Abstract:

BACKGROUND: Avascular necrosis of femoral head can lead to femoral head collapse or hip impairment, but the precise etiological factor and pathogenesis remain poorly understood. Therefore, it is an important mean to study glucocorticoid-induced avascular necrosis of femoral head by establishing animal models.
OBJECTIVE: To establish a stable animal model for glucocorticoid-induced avascular necrosis of femoral head in rabbits, and to explore the mechanism of osteonecrosis femoral head.
METHODS: Healthy adult New Zealand white rabbits were randomly divided into 4 groups. Control group: intramuscular injection of normal saline. Hormone group: hip muscular injection of methyllprednisolone three times. Single endotoxin group: injection of endotoxin followed by three times injections of methyllprednisolone after 24 hours. Double endotoxin group: twice injection of endotoxin and three times injections of methyllprednisolone. X-ray, MRI imaging, histopathological examination, as well as transmission electron microscope were performed prior to and after operation. The rate of empty lacunae was calculated. 
RESULTS AND CONCLUSION: The rate of empty lacunae in the hormone, single endotoxin and double endotoxin groups were obviously increased than that of the control group at 8 weeks after model preparation (P < 0.01), especially highest in the double endotoxin group (P < 0.01). Compared with the hormone and single endotoxin groups, the femoral head osteonecrosis in the double endotoxin group presented earlier and seriously, and the osteonecrosis increased with time prolonged. The findings demonstrated that twice endotoxin injection combined with three times hormone injection induced osteonecrosis of femoral head early and obviously. The rate of the empty lacunae increased with time prolonged.