Periodontal Diseases in the Child and Adolescent

ISSN 0303-6979

Tae-Ju Oh, Robert Eber and Periodontal diseases in the child Hom-Lay Wang Department of Periodontics/Prevention/ Geriatrics, School of Dentistry, University of and adolescent Michigan, Ann Arbor, MI, USA

Oh T-J, Eber R, Wang H-L: Periodontal diseases in the child and adolescent. J Clin Periodontol 2002; 29: 400–410. C Blackwell Munksgaard, 2002.

Abstract Background: Periodontal diseases are among the most frequent diseases affecting children and adolescents. These include gingivitis, localized or generalized aggressive periodontitis (a.k.a., early onset periodontitis which includes generalized or localized prepubertal periodontitis and juvenile periodontitis) and periodontal diseases associated with systemic disorders. The best approach to managing periodontal diseases is prevention, followed by early detection and treatment. Methods: This paper reviews the current literature concerning the most common periodontal diseases affecting children: chronic gingivitis (or dental plaque-induced gingival diseases) and early onset periodontitis (or aggressive periodontitis), including prepubertal and juvenile periodontitis. In addition, systemic diseases Key words: periodontal disease; children; that affect the periodontium and oral lesions commonly found in young children pedodontics; early onset periodontitis; are addressed. The prevalence, diagnostic characteristics, microbiology, host- aggressive periodontitis; localized juvenile periodontitis related factors, and therapeutic management of each of these disease entities are thoroughly discussed. Accepted for publication 15 May 2001

Dental clinicians must be adept at diag- The nomenclature and classification shop classification system includes a nosis and management of periodontal systems we use to describe periodontal greater variety of disease categories that disease in children and adolescents. disease have changed periodically over base the diagnosis on clinical history Periodontal diseases are not limited to the past few decades. This leads to some and findings, relying less on age of on- adults. On the contrary, periodontal confusion when one reviews past litera- set as a major criterion (Table 1). diseases are prevalent among children ture about disease prevalence, treat- This paper primarily follows the and adolescents. For example, gingivitis ment, etc. The Consensus Report of the classification of periodontal disease affects more than 70% of children older 1989 World Workshop in Clinical Peri- from the 1989 World Workshop in Clin- than seven years of age (Page & Schro- odontics used the following criteria to ical Periodontics (AAP 1989) when de- eder 1982, Stamm 1986). Bimstein distinguish various forms of peri- scribing conditions because most clini- (1991) stressed the importance of pre- odontitis: (1) age of onset; (2) rate of cians are familiar with it. For each con- vention, early diagnosis and early treat- disease progression; (3) distribution of dition, we also include the International ment of periodontal diseases in children affected sites; (4) presence or absence of Workshop in Periodontics classification and adolescents because (1) the preva- systemic medical conditions; (5) pres- (Armitage 1999) parenthetically to in- lence of and severity of periodontal dis- ence or absence of specific microbial or troduce readers to the new system and eases are high; (2) incipient periodontal host factors; and (6) response of the dis- to highlight the changes between the diseases in children may develop into ease to therapy (American Academy of two. advanced periodontal diseases in Periodontology: AAP 1989). The classi- The aim of this paper is to review the adults; (3) there is association between fication (AAP 1989) was simplified by current literature concerning the most periodontal and systemic diseases; (4) the Consensus Report of the First common periodontal diseases affecting patients, families, or populations at risk European Workshop on Periodonto- children: chronic gingivitis and early may be identified and included in logy (Attström & van der Velden 1994), onset periodontitis, including prepuber- special prevention or treatment pro- and more recently, a new classification tal and juvenile periodontitis. In ad- grams; and (5) prevention and treat- of periodontal diseases and conditions dition, systemic diseases that affect the ment of most periodontal diseases are was presented at the 1999 International periodontium and oral lesions com- relatively simple and very effective, pro- Workshop on Periodontics (Armitage monly found in young children will be viding lifetime benefits. 1999). The 1999 International Work- addressed. Periodontal diseases in children 401

Table 1. Classifications of periodontitis brushes and antibacterial mouthrinses The 1989 World Workshop in Clinical Periodontics may be useful adjuncts to standard I. Adult periodontitis toothbrushing and flossing for children II. Early-onset periodontitis who are physically challenged, such as A. Prepubertal periodontitis (generalized, localized) children with Downs syndrome, and for B. Juvenile periodontitis (generalized, localized) children undergoing orthodontic care C. Rapidly progressive periodontitis (Trombelli et al. 1995, Grossman & III. Periodontitis associated with systemic disease Proskin 1997, Boyd 1989). IV. Necrotizing ulcerative periodontitis Steroid hormone-related gingivitis is V. Refractory periodontitis associated with elevated sex hormone The 1994 First European Workshop on Periodontology levels that amplify clinical inflamma- I. Early onset periodontitis tory changes of gingivitis (Suzuki II. Adult periodontitis 1988). Increased levels of estrogen and III. Necrotizing periodontitis progesterone during pregnancy (Löe The 1999 International Workshop on Periodontology 1965), during puberty, or in patients I. Gingival diseases medicated with oral contraceptives II. Chronic periodontitis (Kalkwarf 1978) have been reported to III. Aggressive periodontitis