Osteonecrosis of the Femoral Head Explained: Blood Supply Failure, MRI Diagnosis, ARCO Staging, Collapse and Treatment

What Is Osteonecrosis of the Femoral Head?

Terminology

Use:

as the preferred term.

Explain once that commonly used alternative terms include:

• avascular necrosis;
• AVN;
• ischemic necrosis;
• aseptic necrosis.

ARCO adopted osteonecrosis as standardized terminology for these necrotic femoral-head lesions. (PubMed Central (PMC))

For SEO, naturally use both:

osteonecrosis

and:

avascular necrosis / AVN

Central Teaching Concept

Central pathway:

The most important distinction is:

Osteonecrosis can exist while the femoral head is still structurally preserved.

This creates the therapeutic window for:

Opening — Use This Content

A patient receiving long-term glucocorticoid treatment develops deep groin pain.

The hip radiograph looks normal.

Does that exclude major structural bone disease?

The patient may already have:

In early ONFH, bone and marrow cells have died within part of the femoral head, but the overall shape of the femoral head may remain intact.

Plain radiography may therefore still appear normal.

MRI can detect the disease at this stage.

If mechanical failure later develops, the sequence becomes:

The key clinical goal is therefore not merely to ask:

“Is osteonecrosis present?”

It is also to ask:

“Is the femoral head still structurally preservable?”

Normal Femoral-Head Blood Supply

The femoral head depends on a relatively vulnerable vascular network.

In adults, an important blood supply is provided by retinacular vessels arising predominantly from branches of the:

Additional vascular contributions exist, but the educational point is:

This is especially obvious after:

• femoral-neck fracture;
• hip dislocation.

What Is Osteonecrosis?

Osteonecrosis is:

In ONFH, this occurs within a segment of the femoral head.

Histological features include:

• marrow necrosis;
• osteocyte death;
• reparative fibrovascular tissue surrounding the necrotic region. (PubMed Central (PMC))

The necrotic bone does not instantly disappear.

That is crucial.

Dead Bone May Initially Retain Its Shape

Immediately after cellular death, the mineralized structural framework can remain present.

Therefore:

for a period.

The clinical problem develops because normal living bone must withstand repeated mechanical loading.

As repair progresses around necrotic bone, mechanical weakness can develop.

Eventually:

may occur.

That is the major transition toward collapse.

Why The Femoral Head Collapses

The femoral head is repeatedly loaded during:

• standing;
• walking;
• running;
• stair climbing.

The subchondral region beneath the articular cartilage must withstand substantial mechanical stress.

In ONFH:

can eventually exceed structural capacity.

Then:

develops.

Further loading can lead to:

and ultimately:

Causes and Risk Factors

Two Broad Categories

Teach ONFH using:

Traumatic osteonecrosis

A clear mechanical vascular insult occurs.

Examples:

• femoral-neck fracture;
• hip dislocation.

Non-traumatic osteonecrosis

No single major traumatic vascular event explains the disease.

Important associations include:

• glucocorticoid exposure;
• heavy alcohol exposure;
• sickle-cell disease and other hemoglobinopathies;
• autoimmune disease;
• organ transplantation;
• selected coagulation disorders;
• decompression sickness;
• other systemic/metabolic disorders;
• idiopathic disease.

The 2026 ARCO evidence review lists corticosteroids, excessive alcohol exposure, hemoglobinopathies, autoimmune disease, solid-organ transplantation and idiopathic disease among major non-traumatic contexts. (PubMed Central (PMC))

Traumatic ONFH

After a femoral-neck fracture or hip dislocation, vessels supplying the femoral head may be:

• torn;
• compressed;
• disrupted.

Therefore:

The risk depends on the injury pattern and vascular damage.

Non-Traumatic ONFH Is Multifactorial

Non-traumatic ONFH is not explained by thrombosis alone.

or:

“All steroid ONFH is caused by fat emboli.”

Current understanding is more complex.

Potential interacting mechanisms include:

• vascular dysfunction;
• thrombosis/hypercoagulability;
• hypofibrinolysis;
• impaired angiogenesis;
• lipid/fat-cell abnormalities;
• increased intraosseous pressure;
• cellular injury;
• impaired repair;
• genetic susceptibility.

