What happens inside the hip in avascular necrosis

Inside the femoral head — the ball at the top of the thigh bone — a dense network of small blood vessels keeps bone tissue alive. In avascular necrosis (AVN), also called osteonecrosis, that blood supply is cut off. Without it, bone cells begin to die. Over time the structural integrity of the femoral head weakens from the inside, and under normal body weight it may eventually collapse.

The process begins silently. Early on there may be no pain and nothing visible on a standard X-ray — damage is occurring at the level of the bone itself, long before the joint surface is involved. This internal failure is what distinguishes AVN from the wear-and-tear picture most people associate with hip problems.

Four broad categories of cause are recognised:

• Corticosteroid use — prolonged or high-dose steroid treatment (for conditions such as asthma, rheumatoid arthritis, or inflammatory bowel disease) can reduce blood flow to the femoral head; many patients are surprised to learn that a medication prescribed for an entirely different problem may later affect the hip
• Excessive alcohol consumption — alcohol can cause fatty deposits to form within blood vessels, narrowing or blocking the supply to bone
• Traumatic injury — a hip dislocation or fracture can directly sever the vessels feeding the femoral head
• Blood and systemic disorders — conditions such as sickle cell disease, lupus, or clotting disorders may compromise circulation within bone

AVN most commonly affects people between the ages of 40 and 65, and in many cases both hips are involved. This younger demographic matters clinically: the hip joint may have perfectly intact cartilage at the time of diagnosis, because cartilage breakdown is not the cause of AVN — it is a downstream consequence of bony collapse. Understanding that distinction is central to understanding why this condition follows a different course, and demands different management, from degenerative hip arthritis.

Why AVN and osteoarthritis are not the same condition

Osteoarthritis of the hip is a fundamentally different disease, and conflating the two can distort both the sense of urgency and expectations about what happens next.

In osteoarthritis, the primary target is articular cartilage — the smooth tissue lining the ball and socket. Years of loading, age-related change, and mechanical wear gradually thin and roughen that surface; bony changes develop only once cartilage loss is already established. OA is estimated to affect around 240 million people worldwide and is strongly associated with age over 60. Symptoms typically accumulate over years, often with prolonged warning before function is meaningfully curtailed.

Because AVN originates in bone rather than cartilage, the clinical picture can be strikingly different. A patient developing OA usually has a recognisable history of gradual stiffening and worsening discomfort — the hip gives plenty of notice. A patient with AVN may have had no hip symptoms whatsoever before diagnosis; the cartilage surface can remain intact until the femoral head collapses beneath it, which means an absence of prior hip pain offers no reassurance that damage is not already advanced.

Progression timelines also differ. Osteoarthritis typically advances slowly, sometimes across decades. Once the structural integrity of the femoral head is compromised in AVN, collapse can follow more quickly — and it is this difference in tempo, not just mechanism, that makes staging and early specialist assessment more pressing than it would be for uncomplicated degenerative arthritis.

AVN also tends to affect a younger patient group than OA typically does. Where OA is largely a condition of later life, AVN can present well before retirement age — adding a further layer of clinical distinctiveness that shapes both investigation and any subsequent decision-making about the joint.

How AVN is detected and why early imaging matters

Plain X-rays are often the first investigation a GP arranges when a patient reports hip pain — but in AVN, an apparently normal X-ray can be deeply misleading. The bony architecture of the femoral head may look entirely intact on a radiograph even while significant bone death is already under way inside it. By the time X-ray does reveal an abnormality — irregular density, flattening of the femoral head, or joint space changes — the disease is usually at an advanced stage.

MRI is the critical tool. It detects changes in bone marrow signal caused by interrupted blood supply well before any structural failure is visible, making it the standard investigation whenever AVN is clinically suspected. For patients who have been told their X-ray was unremarkable but whose symptoms or risk profile warrant further assessment, MRI is the appropriate next step.

Clinical suspicion matters enormously here. Anyone with a known risk factor — prolonged corticosteroid therapy, alcohol excess, sickle cell disease, or a prior hip fracture or dislocation — should be assessed with that background in mind, even if early imaging looks normal.

Staging systems such as the Ficat and ARCO classifications describe the disease in broad phases: from early pre-collapse changes detectable only on MRI, through a critical transition marked by the 'crescent sign' — a thin subchondral fracture line signalling that the femoral head is close to or beginning to collapse — to established collapse with secondary joint destruction. The stage at which AVN is diagnosed is what determines whether joint-preserving options remain possible, or whether the discussion moves directly to hip replacement.

