Avascular Necrosis of the Hip - Adult

Answer Card

What is avascular necrosis of the hip?

Avascular necrosis (AVN), also termed osteonecrosis, is the ischaemic death of bone tissue in the femoral head due to interruption of its blood supply, leading to progressive structural collapse, deformity, and secondary osteoarthritis if untreated. [1,2]

Who gets it?

Affects predominantly younger adults (age 30-50 years), with bilateral involvement in 40-80% of cases. Major risk factors include high-dose corticosteroid therapy (most common non-traumatic cause), alcohol excess, femoral neck fractures, hip dislocation, sickle cell disease, SLE, Gaucher disease, and organ transplantation. [3,4,5]

How does it present?

Insidious onset of groin pain (may radiate to buttock or knee), worse with weight-bearing and internal rotation. Early stages may be asymptomatic or have normal radiographs despite MRI changes. Progressive stages lead to mechanical pain, restricted range of motion, and limping. Night pain suggests advanced disease. [6,7]

How is it diagnosed?

MRI is the gold standard for early detection (sensitivity > 99%), showing subchondral marrow oedema and characteristic "double-line sign" on T2-weighted images. Plain radiographs may be normal initially, progressing to show sclerosis, crescent sign (subchondral fracture), and eventual collapse. Ficat-Arlet classification stages disease from 0 (normal X-ray, abnormal MRI) to IV (secondary osteoarthritis). [8,9,10]

What is the management?

Early disease (pre-collapse, Ficat I-II): Core decompression reduces intraosseous pressure and may halt progression in 60-80% if lesion less than 30% of femoral head. Bisphosphonates show promise in preventing collapse. Late disease (post-collapse, Ficat III-IV): Total hip arthroplasty is definitive treatment with excellent long-term outcomes. Younger patients (less than 40 years) may benefit from joint-preserving procedures (vascularized fibular grafting, osteotomy) to delay arthroplasty. [11,12,13]

What is the prognosis?

Untreated AVN progresses to femoral head collapse in 80-90% within 2-5 years. Factors predicting poor outcome: larger lesions (> 30% femoral head), lateral location, bilateral disease, and corticosteroid aetiology. Post-arthroplasty outcomes are comparable to standard hip replacement, though revision rates may be higher in younger patients. [14,15]

Clinical Overview

Avascular necrosis of the femoral head represents a devastating condition affecting predominantly young to middle-aged adults, resulting in progressive bone death, structural collapse, and premature osteoarthritis. Unlike degenerative arthritis of the elderly hip, AVN strikes patients during their most productive years, often bilaterally, creating significant functional disability and socioeconomic burden. [1,2]

The pathological hallmark is interruption of the precarious blood supply to the femoral head, which relies on a terminal vascular network with limited collateral circulation. The medial and lateral circumflex femoral arteries, branches of the profunda femoris, form an extracapsular arterial ring at the base of the femoral neck. Ascending cervical branches pierce the hip capsule and traverse the femoral neck to supply the femoral head, making them vulnerable to disruption by intracapsular fractures, dislocation, or intravascular occlusion. [16,17]

The condition exists on a spectrum from early, reversible marrow oedema to late-stage irreversible structural collapse and secondary arthritis. Early detection during the pre-collapse phase, when joint-preserving interventions may succeed, is critical but challenging because initial symptoms are often subtle and radiographs may remain normal for months. MRI has revolutionized early diagnosis, detecting disease at a stage when treatment can potentially alter the natural history. [8,9]

Management strategy hinges on disease stage at presentation. Pre-collapse disease (Ficat stages I-II) may respond to core decompression, pharmacotherapy, or bone grafting procedures, whereas post-collapse disease (Ficat stages III-IV) generally requires arthroplasty. The decision-making process must balance patient age, functional demands, extent of disease, and bilateral involvement against the known high progression rate if left untreated. [11,12]

Understanding the multifactorial aetiology, recognizing high-risk populations, employing appropriate imaging modalities, and implementing timely stage-appropriate intervention are essential for optimizing outcomes in this challenging condition.

Epidemiology

Incidence and Prevalence

AVN affects approximately 10,000-20,000 new patients annually in the United States, accounting for 10-12% of all hip replacements performed. The true incidence is likely underestimated due to asymptomatic early-stage disease and misdiagnosis. [3,4]

Peak incidence occurs in the third to fifth decades of life (age 30-50 years), with a male-to-female ratio of approximately 4:1, though this varies by underlying aetiology. The condition is rare in children except in specific conditions such as sickle cell disease or following high-dose corticosteroid therapy for malignancy. [18]

Bilateral Involvement

Bilateral hip involvement occurs in 40-80% of cases, though often asymmetric in severity and timing. Patients presenting with unilateral disease should undergo bilateral hip MRI screening, as contralateral disease may be asymptomatic initially but progress over time. The high rate of bilateral disease reflects the systemic nature of most non-traumatic aetiologies. [5,19]

Geographic and Ethnic Variation

Higher prevalence is reported in Asian populations, particularly in Japan and South Korea, attributed to increased alcohol consumption patterns and genetic factors influencing lipid metabolism and coagulation. Sickle cell disease-related AVN is more common in African and Afro-Caribbean populations. [20]

Pathophysiology

Vascular Anatomy of the Femoral Head

The blood supply to the adult femoral head is precarious and dependent on extraosseous vessels with limited collateral circulation. The primary arterial supply derives from:

Medial femoral circumflex artery (MFCA) - Provides 60-80% of femoral head blood supply via superior and inferior retinacular arteries that ascend along the posterosuperior and posteroinferior femoral neck
Lateral femoral circumflex artery (LFCA) - Contributes 20-30% via anterior retinacular branches
Artery of ligamentum teres - Branch of obturator or MFCA; minimal contribution in adults but may be more significant in children and in revascularization following AVN [16,17]

The retinacular vessels penetrate the hip capsule at its femoral neck attachment and course beneath the synovial reflection, making them vulnerable to:

Intracapsular fracture with haematoma and tamponade
Hip dislocation with vessel stretch or laceration
Elevated intracapsular pressure from effusion or haemarthrosis
Intravascular occlusion from thromboembolism or vasculitis [21]

Mechanisms of Bone Death

Multiple pathophysiological mechanisms have been proposed, varying by aetiology:

Direct Vascular Injury (Traumatic AVN)

