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Gingivitis and periodontitis in children and adolescents

Gingivitis and periodontitis in children and adolescents
Literature review current through: Sep 2023.
This topic last updated: Jan 28, 2022.

INTRODUCTION — Slowly progressing slight to moderate periodontitis affects most of the adult population, and it often has its incipient beginning in adolescence. Other more severe and rapidly progressing periodontal diseases also are seen occasionally in children, and some of these diseases are signs of systemic diseases or conditions. Definitive diagnosis usually requires a detailed dental examination, including intraoral radiographs and periodontal probing, but signs can be recognized from visual inspection of the gingival and other oral structures.

Periodontal diseases affect the dental supporting structures, primarily the gingiva and alveolar bone (figure 1). They are caused by complex communities of bacteria that grow in a biofilm on the surface of the tooth (dental plaque). Bacteria elicit an inflammatory response that can result in tissue destruction. Both gingivitis and periodontitis occur in children and adolescents. Gingivitis is a reversible dental plaque-induced inflammation limited to the gingiva, and it is common in children as young as five years of age. Periodontitis is usually accompanied by gingivitis but involves irreversible destruction of the supporting tissues surrounding the tooth, including the alveolar bone (figure 1).

Some degree of periodontitis is seen in most adults, in whom periodontitis is a major cause of tooth loss. Slowly progressing forms of periodontitis may not be diagnosed until adulthood. However, they often begin in adolescence and are not detected until destruction of tooth-supporting tissues reaches levels that are easily measured. The more rapidly progressing and rarer forms of periodontitis do produce destruction that is apparent during childhood. The prevalence of these diseases is probably less than 2 percent of the population. (See "Overview of gingivitis and periodontitis in adults" and 'Rapidly progressing (high-grade) periodontitis' below.)

The periodontal examination and the presentation and management of gingivitis and periodontitis in children and adolescents are reviewed here. Other soft tissue lesions, the periodontal manifestations of systemic conditions, and gingivitis and periodontitis in adults are discussed separately. (See "Soft tissue lesions of the oral cavity in children" and "Periodontal disease in children: Associated systemic conditions" and "Overview of gingivitis and periodontitis in adults".)

PERIODONTAL EXAMINATION

Normal findings — The gingival tissues surrounding the teeth in children should appear pink to reddish pink and be firm and resilient. A slight rolling or rounding around the neck of the tooth is normal (picture 1). The root surface of the tooth should be covered by gingiva (with underlying bone), but very little of the crown should be covered. The tooth surface along the gingival margin (gum line) should be free of visible plaque deposits or calculus. The marginal gingiva should be smooth, and no bleeding should be present.

Signs of periodontal disease — Pediatric health care providers should be alert for signs of periodontal disease in children and adolescents. Detailed examination by a dentist is recommended every six months, but several of the signs of periodontal disease are apparent on visual inspection. Heavy plaque (picture 2) or calculus deposits (picture 3); enlargement or edema of the gingival tissues; redness, bleeding, or recession of the gingiva; abnormal change in tooth position; and premature tooth mobility or tooth loss are indications for referral for further evaluation. In addition, smoking status (both tobacco and marijuana) should be determined because smoking is a major risk factor for the development of periodontal disease [1-6]. Less is known about the effects of electronic cigarettes and vaping, but early studies suggest potential risk to periodontal health [7,8]. Patients who smoke or vape should be provided with information about the benefits and methods of quitting. (See "Benefits and consequences of smoking cessation", section on 'Benefits of smoking cessation' and "Management of smoking and vaping cessation in adolescents", section on 'Other sources of behavior support'.)

Calculus, common in adults, is present in approximately 10 percent of children and one-third of adolescents. The typical locations for calculus are the lingual surface of the mandibular incisors (picture 3) and the buccal surface of the maxillary molars. It can be removed only by professional tooth cleaning and should not be allowed to remain on the teeth because it provides a habitat for the bacteria associated with periodontitis. Semiannual tooth cleaning is adequate for most children, but a small number of heavy-calculus formers may require more frequent visits.

GINGIVITIS — Simple gingivitis, characterized by inflammation of the gingival tissues with no loss of attachment or bone (picture 4), is the most common periodontal problem in childhood.

