What avascular necrosis of the hip actually is

Avascular necrosis of the hip — also called osteonecrosis of the femoral head (ONFH) — is a condition in which the bone cells inside the ball of the hip joint die because their blood supply has been cut off. The femoral head, the rounded top of the thigh bone that sits inside the hip socket, depends on a precise network of small blood vessels. When those vessels are blocked or damaged, bone tissue begins to die silently, often before any pain appears.

Without living bone to bear the body's load, the femoral head gradually weakens. Over time it may crack and collapse — a structural failure that converts a metabolic problem into severe joint destruction. AVN is therefore a progressive condition, not a stable one.

The mechanism is fundamentally different from osteoarthritis, where cartilage wears down over decades. In AVN, the cartilage is initially intact; the underlying bone is the primary problem. That distinction shapes how the condition is diagnosed, staged, and treated.

AVN predominantly strikes working-age adults between 35 and 50, which raises the long-term stakes considerably. It also affects both hips in the majority of cases — meaning the unaffected side deserves assessment even when only one hip is causing symptoms.

Causes and risk factors worth knowing

Several well-established factors disrupt the femoral head's blood supply, and knowing which apply to you is one of the most useful things you can bring to a first consultation.

Corticosteroid use is the single most common non-traumatic cause. Steroids — prescribed for conditions ranging from asthma and inflammatory bowel disease to organ transplantation — raise pressure inside the bone by promoting fat-cell growth, which compresses the delicate vessels feeding the femoral head. Heavy alcohol consumption works differently but arrives at the same result: it alters fat metabolism in a way that produces tiny fatty deposits blocking those same microvessels. Together, steroids and alcohol are thought to account for up to 80% of non-traumatic cases, which is why a thorough medication and lifestyle history sits at the centre of any AVN assessment.

Trauma is the dominant cause in younger patients. A hip fracture or dislocation can shear or stretch the blood vessels entering the femoral head mechanically, cutting off supply at the moment of injury. Anyone with a history of significant hip trauma — even if treated successfully at the time — carries a meaningful long-term risk.

An emerging association worth noting is prior COVID-19 infection. Data from one cohort found that 34% of patients presenting with AVN had a documented COVID-19 history before symptom onset. The link is not fully characterised, but it is a risk factor patients may not spontaneously connect to their hip pain.

Systemic conditions including sickle cell disease, lupus (SLE), Gaucher's disease, and decompression sickness can each impair bone blood flow through vascular or haematological mechanisms. In a proportion of cases, no underlying cause is identified at all — idiopathic AVN behaves in the same way and follows the same assessment pathway, so the absence of an obvious trigger does not change what needs to happen next.

What AVN symptoms feel like — and why they're easy to miss early

For many people, the first sign that something is wrong is almost nothing at all. A vague ache in the groin after a long walk, a slight stiffness that fades with rest — symptoms mild enough to be attributed to a pulled muscle, a bad night's sleep, or simply getting older. This early silence is not unusual; it reflects the fact that in Stages I and II, the femoral head is weakening internally while the joint surface remains structurally intact. Mild discomfort that comes and goes is easily dismissed, and diagnostic delay at this stage is common and well-recognised.

The pattern shifts as the disease progresses. Pain begins to feel deeper and more insistent — a throbbing ache centred in the groin that reliably worsens with walking, standing, or any weight-bearing activity. Rest may help initially, but over time the discomfort starts to intrude on sleep. Stiffness develops, turning straightforward movements — getting out of a car, climbing stairs, rising from a low chair — into conscious efforts. A visible limp often follows, the body's attempt to offload an increasingly unreliable joint.

By the time the femoral head approaches collapse, what started as background discomfort has typically become a significant functional problem. Pain score alone is not the most reliable marker; loss of function matters as much. Difficulty walking a useful distance, struggling with basic self-care, or finding that daily tasks now centre around managing hip pain are all clinically significant signals.

If this progression sounds familiar — particularly in the presence of the risk factors described above — imaging rather than further watchful waiting is the appropriate next step. An MRI can detect AVN before any X-ray changes appear, and catching it before collapse opens up a wider range of options.

How AVN is diagnosed and why imaging stage determines your options

Standard X-rays can look entirely normal in early AVN, even when significant bone death is already under way. Plain radiographs detect structural changes — sclerosis, cysts, femoral head flattening — but they cannot reveal the cellular damage that precedes them. By the time the femoral head shows visible changes on film, the window for certain treatment approaches may have already narrowed.

MRI is the investigation that changes the picture. It detects the characteristic signal abnormality within the necrotic segment — typically a low-signal band visible on both T1 and T2 sequences — weeks to months before any radiographic change appears. Requesting an MRI early rather than waiting for plain film confirmation is precisely what keeps options open.

