Effects of glucocorticoids on fracture healing in rats
- VernacularTitle:糖皮质激素对大鼠骨折愈合方式的影响
- Author:
Xiang GAO
;
Zhijun PAN
;
Rongxin HE
;
Jianwei WANG
- Publication Type:Journal Article
- Keywords:
Glucocorticoids;
Fracture healing;
Collagen type Ⅱ
- From:
Chinese Journal of Pathophysiology
2010;26(3):577-580
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To explore the effects of glucocorticoids on fracture healing in a rat model of tibial fracture. METHODS: Sixty three months old female SD rats were divided into control and glucocorticoid-treated group. A glucocorticoid-induced osteoporosis model was established by intramuscular injection of prednisolone acetate (5 mg·kg~(-1)·d~(-1) for 3 weeks), in which the tibial was osteotomized by a wire saw as fracture healing model and internal fixed with a Kirschner pin. The rats were scarified at different time points after operation. The callus formation was monitored over a period of 6 weeks by histological method, bone mineral density (BMD) detection and biomechanical examination. Western blotting was used to measure the expression of type II collagen. RESULTS: A glucocorticoid-induced osteoporosis model was successfully established and conformed by BMD measurement. The formation of primary callus was observed in both groups 3 days after fracture. At 2 weeks after injury, the glucocorticoid-treated group had a lower BMD and less cartilage matrix as compared to control group. An increase in bone callus and chondrogenesis was observed at 4 to 6 weeks after fracture in glucocorticoid-treated group as compared to control group. The expression of type II collagen was delayed in glucocorticoid-treated group. Biomechanical measurement showed that the actual maximum load was increased by 35.8% in control group as compared to glucocorticoid-treated group at 6th week. CONCLUSION: These results indicate that chondrogenesis and transformation from cartilage callus to bony callus are delayed by glucocorticoids. The retardation of collagen Ⅱ production may be the reason for the inhibition of fracture healing.
