Investigation of molecular mechanism of S100A8 in diabetes-associated periodontitis

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K17352
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Periodontology
• Research Institution: The University of Tokushima
• Principal Investigator: HIROSHIMA Yuka 徳島大学, 大学院医歯薬学研究部(歯学域), 助教 (60545143)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: 最終糖化産物 / 歯周病 / S100A8

Outline of Final Research Achievements

Advanced glycation end-products (AGEs) in gingival tissues of diabetes patients aggravate periodontal disease, but the mechanisms are unknown. In this study, we focused on human gingival epithelial cells and examined the effects of S100A8 on periodontal tissue in diabetic conditions. S100A8, which was induced by AGE in human gingival epithelial cells, suppressed inflammatory factors such as IL-6, CCL2 and SAA2. S100A8 did not change the intracellular ROS production. These results suggest that the anti-inflammatory effect of S100A8 may suppress the exacerbation of inflammation in periodontal tissue in diabetic conditions and maintain biological homeostasis.

Free Research Field

歯周病学

Academic Significance and Societal Importance of the Research Achievements

糖尿病病態において歯周組織における最終糖化産物 (AGE)の蓄積は歯周炎の増悪に深く関与している。S100A8は歯肉上皮細胞で恒常的に発現し、炎症マーカーとして知られている。歯肉上皮細胞においてS100A8はAGEで発現が誘導され、AGEとの共存下では炎症性サイトカインを抑制した。糖尿病病態の歯周組織におけるS100A8の抗炎症作用は生体恒常性の維持に関与し、生理的役割の解明に寄与すると考える。