Avascular Necrosis of Hip
Avascular necrosis means bone has died because its blood supply has been interrupted. The hip is the most commonly affected site, because the head of the thigh bone depends on a precarious blood supply that is easily disrupted. The condition matters for two reasons. It affects younger adults—typically people in their thirties, forties, and fifties—rather than the elderly. And it is entirely invisible on X-rays in its early stages, when treatment options are at their best, becoming apparent only once the bone has begun to collapse and the joint is being destroyed. MRI detects it months to years before X-rays do, which makes recognising who should be scanned the single most consequential decision in managing it.
What is it?
Bone is living tissue with its own blood supply, and like any tissue it dies when that supply is cut off. Avascular necrosis—also called osteonecrosis—describes this process in bone.
The head of the thigh bone is particularly vulnerable because of how it is supplied. The main blood vessels reach it by running up along the neck of the bone beneath the joint capsule, forming a ring and then sending small branches into the head itself. There is limited alternative supply. A fracture through the neck, a dislocation, or any process that obstructs these small vessels can deprive a region of the head of its circulation.
What follows unfolds in stages, and understanding this sequence explains both why early detection matters and why treatment changes so abruptly at one particular point.
In the first stage, bone cells die but the architecture of the bone remains intact. The hip looks and feels normal, X-rays are normal, and there may be no symptoms at all. MRI, however, shows the change clearly, because it detects the difference between living and dead marrow.
In the second stage, the body attempts repair. New blood vessels and cells advance into the dead area from the surrounding living bone, resorbing dead bone and laying down new. This repair process is itself part of the problem: resorption temporarily weakens the bone before new bone is laid down, and the region becomes mechanically vulnerable. X-rays may show subtle density changes at this point.
In the third stage, the weakened bone fails beneath the joint surface. A thin fracture line appears just below the cartilage, visible on X-ray as a crescent-shaped lucency. This is the critical transition—the point at which the structure of the femoral head has been compromised.
In the fourth stage, the head flattens and loses its spherical shape. The cartilage, which was never itself affected, is now sitting on a collapsed and irregular surface and begins to fail.
In the final stage, the joint degenerates fully, with the socket also damaged by the now-misshapen head grinding against it.
The practical significance of this sequence is that treatments aimed at preserving the joint work before collapse and largely do not work afterwards. The dividing line is structural failure of the femoral head, and this is why staging matters and why delay in diagnosis has consequences that are not recoverable.
The causes divide into traumatic and non-traumatic.
Traumatic causes directly disrupt the blood supply. Fracture of the femoral neck is the most important, with risk relating to how displaced the fracture was and how promptly it was treated. Hip dislocation similarly tears the vessels, and the risk rises the longer the hip remains dislocated, which is one reason dislocation is treated as an emergency.
Among non-traumatic causes, two dominate.
Corticosteroid use is the most common. The association is strongest with high doses given over extended periods, though cases follow shorter courses and occasionally even single high-dose exposures. The mechanism is thought to involve fat cells within the bone marrow enlarging and raising pressure inside the bone, together with effects on blood clotting and on the small vessels themselves. This is clinically important because corticosteroids are widely prescribed, and because new hip pain in someone taking them should prompt consideration of this diagnosis rather than being attributed to the underlying condition.
Excess alcohol is the other major cause, with risk rising with cumulative intake through similar mechanisms involving marrow fat and vascular effects.
Other causes are well recognised. Sickle cell disease causes repeated vessel blockage by abnormal red cells. Decompression sickness in divers produces nitrogen bubbles obstructing small vessels. Radiotherapy to the pelvis damages the vasculature. Chemotherapy, particularly in childhood leukaemia, is associated. Organ transplantation carries elevated risk, largely but not entirely explained by the corticosteroids used. Clotting disorders, lupus and other autoimmune conditions, HIV infection, Gaucher disease, pancreatitis, and pregnancy are all associated. A proportion occur with no identifiable cause.
The bilateral tendency is practically important. More than half of people with non-traumatic avascular necrosis have both hips affected, frequently with one silent at the time the other is diagnosed. For this reason both hips are imaged when one is identified, and finding early disease on the asymptomatic side offers the best opportunity for intervention.
The symptoms are unremarkable in themselves, which is part of the diagnostic difficulty.
Groin pain is the usual complaint, deep and often radiating into the thigh or knee in the same pattern as any hip joint problem. It may begin gradually or relatively abruptly.
Pain is worse on weight bearing and with activity initially, with rest and night pain developing as the condition advances.
A limp develops.
Restriction of movement, particularly rotation, appears later than the pain, which distinguishes the early presentation from osteoarthritis where stiffness is often an early feature.
The early stage may be entirely silent. This is the crucial point: at the stage when treatment is most likely to preserve the joint, there may be no symptoms at all.
Diagnosis rests on MRI, and the limitations of other imaging deserve direct statement.
X-rays are normal in the early stages. A normal X-ray in a person with hip pain and relevant risk factors does not exclude avascular necrosis, and treating a normal film as reassurance is the most common route to late diagnosis. As the condition progresses, X-rays show patchy density change, then the crescent sign of subchondral fracture, then flattening of the head, and finally secondary joint degeneration.
MRI is the definitive test. It identifies the condition in the earliest stage, before any structural change, and has near-complete sensitivity. The characteristic appearance is a band demarcating the dead segment from surrounding living bone, frequently showing two parallel lines on certain sequences—the double line sign—representing the interface between necrotic bone and the repair tissue advancing into it. MRI also shows the size and location of the affected area, which predicts the likelihood of collapse, and assesses whether collapse has already occurred. It images both hips in the same examination.