Femoral neck fractures, particularly displaced intracapsular fractures, directly disrupt the retinacular vessels. Hip dislocations, especially posterior dislocations, can stretch or tear the MFCA. The risk of post-traumatic AVN correlates with fracture displacement, delay to reduction, and adequacy of fracture fixation. [22]

Intravascular Occlusion (Non-traumatic AVN)

Multiple mechanisms contribute to vessel occlusion:

Thromboembolism: Hypercoagulable states (protein C/S deficiency, antiphospholipid syndrome, Factor V Leiden), sickle cell disease (vaso-occlusion from sickled erythrocytes), fat embolism from marrow (alcohol, corticosteroids, pancreatitis) [23,24]
Vessel wall injury: Vasculitis (SLE, inflammatory bowel disease), radiation, Caisson disease (nitrogen bubble formation in vessels) [25]
Endothelial dysfunction: Corticosteroids cause endothelial apoptosis, increased adipocyte size in marrow with venous stasis, and altered lipid metabolism promoting intravascular coagulation [26]

Extravascular Compression

Elevated intraosseous pressure: Corticosteroids and alcohol increase marrow adipocyte size and number, elevating compartmental pressure within the rigid confines of the femoral head, causing venous stasis, thrombosis, and arterial insufficiency [27]
Bone marrow infiltration: Gaucher disease (glucocerebroside-laden macrophages), haematological malignancies [28]

Osteocyte Toxicity

Direct toxic effects on osteocytes and bone-forming cells:

Corticosteroids: Inhibit osteoblast differentiation, promote osteoblast and osteocyte apoptosis, decrease VEGF production [29]
Alcohol: Direct toxic effect on osteocytes, impaired bone remodelling, altered lipid metabolism [30]
Bisphosphonates (paradoxically): While preventive in some contexts, high-dose or prolonged therapy can impair remodelling and is implicated in atypical osteonecrosis of the jaw [31]

Progression and Structural Failure

Once initiated, AVN follows a progressive natural history:

Ischaemia and cell death (0-48 hours): Bone marrow and haematopoietic elements die first, followed by osteocytes. Bone matrix initially remains intact.
Inflammatory response (days to weeks): Marrow oedema, hyperaemia at the interface between necrotic and viable bone.
Repair attempt (weeks to months): Revascularization from the periphery, osteoclastic resorption of necrotic bone, osteoblastic new bone formation. This "creeping substitution" weakens the structural integrity before new bone is laid down, creating mechanical vulnerability. [32]
Subchondral fracture (months): Repeated loading of mechanically weakened bone causes microfractures in the subchondral plate, visible as the "crescent sign" on radiographs. [33]
Femoral head collapse (months to years): Progressive deformity of the spherical femoral head creates incongruity, point loading, and accelerated cartilage wear.
Secondary osteoarthritis (years): Joint space narrowing, acetabular involvement, osteophyte formation, and end-stage arthritis. [34]

The rate of progression depends on lesion size, location, and ongoing aetiological factors. Small, medial lesions may remain asymptomatic indefinitely, whereas large, lateral lesions (weight-bearing area) typically progress rapidly to collapse. [35]

Aetiology and Risk Factors

Traumatic Causes (20-30%)

Femoral Neck Fractures

Displaced intracapsular fractures: 15-35% AVN risk
Undisplaced fractures: 5-10% AVN risk
Risk increases with delay to fixation > 12-24 hours, fracture comminution, and inadequate reduction [22]

Hip Dislocation

Posterior dislocation: 10-25% AVN risk depending on time to reduction
Anterior dislocation: Lower risk (5-10%)
Fracture-dislocation further increases risk [36]

Surgical Iatrogenic

Intramedullary femoral nailing (3-5% risk from retrograde vessels)
Proximal femoral osteotomies
Excessive screw penetration into femoral head during acetabular fracture fixation [37]

Non-Traumatic Causes (70-80%)

Corticosteroid Therapy (35-40% of non-traumatic cases)

Most common non-traumatic cause. Risk factors:

Dose-dependent: Daily dose > 20mg prednisone equivalent
Duration: Risk increases after 3-6 months of therapy
Cumulative dose: Total dose > 2g prednisone equivalent
Route: Oral > intravenous > intra-articular (though all routes implicated)
Underlying disease: SLE, organ transplantation, inflammatory bowel disease, asthma, nephrotic syndrome [26,38]

Mechanism: Multifactorial - fat emboli from enlarged adipocytes, increased marrow pressure, endothelial dysfunction, osteocyte apoptosis, impaired angiogenesis.

Alcohol Abuse (20-30% of non-traumatic cases)

Chronic heavy consumption (> 400mL/week or > 3 standard drinks/day)
Dose-dependent relationship
Often coexists with corticosteroid use (relative risk multiplicative)
Mechanism: Direct osteocyte toxicity, fat emboli, altered lipid metabolism, hypercoagulability, impaired bone remodelling [30,39]

Haematological Disorders

Sickle Cell Disease and Trait

10-20% lifetime risk in sickle cell disease (HbSS)
3-5% risk in sickle cell trait (HbAS)
Vaso-occlusion from sickled erythrocytes, bone marrow infarction, chronic anaemia with marrow hyperplasia
Often presents at younger age (second to third decade) [40]

Gaucher Disease

Type I (non-neuronopathic): 30-50% lifetime AVN risk
Glucocerebroside accumulation in marrow macrophages causes infiltration, elevated intraosseous pressure, vessel compression
May be first presentation of disease [28]

Myeloproliferative Disorders

Polycythaemia vera, essential thrombocythaemia
Hyperviscosity and hypercoagulable state [41]

Systemic Lupus Erythematosus (SLE)

5-40% of SLE patients develop AVN
Multifactorial: Corticosteroid therapy (primary driver), vasculitis, antiphospholipid antibodies, Raynaud phenomenon
Often bilateral and multifocal (knees, shoulders) [42]

Thrombophilia and Coagulation Disorders

Protein C or S deficiency
Antithrombin III deficiency
Factor V Leiden mutation
Prothrombin G20210A mutation
Antiphospholipid syndrome
Hyperhomocysteinaemia [23,43]

Metabolic and Endocrine

Chronic renal failure: Especially with haemodialysis, secondary hyperparathyroidism
Diabetes mellitus: Weak association, likely multifactorial
Hyperlipidaemia: Controversial independent risk factor; may potentiate steroid-related risk
Pancreatitis: Fat emboli from pancreatic lipase release [44]

