Oxidative stress in steroid-induced necrosis of femoral head: a review revealing new insights into pathogenic mechanisms

Steroid-Induced Necrosis of the Femoral Head (SINFH) has a complex pathogenesis. Disorders of bone metabolism, vascular injury, apoptosis, inflammatory responses, lipid metabolism disturbances, and oxidative stress are all closely related to the occurrence of this condition. Oxidative stress has a broad impact on various physiological functions in the body. Studies have shown that oxidative stress can affect bone metabolic balance, inflammatory responses, vascular injury, and apoptosis, thereby accelerating the progression of SINFH. Therefore, oxidative stress is crucial for the occurrence and development of SINFH. Inhibiting oxidative stress has positive implications for the treatment of steroid-induced avascular necrosis. Different classes of antioxidants exhibit distinct mechanisms of action and therapeutic potential: (1) direct free radical scavengers (e.g., vitamin C, vitamin E) primarily neutralize existing reactive oxygen species (ROS); (2) enzyme modulators (e.g., N-acetylcysteine) enhance endogenous antioxidant systems; (3) natural compounds (e.g., resveratrol, curcumin) activate nuclear factor erythroid 2-related factor 2 (Nrf2) and other signaling pathways. Their application scenarios vary accordingly, with some more suitable for prevention and others for intervention. However, maintaining a dynamic balance between oxidation and antioxidation may be more important than completely suppressing redox reactions.