| Project/Area Number |
01480443
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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 | Nihon University |
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Principal Investigator |
MATSUE Ichiro Nihon University, School of Dentistry at Matsudo, Professor, 松戸歯学部, 教授 (00050021)
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| Co-Investigator(Kenkyū-buntansha) |
OGATA Yorimasa Nihon University, School of Dentistry at Matsudo, Lecturer, 松戸歯学部, 講師(専任扱) (90204065)
TAWARA Hiroshi Nihon University, School of Dentistry at Matsudo, Lecturer, 松戸歯学部, 専任講師 (90197591)
MATSUE Miyoko Nihon University, School of Dentistry at Matsudo, Lecturer, 松戸歯学部, 専任講師 (70165265)
YAMAGUCHI Shinya Nihon University, School of Dentistry at Matsudo, Assistant Lecturer (90158105)
SAKUMOTO Aiko Nihon University, School of Dentistry at Matsudo, Assistant (30215678)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1991: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1990: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1989: ¥5,500,000 (Direct Cost: ¥5,500,000)
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| Keywords | Priodontal disease / Inflammatory involvement / Gingival crevicular fluid / Antibody subclasses patterns / Periodontal disease activity / Periodontal therapy / 歯根膜細胞 / 歯周組織の破壊機序 / 歯肉溝滲出液 / 免疫学的検索 / 細菌学的検索 / 歯周組織の修復機序 |
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| Research Abstract |
Periodontal disease are currently thought to occur with periods of exacerbation and remission. The purpose of this study which composed of three parts, was to clear how to differentiate the inflammatory burst in periodontitis from its gingival counterpart until the bone resorption stage was reached.
First, we had demonstrated the problems associated with clinical and microbial diagnosis.
Second, we had evaluated specific bacteria and their products, host cells and their response to determine active disease sites in periodontitis. It was discussed that gingival crevicular fluid seemed to reflect the inflammatory involvements of periodontal lesions and was becoming increasingly apparent to determine active disease sites. We had evaluate parameters for clinical inflammation and enzymatic, antibacterial both immunologic or non- immunologic response in man. With respect to the host response, there was a strong correlation between antibody subclasses patterns and a variety of enzymes(e. g., collagenase, alkaline pbosphatase)and clinical categorization of periodontal disease.
Finally, we had done(and have continue to do)experimental study in animal, dog models with histological studies to identify active periods of periodontal disease, and to measure the degree of susceptibility to future breakdown for the immediate indication of areas of periodontal disease activity.
Identification of the disease activity is of vital importance to the institution of timely and effective therapy. It might be useful to know responses to periodontal therapy.
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