Objectives: The effects of systemic inflammation on the temporomandibular joint (TMJ) are poorly understood. This study aimed to establish a mouse model to study the effects of systemic inflammation on the TMJ.
Materials and methods: SKG mice, a BALB/c strain with spontaneous onset of rheumatoid arthritis-like symptoms due to a spontaneous point mutation (W163C) in the gene encoding the SH2 domain of ZAP-70, were treated with zymosan (β-1,3-glucan). Synovitis, bone erosion, and cartilage damage in the TMJ were evaluated using established scores for animal models of inflammatory arthritis. Myeloperoxidase-positive areas and numbers of tartrate-resistant acid phosphatase (TRAP)-positive cells were compared between naive and zymosan-treated SKG mice. Correlations between TMJ inflammation scores and clinical scores for extremities were also assessed.
Results: There were significant differences in TMJ inflammation scores, including synovitis, bone erosion, and cartilage damage, between naive and high-dose zymosan-treated mice. There were significant differences in myeloperoxidase-positive areas and numbers of TRAP-positive cells between naive and zymosan-treated mice. There were significant correlations between TMJ inflammation scores and clinical scores for extremities.
Conclusions: Systemic administration of zymosan efficiently induces TMJ inflammation in SKG mice. Zymosan-treated SKG mice offer a useful tool to investigate the effects of systemic inflammation on the TMJ.
Keywords: SKG mice; inflammation; rheumatoid arthritis; temporomandibular joint; zymosan.
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