| Project/Area Number |
10307053
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| Research Category |
Grant-in-Aid for Scientific Research (A).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Periodontal dentistry
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
MAEDA Katsumasa Kyushu University, Dept of Dental Sciences, Professor, 大学院・歯学研究院, 教授 (00117243)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHINO Hiroshi Hiroshima University, Dept of Periodontology, assistant professor, 歯学部, 助手 (50240338)
YOSHIE Hiromasa Niigata University, Dept of Periodontology, Professor, 歯学部, 教授 (20143787)
NEMOTO Eiji Tohoku University, Dept.of Dental sciences, assistant professor, 大学院・歯学研究科, 助手 (40292221)
HIRATA Masato Kyushu University, Dept of Dental Sciences, Professor, 大学院・歯学研究院, 教授 (60136471)
ISHIKAWA Isao Tokyo Medical and Dental University, Dept of Periodontology, Professor, 大学院・医歯学総合研究科, 教授 (10014151)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥25,900,000 (Direct Cost: ¥25,900,000)
Fiscal Year 2000: ¥5,500,000 (Direct Cost: ¥5,500,000)
Fiscal Year 1999: ¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 1998: ¥14,400,000 (Direct Cost: ¥14,400,000)
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| Keywords | bacteria / neutrophil / fibloblast / T cell / macrophage / hyaluronic acid / prostaglandin / doxycycline / インターロイキン1 / Fcレセプター / 分泌型IgA / Ip3結合タンパク質 / 歯周組織再生誘導法 / リポ多糖 / インターロイキン / エムドゲイン / 再生の遺伝子 / 歯周病 / PGE2 / 歯根膜 / 生体防御 / 組織修復 |
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| Research Abstract |
1. Analysis of host defense response in periodontal diseases.
Periodontal diseases are initiated with infection of periodnotopathogenic bacteria in dental plaque. To elucidate the host defense response in the process of disease progression is deeply related with the understanding of the repair reaction in the process of healing from diseases. In this project, we scientifically revealed the role of neutrophils and fibroblasts which are the initial responders in the host defense mechanism. Furthermore, we analyzed the immune response with T-cells which play a central role in the host defense response and we obtained the following results. At the stage of immune response with Th-1 cells and macrophages, a strong bactericidal activity was exhibited, but on the other hand, periodontal tissues were destructed. The immune response with Th-1 cells has a variation among individuals, and it was speculated that this variation may bring about the difference of periodontal diseases among patients.
2. Analysis of tissue repair in periodontal diseases.
We analyzed the hyaluronic acid in the healing process from injury, and we found that at this process, high MVV type hyaluronic acid was produced and it provided the mesenchymal cells with the base for growth and induced the tissue repair. It was also found that eight genes are functioning in the process of healing from injury. Furthermore, when we systemically administer prostaglandin, which is known to promote bone resorption, the bone resorption was found to be inhibited. When we apply the self-resolving membrane with tetracycline on GTR, the formation of new alveolar bone was increased. From these results, we obtained the basic information for the clue from the tissue repair to tissue regeneration.
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