DNA oxidative damage to bone marrow hematopoietic cells and apoptosis of osteocytes in early avascular necrosis of the femoral head induced by glucocorticoids

Zhao Zhen-qun; Liu Wan-lin; Gong Yu-lin; Bai Rui; Wang Wen-xuan

doi:10.3969/j.issn.2095-4344.2015.11.003

Abstract：BACKGROUND:Hormones-induced avascular necrosis of the femoral head is a complex biological process, and its pathogenesis remains unclear. To prove its etiologic mechanism is stil the focus of research in this field. OBJECTIVE:To discuss the pathological changes of hematopoietic cels and osteocytes in early avascular necrosis of the femoral head induced by glucocorticoids . METHODS: Forty Japanese white rabbits, 4 months old, were randomly divided into glucocorticoids+ lipopolysaccharide group (combination group), glucocorticoids group, lipopolysaccharide group and blank control group, with 10 rabbits in each group. Five animals from each group were sacrificed at 2 and 4 weeks after the last dosing, respectively. Vacant bone lacunae were counted under optical microscope, morphology of osteocytes was observed under electron microscope, osteocyte apoptosis was assay by TUNEL, and DNA oxidative damage to hematopoietic cels was detected by immunohistochemistry. <br> RESULTS AND CONCLUSION:Compared with the other three groups, the rates of vacant lacunae and DNA oxidative damage to hematopoietic cels in the combination group were significantly higher at 2 and 4 weeks after treatment as wel as the apoptosis rate of osteocytes at 4 weeks after treatment (P < 0.01); while there were no statistical differences between the other three groups. In the combination group, the vacant rate of bone lacunae and apoptosis rate of osteocytes were positively correlated (r=0.793). These findings indicate that DNA oxidative damage to hematopoietic cels and apoptosis of osteocytes participate in the pathological changes of early avascular necrosis of the femoral head induced by glucocorticoids. The former is prior to the latter, and the death manner of osteocytes is apoptosis.