What Are the Symptoms and Causes of Osteonecrosis of the Hip?

Osteonecrosis of the hip occurs when bone tissue in the femoral head (the ball at the top of the thighbone) dies because its blood supply has been cut off, and it typically announces itself through groin pain that worsens with weight-bearing. The condition affects a surprisingly young population, with the average age at treatment falling between 33 and 38 years, making it one of the leading reasons younger adults end up needing a hip replacement.¹ Its causes range from corticosteroid use and heavy drinking to traumatic hip injuries and inherited clotting disorders, and the symptoms can be deceptively mild in the early stages.

What It Feels Like at Each Stage

Osteonecrosis of the hip is sometimes called a “silent” condition in its earliest phase because bone can be dying without producing any noticeable symptoms. Some people are diagnosed only after an MRI ordered for another reason reveals damage that has already begun. When symptoms do appear, they tend to follow a recognizable pattern.

The first sign is usually a dull ache or throbbing pain deep in the groin or front of the hip. At first, the pain may show up only when you put weight on the affected leg, such as when standing up from a chair or walking uphill. Many people initially mistake it for a pulled muscle or early arthritis. Over weeks to months the pain typically becomes more constant, eventually bothering you at rest or waking you at night. Range of motion gradually decreases: you may notice that rotating the hip inward becomes painful, or that crossing your legs is no longer comfortable.

If the disease progresses to the point where the weakened bone surface collapses, the pain often sharpens suddenly. This collapse of the femoral head changes the shape of the joint, accelerating cartilage wear and leading to secondary arthritis. At that stage, walking even short distances may become difficult, and a noticeable limp can develop. The condition is described as painful, often disabling, and believed to result from temporary or permanent disruption of blood supply to the affected bone.²

How Blood Supply Gets Interrupted

The femoral head is particularly vulnerable to blood-supply problems because of the way it is built. A relatively small network of fine blood vessels feeds the rounded top of the bone, with most of the supply reaching the front and upper portion of the head.¹ When something blocks or damages those vessels, the bone tissue they supply begins to starve. The process is progressive: local ischemia leads to cell death, and eventually the structural integrity of the femoral head gives way, causing collapse and loss of joint function.³

Multiple disease processes can kick off this chain of events, but the final common pathway is the same: nutrients stop reaching the bone in the vulnerable upper part of the femoral head, and bone cells die.⁴ The early steps vary depending on the cause and can involve blood vessel damage, fat cells swelling inside the bone marrow and compressing vessels, clot formation, or a combination of all three.

The Two Most Common Causes

Corticosteroid Use

Long-term or high-dose corticosteroid therapy is the single most frequently identified non-traumatic cause. These medications are prescribed for conditions like lupus, severe asthma, organ transplant rejection, and inflammatory bowel disease. The problem is that corticosteroids can trigger a cascade of changes inside the bone: fat cells in the marrow enlarge, blood vessels get squeezed, clotting activity increases, and the bone’s own repair mechanisms are suppressed. Researchers have identified roles for vascular damage, increased pressure inside the bone, fat-cell dysfunction, abnormal clotting, and impaired cell survival in steroid-related osteonecrosis.⁴ The risk rises with dose and duration, though cases have been reported even after short bursts of high-dose steroids.

Heavy Alcohol Use

Chronic heavy drinking is the other major non-traumatic risk factor. Alcohol and its breakdown products promote fat accumulation inside bone tissue. As fat cells grow abnormally large, they physically compress the small blood vessels in the marrow, cutting off blood flow and triggering cell death. Making things worse, the inflammatory response that would normally clean up dead tissue and start repairs becomes chronically derailed by the ongoing exposure to alcohol, turning what should be a healing process into a destructive one.⁵ The combination of steroid use and alcohol compounds the risk substantially.

Traumatic Causes

A hip dislocation or fracture of the femoral neck can physically tear or kink the blood vessels supplying the femoral head, setting off osteonecrosis weeks to months later. The speed of treatment matters. In one study of patients with posterior hip dislocations, the rate of osteonecrosis climbed from roughly 4% when the hip was put back in place within 6 to 12 hours to about 22% when reduction was delayed beyond 24 hours.⁶ Fractures of the socket (acetabulum) alongside the dislocation made the numbers worse: roughly a third of patients with combined fracture-dislocations developed osteonecrosis, compared with under 5% of those with a dislocation alone. Femoral head fractures with hip dislocation are considered emergencies, with optimal reduction ideally done within six hours to reduce the risk.⁷

Less Obvious Risk Factors

Beyond steroids, alcohol, and trauma, a range of other conditions can predispose someone to osteonecrosis. The connecting thread is anything that either damages blood vessels feeding the femoral head or promotes abnormal clotting inside them.

Clotting disorders: Both inherited conditions (like protein C or protein S deficiency, resistance to activated protein C, and elevated levels of certain clotting factors) and acquired ones (like antiphospholipid antibodies) can promote blood clots in the tiny vessels of the femoral head.⁸ Hereditary thrombophilia in particular has been linked to clot-driven blockage of bone vessels.⁹
Sickle cell disease: Abnormally shaped red blood cells can clog small vessels in bone, making osteonecrosis one of the well-known complications of sickle cell disease.⁸
Autoimmune diseases: Systemic lupus, vasculitis, rheumatoid arthritis, and scleroderma each carry some associated risk, partly through the disease process itself and partly because these conditions are often treated with corticosteroids.¹⁰
Radiation therapy: Pelvic radiation, used for cancers of the cervix, rectum, and prostate, can damage blood vessels in the hip and has been reported as a cause of osteonecrosis.¹⁰
Cushing’s syndrome: Whether from a tumor or from exogenous steroids, chronically elevated cortisol levels create the same bone-marrow environment that drives steroid-associated osteonecrosis.

In roughly 20 to 40 percent of cases, no clear cause is found. These are labeled idiopathic, though some researchers suspect undetected clotting abnormalities or genetic factors play a role in many of them.

How It Is Diagnosed

Plain X-rays are often the first imaging test ordered when someone has persistent hip pain, but they can look completely normal in the early stages of osteonecrosis. By the time changes appear on an X-ray, the disease has usually already progressed. MRI is far more reliable. In differentiating osteonecrosis from other femoral head problems, MRI reaches a sensitivity and specificity of about 97 and 98 percent, respectively, outperforming X-rays, CT, and bone scans.¹¹ MRI is more sensitive and specific than X-rays across a range of hip pathologies, with conventional radiography’s accuracy ranging from about 50 to 90 percent compared with MRI’s 80 to 100 percent.¹²

There is one interesting exception. Once a subchondral fracture (a tiny break just beneath the joint surface) has occurred, CT scans actually detect it better than MRI. In one comparison, CT picked up subchondral fractures in substantially more hips than MRI did at both six-month and twelve-month follow-ups.¹³ So while MRI is the gold standard for catching the disease early, CT has a complementary role once the bone surface starts to crack.

Once osteonecrosis is confirmed, doctors stage it to guide treatment decisions. The two most widely used staging systems, Ficat and ARCO, classify the disease based on imaging findings from early marrow changes all the way through to femoral head collapse and secondary arthritis. These systems have a well-known limitation, however: studies of how consistently different doctors apply them have found poor agreement between observers, which makes comparing results across different hospitals or research studies tricky.¹⁴

What Happens Without Treatment

Left alone, osteonecrosis of the hip has a poor track record. Roughly 70 to 80 percent of untreated patients progress to collapse of the femoral head and secondary arthritis.¹⁵ ¹⁶ A systematic review of studies tracking asymptomatic, untreated hips found that about 59 percent progressed to symptoms or collapse overall.¹⁷

Size and location of the dead-bone area make a big difference, though. Small lesions located toward the inner (medial) part of the femoral head collapsed less than 10 percent of the time, while larger lesions in the weight-bearing zone fared much worse.¹⁷ This is why staging and lesion-size measurement matter so much for deciding how aggressively to treat.

When Both Hips Are Affected

Osteonecrosis frequently strikes both hips. In non-traumatic cases the same systemic risk factors, whether steroids, alcohol, or a clotting disorder, affect the blood supply to both femoral heads. One hip may be diagnosed first, sometimes because the other side is still silent. MRI of both hips is often recommended even when only one side hurts, because it can reveal early-stage disease on the opposite side before symptoms develop.¹⁸

When a patient with bilateral disease undergoes hip replacement on the worse side, there is a meaningful chance the other femoral head will collapse later. In one study of 103 such patients, about 62 percent experienced collapse of the opposite femoral head after the first replacement.¹⁹ Researchers developed a prediction tool based on factors including lesion type and post-surgical hip scores to help clinicians anticipate which patients are most likely to need a second replacement.

