Functional analysis of CXCR4 involved in pulpitis progression and odontoblast differentiation

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K09979
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 57030:Conservative dentistry-related
• Research Institution: Nihon University
• Principal Investigator: KAMIO Naoto 日本大学, 松戸歯学部, 講師 (10508774)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 歯髄 / 炎症 / 細胞・組織 / CXCR4 / シグナル伝達

Outline of Final Research Achievements

We searched for the function of CXCR4 during pulpitis and odontoblast differentiation. Using cultured dental pulp cells, we clarified that IL-1b and bradykinin promote mRNA and protein expression. However, PGE2 had no effect. We examined whether the increase in the intracellular calcium ion concentration was observed in the cells given the inflammatory stimulus. Although CXCL12 and MIF were examined, no significant increase was observed compared to the non-stimulated state. We also examined CX3CR1 as a similar chemokine receptor, confirmed mRNA expression and protein expression in inflammatory stimulation, and suggested that CX3CL stimulation promotes hard tissue formation.

Free Research Field

医歯薬学

Academic Significance and Societal Importance of the Research Achievements

歯髄は一度炎症を起こすと改善が困難な組織である。歯髄の有無が歯の寿命だけでなく認知症や寿命そのものにまで影響を与え、歯髄保存療法の適応拡大は歯科臨床医にとって急務である。CXCR4はケモカイン受容体のひとつで、受容体とそのリガンドは基本的には炎症の拡大時に増強されるが、それと同時に歯髄では治癒機転を促進する可能性がある。本研究で炎症モデルの細胞ではCXCR4の発現が増強されるものの、そのリガンドの作用では治癒機転への影響は確認できなかった。一方で、同様のケモカイン受容体であるCX3CR1は炎症の拡大と治癒機転への影響が確認され、歯髄炎と治癒とを関連付ける因子であることが示唆された。