Intraosseous Arterial Architecture in Nontraumatic Avascular Necrosis of the Femoral Head

Abstract

To determine the vascular architecture of nontraumatic avascular necrosis of the femoral head (ANFH), 38 femoral heads procured from 31 ANFH patients were studied by microangiographic and histologic methods. Microangiography showed that the head was consistently stratified into three zones: the normal vascular, the reparative vascular, and the avascular. Microangiographic abnormalities were closely correlated with the histologic changes in each zone. The extent of the necrotic area proved to depend on the extent and number of involved intraosseous nutrient arteries. Circumscribed necrosis accompanied interruption of the lateral epiphyseal arteries in their intracapital portion. Extensive necrosis resulted from multiple vascular involvement, which included not only the lateral epiphyseal arteries, but also the superior and inferior metaphyseal arteries. Histologic examination of different levels of the nutrient arteries revealed many intraosseous pathologic vascular changes in apposition to the ischemic episode of the femoral head. Interruption of the blood supply causing ANFH occurs in the intracapital arteries probably because of vascular wall damage, and the extent of necrosis depends on the number of the involved nutrient arteries and their proximity to the intracapital site of origin.

Effects of pulse methylprednisolone on bone and marrow tissues. Corticosteroid‐induced osteonecrosis in rabbits

“…First, the histopathologic features of ON in this model are characterized by empty lacunae accompanied by surrounding bone marrow cell necrosis and such resultant reparative changes as granulation tissue and appositional bone formation. These features are analogous to those in humans (5, [18][19][20]27). Second, the multifocal nature of the ON, which includes the femoral condyle and humerus, is also similar to that in humans (5-7).…”

“…In this study, we succeeded for the first time in process (5, [18][19][20]27). Since the relationship between the occurrence of ON and the systemic administration of corticosteroids was first reported in 1957 (4), there have been several experiments that demonstrated many steroid-related histopathologic and pathophysiologic alterations in the bone tissue, such as fat embolism (21,22), an increased pressure of bone marrow in the femoral head (24), an enlargement of the fat cell size (15), and an accumulation of lipid within the osteocytes (1 6).…”

“…The histologic features of ON in humans are characterized by the subchondral necrotic area in the femoral head, namely, osteocytic death resulting in empty lacunae and surrounding bonc marrow necrosis. which commonly accompany the reparative responseappositional bone formation, vascular-rich or cellular granulation tissue, and the infiltration of chronic inflammatory cells-around the necrotic region (3,5, [18][19][20]29). This reparative process depends on the clinical course, including the time after ON onset, steroid treatment, and other factors (18)(19)(20).…”

“…Many experimental studies using corticosteroids have suggested the possible pathogenesis of corticosteroid-induced ON, such as an enlargement of the size of fat cells (15), an accumulation of lipid within the osteocytes (16), and fat emboli (12,13,15,17). However, to our knowledge, the studies have never succeeded in developing histologically definitive ON (18)(19)(20) in animals by the injection of corticosteroids alone (15,16,(21)(22)(23)(24)(25). Perhaps the studies were focusing exclusively on the epiphyseal regions of the femoral and humeral heads that result in subchondral collapse, and were not thoroughly evaluating the metaphyseal and diaphyseal regions.…”

Microvascular obstruction in avascular necrosis Immunohistochemistry of 14 femoral heads

“…However, the nature and the exact location of blood flow obstructions remain controversial (Hungerford and Lennox 1985, Spencer and Brookes 1988, Ohzono et al 1992.…”