Abstract
The limited healing response of articular cartilage has been reported for over three centuries (Hunter 1743; Paget 1853). Healing of cartilage depends on blood clot formation as a provisional matrix for cell migration and a subsequent cascade of chondroprogenitor cells derived from adjacent cartilage, underlying marrow, or synovium, which eventually leads to the formation of reparative tissue in the defect (Buckwalter et al. 1988; Johnson 1991). The persistence of full thickness chondral defects in the articular surface (i.e. those that do not initially penetrate the subchondral bone) is multifactorial: the lack of blood supply, insufficient fibrin clot formation at the area of injury (Buckwalter et al. 1988; Mankin et al. 1994), the low mitotic activity of chondrocytes, inhibition of synovial cell attachment (Langer and Gross 1974), and stimulation of degrading enzymes (Mankin 1982). It is the variability of the repair process that contributes to the difficulty in predicting results of cartilage repair (Buckwalter et al. 1990).
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Nehrer, S., Spector, M. (2000). Tissue Engineering in Cartilage Repair: In Vitro and In Vivo Experiments on Cell-Seeded Collagen Matrices. In: Grifka, J., Ogilvie-Harris, D.J. (eds) Osteoarthritis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-87752-0_10
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DOI: https://doi.org/10.1007/978-3-642-87752-0_10
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