Avascular necrosis of the femoral head is the death of bone tissue at the top of your thighbone, caused by a loss of blood supply. It affects between 10,000 and 20,000 people in the United States each year, most commonly striking in the 30s, 40s, or 50s, with an average age of 38 at diagnosis. Left untreated, the weakened bone gradually collapses and leads to severe arthritis in the hip joint.
Why the Femoral Head Is Vulnerable
The ball-shaped top of your thighbone sits inside the hip socket, and it depends on a surprisingly fragile network of blood vessels to stay alive. Most of its blood supply comes from two arteries that wrap around the neck of the femur and form a ring, sending small branches up into the bone. A second, smaller artery runs through the ligament that tethers the ball to the socket, though this vessel only contributes meaningfully in children.
The problem is that collateral circulation, the backup routes blood can take if the main supply is blocked, is limited in this area. When blood flow is disrupted for any reason, the bone cells (osteocytes) and marrow inside the femoral head begin to die. If circulation isn’t restored quickly, the dead bone weakens from within. Eventually the smooth, rounded surface of the femoral head flattens and crumbles, destroying the joint.
Corticosteroids, Alcohol, and Other Risk Factors
The two most common causes are corticosteroid use and heavy alcohol consumption. Together they account for the majority of cases, though the condition can also follow a hip fracture, radiation therapy, sickle cell disease, or certain autoimmune conditions. In some cases, no clear cause is identified.
With corticosteroids, the risk is dose-dependent. Patients taking more than 40 mg per day of prednisone (or its equivalent) face significantly higher odds, with roughly a 3.6% increase in incidence for every additional 10 mg of daily dose. Most steroid-related cases develop within the first three months of treatment. Long-acting steroid formulations carry a higher risk than short-acting ones, and continuing high doses predicts both new lesions and faster progression to collapse.
Alcohol has a similarly dose-dependent relationship. Occasional drinkers have about three times the odds of developing the condition compared to nondrinkers, while regular heavy drinkers face roughly 13 times the odds. The Association Research Circulation Osseous (ARCO) defines alcohol-related avascular necrosis as consuming more than 320 grams of ethanol per week for over six months, roughly equivalent to about 30 standard drinks per week. But risk begins climbing well below that threshold.
How Symptoms Develop Over Time
Early avascular necrosis often causes no symptoms at all. When pain does appear, it typically starts as a dull ache in the groin, sometimes radiating down the front of the thigh. Some people feel it in the buttock, outer hip, or even the knee, which can lead to misdiagnosis. In one study of untreated cases, the average time from diagnosis to the first onset of pain was 3.4 years, though it ranged widely from under a year to nearly nine years.
As the bone deteriorates, pain tends to worsen with weight-bearing activities like walking or climbing stairs. Range of motion in the hip gradually decreases, particularly internal rotation. Once the femoral head begins to collapse, pain becomes more constant and the joint stiffens further. Collapse was preceded by pain in every case in one long-term study, with an average of eight months of pain before structural failure occurred.
Four Stages of Progression
Doctors classify avascular necrosis into four stages using the Ficat system, which tracks how the bone looks on imaging and what the patient experiences.
- Stage 1: X-rays appear completely normal. The patient may have groin pain, but the damage is only visible on MRI or bone scan.
- Stage 2: X-rays begin to show abnormalities: areas of increased bone density, small cysts, or a mottled appearance. The femoral head still maintains its round shape.
- Stage 3: The femoral head starts to lose its smooth, round contour. A characteristic “crescent sign,” a thin line just beneath the joint surface indicating the bone is separating internally, becomes visible. This stage marks the beginning of structural failure.
- Stage 4: The femoral head has fully collapsed and flattened. The joint space narrows as the cartilage is destroyed, and degenerative arthritis sets in.
Without treatment, nearly 50% of affected hips collapse within four years of diagnosis. The average time to collapse is about 4.1 years, but the range is wide: some hips collapse in just over a year, while others survive almost 12 years.
Why MRI Matters for Early Detection
Standard X-rays cannot detect Stage 0 or Stage 1 disease. Since early intervention offers the best outcomes, MRI is the critical diagnostic tool. It is far more sensitive than plain X-rays and can reveal changes in bone marrow and blood flow before any structural damage appears. If your doctor suspects avascular necrosis based on your symptoms and risk factors, an MRI of both hips is typically the next step, because the condition affects both sides in a significant number of patients.
Treatment Before Collapse
The goal of early treatment is to preserve the natural femoral head and prevent collapse. The most common surgical option for early-stage disease is core decompression, a procedure where a surgeon drills one or more small channels into the femoral head to relieve pressure inside the bone and encourage new blood vessel growth. Success rates depend heavily on the stage at the time of surgery: 84% for Stage 1 hips, 63% for Stage 2, and only 29% for Stage 3. For Stage 1 disease, core decompression significantly outperforms conservative (non-surgical) management, which has a 61% success rate.
Medications also play a role. Bisphosphonates, drugs that slow bone breakdown, have become a standard treatment option. A 20-year study found that bisphosphonate therapy cut radiographic collapse rates roughly in half compared to untreated patients, reducing them from around 76-80% down to 26-30% at three years. The drugs also reduced the eventual need for hip replacement. Pain relief can begin relatively quickly with intravenous forms, though oral bisphosphonates appear more effective at actually preventing collapse.
When Hip Replacement Becomes Necessary
Once the femoral head has collapsed and arthritis has developed, total hip replacement is typically the only option that reliably restores function. The procedure works well: functional outcome scores are comparable to those seen in patients who get hip replacements for standard osteoarthritis. Most patients regain good mobility and significant pain relief.
However, there are important differences for avascular necrosis patients. A large meta-analysis covering over two million hips found that people who received a hip replacement for avascular necrosis had a statistically higher rate of revision surgery, periprosthetic fracture, and joint infection compared to those who had the procedure for osteoarthritis. The likely explanation is age. The average avascular necrosis patient receiving a hip replacement is about 51 years old, compared to roughly 56 for osteoarthritis patients. Younger, more active patients simply put more wear on their implants over more years, increasing the chance they’ll eventually need a second procedure. This is one reason doctors push hard to preserve the natural hip in earlier stages when possible.