Osteonecrosis

Ischemic necrosis of bone is a condition that is secondary to diminished or disrupted blood supply, often subchondral bone, leading to cell death and tissue breakdown. An identical process occurring in the diaphysis or metaphysis of a bone sometimes is called a bone infarct. The pathogenesis of ischemic necrosis of bone is incompletely understood. The deficient blood supply may be secondary to occlusion of arteries, veins, or sinusoidal vessels. Whatever the cause, many believe that a vascular incident may lead to bone marrow edema or hemorrhage, resulting in increased intraosseous pressure, ischemia, and necrosis.

Causes of osteonecrosis include: (1) trauma, (2) systemic disease, (3) steroids, (4) arthritis (increased intracapsular pressure), and (5) idiopathic.

The hip is the most common site of traumatically induced ischemic necrosis, which may be caused by a fracture of the femoral neck or a hip dislocation (Fig. 42). Posttraumatic necrosis also may be seen in the scaphoid, the lunate, and the dome of the talus. Legg-Calve-Perthes disease in a child (Fig. 4) and the idiopathic necrosis of the adult hip (Fig. 71) are additional examples of osteonecrosis. Atraumatic osteonecrosis is bilateral in 50 to 80% of the patients.

Bone infarction is a common finding in the diaphysis and metaphysis of long bones, most frequently in patients receiving corticosteroids and in those with sickle cell anemia. These infarctions appear as irregular regions of marrow calcifications.

Plain film findings of osteonecrosis in an epiphysis occur late in the course of the disease. Early signs are "cystlike" lesions or the "subchondral crescent sign". In addition, segmental collapse of the subchondral bone may be seen.

Bone scan is a most sensitive method to demonstrate osteonecrosis of the femoral head in the immediate posttraumatic period or when a joint effusion is present. MRI also can demonstrate the osteonecrosis at an early stage (Fig. 71), and sequences obtained after intravenous administration of a gadolinium compound play an important role in the assessment of revascularization (Fig. 4).

Niels Egund, Kjell Jonsson, Holger Pettersson and Donald Resnick