## 5 Degradation of Articular Cartilage
The lesions formed in the superficial zone of the AC extend into the deeper layers, resulting in the formation of vertical fissures, increased calcification, and the presence of doubled flow markers. Osteoarthritis leads to significant changes in the mechanical properties of the AC. One of the most important parameters used to assess the biomechanics of this tissue is aggregate modulus. It has been found that in AC affected by OA, the value of this parameter decreases, which may indicate a weakening of the structure of the extracellular matrix, and more precisely, the degradation of proteoglycans and the loss of the ability to transfer loads [291]. Another parameter that decreases with the occurrence of OA is the compressive Young's modulus. The decrease in the value of this parameter is related to the degradation of proteoglycans and increased tissue hydration. As a result, the ECM structure is weakened and the ability to transfer loads is lost. The decrease in E\({}_{\text{C}}\) is estimated to be about 55-68% compared to healthy AC [321]. Collagen structure damage and loss of matrix integrity are reflected in increased hydraulic permeability values. The literature indicates an increase in this parameter by about 60-80% [322]. A slight increase is also noted in the Poisson's ratio, which may indicate changes in the AC structure as well as increased susceptibility to deformation [12]. During OA, the collagen network is damaged and its tensile strength is lost, which is reflected in a reduction of E\({}_{\text{t}}\) by up to 90% [152]. E\({}_{\text{eq}}\) is also reduced by about 40-80%, which also confirms the weakening of the collagen structure and its reduced ability to regenerate [323; 324]. In the course of OA, the integrity of the collagen network is disturbed, as a result of which the risk of cracks and mechanical damage increases. This is reflected in a decrease in the value of the tensile strength parameter [287]. Reduced values are also observed for the complex shear modulus. It is estimated that this parameter decreases by about 70-80%, which increases the susceptibility to shear deformations and reduces the ability to absorb loads [321]. Progression of OA is associated with a significant reduction in the ability of the AC to withstand long-term shear loads, which compromisesthe mechanical stability of the joint. This is reflected by a reduction in \(\rm G_{eq}\). Moreover, OA increases viscosity while reducing AC elasticity, which translates into a reduced ability to transfer mechanical loads and thus increases the shear loss angle. Figure 3 shows a comparison of selected parameters of healthy AC versus AC affected by OA. Age has a significant impact on the composition of the ECM, the spatial organisation of chondrocytes and their response to environmental stimuli, including cytokines [325]. The total number of chondrocytes in the AC does not change, although changes in their distribution within individual zones are observed [2]. With age, the cells tend to disperse in the surface layer, while there is an increased density in the deeper layers. A decrease in the mitotic and synthetic activity of chondrocytes is also observed [129; 326]. The response of chondrocytes to anabolic factors in the form of IFG-I is weakened. This may be related to the increased expression of IGF-binding proteins, which limits the availability of the factor for chondrocyte receptors [327; 328]. The described changes impair the ability to maintain matrix homeostasis and increase the susceptibility to degradation. Ageing of AC is associated with a decrease in its hydration, which increases the compressive stiffness of the matrix. The loss of AC's ability to reversibly deform may ultimately lead to greater loads on the underlying subchondoral bone. It is therefore crucial to maintain the homeostasis of the extracellular matrix environment for the integrity and function of AC.