Toll-like receptor 2 activation primes andupregulates osteoclastogenesis via lox-1

2018 Fiscal Year Final Research Report

• Project/Area Number: 15K11405
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Periodontology
• Research Institution: Fukuoka Dental College
• Principal Investigator: Ohgi Kimiko 福岡歯科大学, 口腔歯学部, 講師 (50610979)
• Co-Investigator(Kenkyū-buntansha): 岡部 幸司 福岡歯科大学, 口腔歯学部, 教授 (80224046)
• Project Period (FY): 2015-04-01 – 2019-03-31
• Keywords: 破骨細胞 / 脂質異常症 / 歯周炎

Outline of Final Research Achievements

Lox-1 is the receptor for oxidized low-density lipoprotein (oxLDL), a mediator in dyslipidemia. Toll-like receptor(TLR)-2 and 4 are receptors of lipopolysaccharide(LPS) from Porphyromonas gingivalis, a major pathogen of chronic periodontitis. Although some reports have demonstrated that periodontitis has an adverse effect on dyslipidemia, little is clear that the mechanism is explained the effects of dyslipidemia on osteoclastogenesis. We have hypothesized that osteoclast oxLDL has directly effect on osteoclasts (OCs), and therefore alveolar bone loss on periodontitis may be increased by dyslipidemia. The present study aimed to elucidate the effect of Lox-1 on osteoclastogenesis associated with TLRs in vitro.
This study supports that osteoclastogenesis is promoted under the coexistence of oxLDL by TLR2-induced upregulation of Lox-1 in BMCs. This indicates that periodontitis could worsen with progression of dyslipidemia.

Free Research Field

骨吸収疾患

Academic Significance and Societal Importance of the Research Achievements

ともに生活習慣病である脂質異常症と歯周病との相互作用を明らかにするため、骨吸収を担う破骨細胞に着目した。
検討の結果、脂質異常症の原因であるoxLDLが存在すると、破骨細胞の形成が促進された。これにより、脂質異常症と歯周炎を併発すると、歯周炎が増悪する可能性が示唆された。
生活習慣病である歯周病と脂質異常症との相互作用の検討を行うことは、骨疾患だけでなく代謝疾患の病因・病態の解明にも繋がり、ひいては口腔から考える全身的な健康へと、国民の口腔領域への関心の向上にも寄与し、「健康社会の実現」へ貢献できると考えた。