Alcohol-induced osteonecrosis

Avascular necrosis, or ostconecrosis, occurs as a result of disruption of blood supply to a segment of bone. The etiology of this disruption is variable and potential causes include trauma, corticosteroids, alcoholism, fat emboli, systemic lupus erythematosus, organ transplantation, dysbaric osteonecrosis, Cushing's disease, pregnancy, cancer, pancreatitis, and infections caused by retroviral agents. The susceptibility of a segment of bone to develop osteonecrosis depends greatly on the vascular supply to that segment; the femoral head is the most common site and accounts for over 50,000 total hip joint replacements/year in the United States. In this review, we discuss the pathogenesis of avascular necrosis based on a review of 383 peer-reviewed manuscripts and including 78 articles selected for discussion. The focus of this article is, also, on the role of alcohol as the third most common cause of avascular necrosis. Alcohol is known to have detrimental effects on many organ systems and alcohol abuse can lead to cirrhosis of the liver. However, multiple studies have demonstrated that alcohol can adversely affect the musculoskeletal, nervous, cardiac, gastrointestinal, and endocrine systems. In genetically susceptible individuals, alcohol has a profound effect on fat metabolism, which directly influences blood supply to marginal areas of arterial perfusion such as the femoral heads. The medical practitioner should be aware that early diagnosis is essential. Conservative therapies, such as heat, massage, ultrasound, diathermy, electrostimulation, and exercise, will not work and may delay the diagnosis. The implications of alcohol usage can be profound, leading to irreversible necrosis, with attendant joint morbidity.