eMedicine Specialties > Radiology > Musculoskeletal

Bone Infarct

Author: Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, Consultant Radiologist, North Manchester General Hospital, The Pennine Acute NHS Trust, Manchester UK
Coauthor(s): Mohammed Jassim Al-Salman, MBBS, Consulting Radiologist, King Abdul Aziz Medical City, National Guard Hospital; Muthusamy Chandramohan, MBBS, DMRD, FRCR, Consultant Radiologist, Bradford Teaching Hospitals, UK; Ian Turnbull, MB, ChB, MD, DMRD, FRCR, Lecturer, Department of Radiology, University of Manchester; Consulting Neuroradiologist, Hope Hospital, Salford, Manchester and North Manchester General Hospital, UK; Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute; Charles Edward Hutchinson, MD, FRCR, Senior Lecturer, Department of Diagnostic Radiology, University of Manchester
Contributor Information and Disclosures

Updated: May 7, 2008

Introduction

Background

Bone infarct refers to ischemic death of the cellular elements of the bone and marrow. A considerable lack of uniformity exists in the use of terminology for bone infarct. At present, the term osteonecrosis is accepted and used widely. In general, bone infarct refers to lesions occurring in the metaphysis and diaphysis of bone. Lesions in the epiphysis are called avascular necrosis (AVN).

Osteonecrosis can be idiopathic or secondary to a number of conditions that reduce blood supply to the bone; such conditions include an intraluminal abnormality, an extrinsic compression, or a combination of both. CT scans, MRIs, and bone scans play a significant role in diagnosing the disease at an early stage and thereby reducing the number and/or severity of complications and morbidity associated with the disease.

Pathophysiology

Ischemic cell death

Ischemic cell death and necrosis are the result of a reduced blood supply to the bone, which in turn can result from either an intrinsic abnormality in the blood vessel supplying part of the bone, an extrinsic abnormality, or a combination of both. The rapidity with which cell death occurs depends on the cell type and the degree and duration of the anoxia. Hematopoietic cells are sensitive to anoxia and are the first to die after reduction or removal of the blood supply; they usually die within 12 hours. Experimental evidence suggests that bone cells composed of osteocytes, osteoclasts, and osteoblasts die within 12-48 hours and that marrow fat cells die within 5 days.

The death of bone does not alter its radiographic opacity. Living bone becomes osteoporotic as a result of osteoclastic bone resorption secondary to reactive hyperemia. Dead bone cannot undergo resorption; therefore, it appears relatively more opaque.

Repair of ischemic bone occurs in 2 phases. First, when dead bone abuts live marrow, capillaries and undifferentiated mesenchymal cells grow into the dead marrow spaces, while macrophages degrade dead cellular and fat debris. Second, mesenchymal cells differentiate into osteoblasts or fibroblasts. Under favorable conditions, layers of new bone form on the surface of dead spongy trabeculae. If sufficiently thickened, these layers may increase the radiopacity of the bone; therefore, the first radiographic evidence of previous necrosis may be patchy sclerosis resulting from repair.

Histologic features

At histologic examination, medullary necrosis appears yellow with occasional flecks of calcium. A serpiginous capsule of grayish glistening collagen may surround the area of necrosis. Minor differences appear in the patterns of response for juxta-articular bone necrosis, but the pattern and sequence of events are similar to those of medullary necrosis. Beneath the articular cartilage in juxta-articular necrosis, the depth of the yellow necrotic marrow varies, and bone trabeculae are devoid of osteocytes. Vascular granulation tissue or grayish glistening collagen separates this dead tissue from underlying living bone. Within this border zone and some distance deep within it, dead bone trabeculae may be broadened by formation of new living bone on their surfaces. This process corresponds to the radiographic sclerotic line or mottled areas of increased opacity.

Trabecular fractures occur in the dead bone immediately beneath the subchondral plate, resulting in a radiographic crescent of subchondral lucency. Later, a wrinkle appears in the articular cartilage at the margin of the dead zone, followed by cracks and fissures leading to structural collapse.

Causes of osteonecrosis

Causes of osteonecrosis and associated conditions include the following:

• Trauma
• Idiopathic causes such as Legg-Calvé-Perthes disease
• Renal transplantation
• Increase in endogenous steroid levels, as in patients with Cushing syndrome
• Collagen vascular disorders such as systemic lupus erythematosus (SLE), rheumatoid arthritis, and scleroderma
• Hemoglobinopathies such as sickle cell disease and thalassemia
• Hemophilia
• Gaucher disease, Fabry disease
• Infection
• Pancreatitis
• Pregnancy
• Gout and hyperuricemia
• Diabetes
• Use of immunosuppressants and other drugs such as exogenous steroids, indomethacin, and phenylbutazone
• Alcohol use
• Dysbaric osteonecrosis
• Radiation therapy
• Arteritis

Frequency

United States

The overall incidence in the United States appears to be the same as that found internationally (see below).

International

Estimates of the rate of steroid-induced osteonecrosis range from 2-4% to more than 25%. AVN of the femoral head occurs in 60-75% of patients with femoral neck fractures, 25% of patients with hip dislocations, and 15-40% of patients with a slipped capital femoral epiphysis. Osteonecrosis is a complicating factor in 10-15% of patients with a scaphoid fracture. Osteonecrosis associated with SLE occurs in 5-6% of patients; some estimates are as high as 40%. Changes within the shoulder girdle are reported in 1-3% of patients undergoing radiation therapy for breast carcinoma.

