Osteonecrosis is the death of bone tissue caused by an interruption of its blood supply. Without steady blood flow, bone cells starve and the internal structure gradually weakens, which can eventually cause the bone surface to collapse and the joint to deteriorate. The hip is the most common site, but the condition also strikes the knee, shoulder, jaw, and smaller bones. Its causes range from steroid use and heavy drinking to fractures, blood disorders, and even deep-sea diving, and whether the bone can be saved often depends on how early the problem is caught.
How Blood Loss to Bone Leads to Tissue Death
Bone is living tissue that depends on a network of small blood vessels to deliver oxygen and nutrients. When that supply is cut off or severely reduced, bone cells and the marrow inside begin to die. The body tries to repair the damage through a process called creeping substitution, where new bone slowly replaces the dead tissue. But in many cases the repair is too slow or too weak to keep up with the structural load the bone carries, and the weakened area starts to give way.
At the cellular level, the loss of blood flow triggers a cascade of problems. Cells lining the small blood vessels inside bone lose their ability to form new vessels and begin to die off at higher rates. Research on steroid-induced osteonecrosis has shown that the endothelial cells in affected bone have reduced ability to migrate and form tube-like structures, while markers of programmed cell death rise sharply.1PubMed Central. Decreased angiogenic and increased apoptotic activities of bone microvascular endothelial cells in patients with glucocorticoid-induced osteonecrosis of the femoral head Disruptions in the balance between bone-building cells and fat cells, combined with impaired blood vessel growth and several forms of cell death, collectively push the tissue toward necrosis.2PubMed Central. The role of post-translational modifications in osteonecrosis of the femoral head
There is also growing evidence that cellular aging plays a role. In the necrotic zone and the surrounding transition zone where the body attempts remodeling, researchers have identified prematurely aged stem cells, bone-forming cells, and bone-maintaining cells. Because these cell types coordinate bone formation and upkeep, their premature aging may help explain why the bone’s self-repair so often falls short.3Scientific Reports. Cellular senescence is associated with osteonecrosis of the femoral head while mesenchymal stem cell conditioned medium inhibits bone collapse
Steroids and Alcohol as Leading Causes
Corticosteroids and heavy alcohol use are the two most frequently identified non-traumatic causes of osteonecrosis. The mechanisms are related but not identical.
When someone takes corticosteroids, especially at high doses or for extended periods, fat cells inside the bone marrow can enlarge and multiply. The swelling fat tissue compresses the tiny blood vessels that feed the bone, choking off circulation. Fat particles may also break loose into the bloodstream and lodge in small vessels, and abnormal blood clotting within bone can compound the blockage. Data on exactly how much steroid exposure is dangerous remain mixed: some research points to cumulative dose as the biggest risk factor, while other studies emphasize peak dose or duration.4PubMed Central. Glucocorticoid-induced avascular bone necrosis: diagnosis and management This inconsistency makes it difficult to set a clear “safe” threshold, though the risk appears to climb with higher and longer exposures.
Alcohol works through a strikingly similar pathway. Chronic heavy drinking promotes fat accumulation in the bone marrow, and as fat cells swell, they compress the surrounding blood vessels. The resulting blockage cuts off blood flow, leading to ischemia, cell death, and clotting within the affected area.5PubMed Central. Osteonecrosis Related to Steroid and Alcohol Use—An Update on Pathogenesis The parallel between steroid-driven and alcohol-driven fat hypertrophy helps explain why the two causes produce nearly identical damage patterns and why combined exposure to both raises the risk further.
Post-Traumatic Osteonecrosis
Fractures are the most straightforward cause of osteonecrosis: break the bone badly enough and you physically sever the blood vessels feeding it. The femoral head, the ball at the top of the thighbone, is especially vulnerable. Roughly 70 to 80 percent of its blood supply comes from a single artery that runs along the outside of the femoral neck, and a fracture through that neck can tear or kink the vessel.6PubMed. Early prediction of femoral head avascular necrosis following neck fracture This makes trauma-induced osteonecrosis of the femoral head the single most common form of bone necrosis at that site.7PubMed. Avascular necrosis of the femoral head after femoral neck fracture
Beyond direct vessel damage, there is a second mechanism at play after fracture. Blood leaking from the broken bone can pool inside the tight joint capsule, and the resulting pressure squeezes the remaining intact vessels shut, a process sometimes called the tamponade effect.8PubMed. Avascular necrosis of the femoral head after femoral neck fracture This means that even if some vessels survive the initial break, swelling and trapped blood can finish the job. Early surgical treatment that restores alignment and relieves pressure can improve outcomes, but osteonecrosis remains a feared complication of hip fractures, particularly in younger patients whose long-term joint function is at stake.
