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Bone toughening through stress-induced non-collagenous protein denaturation

机译:通过应激诱导的非胶原蛋白变性骨骼增韧

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摘要

Bone toughness emerges from the interaction of several multiscale toughening mechanisms. Recently, the formation of nanoscale dilatational bands and hence the accumulation of submicron diffuse damage were suggested as an important energy dissipation processes in bone. However, a detailed mechanistic understanding of the effect of this submicron toughening mechanism across multiple scales is lacking. Here, we propose a new three-dimensional ultrastructure volume element model showing the formation of nanoscale dilatational bands based on stress-induced non-collagenous protein denaturation and quantify the total energy released through this mechanism in the vicinity of a propagating crack. Under tensile deformation, large hydrostatic stress develops at the nanoscale as a result of local confinement. This tensile hydrostatic stress supports the denaturation of non-collagenous proteins at organic-inorganic interfaces, which leads to energy dissipation. Our model provides new fundamental understanding of the mechanism of dilatational bands formation and its contribution to bone toughness.
机译:骨骼韧性出现了几种多尺度增韧机制的相互作用。最近,纳米级扩张带的形成并因此建议亚微米漫射损伤的积累作为骨中的重要能量耗散过程。然而,缺乏对多个尺度跨越多个尺度的亚微米增韧机制的影响的详细机械理解。这里,我们提出了一种新的三维超微结构体积元素模型,显示基于应激诱导的非胶原蛋白变性的纳米级扩张带的形成,并通过该机制在传播裂缝附近进行量化的总能量。在拉伸变形下,由于局部限制,在纳米级上发生大的静压应力。这种拉伸静压应力支持有机无机界面处的非胶原蛋白的变性,这导致能量耗散。我们的型号为扩张频段形成的机制及其对骨骼韧性的贡献提供了新的基础知识。

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