The effect of CXCL9 on bone regeneration and osseointegration process around the implants in mice.

Abstract

This study aimed to investigate the role of CXCL9 during titanium implant osseointegration. Lentivirus-mediated overexpression and knockdown models of Cxcl9 were used in male C57BL/6 mice. Titanium implants were placed in the maxillae of the mice, and the osseointegration process was analyzed using micro-CT to evaluate bone volume and mineral density, histological staining to visualize bone-to-implant contact (BIC), RT-qPCR to detect osteogenic gene expressions, and enzyme-linked immunosorbent assay to assess inflammatory cytokine levels. Results showed that Cxcl9 overexpression significantly impaired osseointegration, as evidenced by reduction in bone volume, bone mineral density, and BIC. This was accompanied by an increase in osteoclast numbers. Moreover, Cxcl9 overexpression suppressed expression of osteogenic genes and resulted in elevated pro-inflammatory cytokines, including TNFα and IL1β. Conversely, Cxcl9 knockdown improved osseointegration, suggesting that CXCL9 is a negative regulator of bone remodeling at implant sites. Further, CXCL9 expression impairs titanium implant osseointegration. This highlights CXCL9 as a potential therapeutic target to improve dental implant osseointegration, particularly in patients with inflammatory conditions.