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

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Osteonecrosis 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, osteonecrosis (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 Fractures, Dislocations, and Sprains: Hip fractures); ON is uncommon after intertrochanteric fractures. The incidence of ON after hip dislocation is high without prompt reduction; the sooner reduction occurs, the lower the incidence. Fracture or dislocation may cause ON by grossly disrupting or compressing nearby blood vessels.

Spontaneous ON of the knee (SPONK) is localized ON of 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).

Nontraumatic ON: Factors causing or contributing to nontraumatic ON are listed in Table 1: Osteonecrosis: Nontraumatic Risk Factors for OsteonecrosisTables. The most common factors are the following:

  • Chronic corticosteroid use
  • Excessive alcohol consumption

The risk of ON is increased when the dose of prednisone Some Trade Names
DELTASONE
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or an equivalent corticosteroid is > 25 mg/day for several weeks or months, resulting in a cumulative dose usually > 3000 mg. The risk of ON also is 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 themselves associated with ON are treated with corticosteroids (eg, SLE), so it is not clear whether risk is increased because of corticosteroid use or the disorder. About 20% of cases are idiopathic. ON of the jaw has recently been reported in several patients who have received high-dose IV bisphosphonate therapy (see Sidebar 1: Osteonecrosis: Osteonecrosis of the JawSidebars). Nontraumatic ON of the hip is bilateral in 60% of patients.

Sidebar 1

Osteonecrosis of the Jaw

Osteonecrosis of the jaw (ONJ) has no unanimously accepted definition but is generally held to be an oral lesion involving bare mandibular or maxillary bone, which usually manifests with pain and purulent discharge, although it may be asymptomatic. ONJ may occur spontaneously or after dental extraction or trauma, radiation therapy to the head and neck (osteoradionecrosis), or high-dose IV bisphosphonate therapy (eg, for cancer treatment). It is not clear whether routine use of oral bisphosphonates for treatment or prevention of osteoporosis increases risk of ONJ. Currently, otherwise appropriate bisphosphonate use should not be discouraged. However, it seems reasonable to accomplish any necessary oral surgery before beginning bisphosphonate therapy and to encourage good oral hygiene while on therapy.

Once established, ONJ is challenging to treat and should be managed by an oral surgeon with experience treating ONJ. Treatment typically involves limited debridement, antibiotics, and oral rinses. Surgical resection of the affected area may worsen the condition and should not be the initial treatment.

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. 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. 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.

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. CT is rarely needed, although it may occasionally be of value to detect joint collapse, which does not appear on plain x-rays.

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.

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 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 done properly. Protected weight bearing is needed for about 6 wk. Most reports indicate satisfactory or good results in 65% of patients, including those whose hips have some degree of collapse, and in 80% of patients whose hips have small, early lesions. Other established procedures include various proximal femoral osteotomies and bone grafting, both vascularized and nonvascularized. These 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 optimum results. An approach currently being evaluated is injection of autologous marrow into the necrotic lesion.

Table 1

Nontraumatic Risk Factors for Osteonecrosis

Alcohol

Asthma

Chemotherapy

Coagulation disorders (eg, antiphospholipid antibodies, disseminated intravascular coagulation, thrombophilia)

Corticosteroids

Cushing's syndrome

Decompression sickness (dysbarism)

Diabetes

Gaucher's disease

Gout

Hemoglobinopathy

Hyperlipidemia

Liver disease

Miscellaneous conditions (eg, chronic renal disease, rare inherited metabolic disorders)

Organ transplantation

Pancreatitis

Radiation

SLE and connective tissue disorders

Smoking

Tumors

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 will last > 15 to 20 yr.

Two alternatives under investigation include surface replacement arthroplasty (SRA) and hemi-SRA. SRA, which can be done instead of total hip replacement, involves the insertion of 2 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.

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

To minimize the risk of ON caused by corticosteroids, they must be used only when essential, should be given in as low a dose as needed, and for as short a duration as possible. To prevent ON caused by decompression sickness (dysbarism), accepted rules for decompression should be followed during 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.

Last full review/revision March 2008 by Marvin E. Steinberg, MD

Content last modified March 2008

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