IV. Periodontitis as a manifestation of systemic diseases result in increased gingival vascularity V. Necrotizing periodontal diseases and inflammation. Removal of local VI. Abscesses of the periodontium factors is the key to the management of VII. Periodontitis associated with endodontic lesions steroid hormone-related gingivitis; VIII. Developmental or acquired deformities and conditions however, it is often necessary to surgic- ally excise unresolved gingival overgrowth. Drug-influenced gingival enlargement increase in gingival activity from early has been observed in patients taking (I). Chronic Gingivitis (Dental Plaque- childhood to adult age. Previously, cyclosporin, phenytoin and calcium induced Gingival Diseases) Matsson (1978) performed a 21-day ex- channel blockers, with higher preva- Chronic gingivitis is the most common perimental gingivitis study comparing 6 lence in children (Mariotti 1999, Seym- periodontal infection among children, children, aged 4 to 5 years, with 6 den- our et al. 2000). Gingival enlargement and adolescents. These may include tal students, aged 23 to 29 years. They was reported in 30% of patients taking plaque-induced chronic gingivitis (the found that the children developed gin- cyclosporin (Seymour & Heasman most prevalent form), steroid hormone givitis less readily than the adults. After 1992), 50% of patients taking phenytoin related gingivitis, drug-influenced gin- 21 days without plaque removal, the (Hassell 1981), and 15% of patients tak- gival overgrowth, and others. It is char- children had less gingival exudate and ing calcium channel blockers such as acterized by inflammation of the mar- a lower percentage of bleeding sites nifedipine (Lederman et al. 1984), vera- ginal gingiva without detectable loss of than the adults. Also, the children had pamil (Pernu et al. 1989), and amlodipi- bone or connective tissue attachment. a smaller increase in gingival crevicular ne (Seymour et al. 1994). Gingival en- The initial clinical findings in gingivitis leukocytes than the adults in response largement starts in the interdental pa- include redness and swelling of mar- to plaque accumulation. The study pilla region and spreads to involve the ginal gingiva, and bleeding upon prob- hypothesized that children may have a marginal gingiva. In severe cases the en- ing. As the condition persists, tissues different vascular response than adults. larged gingiva may cover the incisal and that were initially edematous may be- Gingivitis does not always progress occlusal surfaces of the teeth (Chapple come more fibrotic. Gingival margins, to periodontitis, but periodontitis is 1996). Histologically, the overgrowth is normally knife-edged in contour, may preceded by gingivitis. According to fibroepithelial in nature, with epithelial become rolled, and interdental papillae Marshall-Day et al. (1955), gingivitis acanthosis, increased numbers of may become bulbous and enlarged. without evidence of bone loss was con- fibroblasts and increased collagen pro- Probing depths may increase if signifi- fined to a younger age group, and bone duction. The severity of gingival en- cant hypertrophy or hyperplasia of the loss without gingival alterations was largement is closely related to the level gingiva occurs. rarely found. of plaque control, and therefore reduc- Histologically, ulceration of the sul- Plaque-induced chronic gingivitis is tions in dental plaque can limit the se- cular epithelium and inflammatory cell commonly found in young children and verity of the lesion (Mariotti 1999). infiltration of the underlying connective can be managed by mechanical removal Treatment of drug-influenced gingi- tissue characterize gingivitis. At the of plaque and high levels of oral hy- val enlargement should start with oral microscopic level, T-lymphocytes pre- giene. The etiologic nature of plaque in hygiene instructions, and scaling and dominate in children (Seymour et al. gingivitis was demonstrated by experi- polishing of the teeth to remove bac- 1981) whereas B-cells predominate in mental gingivitis studies in humans terial deposits. This may require several adults (Page & Schroeder 1976). (Löe et al. 1965, Theilade et al. 1986). visits. 2¿ daily chlorhexidine rinses Matsson & Goldberg (1985) sug- Therefore, dentists and dental hygien- (Lang et al. 1982) should be prescribed gested that there is no clear-cut age at ists must educate parents and their when normal brushing and flossing do which the gingival reaction to bacterial children about the importance of oral not achieve the desired level of plaque insult in children becomes similar to hygiene in the prevention of caries and control. Gingivectomy or gingivoplasty that in adults. However, there is gradual periodontal diseases. Electric tooth- may be needed to correct gingival con- 402 Oh et al. tours for hygienic and esthetic reasons. calized and can affect both primary and remain to infect the area or neighboring The patient and parent should be told mixed dentition. Onset occurs between area during eruption of the permanent that gingival enlargement may recur the eruption of the primary dentition teeth, subsequent infection of newly after surgery, and that immaculate and puberty. PP is characterized by se- erupted permanent teeth may occur. home plaque control and regular peri- vere gingival inflammation, rapid bone The coexistence of A.a. in lesions of odontal maintenance are the key to de- loss, tooth mobility, and tooth loss. Su- both PP and localized juvenile peri- creasing the likelihood or severity of re- zuki (1988) reported that PP patients odontitis (LJP) (Zambon et al. 1983) currence. In addition, the patient’s are usually between ages 5 and 8, they may explain the possibility. However, physician should be consulted to deter- have low caries rates, and there is no the possible mechanism of disease pro- mine if the patient could be switched to sex predilection. Page et al. (1983) first gression needs to be re-evaluated since a medication that does not cause gingi- described ‘‘prepubertal periodontitis’’ not all PP develops into JP. val enlargement. The dentist should as a disease entity and further subdi- Although the primary etiology re- never recommend that a patient discon- vided it into a localized form of PP mains bacterial plaque, other factors tinue or change medications without (LPP) and a generalized form of PP may predispose otherwise healthy pa- medical consultation. (GPP). This was based on the clinical tients to PP. These may include ce- description of only three and two cases, mentum defects (Page & Baab 1985), respectively. Diagnostic characteristics functional defects in leukocyte chemo- (II). Early Onset Periodontitis (New for prepubertal periodontitis are listed taxis (Page et al. 1983), and/or presence Classification: Aggressive in Table 2. of bacteriophage (Watanabe 1990). It Periodontitis) Pathogenic bacteria that have been has been generally recognized that GPP Characteristics of early onset peri- associated with PP include Actino- and leukocyte adhesion deficiency odontitis include onset before age 35 bacillus actinomycetemcomitans (A.a.), (LAD) are related. Waldrop et al. years, rapid disease progression, some- Prevotella intermedia (P.i.), Capnocyto- (1987) demonstrated that the molecular what different distribution of lesions phaga species (Delaney & Kornman basis of GPP was leukocyte adhesion than in adult periodontitis, and distinct 1987, Sweeney et al. 1987), Porphyro- deficiency by using monoclonal anti- etiologic characteristics. monas gingivalis (P.g.) (Mishkin et al. bodies against Mac-1, LFA-1, and 1986), and Eikenella corrodens (E. p150,95 surface adhesion molecules. On corrodens) (Delaney & Kornman 1987). the other hand, immunological data 1. Prepubertal periodontitis (PP) (new Delaney & Kornman (1987) found an about LPP have shown that a neutro- classification: aggressive periodontitis) increased proportion of black-pig- phil or monocyte chemotaxis defect, The prevalence of PP ranges from mented anaerobic rods, E. corrodens, but not both, exists in LPP patients. 0.84% to 26.9%, based on a limited Capnocytophaga species, A.a., and Fu- Systemic diseases associated with pre- number of case reports (Jamison 1963, sobacterium nucleatum (F. nucleatum) pubertal periodontitis (new classifi- Sweeney et al. 1987, Bimstein et al. in the cultivable flora in LPP patients cation: periodontitis as a manifestation 1988). Variation in the reported preva- compared to controls. Studies have of systemic diseases) may include insu- lences of PP may depend on genetic fac- tried to determine whether PP ulti- lin dependent diabetes mellitus tors, methodological factors, and the mately progresses to juvenile peri- (IDDM), Papillon-Lefe`vre syndrome, selection of non-random sample popu- odontitis (JP). According to Watanabe hypophosphatasia, neutropenia, Ched- lations (Watanabe 1990). Prepubertal (1990), if pathogenic bacteria around iak-Higashi syndrome, leukemias, periodontitis may be generalized or lo- the deciduous dentition in PP patients histiocytosis X, acrodynia, acquired immunodeficiency syndrome (AIDS), Down syndrome, and leukocyte ad- Table 2. Diagnostic characteristics of prepubertal periodontitis hesion deficiency. Localized prepubertal periodontitis (LPP) Insulin dependent diabetes mellitus O Onset: around 4 years of age or older (IDDM, Juvenile DM) is a relative or O Affected teeth: either few or many teeth absolute decrease in insulin secretion or O Gingival manifestation: minor inflammation, if any availability, caused by a genetic defect O Microbial plaque: minimal O in pancreatic beta cell productivity, de- Alveolar bone destruction: faster than adult periodontitis but much slower than fective insulin release mechanisms generalized form of PP (Johnes & Mason 1980) or by destruc- O Functional defects: either neutrophils or monocytes but not both O tion of beta cells (Jackson & Guthrie Otitis media and upper respiratory infections in some cases O Amenable to mechanical and antibiotic therapy 1986). Bernick et al. (1975), Gislen et al. (1980), and Cianciola et al. (1982) Generalized prepubertal periodontitis (GPP) studied the association between juvenile O Onset: at the time of tooth eruption O diabetes and periodontal diseases in Affected teeth: all primary teeth; the permanent dentition may or may not be affected O Gingival manifestation: fiery red gingiva with acute inflammation around all teeth; young children. Bernick et al. (1975) gingival proliferation, cleft formation, and recession examined 50 diabetic children and 36 O Alveolar bone destruction: rapid healthy control children who were O Functional defects: both neutrophils and monocytes matched for age and oral hygiene sta- O Absence of PMNs in the gingival tissue and marked increase in peripheral blood white tus. They found that gingival inflam- cell count mation was more prevalent in the dia- O Otitis media and upper respiratory infections in most cases O betic group. Furthermore, Gislen et al. Refractory to mechanical and antibiotic therapy (1980) showed that diabetic children Periodontal diseases in children 403 with poor metabolic control appeared blood is below 1000/mm3 in infants, be- terial infections in histiocytosis X pa- to have greater gingival index scores low 1000/mm3 or 1500/mm3 in children, tients may result from PMN defects than children without diabetes. Cianci- and below 1800/mm3 in adults. Neutro- (Tomooka et al. 1986) or decreased ola et al. (1982) investigated prevalence penias associated with oral manifes- monocyte function (Kragballe et al. of periodontal disease in IDDM in 263 tations in children include agranulo- 1981). IDDM patients and 208 control sub- cytosis (malignant neutropenia, rare in Acrodynia is a rare disease character- jects. For children between 11 and 18 children), cyclic neutropenia, chronic ized by a wide variety of clinical signs years old, 9.8 % of the IDDM patients benign neutropenia of childhood, including gingival and mucosal hyper- showed signs of periodontitis versus chronic idiopathic