What Causes Avascular Necrosis and Who’s at Risk?

Avascular necrosis (also called osteonecrosis) happens when bone tissue dies because its blood supply has been cut off. The femoral head, the ball at the top of the thighbone, is the most commonly affected site, though the condition can strike other bones too. The underlying cause is always the same: something interrupts the tiny blood vessels feeding the bone, starving the cells of oxygen. What varies widely is the reason blood flow gets disrupted, and who ends up vulnerable depends on a surprisingly long list of risk factors ranging from a broken hip to heavy drinking to medications prescribed for entirely unrelated conditions.

How Blood Flow to Bone Gets Interrupted

Bone is living tissue, and like every other tissue in your body it needs a steady supply of blood. Deep inside bones, a network of small vessels feeds the cells responsible for maintaining and repairing the hard mineral matrix. When those vessels fail, bone cells begin to die within hours. Over weeks and months, the dead zone weakens, and without treatment the bone surface can eventually collapse under the body’s own weight.

Researchers recognize three broad ways the blood supply to bone can be compromised: physical disruption of blood vessels (typically from a fracture or dislocation), blockage inside the vessels themselves (from blood clots or fat globules lodging in small arteries), and compression of vessels from the outside (when swollen fat cells or other abnormal cells crowd the space inside the bone marrow and squeeze the tiny veins shut).¹ Most cases of avascular necrosis trace back to one or more of these three pathways, even when the triggering event looks very different on the surface.

Why Certain Bones Are Especially Vulnerable

Not every bone in the body faces the same risk. The femoral head, the talus bone in the ankle, the proximal humerus near the shoulder, and the scaphoid bone in the wrist are the most frequent targets. What they share is a precarious blood supply: relatively few arteries reach these bones, and those arteries have limited backup routes.² In the femoral head, for example, most of the blood arrives through a small set of vessels that run along the neck of the femur. A fracture there can sever those vessels in an instant, leaving the ball of the joint with no alternative supply. The hip’s anatomy is the main reason avascular necrosis shows up there far more often than in, say, the shinbone or the pelvis.

Trauma as a Direct Trigger

The most straightforward cause is physical injury. A hip fracture that snaps the femoral neck or a forceful hip dislocation can tear the blood vessels feeding the femoral head outright. How quickly the joint is put back into place matters a great deal. A systematic review of traumatic hip dislocations found that the odds of developing avascular necrosis were more than five times higher when the hip was reduced after twelve hours compared to before.³ In a separate study of posterior hip dislocations with accompanying acetabular fractures, the rate of avascular necrosis was roughly 35%, compared to under 5% for simple dislocations without a fracture.⁴ Those numbers also worsened with longer delays in getting the hip back into its socket. The takeaway for emergency care is that rapid reduction of a dislocated hip is one of the few interventions with strong evidence for reducing avascular necrosis risk.

Corticosteroids and the Dose Question

After trauma, long-term or high-dose corticosteroid use is probably the most well-known nontraumatic risk factor. Drugs like prednisone, dexamethasone, and methylprednisolone are prescribed for a wide range of conditions, including asthma flares, organ transplant rejection, autoimmune diseases, and severe allergic reactions. The problem is that corticosteroids change how fat is stored inside bone marrow. Fat cells enlarge, crowd the marrow space, and eventually compress the tiny blood vessels feeding the bone from within.⁵

One of the frustrating aspects of corticosteroid-related avascular necrosis is that the research on exactly how much steroid is too much remains murky. Some studies point to the total cumulative dose as the most important factor, while others suggest that high peak doses or particular routes of administration matter more. What is clear is that the risk rises with higher doses and longer courses. A brief five-day burst of prednisone for a poison ivy rash is a very different exposure than months of high-dose steroids after a kidney transplant. If you are taking corticosteroids long-term, this is a risk worth discussing with your doctor, though stopping the medication without medical guidance is usually more dangerous than the bone risk itself.

Alcohol and Fatty Marrow Changes

Heavy alcohol consumption is the other major nontraumatic risk factor, and the mechanism overlaps substantially with corticosteroids. Chronic alcohol use disrupts lipid metabolism and drives fat accumulation inside bone marrow. Animal research has shown that sustained alcohol exposure leads to fatty infiltration of both the liver and the bone marrow; the enlarged fat cells fill with triglycerides, swell, and eventually compress surrounding blood vessels. Once blood flow stops, the downstream bone tissue dies.⁶ Heavy drinking also impairs new bone formation and weakens existing bone structure, compounding the damage. The combination of alcohol and corticosteroid use together raises the risk even further, and clinicians treating patients on long-term steroids often counsel reducing alcohol intake for this reason.

