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Osteonecrosis (ON)

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

By

Stuart B. Goodman

, MD, PhD, Stanford University

Last full review/revision May 2020| Content last modified May 2020
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Topic Resources

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 secondary 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 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 osteonecrosis to involve the shoulder or other less commonly affected sites without the hip also being involved. Osteonecrosis of the jaw has been associated rarely with antiresorptive therapy for osteoporosis. Osteonecrosis of the jaw has characteristics that differ from osteonecrosis at other sites.

Etiology

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

Traumatic osteonecrosis

The most common cause of traumatic osteonecrosis is a displaced subcapital fracture of the proximal femur of the hip; osteonecrosis is uncommon after intertrochanteric fractures. The incidence of osteonecrosis 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 osteonecrosis by grossly disrupting or compressing nearby blood vessels.

Nontraumatic osteonecrosis

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

  • Chronic corticosteroid use

  • Excessive alcohol consumption

Table
icon

Nontraumatic Risk Factors for Osteonecrosis

Alcohol

Chemotherapy

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

Corticosteroids

Hemoglobinopathy (eg, sickle cell disease)

Liver disease

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

Radiation

Systemic lupus erythematosus (SLE) and other autoimmune connective tissue disorders

Smoking

Tumors

The risk of osteonecrosis 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, although case reports have described osteonecrosis subsequent to much less corticosteroid exposure. Notably corticosteroid-associated osteonecrosis is often multifocal and can affect both weight-bearing as well as non–weight-bearing joints like the shoulders. The risk of osteonecrosis is also increased when > 3 drinks/day (> 500 mL ethanol/week) are consumed for several years. Some genetic factors increase susceptibility to osteonecrosis. Subtle clotting abnormalities due to deficiencies in protein C, protein S, or antithrombin III or to anticardiolipin antibodies (see Overview of Thrombotic Disorders) can be detected in a high percentage of patients with osteonecrosis.

Some disorders that are associated with osteonecrosis are treated with corticosteroids (eg, systemic lupus erythematosus). Evidence suggests that the risk of osteonecrosis in many of these disorders is related primarily to the corticosteroid use rather than to the disorder. About 20% of cases of osteonecrosis are idiopathic. Osteonecrosis of the jaw has been reported in several patients who have received high-dose IV bisphosphonate therapy. Nontraumatic osteonecrosis of the hip is bilateral in about 60% of patients.

Spontaneous osteonecrosis of the knee (SPONK or SONK) is a process localized to the femoral condyle or tibial plateau in older 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). However, osteonecrosis of the knee can also result from trauma or any of the nontraumatic risk factors of osteonecrosis.

Pathophysiology

Osteonecrosis involves the death of cellular elements of the bone marrow. Mechanisms of nontraumatic osteonecrosis 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, these processes may succeed and the femoral head remains round. However, in about 80% of patients, especially if the infarct is large and in the weightbearing area, collapse of the infarcted area outstrips attempts at repair, and the infarcted area collapses. The femoral head is no longer round.

Because osteonecrosis usually affects the ends (epiphysis and metaphysis) of long bones, the overlying articular cartilage surface becomes flattened and irregular, with areas of collapse that may eventually lead to osteoarthritis and increased pain.

For more information about the pathophysiology of osteonecrosis, see Osteonecrosis: Overview of New Paradigms in the Etiology and Treatment.

Symptoms and Signs

General symptoms

Areas affected by osteonecrosis 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.

Because many of the risk factors for the development of osteonecrosis act systemically (eg, chronic corticosteroid use, excessive alcohol intake, sickle cell disease), osteonecrosis may be multifocal. In sickle cell disease, osteonecrosis may occur throughout different long bones and cause sudden painful crises.

Joint-specific symptoms

Osteonecrosis 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 osteonecrosis. This pain is most often on the medial side of the femoral condyle or tibial plateau and manifests with tenderness, noninflammatory joint effusion, painful motion, and a limp.

