Eswaran Senthil K, Allen Matthew R, Burr David B, Keaveny Tony M
Orthopaedic Biomechanics Laboratory, Department of Mechanical Engineering, University of California, Berkeley, CA 94720, USA.
J Biomech. 2007;40(15):3424-31. doi: 10.1016/j.jbiomech.2007.05.013. Epub 2007 Jul 5.
This study addressed the effects of changes in trabecular microarchitecture induced by suppressed bone turnover-including changes to the remodeling space-on the trabecular bone strength-volume fraction characteristics independent of changes in tissue material properties. Twenty female beagle dogs, aged 1-2 years, were treated daily with either oral saline (n=10 control) or high doses of oral risedronate (0.5mg/kg/day, n=10 suppressed) for a period of 1 year, the latter designed (and confirmed) to substantially suppress bone turnover. High-resolution micro-CT-based finite element models (18-mum voxel size) of canine trabecular bone cores (n=2 per vertebral body) extracted from the T-10 vertebrae were analyzed in both compressive and torsional loading cases. The same tissue-level material properties were used in all models, thus providing measures of tissue-normalized strength due only to changes in the microarchitecture. Suppressed bone turnover resulted in more plate-like architecture with a thicker and more dense trabecular structure, but the relationship between the microarchitectural parameters and volume fraction was unaltered (p>0.05). Though the suppressed group had a greater tissue-normalized strength as compared to the control group (p<0.001) for both compressive and torsional loading, the relationship between tissue-normalized strength and volume fraction was not significantly altered for compression (p>0.13) or torsion (p>0.09). In this high-density, non-osteoporotic animal model, the increases in tissue-normalized strength seen with suppression of bone turnover were entirely commensurate with increases in bone volume fraction and thus, no evidence of microarchitecture-related or "stress-riser" effects which may disproportionately affect strength were found.
本研究探讨了骨转换受抑制所诱导的小梁微结构变化——包括重塑空间的变化——对小梁骨强度-体积分数特征的影响,该影响独立于组织材料特性的变化。20只1 - 2岁的雌性比格犬,每天分别口服生理盐水(n = 10只作为对照组)或高剂量的阿仑膦酸钠(0.5mg/kg/天,n = 10只作为骨转换受抑制组),持续1年,后者旨在(并已证实)大幅抑制骨转换。对从T - 10椎体提取的犬小梁骨芯(每个椎体2个)的基于高分辨率显微CT的有限元模型(体素大小为18μm)进行压缩和扭转加载情况分析。所有模型均使用相同的组织水平材料特性,从而仅根据微结构变化提供组织标准化强度的测量值。骨转换受抑制导致小梁结构更呈板状,小梁结构更厚且更致密,但微结构参数与体积分数之间的关系未改变(p>0.05)。尽管在压缩和扭转加载情况下,与对照组相比,骨转换受抑制组具有更高的组织标准化强度(p<0.001),但对于压缩(p>0.13)或扭转(p>0.09),组织标准化强度与体积分数之间的关系未发生显著改变。在这个高密度、非骨质疏松的动物模型中,骨转换受抑制时所观察到的组织标准化强度增加与骨体积分数的增加完全相称,因此,未发现可能对强度产生不成比例影响的微结构相关或“应力集中器”效应的证据。