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Investigation of the homeostasis retaining mechanism with autophagy in orthodontic tooth movement.

Research Project

Project/Area Number 17K17324
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Orthodontics/Pediatric dentistry
Research InstitutionOkayama University

Principal Investigator

Nakamura Masahiro  岡山大学, 大学病院, 助教 (20708036)

Project Period (FY) 2017-04-01 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords実験的歯牙移動 / オートファジー / 細胞内恒常性維持機構 / 細胞内恒常性維持 / 矯正歯科 / 歯牙移動 / ホメオスタシス
Outline of Final Research Achievements

It is speculated that cell homeostasis is reduced because osteoblasts on the surface of the bone matrix are exposed to various pathological conditions when orthodontic force is applied to teeth. However, details of molecular mechanism for maintaining homeostasis is still unclear. As a result of this study, it was confirmed that osteoblasts on the surface of the alveolar bone during orthodontic tooth movement were in a hypoxic state and were exposed to endoplasmic reticulum stress. In addition, the expression of autophagy markers at the same site was also confirmed, and it was also confirmed that in culture osteoblasts, autophagy was enhanced with respect to hypoxic stress. These findings suggest that autophagy may be involved in maintaining cell homeostasis in osteoblasts exposed to hypoxic and endoplasmic reticulum stress during orthodontic tooth movement.

Academic Significance and Societal Importance of the Research Achievements

本研究成果の学術的意義は、オートファジーが矯正力によるメカニカルストレスだけでなく低酸素や小胞体ストレスに曝された骨芽細胞に対して細胞内恒常性維持機構として機能している可能性を示した点にある。更なる研究を重ねることで歯牙移動の遅延化や歯槽骨以上吸収などの副作用が生じにくい安全な矯正歯科治療を提供することができる点に社会的意義がある。

Report

(3 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Research-status Report

URL: 

Published: 2017-04-28   Modified: 2020-03-30  

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