Treatment Before the Bone Collapses

The strongest consensus in managing osteonecrosis is that early intervention, before the femoral head surface caves in, offers the best outcomes. The most established joint-preserving procedure is core decompression, which involves drilling one or more channels into the femoral head to relieve pressure inside the bone and encourage new blood vessel growth. Results are best in early-stage disease.²⁰

In one large series of over 300 hips treated with core decompression and bone grafting, about 32 percent of pre-collapse hips (stages I and II combined) eventually needed a hip replacement, with outcomes strongly tied to lesion size. Only about 14 percent of hips with small lesions progressed to replacement, compared with roughly 48 percent of those with medium-sized lesions.²¹ These are imperfect numbers, but they show that catching the disease early and with a small area of involvement makes a real difference.

Bisphosphonates, drugs normally used for osteoporosis, have been tried as a way to slow bone breakdown in osteonecrosis. A meta-analysis found a trend toward reduced collapse rates with bisphosphonate therapy, but the difference was not statistically clear-cut.²² These drugs are not a standard-of-care treatment for osteonecrosis, but they are sometimes used off-label, particularly for patients who are not good surgical candidates.

Cell-Based Therapies

There is growing interest in pairing core decompression with biological therapies, especially stem cells. A network meta-analysis comparing six different treatment approaches found that mesenchymal stem cells and bone marrow aspirate concentrate both outperformed core decompression alone in preventing disease progression and reducing the need for hip replacement.²³ The evidence is encouraging, but there is an important caveat: once the femoral head has already collapsed, a separate systematic review found that adding bone marrow aspirate concentrate to core decompression did not improve outcomes compared with decompression alone.²⁴ The window for these biological approaches, at least with current techniques, appears to be before structural collapse.

Hip Replacement in Younger Patients

When the femoral head has already collapsed and joint function is significantly impaired, total hip replacement is the definitive treatment. Because osteonecrosis skews younger than most hip-replacement populations, implant longevity is a central concern. In a study following 135 patients (204 hip replacements) with an average follow-up of 14 years, 10-year implant survival was 86 percent and 20-year survival was 66 percent. Implants lasted longer in patients who were male or over 25 at the time of surgery.²⁵ Those numbers mean a substantial fraction of young patients will need at least one revision surgery in their lifetime, which is why surgeons try hard to delay replacement when feasible.

Timing also matters for post-operative comfort. One study found that patients who had lived with a collapsed femoral head for one to three years before replacement reported worse pain relief after surgery than those who had either a shorter or longer interval before the procedure.²⁶ The functional outcome scores, interestingly, ended up comparable regardless of how long the disease had been present before surgery, suggesting that hip replacement effectively restores mechanics even after prolonged disease, but the pain experience can differ.

For patients whose osteonecrosis was triggered by a bone marrow transplant for a blood cancer or other hematological disease, there is reassuring evidence. A multicenter study comparing hip replacements in bone marrow transplant recipients to those with idiopathic osteonecrosis found no significant differences in complication rates, revision rates, or implant survival at roughly 13 years.²⁷ That finding is relevant because there was previously concern that immunocompromised patients might face higher infection or loosening rates.

Rare and Unusual Presentations

Most cases of osteonecrosis involve a recognizable risk factor, but occasionally the disease shows up in people with rare underlying conditions. One recently documented case involved a young adult with both congenital factor V deficiency and a separate inherited clotting mutation. The combination appeared to be the first reported instance worldwide of bilateral femoral head osteonecrosis linked to that particular dual clotting abnormality.²⁸ Cases like these underscore why clotting workups are sometimes recommended for younger patients diagnosed with osteonecrosis who have no obvious exposure to steroids, alcohol, or trauma. Finding an underlying clotting disorder does not change the hip treatment itself, but it can guide long-term anticoagulation decisions and alert clinicians to watch the other hip or other joints.

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