Femoral head necrosis is a progressive disease that is common between the ages of 20 and 50. If left untreated, the hip joint can be completely destroyed. It used to be called ischemic necrosis, but now it tends to be named osteonecrosis. Simply put, osteonecrosis means “dead bone”. The “ischemic state” of necrotic bone is the result of a loss of circulation and can be caused by a variety of underlying factors. Osteonecrosis describes an end state that is the result of the progression of many possible pathological processes. There are many causes of osteonecrosis, including alcoholism, gout, decompression sickness, Gaucher’s disease, renal bone atrophy, hypercoagulable states, sickle cell anemia, systemic use of adrenocorticotropic hormones, and trauma. However, many patients cannot find a cause, and this group of patients is known as idiopathic osteonecrosis. There are several theories about the pathogenesis of osteonecrosis. These include the following hypotheses: direct cytotoxic effects, abnormal coagulation states, hyperlipidemia, fat embolism, interrupted or abnormal blood supply, and increased bone marrow pressure. All these hypotheses do not explain the full etiology and many people with the above mentioned known risk factors do not develop osteonecrosis, while many people without these risk factors do. The process of osteonecrosis is more likely to be multifactorial. The most common method of staging femoral head necrosis is the Ficat, Arlet method, which stages based on x-ray changes. There are other classification methods, but they are mostly modifications of the Ficat method and are essentially the same.