Attempt of bone regeneration by RANK peptide using alveolar bone resorption model

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K11401
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Periodontology
• Research Institution: Matsumoto Dental University
• Principal Investigator: Koide Masanori 松本歯科大学, 総合歯科医学研究所, 講師 (10367617)
• Co-Investigator(Kenkyū-buntansha): 二宮 禎 日本大学, 歯学部, 准教授 (00360222) ; 宇田川 信之 松本歯科大学, 歯学部, 教授 (70245801)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 歯周病 / RANK / 歯槽骨 / 破骨細胞 / 骨芽細胞 / 骨形成 / 骨吸収

Outline of Final Research Achievements

Osteoblasts express two key molecules for osteoclast differentiation, RANKL and osteoprotegerin (OPG), a soluble decoy receptor for RANKL. RANKL induces osteoclastogenesis, while OPG inhibits it by blocking the binding of RANKL to RANK, a cellular receptor of RANKL. OPG-deficient (OPGKO) mice exhibit severe alveolar bone loss with enhanced bone resorption. RANK peptide (W9) binds to RANKL and blocks RANKL-induced osteoclastogenesis. Here, we show that treatment with W9 restores alveolar bone loss in OPGKO mice by suppressing osteoclastogenesis and enhancing osteoblastogenesis. Administration of W9 to OPGKO mice significantly decreased the osteoclast number and decreased the osteoblast number in the alveolar bone. These results suggest that treatment of OPGKO mice with W9 suppressed osteoclastogenesis by inhibiting RANKL signaling and enhanced osteoblastogenesis in the alveolar bone. Taken together, W9 may be a useful drug to prevent alveolar bone loss in periodontitis.

Free Research Field

医歯薬学