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糖化皮质骨的微观结构疲劳断裂行为

Microstructural fatigue fracture behavior of glycated cortical bone.

作者信息

Maghami Ebrahim, Najafi Ahmad

机构信息

Drexel University, Philadelphia, PA, USA.

出版信息

Med Biol Eng Comput. 2023 Nov;61(11):3021-3034. doi: 10.1007/s11517-023-02901-3. Epub 2023 Aug 16.

DOI:10.1007/s11517-023-02901-3
PMID:37582979
Abstract

The current study aims to simulate fatigue microdamage accumulation in glycated cortical bone with increased advanced glycation end-products (AGEs) using a phase field fatigue framework. We link the material degradation in the fracture toughness of cortical bone to the high levels of AGEs in this tissue. We simulate fatigue fracture in 2D models of cortical bone microstructure extracted from human tibias. The results present that the mismatch between the critical energy release rate of microstructural features (e.g., osteons and interstitial tissue) can alter crack initiation and propagation patterns. Moreover, the high AGEs content through the increased mismatch ratio can cause the activation or deactivation of bone toughening mechanisms under cyclic loading. The fatigue fracture simulations also show that the lifetime of diabetic cortical bone samples can be dependent on the geometry of microstructural features and the mismatch ratio between the features. Additionally, the results indicate that the trapped cracks in cement lines in the diabetic cortical microstructure can prevent further crack growth under cyclic loading. The present findings show that alterations in the materials heterogeneity of microstructural features can change the fatigue fracture response, lifetime, and fragility of cortical bone with high AGEs contents. Cortical bone models are created from microscopy images taken from the cortical cross-section of human tibias. Increased glycation contents in the cortical bone sample can change the crack growth trajectories.

摘要

当前的研究旨在使用相场疲劳框架模拟晚期糖基化终产物(AGEs)增加的糖化皮质骨中的疲劳微损伤积累。我们将皮质骨断裂韧性的材料降解与该组织中高水平的AGEs联系起来。我们在从人类胫骨提取的皮质骨微观结构的二维模型中模拟疲劳断裂。结果表明,微观结构特征(如骨单位和间质组织)的临界能量释放率之间的不匹配会改变裂纹萌生和扩展模式。此外,通过增加不匹配率,高AGEs含量会导致循环加载下骨强化机制的激活或失活。疲劳断裂模拟还表明,糖尿病皮质骨样本的寿命可能取决于微观结构特征的几何形状以及这些特征之间的不匹配率。此外,结果表明,糖尿病皮质微观结构中黏合线中的捕获裂纹可以在循环加载下阻止裂纹进一步扩展。目前的研究结果表明,微观结构特征的材料异质性变化会改变高AGEs含量皮质骨的疲劳断裂响应、寿命和脆性。皮质骨模型是根据从人类胫骨皮质横截面拍摄的显微镜图像创建的。皮质骨样本中糖化含量的增加会改变裂纹扩展轨迹。

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