McNamara L M, Ederveen A G H, Lyons C G, Price C, Schaffler M B, Weinans H, Prendergast P J
Trinity Centre for Bioengineering, School of Engineering, Trinity College, Dublin, Ireland.
Bone. 2006 Aug;39(2):392-400. doi: 10.1016/j.bone.2006.02.070. Epub 2006 Apr 27.
Hormone therapy (HT) drugs and bisphosphonates prevent osteoporosis by inhibiting osteoclastic bone resorption. However, the effects of osteoporosis and anti-resorptive drugs on the mechanical behavior of the bone tissue constituting individual trabeculae have not yet been quantified. In this study, we test the hypothesis that the mechanical properties of bone trabecular tissue will differ for normal, ovariectomized and drug-treated rat bones over the course of ageing. Microtensile testing is carried on individual trabeculae from tibial bone of ovariectomized (OVX) rats, OVX rats treated with tibolone and placebo-treated controls. The method developed minimizes errors due to misalignment and stress concentrations at the grips. The local mineralization of single trabeculae is compared using micro-CT images calibrated for bone mineral content assessment. Our results indicate that ovariectomy in rats increases the stiffness, yield strength, yield strain and ultimate stress of the mineralized tissue constituting trabecular bone relative to normal; we found significant differences (P < 0.05) at 14, 34 and 54 weeks of treatment. These increases are complemented by a significant increase in the mineral content at the tissue level, although overall bone mineral density and mass are reduced. With drug treatment, the properties remain at, or slightly below, the placebo-treated controls levels for 54 weeks. The higher bone strength in the OVX group may cause the trabecular architecture to adapt as seen during osteopenia/osteoporosis, or alternately it may compensate for loss of trabecular architecture. These findings suggest that, in addition to the effects of osteoporosis and subsequent treatment on bone architecture, there are also more subtle processes ongoing to alter bone strength at the tissue level.
激素疗法（HT）药物和双膦酸盐通过抑制破骨细胞的骨吸收来预防骨质疏松症。然而，骨质疏松症和抗吸收药物对构成单个小梁的骨组织力学行为的影响尚未得到量化。在本研究中，我们检验了这样一个假设：在衰老过程中，正常、去卵巢和药物治疗的大鼠骨骼的骨小梁组织力学性能会有所不同。对去卵巢（OVX）大鼠、用替勃龙治疗的OVX大鼠和接受安慰剂治疗的对照组大鼠胫骨的单个小梁进行微拉伸测试。所开发的方法将由于夹具处的不对准和应力集中而导致的误差降至最低。使用经校准用于骨矿物质含量评估的微型计算机断层扫描（micro-CT）图像比较单个小梁的局部矿化情况。我们的结果表明，与正常大鼠相比，大鼠去卵巢会增加构成骨小梁的矿化组织的刚度、屈服强度、屈服应变和极限应力；我们发现在治疗14、34和54周时存在显著差异（P<0.05）。尽管总体骨矿物质密度和质量降低，但这些增加伴随着组织水平矿物质含量的显著增加。经过药物治疗，这些性能在54周内保持在安慰剂治疗对照组水平或略低于该水平。OVX组较高的骨强度可能会导致骨小梁结构如在骨质减少/骨质疏松症期间所见那样发生适应性改变，或者它可能会补偿骨小梁结构的丧失。这些发现表明，除了骨质疏松症及其后续治疗对骨结构的影响外，在组织水平上还存在更微妙的过程在改变骨强度。
