Analysis of leukocyte infiltration mechanism to participate in inflammatory bone resorption in periodontal lesion

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K11834
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Periodontology
• Research Institution: The University of Tokushima
• Principal Investigator: HOSOKAWA Yoshitaka 徳島大学, 病院, 講師 (90346601)
• Co-Investigator(Kenkyū-buntansha): 中西 正 徳島大学, 大学院医歯薬学研究部(歯学域), 准教授 (00217770) ; 細川 育子 徳島大学, 大学院医歯薬学研究部(歯学域), 助教 (50707908)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 歯周炎 / 白血球 / ケモカイン / 歯周組織構成細胞

Outline of Final Research Achievements

CC chemokine receptor (CCR)5 positive leucocytes were involved in bone resorption in periodontal lesion. So, we examined if human periodontal ligament cells (HPDLC) could produce CCR5 ligand {CC chemokine ligand (CCL)3 and CCL5} in this experiment. We found IL-1beta could induce CCL3 and CCL5 production in HPDLC. Next, we will find the material that could inhibit CCL3 or CCL5 production in HPDLC. We focused on alkannin which is extracted from Alkanna tinctoria, a member of the borage family that grows in France. We found alkannin could inhibit CCL3 and CCL5 production in IL-1beta-stimulated HPDLC. Moreover, we reported　alkannin could inhibit nuclear factor (NF)-kappaB activation in IL-1beta-stimulated HPDLC. These results suggest that HPDLC is involved in CCR5-positive leukocytes infiltration because HPDLC could produce CCR5 ligands. Topical application of alkannin might decrease the number of CCR5-positive leucocytes because alkannin could inhibit CCL3 and CCL5 production in HPDLC.

Free Research Field

歯周病態学分野

Academic Significance and Societal Importance of the Research Achievements

本研究ではヒト歯根膜由来細胞が産生するCCR5リガンド産生をアルカンニンが抑制できる事を明らかとした。CCR5陽性白血球が歯周炎病変局所において歯槽骨吸収に関与している事より、アルカンニンを歯周炎局所に投与する事によりCCR5陽性細胞数が減少した結果歯槽骨吸収も抑制できる可能性も考えられ、アルカンニンを歯周炎治療に用いる事が出来る可能性が示唆された。