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The connection between alcohol use and ONFH has been known for almost a century, and, as with corticosteroids, the exact mechanism is unknown. Animal studies of bone marrow treated with alcohol have shown increased pressure and adipogenesis and decreased hematopoiesis, which could lead to osteocyte injury and ONFH. There seems to be a dose-response relationship; however, there is no established threshold beyond which patients are proved more at risk. Given the relatively low prevalence of ONFH among all alcohol users, there is likely a multifactorial relationship between ONFH, genetic susceptibility, environmental factors, and medical comorbidities.