Search for target molecules for the treatment of Idiopathic gingival fibromatosis

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K18536
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 57030:Conservative dentistry-related
• Research Institution: Hiroshima University
• Principal Investigator: Okanobu Ai 広島大学, 病院(歯), 歯科診療医 (00806581)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 特発性歯肉線維腫症

Outline of Final Research Achievements

When periodontitis was induced in NR4A1 knockout mice, marked gingival swelling with dense collagen fibers inside the connective tissue was observed compared to WT mice. Next, RNA sequencing was performed using HGF collected from patients with chronic periodontitis or idiopathic gingival fibromatosis. Consequently, Kegg-pathway analysis showed accumulation of genes with altered expression in ECM-receptor interaction and TGF-beta signaling pathway, but no obvious changes in NR4A1 expression. On the other hand, integrin α8, integrin α11, and transglutaminase 2 (TGM2), which have been reported to be involved in tissue fibrosis, showed fluctuations in their expression.

Free Research Field

歯周病

Academic Significance and Societal Importance of the Research Achievements

本研究の結果から、マウスの歯肉線維化にNR4A1の関与が示唆された一方で、ヒトの特発性歯肉線維腫症では明らかな発現の変動を認めなかった。過去に薬物性歯肉増殖症についてNR4A1の関与が示唆されているが、特発性歯肉線維腫症については、他のメカニズムが関与している可能性がある。今後はNR4A1だけでなく、本研究で発現の変動を認めたインテグリンα8、インテグリンα11、TGM2などにも焦点をあて、その関係性について検討を行うことが、特発性歯肉線維腫症のみならず、種々の線維化疾患のメカニズムの一端を解明することにつながると考える。