Therefore:

ARCO reviews emphasize multifactorial pathogenesis and individual susceptibility. (PubMed Central (PMC))

Glucocorticoids

Glucocorticoid exposure is one of the most important non-traumatic associations.

Potential mechanisms include:

• lipid metabolism changes;
• marrow adipocyte enlargement;
• vascular dysfunction;
• altered coagulation;
• cellular injury;
• impaired osteogenic repair.

Important:

Risk depends on multiple factors, including exposure and individual susceptibility.

Alcohol

Heavy alcohol exposure is another established association.

Potential mechanisms overlap with steroid-associated disease, including:

• altered lipid metabolism;
• marrow changes;
• vascular dysfunction;
• impaired osteogenic differentiation.

Again:

Sickle-Cell Disease

Sickle-cell disease can cause repeated microvascular obstruction.

Therefore:

The femoral head is an important site.

This creates a strong connection between hematology and orthopedic pathology.

Autoimmune Disease

ONFH may occur in patients with systemic autoimmune disease.

Interpret carefully because risk may involve:

• the underlying systemic disease;
• glucocorticoid exposure;
• vascular/coagulation factors;
• combinations of these.

ONFH in a patient with SLE should not automatically be attributed solely to steroid exposure.

Organ Transplantation

Transplant recipients can develop ONFH.

Relevant contributors may include:

• glucocorticoid exposure;
• underlying disease;
• metabolic changes;
• other systemic factors.

Again, avoid reducing a multifactorial problem to one mechanism.

Idiopathic ONFH

Sometimes no definite cause is identified.

This is commonly termed:

“Idiopathic” means:

not:

Bilateral Disease

Non-traumatic ONFH may involve both hips.

Therefore:

A patient can have:

• symptomatic ONFH on one side;
• asymptomatic ONFH on the other.

Contralateral evaluation depends on clinical context.

Symptoms and Examination

Symptoms

Early ONFH may be:

When symptoms develop, the typical complaint is:

Pain may also be perceived in:

• buttock;
• thigh;
• occasionally around the knee.

Symptoms often worsen with weight bearing.

Later disease may produce:

• reduced range of motion;
• limp;
• progressive functional limitation.

Physical Examination

Early disease may have relatively limited examination findings.

As disease progresses, findings can include:

• painful hip movement;
• restricted internal rotation;
• reduced range of motion;
• antalgic gait.

Physical examination does not reliably exclude early ONFH.

Therefore:

Imaging and MRI Diagnosis

Initial Imaging

For clinically suspected osteonecrosis:

The ACR Appropriateness Criteria rate radiography of the area of interest as usually appropriate for initial evaluation. (ACSearch)

For the hip, obtain the standard clinically appropriate hip radiographic views according to local practice.

The Major Limitation Of X-Ray

The most important imaging lesson is:

This is literally incorporated into ARCO stage I:

but:

Therefore a normal X-ray cannot end the investigation when clinical suspicion remains substantial.

When MRI Is Needed

When:

• osteonecrosis is clinically suspected;
• and radiographs are normal or suspicious but nondiagnostic;

the next study should generally be:

The ACR rates MRI without contrast as usually appropriate in this situation. (ACSearch)

Therefore:

This should be one of the article's strongest memory statements.

MRI

MRI is the key imaging modality for:

It can identify the necrotic segment before plain radiographic abnormalities develop.

MRI also helps assess:

• lesion extent;
• lesion location;
• surrounding marrow reaction;
• bilateral disease where imaged.

The 2026 systematic review supporting ARCO guideline development concluded that MRI had the strongest diagnostic performance among evaluated imaging modalities. (PubMed Central (PMC))

MRI is highly useful but not infallible.

T1 Low-Signal Band

A characteristic MRI finding is:

around the necrotic region.

This feature forms part of the revised ARCO stage-I definition. (PubMed Central (PMC))

The band helps demarcate the viable-necrotic interface.

Double-Line Sign

On T2-weighted imaging, the classic:

may be seen.

Conceptually, it represents changes around the reactive interface between necrotic and viable tissue.