Sickle Cell Disease

For people with sickle cell disease, avascular necrosis is one of the most common and painful long-term complications. The connection is intuitive: sickle-shaped red blood cells are rigid and sticky, and they routinely clump together and block small blood vessels throughout the body. When that vaso-occlusion happens inside bone, the result is the same ischemia that leads to bone death from any other cause.⁷ In sickle cell patients, avascular necrosis tends to appear at a younger age than in other populations, and the incidence climbs as patients get older.⁸ It often affects both hips, sometimes the shoulders as well, and standard treatment approaches are not well established. A Cochrane review noted that treatment for avascular necrosis in sickle cell disease remains unstandardized, reflecting how difficult the condition is to manage in this population.⁹

Autoimmune Conditions and Clotting Disorders

Antiphospholipid syndrome is a condition in which the immune system produces antibodies that make the blood prone to clotting. People with this syndrome face a risk of avascular necrosis driven by microvascular thrombosis: tiny clots forming inside the bone’s blood vessels. Reported prevalence varies widely, from under 1% to 20% depending on the study.¹⁰

What makes autoimmune conditions tricky is that corticosteroids are often part of the treatment. In a study of patients with primary antiphospholipid syndrome, every patient who developed avascular necrosis had a history of glucocorticoid use, compared to about a third of those who did not develop it. Patients with avascular necrosis also had low platelet counts far more often.¹¹ So it becomes genuinely hard to separate the disease risk from the treatment risk. People with lupus face a similar double bind: the disease itself promotes clotting and vascular inflammation, while the steroids used to control flares independently raise the risk of bone death.

Gaucher Disease and Rare Storage Disorders

Gaucher disease is a rare inherited condition where a missing enzyme causes certain lipid molecules to accumulate in cells, particularly in bone marrow. Those bloated cells physically crowd out normal marrow and compress the blood vessels running through it. Researchers at a tertiary referral center found a reliable correlation between levels of a specific biomarker (a lipid called GlcSph) and the risk of avascular necrosis. For every unit increase in that biomarker’s level, the risk of osteonecrosis during treatment rose by about 1.2%.¹² Enzyme replacement therapy can reduce that biomarker over time, so monitoring it helps clinicians decide how aggressively to treat the underlying disease and whether to screen for early bone changes.

HIV and Avascular Necrosis

People living with HIV have a higher rate of avascular necrosis than the general population, and the relationship is not fully explained by the other risk factors they may carry. A case report described a 33-year-old woman with HIV who developed avascular necrosis of both femoral heads despite having no history of sickle cell disease, lupus, prolonged steroid use, or trauma.¹³ The virus itself may contribute through chronic inflammation and vascular damage, and some antiretroviral medications have been implicated as well. As people with HIV live longer thanks to modern therapy, avascular necrosis is becoming an increasingly recognized complication.

Divers and Caisson Workers

Dysbaric osteonecrosis is a form of avascular necrosis tied to working or diving under elevated atmospheric pressure. Nitrogen bubbles that form during decompression can block small blood vessels inside bone, damaging tissue over repeated exposures. The risk factors that have been consistently linked to dysbaric osteonecrosis include the frequency, duration, and depth of pressure exposure, inadequate decompression, a history of decompression sickness, and increasing age.¹⁴ This was once considered an occupational disease of commercial divers and tunnel workers, but technical recreational divers performing deep or prolonged dives are now recognized as an at-risk group as well. Fortunately, most recreational diving at moderate depths with standard safety stops carries very low risk.

Genetic Susceptibility

Not everyone exposed to the same risk factor develops avascular necrosis, which has led researchers to look for genetic differences that might make some people more vulnerable. One area of interest is the ABCB1 gene, which encodes a protein that transports substances (including steroids) across cell membranes. A meta-analysis of five studies found that certain variants in this gene were associated with a significantly higher susceptibility to glucocorticoid-induced avascular necrosis of the femoral head.¹⁵ This research is still in its early stages and cannot yet guide individual clinical decisions, but it points toward a future where genetic testing might help identify patients who need extra monitoring when placed on steroid therapy.

