AGGRESSIVE PERIODONTITIS

1. AGGRESSIVE PERIODONTITIS Logien Al Ghazal 17/11/2015

2. General characteristics • Generally affects systemically healthy individuals less than 30 years old. • Aggressive periodontitis may be universally distinguished from • chronic periodontitis by the age of onset, the rapid rate of disease progression. • The nature and composition of the associated subgingival microflora, alterations in the host's immune response, and a familial aggregation of • diseased individuals. • Strong racial influence is observed (African).

3. The two subtypes are: • Localized aggressive periodontitis: • localized juvenile periodontitis (LJP). • Generalized aggressive periodontitis: • Generalized juvenile periodontitis (GJP) and • Rapidly progressive periodontitis (RPP)

4. LOCALIZED AGGRESSIVE PERIODONTITIS

5. Clinical Characteristics • Localized aggressive periodontitis usually has an age of • onset around puberty. • Clinically, it is characterized as having: • "localized first molar/incisor presentation with interproximal attachment loss on at least two permanent teeth, one of which is a first molar, and involving no more than two teeth other than first molars and incisors“ • The localized distribution of lesions in localized aggressive periodontitis is characteristic • .

6. The following possible reasons for the limitation of periodontal destruction to • certain teeth have been suggested: • 1. After initial colonization of the first permanent teeth to erupt (the first molars and incisors), Actinobacillus actinomycetemcomitans evades the host defenses by different mechanisms: • Including production of polymorphonuclear leukocyte chemotaxis-inhibiting factors • endotoxin • Collagenases • leukotoxin • Other factors allow the bacteria to colonize the pocket and initiate the destruction of the periodontal tissues. • A strong antibody response to infecting agents is one characteristic • of localized aggressive periodontitis.

7. 2. Bacteria antagonistic to A. actinomycetemcomitans may colonize the periodontal tissues and inhibit A. actinomycetemcomitans from further colonization of periodontal sites in the mouth. This would localize A. actinomycetemcomitans infection and tissue destruction.“ 3. A. actinomycetemcomitans may lose its leukotoxin producing ability for unknown reasons." If this happens, the progression of the disease may become arrested or retarde 4. The possibility that a defect in cementum formation may be responsible for the localization of the lesions. Root surfaces of teeth extracted from patients with localized aggressive periodontitis have been found to have hypoplastic or aplastic cementum.

8. Clinical Characteristics • A striking feature of localized aggressive periodontitis is the lack of clinical inflammation despite the presence of deep periodontal pockets. • The amount of plaque on the affected teeth is minimal, which seems inconsistent with the amount of periodontal destruction present. • The quantity of plaque may be limited, it often contains elevated levels of A. actinomycetemcomitans, and in some patients, Porphyromonas gingivalis. • Progresses rapidly. • Evidence suggests that the rate of bone loss is about three to four times faster than in chronic periodontitis. • Distolabial migration of the maxillary incisors with concomitant diastema • Formation.

10. Clinical Characteristics • Increasing mobility of the first molars. • Sensitivity of denuded root surfaces to thermal and tactile stimuli. • Deep, dull, radiating pain during mastication, probably because of irritation of the supporting structures by mobile teeth and impacted food. • Periodontal abscesses may form at this stage, and regional lymph node enlargement may occur. • Not all cases of localized aggressive periodontitis progress to the degree described previously. • Some patients, the progression of attachment loss and bone loss may be self-arresting.

12. Radiographic Findings

13. Vertical loss of alveolar bone around the first molars and • incisors. • Beginning around puberty in otherwise healthy teenagers, is a classic diagnostic sign of localized aggressive periodontitis. • Radiographic findings may include an "arc-shaped loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface • of the second molar""

16. Prevalence and Distribution by Age and Sex

17. A clinical and radiographic study of 7266 English adolescents 15 to 19 years old also showed a prevalence rate of 0.1%. In the U.S., a national survey of adolescents age 14 to 17 reported that 0.53% had localized aggressive periodontitis. Gender: Blacks were at much higher risk for localized aggressive periodontitis. Black males were 2.9 times more than females. In contrast, white females were more likely to have localized aggressive periodontitis than white males. Age: puberty and 20 years of age.

18. GENERALIZED AGGRESSIVE PERIODONTITIS

19. Clinical Characteristics Generalized aggressive periodontitis usually affects individuals under the age of 30, but older patients also may be affected. Evidence suggests that individuals affected with generalized aggressive periodontitis produce a poor antibody response to the pathogens present. Characterized by: "generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors" The destruction appears to occur episodically with periods of advanced destruction followed by stages of quiescence of variable length (weeks to months or years). Radiographs often show bone loss that has progressed since the previous Evaluation.

20. Quantitatively, the amount of plaque seems inconsistent with the amount of periodontal destruction. • Qualitatively, P. gingivalis, A. actinomycetemcomitans, and Bacteriodesforsythus frequently are detected in the plaque that is present. • Two gingival tissue responses can be found in cases of generalized aggressive periodontitis: • One is a severe, acutely inflamed tissue, often proliferating, ulcerated, • and fiery red. ,bleeding may occur spontaneously or with slight stimulation. • Suppuration. • 2. In other cases, the gingival tissues may appear pink, free of inflammation, and occasionally with some degree of stippling, although the last feature may be absent.

