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Excessive oxidative stress is another central driver of OA pathogenesis, amplifying inflammation and accelerating chondrocyte apoptosis through ROSinduced cellular injury and activation of degenerative signaling cascades 20,21,22 .Mutual reinforcement between oxidative stress and inflammation establishes a pathological feedback loop that aggravates cartilage damage and joint deterioration 23,24 .In this study, OSR efficiently reduced intracellular ROS accumulation and enhanced intrinsic antioxidant defenses, thereby breaking this pathological feedback loop and improving cellular redox homeostasis

HbA1c, disease duration) and achieved AUC 0.81 in an independent test set, demonstrating utility in risk prediction rather than definitive diagnosis [58]

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Epub 2013 Apr 7

It does not replace nutrition, rest, or injury evaluation