New paradigms for relating the microstructure of cartilage to its large scale mechanics: The Roles of Rigidity-Percolation and Double Gel Network Structure in Non-Linear Response

软骨是一种覆盖在关节骨骼上的光滑组织，是一种非凡的材料，可以持续数十年，并以其独特的材料特性组合胜过任何人造物质。软骨的微观结构有几个方面有助于其长寿。首先，产生这些机械性能的基质由两个互穿聚合物网络组成，这种设计最近已被证明可以抑制裂纹的形成。其次，软骨的机械特性随深度而变化，使得能量阻尼几乎完全发生在其表面附近的薄区域中。 PI最近开发了一种理论模型，解释了聚合物网络浓度的变化如何导致能量吸收定位到组织表面。该项目使用一系列实验技术来测试该模型，并将其适用性扩展到软骨可能受损的极端变形。通过对组织进行化学处理以去除必要的分子成分，并在不存在这些成分的情况下测试组织反应，PI将确定基质的哪些元素对于产生软骨独特的机械特性组合是必不可少的。 更好地了解软骨力学特性的大分子起源将有助于深入了解关节炎等疾病的发展，指导组织修复治疗方法，更广泛地说，为制造能够承受极端载荷的坚固材料提供机械设计标准。关节软骨具有独特的材料特性，使其能够承受每年数百万次的载荷循环，同时保护底层组织。其压缩特性的结构和成分起源已经知道了几十年。然而，有没有相应的理解与其剪切行为的基本机制。最近，研究人员介绍了刚性渗流理论，以前建立的重组聚合物网络的属性，解释软骨剪切力学的线性响应。这个理论是，所观察到的软骨的剪切模量的数量级变化来自于在刚性渗透阈值附近保持平衡的基质成分的小浓度差异。此外，该理论对非线性剪切行为的分子机制做出了新的预测，并对生物化学和机械损伤引起的机械变化提供了新的见解。这个项目将测试这些预测，并确定是否可以使用刚性渗滤作为一个新的范例，关节软骨的机械剪切性能的大分子起源。具体而言，使用化学和机械降解技术，预测模型的关键细胞外基质元素，引起软骨的宏观力学性能将进行测试。最后，这个项目将扩展模型的适用性，以描述软骨的微观结构是如何改变的，当它被剪切超出线性政权。

Cartilage, the smooth tissue that coats bones in joints, is a remarkable material that can last decades and outperform any man-made substance in its unique combination of material properties. There are several aspects of cartilage's microstructure that contribute to its longevity. First, the matrix that gives rise to these mechanical properties is comprised of two interpenetrating polymer networks, a design that has recently been shown to inhibit crack formation. Second, the mechanical properties of cartilage change with depth such that energy damping occurs almost entirely in a thin region near its surface. The PIs have recently developed a theoretical model that explains how variations in the concentration of the polymer networks lead to this localization of energy absorption to the tissue surface. This project uses an array of experimental techniques to test this model and extend its applicability to extreme deformations where cartilage can be damaged. By chemically treating the tissue to remove essential molecular components and testing the tissue response in their absence, the PIs will determine which elements of the matrix are essential for generating cartilage's unique combination of mechanical properties. A better understanding of the macromolecular origins of cartilage mechanical properties will give insight into how diseases such as arthritis develop, guide approaches to tissue repair therapies, and more broadly, provide mechanical design criteria for fabrication of robust materials that can endure extreme loading.Articular cartilage has unique material properties that enable it to endure millions of loading cycles per year while protecting underlying tissues. The structural and compositional origins of its compressive properties have been known for decades. However, there is no equivalent understanding of the underlying mechanisms associated with its shear behavior. Recently the investigators introduced a rigidity percolation theory, previously established to explain the properties of reconstituted polymer networks, to explain the linear response of cartilage shear mechanics. This theory is that the observed orders of magnitude variation in the shear modulus of cartilage arises from small concentration differences of matrix constituents that are poised near a rigidity percolation threshold. Furthermore, the theory makes novel predictions about molecular mechanisms of non-linear shear behavior and gives new insight into mechanical changes that occur from biochemical and mechanical damage. This project will test these predictions and determining if rigidity percolation can be used as a new paradigm for the macromolecular origins of the mechanical shear properties of articular cartilage. Specifically, using chemical and mechanical degradation techniques, predictions made by the model about the critical extracellular matrix elements that give rise to cartilage's macroscale mechanical properties will be tested. Finally, this project will extend the applicability of the model to describe how the microscopic structure of cartilage is altered when it is sheared beyond the linear regime.