Analysis of bone remodeling mechanism between osteoblasts and osteoclasts for the alveolar bone regeneration

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390417
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Functional basic dentistry
• Research Institution: Matsumoto Dental University
• Principal Investigator: UDAGAWA Nobuyuki 松本歯科大学, 歯学部, 教授 (70245801)
• Co-Investigator(Kenkyū-buntansha): KOIDE Masanori 松本歯科大学, 総合歯科医学研究所, 講師 (10367617) ; NAKAMURA Midori 松本歯科大学, 歯学部, 准教授 (90278177) ; NAKAMICHI Yuko 松本歯科大学, 総合歯科医学研究所, 講師 (20350829) ; UEHARA Syunsuke 松本歯科大学, 歯学部, 講師 (90434480) ; TAGUCHI Akira 松本歯科大学, 歯学部, 教授 (70243582)
• Co-Investigator(Renkei-kenkyūsha): ABIKO Yoshimitu 日本大学, 歯学部, 教授 (70050086) ; SHIMODAIRA Shigetaka 信州大学, 医学部, 教授 (80345751)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 骨芽細胞 / 破骨細胞 / 骨代謝共役 / 歯槽骨 / 歯周病 / 骨粗鬆症

Outline of Final Research Achievements

OPG-deficient mice (OPG KO) exhibited severe osteoporosis due to enhanced osteoclastogenesis when they grew to be adults. In RANKL-Tg mice, a soluble form of RANKL is expressed under the control of the human serum amyloid P component promoter. RANKL-Tg mice exhibit osteopenia characterized by excessive bone resorption. Alveolar bone loss in OPG KO mice and RANKL-Tg mice was evaluated using micro computed tomography and histological techniques. We show that OPG KO but not RANKL-Tg mice exhibit severe alveolar bone destruction. OPG was highly expressed in osteocytes in the alveolar bone, suggesting that OPG secreted from osteocytes prevents the alveolar bone loss induced by the excess amount of RANKL in RANKL-Tg mice. Treatment with an anti-RANKL antibody as well as risedronate, a bisphosphonate, significantly inhibited the alveolar bone loss in OPG KO mice. These results suggest that OPG KO mice are a useful model for screening therapeutic agents in periodontology.

Free Research Field

口腔生化学