The pre-collapse and post-collapse divide in AVN management

The staging described in the previous section carries direct clinical weight because one threshold — femoral head collapse — determines which treatments remain on the table.

Before structural collapse occurs, a narrow window may exist for interventions designed to preserve the joint. Core decompression — a procedure in which channels are drilled into the femoral head to relieve pressure and encourage revascularisation — is one approach used in selected pre-collapse cases. Osteotomy, which repositions the femoral head to shift load away from the affected segment, is another option in certain circumstances. Neither intervention is universally appropriate; the extent of bone involvement, how quickly the disease is progressing, and the overall health of the patient all affect whether preservation is realistic. Outcomes vary, and no preservation technique can arrest disease that has already advanced too far.

Once the femoral head collapses, that window closes entirely. The joint surface — which may have remained cartilage-intact right up to the moment of structural failure — is now distorted. A surface that once formed a smooth, spherical bearing becomes irregular, and the cartilage that depended on its geometry deteriorates rapidly under load. Secondary arthritis follows not over years, as it typically might in osteoarthritis, but often over months.

This transition is the single most consequential event in AVN management. Patients who defer assessment, or whose disease advances quickly past the pre-collapse stage, reach the point of specialist review without viable joint-preserving options remaining. The conversation then shifts — necessarily — to what hip replacement can offer.

When total hip replacement becomes the right answer

Collapse plus secondary arthritis — the end-stage picture outlined in the previous section — marks the point at which total hip arthroplasty becomes the most reliable treatment available. Once the femoral head has lost its structural integrity and the joint surface has deteriorated, joint-preserving approaches are no longer viable. In this context, hip replacement is not a reluctant fallback; it is the clinically appropriate answer to a well-defined problem.

Patients in their forties and fifties who develop AVN through corticosteroid therapy, trauma, or haematological disease — rather than through decades of cartilage wear — sometimes resist this conclusion on the grounds that they are too young for an artificial joint. The evidence on modern implants addresses that concern directly. For the right indication, with thorough preparation, a hip replacement can last well beyond 30 years. Most patients reach what surgeons describe as a 'forgotten joint' — a hip that no longer dominates daily awareness or restricts movement. That outcome is achievable for many, though it depends on individual anatomy, preparation, and recovery.

What matters most at this stage is the quality of the assessment that precedes the decision. Replacement should follow careful confirmation that the indication is genuine and the patient is properly prepared — not simply that collapse has occurred. Professor Paul Lee's approach to replacement assessment is built around this principle: his practice includes establishing when to defer as well as when to proceed, which means patients approaching this threshold can expect a recommendation grounded in individual circumstances rather than a reflex to operate. His published work on implant survivorship and revision arthroplasty gives that judgement an evidence base to stand on.

What hip replacement looks like for an AVN patient

For an AVN patient arriving at hip replacement in their late forties or early fifties, the surgical experience differs in one important respect from the typical osteoarthritis presentation: there are likely to be more decades of active life ahead. That longer horizon makes how the replacement is done — not just that it is done — a clinically meaningful question.

The SPAIRE technique takes its name from what it leaves intact: the piriformis and obturator internus tendons at the back of the hip, with repair of the obturator externus. In conventional posterolateral approaches, these structures are divided during the operation. Preserving them may reduce the early dislocation risk historically associated with posterior access, and may support more confident movement in the weeks immediately following surgery — a consideration that carries more weight when the patient expects to remain physically active for three or more decades post-operatively. Professor Lee refined this approach during his fellowship at the Exeter Hip Unit under Professor Timperley.

The structure around the operation — preparation, pain management, and early mobilisation — is organised to support function from the first day rather than rebuild it over subsequent weeks. That design connects directly to soft-tissue handling: when the key posterior tendons are preserved, patients within this pathway may be able to move more confidently from the outset. In suitable, well-prepared cases, same-day or next-day discharge may be achievable; actual outcomes depend on individual fitness, anatomy, and how recovery progresses.

For a patient who developed AVN through corticosteroids, trauma, or haematological disease — not through cartilage wear — this specificity matters. The femoral head collapsed, not the life around it. The surgical question is whether replacement can restore the function that the bone failure interrupted, rather than simply replacing a joint that was already declining.

1. [1] Avascular necrosis. https://en.wikipedia.org/?curid=1498676 https://en.wikipedia.org/?curid=1498676