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Health condition · Clinically reviewed

Avascular necrosis, catch it early, save the joint.

Bone dies quietly when its blood supply fails. Early MRI, treatment of the underlying driver and joint-preserving surgery can change the course before the joint surface collapses.

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A radiographer guides a patient onto the bed of an advanced 3 Tesla MRI scanner in a London imaging suite

Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against NICE, BOA, BSR and peer-reviewed sources you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK guidance on early MRI, joint-preserving surgery and steroid-induced AVN.

Key facts

Avascular necrosis at a glance.

The essentials in plain English. What it is, why it happens, how it is diagnosed and what modern treatment looks like in the UK.

  • What it is

    Bone death caused by loss of blood supply. Also called osteonecrosis or aseptic necrosis. Progresses through stages from marrow oedema to subchondral collapse and secondary arthritis.

  • Where it strikes

    Most commonly the femoral head. Also the humeral head, femoral condyles, talus, scaphoid, lunate (Kienbock), navicular, metatarsal head (Freiberg) and the jaw (MRONJ).

  • Main culprits

    Trauma to end-arterial supply, high-dose corticosteroids, heavy alcohol, sickle cell disease, SLE with antiphospholipid syndrome, radiotherapy and bisphosphonates for jaw disease.

  • Diagnostic gold

    MRI. Detects marrow changes months before X-ray. Classic double-line sign on T2 with a low-signal rim on T1.

  • Early window

    Pre-collapse disease can respond to joint-preserving surgery, core decompression and treatment of the underlying driver.

  • After collapse

    Osteotomy, vascularised bone grafting or joint replacement depending on site, age and stage.

Why this guide matters

Time is bone.

Pre-collapse AVN and post-collapse AVN are different diseases with different treatments. The three points below shape everything else on this page.

  • MRI is the diagnostic gold

    Detects marrow oedema and necrosis months before X-ray change. A normal X-ray does not exclude AVN.

  • The driver matters

    Steroids, alcohol, sickle cell and autoimmune disease need addressing alongside any surgery, or disease progresses.

  • Stage guides surgery

    Pre-collapse disease favours core decompression and joint-preserving options. Post-collapse disease increasingly points to replacement.

How the diagnosis is made

From first pain to a staged plan.

The steps a UK GP, orthopaedic surgeon or rheumatologist will normally follow, in order, so you know what to expect and why each one matters.

  1. 01

    Assessing

    Focused history and risk profile

    Recent trauma, steroid courses (dose and duration), alcohol intake, sickle cell, autoimmune disease, HIV therapy, radiotherapy, bisphosphonates and diving history.

  2. 02

    Assessing

    Clinical examination

    Groin or joint pain on weight-bearing, restricted internal rotation of the hip, antalgic gait, tenderness over the affected bone.

  3. 03

    Assessing

    Plain X-ray both hips or joint

    Often normal early. Later shows crescent sign, subchondral lucency, femoral head flattening and secondary osteoarthritis.

  4. 04

    Confirming

    MRI, the definitive investigation

    Detects marrow oedema and necrosis before X-ray change. Low-signal band on T1 and the double-line sign on T2 are diagnostic.

  5. 05

    Confirming

    CT or bone scan when needed

    CT quantifies subchondral collapse for surgical planning. Bone scan is a fallback when MRI is contraindicated.

  6. 06

    Planning

    Cause workup

    Bloods for lipids, clotting, sickle screen, autoimmune profile including antiphospholipid antibodies, HIV testing and steroid audit.

  7. 07

    Planning

    Staging and MDT referral

    Ficat and Ferkel or ARCO staging drives management. Orthopaedics, rheumatology, haematology and oral surgery input as required.

Typical timeline: a first visit to a staged surgical plan in a few weeks when MRI is prompt.

Symptoms

What avascular necrosis feels like.

The presentation is often insidious. Pain on weight-bearing and loss of internal rotation at the hip are the classic clues. The features that push the case up the queue matter most.

