Avascular Necrosis of the Hip

Avascular necrosis (AVN) — also called osteonecrosis — is what happens when the blood supply to the ball at the top of your thighbone (the femoral head) is interrupted. Bone is living tissue that depends on a constant flow of blood to deliver oxygen and remove waste. The femoral head's supply is especially fragile: most of it enters through a narrow corridor along the neck of the bone, and any disruption — a fracture, a hip dislocation, or damage to the tiny vessels inside the bone itself — can cut off enough flow to kill a patch of bone.

Without blood, the dead bone cannot repair the microscopic fractures that normal daily loading creates. Those microfractures accumulate, the smooth surface of the ball begins to flatten and collapse, and once it collapses the cartilage on top crumbles with it, producing rapid and often severe arthritis of the hip joint. Common risk factors include high-dose or prolonged corticosteroid use (oral steroids for asthma, lupus, or transplant immunosuppression), excessive alcohol use, sickle cell disease, clotting disorders, and prior radiation. In many cases no clear cause is found (idiopathic AVN). The condition is bilateral — affecting both hips — in up to 80% of cases, and it tends to strike adults in their 30s through 50s, earlier in life than typical wear-and-tear arthritis.

Early AVN is often silent, or the pain is so vague that it gets blamed on a muscle strain. The first symptom is usually a dull ache deep in the groin — not on the side of the hip or the buttock, but in the crease where your leg meets your trunk. The pain comes on with weight-bearing and is relieved by rest. Because the damage is inside the bone, the hip may still move normally at this stage, and a physical exam can be surprisingly unremarkable.

As the necrotic area enlarges, pain becomes more persistent. You may start to limp, and your provider may notice that the hip has lost some of its ability to rotate inward (internal rotation) — one of the earliest exam findings. A sudden worsening of pain, sometimes described as a sharp catch or a feeling that the hip "gave way," can signal that the femoral head has begun to collapse. Once collapse occurs, the progression to end-stage arthritis can be rapid — months rather than years.

X-rays of the hip are the first step, but they are often normal in early AVN — the bone has not yet changed shape. By the time the X-ray shows the characteristic crescent sign (a thin bright line just under the surface of the femoral head where the dead bone is separating from the living bone above it) or visible flattening of the ball, the disease is already advanced. That is why MRI is the gold-standard study: it can detect the dead-bone signal months before any X-ray change appears, when the window for preserving the joint is still open.

Once AVN is confirmed, your provider stages it — typically using the Ficat or ARCO classification — based on how much of the femoral head is involved and whether the surface has started to collapse. Staging drives the treatment decision: early stages may respond to protective measures, while a collapsed femoral head almost always requires replacement. If one hip is affected, your provider often orders an MRI of the other hip as well, since the condition is bilateral in a large majority of cases.

Most patients with AVN beyond the earliest stages ultimately require surgery. The choice of procedure depends on the stage, the size of the necrotic lesion, and whether the femoral head has collapsed.

External patient-education references and related OSI pages for additional background:

• Britannica — Hip (anatomy)
• AAOS OrthoInfo — patient education library
• OSI glossary — orthopedic terminology in plain language