neutropenia, and plasia, alveolar bone loss with early loss only 1.7% of the controls. They found familial benign neutropenia. Prichard et of primary teeth, loss of hair, abnormal no periodontitis in children 10 years old al. (1984) and Cohen & Morris (1961) cramps, profuse sweating and sali- or younger in either group. The article reported that cyclic neutropenia was as- vation, and gastrointestinal upsets. argues that probing alone is not suf- sociated with severe gingivitis with ul- Etiology of acrodynia is known to be a ficient to assess periodontitis, particu- ceration and frequent history of recur- mercurial toxicity reaction, either actual larly when applied to the mixed den- rent infections such as otitis media and mercury poisoning or, more likely, an tition. Adjunctive use of radiographs upper respiratory infection. idiosyncracy to mercury (Warkany & was recommended for the assessment of Chediak-Higashi syndrome is a rare Hubbard 1948). periodontitis in children. IDDM pa- autosomal recessive disease associated Acquired immunodeficiency syndrome tients have also been shown to have a with impaired function of cytoplasmic (AIDS) develops as a result of infection reduced PMN response to chemotactic microtubules or microtubule assembly with the human immunodeficiency vi- stimuli (Miller 1972). in PMNs. Diagnostic features include rus (HIV). Children with AIDS may de- Papillon-Lefe`vre syndrome (PLS) is characteristic, abnormally large gran- velop an atypical form of acute necrot- a genetic condition inherited as an ules in granulocytes. According to izing ulcerative gingivitis (ANUG) autosomal recessive trait, characterized Clawson et al. (1978), PMN chemo- (Leggott 1987); however, no reports of by hyperkeratosis of the palms of the tactic defects in Chediak-Higashi syn- prepubertal pediatric AIDS patients hands and soles of the feet and early drome may be due to mechanical inter- presenting with alveolar bone loss exist. onset periodontitis (Johnes & Mason ference in deformability by the giant Down’s syndrome (Trisomy 21 syn- 1980). Severe periodontitis can affect cytoplasmic granules. Moreover, im- drome; Mongolism) is a common and both the primary and permanent den- paired microtubule assembling function easily recognizable chromosomal aber- titions (Smith & Rosenzweig 1967, Gor- (Oliver 1976) and hyperadhesiveness ration. The dentition exhibits a number lin et al. 1964). The prevalence of PMN (Keller et al. 1984) were suggested as of characteristic anomalies including chemotactic defects in the PLS patients the mechanism for PMN chemotactic malformation of the teeth, enamel hy- remains controversial. defects. poplasia, and microdontia. Other com- Hypophosphatasia is a genetic dis- Leukemias are characterized by pro- mon oral manifestations include macro- order. Diagnostic findings include low gressive uncontrolled proliferation of glossia, fissured or pebbly tongue, and levels of serum alkaline phosphatase white blood cells and classified into a high arched palate. Due to a defective and excretion of phosphoethanolamine, acute and chronic lymphocytic leukem- immune system, rampant and pre- the substrate for alkaline phosphatase, ia, acute and chronic granulocytic leu- cocious periodontal disease is prevalent. in the urine. The disorder can be classi- kemia, acute and chronic monocytic Barr-Agholme et al. (1998) compared fied into 3 types: (1) infantile, an auto- leukemia, and other rare forms such as 20 Down’s syndrome patients, aged 9 to somal recessive condition occurring be- plasma cell leukemia. Oral manifes- 21 years, with 19 healthy controls and fore 6 months of age (the most severe tations of leukemias in children are gin- reported that gingival inflammation, form); (2) childhood, an autosomal re- gival hemorrhage, petechiae, lymph- probing depth, calculus, and marginal cessive or autosomal dominant con- adenopathy, gingival hyperplasia or bone loss were significantly greater in dition occurring after 6 months of age; hypertrophy, and gingival pallor. the Down’s syndrome group. No sig- and (3) adult hypophosphatasia, an Bender (1944) and Deasy et al. (1976) nificant differences were found between autosomal dominant condition that is reported association between peri- the two groups, regarding levels of the least severe form (Watanabe 1990). odontal disease and leukemia in serum IgA, IgG2, IgG3, IgG4, IgM, or The most consistent clinical sign is children. albumin. However, the proportion of premature loss of deciduous teeth (Fal- Histiocytosis X represents a disturb- IgG1 in total IgG was significantly lon et al. 1984). The teeth may have ance of the reticulo-endothelial system. higher in the Down’s syndrome group large pulp chambers, and skeletal de- It results from the proliferation and dis- compared to the control group. formities may occur. Baer & Benjamin semination of pathological Langerhans Leukocyte adhesion deficiency (1974) claimed that only deciduous cells and includes three disorders: Let- (LAD) is a genetic disease inherited as teeth are generally affected. Baab et al. terer-Siwe disease (the most severe form an autosomal recessive condition in (1986) reported normal polymorpho- and usually occurs in infants or before which the expression of Mac-1, LFA-1, nuclear leukocyte (PMN) chemotaxis age 3); Hand-Schuller-Christian disease and p150,95 glycoprotein adhesion and abnormal monocyte chemotaxis in (usually occurs before age 5, but can oc- molecules on leukocytes is severely re- 3 children with hypophosphatasia; how- cur in adolescents and even in young duced. Springer et al. (1984) suggested ever, age range was not designated in adults); and eosinophilic granuloma that LAD occurs as a result of a defect the study. (occurs primarily in older children and in the gene that codes for the common Neutropenia is a disorder in which young adults) (Hartman & Colonel beta subunit of cell surface integrins the number of PMNs in the peripheral 1980). Increased susceptibility to bac- which are required for leukocyte diap- 404 Oh et al.

