RIP1 inhibition prevents mechanical stress-induced TMJ OA by regulating apoptosis and late-stage necroptosis of chondrocytes

Abstract Temporomandibular joint osteoarthritis (TMJ OA) is a common degenerative joint disease that has multiple causes. The abnormal stress distribution is known to be an important trigger of TMJ OA. In order to clarify the mechanism of pathological changes in mandibular cartilage under compressive mechanical stress and the function of RIP1 inhibition through Lenti-virus in mechanical stress-induced TMJ OA, we used a compressive mechanical force-induced-TMJ OA rat model and Lenti-virus targeting RIP1 to perform this study. The results identified the characteristics of the spatio-temporal changes in mechanical stress-induced TMJ OA. Under mechanical force, inflammation and apoptosis, which occur in the whole layer of mandibular cartilage, appear on 4th day and persist till 7th day. Necroptosis arises in the late stage of mechanical force and is mainly located in the transition layer. RIP1 plays an essential role in the destruction of mandibular cartilage under mechanical force. RIP1 inhibition through Lenti-virus could protect mechanical stress-induced mandibular cartilage thinning by inhibiting persisted apoptosis and late-stage necroptosis in the transition layer.