Sickle Cell Disease and Other Blood Disorders
Sickle cell disease is one of the best-known non-steroid, non-alcohol causes. The misshapen red blood cells characteristic of the disease can clump and block small blood vessels anywhere in the body, including inside bone. Repeated episodes of vessel blockage gradually damage the bone’s blood supply. Osteonecrosis of the hip is a common and debilitating complication in sickle cell patients, and managing it has proven difficult. A Cochrane review examining treatment options found very low-quality evidence and was unable to confirm that any particular intervention reduced major complications such as hip pain, pain crises, or acute chest syndrome.9PubMed Central. Treatment for avascular necrosis of bone in people with sickle cell disease That uncertainty underscores how challenging osteonecrosis can be to treat once it develops in these patients.
Other blood-related conditions that promote abnormal clotting or impaired clot breakdown can also raise the risk. Research in Poland found that inherited variations in the gene controlling a clot-dissolving enzyme were significantly more common in patients with idiopathic osteonecrosis of the hip, suggesting that sluggish clot breakdown may leave small bone vessels blocked for too long.10PubMed Central. Prevalence of genetic risk factors related with thrombophilia and hypofibrinolysis in patients with osteonecrosis of the femoral head in Poland A study from India similarly found that deficiencies in Protein C and Protein S, both natural blood-thinning proteins, were significantly more common in osteonecrosis patients than in healthy controls.11PubMed Central. Association of Thrombophilic Factors in Pathogenesis of Osteonecrosis of Femoral Head in Indian Population And in patients who develop osteonecrosis in multiple joints at once without an obvious cause, elevated levels of Factor VIII and a variant in the nitric oxide synthase gene have been identified as risk markers.12Journal of Bone and Joint Surgery. Thrombophilia, Hypofibrinolysis, the eNOS T-786C Polymorphism, and Multifocal Osteonecrosis These genetic and clotting factors help explain why some people develop osteonecrosis with no clear external trigger.
Medication-Related Osteonecrosis of the Jaw
The jaw has its own distinct form of osteonecrosis tied to certain medications, particularly bisphosphonates used for osteoporosis and the potent anti-resorptive and anti-angiogenic drugs used in cancer treatment. Unlike hip osteonecrosis, which is driven by blood vessel blockage from fat, clotting, or trauma, jaw osteonecrosis appears to stem from the tight coupling between bone turnover and blood vessel maintenance in the jawbone. When anti-resorptive drugs suppress bone breakdown, they simultaneously reduce the signals that keep the jaw’s blood vessels healthy, effectively starving the bone of circulation from the inside out.13PubMed Central. Mechanisms Underlying Medication‐Related Osteonecrosis of the Jaw
Jaw osteonecrosis typically presents as exposed bone in the mouth that does not heal, often after a tooth extraction or dental procedure. The risk is substantially higher in cancer patients receiving intravenous bisphosphonates at high doses than in osteoporosis patients on lower oral doses. Dental professionals now routinely screen for bisphosphonate use before invasive procedures, and preventive dental care before starting these medications has become standard practice in oncology.
Catching It Early With Imaging
Early-stage osteonecrosis often produces no symptoms or only vague discomfort, and a standard X-ray can miss it entirely. In one study of 45 affected hips, plain X-rays detected osteonecrosis in about 62 percent of cases while missing the rest, whereas MRI picked up every single case.14PubMed Central. The Application of Magnetic Resonance Imaging in the Early and Accurate Diagnosis of Hip Joint Avascular Necrosis A large meta-analysis pooling over 40 studies confirmed MRI’s strong diagnostic performance for early osteonecrosis of the femoral head, with pooled sensitivity around 93 percent and specificity around 91 percent.15PubMed Central. Accuracy of MRI diagnosis of early osteonecrosis of the femoral head: a meta-analysis and systematic review
The practical takeaway is that if you are at elevated risk, say you have been on high-dose steroids or have sickle cell disease, and you start getting hip or groin pain, a normal X-ray does not rule out osteonecrosis. An MRI is the gold standard and can reveal the problem months or even years before the bone shows visible changes on X-ray. That window matters enormously because treatment options are far better before the bone surface collapses.