Prevalence — Gingivitis is uncommon in young children with early primary dentition. It is present in up to one-half of the population by the age of four to five years. The prevalence of gingivitis increases with age, peaking at close to 100 percent at puberty (approximately 10 years of age in females and 13 years of age in males). After puberty, the prevalence declines to 50 percent and remains relatively constant into adulthood [9,10].

Pathogenesis — The inflammation responsible for gingivitis occurs in response to the bacteria that live in biofilms at the gingival margin and in the gingival crevice. These biofilm communities are complex. Levels of many species of bacteria are elevated in gingivitis. Gingivitis resolves when plaque is removed consistently.

Young children have less plaque and appear to be less reactive to plaque than are adults; thus gingivitis is not typical in children with early primary dentition. The diminished reaction may be a result of differences in bacterial colonization and developmental changes in the inflammatory response [11].

Predisposing factors — Inadequate removal of dental plaque is the most common cause of gingivitis, although susceptibility varies with the host. Certain local factors, by interfering with oral hygiene, physiology, or homeostasis, can predispose to development of gingivitis:

Orthodontic appliances, crowding of teeth, and lingually or labially erupted teeth render achieving adequate oral hygiene difficult (picture 2).

Chronic mouth breathing can cause localized gingivitis of the exposed gingiva in the maxillary labial area (picture 5).

Eruption of primary and permanent teeth causes local inflammation and erythema (picture 4).

Hormonal changes during puberty and pregnancy (picture 6) can cause the gingiva to become inflamed and hypertrophic. Puberty gingivitis is thought to be related to increases in steroid hormones and changes in the subgingival microbiota [12,13]. Puberty gingivitis may be severe and may be associated with granulomatous changes (picture 7).

Malnutrition, viral infections, stress, and sleep deprivation can predispose to the development of a very severe and painful form of gingivitis, termed "acute necrotizing ulcerative gingivitis." (See 'Acute necrotizing ulcerative gingivitis' below.)

Longstanding gingivitis can result in chronic inflammatory gingival enlargement (picture 8), which is a particularly common occurrence in patients with orthodontic appliances and poor oral hygiene. The gingival enlargement usually will resolve slowly after effective, regular oral hygiene measures are instituted. (See "Soft tissue lesions of the oral cavity in children", section on 'Gingival overgrowth'.)

Clinical findings — The clinical manifestations of gingivitis are those of inflammation, predominantly edema and erythema (picture 4). In severe cases, the gingival tissues may bleed spontaneously from ulcerations in the sulcus. Tissue hypertrophy also may develop if the inflammation is longstanding. Gingivitis can be described as localized or generalized, marginal or diffuse, hemorrhagic, and even sometimes suppurative.

Treatment — Childhood gingivitis is reversible; it is treated through oral hygiene measures. Recommendations for improving oral hygiene are based on observational studies and small randomized trials [14]. They include:

The use of an appropriately sized toothbrush (smaller heads and larger handles are helpful for children; brushes labeled for specific age groups are available from several manufacturers). Mechanical toothbrushes appropriately sized for children may be beneficial.

The use of toothpaste in flavors that appeal to children.

Parental supervision and assistance in the oral hygiene routine of children younger than 8 to 10 years of age.

Flossing is often recommended, but it can be challenging for caregivers, and evidence does not support its benefit in children.

ACUTE NECROTIZING ULCERATIVE GINGIVITIS — Acute necrotizing ulcerative gingivitis (ANUG) is a painful gingivitis with rapid onset, interproximal and marginal soft tissue necrosis, ulceration, bleeding, and malodor. It is associated with high oral concentrations of spirochetes and Prevotella intermedia. In developed countries, including North America and Europe, ANUG is rare and the incidence peaks in the late teens and early twenties; however, in less developed countries, ANUG commonly occurs in young children. Factors that predispose to development of ANUG include malnutrition, smoking, viral infections, stress, and sleep deprivation. Standard treatment involves local debridement, which usually produces rapid resolution. A number of chemical agents have been tested in small trials, and none appear to surpass simple debridement. Antibiotic therapy with penicillin or metronidazole may be indicated in patients with fever.

PERIODONTITIS — Periodontitis is characterized by gingival inflammation with accompanying (and irreversible) loss of supportive connective tissues, including alveolar bone (figure 1). It results in apical migration of the attachment of the epithelium to the tooth surface and the development of a "periodontal pocket." Periodontitis is classified by stage and grade, according to severity and rate of progression.

