Cx43 expression in the femur of rabbit models of steroid-induced vascular necrosis of the femoral head / 中国组织工程研究

ABSTRACT

BACKGROUND:The mechanism of steroid-induced avascular necrosis of the femoral head is stil unclear, Cx43 protein as the main gap junction in bone tissue, through transmitting information between osteoblasts, regulates bone cel growth and differentiation, compensatory bone increase or decrease. The relationship between Cx43 protein and steroid-induced avascular necrosis of the femoral head is stil rarely reported. OBJECTIVE:To explore the changes in Cx43 expression in rabbit models of steroid-induced vascular necrosis of the femoral head. METHODS:Forty New Zealand rabbits were equal y and randomly divided into model group and control group. Rabbits in the model group were used to establish models of steroid-induced avascular necrosis of the femoral head using endotoxin and hormone. Rabbits in the control group were injected with the same volume of physiological saline at the same time points. RESULTS AND CONCLUSION:At 4 weeks after model establishment, hematoxylin-eosin staining results revealed that in the model group, the trabecula became thin and distributed disorderly in the femoral subchondral area. Empty lacuna increased significantly. Adipocytes increased. Hematopoietic cel s in medul ary cavity apparently diminished. In the control group, trabecula arranged orderly and empty lacuna could be seen. Bone marrow cel s were abundant, but adipocytes were less. Immunohistochemical method demonstrated that Cx43 protein expression was observed in osteoblasts of the edge of trabecula, cytoplasm of osteoblasts of trabecula, and bone marrow stromal cel s. Western blot assay results showed that alkaline phosphatase and Cx43 protein expression was lower in the model group than in the control group (P<0.05). Results indicated that Cx43 protein expression decreased in the model rabbits, which may be the key link of the occurrence and development of steroid-induced avascular necrosis of the femoral head.