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Osteonecrosis

(Avascular Necrosis; Aseptic Necrosis; Ischemic Necrosis of Bone)

by Marvin E. Steinberg, MD

Osteonecrosis (ON) is a focal infarct of bone that may be caused by specific etiologic factors or may be idiopathic. It can cause pain, limitation of motion, joint collapse, and osteoarthritis. Diagnosis is by x-rays and MRI. In early stages, surgical procedures may slow or prevent progression. In later stages, joint replacement may be required for relief of pain and maintenance of function.

In the US, ON affects about 20,000 new patients annually. The hip (femoral head) is most commonly affected, followed by the knee and shoulder (humeral head). The wrist and ankle are less often involved. It is unusual for ON to involve the shoulder or other less commonly affected sites without the hip also being involved.

Etiology

The most common cause of ON is trauma. Nontraumatic ON affects men more often than women, is bilateral in > 60% of cases, and occurs primarily in patients between ages 30 and 50.

Traumatic ON

The most common cause of traumatic ON is a displaced subcapital fracture of the hip (see Hip Fractures); ON is uncommon after intertrochanteric fractures. The incidence of ON after hip dislocation is related primarily to the severity of the initial injury but may be higher if the dislocation is not promptly reduced. Fracture or dislocation may cause ON by grossly disrupting or compressing nearby blood vessels.

Nontraumatic ON

Factors causing or contributing to nontraumatic ON are listed in Nontraumatic Risk Factors for Osteonecrosis. The most common factors are the following:

  • Chronic corticosteroid use

  • Excessive alcohol consumption

Nontraumatic Risk Factors for Osteonecrosis

Alcohol

Chemotherapy

Coagulation disorders (eg, antiphospholipid antibody syndrome, inherited thrombophilia, hypofibrinolytic disorders)

Corticosteroids

Cushing syndrome

Decompression sickness

Gaucher disease

Hemoglobinopathy

Hyperlipidemia

Liver disease

Miscellaneous disorders (eg, chronic kidney disease, rare inherited metabolic disorders)

Organ transplantation

Pancreatitis

Radiation

SLE and other connective tissue disorders

Smoking

Tumors

The risk of ON is increased when the dose of prednisone or an equivalent corticosteroid is > 20 mg/day for several weeks or months, resulting in a cumulative dose usually > 2000 mg. The risk of ON is also increased when > 3 drinks/day (> 500 mL ethanol/wk) are consumed for several years. Some genetic factors increase susceptibility to ON. Subtle clotting abnormalities due to deficiencies in protein C, protein S, or antithrombin III or to anticardiolipin antibodies (see Thrombotic Disorders) can be detected in a high percentage of patients with ON. Some disorders that are associated with ON are treated with corticosteroids (eg, SLE). Evidence suggests that the risk of ON in many of these disorders is related primarily to the corticosteroid use rather than to the disorder. About 20% of cases are idiopathic. ON of the jaw has been reported in several patients who have received high-dose IV bisphosphonate therapy (see Osteonecrosis of the Jaw). Nontraumatic ON of the hip is bilateral in 60% of patients.

Spontaneous ON of the knee (SPONK or SONK) is a process localized to the femoral condyle or tibial plateau in elderly women (occasionally men). SPONK is thought to be caused by an insufficiency fracture (a type of fragility fracture caused by normal wear and tear on osteoporotic bone that occurs without direct trauma).

Pathophysiology

ON involves the death of osteocytes and bone marrow. Mechanisms of nontraumatic ON may include embolization by blood clots or lipid droplets, intravascular thrombosis, and extravascular compression. After the vascular insult, the repair processes attempt to remove necrotic bone and marrow and replace them with viable tissue. If the infarct is small, particularly if it is not subject to major weight bearing, this process may succeed. However, in about 80% of patients, the process is not successful and the infarct gradually collapses. Because ON usually affects the ends of long bones, the overlying articular surface becomes flattened and irregular, causing increased pain and eventually leading to osteoarthritis.

Symptoms and Signs

General symptoms

Affected areas may remain asymptomatic for weeks to months after the vascular insult. Usually pain then develops gradually, although it may be acute. With progressive collapse of the joint, pain increases and is exacerbated by motion and weight bearing and is relieved by rest.

Joint-specific symptoms

ON of the hip causes groin pain that may radiate down the thigh or into the buttock. Motion becomes limited, and a limp usually develops. SPONK usually causes sudden knee pain without preceding trauma; the sudden onset and the location of pain may help differentiate it from classical ON. This pain is most often on the medial side of the femoral condyle or tibial plateau and manifests with tenderness, joint effusion, painful motion, and a limp. ON of the humeral head often causes less pain and disability than hip and knee involvement. With advanced disease, patients have pain and decreased motion, although passive range of motion is less affected than active range of motion. Symptomatic synovial effusions can occur, especially in the knee, and the fluid is noninflammatory.

