Cell Apoptosis and Glucocorticoid‐Induced Osteonecrosis

Glucocorticoids (GCs) are steroid hormones commonly used to treat inflammation, autoimmune diseases, and malignant tumors. By inhibiting bone formation and promoting osteoclast apoptosis, GCs significantly accelerate the onset of femoral head osteonecrosis, leading to structural changes, collapse, or destruction of bone. The mechanisms and pathways involved in glucocorticoid‐induced osteonecrosis (GION) may offer insights for developing new treatments. The pathogenesis of GION is complex and multifaceted, involving multiple pro‐apoptotic signaling pathways that collectively drive bone degradation and osteonecrosis. Specifically, key pathways implicated in GION, including 11β‐HSD enzymes, CD95/CD95L, STAT1‐caspase 3, the Bcl‐2 subfamily, PI3K/Akt, and Wnt/β‐Catenin, represent potential therapeutic targets for preventing and treating GION.