| Project/Area Number |
15K11002
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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 |
Morphological basic dentistry
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
笹野 泰之 東北大学, 歯学研究科, 教授 (30196191)
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| Co-Investigator(Renkei-kenkyūsha) |
TAKAI toshiyuki
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | DAP12 / FcRr / 破骨細胞分化 / 歯の萌出 / 大理石骨病 / c-fos / FcRγ |
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| Outline of Final Research Achievements |
In this study, the teeth and surrounding periodontal tissues in the process of eruption were morphologically examined in DAP12 deficient and DAP12/FcRr double deficient mice with normal tooth eruption in spite of inhibited osteoclast differentiation and c-fos deficient mice with failure of tooth eruption due to impaired osteoclast differentiation. Micro-CT and histological analyses showed that TRAP-positive cells were detected in the mandible of 2-week-old DAP12 deficient mice and mandibular bone volume in DAP12 deficient mice were similar to that in wild type mice at two weeks of age, while mandibular bone volume in 12-week-old DAP12/FcRr deficient mice were higher than wild type mice.
These data suggest that osteoclasts are present in the mandibular bone of DAP12 deficient and DAP12/FcRr deficient mice, and these mice may not exhibit osteopetrosis until they are one month old.
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| Academic Significance and Societal Importance of the Research Achievements |
破骨細胞分化が抑制されたDAP12欠損マウスとDAP12/FcRr二重欠損マウスの顎骨・歯・歯周組織についての詳細な情報はなく、本研究が初めての報告となる。また、網羅的遺伝子解析によりDAP12とFcRrの欠損に対して代償性に働く分子が同定できる可能性がある。
従って、本研究により得られる結果は、破骨細胞分化に関与する新規の分子を特定し、破骨細胞分化の分子メカニズムの解明に貢献するとともに、複雑な歯の萌出メカニズムの一端を解明し、顎口腔領域の発生研究分野に有益な情報を提供できるものと考える。
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