21. Despite the apparently mild clinical gingival appearance, deep pockets • can be demonstrated by probing. • Systemic manifestations such as weight loss, mental depression, and general • Malaise. • Generalized aggressive periodontitis atients must have their medical • histories updated and reviewed.

23. Radiographic Findings

25. The radiographic picture in generalized aggressive periodontitis can range from severe bone loss associated with the minimal number of teeth. • Advanced bone loss affecting the majority of teeth in the dentition • A comparison of radiographs taken at different times illustrates the aggressive • nature of this disease. • Despite the extreme bone loss at certain sites, other sites in the same patient may show no bone loss.

27. Prevalence and Distribution by Age and Sex

28. In a study of untreated periodontal disease conducted in Sri Lanka by Loe and colleagues,36 8% of the population had rapid progression of periodontal disease characterized by a yearly loss of attachment of 0.1 to 1.0 mm. • In the U.S., a national survey of adolescents aged 14 to 17 reported that 0.13% had generalized aggressive periodontitis. • In addition, blacks were at much higher risk than whites for all forms of aggressive periodontitis and males were more likely to have generalized aggressive periodontitis than females.

29. RISK FACTORS FOR AGGRESSIVE PERIODONTITIS

30. 1. Microbiologic Factors Localized aggressive periodontitis (A. actinomycetemcomitans, Capnocytophaga sp., Eikenella corrodens, Prevotella intertnedia, and Campylobacter rectus). A. actinomycetemcomitans has been implicated as the primary pathogen associated with this disease. Tonetti and Mombelli this link is based on the following evidence: (1) A. actinomycetemcomitans is found in high frequency (approximately 90%) in lesions characteristic of localized aggressive periodontitis. (2) Sites with evidence of disease progression often show elevated levels of A. actinomycetemcomitans. .

31. (3) many patients with the clinical manifestations of localized aggressive periodontitis have significantly elevated serum antibody titers to • Actinomycetemcomitans • (4) clinical studies show a correlation between reduction in the subgingival load of A. actinomycetemcomitans during treatment and a successful clinical response. • (5) A. actinomycetemcomitansproduces a number of virulence factors that may contribute to the disease process. • Another study found elevated levels of P. gingivalis, P. intermedia, Fusobacteriumnucleatum, C. rectus, and Treponemadenticola. • Electron microscopic studies of localized aggressive periodontitis have revealed bacterial invasion of connective tissue.

32. 2. Immunologic Factors • The human leukocyte antigens (HLA), which regulate immune responses, • have been evaluated as candidate markers for aggressive periodontitis. • Patients with aggressive periodontitis display functional defects of polymorphonuclear leukocytes (PMNs), monocytes, or both. • These defects can impair either the chemotactic attraction of PMN to the site of infection or their ability to phagocytose and kill microorganisms. • Hyperresponsiveness of monocytes from localized aggressive periodontitis patients with respect to their production of PGE 2 in response to • lipopolysaccharide (LPS).

33. This hyperresponsive phenotype could lead to increased connective tissue or bone loss due to excessive production of these catabolic factors. • Additionally, poorly functional inherited forms of monocyte FcyRII, the receptor for human IgG2 antibodies, have been shown to be disproportionately present in patients with localized aggressive periodontitis. • These PMN and monocyte defects may be induced by the bacterial infection or may be genetic in origin.

34. Autoimmunity : • Host antibodies to collagen, DNA, and immunoglobulin G (IgG). • Possible immune mechanisms include an increase in the expression • of type II major histocompatibility complex (MHC) molecules, • HLA DR43 . • Altered helper or suppressor T-cell function, polyclonal activation of B cells by microbial plaque, and genetic predisposition.

35. 3. Environmental Factors • The amount and duration of smoking are important variables that can influence the extent of destruction seen in young adults . • Patients with generalized aggressive periodontitis who smoke have more affected teeth and more loss of clinical attachment than nonsmoking • patients with generalized aggressive periodontitis. • Smoking may not have the same impact on attachment levels in younger patients with localized aggressive periodontitis.

36. 4. Genetic Factors • All individuals are not equally susceptible to aggressive periodontitis. • Familial pattern of alveolar bone loss and have implicated genetic factors in aggressive periodontitis. • Localized aggressive periodontitis suggest that a major gene plays a role in this disease, which is transmitted through an autosomal dominant mode of • Inheritance. • Familial clustering of the neutrophil abnormalities seen in localized aggressive periodontitis. • The antibody response to periodontal pathogens, particularly A. actinomycetemcomitans, is under genetic control and that the ability to mount high titers of specific, protective antibody (primarily IgG2) against • actinomycetemcomitans may be race dependent. • Gene of major effect exists for aggressive periodontitis.