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Strength of cancellous bone trabecular tissue from normal, ovariectomized and drug-treated rats over the course of ageing

去卵巢大鼠 骨质疏松症 松质骨 骨量减少 内分泌学 骨组织 内科学 替勃龙 医学 骨矿物 骨吸收 老化 骨病 雌激素 化学 解剖
作者
Laoise M. McNamara,A. G. H. Ederveen,Christopher Lyons,Christopher A. Price,Mitchell B. Schaffler,Harrie Weinans,Peter M. Prendergast
出处
期刊:Bone [Elsevier BV]
卷期号:39 (2): 392-400 被引量:70
标识
DOI:10.1016/j.bone.2006.02.070
摘要

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.
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