Last updated: November 4, 2014
Synonyms: Avascular necrosis, aseptic necrosis, ischemic necrosis of bone.
ICD-9 Code: 733.40.
ICD-10 Code: M87
Definition: Osteonecrosis is the ischemic death of bone and bone marrow, clinically manifest as bone pain with distinctive radiographic sequelae.
Etiology: Although a variety of states predispose to osteonecrosis, it may be idiopathic. Underlying mechanisms may include disruption in normal osseous blood flow, thrombosis, fat emboli, endothelial injury, hypercoagulability, increase in intraosseous pressure, and local alterations in tissue architecture (i.e., trauma) or bone stock (osteomalacia).
Risk Factors: Numerous associations have been described, including (in decreasing order of frequency) trauma (with or without adjacent fracture), high-dose corticosteroids, chronic alcoholism, renal failure, organ transplantation, SLE and other connective tissue diseases (e.g., PM), thrombotic states (e.g., sickle cell anemia, hemoglobinopathies), radiation injury, pancreatitis, gout, pregnancy, hyperlipidemia, and caisson disease (decompression sickness in divers).
Pathology: Sequence of events includes cell death, eosinophilic reticulated necrosis, mesenchymal and capillary ingrowth, resorption of bone, collapse, and deposition of new woven bone on ischemic/necrotic trabecular bone.
Demographics: The underlying condition or cause determines the demographics. Osteonecrosis may account for nearly 10% of total hip replacements (>165,000) done in the United States each year. Most commonly seen in third to sixth decades of life, osteonecrosis is more common in men than women (perhaps owing to trauma or alcohol).
Cardinal Findings: Osteonecrosis most commonly affects the proximal femoral head (men), more so than the distal femoral condyles (women). Less common sites include the proximal humeral head, talus, lunate bone of the wrist (Kienböck disease), and tarsal bones. Once clinically recognized, the symptoms and radiographic changes are progressive.
Diagnostic Tests: Laboratory tests have value only in documenting an underlying cause of osteonecrosis.
Imaging: Plain radiographs usually suffice to make a diagnosis. Table 27 demonstrates the correlation between symptoms and typical imaging changes in the course of osteonecrosis. Common early findings on radiographs include alteration in the normal trabecular pattern, with lytic or sclerotic change. Later findings include a crescent sign (subchondral crescent-shaped lucency), collapse, loss of joint space, and secondary osteoarthritic changes (osteophytes). Scintigraphy (bone scan) using technetium-99m may show asymmetric changes, whose nature depends on the stage of disease. The early infarctive stage shows no uptake or a “cold” spot that may be present before the radiographs change. Later, during the reparative stages, the bone scan may show increased areas of uptake. MRI may be more sensitive than bone scanning in picking up earlier lesions but may yield a false-negative result in the first 2 to 3 weeks. The earliest finding is nonspecific marrow edema, later followed by marrow necrosis with changes in cortical bone.
Staging of Osteonecrosis of the Femoral Head
Minimal or no pain
MInimal pain, night pain
Intermitent groin/thigh pain, limitation of motion
Increasing pain, antalgic pain
Increasing pain, severe loss of motion
Sclerosis or cystformation; no collapse, normal joint space
Early subchondral collapse (crescent sign), no flattening, normal joint space
Flattening of femoral head, normal joint space
FLattening of femoral head, joint space narrowing and acetabular changes
|Normal bone scan, MRI
Abnormal MRI or bone scan
Abnormal MRI and bone scan
Keys to Diagnosis: Complaints of vague bone pain (at the ends of long bones), possibly worse at night, in patients with an identifiable risk factor (e.g., steroid use) should suggest osteonecrosis. Remember that clinical symptoms precede radiographic evidence of osteonecrosis by months. The earliest and most reliable diagnosis is made by MRI.
Differential Diagnosis: Monarticular OA, fracture, transient osteoporosis of the hip, osteoidosteoma, sickle cell crisis, osteomyelitis, and primary or metastatic tumor should be considered.
Therapy: Treatment varies according to the stage of disease and whether an underlying cause is identified. For instance, abstinence from alcohol, lowering or discontinuing corticosteroid therapy, lipid-lowering therapy, or avoidance of sickle cell crises may benefit some.
Conservative measures should be aimed at maintaining strength, avoiding contractures or debility (with the assistance of physical and occupational therapy), and pain management.
Pain can be managed with analgesic agents (e.g., acetaminophen) or NSAIDs. Intraarticular steroids are not advisable. Pain may be alleviated with ambulatory assist devices (crutches, cane, or walker).
Surgery: Early stages may benefit from debridement of necrotic bone with subsequent bone grafting. Core decompression, with or without biopsy, is controversial and may be indicated in osteonecrosis of the femoral head when applied early. Joint replacement may be indicated for intractable pain with moderate to severe radiographic changes.
Total joint replacement, unilateral endoprosthesis, and rotational osteotomy have been used to treat advanced painful disease.
Prognosis: Although some patients with osteonecrosis do not progress to bony collapse, most exhibit progressive pain, debility, and radiographic change and may require surgical intervention. Joint replacement surgery for osteonecrosis is less successful than that for other disorders because of a younger population and other comorbid conditions that may result in weaker bone stock.
Chang CC, Greenspan A, Gershwin ME. Osteonecrosis: current perspectives on pathogenesis and treatment. Semin Arthritis Rheum 1993;23:47–69. PMID:8235665
Mankin HJ. Nontraumatic necrosis of bone (osteonecrosis). N Engl J Med 1992;326:1473–1479. PMID:1574093