How Osteonecrosis Is Staged
Doctors use staging systems to describe how far the disease has progressed, which in turn guides treatment decisions. The most widely used is the ARCO (Association Research Circulation Osseous) classification, which was revised in 2019 into four stages. In Stage I, X-rays look normal but MRI or bone scan shows a problem. Stage II shows abnormal X-ray findings like areas of increased density or cyst-like changes, but without any fracture or flattening of the bone surface. Stage III marks the appearance of a fracture in the subchondral bone just beneath the joint surface, subdivided into early (surface depression of 2 mm or less) and late (more than 2 mm). Stage IV indicates full-blown arthritis with joint-space narrowing and damage to the socket side of the joint as well.16PubMed. The 2019 Revised Version of Association Research Circulation Osseous Staging System of Osteonecrosis of the Femoral Head
The stage strongly predicts outcome. In a study testing the reliability of the updated classification, the rate at which the bone surface collapsed was 0 percent for the most favorable type, 19 percent for the intermediate type, and 87 percent for the most severe type. The rates of eventually needing hip replacement followed a similar gradient: roughly 5 percent, 7 percent, and 31 percent, respectively.17PubMed Central. Reliability and repeatability of 2021 ARCO classification and its guiding significance in treatment of nontraumatic osteonecrosis of the femoral head These numbers reinforce why early detection matters so much: the disease caught at an early stage has a fundamentally different trajectory than the disease caught after the surface has already begun to sink.
Why the Bone Collapses
Understanding the collapse is key to understanding why treatment timing is so critical. After the bone cells die, the body sends in repair cells to remodel the necrotic zone. But the remodeling process itself temporarily weakens the bone: old dead bone is resorbed faster than new bone can fill in. Research has shown that what drives collapse is the degree of structural weakening in the spongy cancellous bone deep inside the infarct rather than changes in the thin plate just below the joint surface. Even a fully intact subchondral plate cannot protect a deeply weakened interior from giving way under body weight.18PubMed. Structural consequences of subchondral bone involvement in segmental osteonecrosis of the femoral head
One reason repair falls short may simply be a shortage of raw materials. The proximal femur appears to have fewer bone progenitor cells than other regions of the skeleton, which means the body’s repair crew is working understaffed. This observation has spurred interest in treatments that deliver additional progenitor cells or growth signals to the necrotic zone to boost an otherwise insufficient repair response.19PubMed Central. Cell therapy of hip osteonecrosis with autologous bone marrow grafting
Joint-Preserving Treatments
The goal of early intervention is to prevent or delay collapse so the patient can keep their own joint for as long as possible. The workhorse procedure is core decompression, in which a surgeon drills one or more channels into the necrotic area to relieve the elevated internal pressure and stimulate blood vessel ingrowth and remodeling.20PubMed Central. Stem cell- and growth factor-based regenerative therapies for avascular necrosis of the femoral head On its own, core decompression has a mixed track record: it works reasonably well in early stages but becomes less effective as the necrotic area grows.
To improve on basic drilling, surgeons increasingly augment the procedure with concentrated bone marrow aspirate, which delivers a payload of stem cells and growth factors directly into the lesion. One study tracking this combined approach found that roughly 78 percent of treated hips had not progressed radiographically at two years, dropping to about 53 percent at five years. The risk of progression was lower compared to core decompression alone, though after adjusting for other variables the difference did not quite reach statistical significance.21Journal of Bone and Joint Surgery. Core Decompression and Bone Marrow Aspiration Concentrate Grafting for Osteonecrosis of the Femoral Head That mixed signal is a fair summary of where the field stands: the biological augmentation approach looks promising, but the evidence is not yet strong enough to call it a clear winner.
Other experimental strategies include injectable scaffolds, growth factor delivery systems, and ex vivo expanded stem cell transplants. The regenerative medicine space here is active and optimistic, but most of these approaches are still in relatively early stages of clinical testing.
