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DOI: 10.1055/s-2006-924754
Georg Thieme Verlag KG Stuttgart · New York
Knorpelschaden und Gonarthrose
Teil I: Physiologie und Pathophysiologie des Knorpels und der Gonarthrose Part I: Physiology and Pathophysiology of Cartilage and KneeCartilage Lesions and GonarthritisPublication History
Publication Date:
02 January 2007 (online)
Zusammenfassung
Die Funktion des hyalinen Knorpels hängt entscheidend von der Homöostase der chondralen Matrixbestandteile (vor allem Kollagen II und Proteoglykane) ab. Dieses Gleichgewicht wird durch die abgestimmte Steuerung von Synthese- und Abbauprozessen der Matrixbestandteile gewährleistet. Knorpel ist ein mehrschichtiges Gewebe: oberflächliche Tangentialschicht, mittlere Schicht, Radiärschicht, Tidemark und subchondraler Knochen. Die oberflächliche Schicht ist reich an zur Oberfläche ausgerichteten Kollagenfasern und damit sehr resistent gegenüber den auftretenden Druck- und Scherkräften. Die tieferen Schichten enthalten Proteoglykane in hoher Konzentration, diese binden Wasser und bewirken so die Vorspannung für die Kollagenfasern und können vor allem auftretende Druckkräfte neutralisieren. Der Matrix-Turnover wird hauptsächlich durch Zytokine und die damit verbundene Aktivierung von Matrix-Metallo-Proteasen gesteuert. Charakteristisch für den Knorpel ist die viskoelastische Reaktion auf Belastung. Im Rahmen der Knorpeldegeneration kommt es zum Überwiegen kataboler Prozesse in dessen Folge der Kollagen-II- und Proteoglykangehalt sinkt. Wassereinstrom führt zum Knorpelödem und die Chondrozyten werden apoptotisch. Das führt zur Verminderung der mechanischen Belastbarkeit, infolgedessen Knorpelschäden unterschiedlicher Schweregrade entstehen. Sekundäre Schäden am subchondralen Knochen und der Synovia führen schließlich zur Arthrose.
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 between anabolic morphogens such as cartilage derived morphogenetic 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 viscoelasticity. 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 apoptoptically. 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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