Temporomandibular joint osteoarthritis (TMJ OA) is common degenerative disease with few effective disease-modifying treatments in clinic. Fibroblast growth factor (FGF) signaling is implicated in articular cartilage homeostasis, but the functional roles of FGFR1 in TMJ OA remain largely unknown. In this study, we report that deletion of Fgfr1 in TMJ chondrocytes delayed the TMJ OA progression in age-associated spontaneous OA model and abnormal dental occlusion OA model. Immunohistochemical

more »

... ing revealed that Fgfr1 deficiency decreased the expressions of matrix metalloproteinase-13 (MMP13),A disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) , COL10A1, while increased aggrecan expression level in two TMJ OA models. Furthermore, our data shows that inactivation of FGFR1 signaling may promote autophagic activity in TMJ. FGFR1 inhibitor decreased the expressions of Mmp13, Adamts5, and Runx2 in IL-1β-stimulated condylar chondrocytes, while autophagy inhibitors abrogated the protective effects of FGFR1 inhibitor. Thus, our study indicates inactivated-FGFR1 signaling ameliorates TMJ OA progression partially via promoting autophagic activity. Manipulation of this signaling may be a potential therapeutic approach to modify TMJ OA. Introduction: