ABSTRACT. An animal model of steroid-induced avascular necrosis of the femoral head (SANFH) was established to investigate the roles of osteocyte apoptosis in this process. Forty five-month-old male and female Japanese white rabbits were randomly divided into groups A (hormone + endotoxin), B (hormone alone), C (endotoxin alone), and D (blank control). Animals were sacrificed two and four weeks following the final treatment (N = 5 for each group at each time point). Bilateral femoral heads were fixed and decalcified, and empty lacunae were counted by hematoxylin staining. At weeks 2 and 4, the empty lacunae percentage was significantly higher in group A than that in groups B, C, or D (P < 0.01), while no significant difference was observed between these latter three. At week 2, all osteocyte apoptosis indexes were within normal ranges in all the groups, which therefore did not significantly differ in this respect (P > 0.05). However, at week 4, the apoptotic index was significantly higher in group A than that in groups B, C, or D (P < 0.01), comparisons between which revealed no such differences. Moreover, a positive correlation was observed between the percentage of empty lacunae and the apoptotic index at week 4 in group A (r = 0.893). We conclude that osteocyte apoptosis plays an important role in SANFH.

ABSTRACT. An animal model of steroid-induced avascular necrosis of femoral head (SANFH) was established to investigate the role of oxidative DNA damage of bone marrow hematopoietic cells in SANFH. Forty-fivemonth-old Japanese white rabbits (male or female, 2.5 ± 0.5 kg) were randomly divided into groups A (methylprednisolone + Escherichia coli endotoxin), B (methylprednisolone alone), C (E. coli endotoxin alone), and D (blank control). The animals were sacrificed two and four weeks after administration of the last dose (N = 5 each group and each time). Left and right femoral heads were fixed and decalcified. Empty lacunae were counted by hematoxylin and eosin staining and oxidative DNA damage of bone marrow hematopoietic cells was detected by immunohistochemistry. At week 2, the rate of oxidative DNA damage in bone marrow hematopoietic cells was significantly higher in group A than in groups B, C, and D (P < 0.01), while there was no significant difference between groups B, C, and D. At week 4, the rate of oxidative DNA damage in bone marrow hematopoietic cells was significantly higher in group A than in groups B, C, and D (P < 0.01), while there was no significant difference among groups B, C, and D. Thus, oxidative DNA damage of bone marrow hematopoietic cells appears to play an important role in SANFH.