such as "Introduction", "Conclusion"..etc
Osteoarthritis (OA) has multiple causes and risk factors, but once the articular cartilage is lost, the joint fails. The collagen framework of adult cartilage is turned over very slowly and any severe damage appears to be irreversible and a critical step in the process of joint failure. There is growing evidence that proteolytic damage to cartilage collagen can occur very soon after joint injury (Lohmander et al., 2003).
The material strength and biological properties of articular cartilage depend heavily on its uniquely and extensively cross-linked collagen network and characteristic fibrillar organization that varies with tissue depth and proximity to the cells. Once laid down during development, there appears to be little capacity for articular chondrocytes to recapitulate the overall collagen architecture if the mature tissue is mechanically injured or goes through advanced stages of degeneration. The ability of chondrocytes to remodel the collagen at ultrastructural and molecular levels is poorly understood. There may be greater capacity than previously thought. Potential mechanisms for proteolytic remodelling and molecular repair are of growing interest (Eyre, 2002). In this review, we present what is known of the molecular organization of cartilage collagen as a basis for understanding mechanisms of normal growth, remodelling and potential replacement of the cartilage fibrillar matrix and its proteolytic destruction in osteoarthritis.
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