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Objectives: The present study aimed to elucidate the pathogenesis of temporomandibular joint (TMJ) osteoarthritis (TMJ-OA) in a mouse model. We investigated morphological and histological changes in the head of mandible cartilage and early immunohistochemical (IHC) changes in transforming growth factor (TGF)-β, phosphorylated Smad-2/3 (p-Smad2/3), a TGF-β signaling molecule, and asporin., Methods: TMJ-OA was induced in a mouse model through unilateral partial discectomy. Micro-computed tomography (micro-CT) and safranin-O staining were performed to morphologically and histologically evaluate the degeneration of the head of mandible caused by TMJ-OA. IHC staining for TGF-β, p-Smad2/3, and asporin was performed to evaluate the changes in protein expression., Results: In the experimental group, three-dimensional (3D) morphometry revealed an enlarged head of mandible and safranin-O staining showed degeneration of cartilage tissue in the early stages of TMJ-OA compared to the control group. IHC staining revealed that TGF-β, p-Smad2/3, and asporin expression increased in the head of mandible cartilage before the degeneration of cartilage tissue, and subsequently decreased for a short period., Conclusion: The findings suggested a negative feedback relationship between the expression of asporin and the TGF-β/Smad transduction pathway, which may be involved in the degeneration of the head of mandible in the early stages of TMJ-OA. Asporin is a potential biomarker of the early stages of TMJ-OA, which ultimately leads to the irreversible degeneration of TMJ tissues., Competing Interests: Declaration of competing interest The authors declare no potential conflicts of interest with respect to the authorship or publication of this article., (Copyright © 2024 Japanese Association for Oral Biology. Published by Elsevier B.V. All rights reserved.)

Objectives: Temporomandibular joint osteoarthritis (TMJ-OA) causes degenerative changes in TMJ tissues. The inter-tissue crosstalk that exacerbates illness and organic changes in bone secondary to TMJ-OA potentially affects the muscles; therefore, patients with a muscular disease might also suffer from bone disease. However, knowledge gaps exist concerning muscle pathology at the onset of TMJ-OA. In this study, we documented the pathogeneses of the bone and muscle at the onset of TMJ-OA using a mouse model., Methods: We performed a partial resection of the TMJ disk to establish a mouse model of TMJ-OA. After the onset of TMJ-OA, we performed various measurements at 8, 12, and 16 weeks post-surgery in the defined groups., Results: The volume of the mandibular head in the TMJ-OA group was significantly greater than that in the control group. The temporal muscles in the TMJ-OA group were significantly deformed compared with those in the control group; however, between-group comparisons did not reveal significant differences in the mandibular head or temporal muscles after surgery. Therefore, we hypothesized that the degree of mandibular head hypertrophy would alter the temporal muscles. A subsequent analysis of the correlation between the bone and muscle confirmed that the deformity of the temporal muscle increased with increasing hypertrophy of the mandibular head. Temporal and masseter muscle contact was observed in 25% of surgical groups., Conclusions: This study demonstrates that TMJ-OA progressed when organic changes occurred in bones and muscles, supporting the symbiotic relationship between bones and muscles., Competing Interests: Conflicts of interest All authors declare no conflict of interest., (Copyright © 2021 Japanese Association for Oral Biology. Published by Elsevier B.V. All rights reserved.)