Table 3. Diagnostic characteristics of juvenile periodontitis and 1.3% of white adolescents had EOP. Localized juvenile periodontitis (LJP) Hørmand & Frandsen (1979) explained O Onset: around puberty that the higher incidence of LJP in fe- O Affected teeth: permanent incisors and/or first molars males could result from an earlier oc- O Associated microorganism: Actinobacillus actinomycetemcomitans currence of the disease in females. Stab- O Greater prevalence in blacks holz et al. (1998) reported a high preva- O Neutrophil dysfunction and high IgG2 response O lence of LJP in an Israel population Familial distribution consisting of 86 individuals from 30 Generalized juvenile periodontitis (GJP) families, aged 12 to 20 years. Out of 86 O Onset: during late teen years subjects, 33 individuals from 15 families O Affected teeth: generalized involvement of permanent teeth O showed LJP (38.4%), but none of the Associated microorganism: not clear (P. gingivalis may be involved) subjects showed signs of generalized O Greater prevalence in blacks O juvenile periodontitis. Except for two Neutrophil dysfunction O Familial distribution pairs of families with genetic ties, no familial connections could be traced between the different nuclear families affected by LJP, and there were no dif- edesis. Because emigration of PMNs thia and alveolar bone resorption, but ferences in oral hygiene status between from blood vessels is dependent upon no pathology in gingival tissues. Later, LJP and non-LJP groups. The study adhesion of PMNs to endothelial cell the degenerative process was termed suggests that environmental factors surfaces, patients with LAD have a periodontosis (Orban & Weinmann may influence the occurrence of LJP. poor response to bacterial infections. 1942), who described three stages of the The microflora associated with JP is Therefore, these children are plagued disease: degeneration of PDL fibers; mainly composed of Gram-negative, with recurrent bacterial infections and proliferation of the junctional epithel- capnophilic, and anaerobic rods (Slots impaired wound healing. Patients with ium; and the development of deep 1979, Newman & Socransky 1977). this rare disease present with extremely infrabony pockets. The term ‘‘peri- Actinobacillus actinomycetemcomitans acute inflammation, proliferation of the odontosis’’ was favored by Baer (1971). (A.a.), a Gram-negative, non-motile, gingival tissues, and rapid bone loss. In his article, the disease entity was di- coccobacillus has been well documented An association between generalized pre- vided into two categories, a localized in relation to LJP (Newman & Socran- pubertal periodontitis and LAD was form affecting the first molars and in- sky 1977, Slots et al. 1980, 1982, Korn- demonstrated by Waldrop et al. (1987) cisors, and more generalized form af- man & Robertson 1985). Asikainen et and Page et al. (1987). fecting most of dentition. The term al. (1991) examined A.a. isolates from Treatment for PP has ranged from ‘‘juvenile periodontitis’’, introduced by subgingival sites in 136 subjects in Fin- scaling and root planing or curettage, Butler (1969), accurately describes the land and found that among five sero- with or without systemic antibiotics, to disease as an inflammatory process. types of A.a., serotype b was predomi- the extraction of involved teeth (Watan- Waerhaug (1977) described that the pri- nant in LJP and adult periodontitis, abe 1990). The generalized form, unfor- mary etiology of the disease is subgingi- whereas serotype c predominated in tunately, does not respond as favorably val bacterial plaque. The plaque front is healthy individuals. Wilson & Hamilton to treatment as the localized form. The consistently located within 0.2 mm to (1992) also demonstrated that black majority of cases have been treated by 1.5 mm from the border of loss of subjects with LJP responded to A.a. extraction of involved deciduous teeth attachment. The plaque grows with a serotype b serospecific antigens by the and permanent teeth. Since these pa- faster speed of 3 to 5 microns a day in production of IgG antibodies of the tients may have associated LAD and this disease compared to 0.2 to 1.0 mm IgG2 subclass. Lu et al. (1993, 1994) may be undergoing antibiotic therapy a day in ordinary cases. Diagnostic confirmed this by demonstrating that for recurrent serious infections, it is characteristics of juvenile periodontitis IgG2 was markedly elevated over all necessary to have a consultation with are illustrated in Table 3. other Ig classes reactive with A.a. sero- the treating physician. Estimates of the prevalence of JP type b. Albandar et al. (1997b) found vary from 0.1% to 15% (Sjödin et al. that EOP patients had higher preva- 1993, Hart et al. 1993, Saxeń 1980, lence and levels of P.g., P.i., F. nucleat- 2. Juvenile periodontitis (JP) (new Löe & Brown 1991, Neely 1992), with um., C. rectus, and T. denticola com- classification: aggressive periodontitis) differences attributed to varying cri- pared to healthy controls. P.g., T. Juvenile periodontitis, formerly called teria, geographics, and a diverse data denticola, and P.i., in descending order periodontosis, occurs in children and base. Reports show greater prevalence of importance, were significantly associ- teenagers who are otherwise healthy in African-Americans than in Caucasi- ated with the generalized and/or rapidly and is characterized by a rapid alveolar ans (Burmeister et al. 1984, Löe & progressing disease. bone loss in one or more teeth of the Brown 1991, Melvin et al. 1991). Al- Reports indicate that JP patients permanent dentition (Baer 1971). Ter- bandar et al. (1997a) estimated preva- have defects in neutrophil chemotaxis minology for this disease entity has re- lence of EOP (JP) in a group of school- or phagocytosis (Cianciola et al. 1977, peatedly changed. Gottlieb et al. (1923) children, aged 13 to 17 years, based on Clark et al. 1977, Van Dyke et al. 1987, first described this condition ‘‘diffuse the data of a national survey conducted Suzuki et al. 1984, Kimura et al.1992, atrophy of the alveolar bone.’’ His find- during the 1986–1987 school year. They etc.). Neutrophils in LJP patients have ings in this case included widened peri- showed that approximately 10.0% of fewer receptors on their plasma mem- odontal ligament (PDL), cementopa- African-American, 5.5% of Hispanic, brane for certain chemotaxis-inducing Periodontal diseases in children 405 factors, such as FMLP, C5a, and of A.a. were not significantly reduced by olution of intrabony defects than the GP110 (Van Dyke et al. 1981, 1983, scaling and root planing alone. How- groups that received FDBA alone or 1987). Agarwal et al. (1994) further sug- ever, after flap surgery, the levels of A.a. debridement alone with/without sys- gested that cytokines, such as tumor ne- were significantly reduced, suggesting temic tetracycline. Contrary to these crosis factor (TNF) and interleukin-1 that surgery and/or antibiotics are findings, DiBattista et al. (1995) found (IL-1), present in the serum of LJP pa- necessary to reduce levels of A.a. in no statistically significant differences tients are responsible for priming and young patients with severe generalized between flap debridement alone and inducing altered response in neutro- periodontitis. This result was in agree- various regenerative procedures in 7 phils. In the study, it was found that ment with other studies (Slots & Ro- LJP patients. All patients in this study treatment of neutrophils in healthy sub- sling 1983, Lindhe & Liljenberg 1984, received systemic doxycycline. The re- jects with LJP-sera resulted in a de- Kornman & Robertson 1985). generative procedures utilized were creased neutrophil chemotactic re- Young individuals generally have ex- ePTFE membranes, ePTFE plus root sponse and down regulation of FMLP cellent healing potential. Therefore, in conditioning with doxycycline solution receptors on the cell surface. On the JP patients the combination of systemic (pH: 2.5), and ePTFE π root con- other hand, pretreatment of LJP-sera antibiotics and regenerative surgery is ditioning π composite graft. with anti-TNF and anti-IL-1 antibodies often successful in treating intrabony Based upon the contradictory results, effectively neutralized the ability of defects and early furcation involvement. it is apparent that the results achieved LJP-sera to modulate chemotaxis and Mattout and Roche (1984) found com- with regenerative procedures will vary FMLP receptor levels in healthy sub- plete fill of furcations and significant depending on case selection, the pro- jects. Sigusch et al. (1998) found that supracrestal repair in an 18-year-old JP cedure utilized and operator experience. EOP patients showed reduced expres- patient after treatment with iliac crest Therefore, regenerative procedures sion of monocyte HLA-DR, IFN-g, autografts. Mabry et al. (1985) treated should be selected based on the appro- and IL-2 mRNA, and reduced prolifer- intrabony defects in 16 LJP patients priate selection criteria. ation of peripheral blood monocytes, with a combination of freeze-dried which are known to be positively ex- bone allograft (FDBA) and tetracy- (III). Common Intraoral Lesions pressed by activated TH1 cells. This in- cline. The group that received systemic dicates an impaired TH1 cell response tetracycline therapy and local treatment Dental care providers must be familiar in EOP patients. Ozmeric et al. (1998) with a mixture of tetracycline powder with oral lesions that are commonly further suggested that the IL-8, a and FDBA had significantly better res- found in pediatric patients. The 6 most chemoattractant, produced by LJP patients may be less active than in healthy individuals. Table 4. Therapeutic management of common pediatric oral lesions The etiology of JP can be broadly di- vided into two categories, bacterial Primary herpetic gingivostomatitis O Topical anesthetics/coating agents: plaque and impaired host defense – 1 to 1 mixture of diphenhydramine (Benadryl) elixir & Maalox [OTC] mechanism; therefore, the treatment – diphenhydramine (Benadryl)/lidocaine/Maalox mouth rinse should aim to control pathogenic mi- – Acyclovir elixir croflora and compensate for impaired O Systemic acyclovir antiviral therapy immune function. Systemic approaches Recurrent herpes simplex such as antibiotic therapy are often in- O Avoidance of perpetuating factors dicated in the management of JP. In O Acyclovir (Zovirax) 5% ointment or elixir fact, several studies (Slots & Rosling O Systemic acyclovir as active treatment or prophylaxis for immunosuppressed patients 1983, Christersson et al. 1985, Korn- Recurrent aphthous stomatitis man & Robertson 1985) showed that O Topical anesthetics/coating agents: Zilactin-B [OTC], Orabase-B [OTC], or Oraloe [OTC] scaling and root planing alone failed to O Antimicrobial mouthrinses: 0.12% chlorhexidine gluconate suppress or eliminate A.a. from the dis- O Topical steroids: triamcinolone (Kenalog) in orabase 0.1%, betamethasone valerate 0.1% eased site and failed to improve clinical ointment, dexamethasone (Decadron) elixir 0.5 mg/5ml, or fluocinonide (Lidex) gel 0.05% conditions. Treatment modalities in the Candidiasis management of JP include mechanical O Topical antifungal agents: therapy, such as scaling and root plan- – Nysatin (Mycostatin) oral suspension 100,000 units/ml or popsicles ing and periodontal surgery, local deliv- – Clotrimazole (Mycelex) troches or swabs ery of antimicrobials, and systemic O Antimicrobial mouthrinses: 0.12% chlorhexidine gluconate antibiotics such as tetracycline, doxycy- Angular cheilitis cline, metronidazone, combination of O Topical antifungal agents: nystatin or clotrimazole ointment metronidazole and amoxicillin, or com- O Topical antifungal/steroid agent: nystatin/triamcinolone acetonide (Mucolog II) ointment bination of metronidazole and Aug- O Topical antifungal/antibacterial/steroid agent: hydrocortisone/iodoquinol (Vytone) cream mentin (amoxicillin π clavulanic acid). 