Knorpelschaden und Gonarthrose

G. Spahn1
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Abstract

. Abstract Articular cartilage homoeostasis is critical for joint function. The steady state homoeostasis of articular cartilage matrix composits (above all collagen type II and proteoglycans) is a balance be-tween anabolic morphogens such as cartilage derived morpho-genetic proteins. Cartilage composites of superficial tangential zone, middle zone, deep radial zone, tide mark and subchondral bone. The superior zone is rich on radial orientated collagen fibers. This causes a high mechanical resistance against pressure and shear forces. The deep layers contain more proteoglycans and water. This creates a preload for the collagen fibers as well as neutralizes pressure forces too. The matrix turnover is regulated by cytokines which activate matrix metalloproteinases. The biomechanical property of cartilage is characterized by vis-coelasticity. Cartilage degeneration is caused by the increase of katabolic processes. There is a decrease of matrix composites like collagen type II and proteoglycans. The increases of water content products the edema and the chondrocytes become apoptop-tically. This is conformed by a decreased mechanical resistance. The cartilage defects results from this loss of mechanical properties. Secondary are damages within the subchondral bone and the synovia. This is characteristically for the osteoarthritis.
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软骨损伤和喉炎
. 关节软骨的平衡对关节的功能至关重要。关节软骨基质复合物(尤其是II型胶原和蛋白聚糖)的稳态稳态是合成代谢形态因子(如软骨衍生的形态发生蛋白)之间的平衡。浅表切线带、中间带、深放射状带、潮痕和软骨下骨的软骨复合材料。上区富含径向取向的胶原纤维。这导致了对压力和剪切力的高机械阻力。深层含有更多的蛋白聚糖和水。这为胶原纤维创造了一个预负荷,同时也中和了压力。细胞因子可激活基质金属蛋白酶,调节基质的周转。软骨的生物力学特性以可见共弹性为特征。软骨变性是由代谢过程增加引起的。II型胶原和蛋白聚糖等基质复合材料减少。水含量的增加导致水肿和软骨细胞凋亡。这与减小的机械阻力相一致。软骨缺损就是由于机械性能的丧失而造成的。其次是软骨下骨和滑膜内的损伤。这是骨关节炎的特征。
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