Validation experiment designed to validate causal mechanisms targeting Cx43 in Rats with unilateral anterior crossbite model. Primary outcome: OA-like degeneration in TMJ and Cx43 upregulation
An in vivo animal model study investigating temporomandibular joint osteoarthritis (TMJOA) progression using a unilateral anterior crossbite (UAC) model of malocclusion in rats. The study examined how abnormal occlusion leads to OA-like degeneration in the TMJ, with particular focus on changes in Cx43 expression and Wnt/β-catenin pathway activation in condylar cartilage. The UAC model was used to simulate the mechanical stress and abnormal loading conditions that contribute to TMJOA development in humans.
Induction of unilateral anterior crossbite in rats followed by assessment of TMJ degeneration, Cx43 expression analysis, and Wnt/β-catenin pathway activation in condylar cartilage
UAC would induce OA-like changes with increased Cx43 expression and Wnt pathway activation
Demonstration of TMJ degeneration, upregulated Cx43 expression, and activated Wnt/β-catenin signaling
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