1991 Fiscal Year Final Research Report Summary
Immunohistological study of immune system associated with periodontal tissue breakdown by endotoxin
| Project/Area Number |
02454440
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Conservative dentistry
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| Research Institution | Nagasaki University |
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Principal Investigator |
KATO Ihachi Nagasaki University School of Dentistry, Professor, 歯学部, 教授 (30005087)
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| Co-Investigator(Kenkyū-buntansha) |
ICHIMARU Eiji Nagasaki University School of Dentistry, Research associate, 歯学部, 助手 (60223111)
HARA Yoshitaka Nagasaki University School of Dentistry, Associate Professor, 歯学部, 助教授 (60159100)
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| Project Period (FY) |
1990 – 1991
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| Keywords | Endotoxin / Histopathological study / Node mouse / Bone resorption / Osteoclast / ELISA法 |
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| Research Abstract |
<Purpose> Endotoxin exhibits the toxic and immunological activities, which and associated with the establishment of periodontal disease under the influence of various immune cells. The purpose of this study is to clarify the role of immune cells on the osteoclastic bone resorption and periodontal inflammation induced by endotoxin in immunized (IM), non-immunized (NI) mice and congenital T Lymphocyte deficet (NU) mice.
<Methods and Results> Eight-week-old mice of the BALB/c (+/+) and BALB/c (nu/nu) strains were used for this study. Consecutive infections of E. coli endotoxin into gingival tissue of IM, NI and NU mice were performed. Anti-endotoxin titer of the mouse serum was measured by the ELISA method. IM mice showed osteoclastic bone resorption on alveolar bone and severe inflammation of gingival tissue in earlier period tnan NI mice. The slight inflammation was observed in NU mice compared with IM and NI mice, and was not formed osteoclastic bone resorption. Anti-endotoxin titers of NI and NU mice serum gradually increased, finally overtaked IM mice serum.
<Conclusions> In this study, we could make it clear that the existence of T cell has a great influence on osteoclast formation and periodontal inflammation.
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