Developmet of a Tissue Analog for Cartilage Repair
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DEVELOAPMET OF A TISSUE ANALOG FOR CARTILAGE REPAIR. J.M. Pachence, (ABS LifeSciences, Inc., West Chester, PA), S.R. Frenkel, and H. Lin (Hospital for Joint Diseases/orthoaedic Institute, New York, NY).
ABSTRACT Purified type I collagen was formed into matrices whose pore sizes were defined on the basis of previous results. The first series of in vitro studies measured the metabolisa of cx•rdrvcytes grown in matrices with various pore sizes; results revealed that the growth rate was independent of the average matrix pore size, but that ckmdrocyte infiltration throughout the matrix was optimal for pore sizes of 100 to 150 un. In a second series of studies, type I collagen was combined with hyaluranic acid; the HyA/collagen matrices had little effect on chcrdrocyte cell growth versus A third set of in vitro studies used collagen the collagen matrices. matrices incorporating varying cornentrations of insulin-like growth factor. It was found that the IGF-l/collagen matrices can significantly effect the growth and metabolism of the clxrihrocytes. These experiments were vital in establishing the collagen matrix parameters which will be used in subsequent
in vivo studies.
It has been well documented that injured articular cartilage has only a limited ability for self-repair. As articular cartilage is relatively avascular and aneural, loss of the surface tissue will result in a permanently scarred site; lesions which fracture the subcondral bone, having a greater vascular supply, will undergo an inflammaticn/repair response, with the damaged site filling with fibrocartilage tissue [1]. In either case, function is Inxaired and chronic pain is the usual prognosis as the biochemical and bicaechacal characteristics of the cartilage have been altered. QCurrent treatment protocols call for surgical interventicrn (such as abrasion arthroplasty, excision and drilling, articular cartilage debridement, and arUrSOpic shaving) and will most often lead again to
inadequate repair.
Long-term morbidity such as degereration to arthritic
conditions will often result in patients with chronic cartilage problems. Nevertheless, it seems that articular cartilage does have some intrinsic ability to heal after injury; for example, choxdrocytes are capable of replication when isolated enzymatically from the cartilage matrix [2]. It has been suggested that cartilage repair can be initiated by either replication of ckxidrocytes in the regions adjacent to the defect, or by metaplasia of cftxirocytes from other coriective tissue sten cells within the joint capsule such as from the synovium and msubcldal bone [3]. Given this possibility, investigations of autograft or allograft tissue and tissue analogues to heal cartilage lesions has increased. Initial attempts at transplantation of dxindrocytes for the repair of whole or partial joints met with mixed results (4, 5]. For example, a number of investigators attempted to heal cartilage defects using chordrocytes isolated frao epiPhyseal plates, as well as articular cells, with the hypothesis that th
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