Production of the inflammatory periodontal disease model by the enhanced MAPK signaling

2014 Fiscal Year Final Research Report

• Project/Area Number: 24593132
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Periodontal dentistry
• 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): NINOMIYA Tadashi 松本歯科大学, 総合歯科医学研究所, 講師 (00360222) ; UDAGAWA Nobuyuki 松本歯科大学, 歯学部, 教授 (70245801)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 歯周病 / 歯周病モデル / 歯槽骨吸収 / MAPK / OPG / 歯周免疫機能学

Outline of Final Research Achievements

Periodontitis is caused a chronic inflammatory disease by bacteria infection. But, the condition of a patient is complicated, and pathological condition of periodontitis is not understood well enough. Elucidation of the inflammation of host side is important to progress treatment of periodontitis. MAPK is an intracellular signal transduction of an inflammation. Deficiency of MAPK phosphatase-1 (MAPK inactivating gene, MKP-1) activates constantly inflammation. MKP-1-deficient mice exhibited high sensitivity of inflammation. OPG-deficient mice exhibited severer alveolar bone loss. Our aiming was establishment of the accelerated periodontitis model that reflected the pathological condition. (Result) I got the MKP-1 and OPG double deficient (dKO) mice. The alveolar bone loss is more severe in MKP-1 and OPG dKO mice than OPG-deficient mice using analysis of micro CT.

Free Research Field

医歯薬学