S A Fenwick1, P J Gregg, P Rooney. 1. Glenfield Hospital NHS Trust, University of Leicester, Groby Road, Leicester, LE3 9QP.
Abstract
OBJECTIVE: To determine whether human osteoarthritic (OA) cartilage loses its ability to remain avascular when placed into the in-vivo model of angiogenesis, the chick embryo chorio-allantoic membrane (CAM), and to determine specific changes that occur in the cartilage matrix when the cartilage is exposed to an active vasculature. DESIGN: Articular cartilage from OA and non-OA joints was grafted onto the CAM for up to 5 days before fixing and processing for histological, histochemical and immunological examination for specific changes in proteoglycan and collagen. RESULTS: OA cartilage, but not non-OA cartilage, showed invasion of its matrix by blood vessels from the CAM to various extents. Associated with these blood vessels was a loss of staining for proteoglycans and cartilage specific glycosaminoglycans (GAG). A deposition of collagen types I and X was also visualized around the invasive vessels. CONCLUSIONS: OA cartilage loses or has already lost its ability to remain avascular when placed onto the chick CAM. Changes occur in the matrix around the invasive blood vessels, specifically a loss of proteoglycan and GAG, and the deposition of new collagen types, notably I and X. Copyright 1999 OsteoArthritis Research Society International.
OBJECTIVE: To determine whether humanosteoarthritic (OA) cartilage loses its ability to remain avascular when placed into the in-vivo model of angiogenesis, the chick embryo chorio-allantoic membrane (CAM), and to determine specific changes that occur in the cartilage matrix when the cartilage is exposed to an active vasculature. DESIGN: Articular cartilage from OA and non-OA joints was grafted onto the CAM for up to 5 days before fixing and processing for histological, histochemical and immunological examination for specific changes in proteoglycan and collagen. RESULTS: OA cartilage, but not non-OA cartilage, showed invasion of its matrix by blood vessels from the CAM to various extents. Associated with these blood vessels was a loss of staining for proteoglycans and cartilage specific glycosaminoglycans (GAG). A deposition of collagen types I and X was also visualized around the invasive vessels. CONCLUSIONS: OA cartilage loses or has already lost its ability to remain avascular when placed onto the chick CAM. Changes occur in the matrix around the invasive blood vessels, specifically a loss of proteoglycan and GAG, and the deposition of new collagen types, notably I and X. Copyright 1999 OsteoArthritis Research Society International.
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