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首页> 外文期刊>Osteoarthritis and cartilage >Viscoelasticity of the articular cartilage surface in early osteoarthritis
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Viscoelasticity of the articular cartilage surface in early osteoarthritis

机译：早期骨关节炎中关节软骨表面的粘弹性

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Objective: Structural and biochemical changes in articular cartilage occur throughout the pathogenesis of osteoarthritis (OA). Early changes include proteoglycan loss and collagen network disorganization at or near the articular surface. These changes accompany reductions in mechanical properties of cartilage, yet the relationships between mechanics and structure in early OA are poorly defined. Thus, the overall goal of this work was to measure changes in the microscale mechanics and structure of the articular surface in an . in vivo model of OA to better understand the early pathogenesis of cartilage degeneration in this disease. Design: A canine cranial cruciate ligament transection (CCL x) model was used. The contralateral joint served as an internal control (Ctl). The frequency dependence of the dynamic indentation modulus (E *) was evaluated, and creep behavior was measured to estimate the instantaneous (E i,inst) and equilibrium (E i,eq) indentation moduli and longest creep time-constant (τ). These functional parameters were related to microscopic metrics of cartilage structure and biochemistry, measured by polarized light microscopy and digital densitometry of proteoglycan staining by safranin-O. Results: CCL x and Ctl cartilage exhibited frequency sensitivity. E i,inst, E i,eq, and τ were lower in CCL x vs Ctl cartilage. These mechanical changes were accompanied by a reduction in superficial zone thickness and changes in superficial zone collagen organization, as well as a non-significant reduction in superficial zone proteoglycan staining. Conclusions: Changes in the microscale viscoelastic behavior of the cartilage surface are a functional hallmark of early OA that accompany significant changes to the microstructural organization of the collagenous extracellular matrix.
机译：目的：在整个骨关节炎（OA）的发病机理中都发生了关节软骨的结构和生化变化。早期的变化包括在关节表面处或附近的蛋白聚糖损失和胶原网络的混乱。这些变化伴随着软骨力学性能的降低，但早期OA的力学与结构之间的关系却定义不清。因此，这项工作的总体目标是测量关节的微观结构和关节表面结构的变化。 OA的体内模型可以更好地了解这种疾病的软骨退变的早期发病机理。设计：使用犬颅十字形韧带横断（CCL x）模型。对侧关节用作内部控制（Ctl）。评估了动态压痕模量（E *）的频率依赖性，并测量了蠕变行为，以估算瞬时压痕模量（E i，inst）和平衡压痕（E i，eq）和最长蠕变时间常数（τ）。这些功能参数与软骨结构和生化的微观指标有关，通过偏光显微镜和番红蛋白-O进行蛋白聚糖染色的数字密度法测量。结果：CCL x和Ctl软骨表现出频率敏感性。在CCL x中，E i，inst，E i，eq和τ低于Ctl软骨。这些机械变化伴随着表层厚度的减少和表层胶原组织的变化，以及表层蛋白聚糖染色的无明显减少。结论：软骨表面的微尺度粘弹性行为的变化是早期OA的功能标志，伴随着胶原细胞外基质的微结构组织的显着变化。

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