics classication (Armitage 1999) parenthetically to in- troduce readers to the new systemand to highlight the changes between the two. Theaimof thispaper isto reviewthe current literature concerning the most common periodontal diseases affecting children: chronic gingivitis and early onset periodontitis, includingprepuber- tal and juvenile periodontitis. I n ad- dition, systemic diseases that affect the periodontium and oral lesions com- monly found in young children will be addressed. Periodontal diseases inchildren 401 Table1. Classications of periodontitis The1989WorldWorkshopinClinical Periodontics I . Adult periodontitis I I . Early-onset periodontitis A. Prepubertal periodontitis (generalized, localized) B. J uvenileperiodontitis (generalized, localized) C. Rapidly progressiveperiodontitis I I I . Periodontitis associated with systemic disease I V. Necrotizingulcerativeperiodontitis V. Refractory periodontitis The1994First EuropeanWorkshoponPeriodontology I . Early onset periodontitis I I . Adult periodontitis I I I . Necrotizingperiodontitis The1999International WorkshoponPeriodontology I . Gingival diseases I I . Chronic periodontitis I I I . Aggressiveperiodontitis I V. Periodontitis as a manifestation of systemic diseases V. Necrotizingperiodontal diseases VI . Abscesses of theperiodontium VI I . Periodontitis associated with endodontic lesions VI I I . Developmental or acquired deformities and conditions (I). Chronic Gingivitis (Dental Plaque- induced Gingival Diseases) Chronic gingivitis is themost common periodontal infection among children, and adolescents. These may include plaque-induced chronic gingivitis (the most prevalent form), steroid hormone related gingivitis, drug-inuenced gin- gival overgrowth, and others. I t ischar- acterized by inammation of the mar- ginal gingiva without detectableloss of bone or connective tissue attachment. Theinitial clinical ndings in gingivitis include redness and swelling of mar- ginal gingiva, and bleeding upon prob- ing. As the condition persists, tissues that were initially edematous may be- come more brotic. Gingival margins, normally knife-edged in contour, may becomerolled, and interdental papillae may become bulbous and enlarged. Probing depths may increase if signi- cant hypertrophy or hyperplasia of the gingiva occurs. Histologically, ulceration of the sul- cular epitheliumand inammatory cell inltration of theunderlyingconnective tissue characterize gingivitis. At the microscopic level, T-lymphocytes pre- dominate in children (Seymour et al. 1981) whereas B-cells predominate in adults (Page& Schroeder 1976). Matsson & Goldberg (1985) sug- gested that there is no clear-cut age at which thegingival reaction to bacterial insult in children becomes similar to that inadults. However, thereisgradual increase in gingival activity from early childhood to adult age. Previously, Matsson (1978) performed a21-day ex- perimental gingivitisstudycomparing6 children, aged 4 to 5 years, with 6 den- tal students, aged 23 to 29 years. They found that the children developed gin- givitislessreadily thantheadults. After 21 days without plaque removal, the children had less gingival exudate and a lower percentage of bleeding sites than the adults. Also, the children had a smaller increasein gingival crevicular leukocytes than the adults in response to plaque accumulation. The study hypothesized that children may have a different vascular responsethan adults. Gingivitis does not always progress to periodontitis, but periodontitis is preceded by gingivitis. According to Marshall-Day et al. (1955), gingivitis without evidenceof boneloss was con- ned to a younger agegroup, and bone loss without gingival alterations was rarely found. Plaque-induced chronic gingivitis is commonly found in youngchildren and can bemanaged by mechanical removal of plaque and high levels of oral hy- giene. Theetiologic natureof plaquein gingivitis 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 their children about the importance of oral hygienein theprevention of caries and periodontal diseases. Electric tooth- brushes and antibacterial mouthrinses may be useful adjuncts to standard toothbrushing and ossing for children who are physically challenged, such as childrenwithDownssyndrome, andfor children undergoing orthodontic care (Trombelli et al. 1995, Grossman & Proskin 1997, Boyd 1989). Steroid hormone-related gingivitis is associated with elevated sex hormone levels that amplify clinical inamma- tory changes of gingivitis (Suzuki 1988). I ncreased levels of estrogen and progesterone during pregnancy (Le 1965), during puberty, or in patients medicated with oral contraceptives (Kalkwarf 1978) havebeen reported to result in increased gingival vascularity and inammation. Removal of local factorsis thekey to themanagement of steroid hormone-related gingivitis; however, it is often necessary to surgic- ally excise unresolved gingival over- growth. Drug-inuenced gingival enlargement has been observed in patients taking cyclosporin, phenytoin and calcium channel blockers, with higher preva- lencein children (Mariotti 1999, Seym- our et al. 2000). Gingival enlargement was reported in 30%of patients taking cyclosporin (Seymour & Heasman 1992), 50%of patientstakingphenytoin (Hassell 