Prevention of glucocorticoid-induced fractures is gaining attention, but in fact glucocorticoids are the most long-standing cause of non-traumatic osteonecrosis, which is often overlooked. Osteonecrosis (Glucocorticoid-induced osteonecrosis, GIO) occurs in 9-40% of patients receiving long-term glucocorticoid therapy, while short-term exposure to high doses of glucocorticoids also results in osteonecrosis, but not osteoporosis, such as hormone injections in joint cavities. The name osteonecrosis is actually inaccurate because the underlying histopathological change in GIO is osteoclast apoptosis. Due to the anatomical peculiarities of bone tissue structure, apoptotic osteocytes cannot be phagocytosed and excessive hormones inhibit bone tissue remodeling, which also delays the rate at which apoptotic osteocytes are replaced. The defects caused by glucocorticoid-induced apoptosis in bone tissue are cumulative and irreparable. This defect disrupts the osteocyte-trap-tubule system, which in turn triggers a series of irreversible events leading to femoral head collapse. Available evidence suggests that in patients with osteonecrosis, bisphosphonates can rapidly reduce pain, improve mobility, and delay joint collapse.