When Children Develop Avascular Necrosis

In children, avascular necrosis of the hip has its own name: Legg-Calvé-Perthes disease. It typically strikes between ages four and ten, more often in boys. The cause remains largely unknown, though the leading theory involves disruption of the blood supply to the growing femoral head, possibly combined with biomechanical stress on the immature skeleton.¹⁶ Unlike adult avascular necrosis, Perthes disease in young children has a reasonable chance of healing well on its own, because children’s bones are still growing and can remodel the damaged area. Older children and those with more extensive involvement tend to have worse outcomes and may need surgical intervention to keep the hip functioning properly into adulthood.

A Related but Distinct Problem in the Jaw

Bisphosphonates, medications widely used to treat osteoporosis and bone cancers, have been linked to a different type of bone death: osteonecrosis of the jaw. The mechanism here is not the same as in the hip. Researchers initially assumed bisphosphonate-related jaw lesions were classic avascular necrosis caused by impaired blood supply, but the evidence increasingly points to chronic bone infection (osteomyelitis) as the more accurate description. Bisphosphonates slow the natural turnover of bone by suppressing the cells that break it down. When infection-causing bacteria like Actinomyces or Staphylococcus colonize the jawbone, the bone cannot resorb and replace the contaminated tissue quickly enough, leading to persistent wounds. The fact that similar jaw lesions appear after treatment with denosumab, an entirely different class of drug that also reduces bone turnover, supports this theory.¹⁷ If you are on bisphosphonates, dental hygiene and timely treatment of dental infections are important preventive steps, especially before any invasive dental procedures.

Why Early Detection Changes the Outcome

Avascular necrosis is notoriously quiet in its early stages. Many people have no pain at all until the bone is close to collapsing, which is a problem because treatment works much better before collapse occurs. Standard X-rays are the usual first step, but they miss a substantial portion of early cases. In one study, plain X-rays detected avascular necrosis in about 62% of affected hips, while MRI caught all of them, including clinically silent disease on the opposite side.¹⁸ MRI is considered the gold standard for early diagnosis because it can detect bone marrow changes like swelling and early scarring long before structural collapse shows up on an X-ray.¹⁹ A large meta-analysis of 43 studies put MRI’s sensitivity at about 93% and specificity at about 91% for detecting early disease.²⁰ If you fall into a high-risk group, an MRI ordered proactively can catch the disease at a stage where the joint might still be saved.

What Collapse Looks Like and Why It Matters

Once the bone surface begins to give way, the process accelerates. The “pericollapse” stage, the window just before and during early structural failure, is marked by specific warning signs: worsening hip pain (often sudden), bone marrow swelling visible on MRI, and a crescent-shaped line on X-ray that represents a fracture just beneath the joint surface.²¹ Clinicians consider this the last realistic window for joint-preserving treatment. After the femoral head collapses more than a couple of millimeters, the cartilage surface is irreversibly damaged, and the joint heads toward arthritis and eventual hip replacement.

Treatment Options Before and After Collapse

For early-stage disease, the goal is to halt progression and avoid total hip replacement, particularly in younger patients who would otherwise face multiple replacement surgeries over a lifetime. Core decompression, a procedure where a surgeon drills into the femoral head to relieve internal pressure and encourage new blood vessel growth, is the most established joint-preserving option. Combining core decompression with concentrated bone marrow stem cells has shown improved results: a meta-analysis found that adding stem cell therapy to core decompression was more effective at preventing collapse, slowing disease progression on imaging, and reducing the need for hip replacement.²² These approaches work best when the bone surface is still intact.²³

Hyperbaric oxygen therapy has been explored as a nonsurgical option, with one center reporting stable or improved MRI scans in roughly two-thirds of treated femoral heads over at least six months of follow-up.²⁴ That evidence comes from a small, single-center case series rather than a randomized trial, so it is far from definitive. Still, for patients who are not surgical candidates or whose disease is caught early, it represents an option worth discussing.

Once significant collapse has occurred, total hip replacement becomes the most reliable way to restore function and relieve pain. Modern hip prosthetics last decades in most patients, but for someone in their twenties or thirties, even a long-lasting implant may need to be revised eventually. That prospect is a major reason clinicians push hard for early detection and joint-preserving strategies whenever possible.