| Project/Area Number |
22390351
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Matsumoto Dental University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KOBOYASHI Yasuhiro 松本歯科大学, 総合歯科医学研究所, 准教授 (20264252)
MIZOGUCHI Toshihide 松本歯科大学, 総合歯科医学研究所, 講師 (90329475)
NINOMIYA Tadashi 松本歯科大学, 総合歯科医学研究所, 講師 (00360222)
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| Co-Investigator(Renkei-kenkyūsha) |
UDAGAWA Nobuyuki 松本歯科大学, 歯学部, 教授 (70245801)
NAKAMURA Hiroaki 松本歯科大学, 歯学部, 教授 (50227930)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥19,240,000 (Direct Cost: ¥14,800,000、Indirect Cost: ¥4,440,000)
Fiscal Year 2012: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2011: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
Fiscal Year 2010: ¥7,410,000 (Direct Cost: ¥5,700,000、Indirect Cost: ¥1,710,000)
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| Keywords | 口腔生化学 / 破骨細胞 / 骨芽細胞 / Ｗｎｔ / IL-34 / 破骨細胞前駆細胞 / 破骨細胞ニッチ / Wnt5a / Ror2 / Wnt非古典経路 / OPG / RANKL / M-CSF |
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| Research Abstract |
We examined the role of Wnt signaling for the formation of osteoclast niche, and the results as follows. (1) The osteoclast niche was analyzed and characteristics of osteoclast precursors (quiescent osteoclast precursors, QOP) were clarified. (2) The role of noncanonical Wnt signaling in osteoclastogenesis was examined. Noncanonical Wnt signals (Wnt5a-Ror2 signals) were shown to play important roles in osteoclastogenesis. (3) Wnt5a-Ror2 signals enhanced RANKexpression in QOPs. Canonical Wnt signals did not appear to play a role in osteoclastogenesis. (4) GeneChip analysis was performed on QOPs to identify specific markers of QOPs. But we failed to isolate specific markers of QOPs. However, we found that osteoclasts specifically express Wnt5a.(5) IL-34 was identified as an important cytokine for generation of QOP in hematopoietic tissues. (6) Alveolar bone loss was examined in OPG-deficient (OPG?/?) mice and RANKL-overexpressing transgenic mice. OPG?/? mice were shown to be a use l model of periodontitis. (7) Administration of soluble form of Ror2 into collagen-induced arthritis mice effectively suppressed bone destruction.
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