Compression force and inflammatory factors on the functional regulation of osteoblasts by osteoclasts

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K24130
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0907:Oral science and related fields
• Research Institution: Nihon University
• Principal Investigator: MATSUIKE Rieko 日本大学, 歯学部, 専修医 (10844219)
• Project Period (FY): 2019-08-30 – 2021-03-31
• Keywords: 歯科矯正学 / 破骨細胞 / メカニカルストレス / 骨芽細胞

Outline of Final Research Achievements

Compression force (CF) is continuously applied to alveolar bone via orthodontic appliances. Osteoclast and osteoblast plays an important role in bone remodeling . Semaphorin 4D (Sema4D) derived from osteoclasts suppresses bone formation via its RANK in osteoblast. In the present study, we examined the effects of continuous stimulation of CF on Sema4D expression in osteoclast-like RAW264.7 cells. The cells were continuously stimulated by CF, which was generated by increasing the volume of culture medium in the wells of a 96-well plate, in the presence of RANKL for 4 days. The number of tartrate-resistant acid phosphatase (TRAP) positive multinuclear cells was increased, whereas Sema4D expression was decreased by application of 0.6 and 1.1 g/cm2 CF as compared to 0.3 g/cm2 CF.
Continuous application of CF suppressed Sema4D expression, suggesting that suppressive effects of Sema4D via osteoclast on osteoblastic bone formation might be diminished during orthodontic treatment.

Free Research Field

歯科矯正学

Academic Significance and Societal Importance of the Research Achievements

関節リュウマチや歯周病などに認められる炎症性の骨破壊、ならびに骨粗鬆症など加齢に伴う骨吸収は、患者のQOLを著しく低下させるため、活発な研究が行われている。機械的刺激は、骨芽細胞のみならず骨表層で骨吸収を担う破骨細胞にも負荷される。我々はこれまでに、持続的な圧迫力が破骨細胞に対し促進的に働くことを明らかにした。本研究では、圧迫力が破骨細胞による骨芽細胞の機能調節に及ぼす影響について調べた。これにより持続的な圧迫力が、破骨細胞におけるSema4Dの発現の減少を介し、骨芽細胞に対して促進的に影響することを明らかにした。これにより持続的な圧迫力が骨代謝を促進する可能性が示唆された。