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Query: UMLS:C0003864 (arthritis)
69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunolocalization studies of rheumatoid tissues employing specific synovial collagenase antibody have demonstrated immunoreactive enzyme at the cartilage/pannus junction. Collagenase was not detected in chondrocytes or the cartilage matrix remote from the resorbing front, and relatively little enzyme was observed in the hypertrophied synovial membrane itself. These observations directly support the idea that synovial collagenase participates in cartilage erosion in rheumatoid arthritis.
Arthritis Rheum
PMID:Collagenase at sites of cartilage erosion in the rheumatoid joint. 7 Nov 52

The structure of cartilage in rats with adjuvant disease was investigated lightmicroscopically and by scanning electron microscopy. Severe destruction of the cartilage with formation of lacunae only was observed in areas previously covered by pannus. However, outside the pannus differences between normal animals and animals with arthritis also were observed. In adjuvant treated animals a more fibrillar structure of the surface was seen as compared with untreated rats. This more fibrillar structure may be due to a loss of mucopolysaccharides. The severe destruction of cartilage must be related to the action of collagenase which only acts in areas with a close contact between cartilage and pannus.
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PMID:[Destruction of cartilage in the adjuvants disease of the rat]. 17 Jul 58

Twenty-nine synovial fluids from patients with rheumatoid arthritis (RA) and 10 synovial fluids from patients with other joint diseases were investigated with regard to the presence of antibodies to denatured human collagen and of collagen-anticollagen immune complexes. 12 of the 29 RA synovial fluids showed anticollagen titres from 1:16 to 1:512 in passive haemagglutination. Only one patient in the group with no arthritis had a significant anticollagen titre of 1:32. Digestion of the synovial fluids with bacterial collagenase resulted in an anticollagen titre increase from two to four dilution steps in 9 of the RA fluids, while 6 previously negative RA synovial fluids showed anticollagen titres from 1:32 to 1:28 after digestion with collagenase. These results indicate the existence of collagen-anticollagen immune complexes in 15 of the 29 RA synovial fluids investigated.
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PMID:Demonstration of antibodies to collagen and of collagen-anticollagen immune complexes in rheumatoid arthritis synovial fluids. 18 72

Clinical and experimental data establishing a hypothesis about rheumatoid arthritis (RA) as a collagen auto-immune disease are reviewed, beginning with the demonstration of rheumatoid synovial collagenase, the demonstration of collagen antibodies in the serum and the synovial fluid of patients with RA, the demonstration of collagen inclusion bodies and collagen-anticollagen immune complexes in synovial fluid cells and the synovial fluid of patients with RA, and leading to the in vitro demonstration of the inflammatory effect of such complexes, and the induction of experimental arthritis by these complexes. Each section contains tabular summaries of various investigations. Finally, a relation between these observations and the conclusions deduced from them and the appearance of rheumatoid factors in RA and the pathogenic effect of rheumatoid factor - gammaglobulin aggregates is considered.
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PMID:[Basic studies on chronic polyarthritis as a collagen-autoimmune disease]. 21 Jun 2

Articular cartilage collagenase activity was determined for 28 sections obtained from twelve femoral heads. For each one square centimeter area, a section was graded by a histologic-histochemical grading system for the severity of the arthritis. Collagenase activity was found primarily in those areas of moderately severe disease, but not in mild or end stage arthritis.
Arthritis Rheum
PMID:Correlation between articular cartilage collagenase activity and osteoarthritis. 21 87

A series of intracellular events occurring after treatment of rabbit synovial fibroblasts with 0.01 micrograms/ml phorbol myristate acetate (PMA) were measured. Ten minutes after addition of PMA, there was a temporary increase in intracellular cyclic AMP levels, followed by a transient decrease in incorporation of 3H-thymidine into DNA. Approximately 500 ng/mg cell protein of PGE2 were found in culture medium from the 12- to 24-hour incubation period, but significant collagenase was not detectable until 24 to 36 hours. Treatment with aspirin or indomethacin abolished PGE2 production but did not affect collagenase levels. Production of enzyme was associated with a cessation of cell proliferation, measured by protein content/culture and cell number. No enzyme was detectable in untreated cultures. Synovial fibroblasts treated with phorbol myristate acetate may provide a good model for studies on the mechanism of induction of collagenase production.
Arthritis Rheum 1979 Oct
PMID:Collagenase production by synovial fibroblasts treated with phorbol myristate acetate. 22 97