Important:

This sign alone cannot diagnose or exclude ONFH.

Bone-Marrow Edema

Bone-marrow edema can occur, particularly in symptomatic or more mechanically stressed disease.

But:

It also occurs in:

• insufficiency fracture;
• transient osteoporosis/bone-marrow-edema syndrome;
• arthritis;
• trauma;
• infection;
• other disorders.

Interpret it with lesion morphology and clinical context.

CT

CT is particularly useful for evaluating:

and:

It can complement radiography/MRI when detailed bony architecture is important.

ARCO stage III specifically uses subchondral fracture demonstrated on:

as a defining feature. (PubMed Central (PMC))

The Crescent Sign

The classic:

represents:

It reflects structural failure beneath the articular surface.

“Crescent sign = simply another early MRI sign.”

Instead teach:

This has major prognostic and therapeutic implications.

ARCO Staging

ARCO Staging

Use the 2019 revised ARCO staging system.

Create this table exactly in concept:

The revised system removed the old stage 0 and divided stage III at 2 mm of head depression. (PubMed Central (PMC))

ARCO Stage I

but:

with a characteristic low-signal band.

This is the clearest demonstration that:

At this stage:

ARCO Stage Ii

Stage II has:

Potential findings include:

• sclerosis;
• cystic change;
• focal osteoporotic change.

But critically:

and:

Therefore stage II remains:

ARCO Stage III

Stage III is defined by:

on X-ray or CT, with or without depression/flattening.

This is the major structural turning point.

ARCO IIIa Versus IIIb

Use:

IIIA

IIIB

This distinction comes from the revised 2019 ARCO staging system. (PubMed Central (PMC))

This classification threshold is not an automatic treatment threshold.

ARCO Stage IV

Stage IV means:

Potential findings include:

• joint-space narrowing;
• acetabular changes;
• progressive femoral-head deformity;
• degenerative destruction.

At this point the disease is no longer only a necrotic bone problem.

It has become:

Lesion Size, Location and Prognosis

Stage Is Not Enough

This is an essential section.

ARCO II lesions do not all behave the same.

Prognosis also depends strongly on:

and:

ARCO reviews identify size/location as major predictors of collapse. (PubMed Central (PMC))

Therefore:

Why Lesion Location Matters

The lateral portion of the femoral head contributes heavily to the:

A lesion extending into this region experiences substantial mechanical loading.

Therefore:

generally has greater collapse risk than:

even when both are nominally the same ARCO stage.

ARCO 2021 Size/Location Classification

For advanced students, briefly include the 2021 ARCO early-stage classification described in the updated ARCO literature.

Type 1

Small lesion whose lateral necrotic margin remains medial to the femoral-head apex.

Type 2

Medium lesion with the lateral margin between the apex and lateral acetabular edge.

Type 3

Large lesion extending laterally beyond the lateral acetabular edge.

This classification reinforces:

The ARCO review recommends this approach as a useful unified early-stage size/location classification. (PubMed Central (PMC))

This classification is distinct from the 2019 stage I–IV system.

Modified Kerboul Angle

Mention as an established alternative method for quantifying lesion extent on MRI.

Concept:

Measure the necrotic arc on:

• mid-coronal MRI;
• mid-sagittal MRI;

then combine the angles.

Larger combined necrotic angles correlate with greater collapse risk. (PubMed Central (PMC))

No single classification system is universally mandatory.

The educational message is:

Natural History

Once the osteonecrotic lesion has formed, evidence suggests that its initial:

largely determines its subsequent structural risk.

Small lesions may remain stable.

Large, laterally located lesions are much more likely to progress toward collapse. (PubMed Central (PMC))

Important distinction:

The same necrotic segment can progress from:

to:

to:

Small Lesions

Some small lesions have low collapse risk and may not require operative treatment.

Therefore:

Management depends on:

• symptoms;
• lesion size;
• lesion location;
• stage;
• patient factors.

The ARCO review specifically cautions against unnecessary treatment of small lesions with favorable natural history. (PubMed Central (PMC))

Large Lesions

Large lesions, especially those extending laterally into the weight-bearing region, have substantially greater risk of structural progression.