Etiology — Periodontitis is caused by bacteria residing in biofilms in the gingival sulcus, and therapy is aimed at eradicating or reducing the numbers of these bacteria. 16S rRNA gene-based detection methods have shown that at least 700 species of bacteria commonly reside in the sulcus, some of them not yet cultivable [15]. In the past, cultivation-based studies consistently associated Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola with periodontitis, and they were labeled the "red complex." However, more recent gene-based methods have shown that oral bacterial communities are complex, and several additional disease-associated species have been identified. Although many of these bacteria have been detected in healthy adults and asymptomatic children [16,17], they occur in low numbers. Periodontal disease may be best understood as a dysbiotic shift in the composition of oral microbial communities rather than an acute infection with pathogenic bacteria. The host inflammatory response to this bacterial community results in irreversible destruction of the bone supporting the teeth.

Epidemiology — Loss of periodontal attachment is common in adults, with most adults being affected by periodontitis. However, with increased focus on early detection and prevention of dental disease, early-stage periodontitis is being identified in greater numbers of children. When careful measurements were taken, 20 percent of 14- to 17-year-old adolescents in the United States were found to have attachment loss of at least 2 mm at one or more sites [18], indicating periodontitis often begins in adolescence.

The number and severity of affected sites increases steadily with age as the damage accumulates [9], but the rate of progression of disease in children appears to be similar to that in adults. Smoking is a major risk factor for developing chronic periodontitis.

A distinctive, rapidly progressing form of periodontitis that affects only the molars and incisors is seen almost exclusively in the pediatric population. It is described below. (See 'Rapidly progressing (high-grade) periodontitis' below.)

In addition, childhood periodontitis is associated with several systemic conditions, including Down syndrome, neutropenia, leukocyte adhesion deficiency, diabetes mellitus, and Papillon-Lefèvre syndrome. In addition, the signs of other systemic diseases may mimic those of periodontitis, including leukemia, Langerhans cell histiocytosis, and hypophosphatasia. Although many patients with periodontitis are healthy except for subtle abnormalities in host defenses, children with periodontal disease should be evaluated for the above-mentioned conditions, some of which may be serious or even life-threatening [19]. (See "Periodontal disease in children: Associated systemic conditions".)

Clinical manifestations — The clinical manifestations of late-stage periodontitis are obvious and include attachment loss, gingival recession, periodontal bone loss, tooth mobility, and tooth loss (figure 1).

The early stages of disease may be difficult to detect except by a dental examination that includes measuring the depth of the gingival sulcus. Periodontal bone loss can be localized or more generalized, and is best detected with dental radiographs. Premature tooth mobility or tooth loss is a late sign and may indicate severe periodontal disease, which may be the presenting sign of a serious systemic condition (table 1).

Forms of periodontitis — Classification of periodontal diseases was revised in 2018 with the adoption of a new system of staging and grading according to severity and rate of progression [20].

Slowly progressing (low-grade) periodontitis — A slowly progressing, mild to moderate severity periodontitis (formerly designated "chronic periodontitis") is the most common form of periodontitis. This form of periodontitis usually is not diagnosed until adulthood, although it may have its incipient onset in childhood.

Low-grade periodontitis in the early stages responds well to appropriate periodontal therapy, which must include improved oral hygiene. If detected and treated early, it can be arrested in the early stages, when attachment loss is minimal and deep pockets have not developed. In contrast, the molar/incisor pattern periodontitis that occurs in childhood usually progresses rapidly (high grade) and requires antibiotic therapy.

Rapidly progressing (high-grade) periodontitis — Rapidly progressing forms of periodontitis may be recognized at an early age – although they are rare in childhood. High-grade forms of periodontitis include a molar/incisor pattern of localized periodontitis (previously designated "localized aggressive periodontitis" and "localized prepubertal periodontitis"), periodontitis associated with systemic conditions, and generalized periodontitis (which occurs primarily in adults) [20]. Periodontitis associated with systemic conditions and generalized periodontitis are discussed separately. (See "Periodontal disease in children: Associated systemic conditions" and "Overview of gingivitis and periodontitis in adults".)

