Increased perfusion of the femoral head in transient bone marrow edema syndrome.

The pathophysiology of transient bone marrow edema syndrome is not known. Ischemia has been suggested as the pathophysiologic factor, because the histologic findings are similar to those of early stage osteonecrosis. Angiographic studies of osteonecrotic femoral heads have shown arterial interruption and impaired perfusion. The current report describes the angiographic and scintigraphic findings of transient bone marrow edema syndrome of the hip in a 45-year-old man. The nutrient arteries were dilated, and the femoral head perfusion was increased compared with the unaffected contralateral side. These findings suggest that a vasomotor response plays a role in the pathogenesis of transient bone marrow edema syndrome. The disease might be a reversible process after temporary ischemia of the femoral head.