Therefore:

A large ARCO-I/II lesion can be clinically more concerning than a very small lesion at the same stage.

Treatment Principles

Treatment Philosophy

Treatment should answer two questions:

and:

This creates two broad treatment pathways.

Pre-Collapse Disease

For appropriately selected:

disease, the therapeutic objective is:

Potential strategies include:

• observation in selected low-risk lesions;
• addressing modifiable risk factors;
• symptom management;
• selected joint-preserving surgery;
• core decompression;
• selected grafting/biologic augmentation procedures;
• selected osteotomy approaches.

Choice depends on lesion characteristics and patient factors.

The 2026 evidence review describes core decompression and other joint-preserving interventions as approaches used in pre-collapse disease, while emphasizing that no single intervention has demonstrated superiority across all subgroups. (PubMed Central (PMC))

Observation

Observation may be appropriate for selected:

particularly when asymptomatic.

Not every MRI-positive hip requires intervention.

Conversely:

Management must be risk-based.

Risk-Factor Modification

Where clinically appropriate:

• minimize avoidable glucocorticoid exposure in coordination with the treating specialist;
• address harmful alcohol exposure;
• optimize management of associated systemic disease;
• address relevant modifiable vascular/metabolic factors.

Important:

The underlying disease may require them.

Medication decisions belong with the relevant treating clinician.

Weight Bearing

Mechanical loading matters, but:

Activity/weight-bearing recommendations should be individualized according to:

• pain;
• stage;
• lesion;
• fracture/collapse risk;
• orthopedic plan.

Core Decompression

Core decompression is a joint-preserving procedure most often considered in:

The conceptual aim is to:

• reduce intraosseous pressure;
• create channels through necrotic bone;
• encourage vascular/biological repair.

The most important principle is:

Outcome is influenced by:

• lesion size;
• lesion location;
• disease stage;
• patient selection.

Core Decompression Is Not A Universal Answer

ARCO stage I or II does not automatically require core decompression.

Some small lesions may have favorable natural history without intervention.

Conversely, very large high-risk lesions may have poorer results despite decompression.

The ARCO review concluded that conventional core decompression has inconsistent outcomes and that effectiveness decreases in larger lesions. (PubMed Central (PMC))

Therefore:

Biologic Augmentation

Core decompression has been combined with approaches such as:

• bone-marrow aspirate concentrate;
• cellular therapy;
• grafting;
• other biologic strategies.

Evidence remains heterogeneous.

not:

The 2026 evidence review found no single intervention clearly superior across patient groups/stages. (PubMed Central (PMC))

Bone Grafting

Various vascularized and nonvascularized bone-grafting techniques have been used in selected joint-preservation strategies.

The theoretical goals include:

• removing/supporting necrotic bone;
• improving structural support;
• providing biological repair potential.

These are specialist procedures.

Osteotomy

Selected osteotomies attempt to:

and place more viable femoral-head surface under load.

These procedures require careful selection and substantial expertise.

They are not universal treatment for ONFH.

The ARCO literature describes them primarily as selected joint-preserving options. (PubMed Central (PMC))

Pharmacological Treatment

Many medications have been investigated, including:

• bisphosphonates;
• statins;
• anticoagulants;
• vasodilator approaches;
• antiplatelet/vascular strategies;
• other agents.

But:

The ARCO review concluded that pharmacological prevention/treatment had not been proven sufficiently effective for general recommendation. (PubMed Central (PMC))

The newer evidence synthesis similarly shows continuing uncertainty rather than one universally superior treatment. (PubMed Central (PMC))

Bisphosphonates

Bisphosphonates have been studied because suppression of bone resorption might theoretically reduce mechanical weakening during repair.

However evidence is inconsistent.

Therefore:

Available evidence does not support promising prevention of collapse.

Anticoagulation

Anticoagulation has been studied in selected patients, particularly where thrombophilic mechanisms may be relevant.

But:

This belongs to individualized specialist assessment.

Statins

Statins have been investigated, particularly around steroid-associated disease and lipid pathways.

Current evidence does not justify teaching:

Universal prophylactic statin treatment is not recommended.

After Subchondral Fracture

Once:

has developed, the mechanical situation changes fundamentally.

