2020 Volume 61 Issue 1 Pages 9-19
Mechanical overloading of the temporomandibular joint (TMJ) promotes both the initiation and progression of TMJ osteoarthritis (OA). New preclinical animal models are needed for the evaluation of the molecular basis of cellular load transmission. This would allow a better understanding of the underlying mechanisms of TMJ-OA pain and disability, and help identify new therapeutics for its early diagnosis and management. The purpose of this study was to evaluate the role of mechanical loading in the progression of TMJ-OA in surgical instability arising from unilateral partial discectomy (UPD) in a murine model. In the theoretical modelling employed, lower joint reaction forces were observed on the chewing (working) side of the TMJ in the murine craniomandibular musculoskeletal system. Hypofunction was induced secondary to UPD through surgically manipulating the working side using an unopposed molar model. When the working side was restricted to the same side as that on which UPD was performed, late-stage degeneration of the cartilage showed a significant reduction (p<0.05), with diminished fibrillation and erosion of the articular cartilage, cell clustering, and hypocellularity. Condylar remodelling and proteolysis of proteoglycans were less affected. Thus, select and specific late-stage changes in TMJ-OA were contextually linked with the local mechanical environment of the joint. These data underscore the value of the UPD mouse model in studying mechanobiological pathways activated during TMJ-OA, and suggest that therapeutically targeting mechanobiological stimuli is an effective strategy in improving long-term biological, clinical, and patient-based outcomes.