Osteonecrosis of the humeral head often causes less pain and disability than hip and knee involvement.

With advanced osteonecrosis, 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

Osteonecrosis should be suspected in patients with the following:

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

  • Persistent spontaneous hip, knee, or shoulder pain, particularly if risk factors for osteonecrosis 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 due to a fracture in the epiphysis may appear. Then, gross collapse and flattening of the articular surface is seen, followed by advanced degenerative changes.

When clinical suspicion is high but 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 osteonecrosis. However, they might help detect an underlying disorder (eg, coagulation defects, hemoglobinopathies, lipid abnormalities).

Treatment

  • Symptomatic measures (eg, rest, physical therapy, nonsteroidal anti-inflammatory drugs [NSAIDs])

  • Surgical decompression or other procedures to stimulate healing

  • Hip replacement

Nonsurgical treatments

Small, asymptomatic lesions, especially those in non-weightbearing areas, 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 long-term outcome. Small lesions may heal without treatment if osteonecrosis is diagnosed early, if the lesion is not in the weight-bearing area, and contributing factors can be mitigated (eg, stopping corticosteroid use). However, osteonecrosis is often treated (for example, with a simple procedure such as core decompression) to improve the chance that lesions heal without joint collapse.

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

Surgical treatments

Surgical treatments for osteonecrosis are most effective when done before joint collapse. They have been used most often in treating osteonecrosis 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 weeks. Most reports indicate satisfactory or good results in 65% of patients overall and in 80% of patients whose hips have smaller lesions that are dealt with early; however, reported outcomes and, thus, the need for total hip replacement, can vary widely. In general, about 20 to 35% of patients require total hip replacement.

The injection of concentrated autologous cells harvested from the iliac crest into the core decompression track at surgery has recently been shown to improve the clinical outcome and imaging appearance of osteonecrosis of the femoral head (1-3).

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 months, 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.

If extensive collapse of the femoral head and degenerative changes in the acetabulum cause sufficient pain and disability, an arthroplasty usually is the most reliable 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 months. Most prosthetic hips and knees last > 15 to 20 years.

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. These procedures are rarely indicated because of an increasing incidence of local complications, prosthesis failure, and concerns about possible long-term systemic effects of metal ions.

Osteonecrosis of the knee and shoulder can be managed nonsurgically more often than osteonecrosis of the hip. Limited experience with core decompression and bone grafting has been promising. In advanced stages, partial or total joint replacement may be indicated. However, SPONK usually resolves without surgical treatment.

Treatment references

  • 1. Atilla B, Bakırcıoğlu S, Shope AJ, et al: Joint-preserving procedures for osteonecrosis of the femoral head. J.EFORT Open Rev 4(12):647-658, 2020. doi: 10.1302/2058-5241.4.180073. 

  • 2. Hernigou P, Dubory A, Homma Y, et al: Cell therapy versus simultaneous contralateral decompression in symptomatic corticosteroid osteonecrosis: A thirty-year follow-up prospective randomized study of one hundred and twenty-five adult patients. Int Orthop 42(7):1639−1649, 2018. doi: 10.1007/s00264-018-3941-8. Epub 2018 May 9.

  • 3. Zhang C, Fang X, Huang Z, et al: Addition of bone marrow stem cells therapy achieves better clinical outcomes and lower rates of disease progression compared with core decompression alone for early stage osteonecrosis of the femoral head: A systematic review and meta-analysis. J Am Acad Orthop Surg, 2020. doi: 10.5435/JAAOS-D-19-00816. Epub 2020 February 28.

Prevention

Risk of osteonecrosis 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 osteonecrosis 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 osteonecrosis in patients at high risk.

Key Points

  • Osteonecrosis is most often a complication of displaced hip fracture, but factors that compromise bone blood flow (eg, sickle cell disease) increase risk of nontraumatic osteonecrosis.

  • Osteonecrosis 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 osteonecrosis of the hip.

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