Osteonecrosis of the femoral head involves the hip joint, with osteocytes of the femoral head dying along with the bone marrow; resorption of the dead tissue by new but weaker osseous tissue can then lead to subchondral fracture and collapse. There are 2 forms of osteonecrosis: traumatic (the most common form) and atraumatic. Other terms to describe this disorder are avascular necrosis and ischemic necrosis to denote vascular etiology. The term aseptic necrosis also has been used to indicate that infection does not play a causative role.
Alexander Munro first identified the condition in 1738. In the mid 1800s, Cruveilhier was the first to attribute the disorder to an aberration of circulation in the femoral head. Diagnosis of this disorder has increased because of improved technology and increased awareness.
Osteonecrosis is now a commonly recognized disorder with significant morbidity. The end stage of the process is severe destruction of the femoral head with resultant degeneration of the hip joint. In many patients, even early identification and intervention do not alter the result. Unfortunately, patients who are affected with osteonecrosis are young, usually in the third to sixth decades of life.
Traumatic and atraumatic osteonecrosis are essentially 2 distinct problems. The traumatic form has a definitive causal event and is isolated to the particular injured bone. The atraumatic form has multiple etiologies and can involve multiple bones. The main focus of this article is atraumatic osteonecrosis.
Approximately 10,000-20,000 new cases are identified each year in the United States. The traumatic form of hip osteonecrosis occurs in 10% of undisplaced femoral neck fractures, 15-30% of displaced femoral neck fractures, and 10% of hip dislocations.
Corticosteroid use contributes to the atraumatic form of osteonecrosis in 5-25% of patients. The male-to-female ratio is about 4:1. At least 50% of patients with atraumatic hip osteonecrosis are thought to have bilateral involvement. Other bones often are involved in the atraumatic form, including the shoulder, knee, and talus.
As the name implies, traumatic osteonecrosis is secondary to direct injury to the femoral head with resultant damage of the blood supply. Fracture of the femoral head or neck and hip dislocation are the primary mechanisms of injury.
Atraumatic osteonecrosis has many risk factors. The 2 most commonly associated problems are corticosteroid use and alcohol abuse. [1, 2] The idiopathic cases make up the third most common category. Other factors include sickle cell anemia, Gaucher disease, systemic lupus erythematosus, coagulopathies, hyperlipidemia, organ transplantation, caisson disease, and thyroid disorders. Genetic factors may also play a role.
Hip osteonecrosis resulting from corticosteroid use or alcohol abuse is associated with the worst prognosis. Frequently, steroid-induced osteonecrosis involves multiple bones and, in the case of the hip, results in nearly 100% bilateral involvement. The exact dose required to induce osteonecrosis remains an enigma, but most studies indicate that higher doses, even over a short duration, present the highest risk. Often, patients on steroids have other associated risk factors.
Osteonecrosis associated with alcohol abuse usually occurs in those who drink more than 400 mL of alcohol per week. It is more common in those with a long-term history of heavy consumption.
Traumatic osteonecrosis is a direct result of disruption of the blood supply to the femoral head. Death of bone marrow occurs within 6-12 hours after vascular insult. Death of the bone becomes apparent several days later.
The pathophysiology in atraumatic osteonecrosis remains controversial.  Fat cell hypertrophy with resultant pressure increase within the femoral head, leading to vascular collapse and then necrosis, has been proposed as a mechanism for steroid-induced osteonecrosis. A fat embolism phenomenon with resultant vascular occlusion is another proposed mechanism. A hyperlipidemic state seems to be related to causation, but the exact mechanism is unknown. Similarly, the lipid hypothesis has also been applied to cases associated with alcohol abuse.
Studies have shown evidence of acquired hypercoagulabiltiy. This effect appears to be augmented by tobacco abuse.  Recent studies have also shown elevated cryofibrinogen levels in atraumatic osteonecrosis. 
In caisson disease, circulating nitrogen bubbles occlude blood vessels in response to reduction in ambient pressure during decompression. Sickle cell anemia results in bone death secondary to the sickling process and subsequent vascular occlusion.
Increased intraosseous pressure contributes directly to the propagation of necrosis, regardless of etiology. As bone death occurs, a repair process takes place as dead bone is removed and replaced by new bone. During this phase, the bone underlying the joint surface is weakened. In most patients, subchondral fracture alters the articular surface, resulting in abnormal mechanics and arthritic alterations to the joint.
The disease affects both sides of the joint, as confirmed by PET scan imaging showing earlier involvement in the acetabulum than is discernible by other radiographic modalities.
Patients with osteonecrosis usually are men in the sixth decade of life who experience pain primarily in the groin but occasionally the buttocks. Pain usually is deep and throbbing and is worse with ambulation, but it also is significant at night. Onset often can be described as acute. Patients frequently describe a catching or popping sensation with motion. A history of trauma, steroid use, alcohol abuse, and other risk factors should be sought.
Physical examination reveals pain with range of motion and ambulation. Limitation of internal rotation in both flexion and extension are prevalent, with passive internal rotation in extension being particularly painful. A Trendelenburg gait often is present.
Plain radiographic findings frequently are normal. Therefore, a high index of suspicion should arise based on the history and physical.
History and physical examinations are paramount for diagnosis. Treatment is indicated after diagnosis is confirmed with radiographic studies. Most studies indicate that the risk for disease progression is greater with nonsurgical treatment than with surgical intervention. The natural history is not well understood in atraumatic osteonecrosis, but it has been recently shown that approximately 56% of asymptomatic patients eventually become symptomatic. 
Blood is supplied to the femoral head primarily from branches of the medial and lateral circumflex vessels, which arise from the femoral artery. The retinacular branches deep to the posterior capsule are the most important. Blood also is supplied from the obturator artery.
There are few contraindications to surgical treatment of osteonecrosis. Obvious disorders aside (eg, severe systemic disease, systemic sepsis), those afflicted often are young and have few surgical contraindications.
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