Dysbaric Osteonecrosis (Caisson Disease)

Decompression sickness in divers, compressed air workers, aviators
Nitrogen bubble formation in blood and marrow causes vessel occlusion
Often multifocal (shoulders, knees) and bilateral
Preventable with proper decompression protocols [25,45]

Radiation Therapy

High-dose pelvic radiation (> 30-50 Gy)
Direct endothelial and osteocyte damage, vessel obliteration
Latency period of months to years [46]

Idiopathic (20-40% of cases)

Despite thorough investigation, many cases have no identifiable cause. Genetic predisposition (polymorphisms in genes regulating coagulation, lipid metabolism, angiogenesis) may play a role and is an area of active research. [47]

Multifactorial Risk

Multiple risk factors often coexist and have synergistic effects. A patient with SLE on high-dose corticosteroids who consumes alcohol has exponentially higher risk than any single factor alone. Screening high-risk asymptomatic populations with MRI is controversial but may be considered in selected cases (e.g., new high-dose steroid therapy in SLE, post-transplant patients). [48]

Clinical Presentation

Symptom Onset and Characteristics

Early Disease (Pre-collapse, Ficat I-II)

The insidious nature of early AVN often delays diagnosis. Patients may be asymptomatic despite MRI evidence of disease, or present with:

Groin pain: Dull, aching, worse with weight-bearing (walking, stairs, rising from seated position)
Referred pain: Buttock (L5-S1 distribution), lateral hip, anterior thigh, or knee (can mimic knee pathology)
Pain pattern: Mechanical pain initially (activity-related, relieved by rest); progresses to pain at rest and night pain as disease advances
Onset: Gradual over weeks to months; rarely acute (may suggest subchondral fracture event)
Functional limitation: Difficulty with prolonged walking, impact activities, stair climbing [6,7]

Late Disease (Post-collapse, Ficat III-IV)

Progressive symptoms reflect structural failure:

Constant pain: Mechanical pain from joint incongruity, inflammatory pain from synovitis
Night pain: Suggests advanced collapse or secondary arthritis
Stiffness: Particularly after rest, reduced range of motion
Limping: Antalgic gait, Trendelenburg gait if abductor weakness develops
Functional disability: Difficulty with shoe/sock donning, nail cutting, sexual activity, prolonged sitting [49]

Physical Examination

Gait

Antalgic gait: Shortened stance phase on affected side to minimize loading
Trendelenburg gait: Pelvic drop on contralateral side during stance if abductor insufficiency (late finding)

Range of Motion

Early disease: May be normal or subtle restriction in internal rotation and abduction
Provocation tests: Pain with passive internal rotation in flexion (most sensitive early finding); FABER test (Flexion-Abduction-External Rotation) reproduces groin pain
Late disease: Global restriction of all movements, particularly internal rotation and flexion; fixed flexion deformity may develop [50]

Leg Length

True leg length discrepancy rare unless severe collapse with femoral head resorption
Apparent shortening if fixed adduction or flexion deformity

Special Tests

Log roll test: Gentle internal-external rotation of hip in extension; pain suggests intra-articular pathology
Stinchfield test: Resisted straight leg raise reproduces hip pain (differentiates from lumbar spine)
Trendelenburg test: Pelvic drop when standing on affected leg (abductor weakness, late finding)

Neurovascular Examination

Typically normal; exclude lumbar radiculopathy, peripheral vascular disease

Bilateral Assessment

Always examine both hips given 40-80% bilateral involvement

Red Flag Symptoms

Groin pain with normal radiographs: High index of suspicion for early AVN; proceed to MRI
Young patient with hip pain and risk factors: Corticosteroids, alcohol, SLE, sickle cell disease
Acute worsening of chronic groin pain: May indicate subchondral fracture (crescent sign)
Bilateral hip pain: Suggests systemic aetiology (steroids, alcohol, coagulopathy) [51]

Differential Diagnosis

Groin pain in a young to middle-aged adult has a broad differential:

Intra-articular Hip Pathology

Acetabular labral tear: Catching/clicking, C-sign (cupping hand over lateral hip), positive FABER and FADIR tests, MR arthrography diagnostic
Femoroacetabular impingement (FAI): Cam (femoral head-neck offset loss) or pincer (acetabular overcoverage) morphology, anterior groin pain with flexion/internal rotation
Osteoarthritis: Older age, gradual onset, radiographic joint space narrowing
Inflammatory arthritis: Rheumatoid arthritis, seronegative spondyloarthropathies; systemic features, raised inflammatory markers
Septic arthritis: Acute onset, fever, systemic upset, elevated WCC/CRP, joint aspiration diagnostic
Transient osteoporosis of hip (regional migratory osteoporosis): Self-limiting, often in third trimester pregnancy or middle-aged men, MRI shows diffuse marrow oedema (vs. focal in AVN), resolves spontaneously in 6-12 months [52]

Peri-articular Pathology

Trochanteric bursitis: Lateral hip pain, tenderness over greater trochanter
Iliopsoas bursitis/tendinopathy: Anterior groin pain, worse with hip flexion
Athletic pubalgia (sports hernia): Groin pain in athletes, worse with sit-ups/twisting
Adductor tendinopathy: Medial groin pain, worse with resisted adduction

Bone Pathology

Stress fracture of femoral neck: Insidious groin pain in runners/military recruits; radiographs may be normal initially, MRI shows fracture line
Atypical femoral fracture: Long-term bisphosphonate use, lateral femoral cortex thickening, prodromal thigh pain
Bone tumours: Primary (osteoid osteoma, chondrosarcoma) or metastatic; night pain, constitutional symptoms

Referred Pain

Lumbar spine pathology: L2-L4 radiculopathy can mimic hip pain; check for lumbar spine signs, dermatomal distribution
Sacroiliac joint dysfunction: Posterior pelvic pain, positive sacroiliac provocation tests
Intra-abdominal pathology: Inguinal/femoral hernia, ovarian pathology, appendicitis (rarely), renal calculi

Key Discriminators

MRI is essential to differentiate AVN from other causes of hip pain in young adults, particularly when radiographs are normal. The characteristic MRI appearance (band-like signal change, double-line sign) distinguishes AVN from transient osteoporosis (diffuse oedema) and stress fracture (fracture line). [53]

