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聚合物力学作为短期和与流动无关的软骨粘弹性模型

Polymer Mechanics as a Model for Short-Term and Flow-Independent Cartilage Viscoelasticity.

作者信息

June R K, Neu C P, Barone J R, Fyhrie D P

机构信息

Department of Cellular and Molecular Medicine, University of California, San Diego, San Diego, CA, 92093.

出版信息

Mater Sci Eng C Mater Biol Appl. 2011 May 10;31(4):781-788. doi: 10.1016/j.msec.2010.11.029.

DOI:10.1016/j.msec.2010.11.029
PMID:21552375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3087607/
Abstract

Articular cartilage is the load bearing soft tissue that covers the contacting surfaces of long bones in articulating joints. Healthy cartilage allows for smooth joint motion, while damaged cartilage prohibits normal function in debilitating joint diseases such as osteoarthritis. Knowledge of cartilage mechanical function through the progression of osteoarthritis, and in response to innovative regeneration treatments, requires a comprehensive understanding of the molecular nature of interacting extracellular matrix constituents and interstitial fluid. The objectives of this study were therefore to (1) examine the timescale of cartilage stress-relaxation using different mechanistic models and (2) develop and apply a novel (termed "sticky") polymer mechanics model to cartilage stress-relaxation based on temporary binding of constituent macromolecules. Using data from calf cartilage samples, we found that different models captured distinct timescales of cartilage stress-relaxation: monodisperse polymer reptation best described the first second of relaxation, sticky polymer mechanics best described data from ∼1-100 seconds of relaxation, and a model of inviscid fluid flow through a porous elastic matrix best described data from 100 seconds to equilibrium. Further support for the sticky polymer model was observed using experimental data where cartilage stress-relaxation was measured in either low or high salt concentration. These data suggest that a complete understanding of cartilage mechanics, especially in the short time scales immediately following loading, requires appreciation of both fluid flow and the polymeric behavior of the extracellular matrix.

摘要

关节软骨是覆盖在关节中长骨接触表面的承重软组织。健康的软骨能使关节运动顺畅,而受损的软骨会导致诸如骨关节炎等使人衰弱的关节疾病出现功能异常。要了解骨关节炎发展过程中以及对创新再生治疗作出反应时软骨的力学功能,就需要全面了解细胞外基质成分与组织液相互作用的分子本质。因此,本研究的目的是:(1)使用不同的力学模型研究软骨应力松弛的时间尺度;(2)基于组成大分子的临时结合,开发并应用一种新颖的(称为“粘性”)聚合物力学模型来描述软骨应力松弛。利用来自小牛软骨样本的数据,我们发现不同的模型捕捉到了软骨应力松弛的不同时间尺度:单分散聚合物链爬行最能描述松弛的前一秒,粘性聚合物力学最能描述约1至100秒松弛过程中的数据,而无粘性流体通过多孔弹性基质的模型最能描述100秒至平衡阶段的数据。在低盐或高盐浓度下测量软骨应力松弛的实验数据也进一步支持了粘性聚合物模型。这些数据表明,要全面理解软骨力学,尤其是在加载后的短时间尺度内,需要同时考虑流体流动和细胞外基质的聚合物行为。

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Adv Healthc Mater. 2021 May;10(9):e2002030. doi: 10.1002/adhm.202002030. Epub 2021 Mar 18.
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Aggrecan nanoscale solid-fluid interactions are a primary determinant of cartilage dynamic mechanical properties.聚集蛋白聚糖的纳米级固液相互作用是软骨动态力学性能的主要决定因素。
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本文引用的文献

1
Stress-relaxation behavior in gels with ionic and covalent crosslinks.具有离子交联和共价交联的凝胶中的应力松弛行为。
J Appl Phys. 2010 Mar 15;107(6):63509. doi: 10.1063/1.3343265. Epub 2010 Mar 23.
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A missense mutation in the aggrecan C-type lectin domain disrupts extracellular matrix interactions and causes dominant familial osteochondritis dissecans.一种聚集蛋白聚糖 C 型凝集素结构域的错义突变破坏细胞外基质相互作用,并导致显性家族性剥脱性骨软骨炎。
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Cartilage stress-relaxation is affected by both the charge concentration and valence of solution cations.软骨应力松弛受溶液阳离子的电荷浓度和价态影响。
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The structure and function of cartilage proteoglycans.软骨蛋白聚糖的结构与功能。
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Aggrecan, aging and assembly in articular cartilage.聚集蛋白聚糖、衰老与关节软骨中的组装
Cell Mol Life Sci. 2005 Oct;62(19-20):2241-56. doi: 10.1007/s00018-005-5217-x.
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The role of viscoelasticity of collagen fibers in articular cartilage: axial tension versus compression.胶原纤维粘弹性在关节软骨中的作用:轴向拉伸与压缩
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Separation of chondroitin sulfate from cartilage.从软骨中分离硫酸软骨素。
J Biol Chem. 1950 Aug;185(2):725-30.
9
Polymer dynamics as a mechanistic model for the flow-independent viscoelasticity of cartilage.聚合物动力学作为软骨非流动依赖粘弹性的一种机理模型。
J Biomech Eng. 2003 Oct;125(5):578-84. doi: 10.1115/1.1610019.
10
Collagen of articular cartilage.关节软骨的胶原蛋白。
Arthritis Res. 2002;4(1):30-5. doi: 10.1186/ar380. Epub 2001 Oct 5.