1981), and15%of patientstak- ing calcium channel blockers such as nifedipine(Lederman et al. 1984), vera- pamil (Pernuet al. 1989), andamlodipi- ne (Seymour et al. 1994). Gingival en- largement starts in the interdental pa- pilla region and spreads to involve the marginal gingiva. I nseverecasestheen- largedgingivamaycover theincisal and occlusal surfaces of the teeth (Chapple 1996). Histologically, theovergrowth is broepithelial in nature, with epithelial acanthosis, increased numbers of broblasts and increased collagen pro- duction. The severity of gingival en- largement is closely related to the level of plaquecontrol, and thereforereduc- tions in dental plaque can limit the se- verity of thelesion (Mariotti 1999). Treatment of drug-inuenced gingi- val enlargement should start with oral hygiene instructions, and scaling and polishing of the teeth to remove bac- terial deposits. Thismay requireseveral visits. 2 daily chlorhexidine rinses (Lang et al. 1982) should beprescribed when normal brushing and ossing do not achieve the desired level of plaque control. Gingivectomy or gingivoplasty may beneeded to correct gingival con- 402 Ohet al. tours for hygienic and esthetic reasons. The patient and parent should be told that gingival enlargement may recur after surgery, and that immaculate home plaque control and regular peri- odontal maintenancearethekey to de- creasingthelikelihood or severity of re- currence. I n addition, the patients physician should beconsulted to deter- mineif thepatient could beswitched to a medication that does not causegingi- val enlargement. The dentist should never recommend that apatient discon- tinue or change medications without medical consultation. (II). Early Onset Periodontitis (New Classication: Aggressive Periodontitis) Characteristics of early onset peri- odontitis include onset before age 35 years, rapid disease progression, some- what different distribution of lesions than in adult periodontitis, and distinct etiologic characteristics. 1. Prepubertal periodontitis (PP) (new classication: aggressive periodontitis) The prevalence of PP ranges from 0.84% to 26.9%, based on a limited number of case reports (J amison 1963, Sweeney et al. 1987, Bimstein et al. 1988). Variation in the reported preva- lencesof PP maydependongeneticfac- tors, methodological factors, and the selection of non-randomsample popu- lations (Watanabe 1990). Prepubertal periodontitis may be generalized or lo- Table2. Diagnostic characteristics of prepubertal periodontitis Localizedprepubertal periodontitis(LPP) O Onset: around 4years of ageor older O Affected teeth: either fewor many teeth O Gingival manifestation: minor inammation, if any O Microbial plaque: minimal O Alveolar bonedestruction: faster than adult periodontitis but much slower than generalized formof PP O Functional defects: either neutrophils or monocytes but not both O Otitis media and upper respiratory infections in somecases O Amenableto mechanical and antibiotic therapy Generalizedprepubertal periodontitis(GPP) O Onset: at thetimeof tooth eruption O Affected teeth: all primary teeth; thepermanent dentition may or may not beaffected O Gingival manifestation: ery red gingiva with acuteinammation around all teeth; gingival proliferation, cleft formation, and recession O Alveolar bonedestruction: rapid O Functional defects: both neutrophils and monocytes O Absenceof PMNs in thegingival tissueand marked increasein peripheral blood white cell count O Otitis media and upper respiratory infections in most cases O Refractory to mechanical and antibiotic therapy calizedandcanaffect bothprimaryand mixed dentition. Onset occurs between the eruption of the primary dentition and puberty. PP is characterized by se- vere gingival inammation, rapid bone loss, tooth mobility, and tooth loss. Su- zuki (1988) reported that PP patients are usually between ages 5 and 8, they have low caries rates, and there is no sex predilection. Pageet al. (1983) rst described prepubertal periodontitis as 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 clinical description of only threeand two cases, respectively. Diagnostic characteristics for prepubertal periodontitis are listed in Table2. Pathogenic bacteria that have been associated with PP include Actino- bacillus actinomycetemcomitans (A.a.), Prevotellaintermedia(P.i.), Capnocyto- phaga species (Delaney & Kornman 1987, Sweeney et al. 1987), Porphyro- monas gingivalis (P.g.) (Mishkin et al. 1986), and Eikenella corrodens (E. corrodens) (Delaney& Kornman1987). Delaney & Kornman (1987) found an increased proportion of black-pig- mented anaerobic rods, E. corrodens, Capnocytophaga species, A.a., and Fu- sobacterium nucleatum (F. nucleatum) in the cultivable ora in LPP patients compared 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 around the deciduous dentition in PP patients remainto infect theareaor neighboring area during eruption of the permanent teeth, subsequent infection of newly erupted permanent teeth may occur. The coexistence of A.a. in lesions of both PP and localized juvenile peri- odontitis (LJ P) (Zambon et al. 1983) may explain the possibility. However, thepossiblemechanismof diseasepro- gression needs to be re-evaluated since not all PP develops into J P. Although the primary