Diagnosis

  • X-rays

  • MRI

ON should be suspected in patients with the following:

  • Fractures associated with an increased incidence of ON, particularly if pain persists or worsens

  • Persistent spontaneous hip, knee, or shoulder pain, particularly if risk factors for ON are present

Plain x-rays should be done initially. They may show no abnormalities for months. The earliest findings are localized areas of sclerosis and lucency. Later, a subchondral crescent sign may appear. Then, gross collapse and flattening of the articular surface is seen, followed by advanced degenerative changes.

When x-rays are normal or nondiagnostic, an MRI, which is much more sensitive and more specific, should be done. Both hips should be imaged. Bone scans are less sensitive and less specific than MRI and are seldom done today. CT is rarely needed, although it may occasionally be of value to detect joint collapse, which does not appear on plain x-rays and sometimes may not appear on MRI.

Laboratory studies are usually normal and of little value in detecting ON. However, they might help detect an underlying disorder (eg, coagulation defects, hemoglobinopathies, lipid abnormalities).

Treatment

  • Symptomatic measures (eg, rest, physical therapy, NSAIDs)

  • Surgical decompression or other procedures to stimulate healing

  • Hip replacement

Nonsurgical treatments

Small, asymptomatic lesions may heal spontaneously and may not need treatment.

Larger lesions, both symptomatic and asymptomatic, have a poor prognosis if untreated, especially when in the femoral head. Therefore, early treatment to slow or prevent progression and save the joint is desirable. No completely effective treatment is yet available. Nonsurgical treatments include drugs (eg, bisphosphonates) and physical modalities (eg, electromagnetic fields and acoustic waves). Drug therapy and physical modalities have shown promise in limited studies but are not currently in general use. Limited weight bearing or non–weight bearing alone has not been shown to improve outcome.

SPONK is usually treated without surgery, and pain usually resolves.

Surgical treatments

Surgical treatments are most effective when done before joint collapse. They have been used most often in treating ON of the hip where the prognosis without treatment is worse than that for other regions.

Core decompression is the procedure most frequently done; one or more cores of bone are removed from the necrotic region or multiple small tracks or perforations are made in an attempt to decrease intraosseous pressure and stimulate repair. Core decompression is technically simple, and the complication rate is very low if the procedure is done correctly. Protected weight bearing (bearing weight only as tolerated and with a mobility aid, such as crutches or a walker) is needed for about 6 wk. Most reports indicate satisfactory or good results in 65% of patients overall and in 80% of patients whose hips have small, early lesions; however, reported outcomes can vary widely.

Other established procedures include various proximal femoral osteotomies and bone grafting, both vascularized and nonvascularized. These procedures are technically demanding, require protected weight bearing for up to 6 mo, and have not been done often in the US. Reports vary as to their indications and effectiveness. They should be done primarily at selected centers that have the surgical experience and facilities to achieve optimal results. An approach currently being evaluated is injection of autologous marrow into the necrotic lesion; early results are promising.

If extensive collapse of the femoral head and degenerative changes in the acetabulum cause sufficient pain and disability, an arthroplasty usually is the only way to effectively relieve pain and increase range of motion. The conventional approach is total hip replacement. Good to excellent results are achieved in 95% of total hip and total knee replacements, complication rates are low, and patients resume most activities of daily living within 3 mo. Most prosthetic hips and knees last > 15 to 20 yr.

Two alternatives to total hip replacement include surface replacement arthroplasty (SRA) and hemi-SRA. SRA involves the insertion of two metal caps, one into the acetabulum and one onto the femoral head, producing a metal-on-metal articulation. Hemi-SRA involves placement of a metal cap onto only the femoral head. It is done only if disease is limited to the femoral head and is considered a temporizing procedure. These procedures are done less often now than a few years ago because of an increasing incidence of local complications, prosthesis failure, and concerns about possible long-term systemic effects of metal ions.

ON of the knee and shoulder can be managed nonsurgically more often than ON of the hip. Limited experience with core decompression has been promising. In advanced stages, partial or total joint replacement may be indicated.

Prevention

Risk of ON caused by corticosteroids can be minimized by using them only when essential and by giving them in as low a dose as needed and for as short a duration as possible. To prevent ON caused by decompression sickness, people should follow accepted rules for decompression when diving and when working in pressurized environments. Excessive alcohol use and smoking should be discouraged. Various drugs (eg, anticoagulants, vasodilators, lipid-lowering drugs) are being evaluated for prevention of ON in patients at high risk.

Key Points

  • ON is most often a complication of displaced hip fracture, but factors that compromise bone blood flow (eg, chronic corticosteroid use, excessive alcohol use) increase risk of nontraumatic ON.

  • ON should be suspected in patients with unexplained nontraumatic pain in the hip, knee, or shoulder (sometimes the wrist or ankle) and after certain fractures if pain persists or worsens.

  • Although x-rays may be diagnostic, MRI is more sensitive and specific.

  • Smaller lesions may heal spontaneously, but most larger lesions, especially in the hip, progress without treatment.

  • Nonsurgical treatments are not widely used because efficacies are not clearly proved.

  • Surgical treatment is often indicated to limit progression and/or relieve symptoms, particularly for ON of the hip.

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