Abstract
Temporomandibular joint osteoarthritis (TMJOA) is a degenerative disorder affecting the temporomandibular joint (TMJ), marked by persistent inflammation and structural damage to the joint. Only symptomatic treatment is available for managing TMJOA. Human umbilical cord mesenchymal stem cells (hUC-MSCs) show potential for treating TMJOA via their immune-modulating actions in the disease area. In addition, stimulation of inflammatory cytokines such as interferon-gamma in hUC-MSCs improves the therapeutic activity of naïve stem cells. Emerging evidence indicates that macrophages play significant roles in regulating joint inflammation through diverse secreted mediators in the pathogenesis of TMJOA. This study was conducted to evaluate the effects of inflammatory cytokine-stimulated hUC-MSCs in repairing TMJOA-induced cartilage lesions and the role of macrophages in the disease. Our in vitro data showed that stimulated hUC-MSCs induce M2 polarization of macrophages and enhance the expression of anti-inflammatory molecules. These effects were subsequently validated in vivo. In a rat model of TMJOA, stimulated hUC-MSCs ameliorated inflammation and increased M2 macrophages ratio. Our results indicate that hUC-MSCs stimulated by inflammatory cytokines modulate the activation of M2 macrophages, thereby shifting the local osteoarthritis microenvironment toward a prochondrogenic state and facilitating cartilage repair in inflammatory conditions. Stimulating hUC-MSCs with inflammatory cytokines could potentially offer an effective therapeutic approach for TMJOA, with macrophages playing a pivotal role in immune modulation.
Impact Statement
Temporomandibular joint osteoarthritis (TMJOA) is marked by chronic inflammation and degeneration of the joint. This research focuses on human umbilical cord stem cells (hUC-MSCs), stimulated with inflammatory cytokines, to repair osteoarthritis (OA)-related cartilage lesions. In vitro results show that these stimulated cells promote M2 polarization of macrophages, leading to improved chondrocyte microenvironments and cartilage repair, validated in an in vivo rat model. This suggests a promising treatment strategy, as inflammatory cytokine-stimulated hUC-MSCs could shift the local OA environment toward cartilage repair, offering potential therapeutic benefits for TMJOA.
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