Monosodium Iodoacetate Induced Subchondral Bone Microstructure and Inflammatory changes in an Animal Model of Osteoarthritis

Abstract Objective: To verify the presence of histopathological injury and cartilage degeneration in MIA induced joints. To investigate the correlation between inflammatory reaction and subchondral bone remodeling in a rodent osteoarthritic model.Method: Intra-articular injection of MIA was performed in Wistar rats to induce OA. After 4 weeks intervention, the animals were sacrificed, changes in intrinsic structural properties of the subchondral bones were measured using micro-CT scanning. Moreover, the histological evaluation and biochemical analysis was conducted using histochemical staining, immunofluorescence, real-time polymerase chain reaction, and western blot analysis.Results: This study demonstrated that intra-articular injection of MIA increased chondrocyte apoptosis and promoted cartilage matrix degradation, such as cartilage surface defects and shallow or even disappeared staining. MIA also induced the inflammatory process, improved the expression of IL-1β, TNF-α, matrix metalloproteinase, and decreased the expression of cartilage specific proteins with the extension of modeling time. Meanwhile, the MIA also significantly accelerated the subchondral bone remodeling at both week two and week four, as shown by the decreased subchondral bone density, thinning of trabeculae, disordered cartilage structure and morphology.Conclusion: Intra-articular injection of MIA can lead to articular cartilage degeneration and subchondral bone remodeling in the rat model of OA. MIA induced rodent osteoarthritic model would cause decreased subchondral bone density, sparse trabecular bone, and other manifestations of osteoporosis accompanied by an inflammatory response, which would worsen with the progression of modelling time.