etiology re- mains bacterial plaque, other factors may predispose otherwise healthy pa- tients to PP. These may include ce- mentum defects (Page & Baab 1985), functional defects in leukocyte chemo- taxis (Pageet al. 1983), and/or presence of bacteriophage (Watanabe 1990). I t hasbeen generally recognized that GPP and leukocyte adhesion deciency (LAD) are related. Waldrop et al. (1987) demonstrated that themolecular basis of GPP was leukocyte adhesion deciency by using monoclonal anti- bodies against Mac-1, LFA-1, and p150,95surfaceadhesionmolecules. On the other hand, immunological data about LPP have shown that a neutro- phil or monocyte chemotaxis defect, but not both, exists in LPP patients. Systemic diseasesassociatedwithpre- pubertal periodontitis (new classi- cation: periodontitis as a manifestation of systemic diseases) may include insu- lin dependent diabetes mellitus (I DDM), Papillon-Lefe`vre syndrome, hypophosphatasia, neutropenia, Ched- iak-Higashi syndrome, leukemias, histiocytosisX, acrodynia, acquiredim- munodeciency syndrome (AI DS), Down syndrome, and leukocyte ad- hesion deciency. I nsulin dependent diabetes mellitus (I DDM, J uvenile DM) is a relative or absolutedecreasein insulin secretion or availability, caused by a genetic defect in pancreatic beta cell productivity, de- fective insulin release mechanisms (J ohnes & Mason 1980) or by destruc- tion of beta cells (J ackson & Guthrie 1986). Bernick et al. (1975), Gislen et al. (1980), and Cianciola et al. (1982) studied theassociationbetween juvenile diabetes and periodontal diseases in young children. Bernick et al. (1975) examined 50 diabetic children and 36 healthy control children who were matched for age and oral hygiene sta- tus. They found that gingival inam- mation was more prevalent in the dia- betic group. Furthermore, Gislen et al. (1980) showed that diabetic children Periodontal diseases inchildren 403 with poor metabolic control appeared to have greater gingival index scores than children without diabetes. Cianci- ola et al. (1982) investigated prevalence of periodontal diseasein I DDM in 263 I DDM patients and 208 control sub- jects. For children between 11 and 18 years old, 9.8 %of theI DDM patients showed signs of periodontitis versus only 1.7% of the controls. They found no periodontitisinchildren10yearsold or younger in either group. The article argues that probing alone is not suf- cient to assess periodontitis, particu- larly when applied to the mixed den- tition. Adjunctive use of radiographs wasrecommendedfor theassessment of periodontitis in children. I DDM pa- tients have also been shown to have a reduced PMN response to chemotactic stimuli (Miller 1972). Papillon-Lefe`vre syndrome (PLS) is a genetic condition inherited as an autosomal recessivetrait, characterized by hyperkeratosis of the palms of the hands and soles of the feet and early onset periodontitis (J ohnes & Mason 1980). Severe periodontitis can affect both the primary and permanent den- titions(Smith& Rosenzweig1967, Gor- lin et al. 1964). Theprevalenceof PMN chemotactic defects in thePLS patients remains controversial. Hypophosphatasia is a genetic dis- order. Diagnostic ndings include low levels of serum alkaline phosphatase and excretion of phosphoethanolamine, the substrate for alkaline phosphatase, in theurine. Thedisorder can beclassi- ed into 3 types: (1) infantile, an auto- somal recessivecondition occurringbe- fore 6 months of age (the most severe form); (2) childhood, an autosomal re- cessive or autosomal dominant con- dition occurring after 6 months of age; and (3) adult hypophosphatasia, an autosomal dominant condition that is the least severe form(Watanabe 1990). The most consistent clinical sign is prematureloss of deciduous teeth (Fal- lon et al. 1984). The teeth may have large pulp chambers, and skeletal de- formities may occur. Baer & Benjamin (1974) claimed that only deciduous teeth aregenerally affected. Baab et al. (1986) reported normal polymorpho- nuclear leukocyte (PMN) chemotaxis and abnormal monocytechemotaxis in 3childrenwithhypophosphatasia; how- ever, age range was not designated in thestudy. Neutropenia is a disorder in which thenumber of PMNs in theperipheral blood isbelow1000/mm 3 in infants, be- low1000/mm 3 or 1500/mm 3 in children, and below1800/mm 3 in adults. Neutro- penias associated with oral manifes- tations in children include agranulo- cytosis (malignant neutropenia, rare in children), cyclic neutropenia, chronic benign neutropenia of childhood, chronic idiopathic neutropenia, and familial benignneutropenia. Prichardet al. (1984) and Cohen & Morris (1961) reportedthat cyclicneutropeniawasas- sociated with severe gingivitis with ul- ceration and frequent history of recur- rent infections such as otitis media and upper respiratory infection. Chediak-Higashi syndrome is a rare autosomal recessive disease associated with impaired function of cytoplasmic microtubules or microtubule assembly in PMNs. Diagnostic features include characteristic, abnormally large gran- ules in granulocytes. According to Clawson et al. (1978), PMN chemo- tactic defects in Chediak-Higashi syn- dromemay bedueto mechanical inter- ference in deformability by the giant cytoplasmic granules. Moreover, im- paired microtubuleassemblingfunction (Oliver 1976) and hyperadhesiveness (Keller et al. 1984) were suggested as the mechanism for PMN chemotactic defects. Leukemias are characterized by pro- gressive uncontrolled proliferation of white blood cells and classied into acuteand chronic lymphocytic leukem- ia, acute and chronic granulocytic leu- kemia, acute and chronic monocytic leukemia, and other rareforms such as plasma cell leukemia. Oral manifes- tationsof leukemiasin children aregin- gival hemorrhage, petechiae, lymph- adenopathy, gingival hyperplasia or hypertrophy, and gingival pallor. Bender (1944) and Deasy et al. (1976) reported association between peri- odontal disease and leukemia in children. Histiocytosis X represents a disturb- anceof thereticulo-endothelial system. I t resultsfromtheproliferationanddis- semination of pathological Langerhans cells and includes three disorders: Let- terer-Siwedisease(themost severeform and usually occurs in infants or before age3); Hand-Schuller-Christian disease (usuallyoccursbeforeage5, but canoc- cur in adolescents and even in young adults); and eosinophilic granuloma (occurs primarily in older children and young adults) (Hartman & Colonel 1980). I ncreased susceptibility to bac- terial infections in histiocytosis X pa- tients may result from PMN defects (Tomooka et al. 1986) or decreased monocyte function (Kragballe et al. 1981). Acrodyniaisararediseasecharacter- ized by a wide variety of clinical signs including gingival and mucosal hyper- plasia, alveolar bonelosswithearlyloss of primary teeth, lossof hair, abnormal cramps, profuse sweating and sali- vation, and gastrointestinal upsets. Etiology of acrodynia is known to bea mercurial toxicityreaction, either actual mercury poisoning or, more likely, an idiosyncracy to mercury (Warkany & Hubbard 1948). Acquiredimmunodeciencysyndrome (AI DS) developsasaresult of infection with the human immunodeciency vi- rus(HI V). ChildrenwithAI DSmayde- velop an atypical formof acutenecrot- izing ulcerative gingivitis (ANUG) (Leggott 1987); however, no reports of prepubertal pediatric AI DS patients presentingwith alveolar bonelossexist. Downs syndrome (Trisomy 21 syn- drome; Mongolism) is a common and easily recognizable chromosomal aber- ration. Thedentition exhibits anumber of characteristic anomalies including malformation of the teeth, enamel hy- poplasia, and microdontia. Other com- monoral manifestationsincludemacro- glossia, ssured or pebbly tongue, and ahigh arched palate. Dueto adefective immune system, rampant and pre- cociousperiodontal diseaseisprevalent. Barr-Agholme et al. (1998) compared 20Downssyndromepatients, aged9to 21 years, with 19 healthy controls and reported that gingival inammation, probing depth, calculus, and marginal bone loss were signicantly greater in the Downs syndrome group. No sig- nicant differences werefound between the two groups, regarding levels of serumI gA, I gG 2 , I gG 3 , I gG 4 , I gM, or albumin. However, the proportion of I gG 1 in total I gG was signicantly higher in the Downs syndrome group compared to thecontrol group. Leukocyte adhesion deciency (LAD) is a genetic diseaseinherited as an autosomal recessive condition in which theexpression of Mac-1, LFA-1, and p150,95 glycoprotein adhesion molecules on leukocytes is severely re- duced. Springer et al. (1984) suggested that LAD occurs as a result of a defect in thegenethat codes for thecommon beta subunit of cell surface integrins which are required for leukocyte diap- 404 Ohet al. Table3. Diagnostic characteristics of juvenileperiodontitis Localizedjuvenileperiodontitis(LJ P) O Onset: around puberty O Affected teeth: permanent incisors and/or rst molars O Associated microorganism: Actinobacillus actinomycetemcomitans O Greater prevalencein blacks O Neutrophil dysfunction and high I gG2response O Familial distribution Generalizedjuvenileperiodontitis(GJ P) O Onset: duringlateteen years O Affected teeth: generalized involvement of permanent teeth O Associated microorganism: not clear (P. gingivalis may beinvolved) O Greater prevalencein blacks O Neutrophil dysfunction O Familial distribution edesis. Because emigration of PMNs from blood vessels is dependent upon adhesion of PMNs to endothelial cell surfaces, patients with LAD have a poor response to bacterial infections. Therefore, these children are plagued with recurrent bacterial infections and impaired wound healing. Patients with this rarediseasepresent with extremely acuteinammation, proliferation of the gingival tissues, and rapid bone loss. Anassociationbetweengeneralizedpre- pubertal periodontitis and LAD was demonstrated by Waldrop et al. (1987) and Pageet al. (1987). Treatment for PP has ranged from scaling and root planing or curettage, with or without systemic antibiotics, to theextraction of involved teeth (Watan- abe1990). Thegeneralizedform, unfor- tunately, does not respond as favorably to treatment as thelocalized form. The majority of cases have been treated by extraction of involved deciduous teeth and permanent teeth. Since these pa- tients may have associated LAD and may be undergoing antibiotic therapy for recurrent serious infections, it is necessary to have a consultation with thetreatingphysician. 