Aseptic Necrosis (Avascular Necrosis)
Aseptic necrosis, also known as osteonecrosis or avascular necrosis, is a degenerative condition in which living bone cells die because of reduced or interrupted blood supply to the subchondral region. This ischemia most often affects the epiphysis of weight-bearing joints such as the hip, knee and ankle, but it may also occur in the shoulder and wrist. As blood supply decreases, osteocytes and bone marrow die and the bone structure gradually weakens, which may lead to subchondral collapse and subsequent joint destruction. This represents a significant threat to joint function and integrity¹.
In non-traumatic cases, patients often present with mechanical pain that may vary in onset and intensity. The pain is frequently diffuse and difficult to localize precisely. In the early stages, clinical examination may appear normal, which often delays diagnosis and therefore the initiation of necessary management¹.
Causes and Risk Factors
Osteonecrosis occurs most commonly in the femoral head, but may also affect the humerus, femoral condyles, talus and, more rarely, carpal bones such as the lunate or scaphoid¹. The condition can be caused by both traumatic and non-traumatic mechanisms.
Traumatic triggers include:
Joint dislocation or fracture, particularly involving the hip, which may compromise local blood vessels.
Proximal femoral fracture that affects circulation to the femoral head.
Radiation therapy involving the skeleton, which may weaken bone structure and vascular supply.
Non-traumatic factors include:
High alcohol intake³, which is associated with fat accumulation in bone marrow and reduced perfusion.
Long-term glucocorticoid use, which has a stronger association with osteonecrosis than alcohol exposure alone.
Hyperlipidemia, which increases marrow fat volume and may cause microcirculatory failure.
Smoking, which reduces nitric-oxide availability, increases oxidative stress and contributes to endothelial dysfunction.
Overweight and obesity, often associated with hyperlipidemia and increased bone-marrow fat.
Conditions such as sickle-cell anemia and systemic lupus erythematosus, which may cause vascular occlusion or inflammation within bone tissue.
The condition occurs more frequently in men, which may partly be explained by higher rates of smoking and alcohol use in this group⁴. Some studies also suggest a higher incidence in areas with large climatic variations⁴.
Clinical Presentation and Symptoms
Symptoms vary according to disease stage. In the early phases, the disease is often asymptomatic and may be discovered incidentally on imaging. When symptoms occur, they are commonly described as deep, aching pain localized to the affected joint, most often the hip, knee or shoulder³. Pain typically worsens with activity and particularly with internal rotation of the hip in flexion, while in later stages it may also occur at rest.
Joint range of motion gradually decreases, and when the hip is affected, limping and stiffness may develop. Segmental collapse can occur without the patient being aware of it, contributing to the often delayed diagnosis.
Osteonecrosis can be classified into five stages based on clinical and radiological findings⁵:
Stage 1: No visible changes on X-ray. MRI may show bone-marrow edema. The disease is often asymptomatic.
Stage 2: X-ray demonstrates sclerosis, osteopenia or subchondral cysts, particularly in the central superior portion of the epiphysis.
Stage 3: The articular surface begins to collapse, causing deformity of the joint contour and narrowing of the joint space. A crescent sign is often visible on X-ray.
Stage 4: Marked collapse of the subchondral bone and destruction of the trabecular pattern. Secondary osteoarthritis may develop.
Stage 5: Both joint surfaces are affected. The joint becomes painful and loses functional capacity.
In osteonecrosis of the femoral head, which accounts for more than 72% of cases, pain in the groin, buttock and medial thigh is common. X-rays may be normal in the early stage, and MRI should be used when there is clinical suspicion. Without treatment, 85% may progress to joint collapse and require total hip arthroplasty⁶.
Diagnostic Investigations
Diagnosis requires a detailed medical history and thorough clinical examination. Known risk factors such as steroid exposure and alcohol misuse should be identified. Osteonecrosis generally occurs in younger patients than osteoarthritis and should be considered in this group when unexplained joint pain is present³.
Early in the disease course, clinical detection can be very difficult, making imaging important. MRI is the most sensitive method and may demonstrate the characteristic "double-line sign" of osteonecrosis. This consists of a bright inner line representing granulation tissue and a dark outer line representing sclerotic bone⁷. MRI also provides information about lesion size and location, which is important when assessing the risk of collapse and prognosis.
In more advanced disease, X-ray can confirm the diagnosis. Necrotic bone often appears denser (whiter), with sclerotic or patchy changes⁸. Subchondral radiolucency—the crescent sign—may also be visible and indicates impending collapse of the articular surface and therefore severe disease.
Outcome Measures in Osteonecrosis
Functional outcome measures are important for documenting the patient's baseline function and defining measurable treatment endpoints. The choice of instrument should depend on the joint affected. For hip involvement, the following tools may be used:
1. Harris Hip Score (HHS): A structured tool that measures pain, function and hip range of motion. It produces a total score from 0 to 100, with higher scores indicating better function. HHS is used in both clinical practice and research to evaluate treatment outcomes.
2. Pain scales: When pain is present, the patient can be assessed with the 4-Item Pain Intensity Measure (P4), Numeric Pain Rating Scale (NPRS) or Visual Analogue Scale (VAS). These scales are simple to use and provide reliable information about pain intensity over time.
3. HOOS (Hip disability and Osteoarthritis Outcome Score): A validated patient-reported outcome measure developed for people with hip problems, including osteonecrosis. HOOS covers five domains: pain, symptoms, activities of daily living, sport/recreation and hip-related quality of life. It is suitable for both conservative and postoperative follow-up.
