Elucidation of the Immune Regulatory Dysfunction Mechanisms of Intrinsic MSCs and Novel Therapeutic Strategies for Peri-implantitis

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K23109
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0907:Oral science and related fields
• Research Institution: Okayama University
• Principal Investigator: Kohno Teisaku 岡山大学, 大学病院, 医員 (60882644)
• Project Period (FY): 2020-09-11 – 2023-03-31
• Keywords: マクロファージ / オートファジー / 間葉系幹細胞 / 歯周炎

Outline of Final Research Achievements

In this study, using a mouse ligature model that induces acute periodontal inflammation, we compared 5-week-old mice with immature immune systems to 50-week-old mice with aged immune systems and found that age-related exacerbation of alveolar bone destruction occurs. Our results suggest that the decline in MSCs function with age may contribute to the progression of alveolar bone destruction by inhibiting macrophage autophagy activity. We obtained new insights indicating that the age-related increase in macrophage autophagy activity and the decline in mesenchymal stem cell function may exacerbate periodontal disease.

Free Research Field

分子生物学

Academic Significance and Societal Importance of the Research Achievements

本研究では、急性の歯周炎症を惹起させるマウス結紮モデルを用いて、免疫系が未成熟である5週齢と中高齢である50週齢を比較したところ、加齢によって歯槽骨破壊が重症化することが分かった。本研究の結果より加齢に伴うMSCs機能の低下が、マクロファージのオートファジー活性を抑制できずに歯槽骨破壊進行を助長させる可能性が示唆された。本研究では、加齢に伴うマクロファージのオートファジー活性亢進と間葉系幹細胞機能の低下が歯周病を重症化させる可能性を示す新しい知見を得た。