2017 Fiscal Year Final Research Report
Functional analysis of Runx2 in bone resorption in the animal model of Cleidocranial dysplasia
| Project/Area Number |
15K11335
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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 |
Orthodontics/Pediatric dentistry
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
山本 照子 東北大学, 歯学研究科, 名誉教授 (00127250)
北浦 英樹 東北大学, 歯学研究科, 准教授 (60295087)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 歯学 / 歯の移動 / 先天異常 / Runx2 |
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| Outline of Final Research Achievements |
Cleidocranial dysplasia (CCD) is caused by mutations of RUNX2. However, the mechanism of orthodontic tooth movement in CCD patients has not been clarified. We examined the amount of experimental tooth movement in hetero mice deficient in RUNX2 gene (hetero KO mice), the animal model of CCD. Compared to wild-type mice, the hetero KO mice exhibited delayed experimental tooth movement, and osteoid formation. Moreover, we applied continuous mechanical tensile force to bone marrow stromal cells (BMSCs) as an in vitro model of the tension side of tooth movement. Runx2 hetero deficiency delayed tensile force-induced increase of DNA content in BMSCs, and also delayed and reduced tensile force-induced ALP activity, calcium content, and OSC mRNA expression of BMSCs in osteogenic medium compared to wild-type BMSCs.
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| Free Research Field |
歯科矯正学
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