Investigations

Imaging

Plain Radiographs

Initial Investigation

AP pelvis and lateral hip: First-line imaging; bilateral comparison essential
Sensitivity/specificity: Low sensitivity (30-50%) in early disease; specificity increases as disease progresses
Early findings (may be normal for months despite MRI changes):
- Subtle sclerosis in femoral head
- Osteopenia (differential density between necrotic and viable bone)
Intermediate findings:
- "Crescent sign: Subchondral lucency representing separation of necrotic segment (pathognomonic but indicates advanced pre-collapse disease)"
- "Sclerosis: Reactive bone formation at interface between necrotic and viable bone"
- Cyst formation
Late findings:
- Femoral head flattening and collapse
- Loss of sphericity
- Joint space narrowing
- Acetabular changes (secondary OA)
- Osteophyte formation [8,54]

Magnetic Resonance Imaging (MRI)

Gold Standard for Diagnosis

Sensitivity: > 99% for detecting AVN, including preclinical disease
Specificity: 95-99%
Protocol: T1-weighted, T2-weighted, and STIR (Short Tau Inversion Recovery) sequences; bilateral hip imaging mandatory
Characteristic findings:
- Band-like serpentine low signal on T1 and T2 at interface between necrotic and viable bone
- "Double-line sign on T2: Inner hyperintense line (granulation tissue) and outer hypointense line (sclerotic bone) - highly specific (90-100%) [9,55]"
- "Bone marrow oedema: Diffuse high signal on STIR/T2 in surrounding viable bone (reactive oedema)"
- "Geographic distribution: Typically anterosuperior femoral head (weight-bearing zone)"

Advantages:

Detects disease 3-6 months before radiographic changes
Assesses extent and location of necrosis (treatment planning)
Identifies bilateral disease
Monitors disease progression

Limitations:

Cost, availability
Contraindications (pacemakers, metallic implants)
Cannot be performed in claustrophobic or uncooperative patients

Computed Tomography (CT)

Role: Limited; less sensitive than MRI but more sensitive than radiographs
Indications: When MRI contraindicated or unavailable; pre-operative planning for osteotomy or arthroplasty
Findings: Sclerosis, crescent sign, collapse more visible than on radiographs; 3D reconstruction for surgical planning [56]

Bone Scintigraphy (Technetium-99m)

Historical importance: Previously used for early detection; now superseded by MRI
Findings: "Cold-on-cold" pattern (photopenic area within photopenic femoral head) in early disease; "hot-on-cold" in later stages (peripheral hyperaemia surrounding cold necrotic core)
Sensitivity: 70-85% (inferior to MRI)
Specificity: Lower than MRI; non-specific uptake patterns
Current role: Extremely limited; occasionally used if MRI unavailable [57]

Laboratory Tests

No Specific Diagnostic Tests for AVN

Laboratory investigations aim to identify underlying aetiology and risk factors:

Baseline Haematology and Biochemistry

Full blood count: Anaemia (sickle cell, Gaucher), polycythaemia
ESR/CRP: Usually normal in AVN; elevated suggests infection or inflammatory arthritis
Renal function: Chronic kidney disease
Liver function: Alcohol-related disease
Lipid profile: Hyperlipidaemia (controversial risk factor)
Glucose: Diabetes mellitus

Haematological Screen (if non-traumatic AVN without obvious cause)

Haemoglobin electrophoresis: Sickle cell disease/trait
Protein C, protein S, antithrombin III levels
Factor V Leiden mutation
Prothrombin G20210A mutation
Anticardiolipin antibodies, lupus anticoagulant, anti-β2 glycoprotein I (antiphospholipid syndrome)
Homocysteine level [23,43]

Autoimmune Screen (if clinical suspicion)

ANA, anti-dsDNA: SLE
Rheumatoid factor, anti-CCP: Rheumatoid arthritis
HLA-B27: Seronegative spondyloarthropathies

Metabolic Screen

Lipid panel
Gaucher enzyme assay (glucocerebrosidase) if appropriate clinical context [28]

Endocrine

Cortisol, dexamethasone suppression test: Cushing syndrome (rare)

Joint Aspiration

Indication: If septic arthritis or inflammatory arthritis suspected
Findings in AVN: Clear, yellow synovial fluid; cell count less than 2000/μL (non-inflammatory); negative culture
Not routinely performed in typical AVN presentation

Classification Systems

Ficat-Arlet Classification (Radiographic Staging)

The most widely used classification, based on plain radiographs and clinical findings:

Stage	Radiographic Findings	MRI Findings	Symptoms	Treatment Implications
0	Normal	Abnormal (marrow oedema, early necrosis)	Asymptomatic or minimal pain	Joint-preserving surgery may succeed; high success rate for core decompression
I	Normal or subtle osteopenia	Band-like signal change, double-line sign	Pain with activity	Joint-preserving preferred; core decompression ± bone grafting
II	Sclerosis, cysts; no collapse	Necrotic segment well-defined	Progressive pain	Joint-preserving may succeed if lesion less than 30% femoral head; consider vascularized graft
III	Crescent sign or early collapse	Subchondral fracture, collapse	Constant pain, limited ROM	Joint-preserving poor outcomes; consider arthroplasty in older patients; complex reconstruction (osteotomy, graft) in young
IV	Femoral head collapse, joint space narrowing, acetabular changes	Secondary OA	Severe pain, marked functional limitation	Total hip arthroplasty

Limitations: Radiograph-based staging misses early disease; progression not always linear; does not account for lesion size or location. [8,58]

Steinberg (University of Pennsylvania) Classification

Refinement of Ficat system incorporating lesion size:

Stage 0: Normal radiographs and MRI
Stage I: Normal radiographs, abnormal MRI
- "IA: less than 15% femoral head involved"
- "IB: 15-30%"
- "IC: > 30%"
Stage II: Sclerosis/cysts on radiographs, no collapse
- "IIA, IIB, IIC: Same size subdivisions"
Stage III: Crescent sign, subchondral collapse
- "IIIA: less than 15% depression"
- "IIIB: 15-30%"
- "IIIC: > 30%"
Stage IV: Femoral head flattening
- IVA, IVB, IVC
Stage V: Joint space narrowing
Stage VI: Advanced degenerative changes [59]

Prognostic Value: Lesion size > 30% femoral head (stage C) has high progression risk; lateral lesion location (weight-bearing) worse than medial.