The femoral head has begun to fail.

Joint-preserving procedures generally become less predictable.

Therefore:

Arthroplasty

For advanced symptomatic disease with:

• substantial collapse;
• deformity;
• secondary osteoarthritis;

is the definitive reconstructive treatment for many patients.

Modern THA outcomes in ONFH have improved substantially with contemporary implants and bearing surfaces. (PubMed Central (PMC))

Do Not Oversimplify The Treatment Threshold

Avoid:

“Stage III always means THA.”

and:

“Stage II always means core decompression.”

Treatment depends on:

The 2026 ARCO evidence synthesis emphasizes individualized care because no single intervention has proved best across all subgroups. (PubMed Central (PMC))

Differential Diagnosis

Differential Diagnosis

Important differential diagnoses include:

• subchondral insufficiency fracture;
• transient osteoporosis/bone-marrow-edema syndrome;
• hip osteoarthritis;
• occult fracture;
• femoroacetabular impingement;
• inflammatory arthritis;
• septic arthritis;
• stress injury;
• referred pain.

because imaging can overlap.

ONFH Versus Subchondral Insufficiency Fracture

Bottom:

ONFH Versus Transient Osteoporosis / Bmes

Marrow edema itself does not equal osteonecrosis.

ONFH Versus Osteoarthritis

ARCO IV represents the point where ONFH has progressed to secondary osteoarthritis.

ONFH Versus Osteonecrosis Elsewhere

Osteonecrosis can affect other skeletal sites.

But this article owns:

• knee osteonecrosis;
• humeral-head osteonecrosis;
• jaw osteonecrosis;
• medication-related osteonecrosis of the jaw.

Those are distinct topics and would dilute search intent.

Master Pathophysiology Algorithm

Two possibilities:

Favorable structural course

especially with favorable lesion characteristics.

Progressive mechanical failure

Bottom:

Master Diagnostic Algorithm

Diagnostic structural ONFH changes?

Normal or nondiagnostic but suspicion persists?

Pre-collapse?

Assess collapse risk and joint-preserving strategy.

Subchondral fracture/collapse?

Assess structural failure and reconstructive options.

Bottom:

ACR supports MRI without contrast as the next study when radiographs are normal or suspicious in clinically suspected osteonecrosis. (ACSearch)

Master Treatment Algorithm

NO — ARCO I–II

Assess:

Lesion size

Lesion location

Symptoms

Patient factors

Small / favorable low-risk lesion

Clinically important higher-risk pre-collapse lesion

including selected core decompression ± specialist augmentation strategies.

YES — ARCO III–IV

Assess:

Amount of collapse

Symptoms

Age

Joint degeneration

Patient factors

Selected joint-preservation procedure in appropriate circumstances

or:

Bottom:

Most Important Prognostic Equation

Create a callout:

Not a literal mathematical equation.

It is a memory tool.

Students should understand:

Small + medial + intact

Generally more favorable.

Large + lateral + intact

Higher risk despite pre-collapse stage.

Subchondral fracture

Structural failure has already begun.

Worked Clinical Cases

Case 1 — Normal X-ray after steroids

A patient treated with systemic glucocorticoids develops persistent groin pain.

X-ray is normal.

Wrong conclusion

“No AVN.”

Correct next thought

Early ARCO-I disease can have a normal radiograph.

Case 2 — ARCO I

MRI shows a characteristic low-signal boundary around a necrotic segment.

Radiograph remains normal.

Stage

Key:

Case 3 — Asymptomatic other hip

Patient has symptomatic non-traumatic ONFH on the right.

MRI also demonstrates a small lesion on the asymptomatic left side.

Lesson

Management of the second hip depends on its lesion characteristics and risk.

Case 4 — ARCO II

Radiograph shows sclerosis and cystic change.

Femoral-head contour is preserved and no subchondral fracture is identified.

Stage

This is still:

Case 5 — Crescent sign

Radiograph demonstrates a crescent-shaped subchondral lucency.

Meaning

This is not merely another nonspecific sign of AVN.

It means:

Case 6 — IIIA versus IIIB

Two patients have subchondral fracture.

Patient A has 1.5-mm head depression.