2. Juvenile periodontitis (JP) (new classication: aggressive periodontitis) J uvenile periodontitis, formerly called periodontosis, occurs in children and teenagers who are otherwise healthy and is characterized by a rapid alveolar bone loss in one or more teeth of the permanent dentition (Baer 1971). Ter- minology for this diseaseentity has re- peatedly changed. Gottlieb et al. (1923) rst described this condition diffuse atrophy of thealveolar bone. His nd- ings in this caseincluded widened peri- odontal ligament (PDL), cementopa- thia and alveolar bone resorption, but no pathology in gingival tissues. Later, the degenerative process was termed periodontosis (Orban & Weinmann 1942), who describedthreestagesof the disease: degeneration of PDL bers; proliferation of the junctional epithel- ium; and the development of deep infrabony pockets. The term peri- odontosis was favored by Baer (1971). I n his article, thediseaseentity was di- vided into two categories, a localized form affecting the rst molars and in- cisors, and more generalized form af- fecting most of dentition. The term juvenile periodontitis, introduced by Butler (1969), accurately describes the disease as an inammatory process. Waerhaug(1977) describedthat thepri- maryetiologyof thediseaseissubgingi- val bacterial plaque. Theplaquefront is consistently located within 0.2 mm to 1.5 mm from the border of loss of attachment. The plaque grows with a faster speed of 3 to 5 microns a day in this disease compared to 0.2 to 1.0 mm a day in ordinary cases. Diagnostic characteristics of juvenile periodontitis areillustrated in Table3. Estimates of the prevalence of J P vary from 0.1% to 15% (Sjdin et al. 1993, Hart et al. 1993, Saxen 1980, Le & Brown 1991, Neely 1992), with differences attributed to varying cri- teria, geographics, and a diverse data base. Reports show greater prevalence in African-Americans than in Caucasi- ans (Burmeister et al. 1984, Le & Brown 1991, Melvin et al. 1991). Al- bandar et al. (1997a) estimated preva- lenceof EOP (J P) in agroup of school- children, aged 13 to 17 years, based on thedataof anational survey conducted duringthe19861987school year. They showed that approximately 10.0% of African-American, 5.5% of Hispanic, and1.3%of whiteadolescentshadEOP. Hrmand & Frandsen (1979) explained that the higher incidence of LJ P in fe- males could result from an earlier oc- currenceof thediseaseinfemales. Stab- holz et al. (1998) reported ahigh preva- lence of LJ P in an I srael population consisting of 86 individuals from 30 families, aged 12to 20years. Out of 86 subjects, 33individualsfrom15families showed LJ P (38.4%), but none of the subjects showed signs of generalized juvenile periodontitis. Except for two pairs of families with genetic ties, no familial connectionscouldbetracedbe- tween the different nuclear families affected by LJ P, and therewereno dif- ferences in oral hygiene status between LJ P and non-LJ P groups. The study suggests that environmental factors may inuencetheoccurrenceof LJ P. The microora associated with J P is mainly composed of Gram-negative, capnophilic, and anaerobic rods (Slots 1979, Newman & Socransky 1977). Actinobacillus actinomycetemcomitans (A.a.), a Gram-negative, non-motile, coccobacillushasbeenwell documented in relation to LJ P (Newman & Socran- sky 1977, Slots et al. 1980, 1982, Korn- man & Robertson 1985). Asikainen et al. (1991) examined A.a. isolates from subgingival sites in 136subjects in Fin- land and found that among ve sero- types of A.a., serotype b was predomi- nant in LJ P and adult periodontitis, whereas serotype c predominated in healthyindividuals. Wilson& Hamilton (1992) also demonstrated that black subjects with LJ P responded to A.a. serotype b serospecic antigens by the production of I gG antibodies of the I gG2 subclass. Lu et al. (1993, 1994) conrmed this by demonstrating that I gG2 was markedly elevated over all other I g classes reactivewith A.a. sero- type b. Albandar et al. (1997b) found that EOP patients had higher preva- lenceand levels of P.g., P.i., F. nucleat- um., C. rectus, and T. denticola com- pared to healthy controls. P.g., T. denticola, and P.i., in descending order of importance, weresignicantlyassoci- atedwiththegeneralizedand/or rapidly progressingdisease. Reports indicate that J P patients have defects in neutrophil chemotaxis or phagocytosis (Cianciola et al. 1977, Clark et al. 1977, Van Dykeet al. 1987, Suzuki et al. 1984, Kimura et al.1992, etc.). Neutrophils in LJ P patients have fewer receptors on their plasma mem- brane for certain chemotaxis-inducing Periodontal diseases inchildren 405 factors, such as FMLP, C5a, and GP110 (Van Dyke et al. 1981, 1983, 1987). Agarwal et al. (1994) further sug- gestedthat cytokines, suchastumor ne- crosis factor (TNF) and interleukin-1 (I L-1), present in theserumof LJ P pa- tients are responsible for priming and inducing altered response in neutro- phils. I n the study, it was found that treatment of neutrophilsin healthy sub- jects with LJ P-sera resulted in a de- creased neutrophil chemotactic re- sponse and down regulation of FMLP receptors on the cell surface. On the other hand, pretreatment of LJ P-sera withanti-TNF andanti-I L-1antibodies effectively neutralized the ability of LJ P-sera to modulate chemotaxis and FMLP receptor levels in healthy sub- jects. Sigusch