Potential pathological and molecular mechanisms of temporomandibular joint osteoarthritis

Temporomandibular joint osteoarthritis (TMJ OA) is a progressive degenerative disease of the temporomandibular joint (TMJ). The unclear etiology and mechanisms of TMJ OA bring great difficulties to early diagnosis and effective treatment, causing enormous burdens to patients’ life and social economics. In this narrative review, we summarized the main pathological changes of TMJ OA, including inflammatory responses, degeneration of extracellular matrix (ECM), abnormal cell biological behaviors (apoptosis, autophagy, and differentiation) in TMJ tissue, and aberrant angiogenesis. All pathological features are closely linked to each other, forming a vicious cycle in the process of TMJ OA, which results in prolonged disease duration and makes it difficult to cure. Various molecules and signaling pathways are involved in TMJ OA pathogenesis, including nuclear factor kappa-B (NF-κB), mitogen-activated protein kinases (MAPKs), extracellular regulated protein kinases (ERKs) and transforming growth factor (TGF)-β signaling pathways et al. One molecule or pathway can contribute to several pathological changes, and the crosstalk between different molecules and pathways can further lead to a complicated condition TMJ OA. TMJ OA has miscellaneous etiology, complex clinical status, depressed treatment results, and poor prognosis. Therefore, novel in-vivo and in-vitro models, novel medicine, materials, and approaches for therapeutic procedures might be helpful for further investigation of TMJ OA. Furthermore, the role of genetic factors in TMJ OA needs to be elucidated to establish more reasonable and effective clinical strategies for diagnosing and treating TMJ OA.