Hyperlipidemia is demonstrated in 80% of patients with idiopathic osteonecrosis; approximately 60% and 40% of the cases of idiopathic osteonecrosis are associated with alcohol ingestion and hyperuricemia, respectively. The incidence of osteonecrosis after renal transplantation varies from 3-41%; usually, it is less than 20%. In deep-sea divers, the incidence is 5-10%. About 40-50% of patients with AVN of the talus have an associated talar fracture with a subtalar dislocation.

Mortality/Morbidity

Morbidity and mortality related to a bone infarct depend on the site of involvement, stage of disease, and possible complications.

• Secondary osteoarthritis develops after structural failure and collapse.
• Bone infarcts complicated by malignant degeneration are reported; these cases are associated with significant mortality.

Race

Bone infarct associated with sickle cell disease is common in black people of African origin. Bone infarcts associated with Gaucher disease are predominant in the Jewish population.

Sex

• Posttraumatic osteonecrosis is more common in young males than in other groups.
• Osteonecrosis related to an osteoporotic fracture is common in elderly women.
• Idiopathic osteonecrosis, such as is associated with Legg-Calvé-Perthes syndrome and slipped femoral capital epiphysis, is predominant in boys, with male-to-female ratios of 4:1 and 3:1, respectively.
• In adults, spontaneous osteonecrosis of the femoral head and sarcomas arising from bone infarct are more common in men than in women.
• Spontaneous osteonecrosis around the knee in adults is much more common in women than in men.
• AVN of the carpal lunate is common in males, with a male-to-female ratio of 2:1.

Age

• Idiopathic osteonecrosis related to Legg-Calvé-Perthes disease or slipped femoral capital epiphysis is seen in children aged 3-12 years or those aged 10-16 years, respectively.
• Spontaneous osteonecrosis in adults and malignant degeneration of bone infarct are common in persons aged 40-70 years.
• Osteochondritis dissecans affects adolescents.
• Posttraumatic osteonecrosis is more common in young adults, and osteonecrosis related to an osteoporotic fracture occurs in elderly women.
• Osteonecrosis of the second metatarsal head is common in those aged 10-20 years, and osteonecrosis of the lunate is common in those aged 10-30 years.
• AVN of the lunate is common in persons aged 20-40 years.

Anatomy

The blood supplies to the humeral and femoral heads, talus, and scaphoid bone are critical to the development of AVN at these sites (see Images below and Images 1-5 in Multimedia).

Presentation

Clinical features of bone infarct depend on the stage of the disease and the site of involvement. Patients with medullary infarcts are usually asymptomatic.¹ If present, symptoms are nonspecific in the early stages of the disease. Patients with juxta-articular lesions may have disability. Before the onset of structural failure and collapse, patients with juxta-articular bone infarcts are usually asymptomatic.

Localized pain is the most common presentation for both medullary and juxta-articular infarcts. Patients with juxta-articular infarcts can present with joint pain and limitation of movement. If unrecognized and untreated, the affected bone is liable to disintegrate further, with a consequent increase in pain and disability.

In sickle cell disease, the patient may present with severe bone and abdominal pain associated with sickle cell crisis.² In Legg-Calvé-Perthes syndrome and slipped femoral capital epiphysis, the presenting feature can be groin pain and limping, and the pain may be referred to the thigh and knee.³ In spontaneous osteonecrosis of the tibia, pain may be localized to the knee joint level, particularly over the medial condyle. Spontaneous osteonecrosis is often associated with pain, tenderness, swelling, and restriction of movement. In osteochondritis dissecans, symptoms may vary or be absent; it usually affects the non–weight-bearing surface of the medial femoral condyle.

Preferred Examination

Plain radiography is not sensitive in the detection of bone infarction. However, plain radiography has a role in the differential diagnosis. Radionuclide imaging and MRI are much more sensitive than plain radiography and may show changes caused by altered hemodynamics early in the course of disease. CT scanning is complementary to the other techniques, but it is not as sensitive as radionuclide imaging or MRI. CT scans may demonstrate subtle trabecular irregularity with bone necrosis when plain radiographic findings are normal. Ultrasonography may be useful in differentiating bone infarction from osteomyelitis in patients with sickle cell disease.^{4,5,6,7,8,9,10}

Limitations of Techniques

No radiologic findings are specific for bone infarction. A variety of pathologies may mimic bone infarction, including stress fractures, infections, inflammations, and metabolic and neoplastic processes. A bone infarct may mimic a bone tumor on imaging. The limitations apply to all imaging modalities, including plain radiography, radionuclide studies, CT, and MRI. However, when the global picture is considered, including the history, clinical findings, and course of events, the diagnosis can be achieved with the help of imaging in most patients.¹¹

Differential Diagnoses

Calcium Pyrophosphate Deposition Disease
Legg-Calve-Perthes Disease
Neuropathic Arthropathy (Charcot Joint)
Osteochondritis Dissecans
Stress Fracture

Other Problems to Be Considered

Inflammations
Metabolic and neoplastic processes
Fragmentation and collapse of the femoral head, which may be related to osteochondrosis (Legg-Calvé-Perthes syndrome) and hypothyroidism in younger patients
Transient osteoporosis in cases of spontaneous osteonecrosis of the knee
Secondary osteoarthritis

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