Abstract:

BACKGROUND: Slather of glucocorticoid (GC) is the most common non-traumatic cause for necrosis of the femoral head. Though there are close association between GC and necrosis of the femoral head, the underlying mechanisms remain unclear.
OBJECTIVE: To establish an experimental model of avascular necrosis of the femoral head (ANFH) caused by corticosteroid in adult rabbits and to observe the metabolism of fatty substance.
METHODS: Twenty healthy Japanese rabbits were randomly divided into the control and the experiment groups. In the experiment group, ANFH was induced by injection of horse serum and a high dose of corticosteroid. In the control group, normal saline was injection with the same volume. Contents of total cholesterol (TC) and triacylglycerol (TG) of the blood serum were measured at 2, 4, 6 and 8 weeks after injection. Animals were sacrificed at 2, 4 and 6 weeks and the pathological changes were detected with hematoxylin-eosin staining. Digital radiography (DR) and computed tomography (CT) were performed at 8 weeks before killing the remaining rabbits.
RESULTS AND CONCLUSION: In experiment group: DR showed bilaterally decreased bone density, an unclear epiphyseal line, and blurred texture of cancellous bone. CT showed spot-like low-density imaging of cancellous bone, thinner cortical bone, osteoporosis, and an unclear epiphyseal line. Hematoxylin-eosin staining of pathological sections showed fewer trabeculae and thin bone, an increased proportion of empty osteocyte lacunae, decreased hematopoiesis, thrombosis, and fat cell hypertrophy. No obviously change was found in the control group. The contents of TC and TG in experiment group were increased after model preparation (P < 0.05), which was apparently greater than that of the control group (P < 0.01). Rabbit model of ANFH can be successfully established by combination of horse serum and corticosteroid. Metabolic disorder of fatty substance is a very important pathogenesis of steroid-induced avascular necrosis of femoral head.