LAUSR

OBJECTIVE TMJOA is a chronic degenerative joint disorder with multiple etiologies that significantly impair patients' quality of life. Autophagy and apoptosis are critical to the pathogenesis of TMJOA. Trehalose is a novel autophagy activator and has significant therapeutic efficacy in mitigating diseases. This study investigated trehalose's role and possible mechanisms in TMJOA evolution, both in vitro and in vivo. METHODS Rat condylar chondrocytes were identified by toluidine blue and type I/II collagen immunofluorescence staining. Methods such as CCK-8 assay and immunofluorescence were used to detect the protective effect of trehalose on interleukin-1β (IL-1β)-induced chondrocytes. Histological staining and other techniques were applied to evaluate its therapeutic effect on monosodium iodoacetate (MIA)-induced TMJOA in rats and its underlying mechanism. RESULTS Trehalose can suppress IL-1β-induced apoptosis in condylar chondrocytes by stimulating autophagy through the activation of AMP-activated kinase (AMPK) and UNC51-like kinase-1 (ULK1). The inhibition of the AMPK signaling pathway negated the preventive effect of trehalose on TMJOA. TMJOA rats treated with trehalose exhibited phosphorylation of the AMPK/ULK1 pathway and activation of autophagy, accompanied by cartilage protection. CONCLUSIONS This study demonstrates the potential of trehalose as a novel treatment agent to impede the evolution of TMJOA.