  • Groin or deep hip pain

    Insidious ache, worse on weight-bearing and stairs, often referred to the buttock or thigh. Classic first symptom of hip AVN.

  • Restricted rotation

    Loss of internal rotation is an early sign at the hip. Shoulder AVN reduces overhead reach and rotation.

  • Night pain and rest pain

    Marrow pressure and inflammation cause pain that disturbs sleep, distinguishing AVN from simple mechanical strain.

  • Progressive loss of function

    Difficulty walking, climbing stairs or putting on shoes. Function declines faster than in typical osteoarthritis.

  • Sudden step-off or clunk

    A sharp deterioration can signal subchondral collapse. Warrants urgent imaging and specialist review.

  • Wrist or foot involvement

    Kienbock disease at the lunate, scaphoid AVN after fracture, Freiberg at the metatarsal head, or talar AVN after ankle trauma.

  • Jaw exposure (MRONJ)

    Exposed bone in the mouth for over eight weeks in a patient on bisphosphonates or denosumab. Painful, slow to heal.

  • Red flag - bilateral disease

    Both hips affected together strongly suggests a systemic driver such as steroids, alcohol, sickle cell or SLE.

Treatment

How avascular necrosis is treated in the UK.

Treat the driver, protect the joint, and match the surgery to the stage. Early disease favours joint-preserving options. Post-collapse disease increasingly points to replacement.

  • Protected weight-bearing

    Crutches and activity modification while investigations and definitive plans are put in place. Rarely enough on its own.

  • Treat the driver

    Reduce steroid dose where safe, address alcohol, initiate sickle cell exchange transfusion, treat coagulopathy, stop smoking, control lipids.

  • Bisphosphonates and statins

    May slow progression in early pre-collapse disease. Evidence is strongest in steroid-related AVN. Not appropriate for MRONJ.

  • Hyperbaric oxygen

    Selective use in early hip AVN and MRONJ. Improves oxygenation of ischaemic bone and can reduce pain in specialist protocols.

  • Core decompression

    Drilling the necrotic segment to relieve pressure. Often combined with bone graft, BMP or stem cell augmentation for early disease.

  • Vascularised bone grafting

    Free fibular graft brings living blood supply to the femoral head. A joint-preserving option in younger patients after early collapse.

  • Osteotomy

    Rotational transtrochanteric or angular osteotomy shifts load away from the necrotic segment. Selected younger patients with focal disease.

  • Joint replacement

    Hip resurfacing or total hip arthroplasty for advanced disease. Excellent pain relief. Younger patients may need revision later.

Multidisciplinary care

AVN rarely sits with one team.

Orthopaedics leads the joint. Rheumatology helps with steroid and autoimmune drivers. Haematology manages sickle cell and coagulopathy. Oral and maxillofacial surgery leads on jaw disease. Physiotherapy, pain services and social support round out the plan.

What this guide is based on

The sources behind every claim on this page.

UK national guidance and specialist society standards, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your GP, orthopaedic surgeon, rheumatologist or oral surgeon knows your history and imaging and can tell you which parts apply to you. If in doubt, get seen.

  • NICE. Osteonecrosis: assessment and referral guidance.

  • British Orthopaedic Association (BOA). Standards for the management of avascular necrosis of the femoral head.

  • British Society for Rheumatology (BSR). Guidance on steroid-related osteonecrosis.

  • MHRA and SDCEP. Guidance on medication-related osteonecrosis of the jaw (MRONJ).

  • ARCO. International classification of osteonecrosis of the femoral head.

Red flags

When AVN needs urgent attention.

Most cases can be worked up through the standard pathway. These situations should not wait.

  • Sudden severe pain and step-off

    Rapid deterioration with a mechanical clunk suggests subchondral collapse. Needs urgent orthopaedic review and imaging.

  • Bilateral hip pain on steroids

    A red flag for bilateral steroid-induced AVN. Refer for MRI even if X-rays are normal.

  • Exposed jaw bone on bisphosphonates

    Persistent oral bone exposure in a patient on bisphosphonates or denosumab is MRONJ until proven otherwise. Refer to maxillofacial.

