The functional analysis of SOD2, antioxidantdefense in periodontal tissue

2015 Fiscal Year Final Research Report

• Project/Area Number: 25463221
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Periodontology
• Research Institution: Kyushu Dental College
• Principal Investigator: USUI MICHIHIKO 九州歯科大学, 歯学部, 准教授 (10453630)
• Co-Investigator(Kenkyū-buntansha): TAKAHIKO SHIMIZU 千葉大学, 医学科研究院, 准教授 (40301791)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 酸化ストレス / セメント質 / ＳＯＤ２

Outline of Final Research Achievements

SOD (Superoxide dismutase) is an enzyme that alternately catalyzes the dismutation of the superoxide (O2－) radical into either ordinary molecular oxygen (O2) or hydrogen peroxide (H2O2). Thus, SOD is an important antioxidantdefense in nearly all living cells exposed to oxygen. We generated DMP1 cre SOD2 KO mice and conditionally inactivated SOD2 in osteocytes and odontoblasts. We found that loss of SOD2 enhanced thickness of cementum in teeth. In the other hands, periodontal ligament and alveolar bone in DMP1 cre SOD2 KO mice were normal compared with wild type mice. Overexpression of SOD2 in cementoblasts decreased the expression of DMP1 and CP23, which were differentiation markers of cementum. On the contrary, knockdown of SOD2 using siRNA increased both proliferation and differentiation in cementoblasts. These data suggested that SOD2 supressed proliferation and differentiation in cementoblasts.

Free Research Field

歯周病学分野