CCR2 is a potential therapeutic target in peri‐implantitis

Abstract Aim CCR2 (C‐C chemokine receptor type 2) plays a crucial role in inflammatory and bone metabolic diseases; however, its role in peri‐implantitis remains unclear. This study aimed to explore whether CCR2 contributes to peri‐implantitis and the treatment effects of cenicriviroc (CVC) on peri‐implant inflammation and bone resorption. Materials and Methods The expression of CCR2 was studied using clinical tissue analysis and an in vivo peri‐implantitis model. The role of CCR2 in promoting inflammation and bone resorption in peri‐implantitis was evaluated in Ccr2 −/− mice and wild‐type mice. The effect of CVC on peri‐implantitis was evaluated using systemic and local dosage forms. Results Human peri‐implantitis tissues showed increased CCR2 and CCL2 levels, which were positively correlated with bone loss around the implants. Knocking out Ccr2 in an experimental model of peri‐implantitis resulted in decreased monocyte and macrophage infiltration, reduced pro‐inflammatory cytokine generation and impaired osteoclast activity, leading to reduced inflammation and bone loss around the implants. Treatment with CVC ameliorated bone loss in experimental peri‐implantitis. Conclusions CCR2 may be a potential target for peri‐implantitis treatment by harnessing the immune‐inflammatory response to modulate the local inflammation and osteoclast activity.