Altered architecture and cell populations affect bone marrow mechanobiology in the osteoporotic human femur.

Altered architecture and cell populations affect bone marrow mechanobiology in the osteoporotic human femur.
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结构和细胞群的改变影响骨质疏松人类股骨的骨髓力学生物学。

DOI:
10.1007/s10237-016-0856-4
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发表时间:
2017
影响因子:
3.5
通讯作者:
Niebur,GlenL
Niebur,GlenL
中科院分区:
工程技术2区
文献类型:
--
作者:
Metzger,ThomasA;Vaughan,TedJ;McNamara,LaoiseM;Niebur,GlenL

文献摘要

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骨质疏松症中骨小梁孔隙率的增加不仅影响骨的强度和刚度,还可能影响骨的机械生物学反应。骨小梁和骨髓之间的机械相互作用是机械生物学信号的来源之一,因为骨髓中的许多细胞群是机械敏感的。然而,由于骨小梁的长度尺度和几何复杂性,测量这种相互作用的力学是困难的。在这项研究中,一个多尺度的计算方案,结合高分辨率,组织水平,流体-结构相互作用模拟与离散细胞水平的模型被应用到表征骨小梁孔隙率和骨髓成分对骨髓机械生物学在人股骨的潜在影响。首先,四个不同体积分数(BV/TV)的组织水平的模型进行循环压缩,以确定在骨髓中的连续水平的剪切应力。将计算的应力应用于三个详细的模型,其中包含单个细胞并具有不同的脂肪细胞分数。在组织水平上,骨沿着其主要机械轴的压缩在骨髓中引起范围从2.0到5.6 Pa的剪切应力,其随着骨体积分数和应变率而增加。剪切应力在细胞水平上被放大,超过90%的非脂肪细胞经历比施加的组织水平应力更高的剪切应力。当脂肪细胞体积分数(AVF)从30%(如年轻健康骨髓中所见)增加到45%或60% AVF时,最大剪切应力降低了20%,这通常见于骨质疏松患者。结果表明,增加AVF对骨髓中的机械生物学信号的影响与体积分数降低相似。
Age-related increases in trabecular bone porosity, as seen in osteoporosis, not only affect the strength and stiffness, but also potentially the mechanobiological response of bone. The mechanical interaction between trabecular bone and bone marrow is one source of mechanobiological signaling, as many cell populations in marrow are mechanosensitive. However, measuring the mechanics of this interaction is difficult, due to the length scales and geometric complexity of trabecular bone. In this study, a multi-scale computational scheme incorporating high-resolution, tissue-level, fluid–structure interaction simulations with discrete cell-level models was applied to characterize the potential effects of trabecular porosity and marrow composition on marrow mechanobiology in human femoral bone. First, four tissue-level models with different volume fractions (BV/TV) were subjected to cyclic compression to determine the continuum level shear stress in the marrow. The calculated stress was applied to three detailed models incorporating individual cells and having differing adipocyte fractions. At the tissue level, compression of the bone along its principal mechanical axis induced shear stress in the marrow ranging from 2.0 to 5.6 Pa, which increased with bone volume fraction and strain rate. The shear stress was amplified at the cell level, with over 90% of non-adipocyte cells experiencing higher shear stress than the applied tissue-level stress. The maximum shear stress decreased by 20% when the adipocyte volume fraction (AVF) increased from 30%, as seen in young healthy marrow, to 45 or 60% AVF typically found in osteoporotic patients. The results suggest that increasing AVF has similar effects on the mechanobiological signaling in bone marrow as decreased volume fraction.