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首页> 外文期刊>Journal of Biomechanics >Failure of mineralized collagen fibrils: Modeling the role of collagen cross-linking.
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Failure of mineralized collagen fibrils: Modeling the role of collagen cross-linking.

机译:矿化胶原蛋白原纤维的失效:模拟胶原蛋白交联的作用。

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摘要

Experimental evidence demonstrates that collagen cross-linking in bone tissue significantly influences its deformation and failure behavior yet difficulties exist in determining the independent biomechanical effects of collagen cross-linking using in vitro and in vivo experiments. The aim of this study is to use a nano-scale composite material model of mineral and collagen to determine the independent roles of enzymatic and non-enzymatic cross-linking on the mechanical behavior of a mineralized collagen fibril. Stress-strain curves were obtained under tensile loading conditions without any collagen cross-links, with only enzymatic cross-links (modeled by cross-linking the end terminal position of each collagen domain), or with only non-enzymatic cross-links (modeled by random placement of cross-links within the collagen-collagen interfaces). Our results show enzymatic collagen cross-links have minimal effect on the predicted stress-strain curve and produce a ductile material that fails through debonding of the mineral-collagen interface. Conversely, non-enzymatic cross-links significantly alter the predicted stress-strain response by inhibiting collagen sliding. This inhibition leads to greater load transfer to the mineral, which minimally affects the predicted stress, increases modulus and decreases post-yield strain and toughness. As a consequence the toughness of bone that has more non-enzymatically mediated collagen cross-links will be drastically reduced.
机译:实验证据表明,骨组织中的胶原蛋白交联会显着影响其变形和破坏行为,但在使用体外和体内实验确定胶原蛋白交联的独立生物力学效果方面存在困难。这项研究的目的是使用矿物质和胶原蛋白的纳米级复合材料模型来确定酶促和非酶促交联对矿化胶原蛋白原纤维力学行为的独立作用。应力-应变曲线是在拉伸载荷条件下获得的,没有任何胶原蛋白交联,仅具有酶促交联(通过交联每个胶原蛋白域的末端位置进行建模),或者仅具有非酶促交联(进行了建模)通过在胶原蛋白-胶原蛋白界面内随机放置交联键)。我们的结果表明,酶促胶原蛋白交联对预测的应力-应变曲线的影响最小,并产生了一种可延展的材料,该材料会由于矿物-胶原蛋白界面的脱粘而失效。相反,非酶交联通过抑制胶原蛋白的滑动显着改变了预期的应力-应变反应。这种抑制会导致更大的载荷传递到矿物上,从而最小程度地影响预测应力,增加模量并降低屈服后应变和韧性。结果,具有更多非酶介导的胶原蛋白交联的骨骼的韧性将大大降低。

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