Osteonecrosis is not a discrete disease but represents the final common pathway of multiple conditions, most of which result in impaired blood supply to bone. Proposed mechanisms include occlusion of smaller arteries of the femoral head by lipid droplets, sickled red blood cells, or nitrogen bubbles from caisson disease. Alternatively, structural damage to the arterial or venous walls from trauma, vasculitis, radiation, or release of vasoactive substances may lead to ischemia. In some conditions, increased intraosseous pressure from enlargement of intramedullary fat cells or osteocytes may play a role. Through one or more of these pathways, osteonecrosis begins with interruption of the blood supply to bone; subsequently, the adjacent area becomes hyperemic, leading to demineralization, trabecular thinning and, if stressed, bony collapse. The process is usually progressive, resulting in joint destruction within 3–5 years if left untreated.