ARCO (Association Research Circulation Osseous) Classification

International classification incorporating imaging, location, and extent:

Stage 0: Risk factors present, no imaging changes
Stage I: MRI/bone scan positive, X-ray normal
Stage II: X-ray shows sclerosis/cysts, no collapse
Stage III: Subchondral collapse (crescent sign), femoral head intact
Stage IV: Femoral head collapse, acetabular involvement

Substages: A, B, C based on location (medial, central, lateral) and extent (less than 15%, 15-30%, > 30%). [60]

Clinical Utility

Ficat I-II: Pre-collapse disease; joint preservation feasible
Ficat III-IV: Post-collapse; arthroplasty usually required
Lesion size > 30% and lateral location: Poor prognosis regardless of stage
Bilateral staging: Each hip staged independently; treatment often staged temporally

Management

Treatment strategy depends on disease stage, lesion size and location, patient age and functional demands, and bilateral involvement. The goals are to relieve pain, preserve the native joint when feasible, and delay or avoid arthroplasty, particularly in younger patients.

Conservative Management

Observation

Indication: Very small lesions (less than 15% femoral head), medial location (non-weight-bearing), asymptomatic incidental finding
Protocol: Serial MRI every 6-12 months to monitor progression; symptom surveillance
Limitation: 80-90% of AVN progresses to collapse without intervention; observation rarely appropriate as definitive strategy [14,15]

Protected Weight-Bearing

Rationale: Reduce mechanical stress on weakened subchondral bone to prevent collapse
Protocol: Non-weight-bearing or partial weight-bearing with crutches for 6-12 weeks
Evidence: Historical approach with poor outcomes; prolonged immobilization causes muscle atrophy, stiffness; does not address underlying pathophysiology; not recommended as sole therapy [61]

Pharmacotherapy

Bisphosphonates

Mechanism: Inhibit osteoclastic bone resorption during "creeping substitution" phase, potentially reducing mechanical weakening
Evidence: Multiple RCTs show reduced collapse rates in early AVN (Ficat I-II)
- "Alendronate 70mg weekly for 12-24 months: 20-40% reduction in progression vs. placebo in meta-analyses [62,63]"
- Most effective in small-medium lesions (less than 30% femoral head)
Limitation: Effect modest; does not reverse necrosis; not a substitute for surgical intervention in high-risk lesions
Current role: Adjunct to core decompression or in patients unfit for surgery

Anticoagulation

Indication: Thrombophilic disorders (protein C/S deficiency, antiphospholipid syndrome)
Evidence: Case series suggest benefit in preventing progression and contralateral involvement; no RCTs
Protocol: Therapeutic anticoagulation with warfarin or DOAC; duration unclear (often long-term) [64]

Statins

Rationale: Lipid-lowering, endothelial protection, anti-inflammatory effects
Evidence: Observational studies suggest reduced AVN incidence in statin users; no RCTs for treatment of established AVN
Current role: Investigational; may be considered in hyperlipidaemia [65]

Iloprost (Prostacyclin Analogue)

Mechanism: Vasodilator, antiplatelet effects
Evidence: Small European studies show pain reduction and reduced progression in early AVN; not widely available
Current role: Not standard in UK/US practice [66]

Risk Factor Modification

Corticosteroid minimization: Lowest effective dose, shortest duration, alternate-day regimens if feasible
Alcohol cessation: Mandatory; continued use worsens prognosis
Management of underlying disease: Optimal control of SLE, sickle cell disease, coagulopathy

Surgical Management

Joint-Preserving Procedures (Pre-Collapse Disease, Ficat I-II)

Core Decompression

Most common joint-preserving procedure for early AVN

Rationale: Reduce elevated intraosseous pressure, promote revascularization, provide stimulus for bone healing
Technique:
- Percutaneous or mini-open approach
- Single or multiple trephine cores (8-10mm diameter) drilled from lateral femoral cortex through femoral neck into necrotic area
- Fluoroscopic guidance to avoid subchondral bone violation
- May be combined with bone marrow aspirate concentrate (BMAC) injection [67]
Outcomes:
- "Success rate (avoidance of collapse/arthroplasty at 2-5 years):"
  - Small lesions (less than 15%): 80-90%
  - Medium lesions (15-30%): 60-70%
  - Large lesions (> 30%): 30-50%
- "Predictors of failure: Lesion size > 30%, lateral location, Ficat stage IIB/C, collapsed crescent sign"
- "Meta-analyses: Moderate quality evidence supports core decompression vs. observation in early disease; benefit over non-operative management most robust in Ficat I-IIA [11,68]"
Complications: Subtrochanteric fracture (1-3%, risk reduced with smaller/multiple cores vs. single large core), femoral neck fracture (rare), infection (less than 1%)

Bone Grafting Procedures

Vascularized Fibular Graft

Indication: Younger patients (less than 40 years), larger lesions (> 30%), failed core decompression, pre-collapse or early collapse (Ficat IIA-IIIA)
Technique:
- Harvest vascularized fibular segment (8-12cm) with peroneal artery pedicle
- Core decompression of femoral head with larger diameter core (> 10mm)
- Insert vascularized fibular graft through femoral neck into necrotic area
- Microvascular anastomosis of peroneal vessels to lateral femoral circumflex artery/vein
- Provides structural support and revascularization [69]
Outcomes:
- "Success rate (5-10 year): 60-80% in Ficat II, 40-60% in Ficat III"
- Better than non-vascularized graft in comparative studies
- Technically demanding; requires microsurgical expertise
Complications: Donor site morbidity (ankle instability, foot drop from peroneal nerve injury, chronic pain), graft fracture, vascular thrombosis, prolonged rehabilitation

Non-vascularized Bone Grafting

Techniques: Autograft (iliac crest) or allograft (femoral head from THR) packed into core decompression tract
Outcomes: Inferior to vascularized graft in most studies; limited role
Advantage: Simpler procedure, no microvascular anastomosis [70]

Osteotomy

Transtrochanteric Rotational Osteotomy

Rationale: Rotate necrotic segment away from weight-bearing zone, position viable bone under acetabular dome
Indication: Younger patients, medial or anterior necrotic lesion with viable lateral/posterior bone, pre-collapse or early collapse
Technique: Complex 3D rotational osteotomy of proximal femur; requires precise pre-operative planning with CT/MRI
Outcomes:
- "Success rate: 60-75% at 10 years in selected cases"
- High technical demand; results dependent on precise execution
- More popular in Japan; less commonly performed in West [71]
Complications: Non-union, malunion, limb length discrepancy, conversion to THR technically challenging