Pharmacological Treatment
Pharmacological treatment is mainly used in early stages in an attempt to slow disease progression, although the evidence remains limited. Possible medications include:
Anticoagulants, statins and vasodilators, which may potentially improve microcirculation and reduce further joint degeneration. Evidence of effectiveness is limited and of low certainty⁹.
Bisphosphonates have a theoretical effect through inhibition of osteoclast activity and may therefore delay subchondral collapse. Their use remains experimental but may be considered in patients with early-stage disease⁹.
Surgical Treatment
When conservative treatment is insufficient, different surgical procedures may be considered depending on disease stage, patient age and general health.
Core decompression:
Used mainly in stages 1 and 2. A channel is drilled into the bone, for example the femoral head, to reduce intramedullary pressure and improve blood flow. This may stimulate revascularization and new bone formation. The procedure can be combined with vascularized bone grafting, often using a fibular graft with anastomosis to the lateral femoral circumflex artery to promote callus formation and regeneration.
Osteotomy:
In this procedure, the bone is cut to shift weight-bearing away from the necrotic area, either by rotating the femoral head and neck or by creating valgus or varus angulation of the proximal femur. The treatment is generally reserved for younger patients without comorbidities that impair bone healing. Long-term studies in the United States report success rates of 70–90% in stages 2 and 3⁶.
Total hip arthroplasty:
In stages 3 and 4, when the joint has been substantially damaged, total joint replacement may be the final option. The procedure involves:
Removal of the femoral head and insertion of a metal stem into the femoral shaft.
Placement of a ceramic or metal ball to replace the femoral head.
Preparation and replacement of the acetabulum with a metal cup.
Insertion of a plastic, metal or ceramic bearing surface to allow low-friction movement.
Long-term follow-up of patients with 32 mm alumina-on-alumina prostheses has shown good outcomes, including higher Harris Hip Scores and substantial pain relief after surgery¹⁰.
Physiotherapy Treatment
Physiotherapy does not aim to cure osteonecrosis, but it plays an important role in slowing functional decline and reducing pain. In patients with stage 1 or 2 disease, exercise may help maintain mobility and strength⁵. In many cases, surgery may eventually be required, but physiotherapy is also central to postoperative rehabilitation³.
The main goals of conservative treatment are:
Pain relief
Prevention of progression
Improvement of function
Patient education is the first step. Risk factors such as smoking and alcohol misuse should be addressed, and glucocorticoid exposure reduced where medically appropriate⁵. Unloading the affected joint may be important, and a physiotherapist can instruct the patient in the use of crutches or walking aids. Although reduced weight-bearing alone does not prevent progression, it has value as part of a multifactorial treatment approach⁹.
Exercise programs should be individualized and may include:
Passive and active range-of-motion exercises, including hip rotations, stretching and circular movements in different starting positions.
Strength training for the hip, thigh and core musculature to support the joint and reduce joint loading.
Endurance training, such as low-load treadmill walking or cycling, and
Coordination training, for example balance training and walking on varying surfaces and at different speeds.
Movement should be performed with consideration of joint biomechanics, and excessive compressive and shear forces should be avoided to reduce the risk of further damage. Treatment response depends on lesion size and disease stage at the start of rehabilitation.
After surgery, physiotherapy begins immediately:
The patient is instructed in daily activities such as getting out of bed, walking with a walker or crutches and performing necessary mobility tasks⁵.
In later rehabilitation, treatment focuses on strengthening, improving mobility, normalizing gait and gradually restoring function, while observing relevant hip precautions.
Rehabilitation is combined with a home exercise program, and exercise intensity is increased gradually in line with healing progress¹³.
Sources:
Matthews AH, Stitson D. Osteonecrosis. InStatPearls. 2019. StatPearls Publishing. : https://www.ncbi.nlm.nih.gov/books/NBK537007/
Dr ER tv Avascular necrosis : https://www.youtube.com/watch?v=w2ZOTDbEe-0
Gruson K, Kwon Y. Atraumatic osteonecrosis of the humeral head. Bulletin of the NYU Hospital for Joint Diseases. 2009;67(1):6-14.
Zhao DW, Yu M, Hu K, Wang W, Yang L, Wang BJ, 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(21) : 2843-2850
Lee MS, Hsieh PH, Shih CH, Wang CJ. Non-traumatic osteonecrosis of the femoral head – from clinical to bench. Chang Gung Med J 2010;33(4):351-360
Bentley G. 2012. European Instructional. Lectures13th EFORT Congress. Berlin,Germany. 2012; 12: 148 e.v.
Niknejad MT, Gaillard F. Crescent sign of avascular necrosis. https://radiopaedia.org/articles/crescent-sign-of-avascular-necrosis-1'
Magee DJ. Orthopedic physical assessment. Saunders:St Louis, MO;2008.
Klumpp R, Trevisan C. Aseptic osteonecrosis of the hip in the adult: current evidence on conservative treatment. Clinical Cases in Mineral and Bone Metabolism. 2015;12(Suppl 1):39–42.
Garino JP, Steinberg ME. Total Hip Arthroplasty in Patients with Avascular Necrosis of the Femoral Head; A 2-to 10-Year Followup. Clinical orthopaedics and related research. 1997; 334: 108-115.
Neumayr LD, Aguilar C, Earles AN, Jergesen HE, Haberkern CM, Kammen BF, et al. Physical therapy alone compared with core decompression and physical therapy for femoral head osteonecrosis in sickle cell disease. J Bone Joint Surg Am. 2006; 88(12): 2573-2582.
Mass general, Total Hip Replacement, Rehabilitation & Physical Therapy Protocols 'http://www.massgeneral.org/ortho-hip-knee/patient-education/pt-ed-hiprehab.pdf'
Paula Miller, Treating Avascular Necrosis, 21(17):23
