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纳米级增韧机制在骨质疏松症中的作用。

The role of nanoscale toughening mechanisms in osteoporosis.

作者信息

Thurner Philipp J, Katsamenis Orestis L

机构信息

Institute for Lightweight Design and Structural Biomechanics, Vienna University of Technology, Gusshausstrasse 27-29 A-1040, Vienna, Austria,

出版信息

Curr Osteoporos Rep. 2014 Sep;12(3):351-6. doi: 10.1007/s11914-014-0217-0.

Abstract

Strength is the most widely reported parameter with regards to bone failure. However, bone contains pre-existing damage and stress concentration sites, perhaps making measures of fracture toughness more indicative of the resistance of the tissue to withstand fracture. Several toughening mechanisms have been identified in bone, prominently, at the microscale. More recently, nanoscale toughness mechanisms, such as sacrificial-bonds and hidden-length or dilatational band formation, mediated by noncollagenous proteins, have been reported. Absence of specific noncollagenous proteins results in lowered fracture toughness in animal models. Further, roles of several other, putative influencing, factors such as closely bound water, collagen cross-linking and citrate bonds in bone mineral have also been proposed. Yet, it is still not clear if and which mechanisms are hallmarks of osteoporosis disease and how they influence fracture risk. Further insights on the workings of such influencing factors are of high importance for developing complementary diagnostics and therapeutics strategies.

摘要

强度是关于骨失效报道最为广泛的参数。然而,骨中存在预先存在的损伤和应力集中部位,这或许使得断裂韧性的测量更能体现组织抵抗骨折的能力。已在骨中识别出几种增韧机制,显著的是在微观尺度上。最近,由非胶原蛋白介导的纳米尺度增韧机制,如牺牲键以及隐藏长度或膨胀带的形成,也已被报道。在动物模型中,特定非胶原蛋白的缺失会导致断裂韧性降低。此外,还提出了其他一些假定的影响因素的作用,如紧密结合水、胶原蛋白交联以及骨矿物质中的柠檬酸盐键。然而,目前仍不清楚是否以及哪些机制是骨质疏松症的特征,以及它们如何影响骨折风险。对这些影响因素作用机制的进一步深入了解对于开发补充性诊断和治疗策略至关重要。

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