Development of jawbone fusion induction method by elucidating the crosstalk mechanism of inflammation and bone formation

2021 Fiscal Year Final Research Report

• Project/Area Number: 20K18682
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 57060:Surgical dentistry-related
• Research Institution: Nihon University (2021); Tokai University (2020)
• Principal Investigator: AOKI Junya 日本大学, 歯学部, 専修医 (20867030)
• Project Period (FY): 2020-04-01 – 2022-03-31
• Keywords: 骨欠損修復 / p53 / 骨芽細胞 / 骨細胞

Outline of Final Research Achievements

This study investigated the role of p53 in bone regeneration using p53KO mice. As a result, the osteoblast proliferation ability of the p53KO mouse was higher and the bone defect repair was faster than that of the wild-type mouse. In p53KO mice, the expression of runx2 and osterix was high, while the expression level of sclerostin, which suppresses the function of osteoblasts, was low. In addition, p53KO mice-derived macrophages had a low ability of osteoclast differentiation. These effects of p53 deficiency induced that the bone defect in p53KO mice is considered to have been repaired at an early stage.

Free Research Field

口腔外科学

Academic Significance and Societal Importance of the Research Achievements

本研究はp53欠損が骨芽細胞の増殖を促進することに加え、骨細胞のスクレロスチン発現を一時的に阻害することで、骨欠損部に骨形成が促される環境になることを明らかにした。この得られた結果は、これまで知られていた腫瘍抑制作用だけでなく、骨形成促進に働くというp53の新たな役割を示したことは学術的意義がある。さらに、これらの結果は、今後の口腔外科学ならびに関連歯科医学の発展に寄与するところが大きいため、社会的意義は高いと考えられる。