What MRI also enables is staging. Both the Ficat-Arlet and ARCO classification systems grade AVN from early disease (abnormal MRI, normal X-ray) through to advanced collapse with secondary joint destruction. The precise staging criteria involve clinical detail best reviewed with your surgeon, but the practical principle is clear: earlier stages retain the possibility of joint-preserving procedures such as core decompression; later stages — where the femoral head has already collapsed and the articular surface is damaged — shift the discussion toward hip replacement. Staging is not simply a label; it is the mechanism by which the imaging finding translates directly into which treatment doors remain open.

Because AVN affects both hips in the majority of cases, often without symptoms on the second side, imaging the contralateral hip at the same assessment is standard practice — not an optional extra.

Non-surgical care, early intervention, and the shift toward hip replacement

Non-surgical management — anti-inflammatories, physiotherapy, weight control, and walking aids to reduce load on the joint — can meaningfully reduce discomfort in early-stage AVN. What it cannot do is reverse bone death already under way or prevent the femoral head from eventually collapsing if the disease progresses. It is a holding measure, appropriate while staging is being clarified or overall health is being optimised; not a curative pathway.

In Stages I and II, before structural collapse has occurred, selected patients may be considered for a joint-preserving procedure. Core decompression — in which a channel is drilled into the necrotic segment to relieve elevated intraosseous pressure and encourage revascularisation — may slow or prevent collapse in appropriate candidates, often combined with bone grafting for added structural support. These options carry honest caveats: they are most likely to help when the necrotic area is small and detected early, and they do not guarantee that progression is halted. Where they are appropriate, they may allow a meaningful interval before any replacement discussion arises.

Once the femoral head has collapsed — Stage III onwards — the structural damage is irreversible. Preservation procedures are no longer viable at this point, and attempting to delay replacement typically means accepting continued functional deterioration without clinical benefit.

The shift toward total hip arthroplasty is not triggered by imaging stage alone. Persistent pain that disrupts sleep, inability to manage basic daily tasks — dressing, walking a reasonable distance, climbing stairs — and progressive loss of mobility all contribute to when the balance tips. These functional markers matter alongside what the scan shows.

Professor Paul Lee — Consultant Orthopaedic Surgeon at the Royal London Hospital and in private practice at 108 Harley Street — works at precisely this decision junction. His assessment draws together imaging stage, symptom trajectory, activity level, and individual anatomy to evaluate which patients may still benefit from conservative management and which are losing function unnecessarily by deferring a well-timed replacement.

Hip replacement for AVN: what makes it different and what to expect

Replacing a hip in a 40-year-old with AVN is a different calculation from replacing one in a 68-year-old with osteoarthritis — and the honest version of that conversation is worth having before surgery, not after.

The central difference is the time horizon. AVN patients are younger, typically more physically active, and will place far greater cumulative demand on an implant over decades. One study reporting outcomes at a mean follow-up of seven years found a major revision rate of 28% in AVN patients compared with 6% in those operated on for osteoarthritis. That gap deserves acknowledgement rather than minimising. It also explains why implant choices — cementless fixation for reliable biological bonding, and advanced bearing surfaces such as highly cross-linked polyethylene or ceramic-on-ceramic — are weighted toward longevity in this patient group rather than cost or simplicity.

Surgical technique carries its own importance here. The posterolateral approach to the hip has traditionally required detaching the external rotator tendons to gain access, then repairing them under tension — a repair that, if it stretches or fails, leaves the hip relying on the prosthesis geometry alone for stability. The SPAIRE technique, which Professor Paul Lee performs at 108 Harley Street, takes a different route: the piriformis and obturator internus tendons are preserved rather than divided, and the obturator externus is formally repaired, keeping the posterior soft-tissue sleeve intact. The clinical purpose is a hip that retains its natural posterior stabilisers from the moment the patient wakes from anaesthesia — which may support early confident mobilisation within a structured recovery pathway, and can allow selected patients to go home within a day of surgery.

For patients who have reached Stage III or IV and lost meaningful function, THA for AVN consistently delivers what matters most: freedom from the deep, weight-bearing pain that has been narrowing daily life. Published survivorship at five to ten years runs at roughly 92%, and the general evidence base for modern hip replacement supports longevity well beyond that horizon — though long-term data specific to AVN cohorts remain limited. The goal, as Professor Paul Lee frames it, is a hip the patient stops thinking about.

1. [1] Avascular Necrosis – Wikipedia. https://en.wikipedia.org/?curid=1498676 https://en.wikipedia.org/?curid=1498676