CT is better than X-ray at detecting subtle collapse of the joint surface, which can be difficult to appreciate on plain films, and this distinction directly affects whether joint-preserving surgery remains an option.
Bone scan was historically used but is less sensitive than MRI and has largely been superseded.
The extent and location of involvement are assessed because they predict outcome. Lesions that are small and located away from the main weight-bearing area may remain stable, while large lesions involving the superior weight-bearing portion of the head have a high likelihood of collapsing.
The key clinical message is about who should be imaged. Anyone with unexplained hip pain who has relevant risk factors—particularly corticosteroid use, significant alcohol intake, sickle cell disease, previous hip fracture or dislocation, lupus, or transplantation—should have an MRI rather than being reassured by a normal X-ray. This single step accounts for most of the difference between diagnosing the condition when it can be treated and diagnosing it when only replacement remains.
Important to Know
The central principle in avascular necrosis is that treatment options change fundamentally once the femoral head collapses, so the aim is to identify and act on the condition before that point. Care is managed by orthopaedic surgeons, ideally those with specific experience in hip preservation, alongside the specialists managing any underlying condition.
For anyone with risk factors, the practical implication is straightforward: new hip or groin pain warrants MRI rather than X-ray alone. This applies particularly to people taking corticosteroids, where hip pain is easily attributed to the condition being treated, and to those with sickle cell disease, lupus, or a transplant.
Where one hip is diagnosed, the other should be imaged, since bilateral involvement is common and the second hip is frequently affected but silent.
Treatment before collapse aims to preserve the joint.
Core decompression is the most established procedure. One or more channels are drilled into the affected segment of the femoral head, which relieves the raised pressure within the bone and creates a pathway for new blood vessels to grow in. It reduces pain in the majority and, in appropriately selected cases with smaller lesions diagnosed before collapse, can prevent or substantially delay progression. Its effectiveness falls sharply in larger lesions and is minimal once collapse has occurred.
Variations are widely used, including filling the decompressed area with bone graft, inserting structural support, or augmenting with bone marrow concentrate containing cells intended to assist regeneration. Evidence for the added benefit of these augmentations is encouraging but not definitive, and they are not uniformly available.
Vascularised bone grafting, in which bone with its own blood supply is transferred into the femoral head, is performed at a small number of specialist centres and can be effective in younger people, though it is technically demanding with a longer recovery.
Osteotomy, rotating the femoral head so that an unaffected portion bears the load, is used selectively and more commonly in some countries than others.
Reducing weight bearing with crutches is frequently advised but does not by itself alter the natural course, and should not be relied upon as treatment.
Medication has been studied extensively with mixed results. Bisphosphonates, which reduce bone resorption and might therefore limit the weakening phase, showed promise in early studies but have not consistently prevented collapse in larger trials. Anticoagulants, statins, and vasodilators have been investigated. Extracorporeal shockwave therapy and hyperbaric oxygen have some supporting evidence. None is established as standard, and a person offered these should ask what the evidence shows.
After collapse, total hip replacement is the definitive treatment and produces excellent results, with pain relief and function comparable to replacement for osteoarthritis. The consideration specific to this group is age: people with avascular necrosis are typically considerably younger than those having replacement for osteoarthritis, so they face a longer period during which revision may become necessary. Modern bearing surfaces have improved durability substantially, and this concern is less than it once was, but it influences timing and the choice of implant.
Hip resurfacing is generally unsuitable where the femoral head is extensively necrotic, since the procedure relies on the head providing a sound foundation.
Addressing the underlying cause matters where possible. Corticosteroid dose should be minimised where the treated condition allows, in consultation with the prescribing specialist rather than independently. Alcohol intake should be reduced. Underlying conditions such as clotting disorders should be managed.
A point about corticosteroids deserves care. They are prescribed for conditions where they are genuinely necessary, and the possibility of avascular necrosis is not a reason to stop them abruptly or without advice. The appropriate response is awareness—knowing that new hip pain should be investigated promptly rather than dismissed—and discussion with the prescribing clinician about whether the dose can be reduced.
Avascular necrosis affects other sites, and someone diagnosed in the hip may have involvement elsewhere. The knee, shoulder, and the small bones of the wrist and foot are affected, with similar principles applying. The jaw is affected by a distinct condition related to certain bone medications and dental procedures, which is a separate entity despite the shared name.
Outcomes depend substantially on the stage at diagnosis and the size of the affected area. Small lesions found early and treated may never progress. Large lesions in the weight-bearing area frequently collapse within two to three years regardless of treatment, and planning should be realistic about this. Being told the likely course based on the specific findings is more useful than general reassurance, and it is reasonable to ask.
Care is managed by orthopaedics, with rheumatology, haematology, or transplant teams involved according to the underlying cause. MRI is central to diagnosis and staging, and both hips are assessed.
Patient education plays an important role. Understanding that X-rays are normal early and do not exclude the diagnosis, that MRI is required where risk factors are present, that both hips should be checked, that joint-preserving treatment works before collapse and not after, and that new hip pain on corticosteroids should be investigated promptly all contribute to appropriate care.
Red flag symptoms include new or worsening hip or groin pain in anyone taking corticosteroids, with sickle cell disease, lupus, or a transplant, which warrants prompt MRI rather than reassurance from a normal X-ray; sudden severe hip pain or inability to bear weight, which may indicate fracture or acute collapse; hip pain following previous hip fracture or dislocation; fever with a hot, painful hip, suggesting infection; and progressive loss of movement with increasing night pain. These warrant prompt medical evaluation.