Molar/incisor pattern periodontitis — Molar/incisor pattern periodontitis was previously recognized as a separate form of disease called localized aggressive periodontitis. The 2018 nomenclature no longer gives it a separate designation [20], despite considerable controversy.

Molar/incisor pattern periodontitis is characterized by isolated, bilateral loss of attachment and bone around the young permanent incisors and permanent molars [21]. The attachment loss occurs rapidly, typically at three times the rate of loss in adult-onset disease. The radiographic appearance is distinctive.

The prevalence of the molar/incisor pattern periodontitis is estimated to be approximately 1 percent, and in the United States it is most commonly seen in the African American population. The etiology is not entirely clear. At least some cases appear to be inherited as an autosomal dominant trait [22,23]. Molar/incisor pattern periodontitis has been linked to a neutrophil chemotactic defect and to defects in repressing inflammation [24-27]. In addition to the inflammatory component, it clearly is linked to the presence of high numbers of Aggregatibacter actinomycetemcomitans, and successful treatment outcomes correlate well with eradication of the bacteria [28-31].

Molar/incisor pattern periodontitis usually is detected in early adolescence. However, retrospective examination of earlier radiographs sometimes reveals undiagnosed disease in the primary dentition. These observations suggest that localized bone loss in children around the primary molars (primary molar pattern periodontitis, previously designated "localized prepubertal periodontitis") is the same entity as molar/incisor pattern periodontitis.

Inflammation and accumulation of plaque in children with molar/incisor pattern periodontitis occur to a greater extent than they do in the average teenager. In contrast, the inflammation in molar/incisor periodontitis is usually not as extreme as that seen in the forms of periodontitis associated with systemic disease. (See "Periodontal disease in children: Associated systemic conditions".)

Treatment of molar/incisor pattern periodontitis consists of local debridement combined with systemic antibiotic therapy and clinical monitoring. Effective oral antibiotic regimens include azithromycin, metronidazole alone or in combination with amoxicillin, and tetracycline [32-34]. Azithromycin often is preferred because of its simple regimen (once a day for three to five days) and relative safety. Although metronidazole or combination metronidazole and amoxicillin appears to be more effective than tetracycline, there are concerns that metronidazole may be carcinogenic [35].

Reattachment and resolution of the periodontal defects may occur after antibiotic therapy. However, periodontal surgery often is necessary to repair the residual defects.

Primary molar pattern periodontitis — A pattern of bone loss around the primary molars, previously designated "localized prepubertal periodontitis," is a high-grade form of periodontitis that occurs in the primary dentition of children in the absence of systemic disease. It is not given a specific designation in the 2018 nomenclature, but it is well documented in the literature [36,37]. In the United States, it occurs most commonly in the African American population. An autosomal dominant pattern of inheritance has been described in one extended family [38].

Primary molar pattern periodontitis is characterized by bilateral, symmetric, localized loss of attachment in the primary dentition, typically involving the molar area [21]. It typically is accompanied by greater-than-average plaque deposits, calculus, and mild to moderate inflammation.

Primary molar pattern periodontitis usually is diagnosed in the late primary or early transitional dentition. It may progress to molar/incisor pattern periodontitis in the permanent dentition. Both entities probably are the same disease, differing only in age of onset or detection. The distinctive tooth patterns probably are determined by sequence of tooth eruption and time of onset of disease. Primary molar pattern periodontitis has not been as extensively studied as permanent molar/incisor pattern periodontitis.

Treatment involves local debridement and antibiotic therapy. Based upon studies of the efficacy of treatment of molar/incisor pattern periodontitis, azithromycin may be the antibiotic agent of choice in the treatment of primary molar bone loss pattern periodontitis. Tetracyclines are contraindicated in the management of primary molar bone loss because of the potential for staining the permanent teeth.

SUMMARY

Pediatric health care providers should be alert for signs of periodontal disease in children and adolescents. Signs of periodontitis that are apparent on visual inspection include heavy plaque (picture 2); calculus deposits (picture 3); enlargement or edema of the gingival tissues; redness, bleeding, or recession of the gingiva (picture 4); abnormal change in tooth position; and premature tooth mobility or tooth loss. (See 'Periodontal examination' above.)

Simple gingivitis is the most common periodontal problem in childhood, and inadequate removal of dental plaque is the most common cause. Predisposing factors may include orthodontic appliances (picture 2), dental crowding, chronic mouth breathing, and hormonal changes. The predominant clinical manifestations are edema and erythema (picture 4). In severe cases, the gingival tissues may bleed spontaneously. Childhood gingivitis is reversible and is treated through improved oral hygiene. (See 'Gingivitis' above.)

Acute necrotizing ulcerative gingivitis is a painful gingivitis with rapid onset, interproximal and marginal soft tissue necrosis, ulceration, bleeding, and malodor. Predisposing factors include malnutrition, smoking, viral infections, stress, and sleep deprivation. Treatment involves local debridement, which usually produces rapid resolution. (See 'Acute necrotizing ulcerative gingivitis' above.)

Periodontitis is characterized by gingival inflammation with accompanying (and irreversible) loss of supportive connective tissues, including alveolar bone (figure 1). It results in apical migration of the attachment of the epithelium to the tooth surface and the development of a "periodontal pocket." The slowly progressing periodontitis that occurs in most adults may have its incipient onset in young patients, although it does not advance to significant later-stage disease until adulthood. Early-stage disease is treated by professional debridement and improved home oral hygiene. (See 'Periodontitis' above.)

Molar/incisor pattern periodontitis, although rare, occurs in adolescents and prepubertal children and involves rapid destruction of the periodontal tissues. It is associated with a single species of bacteria (Aggregatibacter actinomycetemcomitans) residing in biofilms in the gingival sulcus. Therapy consists of local debridement and systemic antibiotic therapy. (See 'Rapidly progressing (high-grade) periodontitis' above.)

