Suppr超能文献

用于研究关节软骨中机械诱导损伤起始和进展的数值模型。

A numerical model to study mechanically induced initiation and progression of damage in articular cartilage.

机构信息

Department of Biomedical Engineering, Gem-Z 4.101, Eindhoven University of Technology, PO Box 513, 5600 MB Eindhoven, The Netherlands.

出版信息

Osteoarthritis Cartilage. 2014 Jan;22(1):95-103. doi: 10.1016/j.joca.2013.10.010. Epub 2013 Nov 1.

Abstract

OBJECTIVE

Proteoglycan (PG) loss and surface roughening, early signs of osteoarthritis (OA), are likely preceded by softening of the ground substance and the collagen network. Insight in their relative importance to progression of OA may assist the development of treatment strategies for early OA. To support interpretation of experimental data, a numerical model is proposed that can predict damage progression in cartilage over time, as a consequence of excessive mechanical loading. The objective is to assess the interaction between ground substance softening and collagen fiber damage using this model.

DESIGN

An established cartilage mechanics model is extended with the assumption that excessive strains may damage the ground substance or the collagen network, resulting in softening of the overstrained constituent. During subsequent loading cycles the strain may or may not cross a threshold, resulting in damage to stabilize or to progress. To evaluate how softening of the ground substance and collagen may interact, damage progression is computed when either one of them, or both together are allowed to occur during stepwise increased loading.

RESULTS

Softening in the ground substance was predicted to localize in the superficial and transitional zone and resulted in cartilage softening. Collagen damage was most prominent in the superficial zone, with more diffuse damage penetrating deeper into the tissue, resulting in adverse strain gradients. Effects were more pronounced if both constituents developed damage in parallel.

CONCLUSION

Ground substance softening and collagen damage have distinct effects on cartilage mechanopathology, and damage in either one of them may promote each other.

摘要

目的

蛋白聚糖(PG)流失和表面粗糙,骨关节炎(OA)的早期迹象,很可能是由于基质和胶原网络变软所致。了解它们对 OA 进展的相对重要性可能有助于开发早期 OA 的治疗策略。为了支持实验数据的解释,提出了一个数值模型,该模型可以预测由于过度机械加载而导致软骨中损伤随时间的进展。目的是使用该模型评估基质软化和胶原纤维损伤之间的相互作用。

设计

用假设来扩展已建立的软骨力学模型,即过大的应变可能会损坏基质或胶原网络,从而导致过度应变的成分变软。在随后的加载循环中,应变可能会或不会超过阈值,从而导致损伤稳定或进展。为了评估基质和胶原的软化如何相互作用,当它们中的一个或两个在逐步增加的加载过程中被允许发生时,计算了损伤的进展情况。

结果

基质软化被预测会局限于浅层和过渡区,从而导致软骨软化。胶原损伤在浅层最为明显,更弥散的损伤会更深地穿透组织,导致不良的应变梯度。如果两个成分同时发生损伤,效果更为明显。

结论

基质软化和胶原损伤对软骨病理力学有明显的影响,它们中的任何一个损伤都可能相互促进。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验