Tantalum Rod Implantation

Technique: Porous tantalum rod inserted via core decompression tract to provide structural support and scaffold for bone ingrowth
Evidence: Limited; some studies show benefit in small-medium lesions; no clear advantage over standard core decompression
Current role: Not widely adopted; investigational [72]

Stem Cell Therapy (Bone Marrow Aspirate Concentrate)

Rationale: Augment healing by delivering mesenchymal stem cells, growth factors into necrotic area
Technique: Bone marrow aspiration from iliac crest, concentration, injection into femoral head via core decompression tract
Evidence: Multiple small RCTs suggest improved outcomes when combined with core decompression vs. core decompression alone; meta-analyses show modest benefit
Current role: Adjunct to core decompression; not standalone therapy; optimal cell dose, processing unclear [73,74]

Joint Replacement (Post-Collapse Disease, Ficat III-IV)

Total Hip Arthroplasty (THA)

Definitive treatment for late-stage AVN with femoral head collapse

Indication: Ficat III-IV, failed joint-preserving surgery, severe pain/functional limitation, age > 40-50 years (relative)
Outcomes:
- Excellent pain relief and functional improvement in > 90%
- "Survivorship (implant retention): 90-95% at 10 years, 80-85% at 20 years"
- Comparable to THA for osteoarthritis in short-medium term
- Higher revision risk in younger patients (less than 50 years), particularly if bilateral disease, corticosteroid aetiology, or excessive activity level [75,76]
Technical Considerations:
- Acetabular bone stock usually preserved (vs. dysplasia or Perthes sequelae)
- Femoral canal may be narrow (younger patients); templating critical
- "Implant selection:"
  - Younger patients: Uncemented fixation (cementless acetabular cup, uncemented femoral stem)
  - Large femoral head (36-40mm) to reduce dislocation risk, improve range of motion
  - Bearing surface: Ceramic-on-ceramic or ceramic-on-polyethylene for younger patients (lower wear)
- "Bilateral disease: Stage procedures 3-6 months apart to allow rehabilitation; simultaneous bilateral THA rarely indicated [77]"
Complications:
- Dislocation (1-3%)
- Infection (0.5-1%)
- Aseptic loosening (leading cause of long-term failure)
- Periprosthetic fracture
- Leg length discrepancy
- Osteolysis from polyethylene wear (reduced with modern bearings)

Hip Resurfacing Arthroplasty

Rationale: Bone-conserving alternative to THA; metal-on-metal bearing resurfaces femoral head and acetabulum
Indication: Young (less than 60 years), active males with good bone quality, large femoral head size
Contraindications: Women of childbearing age (metal ion concerns), renal impairment, small femoral head, cystic changes (increased fracture risk)
Outcomes:
- Good short-medium term results in selected patients
- "Concerns: Metal ion release (cobalt/chromium), pseudotumor formation, femoral neck fracture (5-10% at 5 years)"
- Declining popularity due to metal-on-metal concerns; many surgeons prefer uncemented THA with large head [78,79]

Hemiarthroplasty

Role: Very limited in AVN; rarely indicated
Potential indication: Extremely elderly, low-demand patient with isolated femoral head involvement and intact acetabulum (unusual scenario)
Limitation: Acetabular cartilage wear leads to groin pain; not suitable for active patients

Algorithm for Management

Ficat Stage 0-I (Normal X-ray, Abnormal MRI)

Lesion less than 15% medial: Consider observation vs. core decompression + bisphosphonates
Lesion 15-30% or any lateral: Core decompression ± BMAC ± bisphosphonates
Lesion > 30%: Core decompression + vascularized fibular graft (young) vs. THA (older)

Ficat Stage II (Sclerosis, No Collapse)

Lesion less than 30%: Core decompression ± bone grafting ± bisphosphonates
Lesion > 30%: Vascularized fibular graft (young, high demand) vs. THA (older, lower demand)
Consider osteotomy in select young patients with favourable lesion location

Ficat Stage III (Crescent Sign, Collapse)

Age less than 40, high demand: Vascularized fibular graft or complex reconstruction (osteotomy) vs. THA
Age > 40 or lower demand: THA

Ficat Stage IV (Secondary OA)

THA (definitive treatment)

Bilateral Disease

Stage more symptomatic hip first
Consider prophylactic intervention on asymptomatic contralateral hip if high-risk lesion (controversial)
Stage arthroplasties 3-6 months apart [12,80]

Prognosis and Natural History

Untreated Disease

AVN is a progressive condition with high rates of femoral head collapse and secondary arthritis without intervention:

Progression to collapse: 80-90% within 2-5 years in Ficat I-II lesions
Time to collapse: Median 1-3 years; influenced by lesion size, location, aetiology
Bilateral progression: 40-80% develop contralateral hip involvement, often within 1-2 years of index diagnosis [14,15]

Prognostic Factors

Poor Prognosis (High Collapse Risk)

Lesion size > 30% of femoral head
Lateral (weight-bearing) location
Advanced Ficat stage (IIC, III)
Corticosteroid aetiology (vs. traumatic or idiopathic)
Bilateral involvement
Younger age at onset (longer disease exposure)
Continued risk factor exposure (ongoing steroids, alcohol) [35,81]

Better Prognosis

Small lesion (less than 15%)
Medial (non-weight-bearing) location
Early detection (Ficat 0-I)
Single well-defined necrotic area (vs. multifocal)
Traumatic aetiology (if revascularization occurs)
Risk factor cessation (alcohol abstinence, steroid discontinuation)

Outcomes by Treatment

Core Decompression

Small lesions: 80-90% success (no collapse/THA at 5 years)
Medium lesions: 60-70% success
Large lesions: 30-50% success
Failures typically occur within 2-3 years post-procedure [68]

Vascularized Fibular Graft

5-10 year joint preservation: 60-80% in pre-collapse disease
Higher success in younger, more active patients
Technically demanding; outcomes surgeon-dependent [69]

Total Hip Arthroplasty

10-year survivorship: 90-95%
20-year survivorship: 80-85%
Pain relief and functional improvement excellent in > 90%
Revision risk higher in younger patients; expect 1-2 revisions over lifetime if THA performed less than 50 years [75,76]

Quality of Life

Untreated late-stage AVN: Severe functional limitation, inability to work, depression, chronic pain
Post-THA: Significant QOL improvement; return to low-impact activities (walking, swimming, cycling); high-impact sports generally discouraged
Bilateral disease: Cumulative disability; both hips often require eventual arthroplasty with prolonged rehabilitation [82]