1% Gunsolley et al. (1994) compared Geographic tongue nonsurgical and surgical periodontal O Topical anesthetic/analgesic mouth rinse: Ulcer-Ease [OTC] treatment in 23 young patients with se- O Topical antifungal/steroid agent: triamcinolone acetonide 0.1% in nystatin suspension O Alkaline saline mouth rinse vere generalized periodontitis. They O found that P.g. was virtually eliminated Topical anesthetics/coating agents: 1 to 1 mixture of diphenhydramine (Benadryl) elixir & by scaling and root planing while levels Maalox [OTC] 406 Oh et al. commonly found pediatric oral lesions Vesicles often develop at the same site adults on long-term antibiotics or ster- are: primary herpetic gingivostomatitis, and are usually present in small clusters oid therapy are frequently affected. In recurrent herpes simplex infection, re- following the distribution of the infected addition, individuals with diabetes, hy- current aphthous stomatitis, diffuse in- nerve. In healthy individuals, the disease poparathyroidism, immunodeficiency, traoral candidiasis, angular cheilitis, is limited to periosteal-bound, keratiniz- or those undergoing chemotherapy are and geographic tongue. Table 4 sum- ed mucosa whereas recurrences in the also often affected. Particularly, marizes the therapeutic management of buccal mucosa and tongue may develop children and adolescents with HIV-in- each of these conditions. in immunocomprimised patients. The fection are predisposed to the develop- lesions are most frequently seen as her- ment of oral candidiasis (Flaitz & Hicks pes labialis, where lesions occur at the 1999). Like other forms of Candida in- Primary herpetic gingivostomatitis (PHG) vermillion border of the lip. fection, such as angular cheilitis and The primary etiology of this disease is geographic tongue, the lesions can be herpes simplex virus (HSV) type 1. managed by both topical and systemic Recurrent aphthous stomatitis (RAS) Viral transmission may occur via oral- treatment with antifungal medications, genital or oral-oral direct mucocutane- RAS is the most common oral mucosal such as Nystatin ointment. ous contact of infected secretions. The disease in North America (Murray & initial infection of PHG primarily af- Amedee 2000). Approximately 20% of fects children under 10 years of age with population experiences minor apthae, Angular cheilitis a peak incidence at 2–4 years of age, which is the most common form of and secondarily young adults, aged 15 childhood RAS (Field et al. 1992). Angular cheilitis, perleche, is a painful to 25 years (Main 1989). The incuba- These ulcerative lesions are often re- condition beginning as an inflammation tion period of HSV infection ranges ap- ferred as ‘‘canker sores’’ by the patient. of the commissure of the lips, followed proximately 3 to 10 days. Clinical mani- RAS lesions range from occasional by erosion, ulceration, and fissuring. It festations include fever, malaise, irrita- small (0.5 to 1.0 cm in diameter), well- is known to be associated with Candida bility, lymphadenopathy, widespread defined round or ovoid shallow ulcers albicans and Staphylococcus aureus. inflammation in the marginal and at- with a gray-yellowish central area sur- The possible predisposing factors may tached gingiva, and small clusters of rounded by an erythematous halo to include immunodeficiency, riboflavin vesicles throughout the mouth. The ves- larger (1 to 3 cm in diameter) oval or (vitamin B2) deficiency, trauma, and icles often coalescence and burst, form- irregular ulcers. Small lesions heal in 7 loss of vertical dimension. According to ing large ulcers. It often causes severe to 10 days without scarring whereas Flaitz & Hicks (1999), oral candidiasis, pain and debilitation. Consequently, larger lesions persist for weeks and heal including angular cheilitis, is the most mastication and swallowing may be too with scarring (Eversole 1989). The common oral manifestation in HIV-in- painful, resulting in dehydration. This etiology is unknown, yet suggested fected children. Treatment may include can be managed by supportive treat- etiologies include the L-form of strepto- removal, if possible, of predisposing ment with high oral fluid intake or in- coccus and/or an immunopathic pro- factors and application of antifungal travenous fluid infusion (Dohvoma cess involving cell-mediated cytolytic medications. 1994). PHG is a contagious disease that activity in response to HLA or foreign usually regresses spontaneously within antigens. Precipitating factors may in- 12 to 20 days. Amir et al. (1997) re- clude trauma, stress, menstruation, nu- ported that acyclovir oral suspension tritional deficiencies, food allergies, and Geographic tongue (benign migratory glossitis) treatment (15 mg/kg 5 times a day) for endocrinopathies. In children with herpetic gingivostomatitis, started Behcet’s disease and HIV infection, Geographic tongue is a benign in- within 3 days of onset, significantly re- RAS lesions are frequently found flammatory condition that is character- duced the duration of clinical manifes- (Krause et al. 1999, Ramos-Gomez et ized by desquamation of superficial tations and infectivity of affected al. 1999). Clinical management of RAS keratin and the filiform papillae. It af- children. may include mouthrinses such as chlor- fects approximately 1 to 2% of popula- hexidine gluconate, topical cortico- tion. Kleinman et al. (1994) reported steroids, topical tetracyclines, immuno- 0.6% prevalence of geographic tongue Recurrent herpes simplex (RHS) modulators, and others (Porter et al. in 39,206 U.S. schoolchildren, aged 5– Following primary infection by herpes 1998). 