et al. (1998) found that EOP patients showed reduced expres- sion of monocyte HLA-DR, I FN-g, and I L-2mRNA, and reduced prolifer- ation of peripheral blood monocytes, which are known to be positively ex- pressed by activated T H 1 cells. This in- dicates an impaired T H 1 cell response in EOP patients. Ozmeric et al. (1998) further suggested that the I L-8, a chemoattractant, produced by LJ P pa- tients may beless activethan in healthy individuals. Theetiology of J P can bebroadly di- vided into two categories, bacterial plaque and impaired host defense mechanism; therefore, the treatment should aim to control pathogenic mi- croora and compensate for impaired immunefunction. Systemic approaches such as antibiotic therapy areoften in- dicated in the management of J P. I n fact, several studies (Slots & Rosling 1983, Christersson et al. 1985, Korn- man & Robertson 1985) showed that scalingand root planingalonefailed to suppress or eliminateA.a. fromthedis- eased siteand failed to improveclinical conditions. Treatment modalities in the management of J P include mechanical therapy, such as scaling and root plan- ingandperiodontal surgery, local deliv- ery of antimicrobials, and systemic antibiotics such as tetracycline, doxycy- cline, metronidazone, combination of metronidazoleand amoxicillin, or com- bination of metronidazole and Aug- mentin (amoxicillin clavulanic acid). Gunsolley et al. (1994) compared nonsurgical and surgical periodontal treatment in 23 young patients with se- vere generalized periodontitis. They foundthat P.g. wasvirtually eliminated by scalingand root planingwhilelevels of A.a. werenot signicantlyreducedby scaling and root planing alone. How- ever, after apsurgery, thelevelsof A.a. were signicantly reduced, suggesting that surgery and/or antibiotics are necessary to reduce levels of A.a. in young patients with severe generalized periodontitis. This result was in agree- ment with other studies (Slots & Ro- sling 1983, Lindhe & Liljenberg 1984, Kornman & Robertson 1985). Young individuals generally haveex- cellent healing potential. Therefore, in J P patientsthecombinationof systemic antibiotics and regenerative surgery is often successful in treating intrabony defectsandearlyfurcationinvolvement. Mattout and Roche(1984) found com- plete ll of furcations and signicant supracrestal repair in an 18-year-old J P patient after treatment with iliac crest autografts. Mabry et al. (1985) treated intrabony defects in 16 LJ P patients with a combination of freeze-dried bone allograft (FDBA) and tetracy- cline. The group that received systemic tetracyclinetherapyandlocal treatment with a mixture of tetracycline powder and FDBA had signicantly better res- Table4. Therapeutic management of common pediatric oral lesions Primaryherpeticgingivostomatitis O Topical anesthetics/coatingagents: 1to 1mixtureof diphenhydramine(Benadryl) elixir & Maalox [OTC] diphenhydramine(Benadryl)/lidocaine/Maalox mouth rinse Acyclovir elixir O Systemic acyclovir antiviral therapy Recurrent herpessimplex O Avoidanceof perpetuatingfactors O Acyclovir (Zovirax) 5%ointment or elixir O Systemic acyclovir as activetreatment or prophylaxis for immunosuppressed patients Recurrent aphthousstomatitis O Topical anesthetics/coatingagents: Zilactin-B [OTC], Orabase-B [OTC], or Oraloe[OTC] O Antimicrobial mouthrinses: 0.12%chlorhexidinegluconate O Topical steroids: triamcinolone (Kenalog) in orabase 0.1%, betamethasone valerate 0.1% ointment, dexamethasone(Decadron) elixir 0.5mg/5ml, or uocinonide(Lidex) gel 0.05% Candidiasis O Topical antifungal agents: Nysatin (Mycostatin) oral suspension 100,000units/ml or popsicles Clotrimazole(Mycelex) troches or swabs O Antimicrobial mouthrinses: 0.12%chlorhexidinegluconate Angular cheilitis O Topical antifungal agents: nystatin or clotrimazoleointment O Topical antifungal/steroid agent: nystatin/triamcinoloneacetonide(MucologI I ) ointment O Topical antifungal/antibacterial/steroid agent: hydrocortisone/iodoquinol (Vytone) cream 1% Geographictongue O Topical anesthetic/analgesic mouth rinse: Ulcer-Ease[OTC] O Topical antifungal/steroid agent: triamcinoloneacetonide0.1%in nystatin suspension O Alkalinesalinemouth rinse O Topical anesthetics/coating agents: 1 to 1 mixtureof diphenhydramine(Benadryl) elixir & Maalox [OTC] olution of intrabony defects than the groups that received FDBA alone or debridement alone with/without sys- temic tetracycline. Contrary to these ndings, DiBattista et al. (1995) found no statistically signicant differences between ap debridement alone and various regenerative procedures in 7 LJ P patients. All patients in this study received systemic doxycycline. The re- generative procedures utilized were ePTFE membranes, ePTFE plus root conditioning with doxycycline solution (pH: 2.5), and ePTFE root con- ditioning compositegraft. Baseduponthecontradictoryresults, it is apparent that the results achieved with regenerative procedures will vary depending on case selection, the pro- cedureutilizedandoperator experience. Therefore, regenerative procedures should beselected based on theappro- priateselection criteria. (III). Common Intraoral Lesions Dental care providers must be familiar with oral lesions that are commonly found in pediatric patients. The6most 