Osteonecrosis (Avascular Necrosis)

Also known as: Avascular necrosis, AVN (avascular necrosis), Osteonecrosis, Ischemic bone necrosis, Bone infarction, Aseptic necrosis, Femoral head osteonecrosis, Dead bone (bone tissue death)

Last updated: December 18, 2024

Osteonecrosis (avascular necrosis) is the death of bone tissue when blood flow to part of a bone is reduced or interrupted. It often affects the bone end near a joint, such as the femoral head, and weakened bone may collapse and change joint alignment, sometimes leading to osteoarthritis. Symptoms include deep joint pain, often worse with activity, and reduced range of motion that can progress over time. Prognosis varies by size, location, and stage.

Key Facts

•Osteonecrosis, also called avascular necrosis, describe death of bone tissue that occurs when blood flow to a segment of bone becomes reduced or interrupted
•Deep joint pain that worsens with weight-bearing or activity and later occur at rest, described in the groin for hip involvement
•Diagnosed through history, physical exam, and imaging
•First-line treatment includes exercise, weight management, and activity modification

What It Is

Osteonecrosis, also called avascular necrosis, may describe death of bone tissue that can occur when blood flow to a segment of bone becomes reduced or interrupted. The loss of perfusion can lead to death of osteocytes and marrow elements, and the weakened subchondral bone can collapse under normal joint loading. This process often involves the epiphysis near a joint surface, so articular congruity can become altered and secondary osteoarthritis may develop. The femoral head is commonly affected, although the knee, shoulder, and other sites can also be involved.

Affected Anatomy

This condition affects several structures in and around the joint:

•Femoral head subchondral bone (hip)
•Femoral head articular cartilage and adjacent joint surface (hip)
•Acetabular cartilage and labrum (hip joint secondary involvement)
•Medial femoral condyle subchondral bone (knee)
•Tibiofemoral articular cartilage (knee joint surface affected after collapse)
•Humeral head subchondral bone (shoulder)
•Glenoid articular cartilage (shoulder joint secondary degeneration)
•Bone marrow and intraosseous microcirculation (sinusoidal and small vessel network)

Common Symptoms

Symptoms can vary in intensity and may change over time. Common experiences include:

•Deep joint pain that may worsen with weight-bearing or activity and can later occur at rest, often described in the groin for hip involvement
•Reduced range of motion that can progress over time, typically affecting internal rotation and abduction at the hip
•Limping or altered gait that may reflect pain inhibition and mechanical changes after subchondral collapse
•Mechanical symptoms such as catching or stiffness that can occur when joint surface irregularity develops
•Referred pain that may radiate to the thigh, buttock, or knee in hip disease, which can complicate localization
•Pain with overhead motion and decreased shoulder function when the humeral head is involved
•Minimal or absent symptoms in early stages, as small lesions can be clinically silent until structural compromise occurs

Causes and Risk Factors

Multiple factors can contribute to the development of this condition:

Causes

•Trauma-related vascular disruption, such as femoral neck fracture or hip dislocation, which can compromise blood supply to the femoral head
•Glucocorticoid-associated osteonecrosis, which may involve lipid metabolism changes, marrow fat hypertrophy, and microvascular compromise
•Alcohol-associated osteonecrosis, which can be linked to fatty infiltration of marrow and impaired microcirculation
•Sickle cell disease and other hemoglobinopathies, where vaso-occlusion can reduce perfusion and promote bone infarction
•Decompression sickness (dysbaric osteonecrosis), where gas emboli and vascular injury can contribute to ischemia
•Idiopathic osteonecrosis, where a clear precipitating factor may not be identified despite evaluation

Risk Factors

•High-dose or prolonged systemic corticosteroid exposure, which can be associated with nontraumatic osteonecrosis
•Heavy alcohol use, which may increase risk through metabolic and vascular mechanisms
•Prior joint trauma (e.g., hip dislocation, femoral neck fracture, knee injury) that can disrupt local blood supply
•Sickle cell disease or other conditions with hypercoagulability or vaso-occlusive phenomena
•Organ transplantation and associated immunosuppression, which can correlate with steroid exposure and metabolic risk
•Autoimmune or inflammatory disorders (e.g., systemic lupus erythematosus), often in the context of corticosteroid therapy
•Coagulation abnormalities or thrombophilia, which can promote microthrombi and reduced intraosseous perfusion
•Decompression exposure (e.g., diving or compressed-air work), which can be associated with dysbaric osteonecrosis

How It's Diagnosed

Diagnosis typically involves a combination of clinical assessment and imaging studies:

