Phorphyromonas gingivalis感染による実験的歯周炎モデル

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The murine system offers an exciting opportunity for investigating the capacity of the host immune system to protect against or contribute to periodontal bone loss. Periodontal diseases are inflammatory responses through to be triggered by specific microorganisms including Porphyromonas gingivalis colonizing in the gingival crevice. However, colonization of P. gingivalis in the murine mouth subgingival area has not been well demonstrated. The purpose of this study was to examine whether P. gingivalis could colonize in the murine mouth and induce alveolar bone loss. Conventional, specific pathogen-free C3H/HeN mice (7 weeks old, male) were purchased, and maintained in horizontal flow cabinets and provided food and tap water ad libitum in the animal facility of Fukuoka Dental Collage. In this study, mice were divided into three groups, i. e., infected, sham-infected and control groups. The mice in infected group were immunized orally inoculated with 10^6 (colony forming units ; CFU) viable P. gingivalis 381 during ligation of the maxillary first molars in one quadrant withbacterium-soaked silk ligature. The sham-infected mice received silk ligature without bacteria, and the control mice were not ligated nor infected with the bacterium. Mice were sacrificed on 1 to 15 weeks after infection by 2 weeks' interval. The plaque samples from each site were collected at the time of killing. The molar segments were then dissected for the examination of alveolar bone loss. The total cultivable counts of bacteria and the black-pigmented bacteria were examined by the culture of the plaque sample on the blood agar plate and the blood agar plate supplemented with hemin and menadion, respectively. Furthermore, P. gingivalis was identified by microbiologically (black-pigmented colonies and Gram-stain) and immunologically (Western blot analysis with antibody to P. gingivalis 381 fimbriae). For the measurement of alveolar bone loss, the dissected upper jaw was stained. The alveolar bone loss was expressed by the distance from the cement-enamel junction to the alveolar crest. The results indicated that P. gingivalis was not isolated in all the groups before infection, and was not recovered in sham-infected and control groups through the experimental period. In contrast, significant number of P. gingivalis were identified in infected mice until the end of the experimental period (15 weeks after infection). Regarding the alveolar bone loss, sham-infected mice as well as infected mice showed significant bone loss around the maxillary second molars after 3 weeks of infection. Since sham-infected mice received sham-infection (ligation without bacteria), the alveolar bone loss could be induced by the ligation irrespective of bacterial infection. After 11 to 15 weeks, however, infected mice showed significant higher amount of bone loss (both horizontal and vertical) around the maxillary second molars than that of sham-infected mice, suggesting that P. gingivalis infection could cause the further enhancement of the alveolar bone loss. Taken together, the present findings suggest that it is possible to establish P. gingivalis in conventional mouse oral flora by means of the bacteria-soaked ligature at least until 15 weeks after infection. It is also suggested tnat the P. gingivalis-associated alveolar bone breakdown could be induced in this model system.
福岡歯科大学学会の論文
1998-03-31

Phorphyromonas gingivalis感染による実験的歯周炎モデル

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