Long-Term Surveillance

Post-core decompression: Clinical + radiographic follow-up at 3, 6, 12 months, then annually for 5 years; MRI at 6-12 months to assess revascularization
Contralateral hip: Bilateral MRI at diagnosis; repeat imaging if symptoms develop; controversial role for prophylactic surveillance MRI
Post-THA: Standard arthroplasty follow-up; radiographs at 1, 5, 10 years to monitor for loosening/osteolysis [83]

Prevention

Primary Prevention

Corticosteroid Use

Lowest effective dose for shortest duration
Alternate-day regimens where feasible (reduces cumulative dose)
Consider steroid-sparing agents (methotrexate, azathioprine, biologics) in SLE, inflammatory bowel disease
Prophylactic strategies (controversial; no RCT evidence):
- Lipid-lowering therapy (statins)
- Anticoagulation in thrombophilic patients
- Bisphosphonates (some retrospective data suggest reduced AVN incidence in renal transplant patients on prophylactic alendronate) [84,85]

Alcohol

Public health messaging on safe limits
Alcohol cessation programs for at-risk individuals

Sickle Cell Disease

Hydroxyurea therapy reduces vaso-occlusive crises, may reduce AVN risk (limited evidence)
Chronic transfusion programs in severe disease
Prompt treatment of vaso-occlusive crises [86]

Diving and Hyperbaric Exposure

Strict adherence to decompression protocols
Pre-dive medical screening
Avoid rapid ascent

Trauma

Urgent reduction of hip dislocation (less than 6 hours preferred)
Anatomic reduction and stable fixation of femoral neck fractures
Minimize time to surgery (less than 12-24 hours) [22,36]

Secondary Prevention

High-Risk Patient Monitoring

Screening MRI in asymptomatic high-risk patients (e.g., high-dose steroids for SLE, renal transplant) is controversial; no consensus guidelines
Low threshold for MRI in high-risk patients with hip pain despite normal radiographs
Bilateral MRI if unilateral AVN diagnosed (detect subclinical contralateral disease)

Risk Factor Modification

Mandatory alcohol cessation
Minimization/discontinuation of corticosteroids where medically safe
Anticoagulation in thrombophilic disorders [87]

Special Populations

Pregnancy

AVN rare in pregnancy; transient osteoporosis of hip more common
Third trimester presents diagnostic challenge (weight gain, mechanical low back/hip pain common)
MRI safe in pregnancy (no gadolinium contrast needed for AVN diagnosis)
Management: Conservative in pregnancy; definitive surgical treatment post-partum [88]

Paediatric

AVN in children most often related to:
- Sickle cell disease
- High-dose corticosteroids (ALL, leukaemia treatment, transplant)
- Developmental dysplasia of hip (iatrogenic from treatment)
- Perthes disease (distinct entity; idiopathic AVN of femoral head in children age 4-10)
Management differs from adults; joint preservation paramount given decades of anticipated loading
Refer to specialist paediatric orthopaedic centre [89]

Bilateral Disease

40-80% of AVN patients have bilateral involvement
Often asymmetric in stage and symptoms
Staging surgical interventions:
- "If both require THA: Stage 3-6 months apart to allow rehabilitation"
- Simultaneous bilateral THA rarely indicated (high complication risk, prolonged anaesthesia, massive blood loss)
- May perform core decompression bilaterally in single setting if both early stage [90]

Key References and Evidence Base

Landmark Studies

Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am 1995;77:459-474. [Classic review of natural history and risk factors]
Zhao DW, Yu M, Hu K, et al. Prevalence of nontraumatic osteonecrosis of the femoral head and its associated risk factors in the Chinese population: results from a nationally representative survey. Chin Med J 2015;128:2843-2850. [Large epidemiological study]
Lieberman JR, Berry DJ, Mont MA, et al. Osteonecrosis of the hip: management in the 21st century. J Bone Joint Surg Am 2002;84:834-853. [Comprehensive management review]
Marker DR, Seyler TM, Ulrich SD, et al. Do modern techniques improve core decompression outcomes for hip osteonecrosis? Clin Orthop Relat Res 2008;466:1093-1103. [Systematic review of core decompression]
Lieberman JR, Conduah A, Urist MR. Treatment of osteonecrosis of the femoral head with core decompression and human bone morphogenetic protein. Clin Orthop Relat Res 2004;429:139-145. [Biologic augmentation]
Zalavras CG, Lieberman JR. Osteonecrosis of the femoral head: evaluation and treatment. J Am Acad Orthop Surg 2014;22:455-464. [Practical clinical review]
Yoon BH, Mont MA, Koo KH, et al. The 2019 Revised Version of Association Research Circulation Osseous Staging System of Osteonecrosis of the Femoral Head. J Arthroplasty 2020;35:933-940. [Updated ARCO classification]
Moya-Angeler J, Gianakos AL, Villa JC, et al. Current concepts on osteonecrosis of the femoral head. World J Orthop 2015;6:590-601. [Contemporary review]
Koo KH, Kim R. Quantifying the extent of osteonecrosis of the femoral head: a new method using MRI. J Bone Joint Surg Br 1995;77:875-880. [Quantitative MRI assessment]
Mitchell DG, Rao VM, Dalinka MK, et al. Femoral head avascular necrosis: correlation of MR imaging, radiographic staging, radionuclide imaging, and clinical findings. Radiology 1987;162:709-715. [Classic imaging correlation study]
Mont MA, Carbone JJ, Fairbank AC. Core decompression versus nonoperative management for osteonecrosis of the hip. Clin Orthop Relat Res 1996;324:169-178. [RCT of core decompression]
Mont MA, Ragland PS, Etienne G. Core decompression of the femoral head for osteonecrosis using percutaneous multiple small diameter drilling. Clin Orthop Relat Res 2004;429:131-138. [Technical refinement]
Lai KA, Shen WJ, Yang CY, et al. The use of alendronate to prevent early collapse of the femoral head in patients with nontraumatic osteonecrosis: a randomized clinical study. J Bone Joint Surg Am 2005;87:2155-2159. [Bisphosphonate RCT]
Hernigou P, Beaujean F. Treatment of osteonecrosis with autologous bone marrow grafting. Clin Orthop Relat Res 2002;405:14-23. [Stem cell therapy series]
Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg Br 1995;77:34-41. [Steinberg classification]
Trueta J, Harrison MH. The normal vascular anatomy of the femoral head in adult man. J Bone Joint Surg Br 1953;35:442-461. [Classic vascular anatomy]
Gautier E, Ganz K, Krügel N, et al. Anatomy of the medial femoral circumflex artery and its surgical implications. J Bone Joint Surg Br 2000;82:679-683. [Surgical anatomy]
Assouline-Dayan Y, Chang C, Greenspan A, et al. Pathogenesis and natural history of osteonecrosis. Semin Arthritis Rheum 2002;32:94-124. [Natural history review]
Cheng EY, Thongtrangan I, Laorr A, Saleh KJ. Spontaneous resolution of osteonecrosis of the femoral head. J Bone Joint Surg Am 2004;86:2594-2599. [Rare spontaneous resolution]
Zhao FC, Guo KJ, Li ZR. Osteonecrosis of the femoral head in SARS patients: seven years later. Eur J Orthop Surg Traumatol 2013;23:671-677. [SARS-related AVN follow-up]

