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2020 Fiscal Year Final Research Report

Clarification of novel tissue destruction mechanism induced by mechanobiology breakdown

Research Project

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Project/Area Number 18H02975
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Review Section Basic Section 57030:Conservative dentistry-related
Research InstitutionTohoku University

Principal Investigator

Saito Masahiro  東北大学, 歯学研究科, 教授 (40215562)

Co-Investigator(Kenkyū-buntansha) 吉田 恭子 (今中恭子)  三重大学, 医学系研究科, 教授 (00242967)
山田 聡  東北大学, 歯学研究科, 教授 (40359849)
半田 慶介  神奈川歯科大学, 大学院歯学研究科, 教授 (40433429)
Project Period (FY) 2018-04-01 – 2021-03-31
Keywords細胞外マトリックス / 結合組織 / 炎症 / 弾性線維
Outline of Final Research Achievements

In order to investigate the effect of mechanical force on the development of connective tissue disease, we generated ADAMTSL6-deficient mice, which are polymerization regulators of elastic fibers that play a critical for regulating tissue strength. ADAMTSL6 is an extracellular matrix that promotes the polymerization of fibrillin-1microfibril, which is essential to elastic fiber formation. ADAMTSL6 has two types, alpha and beta, and that alpha knockout mice is embryonic lethality and beta knockout mice able to survive. An apical periodontitis model was performed to investigate if ADAMTSL6 beta knockout mice the effects of connective tissue disease. Result indicated that ADAMTSL6 beta knockout mice clearly induced bone destruction in this model. From these result, reduction of elastic fibers strength may cause connective tissue disease.

Free Research Field

歯科

Academic Significance and Societal Importance of the Research Achievements

本研究は機械的外力が病気の発症に係るかを調べた研究である。機械的外力の低下で発症する病気の代表例で解離性大動脈瘤が知られているが、歯科領域でも歯周病、根尖性歯周炎などの炎症性疾患の原因になりことが報告されてきた。しかし機械的外力がどのように体内で調整され、病気に関わるかは全く不明であった。本研究では人為的に機械的強度を弱めた実験モデルを用いて顎骨破壊が促進することを証明した。これらの成果により機械的強度の維持を目指した治療が病気予防に重要な働きをすることが示された。

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Published: 2022-01-27  

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