The leukocyte adherence inhibition assay in rheumatoid arthritis.
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Peripheral blood leukocytes (PBL) from patients with rheumatoid arthritis (RA) and from control subjects were exposed to rheumatoid and osteoarthritic synovial membrane extracts. The number of nonadherent PBL in the presence of each extract was monitored in a test tube leukocyte adherence inhibition (LAI) assay. Six of 7 rheumatoid synovial extracts produced significantly greater nonadherence values when RA leukocytes were used as the test cell (36 +/- 5) compared with values obtained when control leukocytes were used (-5 +/- 3). Preincubation of LAI reactive leukocytes from RA patients with the RA synovial extracts abrogated the positive response, whereas preincubation with the OA extract had no effect. These studies indicate that leukocytes from RA subjects respond to a greater degree to extracts derived from rheumatoid synovium than to extracts derived from osteoarthritic synovium and add further support to the concept that unique substances (putative neoantigens?) are present in RA synovium.Cite
N-acetyl-beta-hexosoaminidase (Hex) is a lysosomal enzyme which releases N-acetylaminohexose from non reducing end of glycosaminoglycans, glycoproteins and glycolipids, taking part in degradation of these substances. It is not known what role Hex plays in the degradation of joints in rheumatoid arthritis and osteoarthritis. The aim of our work was evaluation of Hex activity in synovial fluid and serum of patients with rheumatoid arthritis and osteoarthritis. The investigation was performed on material taken from 28 patients with rheumatoid arthritis aged 22-74 years with III or IV stage of disease and 26 patients with osteo-arthritis aged 41-75 years. The synovial fluid was collected from the knee joint during puncture. Hex activity was also determined in serum of healthy people at the age 25-40 years which constitute a control group. Hex activity was determined by the method of Chatterjee et al. modified by Zwierz et al. The concentration of Hex activity in synovial fluid of patients with rheumatoid arthritis was 15.2 nmol/ml/min and 3-4 times excedeed the serum value in these patients. In osteoarthrosis patients Hex concentration in synovial fluid was 6.15 nmol/ml/min. In serum of all investigated groups, concentration of Hex activity was 4.0-4.7 nml/ml/min. The specific activity of Hex (calculated as a constant amount of protein) in synovial fluid of patients with rheumatoid arthritis was significantly higher than in serum of these persons (p<0.017 and 0.014 respectively).
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The metabolism of the synovial lining cells of the normal and chronically inflamed joints of rabbits, in the Dumonde and Glynn model of rheumatoid arthritis, has been examined by quantitative cytochemistry. Significant alterations in metabolic activity were found in the synovial lining cells of the chronically inflamed joints. These alterations in metabolic activity closely resemble the pattern of metabolic changes found in human synovial lining cells in rheumatoid arthritis.
Metabolic activity
Cytochemistry
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Summary Horse articular cartilage glycosaminoglycans (GAGs) were measured in synovial fluids from 48 joints affected with osteoarthritis (OA), 22 normal joints, four joints with osteochondritis, three joints with traumatic arthritis and seven joints infected with bacteria. Serum and urine from individual horses were also examined for the presence of GAGs. High levels of GAGs were found in synovial fluids (SF) from horses with OA. In each case, the level was higher in the synovial fluid than in the serum or urine from the same horse. Horses with OA showed high GAG levels in SF, serum and urine compared to horses with normal and infected joints. High levels were also found in horses with osteochondritis and traumatic arthritis. Levels of synovial fluid GAG reflect cartilage destruction in arthritis and may be useful for monitoring disease progression in the equine species.
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A case of acute hip pain in rheumatoid arthritis is presented, with synovial membrane findings. A patient with classical rheumatoid arthritis suffered three unusual bouts of sudden, severe but transient hip pain. The hips were clinically normal between these episodes. The clinical picture on two of these occasions strongly suggested septic arthritis. Although the synovial fluid was highly inflammatory, cultures were negative. The synovial membrane showed mild lining cell hyperplasia, vascular congestion, and scattered inflammatory cells, predominantly lymphocytes. These findings were not compatible with either pyogenic infection or longstanding rheumatoid arthritis. The clinical and pathological features of acute non-infectious arthritis of the hip appear to delineate a distinct syndrome.
Inflammatory arthritis
Hip pain
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Synovectomy
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MRL/l mice spontaneously develop an arthritis very similar in many respects to human rheumatoid arthritis. A detailed morphologic and serologic analysis of this disease revealed the following: (a) a 75% incidence of synovial and periarticular inflammation, very similar to human rheumatoid arthritis, in 5-6 mo-old females, (b) close associations between presence of joint inflammation and subsynovial and/or periarticular vasculitis, and (c) a close correlation between presence of circulating IgM rheumatoid factor (RF) and demonstrable synovial and/or joint pathology, i.e., 95% of mice with significant levels of IgMRF had synovitis and/or arthritis.
Rheumatoid factor
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Objectives Mutation of p53 may play a role in manifestation of rheumatoid arthritis synovium, but several studies on p53 expression in synovial tissues of rheumatoid arthritis showed conflicting results. We investigated the amount and pattern of p53 positive cells in rheumatoid arthritis synovium, in comparison with osteoarthritis synovium, by using immunohistochemistry with two other monoclonal antibodies for p53. Methods Synovial tissues from 9 patients with rheumatoid arthritis and 5 patients with osteoarthritis were examined for p53 expression by immunohistochemistry with 2 monoclonal antibodies for p53, DO-1 and DO-7. Histologic features of inflammation were also scored and compared with p53 expression. Results There was no significant difference between inflammatory scores in both groups. In the synovial tissues of rheumatoid arthritis patients, p53 positive cells were detected in 3 out of 9 samples(33%) and p53 expressions were restricted to inflammatory mononuclear cells, but synovial lining cells, subsynovial fibroblast-like cells and vascular endothelial cells were p53 negative. p53 expressions in osteoarthritis synovial tissues as control were observed in 2 out of 5 samples(40%) and the amount and pattern of p53 positive cells were comparable to those seen in rheumatoid arthritis synovial tissues. There was no demonstrable correlation between the synovial tissues of both groups with respect to inflammation scores and expression of p53 protein. Conclusion Our findings suggest that altered p53 expression may not play a significant role in the manifestation of rheumatoid arthritis synovium. However these data need to be strengthened by increasing the number of samples and molecular biology approaches.
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Adenosine deaminase activity was determined in paired samples of serum and synovial fluid taken from patients with rheumatoid arthritis (n = 12), reactive arthritis (n = 13), and osteoarthritis (n = 7), and the value of this investigation in the diagnosis of synovial swellings was assessed. Increased activity was found in the synovial fluid taken from patients with rheumatoid disease and reactive arthritis, though values were less raised in the latter. Synovial fluid taken from patients with osteoarthritis did not show significantly raised adenosine deaminase activity as compared with that of normal controls (n = 3).
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