Cultured mononuclear cells from human peripheral blood produce a soluble factor (MCF) that stimulates collagenase and prostaglandin E2 (PGE2) release by cultured rheumatoid synovial cells up to several hundred fold. These target rheumatoid synovial cells lack conventional macrophage markers. To determine which mononuclear cells are the source of MCF, purified populations of monocyte-macrophages, thymus-derived (T) lymphocytes, and bone marrow-derived (B) lymphocytes were prepared. The monocyte-macrophages alone produced levels of MCF that were proportional to cell density but unaffected by phytohemagglutinin or pokeweed mitogen. No detectable collagenase activity was produced by the cultured monocyte-macrophages or lymphocytes. Purified T lymphocytes produced levels of MCF approximately or equal to 1--3% those of purified monocyte-macrophages in the presence or absence of the above lectins. Purified T lymphocytes modulated the production of MCF by the monocyte-macrophages, however, in a manner dependent upon relative cell densities and the presence of lectins. For example, at optimal ratios of T lymphocytes: monocyte-macrophages, MCF production was markedly stimulated by pokeweed mitogen. Thus, interactions of T lymphocytes and monocyte-macrophages could be important in determining levels of MCF, which regulate collagenase and PGE2 production by target synovial cells in inflammatory arthritis.
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PMID:Participation of monocyte-macrophages and lymphocytes in the production of a factor that stimulates collagenase and prostaglandin release by rheumatoid synovial cells. 22 33

Connective tissue cells are capable of both synthesizing and degrading the macromolecular components of the extracellular matrix. The degradation of proteoglycan and collagen has been shown to be associated with the extracellular release of proteolytic enzymes, some of which are of lysosomal origin. The identity in carilage of two previously unrecognized proteases, capable of proteoglycan breakdown (CPGases), has recently been achieved by the use of a new assay for proteoglycan degradation. These enzymes have been shown to be synthesized and released in response to vitamin A. The third proteoglycan degrading enzyme of connective tissue cells, cathepsin D, has been located in the pericellular environment by trapping with specific antibody and the pattern of release studied in organ culture, experimental arthritis and in human rheumatoid tissues. The secretion of this enzyme and possibly also of the other CPGases is thought to be of importance in the local (pericellular) turnover of matrix macromolecules and, in association with collagenase, to be the cause of the excessive degradation in the pannus erosion of articular cartilage in rheumatoid arthritis.
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PMID:The secretion of enzymes into the pericellular environment. 23 25

The Freund's adjuvant-injected rat shares a number of features with the arthritis patient, viz the presence of a proliferative synovitis, joint swelling, and cartilage and bone erosion. Naproxen, a prostaglandin synthetase inhibitor which is an effective antiinflammatory agent in laboratory animals and humans, was evaluated as an inhibitor of connective tissue destruction in this model by use of radiologic and histopathologic analyses. Sixteen days after rats were injected with Freund's complete adjuvant, marked joint swelling was noted. On day 17, vehicle or naproxen, 7 mg/kg/day, was administered orally. Twenty-eight days later vehicle-treated animals demonstrated the following pathologic changes in their hindpaws; swelling, cartilage loss, large amounts of pannus within the joint spaces, osteoporosis, bone erosions, periosteal new bone formation, heterotopic ossification, and bony ankylosis. Rats treated 28 days with naproxen had significantly milder disease than the vehicle controls. The incidence of severe juxtaarticular bone destruction was 10/10 in the vehicle controls versus 2/10 of the drug-treated group (P less than 0.01). A comparable reduction in cartilage erosion, incidence of pannus, and new bone formation was noted in the drug-treated group. These effects may relate to an inhibition of prostaglandin biosynthesis; prostaglandins have been shown to: 1) stimulate collagenase secretion from macrophages, 2) stimulate bone resorption in vivo and in vitro, and 3) diminish proteoglycan synthesis in cartilage.
Arthritis Rheum 1979 Dec
PMID:Effects of naproxen on connective tissue changes in the adjuvant arthritic rat. 51 18

The synovium removed from the knee of a 10-year-old with hemophilia A was characterized morphologically and biochemically. The specimen showed villous hypertrophy with hyperplasia of synovial lining cells which contained abundant intracytoplasmic granules of hemosiderin. Monolayer cultures prepared from enzymatically dispersed tissue were characterized by pigment-laden fibroblast-like cells and round cells. Both explants of synovium and adherent cells secreted a large amount of latent collagenase and neutral proteinase into the culture medium. The secretion of these enzymes dropped sharply and intracellular pigment decreased with passage of these cultures. Lysozyme was secreted by the explants but was not detected in the monolayer culture medium. These data establish the degradative potential of the synovitis found in hemophilia and support the concept that recurrent hemarthrosis without inflammation is sufficient in and of itself to produce proliferative synovitis.
Arthritis Rheum
PMID:Proliferative synovitis in hemophilia: biochemical and morphologic observations. 62 83


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