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Many people think of periodontal disease as an adult problem. However, studies indicate that nearly all children and adolescents have gingivitis, the first stage of periodontal disease. So periodontal disease can be a problem for all children and young adults.Generalized juvenile periodontitis which includes early onset adult periodontitis, recurrent necrotizing ulcerative periodontitis and the true generalized form of juvenile periodontitis. Periodontitis in systemically diseased individuals can be divided into three subgroups: juvenile periodontitis associated with primary neutrophil disorders, juvenile periodontal disease in which neutrophils are secondarily abnormal, and juvenile periodontitis associated with other diseases. Juvenile periodontitis is perhaps the best understood form of periodontal disease. As always, it should be accepted practice not only for adults but also for children to visit the dentist at least once every six months.

Juvenile periodontitis.
A degenerative periodontal disease of adolescents in which the periodontal destruction is out of proportion to the local irritating factors present on the adjacent teeth; inflammatory changes become superimposed, and bone loss, migration, and extrusion are observed. Two forms are recognized: localized, in which the destruction is limited to the incisors and first molars; and generalized, involving all the teeth. Juvenile periodontosis is defined as a disease of the periodontium occurring in otherwise healthy adolescents (onset as low as 11 and as high as 20 years of age) and characterized by rapid alveolar bone loss in one or more permanent teeth (2:73). The disease has been classification (3:268) and usually occurs in young adults, though much earlier onset, around puberty, has been observed (1:58). Localized Juvenile Periodontitis (LJP)

LJP is different from all other periodontal infections, as it is not associated with plaque

accumulations or calculus (in fact the absence of such led early investigators to consider it as a degenerative condition), is localized to certain anterior or front teeth and first molars, and is seen following puberty. It is a rather rare entity, occurring in about 0.1 to 0.5% of teenagers, but when found, is often clustered within families. This familial background suggested a genetic predisposition, which subsequently has been identified as a neutrophil defect associated with reduced chemotaxis. Bacterial examinations of subgingival plaque from affected teeth and adjacent healthy teeth, revealed that the diseased teeth were colonized by an essentially Gram-negative flora dominated by organisms subsequently identified as various Capnocytophaga and Wolinella species and Actinobacillus actinomycetemcomitans. It is A actinomycetemcomitans that appears to be the etiologic agent of LJP, and the arguments for its involvement are illustrative of the arguments made to implicate other species in other forms of periodontitis. Once LJP has been recognized clinically, most of the tissue damage has already occurred, thereby permitting only a retrospective diagnosis of an A actinomycetemcomitans infection. A actinomycetemcomitans is found at a higher prevalence in tooth sites associated with LJP and at a lower prevalence in healthy sites in the same mouth, or at sites in periodontally healthy individuals.

It is often found among other family members in a household with an LJP individual, and indeed among siblings at risk to LJP, there is suggestive data that colonization by A actinomycetemcomitans precedes the development of a pocket and subsequent bone loss. But what has been the most important reason for implicating A actinomycetemcomitans as a periodontopathogen, is its killing effect on neutrophils.

A actinomycetemcomitans produces a leukotoxin that kills neutrophils in vitro. It is clear that this leukotoxin is expressed in vivo, because patients with LJP have developed circulating antibodies which can neutralize this toxin in vitro. From this finding, a scenario can be developed that explains the localized nature of LJP. Children with a neutrophil chemotactic defect become colonized by A actinomycetemcomitans in early life, presumably by contact with infected household members. The colonization spreads to those permanent teeth that erupted at ages 5 to 7, but remains quiescent as an infection during the time that the primary or baby teeth are lost, and new permanent teeth appear at about ages 11 to 13. The individual entering puberty, has a dentition composed of first molars and incisors that are colonized by A actinomycetemcomitans and newly erupted teeth that either are not colonized or only minimally colonized. Something then triggers the relative overgrowth of A actinomycetemcomitans in the subgingival plaque, and some of these organisms invade the gingival tissue and cause attachment and bone loss in the absence of an obvious inflammatory response. The latter can be explained by both a sluggish neutrophil response to the bacteria and by the leukotoxin inhibiting the neutrophils, and thereby preventing a protective host response in the pocket microenvironment. The leukotoxin is antigenic and elicits an antibody response which may neutralize the leukotoxin at other tooth sites, thereby limiting the infection to the originally colonized molars and incisors. This scenario, while incomplete, does explain the localized nature of LJP, partially explains the absence of an inflammatory response in the tissue, and demonstrates the

dynamic role of neutrophils and circulating antibodies in defending the periodontium. Presumably, this theme is operating in the more commonly found cases of adult periodontitis. Certainly, the central role of the neutrophils in host defense is unquestioned, as individuals with neutropenias, chronic granulomatous disease and various leukemias often present with advanced forms of periodontal disease. Generalized juvenile periodontitis

Generalized juvenile periodontitis which includes early onset adult periodontitis, recurrent necrotizing ulcerative periodontitis and the true generalized form of juvenile periodontitis. Periodontitis in systemically diseased individuals can be divided into three subgroups: juvenile periodontitis associated with primary neutrophil disorders, juvenile periodontal disease in which neutrophils are secondarily abnormal, and juvenile periodontitis associated with other diseases. Juvenile periodontitis is perhaps the best understood form of periodontal disease. A major infecting organism, Actinobacillus actinomycetemcomitans, is strongly associated with the disease, and may be an exogenous pathogen since it is not found in healthy individuals or in healthy sites in LJP patients. It is virulent with marked leukaggressive properties and it induces a marked antibody response in infected patients. Eradication of Actinobacillus actinomycetemcomitans requires attention to the fact that it invades the tissue and hence systemic antimicrobials or surgical excision of the tissues is necessary for eradication. Marked suppression of the organism from subgingival sites is associated with healing.

Host responses in LJP have also been well described and most immune functions studied appear to be normal. The notable exception is neutrophil chemotaxis which is depressed. Associated with depressed neutrophil chemotaxis is a reduction of neutrophil receptors for several chemotactic factors including C5a, the fifth component of complement. Conclusion

Many people think of periodontal disease as an adult problem. However, studies indicate that nearly all children and adolescents have gingivitis, the first stage of periodontal disease. Advanced forms of periodontal disease are more rare in children than adults, but can occur. Types of periodontal diseases in children Chronic gingivitis is common in children. It usually causes gum tissue to swell, turn red and bleed easily. Gingivitis is both preventable and treatable with a regular routine of brushing, flossing and professional dental care. However, left untreated, it can eventually advance to more serious forms of periodontal disease. Aggressive periodontitis can affect young people who are otherwise healthy. Localized aggressive periodontitis is found in teenagers and young adults and mainly affects the first molars and incisors. It is characterized by the severe loss of alveolar bone, and ironically, patients generally form very little dental plaque or calculus.

Generalized aggressive periodontitis may begin around puberty and involve the entire mouth. It is marked by inflammation of the gums and heavy accumulations of plaque and calculus. Eventually it can cause the teeth to become loose. Periodontitis associated with systemic disease occurs in children and adolescents as it does in adults. Conditions that make children more susceptible to periodontal disease include:

Type I diabetes Down syndrome Kindler syndrome Papillon-Lefevre syndrome

It is good practice for adults as well as children to make regular visits to their dentist (at least once every six months). The problem of juvenile periodontitis can be eliminated through good oral hygiene habits and dental care.