406 Ohet al. commonly found pediatric oral lesions are: primary herpetic gingivostomatitis, recurrent herpes simplex infection, re- current aphthous stomatitis, diffusein- traoral candidiasis, angular cheilitis, and geographic tongue. Table 4 sum- marizes thetherapeutic management of each of theseconditions. Primary herpetic gingivostomatitis (PHG) The primary etiology of this disease is herpes simplex virus (HSV) type 1. Viral transmission may occur via oral- genital or oral-oral direct mucocutane- ous contact of infected secretions. The initial infection of PHG primarily af- fectschildrenunder 10yearsof agewith a peak incidence at 24 years of age, and secondarily young adults, aged 15 to 25 years (Main 1989). The incuba- tionperiodof HSV infectionrangesap- proximately3to 10days. Clinical mani- festations include fever, malaise, irrita- bility, lymphadenopathy, widespread inammation in the marginal and at- tached gingiva, and small clusters of vesiclesthroughout themouth. Theves- icles often coalescenceand burst, form- ing large ulcers. I t often causes severe pain and debilitation. Consequently, mastication and swallowingmay betoo painful, resulting in dehydration. This can be managed by supportive treat- ment with high oral uid intake or in- travenous uid infusion (Dohvoma 1994). PHG isacontagiousdiseasethat usually regresses spontaneously within 12 to 20 days. Amir et al. (1997) re- ported that acyclovir oral suspension treatment (15 mg/kg 5 times a day) for herpetic gingivostomatitis, started within 3 days of onset, signicantly re- duced the duration of clinical manifes- tations and infectivity of affected children. Recurrent herpes simplex (RHS) Following primary infection by herpes simplexvirus, thevirusascendsthrough sensory or autonomic nerves and per- sists in neuronal ganglia. I t becomes dominant withinthenucleusandispres- ent as a latent HSV (Corey & Spear 1986). I nabout 30to40%of population, secondary manifestations may occur as a result of precipitating factors such as sunlight, trauma, fever, immunosup- pression, or stress. These secondary manifestations are recurrent herpes la- bialis, herpes genitalis, ocular herpes, and herpes encephalitis (Park 1988). Vesicles often develop at the same site and areusually present in small clusters followingthedistributionof theinfected nerve. I nhealthyindividuals, thedisease islimitedtoperiosteal-bound, keratiniz- ed mucosa whereas recurrences in the buccal mucosaand tonguemay develop in immunocomprimised patients. The lesions aremost frequently seen as her- pes labialis, where lesions occur at the vermillionborder of thelip. Recurrent aphthous stomatitis (RAS) RAS is themost common oral mucosal disease in North America (Murray & Amedee 2000). Approximately 20% of population experiences minor apthae, which is the most common form of childhood RAS (Field et al. 1992). These ulcerative lesions are often re- ferred as canker sores by thepatient. RAS lesions range from occasional small (0.5 to 1.0 cmin diameter), well- dened round or ovoid shallow ulcers with a gray-yellowish central area sur- rounded by an erythematous halo to larger (1 to 3 cm in diameter) oval or irregular ulcers. Small lesions heal in 7 to 10 days without scarring whereas larger lesionspersist for weeksand heal with scarring (Eversole 1989). The etiology is unknown, yet suggested etiologiesincludetheL-formof strepto- coccus and/or an immunopathic pro- cess involving cell-mediated cytolytic activity in response to HLA or foreign antigens. Precipitating factors may in- cludetrauma, stress, menstruation, nu- tritional deciencies, foodallergies, and endocrinopathies. I n children with Behcets disease and HI V infection, RAS lesions are frequently found (Krause et al. 1999, Ramos-Gomez et al. 1999). Clinical management of RAS may includemouthrinses such as chlor- 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 theoral mucosa. I t is causedbyanovergrowthof asupercial fungus, Candida albicans, opportunistic fungus found in theoral cavity, gastro- intestinal tract, and vagina. Clinically, it appears as diffuse, curdy, or velvety whitemucosal plaques that can bewip- ed off. I nfants whose mothers display vaginal thrush at thetimeof birth and adults on long-termantibiotics or ster- oid therapy are frequently affected. I n addition, individuals with diabetes, hy- poparathyroidism, immunodeciency, or those undergoing chemotherapy are also often affected. Particularly, children and adolescents with HI V-in- fection are predisposed to the develop- ment of oral candidiasis(Flaitz & Hicks 1999). Likeother forms of Candida in- fection, such as angular cheilitis and geographic tongue, the lesions can be managed by both topical and systemic treatment with antifungal medications, such as Nystatin ointment. Angular cheilitis Angular cheilitis, perleche, is a painful conditionbeginningasaninammation of thecommissureof thelips, followed by erosion, ulceration, and ssuring. I t is known to beassociated with Candida albicans and Staphylococcus aureus. The possible predisposing factors may include immunodeciency, riboavin (vitamin B 2 ) deciency, trauma, and lossof vertical dimension. Accordingto Flaitz & Hicks (1999), oral candidiasis, including angular cheilitis, is the most common oral