•Clinical history and physical examination, which can include assessment of pain location, gait, range of motion, strength testing, and provocative maneuvers to evaluate hip, knee, or shoulder involvement
•Plain radiographs (X-rays), which can be used to evaluate late-stage changes such as sclerosis, cystic change, subchondral lucency (crescent sign), and femoral head flattening
•Magnetic resonance imaging (MRI), which can often detect early osteonecrosis before radiographic changes and can help define lesion size, location, and marrow edema patterns
•Computed tomography (CT), which can help characterize subchondral fracture, collapse, and bony architecture when surgical planning is considered
•Bone scintigraphy (nuclear medicine bone scan), which can sometimes identify altered perfusion and bone turnover when MRI is not available or is contraindicated
•Laboratory evaluation for contributing conditions, which can include tests that may assess hemoglobinopathies, inflammatory disease, lipid abnormalities, or coagulation disorders depending on clinical context
•Staging and lesion quantification, which can use commonly referenced systems (e.g., imaging-based staging) to correlate extent of involvement with management options and prognosis

Treatment Options

Treatment approaches range from conservative measures to surgical interventions, often starting with the least invasive options:

Self-Care and Activity Modification

•Activity modification and load reduction strategies, which may help limit pain and mechanical stress on the affected joint in earlier stages
•Bisphosphonate therapy, which has been studied for potential reduction of collapse risk in selected early-stage cases, although evidence can vary by stage and study design
•Bone grafting procedures (nonvascularized or vascularized), which can be used to support subchondral bone and attempt to restore structural integrity in selected patients

Physical Therapy and Exercise

•Physical therapy approaches, which can focus on maintaining range of motion, strengthening surrounding musculature, and optimizing gait mechanics

Medications

•Analgesic and anti-inflammatory medications, which can be used for symptom control while underlying disease course is evaluated

Injections and Office-Based Procedures

•Management of contributing factors, which can include addressing alcohol exposure, reviewing corticosteroid exposure, and treating associated systemic conditions when present

Surgery

•Core decompression, which can be used in pre-collapse or early-collapse disease to reduce intraosseous pressure and potentially improve perfusion, sometimes combined with bone grafting
•Osteotomy, which can be used in some cases to shift load away from the necrotic segment, depending on lesion location and joint anatomy
•Joint replacement (e.g., total hip arthroplasty, shoulder arthroplasty, or knee arthroplasty), which can be considered when collapse and secondary arthritis lead to persistent pain and functional limitation

Prognosis and Recovery

The course of this condition varies between individuals:

•Prognosis can vary by lesion size, location (weight-bearing dome involvement), and stage at diagnosis, with earlier-stage disease generally associated with more joint-preserving options.
•Small, medially located lesions may progress more slowly, while larger lesions involving the weight-bearing surface can be associated with higher likelihood of subchondral collapse.
•Once collapse and secondary osteoarthritis develop, symptoms can become more persistent and joint replacement may become a more common management pathway.
•Outcomes after joint-preserving procedures can vary, and durability may depend on stage, underlying cause (e.g., steroid-associated disease), and extent of necrosis.
•Bilateral or multifocal disease can occur, particularly in nontraumatic etiologies, and can influence long-term function and monitoring strategies.

Total Hip Arthroplasty (Total Hip Replacement)(Procedure)
Bone Grafting(Procedure)
Hip Osteoarthritis(Condition)

Frequently Asked Questions

Common symptoms include: Deep joint pain that may worsen with weight-bearing or activity and can later occur at rest, often described in the groin for hip involvement; Reduced range of motion that can progress over time, typically affecting internal rotation and abduction at the hip; Limping or altered gait that may reflect pain inhibition and mechanical changes after subchondral collapse; Mechanical symptoms such as catching or stiffness that can occur when joint surface irregularity develops; Referred pain that may radiate to the thigh, buttock, or knee in hip disease, which can complicate localization.

Diagnosis typically involves: Clinical history and physical examination, which can include assessment of pain location, gait, range of motion, strength testing, and provocative maneuvers to evaluate hip, knee, or shoulder involvement; Plain radiographs (X-rays), which can be used to evaluate late-stage changes such as sclerosis, cystic change, subchondral lucency (crescent sign), and femoral head flattening; Magnetic resonance imaging (MRI), which can often detect early osteonecrosis before radiographic changes and can help define lesion size, location, and marrow edema patterns; Computed tomography (CT), which can help characterize subchondral fracture, collapse, and bony architecture when surgical planning is considered.

Treatment options range from conservative measures to surgical interventions, including: Activity modification and load reduction strategies, which may help limit pain and mechanical stress on the affected joint in earlier stages; Analgesic and anti-inflammatory medications, which can be used for symptom control while underlying disease course is evaluated; Physical therapy approaches, which can focus on maintaining range of motion, strengthening surrounding musculature, and optimizing gait mechanics; Management of contributing factors, which can include addressing alcohol exposure, reviewing corticosteroid exposure, and treating associated systemic conditions when present; Bisphosphonate therapy, which has been studied for potential reduction of collapse risk in selected early-stage cases, although evidence can vary by stage and study design.