We have obtained Chinese hamster ovary cell mutants defective in the biosynthesis of glycosaminoglycans by screening replicate colonies immobilized on polyester cloth. Depending upon the strain, the mutants accumulated less 35S-labeled glycosaminoglycans per ,ug of cell protein by a
We were able to demonstrate type I1 collagen in synovial phagocytes of osteoarthritis (OA) and rheumatoid arthritis (RA) patients, using a monoclonal antibody to human type I1 collagen and immunoperoxidase staining. In addition, using immunoelectron microscopy, we demonstrated labeled fragments in synovial phagocytes of both RA and OA patients. This immunohistoehemical assay may prove to be a sensitive indicator of cartilage erosion in patients with OA and RA.There is currently no sensitive indicator of active cartilage destruction in patients with arthritis. Radiographs provide only a historical record of severe damage. Clinical assessment of osteoarthritis (OA) and rheumatoid arthritis (RA) is also often inadequate; subjective assessment of pain is often the measurement used. Laboratory tests, such as erythrocyte sedimentation rate (ESR) and C-reactive protein values, are indirect measures of joint inflammation. In an effort to find markers for cartilage and joint destruction in various forms of connective tissue diseases, numerous investigators have studied bone and cartilage components, such as hydroxyproline (l), pyridinoline (2), type 111 procollagen peptide (3), proteoglycans (4), and cartilage matrix glycoprotein (3, in serum and urine. However, none of these investigations has thus far led to wider clinical use and application.Of the 5 main components of cartilage, i.e., collagen, proteoglycans, water, noncollagenous proteins, and cells, type I1 collagen makes up about half the dry weight of adult articular cartilage (6). Based on the fact that normal synovial fluid (SF) does not contain collagen, the existence of type I1 collagen in SF indicates either current ongoing or recent degradation of articular cartilage. With this in mind, we sought to detect type I1 collagen in synovial phagocytes and SF of patients with RA and OA using a monoclonal antibody (MAb) directed against human type I1 collagen. The ability to identify type I1 collagen in SF may be helpful not only in evaluating the extent of initial joint damage, but also in following the progression of joint disease.
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