Summary

Avascular necrosis of the hip is a challenging condition affecting predominantly younger adults, with corticosteroid therapy and alcohol excess being the leading non-traumatic causes. The precarious blood supply of the femoral head renders it vulnerable to ischaemic insult from traumatic disruption or intravascular/extravascular compromise. Early diagnosis with MRI before radiographic collapse is critical, as joint-preserving procedures (core decompression, vascularized fibular grafting) have highest success in pre-collapse disease. Post-collapse disease generally requires total hip arthroplasty with excellent pain relief but higher revision risk in young patients. Bilateral involvement is common, necessitating bilateral imaging at diagnosis. Understanding risk factors, employing appropriate imaging, staging disease accurately, and tailoring treatment to patient age, lesion characteristics, and disease stage are essential for optimizing outcomes.

Basic Cards

Q: What is the most common non-traumatic cause of AVN of the hip? A: High-dose corticosteroid therapy (35-40% of non-traumatic cases). Dose > 20mg prednisone/day for > 3 months and cumulative dose > 2g are risk factors.

Q: What percentage of AVN cases are bilateral? A: 40-80% have bilateral involvement, though often asymmetric in stage and symptoms.

Q: What is the gold standard imaging modality for early AVN diagnosis? A: MRI with sensitivity > 99%. Shows band-like signal change and "double-line sign" on T2 before radiographic changes appear.

Q: What is the "crescent sign" and what does it indicate? A: Subchondral lucency on radiographs representing separation of necrotic bone segment from underlying viable bone. Indicates advanced pre-collapse disease (Ficat stage III) with high progression risk.

Q: What is the success rate of core decompression in small lesions (less than 15% femoral head)? A: 80-90% success (avoidance of collapse/arthroplasty at 5 years) in small, early-stage lesions.

Q: What lesion size predicts poor prognosis in AVN? A: Lesions involving > 30% of the femoral head have high collapse risk and poor outcomes with joint preservation.

Q: What is the most common clinical presentation of early AVN? A: Insidious groin pain worse with weight-bearing and internal rotation; early stages may have normal radiographs.

Q: What is the natural history of untreated AVN? A: 80-90% progress to femoral head collapse within 2-5 years.

Q: What is the Ficat classification used for? A: Radiographic staging of AVN from stage 0 (normal X-ray, abnormal MRI) to stage IV (secondary osteoarthritis with acetabular involvement).

Q: What are the indications for total hip arthroplasty in AVN? A: Ficat stage III-IV (post-collapse disease), failed joint-preserving surgery, severe pain/functional limitation, typically age > 40-50 years.

Clinical Scenario Cards

Q: A 35-year-old woman with SLE on prednisolone 40mg/day for 4 months presents with bilateral groin pain. X-rays are normal. Next step? A: Bilateral hip MRI (gold standard for early AVN detection in high-risk patient with normal radiographs).

Q: MRI shows AVN involving 25% of right femoral head, Ficat stage I. Management? A: Core decompression ± bone marrow aspirate concentrate ± bisphosphonates (alendronate). Lesion less than 30%, pre-collapse, favourable for joint preservation.

Q: A 28-year-old man has AVN (35% femoral head, lateral location, Ficat IIB). Core decompression failed. Options? A: Vascularized fibular graft (young, high-demand patient with large lesion) vs. total hip arthroplasty. Complex decision balancing joint preservation (delay THA) vs. definitive treatment.

Q: Post-THA for AVN, what is 10-year implant survivorship? A: 90-95%, comparable to THA for OA, though higher revision risk in younger patients.

Image Interpretation Cards

Q: MRI T2-weighted image shows hyperintense line (inner) and hypointense line (outer) forming band in femoral head. Diagnosis? A: "Double-line sign" pathognomonic for AVN. Inner line = granulation tissue, outer line = sclerotic bone.

Q: What radiographic finding is shown: subchondral lucency in superolateral femoral head? A: Crescent sign (subchondral fracture), indicating Ficat stage III disease.

Viva-Style Cards

Q: Describe the blood supply to the adult femoral head. A: Predominantly medial femoral circumflex artery (60-80%) via superior and inferior retinacular arteries ascending posterosuperior and posteroinferior femoral neck. Lateral femoral circumflex artery contributes 20-30% via anterior retinacular branches. Artery of ligamentum teres has minimal contribution in adults. Terminal circulation with limited collaterals.

Q: What are the pathophysiological mechanisms of corticosteroid-induced AVN? A: Multifactorial: (1) fat emboli from enlarged adipocytes; (2) elevated intraosseous pressure from marrow adipocyte expansion; (3) endothelial dysfunction and apoptosis; (4) osteocyte and osteoblast apoptosis; (5) impaired angiogenesis (reduced VEGF).

Q: A patient has Ficat stage IIIC AVN. Explain why joint preservation is unlikely to succeed. A: Stage III = established collapse (crescent sign); C = > 30% femoral head involved. Collapse indicates structural failure with joint incongruity. Large lesion size predicts high progression. Core decompression success rates less than 30-50% in large lesions, and nearly zero post-collapse. Arthroplasty typically required.

Q: Compare outcomes of vascularized vs. non-vascularized fibular graft. A: Vascularized graft superior in comparative studies: 60-80% joint preservation at 5-10 years in pre-collapse disease vs. lower rates with non-vascularized. Vascularized graft provides both structural support and revascularization via microvascular anastomosis. Technically demanding, requires microsurgical expertise, donor site morbidity.