  1. Position paper: epidemiology of periodontal diseases. American Academy of Periodontology. J Periodontol 1996; 67:935.
  2. Grossi SG, Genco RJ, Machtei EE, et al. Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss. J Periodontol 1995; 66:23.
  3. Genco RJ. Current view of risk factors for periodontal diseases. J Periodontol 1996; 67:1041.
  4. Thomson WM, Poulton R, Broadbent JM, et al. Cannabis smoking and periodontal disease among young adults. JAMA 2008; 299:525.
  5. Hujoel PP. Destructive periodontal disease and tobacco and cannabis smoking. JAMA 2008; 299:574.
  6. Torpy JM, Burke AE, Glass RM. JAMA patient page. Periodontal disease. JAMA 2008; 299:598.
  7. Javed F, Abduljabbar T, Vohra F, et al. Comparison of Periodontal Parameters and Self-Perceived Oral Symptoms Among Cigarette Smokers, Individuals Vaping Electronic Cigarettes, and Never-Smokers. J Periodontol 2017; 88:1059.
  8. Sundar IK, Javed F, Romanos GE, Rahman I. E-cigarettes and flavorings induce inflammatory and pro-senescence responses in oral epithelial cells and periodontal fibroblasts. Oncotarget 2016; 7:77196.
  9. Oliver RC, Brown LJ, Löe H. Periodontal diseases in the United States population. J Periodontol 1998; 69:269.
  10. Brown LJ, Oliver RC, Löe H. Periodontal diseases in the U.S. in 1981: prevalence, severity, extent, and role in tooth mortality. J Periodontol 1989; 60:363.
  11. Matsson L. Factors influencing the susceptibility to gingivitis during childhood--a review. Int J Paediatr Dent 1993; 3:119.
  12. Nakagawa S, Fujii H, Machida Y, Okuda K. A longitudinal study from prepuberty to puberty of gingivitis. Correlation between the occurrence of Prevotella intermedia and sex hormones. J Clin Periodontol 1994; 21:658.
  13. Gusberti FA, Mombelli A, Lang NP, Minder CE. Changes in subgingival microbiota during puberty. A 4-year longitudinal study. J Clin Periodontol 1990; 17:685.
  14. Worthington HV, MacDonald L, Poklepovic Pericic T, et al. Home use of interdental cleaning devices, in addition to toothbrushing, for preventing and controlling periodontal diseases and dental caries. Cochrane Database Syst Rev 2019; 4:CD012018.
  15. Paster BJ, Boches SK, Galvin JL, et al. Bacterial diversity in human subgingival plaque. J Bacteriol 2001; 183:3770.
  16. Lamell CW, Griffen AL, McClellan DL, Leys EJ. Acquisition and colonization stability of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in children. J Clin Microbiol 2000; 38:1196.
  17. Tanner AC, Milgrom PM, Kent R Jr, et al. The microbiota of young children from tooth and tongue samples. J Dent Res 2002; 81:53.
  18. Bhat M. Periodontal health of 14-17-year-old US schoolchildren. J Public Health Dent 1991; 51:5.
  19. Watanabe K. Prepubertal periodontitis: a review of diagnostic criteria, pathogenesis, and differential diagnosis. J Periodontal Res 1990; 25:31.
  20. Papapanou PN, Sanz M, Buduneli N, et al. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol 2018; 89 Suppl 1:S173.
  21. Carranza FA. Prepubertal and juvenile periodontitis. In: Clinical Peridontology, WB Saunders, Philadelphia 1996. p.336.
  22. Aggressive periodontitis. In: Online Mendelian Inheritance in Man. Johns Hopkins University. http://omim.org/entry/170650 (Accessed on November 02, 2012).
  23. Boughman JA, Halloran SL, Roulston D, et al. An autosomal-dominant form of juvenile periodontitis: its localization to chromosome 4 and linkage to dentinogenesis imperfecta and Gc. J Craniofac Genet Dev Biol 1986; 6:341.
  24. Perez HD, Kelly E, Elfman F, et al. Defective polymorphonuclear leukocyte formyl peptide receptor(s) in juvenile periodontitis. J Clin Invest 1991; 87:971.
  25. Page RC, Beatty P, Waldrop TC. Molecular basis for the functional abnormality in neutrophils from patients with generalized prepubertal periodontitis. J Periodontal Res 1987; 22:182.
  26. Van Dyke TE, Levine MJ, Tabak LA, Genco RJ. Reduced chemotactic peptide binding in juvenile periodontitis: a model for neutrophil function. Biochem Biophys Res Commun 1981; 100:1278.
  27. Bowen TJ, Ochs HD, Altman LC, et al. Severe recurrent bacterial infections associated with defective adherence and chemotaxis in two patients with neutrophils deficient in a cell-associated glycoprotein. J Pediatr 1982; 101:932.
  28. Tinoco EM, Beldi MI, Campedelli F, et al. Clinical and microbiological effects of adjunctive antibiotics in treatment of localized juvenile periodontitis. A controlled clinical trial. J Periodontol 1998; 69:1355.
  29. Christersson LA, Zambon JJ. Suppression of subgingival Actinobacillus actinomycetemcomitans in localized juvenile periodontitis by systemic tetracycline. J Clin Periodontol 1993; 20:395.
  30. Haubek D, Ennibi OK, Poulsen K, et al. Risk of aggressive periodontitis in adolescent carriers of the JP2 clone of Aggregatibacter (Actinobacillus) actinomycetemcomitans in Morocco: a prospective longitudinal cohort study. Lancet 2008; 371:237.
  31. Shaddox LM, Huang H, Lin T, et al. Microbiological characterization in children with aggressive periodontitis. J Dent Res 2012; 91:927.
  32. Seymour RA, Heasman PA. Pharmacological control of periodontal disease. II. Antimicrobial agents. J Dent 1995; 23:5.
  33. Saxén L, Asikainen S. Metronidazole in the treatment of localized juvenile periodontitis. J Clin Periodontol 1993; 20:166.
  34. Haas AN, de Castro GD, Moreno T, et al. Azithromycin as an adjunctive treatment of aggressive periodontitis: 12-months randomized clinical trial. J Clin Periodontol 2008; 35:696.
  35. National Toxicology Program. Metronidazole. Rep Carcinog 2011; 12:269.
  36. Miller K, Treloar T, Guelmann M, et al. Clinical Characteristics of Localized Aggressive Periodontitis in Primary Dentition. J Clin Pediatr Dent 2018; 42:95.
  37. Fine DH, Armitage GC, Genco RJ, et al. Unique etiologic, demographic, and pathologic characteristics of localized aggressive periodontitis support classification as a distinct subcategory of periodontitis. J Am Dent Assoc 2019; 150:922.
  38. Shapira L, Schlesinger M, Bimstein E. Possible autosomal-dominant inheritance of prepubertal periodontitis in an extended kindred. J Clin Periodontol 1997; 24:388.
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