Orthopaedic Research Laboratory, Department of Orthopaedics and Traumatology, Odense University Hospital, Institute of Clinical Research, University of Southern Denmark, Odense, Denmark.
J Tissue Eng Regen Med. 2012 Jun;6(6):443-50. doi: 10.1002/term.448. Epub 2011 Jul 13.
In this study, 18 female skeletally mature sheep were randomly allocated into three groups of six each. Group 1 (glucocorticoid-1) received prednisolone treatment (0.60 mg/kg/day, five times weekly) for 7 months. Group 2 (glucocorticoid-2) received the same treatment regime followed by observation of 3 months without treatment. Group 3 was left untreated and served as controls. All sheep received a restricted diet with low calcium and phosphorus. At sacrifice, cortical bone samples from the femur midshaft of each sheep were harvested, micro-CT scanned and subjected to three-point bending and tensile strength testing. Bone collagen and mineral were determined. Cortical porosity was significantly increased in the glucocorticoid-2 compared with the glucocorticoid-1 and control groups. Apparent density was significantly decreased in the glucocorticoid-2 compared with the glucocorticoid-1 group. Collagen content was significantly increased in the glucocorticoid-2 compared with the glucocorticoid-1 and control groups. Bone mineral content did not differ between the groups. Neither the three-point bending mechanical properties nor the tensile mechanical properties differed significantly between the groups, while there was a trend towards decreasing bending mechanical properties in the glucocorticoid-2 group. In conclusion, 7 months of glucocorticoid treatment with malnutrition had a significant impact on the cortical microarchitecture of the sheep femur midshaft. These observed changes occurred 3 months after glucocorticoid cessation, suggesting a delayed effect of glucocorticoid on cortical bone. Thus, changes in cortical bone beyond cancellous bone might further increase fracture risk in patients treated with glucocorticoids. This model might be used as a glucocorticoid-induced osteoporotic model for orthopaedic biomaterial, joint prosthesis and medical device researches.
在这项研究中，18 只骨骼成熟的雌性绵羊被随机分为三组，每组 6 只。第 1 组（糖皮质激素 1）接受泼尼松龙治疗（0.60mg/kg/天，每周 5 次）7 个月。第 2 组（糖皮质激素 2）接受相同的治疗方案，然后观察 3 个月不治疗。第 3 组未接受治疗，作为对照。所有绵羊均接受低钙磷限制饮食。处死时，从每只绵羊的股骨中段采集皮质骨样本，进行微 CT 扫描，并进行三点弯曲和拉伸强度测试。测定骨胶原和矿物质。与糖皮质激素 1 组和对照组相比，糖皮质激素 2 组的皮质骨孔隙率显著增加。与糖皮质激素 1 组相比，糖皮质激素 2 组的表观密度显著降低。与糖皮质激素 1 组和对照组相比，糖皮质激素 2 组的胶原含量显著增加。各组间骨矿含量无差异。三组弯曲力学性能和拉伸力学性能无显著差异，而糖皮质激素 2 组弯曲力学性能呈下降趋势。结论：营养不良 7 个月的糖皮质激素治疗对绵羊股骨中段皮质微观结构有显著影响。这些观察到的变化发生在糖皮质激素停止后 3 个月，表明糖皮质激素对皮质骨有延迟作用。因此，接受糖皮质激素治疗的患者，皮质骨的变化可能会进一步增加骨折风险，而松质骨的变化可能会增加。这种模型可能被用作骨科生物材料、关节假体和医疗器械研究的糖皮质激素诱导骨质疏松模型。
