| Project/Area Number |
24592279
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Keio University |
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Principal Investigator |
SATO KAZUKI 慶應義塾大学, 医学部, 講師 (60235322)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAMOTO Takeshi 慶應義塾大学, 医学部, 講師 (70383768)
三戸 一晃 慶應義塾大学, 医学部, 助教 (10445223)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 骨代謝 / ニコチン / 破骨細胞 / 骨質 |
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| Outline of Final Research Achievements |
(1) To examine the influence of nicotine on ossification, a mouse bone restoration model was adopted. As the result performed after having maintained high density of internal nicotine for a long duration, the callus bridging formation was significantly worse than control group in two weeks. Additionally, few callus formation implied that the enchondral ossification was impaired. (2)We cultured the mouse thighbone and measured intraosseous pentosidine, one of AGEs. The result was that, not in α7nAchR knockout mouse (KO), but in wild type mouse (WT), pentosidine level was significantly higher in nicotine group, which indicated nicotine affects bone quality. (3)As a result of bone morphometry for WT and KO, in KO the bone density was significantly higher and osteoclasts were fewer. There was no difference in the histological examination of osteogenesis and chondrogenesis between them, by which it was supposed that α7nAchR activated osteoclasts in physiological bone metabolism.
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