A study of mechanism of adherence to the oral cavity in periodontopathic bacteria by animal model.

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We previously reported that the presence of two different kinds of fimbriae expressed on the cell surface of Porphyromonas gingivalis ATCC 33277. The initial event in most infectious diseases involves adhesion of pathogens to host tissues and subsequent invasion by the pathogens. To define the role of fimbriae in Porphyromonas gingivalis adherence to and invasion of epithelial cells, we have constructed fimbrial mutants. The involvement of P.gingivalis fimbriae in the invasion process and alveolar bone resorption in rats were examined. Inactivated mutants of 41-K fimbrillin gene (fimA) and/or the 67-K fimbrillin gene (mfa1) by a homologous recombination technique and compared among fimA mutant (MPG1), mfa1 mutant (MPG67), and double knockout mutant (MPG4167). Adherence and invasion of P.gingivalis was assessed in human oral epithelial KB cells. We used a rat model to examine the role of each type of fimbriae in alveolar bone loss by oral infection. The adherence and invasion levels of the mutants were lower than the wild-type strain. The bone loss of rats infected with the MPG1 was higher than that of those infected with MPG67. Moreover, the bone loss of rats infected with the double knockout mutant was significantly decreased compared to that of rats infected with the wild-type strain. Data from this study suggest that not only the 41-K fimbrial protein, but also the 67-K fimbrial protein play important roles in the pathogenesis of periodontal disease.