Abstract

Bacterial biofilm have been shown to be the primary etiological factor in the initiation of gingival inflammation and subsequent destruction of periodontal tissues. At the same time, there is strong evidence that indicates that periodontal disease is not a conventional infectious disease, but an inflammatory disease triggered by host immune response to a constellation of periodontal biofilm-associated microorganisms. Earlier studies showed that adult periodontitis and advanced destructive periodontitis patients had significantly higher levels of IgG antibodies to P. gingivalis. In patients with localized aggressive periodontitis, elevation of IgG antibody was also found in response to Aggregatibacter actinomycetemcomitans. Serum IgG antibody was elevated in periodontitis subjects, with unique antigens on P. gingivalis and A. actinomycetemcomitans by the patient sera, indicating the antigenic specificities of antibody response. These antibodies against periodontopathic bacteria have been shown to function in antibacterial immunity by a variety of mechanisms like inhibition of adherences and colonization, lyses of bacteria, and the abilities to aggregate the bacteria and detoxify endo- and exotoxins. Both human and experimental animal studies have shown that there is considerable potential for intervention or interference with periodontitis by interference with the host immune system. Advances in our understanding, the critical role of host responses in the progression of periodontal disease, immunization strategies against periodontopathic bacterial infection may be feasible and may raise protective immunity against periodontitis.

Full Text
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