  • Sickle cell crisis with hip pain

    New or worsening hip pain in sickle cell disease needs early MRI. AVN is common and often silent until collapse.

  • Post-fracture pain that persists

    Ongoing pain months after a scaphoid, femoral neck or talar fracture may signal AVN in the proximal fragment.

  • Autoimmune disease with new joint pain

    SLE with antiphospholipid syndrome is a strong risk. New hip or shoulder pain warrants low-threshold MRI.

  • Systemic upset with bone pain

    Fever, weight loss or night sweats with bone pain needs urgent workup to exclude infection or malignancy first.

  • Rapid progression in a young patient

    Aggressive AVN under 40 should prompt haematology and rheumatology review to identify a treatable driver.

  • Post-transplant patient with hip pain

    High steroid exposure after solid organ transplant makes AVN common. Have a low threshold for imaging.

Living with it

A serious diagnosis, with a clear plan.

Four things make the biggest day-to-day difference. Respect the load on the bone, tackle the driver, keep moving with guidance and stay in the follow-up loop.

A quiet reminder

Silent progression is the enemy.

Pain that settles for a while does not mean the bone has healed. Keep the imaging and the review appointments in the diary.

  1. 01 Load

    Respect the bone

    Protected weight-bearing while investigations run buys the femoral head time. Follow the plan even when pain settles.

  2. 02 Drivers

    Tackle the cause

    Steroid reduction where safe, alcohol reduction, sickle cell care, lipid control and stopping smoking all matter.

  3. 03 Rehab

    Move with guidance

    Physiotherapy protects range and strength before and after any surgery. Aquatic therapy is often kinder than land-based work.

  4. 04 Follow-up

    Stay on the radar

    Serial MRI or X-ray tracks progression. Early re-referral if pain escalates prevents avoidable collapse.

Frequently asked

Everything we get asked about avascular necrosis.

Quick answers on causes, MRI, joint-preserving surgery, MRONJ and joint replacement.

  • What is avascular necrosis?

    Avascular necrosis, also called osteonecrosis, is bone death caused by loss of blood supply. It most often affects the femoral head at the hip but can affect the shoulder, knee, wrist, ankle, foot and jaw. Without intervention it progresses to subchondral collapse and secondary arthritis.

  • What causes avascular necrosis?

    Traumatic causes include displaced femoral neck fracture, hip dislocation and scaphoid fracture. Non-traumatic causes include corticosteroids (even short high-dose courses), heavy alcohol, sickle cell disease, SLE with antiphospholipid syndrome, HIV therapy, radiotherapy, chemotherapy, bisphosphonates for jaw AVN, Gaucher disease, decompression sickness, coagulopathy, transplantation, pancreatitis, hyperlipidaemia and smoking.

  • How is avascular necrosis diagnosed?

    MRI is the gold standard and detects marrow changes months before X-ray. The classic findings are a low-signal band on T1 and the double-line sign on T2. X-ray, CT and bone scan have supporting roles. Staging follows Ficat and Ferkel or ARCO systems and drives treatment.

  • Can avascular necrosis be reversed?

    Early pre-collapse disease can be halted or improved with treatment of the underlying driver combined with core decompression, sometimes augmented with bone graft, BMP or stem cells. Once the joint surface collapses, the changes are structural and joint-preserving or joint-replacing surgery is needed.

  • What is medication-related osteonecrosis of the jaw (MRONJ)?

    MRONJ is exposed jaw bone for more than eight weeks in a patient on bisphosphonates or denosumab, usually after dental extraction or trauma. Management involves pausing the drug where possible before dental surgery, antibiotics, conservative debridement and specialist maxillofacial care.

  • When is joint replacement needed?

    Total hip arthroplasty or hip resurfacing is offered when the joint surface has collapsed and pain and function no longer respond to conservative or joint-preserving measures. Modern implants give excellent pain relief but younger patients should expect revision surgery later in life.

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