Fracture resistance of human cortical bone across multiple length-scales at physiological strain rates.
Fracture resistance of human cortical bone across multiple length-scales at physiological strain rates.
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DOI：
10.1016/j.biomaterials.2014.03.066
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发表时间：
2014-07
期刊：
影响因子：
14
通讯作者：
E. Zimmermann;B. Gludovatz;E. Schaible;B. Busse;R. Ritchie
中科院分区：
文献类型：
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作者：
E. Zimmermann;B. Gludovatz;E. Schaible;B. Busse;R. Ritchie
虽然大多数骨的骨力学研究都是在低应变率下进行的，但生理性骨折总是发生在较高的加载速率下。在这里，在10 - 5到10 - 1 s-1的应变速率下，我们研究了骨的变形和断裂，在小的长度尺度上使用原位小角X射线散射（SAXS）来研究矿化胶原纤维的变形，并通过骨力学实验在微观结构水平上研究通过裂纹尖端屏蔽产生韧性的增韧机制。我们的研究结果表明，随着应变率的增加，骨韧性降低，因为裂纹以较高的应变率穿透骨单位，而不是在骨水泥线处偏转，这是骨在低应变率下的主要增韧机制。较高应变率下不存在裂纹偏转机制与较低的内在骨基质韧性一致。在SAXS实验中，在较高的应变速率下较高的原纤应变表明较少的非弹性变形，从而支持较低的内在韧性。由高应变速率引起的断裂发生率增加可能与由应变速率引起的原纤维延展性硬化引起的基质韧性损失有关，即，粘性滑动和牺牲性结合机制的“锁定”，这是小长度尺度下骨中非弹性变形（和韧性）的起源。
While most fracture-mechanics investigations on bone have been performed at low strain rates, physiological fractures invariably occur at higher loading rates. Here, at strain rates from 10−5to 10−1s−1, we investigate deformation and fracture in bone at small length-scales usingin situsmall-angle x-ray scattering (SAXS) to study deformation in the mineralized collagen fibrils and at the microstructural level via fracture-mechanics experiments to study toughening mechanisms generating toughness through crack-tip shielding. Our results show diminished bone toughness at increasing strain rates as cracks penetrate through the osteons at higher strain rates instead of deflecting at the cement lines, which is a prime toughening mechanism in bone at low strain rates. The absence of crack deflection mechanisms at higher strain rates is consistent with lower intrinsic bone matrix toughness. In the SAXS experiments, higher fibrillar strains at higher strain rates suggest less inelastic deformation and thus support a lower intrinsic toughness. The increased incidence of fracture induced by high strain rates can be associated with a loss in toughness in the matrix caused by a strain rate induced stiffening of the fibril ductility,i.e., a “locking-up” of the viscous sliding and sacrificial bonding mechanisms, which are the origin of inelastic deformation (and toughness) in bone at small length-scales.