When Hip Replacement Is Needed
Once the femoral head has collapsed and arthritis has set in, joint-preserving strategies are usually off the table. Total hip arthroplasty, or hip replacement, becomes the standard treatment. Osteonecrosis is one of the leading reasons younger adults end up needing a hip replacement, which creates a particular concern because younger patients will live with the implant longer and may eventually need revision surgery.
Some patients first undergo joint-preserving procedures like vascularized fibular grafting, in which a segment of the smaller leg bone, complete with its blood supply, is transplanted into the femoral head to provide structural support and new circulation. When these grafts eventually fail, the question is whether the prior surgery makes a subsequent hip replacement more difficult or less successful. Research suggests the answer is generally reassuring: hip replacement after a failed fibular graft has shown functional results comparable to primary hip replacement in osteonecrosis patients, at least over five or more years of follow-up.22PubMed. Hip arthroplasty after failed free vascularized fibular grafting for osteonecrosis in young patients More recent data have echoed that finding, confirming similar short- to mid-term outcomes once the residual graft material is removed and the femoral component is positioned correctly.23PubMed. Outcomes of total hip arthroplasty after failed free vascularized fibular grafting for osteonecrosis of the femoral head This is useful news for patients considering a joint-sparing procedure: trying to save the hip first does not appear to burn bridges if replacement becomes necessary later.
Dysbaric Osteonecrosis in Divers and Compressed Air Workers
One of the more unusual causes of osteonecrosis has nothing to do with medications or fractures. Divers and workers who spend time in pressurized environments, such as caisson workers building underwater tunnels, can develop bone lesions from repeated exposure to raised ambient pressure. The condition was first radiologically confirmed in compressed air workers in the early 1900s, with the first case reported in an underwater diver appearing in 1936.24PubMed. Dysbaric osteonecrosis: a reassessment and hypothesis It is now called dysbaric osteonecrosis.
The frequency, duration, and depth of pressure exposure all contribute to the risk, along with inadequate decompression, a history of decompression sickness, and advancing age.25PubMed Central. Dysbaric osteonecrosis in technical divers: The new ‘at-risk’ group? Gas bubbles that form in the blood during decompression are thought to block small bone vessels in much the same way that fat emboli do in steroid-related disease. Many dysbaric lesions occur in the shafts of long bones rather than near joints, and those deep lesions may never cause symptoms. The dangerous ones are the lesions near the joint surface, where weakening and collapse follow the same pattern seen in other forms of osteonecrosis. Recreational divers have historically been considered low-risk, but technical divers who push deeper and longer have drawn increasing attention as a potentially undermonitored group.
Osteonecrosis in Dogs
Osteonecrosis is not a uniquely human problem. Small-breed dogs develop a strikingly similar condition of the femoral head, called Legg-Calvé-Perthes disease (the same name used for the pediatric version in children). In a retrospective study of 43 affected dogs, nearly all presented with lameness and pain in the hip joint, and the vast majority weighed under five kilograms. Females were slightly more affected, and over half were diagnosed before four months of age. The most common treatment was surgical removal of the femoral head and neck, after which about 43 percent of dogs achieved full functional recovery while another quarter required additional rehabilitation.26Acta Scientiae Veterinariae. Avascular Necrosis of the Femoral Head in Dogs – Retrospective Study
Veterinary research on osteonecrosis has actually contributed to human medicine. Canine models have been used to test whether advanced MRI techniques can detect early osteonecrosis before conventional imaging shows any abnormality. Dynamic contrast-enhanced MRI, which tracks how quickly blood flows into bone marrow, was able to distinguish healthy femoral heads from ischemic ones in dogs even when standard MRI sequences showed nothing.27PubMed. Detection of acute avascular necrosis of the femoral head in dogs: dynamic contrast-enhanced MR imaging vs spin-echo and STIR sequences Canine models have also been used to study core decompression, revealing that the procedure’s effectiveness depends heavily on the type of blood-flow disruption. In dogs with osteonecrosis caused by venous congestion, decompression showed signs of restoring the bone, but in dogs whose arterial supply was cut off, it barely slowed the damage.28PubMed. Efficacy of core decompression for treatment of canine femoral head osteonecrosis induced by arterial ischaemia and venous congestion That distinction, between venous and arterial causes, may eventually help clinicians predict which human patients are most likely to benefit from joint-preserving surgery.