Department of Materials Science and Engineering, University of California, Berkeley, CA 94720, USA.
Proc Natl Acad Sci U S A. 2011 Aug 30;108(35):14416-21. doi: 10.1073/pnas.1107966108. Epub 2011 Aug 22.
The structure of human cortical bone evolves over multiple length scales from its basic constituents of collagen and hydroxyapatite at the nanoscale to osteonal structures at near-millimeter dimensions, which all provide the basis for its mechanical properties. To resist fracture, bone's toughness is derived intrinsically through plasticity (e.g., fibrillar sliding) at structural scales typically below a micrometer and extrinsically (i.e., during crack growth) through mechanisms (e.g., crack deflection/bridging) generated at larger structural scales. Biological factors such as aging lead to a markedly increased fracture risk, which is often associated with an age-related loss in bone mass (bone quantity). However, we find that age-related structural changes can significantly degrade the fracture resistance (bone quality) over multiple length scales. Using in situ small-angle X-ray scattering and wide-angle X-ray diffraction to characterize submicrometer structural changes and synchrotron X-ray computed tomography and in situ fracture-toughness measurements in the scanning electron microscope to characterize effects at micrometer scales, we show how these age-related structural changes at differing size scales degrade both the intrinsic and extrinsic toughness of bone. Specifically, we attribute the loss in toughness to increased nonenzymatic collagen cross-linking, which suppresses plasticity at nanoscale dimensions, and to an increased osteonal density, which limits the potency of crack-bridging mechanisms at micrometer scales. The link between these processes is that the increased stiffness of the cross-linked collagen requires energy to be absorbed by "plastic" deformation at higher structural levels, which occurs by the process of microcracking.
人类皮质骨的结构在多个长度尺度上从其基本组成部分——纳米尺度的胶原蛋白和羟磷灰石——发展到近毫米尺寸的骨单位结构，所有这些都为其力学性能提供了基础。为了抵抗断裂，骨骼的韧性本质上是通过结构尺度通常低于一微米的塑性（例如，纤维滑动）获得的，而外在则是通过较大结构尺度产生的机制（例如，裂纹偏转/桥接）获得的。衰老等生物因素会导致骨折风险明显增加，这通常与与年龄相关的骨量（骨量）损失有关。然而，我们发现与年龄相关的结构变化会显著降低多个长度尺度上的抗断裂能力（骨质量）。我们使用原位小角 X 射线散射和广角 X 射线衍射来表征亚微米结构变化，以及同步加速器 X 射线计算机断层扫描和原位断裂韧性测量在扫描电子显微镜中以表征微米尺度的影响，我们展示了这些不同尺寸尺度的与年龄相关的结构变化如何降低骨骼的内在和外在韧性。具体来说，我们将韧性的损失归因于非酶促胶原蛋白交联的增加，这抑制了纳米尺度的塑性，以及骨单位密度的增加，这限制了微米尺度上裂纹桥接机制的效力。这些过程之间的联系是，交联胶原蛋白的增加刚性需要通过更高结构水平的“塑性”变形来吸收能量，这是通过微裂纹过程发生的。