17 years. The etiology is unknown, but simplex virus, the virus ascends through correlation with nutritional deficiencies sensory or autonomic nerves and per- and/or emotional stress has been sug- Candidiasis sists in neuronal ganglia. It becomes gested. The condition is often restricted dominant within the nucleus and is pres- Candidiasis is the most prevalent my- to the dorsum and lateral borders of the ent as a latent HSV (Corey & Spear cotic infection in the oral mucosa. It is tongue. Sometimes these usually benign 1986). In about 30 to 40% of population, caused by an overgrowth of a superficial lesions can become symptomatic ex- secondary manifestations may occur as fungus, Candida albicans, opportunistic hibiting a burning sensation. Palliative a result of precipitating factors such as fungus found in the oral cavity, gastro- treatment, including avoidance of acidic sunlight, trauma, fever, immunosup- intestinal tract, and vagina. Clinically, and spicy foods and drinks is advisable pression, or stress. These secondary it appears as diffuse, curdy, or velvety for those cases exhibiting symptoms. manifestations are recurrent herpes la- white mucosal plaques that can be wip- Topical and systemic antihistamine may bialis, herpes genitalis, ocular herpes, ed off. Infants whose mothers display be used to manage the lesions of geo- and herpes encephalitis (Park 1988). vaginal thrush at the time of birth and graphic tongue (Sigal & Mock 1992). Periodontal diseases in children 407

rodontitis), einschließlich pra¨pubertale und randomized double blind placebo con- Summary juvenile Parodontitis. Zusa¨tzlich werden sy- trolled study. Br Med J 314, 1800–1803. Periodontal diseases are among the stemische Erkrankungen, die das Parodonti- Armitage, G. C. (1999) Development of a most frequent diseases affecting um und die orale Schleimhaut betreffen und classification system for periodontal dis- bei jungen Kindern gewo¨hnlich gefunden eases and conditions. Ann Periodontol 4, children and adolescents. Dental clini- werden, behandelt. Die Pra¨valenz, die dia- 1–6. cians must be aware of the prevalence, gnostischen Merkmale, die Mikrobiologie, Asikainen, S., Lai, C. C., Alaluusua, S. & diagnostic characteristics, micro- die Wirtsfaktoren und das therapeutische Slots, J. (1991) Distribution of Actino- biology, host-related factors, and thera- Management von jeder dieser Erkrankungen bacillus actinomycetemcomitans serotypes peutic management of each of these dis- werden gru¨ndlich diskutiert. in periodontal health and disease. Oral ease entities. It is well known that the Microbiol Immunol 6, 115–118. primary etiology of periodontal dis- Attström, R. & van der Velden, U. (1994) eases is bacterial plaque. However, pa- Re«sume« Consensus report on epidemiology. Pro- ceedings of the 1st European Workshop on tients affected by early onset peri- Maladies parodontales chez l’enfant et l’ado- periodontology, p. 120. London: Quintess- odontitis (or aggressive periodontitis) lescent ence. Origine: Les maladies parodontales sont par- often present with impaired immune Baab, D. D., Page, R.C., Ebersole, J. J., Willi- mi les maladies les plus fre´quentes affectant function, mainly neutrophil dysfunc- ams, B. L. & Scott, C. R. 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J Periodontol 42, 516– parodontales est la pre´vention suivie par une titis, recurrent herpes simplex, recurrent 519. de´tection prećoce et un traitement. aphthous stomatitis, diffuse intraoral Barr-Agholme, M., Dahllof, G., Modeer, T., Me´thodes: Ce manuscrit revoit la litte´rature candidiasis, angular cheilitis, and geo- Engstrom, P. & Engstrom, G. N. (1998) actuelle concernant les maladies parodonta- graphic tongue should be promptly Periodontal conditions and salivary im- les les plus communes affectant les enfants: munoglobulins in individuals with Down identified and treated if necessary. It is gingivite chronique (ou maladie gingivale in- syndrome. J Periodontol 69, 1119–1123. believed that the best approach to man- duite par la plaque dentair) et parodontite Bender, I. B. (1944) Bone changes in leucem- age periodontal diseases is prevention, prećoce (ou parodontite agressive) incluant ia. Am J Orthodon Oral Surg 30, 556–563. followed by early detection and treat- les parodontites pre´pubertaire et juveńile. De Bernick, S., Cohen, D. D., Baker, L. & Las- ment. To achieve this, profound knowl- plus, les maladies syste´miques qui affectent le ter, L. (1975) Dental disease in children parodonte et les le´sions orales commune´ment edge about periodontics and pedodont- with diabetes mellitus. J Periodontol 46, trouveés chez les jeunes enfants sont reprises. ics as well as intimate periodontal-pe- 241–245. La fre´quence globale, les caracte´ristiques du dodontics interactions are essential. Bimstein, E. (1991) Periodontal health and diagnostic, la microbiologie, les facteurs de disease in children and adolescents. Pedi- l’hoˆte et l’approche the´rapeutique de chacu- atr Clin North Am 38, 1183–1207. ne de ces entite´s de maladie sont discute´sen Acknowledgements Bimstein, E., Delaney, J. J., Sweeney, E. A. profondeur. 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munoglobulin Gsubclass response of local- (1983) Actinobacillus actinomycetem- Address: ized juvenile periodontitis patients to A.a. comitans in human periodontal disease: Hom-Lay Wang Y4 lipopolysaccharide. Infect Immun 60, prevalence in patient groups and distri- Department of Periodontics/Prevention/ 1806–1812. bution of biotypes and serotypes within Geriatrics Zambon, J. J., Christersson, L. A. & Slots, J. families. J Periodontol 54, 707–711. University of Michigan School of Dentistry 1011 North University Avenue Ann Arbor, Michigan 48109-1078 USA Fax: π1 734 936 0374 e-mail: homlay/umich.edu