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首页> 外文期刊>IFAC PapersOnLine >Coupling cellular phenotype and mechanics to understand extracellular matrix formation and homeostasis in osteoarthritis * * financial support through BMBF project OVERLOAD-PrevOp, grant number 01EC1408H is acknowledged.
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Coupling cellular phenotype and mechanics to understand extracellular matrix formation and homeostasis in osteoarthritis * * financial support through BMBF project OVERLOAD-PrevOp, grant number 01EC1408H is acknowledged.

机译：耦合细胞表型和力学机制以了解骨关节炎中的细胞外基质形成和体内稳态 * * 通过BMBF项目OVERLOAD-PrevOp提供资金支持，授予号码01EC1408H被确认。

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Abstract: Osteoarthritis of the knee is a common degenerative disease during aging. It is typically caused by articular cartilage degeneration. Cartilage, which is located between bone surfaces, is a viscoelastic material aiming to absorb, redirect and transmit mechanical forces during movement. Without the cartilages’ buffering capacity, bones come into direct contact inducing severe pain up to the stage where affected individuals loose mobility. The mechanisms of cartilage remodeling are poorly understood, and there is currently no effective method to reconstitute damaged cartilage. Cartilage consists of extracellular matrix (ECM) and a low density of cells (chondrocytes), which generate matrix proteins. The composition of the matrix gives the cartilage specific viscoelastic properties, which are sensed by chondrocytes feeding back on ECM remodeling. The aim of this study is to build a mathematical model that couples mechanical ECM properties with chondrocyte phenotype in the upkeep of cartilage homeostasis. We model the viscoelastic properties of the cartilage in terms of a linear Kelvin-Voigt model, where the dampening ratio feeds back on the phenotypic switching behaviour in chondrocytes. The chondrocytes, depending on their phenotypic state, may either produce proteoglycans or collagens or both, which alters the viscoelastic properties of the cartilage. We formulate a coupled system of equations integrating mechano-sensitive phenotypic switching behaviour of chondrocytes with respect to ECM remodelling. We define cartilage homeostasis as the fixed point of the derived systems of equations. Using this framework we can reproduce the long term changes in cartilage composition during aging.
机译：摘要：膝骨关节炎是衰老过程中常见的变性疾病。它通常是由关节软骨变性引起的。位于骨表面之间的软骨是一种粘弹性材料，旨在吸收，重定向和传递运动过程中的机械力。没有软骨的缓冲能力，骨头直接接触会引起严重的疼痛，直至受影响的个体失去活动能力。软骨重塑的机制了解甚少，目前还没有有效的方法来重建受损的软骨。软骨由细胞外基质（ECM）和低密度的细胞（软骨细胞）组成，可产生基质蛋白。基质的组成赋予了软骨特定的粘弹性质，软骨细胞在ECM重塑时反馈，可以感知软骨的粘弹性质。这项研究的目的是建立一个数学模型，将机械ECM特性与软骨稳态中软骨细胞表型结合起来。我们用线性Kelvin-Voigt模型对软骨的粘弹性进行建模，其中阻尼比反馈软骨细胞的表型转换行为。软骨细胞，根据其表型状态，可能产生蛋白聚糖或胶原蛋白，或两者都产生，从而改变软骨的粘弹性。我们制定了一个耦合的方程式系统，整合了软骨细胞相对于ECM重塑的机械敏感表型转换行为。我们将软骨动态平衡定义为导出的方程组的不动点。使用此框架，我们可以再现衰老过程中软骨成分的长期变化。

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