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Corticosteroids are considered the most common cause of atraumatic ONFH, and the exact mechanism is unknown. A 2015 meta-analysis by Mont and colleagues found a statistically significant association between high-dose corticosteroid use (20 mg prednisone or equivalents per day) and ONFH, but cases have been reported from long-term and short-term doses and after oral, intravenous, topical, and intra-articular application. The most commonly accepted theory surrounding corticosteroids and ONFH involves fat accumulation in marrow, leading to increased intraosseous hypertension and decreased blood flow. This concept has been extrapolated into a multiple-hit theory by which corticosteroids alter bone homeostasis, injure bone cells, impair blood flow, and suppress bone cell precursors in susceptible patients. In support of the multiple-hit theory, Wang and colleagues found increased differentiation of pluri potential stem cells into adipocytes and reduced expression of type I collagen and osteocalcin messenger RNA in an animal model. Corticosteroids inhibit angiogenesis and promote a hypercoaguable state, which could contribute to the formation of intravascular thrombosis leading to ONFH. Also, studies have investigated whether there is a genetic susceptibility to corticosteroid-induced ONFH. Because not all patients receiving corticosteroids develop ONFH, it is most likely due to a combination of factors, including genetic susceptibility, dosage, and underlying condition