manifestation in HI V-in- fected children. Treatment may include removal, if possible, of predisposing factors and application of antifungal medications. Geographic tongue (benign migratory glossitis) Geographic tongue is a benign in- ammatory condition that is character- ized by desquamation of supercial keratin and the liformpapillae. I t af- fects approximately 1 to 2%of popula- tion. Kleinman et al. (1994) reported 0.6% prevalence of geographic tongue in 39,206 U.S. schoolchildren, aged 5 17 years. Theetiology is unknown, but correlation with nutritional deciencies and/or emotional stress has been sug- gested. Thecondition is often restricted to thedorsumandlateral bordersof the tongue. Sometimestheseusually benign lesions can become symptomatic ex- hibiting a burning sensation. Palliative treatment, includingavoidanceof acidic and spicy foods and drinks is advisable for those cases exhibiting symptoms. Topical andsystemicantihistaminemay be used to manage the lesions of geo- graphic tongue(Sigal & Mock 1992). Periodontal diseases inchildren 407 Summary Periodontal diseases are among the most frequent diseases affecting children and adolescents. Dental clini- cians must be aware of the prevalence, diagnostic characteristics, micro- biology, host-related factors, and thera- peuticmanagement of eachof thesedis- ease entities. I t is well known that the primary etiology of periodontal dis- eases is bacterial plaque. However, pa- tients affected by early onset peri- odontitis (or aggressive periodontitis) often present with impaired immune function, mainly neutrophil dysfunc- tion. Therefore, it is important when managing periodontal diseases in young individuals, the dentist should rule out systemic diseases that can af- fect host defense mechanisms. I n ad- dition, commonly found oral lesions such asprimary herpetic gingivostoma- titis, recurrent herpessimplex, recurrent aphthous stomatitis, diffuse intraoral candidiasis, angular cheilitis, and geo- graphic tongue should be promptly identied and treated if necessary. I t is believed that thebest approach to man- age periodontal diseases is prevention, followed by early detection and treat- ment. To achievethis, profound knowl- edgeabout periodontics and pedodont- ics as well as intimate periodontal-pe- dodontics interactions areessential. Acknowledgements This article was partially supported by theUniversityof Michigan, Periodontal GraduateStudent Research Fund. Zusammenfassung Parodontale Erkrankungen bei Kindern und Heranwachsenden Hintergrund: Parodontale Erkrankungen ge- horen zu den haugsten Erkrankungen, die Kinder und Heranwachsendebetreffen. Dies bezieht die Gingivitis, die lokalisierte oder generalisierte aggressive Parodontitis (fruh einsetzendeParodontitis, diediegeneralisier- teoder lokalisierteprapubertaleParodontitis und diejuvenileParodontitis einbezieht) und parodontale Erkrankungen verbunden mit systemischen Storungen ein. Der beste Weg fur die Beschaftigung mit parodontalen Er- krankungen ist die Pravention, gefolgt von der fruhen Entdeckungund der Behandlung. Methoden: Diese Arbeit bewertet die gegen- wartigeLiteratur diesich mit den haugsten parodontalen Erkrankungen bei Kindern be- schaftigt: chronischeGingivitis (oder Plaque induziertegingivaleErkrankungen) und fruh einsetzendeParodontitis (oder aggressivePa- rodontitis), einschlielich prapubertale und juvenile Parodontitis. Zusatzlich werden sy- stemischeErkrankungen, diedas Parodonti- umund dieoraleSchleimhaut betreffen und bei jungen Kindern gewohnlich gefunden werden, behandelt. Die Pravalenz, die dia- gnostischen Merkmale, die Mikrobiologie, die Wirtsfaktoren und das therapeutische Management von jeder dieser Erkrankungen werden grundlich diskutiert. Re sume Maladies parodontales chez lenfant et lado- lescent Origine: Lesmaladiesparodontalessont par- mi les maladies les plus frequentes affectant les enfants et les adolescents. Elles compren- nent la gingivite, la parodontiteagressivelo- calisee ou generalisee (parodontite precoce qui inclut les formes generalisees ou locali- sees deparodontiteprepubertaireet la paro- dontitejuvenile) et lesmaladiesparodontales associees aux proble`mes systemiques. La meilleure approche pour traiter les maladies parodontales est la prevention suiviepar une detection precoceet un traitement. Methodes: Ce manuscrit revoit la litterature actuelle concernant les maladies parodonta- les les plus communes affectant les enfants: gingivitechronique(ou maladiegingivalein- duite par la plaque dentair) et parodontite precoce (ou parodontite agressive) incluant lesparodontitesprepubertaireet juvenile. De plus, lesmaladiessystemiquesqui affectent le parodonteet leslesionsoralescommunement trouveeschez lesjeunesenfantssont reprises. La frequenceglobale, les caracteristiques du diagnostic, la microbiologie, les facteurs de lhoteet lapprochetherapeutique dechacu- nedeces entites demaladiesont discutes en profondeur. References AAP (TheAmerican Academy of Periodon- tology) (1989) Consensus report on peri- odontal diagnosis and diagnostic aids. Proceedings of the World Workshop in Clinical periodontics. Chicago: American Academy of Periodontology 1, 231:31. Agarwal, S., Suzuki, J . B. & Riccelli, A. E. 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