| Project/Area Number |
17591932
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | National Institute for Longevity Sciences,NCGG |
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Principal Investigator |
NIIDA Shumpei National Institute for Longevity Sciences,NCGG, Research Institution, National Center for Geriatrics and Gerontology, 室長 (10137630)
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| Co-Investigator(Kenkyū-buntansha) |
森脇 佐和子 国立長寿医療センター, (研究所)・運動器疾患研究部, 流動研究員 (90399593)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,370,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2006: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | γ-GTP / osteoclast / bone resorption / alveolar bone / periodontitis / 歯槽骨破壊 / 歯周病原因菌 / ガンマGTP / 炎症性サイトカイン / 歯周病菌 / RANKL |
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| Research Abstract |
γ-Glutamyl transpeptidase(GGT) is a newly identified bone-resoibing factor which stimulates osteoclast formation. In this project, we revealed the involvements of GGT in the osteoclastic bone resorption as following :
1. GGT expression has been detected in CD45- and CD20-positive lymphocytes and plasma cells in the inflammation sites.
2. Application of GGT into rat gingival sulcus caused acute osteoclastic alveolar bone destruction.
3. We generated the monoclonal Ab against GGT, and injected them into the arthritis mice. GGT-mAb significantly diminished the number of osteoclasts and the seventy of joint destruction in arithritis mice.
4. Several bacteria(18 strains) implicated in periodontitis produced GGT.
5. We generated recombinant H. Pylori- and T. denticola GGT. Pylori GGT possessed osteoclastogenic activity in bone marrow cultures.
6. However, T. denticola GGT did not induce osteoclast formation.
These results indicate that endogenous GGT(produced by lymphocytes) acts as an enhancer for pathological osteoclast formation. GGT antagonists might be novel therapeutic agents for attenuating the bone erosion such as arthritis and periodontitis. In addition, the result that bactenal GGT stimulate osteoclastogenesis suggests that GGT generated in bacteria is involved in perodontitis-induced osteolysis. The structure of T. denticola GGT was different from that of human and Pylori's ; small molecule and short A. A. length. Since, however, GGT structures of other bacterial species are unknown, further studies are required to understand the pathology of the periodontitis.
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