Toll‐like receptor 2 mediates the degeneration of cartilage in experimental inflammatory TMJOA

Abstract Objective Synovial inflammation and intra‐articular excessive pressure were accepted as two predominant etiologies for temporomandibular joint osteoarthritis (TMJOA). Toll‐like receptor 2 (TLR2) exerts roles both in certain inflammation‐ and pressure‐induced diseases. We aim to detect the role of TLR2 in the synovitis‐ or discectomy‐induced TMJOA mice. Materials and methods Complete Freund's adjuvant (CFA)‐ and discectomy‐induced TMJOA mice were established, and pretreated with TLR2 inhibitor CU‐CPT22. Synovial inflammation, deterioration of cartilage and subchondral bone were measured by H&E and Safranin‐O staining, as well as micro‐CT. Western blotting was utilized to quantify TLR2's effect in inflammation‐ or pressure‐stimulated chondrocytes derived from rat TMJs. Results Obvious synovitis occurred in CFA‐injection mice, while unapparent inflammatory change in discectomy mice. TLR2 elevated in cartilage and synovium of CFA‐injection mice, whereas no alterations in discectomy mice. TLR2 contributed to the synovitis, deterioration of cartilage and subchondral bone in CFA‐injection mice instead of discectomy mice. TLR2 induced the production of inflammatory and catabolic factors in rat chondrocytes by IL‐1β other than pressure. Conclusion Toll‐like receptor 2 mediates synovitis, damage of cartilage and subchondral bone in CFA‐induced TMJOA model, but not discectomy‐induced TMJOA. TLR2 could be a potential target to prevent the deterioration of early phase TMJOA.