Articular cartilage is a complex structure with an architecture in which fluid-swollen proteoglycans constrained within a 3D network of collagen fibrils. Because of the complexity of the cartilage structure, the relationship between its mechanical behaviours at the macroscale level and its components at the micro-scale level are not completely understood.ududThe research objective in this thesis is to create a new model of articular cartilage that can be used to simulate and obtain insight into the micro-macro-interaction and mechanisms underlying its mechanical responses during physiological function. The new model of articular cartilage has two characteristics, namely: i) not use fibre-reinforced composite material idealization ii) Provide a framework for that it does probing the micro mechanism of the fluid-solid interaction underlying the deformation of articular cartilage using simple rules of repartition instead of constitutive / physical laws and intuitive curve-fitting.ududEven though there are various microstructural and mechanical behaviours that can be studied, the scope of this thesis is limited to osmotic pressure formation and distribution and their influence on cartilage fluid diffusion and percolation, which in turn governs the deformation of the compression-loaded tissue.ududThe study can be divided into two stages. In the first stage, the distributions and concentrations of proteoglycans, collagen and water were investigated using histological protocols. Based on this, the structure of cartilage was conceptualised as microscopic osmotic units that consist of these constituents that were distributed according to histological results. These units were repeated three-dimensionally to form the structural model of articular cartilage. In the second stage, cellular automata were incorporated into the resulting matrix (lattice) to simulate the osmotic pressure of the fluid and the movement of water within and out of the matrix; following the osmotic pressure gradient in accordance with the chosen rule of repartition of the pressure.ududThe outcome of this study is the new model of articular cartilage that can be used to simulate and study the micromechanical behaviours of cartilage under different conditions of health and loading. These behaviours are illuminated at the microscale level using the socalled neighbourhood rules developed in the thesis in accordance with the typical requirements of cellular automata modelling. Using these rules and relevant Boundary Conditions to simulate pressure distribution and related fluid motion produced significant results that provided the following insight into the relationships between osmotic pressure gradient and associated fluid micromovement, and the deformation of the matrix. For example, it could be concluded that: 1. It is possible to model articular cartilage with the agent-based model of cellular automata and the Margolus neighbourhood rule.udud2. The concept of 3D inter connected osmotic units is a viable structural model for the extracellular matrix of articular cartilage.udud3. Different rules of osmotic pressure advection lead to different patterns of deformation in the cartilage matrix, enabling an insight into how this micromechanism influences macromechanical deformation.udud4. When features such as transition coefficient were changed, permeability (representing change) is altered due to the change in concentrations of collagen, proteoglycans (i.e.ududdegenerative conditions), the deformation process is impacted.udud5. The boundary conditions also influence the relationship between osmotic pressure gradient and fluid movement at the micro-scale level.ududThe outcomes are important to cartilage research since we can use these to study the microscale damage in the cartilage matrix. From this, we are able to monitor related diseases and their progression leading to potential insight into drug-cartilage interaction for treatment. This innovative model is an incremental progress on attempts at creating further computational modelling approaches to cartilage research and other fluid-saturated tissues and material systems.
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机译：关节软骨是具有复杂结构的结构，其中液体溶胀的蛋白聚糖被限制在胶原纤维的3D网络内。由于软骨结构的复杂性，人们尚未完全了解其在宏观水平上的力学行为与在微观水平上的成分之间的关系。 ud ud本论文的研究目的是建立一种新的关节模型可以用来模拟并获得对微宏相互作用及其在生理功能过程中机械反应基础的机理的了解的软骨。新的关节软骨模型具有两个特征，即：i）不使用纤维增强的复合材料理想化； ii）提供一个框架，使它确实使用简单的规则来探究关节软骨变形背后的流固相互作用的微观机理。 ud ud尽管可以研究各种微观结构和力学行为，但本文的研究范围仅限于渗透压的形成和分布及其对软骨液的影响扩散和渗滤，进而控制受压组织的变形。 ud ud这项研究可以分为两个阶段。在第一阶段，使用组织学方案研究蛋白聚糖，胶原蛋白和水的分布和浓度。基于此，将软骨的结构概念化为微观渗透单元，该渗透单元由根据组织学结果分布的这些成分组成。这些单元在三维上重复，以形成关节软骨的结构模型。在第二阶段，将细胞自动机整合到生成的基质（晶格）中，以模拟流体的渗透压以及水在基质内外的移动。根据所选的压力分配规则遵循渗透压梯度。 ud ud这项研究的结果是一种新的关节软骨模型，可用于模拟和研究不同健康状况下软骨的微机械行为。和加载。根据细胞自动机建模的典型要求，使用本文中开发的邻域规则在微观尺度上阐明了这些行为。使用这些规则和相关的边界条件来模拟压力分布和相关的流体运动产生了重要的结果，为渗透压梯度和相关的流体微运动与基质变形之间的关系提供了以下见解。例如，可以得出以下结论：1.可以使用基于代理的细胞自动机模型和Margolus邻域规则来建模关节软骨。 3D互连渗透单元的概念是关节软骨细胞外基质的可行结构模型。渗透压对流的不同规则导致软骨基质变形的方式不同，从而使人们能够深入了解这种微观机制如何影响宏观力学变形。 ud ud4。当诸如过渡系数之类的特征发生变化时，由于胶原蛋白，蛋白聚糖的浓度（即 ud uddegeneration性条件）的变化，通透性（代表变化）也发生了变化，从而影响了变形过程。边界条件还在微观水平上影响渗透压梯度与流体运动之间的关系。 ud ud结局对于软骨研究很重要，因为我们可以使用这些结果来研究软骨基质中的微观损伤。由此，我们能够监控相关疾病及其进展，从而潜在地了解药物-药物相互作用以进行治疗。这种创新模型是在尝试创建用于软骨研究以及其他流体饱和的组织和材料系统的进一步的计算建模方法时所取得的进步。
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