作者: A. Robin Poole , G. Rizkalla , A. Reiner , M. Ionescu , E. Bogoch
DOI: 10.1007/978-4-431-68192-2_1
关键词:
摘要: Articular cartilage is carefully organized to provide an articulating surface that provides almost frictionless movement and the ability absorb dissipate compressive load resist tensile forces. The into zones, structures of which reflect mechanical forces acting upon cartilage. Type II collagen, together with type IX XI collagens, forms a fibrillar network throughout matrix secreted by chondrocytes. large aggregating proteoglycans smaller interact directly or indirectly this network. collagen can be degraded metalloproteinases produced In osteoarthritis, early damage seen at articular in upper mid-zone. It accompanied local loss proteoglycan small proteoglycans. Large exhibit degradative changes stage. With further progression disease, fibrillation occurs are lost replaced larger more intact molecules different glycosaminoglycan chains. Collagen now extends There also significant organization proteoglycans, decorin biglycan, osteoarthritic Overall, major reorganization net damage. We know proteases degrade both how their synthesis, secretion activity may stimulated. arthritis probably results from stimulation protease impaired fibril assembly although synthesis continues actively. Thus, key survival cartillage protection preservation inact Clearly, there no evidence but retention prevented when damaged.