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GENERAL PRINCIPLES OF BONE ISCHEMIA

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The pathophysiological consequence of bone ischemia is avascular necrosis (osteonecrosis) or bone infarction. Interruption of the blood supply to the bone can result from acute thrombosis, trauma, an underlying vascular disease, or a predisposing osseous disorder. A process that leads to elevation of the intramedullary pressure (e.g., pyogenic infection) can impede perfusion to the point that ischemic necrosis occurs. In addition to infection, conditions that are commonly associated with ischemic bone disease in children include sickle cell disease, steroid therapy, trauma, hemophilia, irradiation, collagen vascular disease, Gaucher disease, and Cushing syndrome. Various sites in the pediatric skeleton can also be involved with idiopathic ischemic necrosis; the most common of these is the hip, that is, Legg-Calvé-Perthes disease. Ischemia in the developing epiphysis of a child can result in growth disturbance due to chondrocyte injury or death in the germinal zone of the primary physis and in the physis of the secondary ossification center. The term ischemic necrosis generally refers to involvement of an epiphysis or subarticular area, whereas bone infarct indicates the consequence of ischemia in the metaphysis or diaphysis.

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The pathophysiological consequences of bone infarction tend to follow a similar sequence, irrespective of the cause of ischemia and the site of skeletal involvement. The ischemic insult leads to death of the cellular components of the bone. There is subsequent revascularization, reossification, and concomitant resorption of dead bone. The radiographic appearance of infarcted bone is indistinguishable from that of viable bone. Potential findings in this acute phase include local soft tissue swelling or osteoporosis adjacent to the necrotic bone due to disuse or hyperemia. Skeletal scintigraphy and MR allow accurate diagnosis of bone ischemia in the early, radiographically occult, phase.

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Beginning several days to several weeks after the ischemic event, radiographs often show increased radiodensity in the involved portion of bone. Several mechanisms apparently contribute to this finding. As described above, there may be apparent increase in density due to regional demineralization of adjacent structures. True increased radiodensity of the ischemic bone occurs during revascularization, as new bone is laid down on residual ischemic trabeculae. Eventual resorption of the nonviable bone may result in a return to normal radiodensity. Increased density of ischemic bone can also be caused by collapse and compression of necrotic trabeculae. Focal areas of diminished radiodensity often occur in response to bone ischemia, usually due to revascularization and resorption of necrotic bone. Radiolucent areas may also occur due to fibrosis or extension of cartilage into the bone.

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The earliest MR findings of bone ischemia are increased diffusion in the involved marrow and lack of normal contrast enhancement. There is often local soft tissue edema. Within a few days, marrow edema causes diminished signal on T1-weighted images and slightly elevated signal intensity on fat-suppressed T2-weighted images. The lack of contrast enhancement persists until revascularization. In the subacute to late stages, MR shows reactive changes at the ...

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