Patient B has 3-mm depression.

Classification

Patient A:

Patient B:

because the revised ARCO dividing point is 2 mm. (PubMed Central (PMC))

Case 7 — ARCO IV

Patient has femoral-head collapse, joint-space narrowing and acetabular degenerative changes.

Stage

The process has progressed to:

Case 8 — Same stage, different prognosis

Two patients have ARCO-II ONFH.

Patient A has a small medial lesion.

Patient B has a large lesion extending into the lateral weight-bearing region.

Wrong conclusion

“They have the same prognosis because both are stage II.”

Correct principle

Patient B has substantially greater structural concern.

Case 9 — Trauma

Patient sustains a major femoral-neck injury and later develops ONFH.

Mechanism

This differs etiologically from steroid-associated disease even though the final femoral-head pathology is osteonecrosis.

Case 10 — Sickle-cell disease

Young adult with sickle-cell disease develops persistent hip pain.

Mechanism to remember

Pain should not be dismissed as a transient pain crisis when clinical features suggest structural hip disease.

Case 11 — Insufficiency fracture

Older patient without typical ONFH risk factors develops acute hip pain and a subchondral MRI abnormality.

Wrong action

Automatically label every subchondral low-signal band as ONFH.

Correct thought

Interpret morphology and clinical context.

Case 12 — “Can medicine restore the dead bone?”

Patient asks for medication guaranteed to reverse ONFH.

Answer

No pharmacological therapy has been established to universally reverse ONFH or reliably prevent collapse in all patients.

Treatment is based on:

Common Mistakes

Mistake 1

Osteonecrosis and osteoporosis are the same disease. Wrong.

Mistake 2

AVN means infection of bone. Wrong.

Mistake 3

Normal X-ray excludes early ONFH. Wrong.

Mistake 4

MRI is unnecessary when X-ray is normal. Wrong when meaningful suspicion persists.

Mistake 5

Every steroid-treated patient develops ONFH. Wrong.

Mistake 6

All non-traumatic ONFH is caused by steroids. Wrong.

Mistake 7

Alcohol is the only other major cause. Wrong.

Mistake 8

ONFH must be symptomatic. Wrong.

Mistake 9

Unilateral pain means disease is necessarily unilateral. Wrong.

Mistake 10

Bone-marrow edema alone diagnoses ONFH. Wrong.

Mistake 11

The double-line sign must be present in every patient. Wrong.

Mistake 12

The crescent sign is merely an early nonspecific sign. Wrong — it indicates subchondral fracture.

Mistake 13

All ARCO-II lesions have the same prognosis. Wrong.

Mistake 14

ARCO stage alone determines treatment. Wrong.

Mistake 15

Every small MRI lesion requires surgery. Wrong.

Mistake 16

Every pre-collapse lesion requires core decompression. Wrong.

Mistake 17

Core decompression works equally well after major collapse. Wrong.

Mistake 18

Bisphosphonates reliably prevent collapse in every patient. Wrong.

Mistake 19

Weight-bearing restriction alone cures ONFH. Wrong.

Mistake 20

Once necrosis occurs, arthroplasty is immediately inevitable. Wrong.

ONFH in One Minute

Important risk contexts:

Trauma

Steroids

Alcohol

Sickle cell

Systemic disease

Imaging:

but:

If suspicion remains:

ARCO:

I = X-ray normal, MRI abnormal

II = X-ray abnormal, no fracture/collapse

III = subchondral fracture ± collapse

IIIA ≤2 mm

IIIB >2 mm

IV = secondary OA

Then remember:

Also assess:

Treatment:

Pre-collapse

Advanced collapse/OA

Final:

Frequently Asked Questions

Key Take-Home Messages

Osteonecrosis of the femoral head begins with:

The key sequence is:

But:

This creates an important:

Early disease may have:

Therefore:

When suspicion remains:

The revised ARCO staging system teaches the structural progression:

But:

Always consider:

because these strongly influence collapse risk. (PubMed Central (PMC))

The therapeutic question is:

In selected pre-collapse disease:

Once major structural collapse and secondary OA develop:

No medication should be presented as a universal cure.

Final memory: