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At least 631 records · Page 35Linked to original sources
PubMed1991

C1q-bearing immune complexes detected by a monoclonal antibody to human C1q in rheumatoid arthritis sera and synovial fluids.

Using a monoclonal antibody directed against the C-chain of human C1q, we detected C1q-bearing immune complexes (IC) in sera and synovial fluids of rheumatoid arthritis (RA) patients. In a sandwich-ELISA, C1q-bearing IC were captured by the solid-phase monoclonal antibody and then detected with peroxidase-labeled F(ab')2-antibodies to either human IgG or IgM. The results of this assay were compared to an ELISA-modification of the C1q-solid-phase binding assay (C1q-SPBA). C1q-bearing IC were detected in 81.1% of RA-sera and the 65.2% of RA-synovial fluids. IgG as well as IgM was present in 72.6% of the sera and 70% of the synovial fluids which were positive in both assays. Most RA sera that were only positive for C1q-bearing IC, contained IgG alone (81.5%). The corresponding synovial fluids showed IgG alone (53%) or both IgG and IgM (41.1%). IgM alone (25%) could be detected in sera, e.g. in juvenile forms of RA. The levels of IC were higher in synovial fluid than in paired serum. In comparison to normal human serum (NHS) and patients with osteoarthritis, complement activity (CH50 titers) and C1q-values in patients with RA were frequently elevated. Since the formation of C1q-bearing IC is an indicator for the classical complement pathway activation, an assay with monoclonal anti-C1q antibody may be a useful tool in the diagnosis of rheumatoid diseases.

Antibodies, Monoclonal↗
PubMed1977

Reduced Fc-receptor bearing cells in peripheral bloods of patients with systemic lupus erythematosus and in rheumatoid synovial fluids.

Previous reports described that human red cells sensitized with one of Rh antisera (Ripley) make rosette formations (Fc-rosette with some lymphocytes. These Fc-rosettes were well inhibited by aggregated human IgG as well as hypocomplementemic systemic lupus erythematosus (SLE) sera and rheumatoid synovial fluids. In the present study, Fc-receptor bearing lymphocytes were considerably reduced in peripheral bloods of SLE (16.0 +/- 7.6%) and rheumatoid synovial fluids (15.6 +/- 5.3%). On the other hand, EAC-rosette formation rates of peripheral bloods of SLE (32.0 +/- 13.2%) and rheumatoid synovial fluids (30.3 +/- 11.2%) did not significantly differ from normal peripheral bloods (28.3 +/- 2.9%). E-rosette forming lymphocytes were reduced in peripheral bloods of SLE (48.7 +/- 15.7%) and in rheumatoid synovial fluids (49.0 +/- 14.6%) whereas 61.7 +/- 8.6% in normal peripheral bloods. Reduced Fc-rosette formation rates correlated well with the Fc-rosette inhibitory rates. In addition, eluates from the lymphocytes in rheumatoid synovial fluids also inhibited Fc-rosette formation. These results suggested that immune complexes present in peripheral bloods of SLE and rheumatoid synovial fluids are bound to the Fc-receptors on the lymphocytes, block the additional binding of the sensitized red cells, and result in the reduction of Fc-rosette formation.

Antigen-Antibody Complex↗
PubMed1997

[Levels of matrix metalloproteinase-3 and urokinase-type plasminogen activator in knee synovial fluids from patients with rheumatoid arthritis and osteoarthritis].

The objective of this study is to determine the levels of matrix metalloproteinase-3 (MMP-3) and urokinase-type plasminogen activator (uPA) in knee synovial fluids from patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Knee synovial fluids were collected from patients with RA and OA. Concentrations of MMP-3 were determined by enzyme immunoassay using a pair of monoclonal antibodies against human proMMP-3, and activities of uPA were measured by immunocapture assay using a polyclonal antiserum against human uPA. The median concentration of MMP-3 in synovial fluids was 97.5 +/- 82.6 micrograms/ml (range 1.06-336 micrograms/ml) for RA group and 20.5 +/- 11.3 micrograms/ml (range 6.19-42.8 micrograms/ml) for OA group. Levels of MMP-3 were significantly higher in RA group than in OA group. The median activity of uPA in synovial fluids was 0.053 +/- 0.052 i.u./ml (range 0.003-0.187 i.u./ml) for RA group and 0.072 +/- 0.059 i.u./ml (range 0.006-0.169 i.u./ml) for OA group. No significant difference of uPA activity was observed between RA and OA group. Significant correlation of the levels of MMP-3 with those of uPA was observed in RA group, however not in OA group. The increased levels of MMP-3 in synovial fluids in RA group may reflect an elevated matrix degrading activity due to joint inflammation. The significant correlation of MMP-3 with uPA in RA group suggests that MMP-3 could degrade cartilage matrix more actively in conjunction with PA-plasmin system than MMP-3 alone.

Aged↗
PubMed1984

Different synovial fluid fibronectin levels in rheumatoid variants.

A circulating high-molecular-weight glycoprotein called fibronectin plays a part in cell adhesion and migration before phagocytosis and in morphology, differentiation, and metabolism in inflammatory synovial effusions of patients with rheumatic diseases. A technique of nephelometric immunoassay, based on the measurement of an antigen-antibody reaction, was applied to the analysis of fibronectin concentrations in synovial fluids from 20 patients with rheumatoid arthritis (RA) and other diseases (non-RA). RA synovial fluids have a significantly higher concentration than the specimens obtained from Yersinia arthritis patients (n = 12). The mean concentration of other synovial fluids, from 12 patients with osteoarthritis of the knees, did not significantly differ from the synovial fluids of control values obtained from patients who underwent meniscectomy. There was a considerably negative correlation between fibronectin levels and overall indices of inflammatory activity, such as Ritchie articular indices or a whole number of painful rheumatoid arthritis joints. However, a particularly distinct correlation was obtained when raised fibronectin levels were compared with the inflammatory activity of the knee joint, from which the specimen was aspirated. Thus, these findings suggest that the measurements of fibronectin in synovial fluid may be of some differential-diagnostic value in rheumatoid variants, but may only serve as an indicator of inflammatory activity if the joint, from which the specimen is obtained, is taken into account.

Adult↗
PubMed1991

Isolation of Yersinia-specific T cell clones from the synovial membrane and synovial fluid of a patient with reactive arthritis.

Synovial fluid (SF) mononuclear cells from patients with reactive arthritis (ReA) proliferate in vitro when challenged with ReA-associated bacteria, the maximal response being for the organism causing the triggering infection. We report the results of a study of the antigenic specificity of synovial T lymphocytes from an HLA-B27 positive ReA patient whose SF mononuclear cells responded preferentially to Yersinia antigens. This is the first report of the isolation of Yersinia-specific T cell clones from synovial membrane (obtained by closed-needle synovial biopsy). We present a detailed analysis of these clones, together with others obtained from the SF.

Adult↗
PubMed1983

Complement C3c and C3d in plasma and synovial fluid in rheumatoid arthritis.

By means of recently developed immunochemical assays increased levels of the complement C3c and C3d split products were found in synovial fluids of patients with rheumatoid arthritis (RA) as compared with synovial fluids of patients with traumatic synovitis (TS). In plasma, only the C3d levels were significantly increased compared with plasma levels of patients with TS. Both split products were higher in RA synovial fluids (SF) than in RA plasma. A positive correlation between the C3d concentrations in plasma and the presence of IC in serum was found, and between the C3c levels and the concentration of polymorphonuclear cells in SF of RA patients. Due to differences in turn-over of C3c and C3d determination of plasma C3d levels may be a useful parameter for the evaluation of immunological activity in RA, while measurement of C3c in the synovial fluid may elucidate the actual inflammatory activity in the synovial membranes.

Antigen-Antibody Complex↗
PubMed1982

Synovial fluid and plasma fibronectin levels in rheumatoid arthritis.

1. Plasma fibronectin levels were similar in 60 healthy subjects and 88 with the rheumatoid arthritis. 2. In 42 patients with rheumatoid arthritis synovial fluid fibronectin levels were significantly higher than plasma levels (P less than 0.001). Intermediate fibronectin levels were found in synovial fluid from six patients with psoriatic arthritis, eight patients with osteoarthritis and seven with seronegative arthritis. 3. Plasma and synovial fluid fibronectin levels were not related to indices of inflammatory activity such as the erythrocyte sedimentation rate, the Ritchie articular index or synovial fluid cell counts. Nor did fibronectin behave as an acute-phase protein. 4. Immunofluorescent studies showed that fibronectin was adsorbed on fibrinous debris in rheumatoid arthritic joints. 5. These findings suggest that there is local production of fibronectin by the synovium and suggest that measurement of fibronectin levels in the synovial fluid may serve as an indicator of the tissue response to rheumatoid arthritis.

Adolescent↗
PubMed1994

Determination of non-protein-bound iron in human synovial fluid by high-performance liquid chromatography with electrochemical detection.

Non-protein-bound iron in human synovial fluid was determined using high-performance liquid chromatography with electrochemical detection. The procedure was based on the separation of the iron-diethylenetriaminepentaacetic acid (DTPA) complex formed directly on a chromatographic column containing an anion-exchange resin followed by electrochemical detection. The method enabled more than 0.1 microM Fe(III) to be determined with an injection volume of 10 microliters. A mixture of synovial fluid, 20 microM DTPA and acetate buffer was incubated in the presence and absence of superoxide (O2-) generated by a xanthine-xanthine oxidase system and was ultrafiltered through a 30,000 molecular mass cut-off filter. No iron was detected in the ultrafiltrate at physiological pH. However, the presence of iron was observed in the ultrafiltrate at low pH, and O2- facilitated the release of iron into the synovial fluid. This result suggested that in an inflamed joint with generated O2- and decreased pH, iron may be released into the synovial fluid.

Arthritis, Rheumatoid↗
PubMed1991

Hypoxanthine, xanthine, and urate in synovial fluid from patients with inflammatory arthritides.

As nucleotide catabolism increases during tissue injury the appearance of purine metabolites in inflamed synovial fluid might be of value in understanding the joint damage in inflammatory arthritides. In this study, therefore, synovial and plasma concentrations of hypoxanthine, xanthine, and urate in 16 patients with rheumatoid arthritis (three with psoriatic arthropathy) were analysed. It was found that their plasma concentrations of hypoxanthine were greater than those of a reference group of healthy subjects. The synovial fluid concentrations of hypoxanthine, xanthine, and urate were higher than corresponding concentrations in plasma. Positive correlations were found between the respective plasma and synovial fluid values of xanthine and urate. These findings indicate a local enhanced purine metabolism in inflamed joint tissue and diffusion of oxypurines from joint cavity to plasma. No relation was found between measured metabolites and disease duration, radiological joint findings, or synovial fluid cells. Except for a weak correlation between plasma urate and serum haptoglobin, measured purine metabolites were not related to laboratory measures of systemic inflammation.

Adult↗
PubMed2001

Activities of plasminogen activator, plasmin and kallikrein in synovial fluid from patients with temporomandibular joint disorders.

To measure the activities of plasminogen activator (PA), plasmin and kallikrein, multiple synovial fluid samples were taken from 32 patients with internal derangement (ID) and osteoarthrosis (OA), and nine asymptomatic volunteers. The enzyme activity in synovial fluid from the temporomandibular joint (TMJ) was quantitated by a fluorogenic substrate assay using an enzyme substrate. In fluid samples from the patient group, PA was detected in 24 (31.5%), plasmin in 20 (26.3%) and kallikrein in 53 (96.4%), while none of these enzymes were found in the synovial fluid samples from the control group. There were positive correlations found among PA, plasmin and kallikrein. These results clearly demonstrated increased levels of PA, plasmin and kallikrein activities in the synovial fluid of patients with ID and OA, and suggest that these enzymes may be involved in the pathogenesis of synovitis, as well as the resorption of cartilage and bone in TMJ.

Adolescent↗
PubMed2006

Synovial fluid metabolites in osteonecrosis.

OBJECTIVES: Osteonecrosis of the femoral head results from interruption of the vascular supply and eventual death of the cellular portion of bone. Effective methods of monitoring response to treatment are needed. Our aim was to evaluate synovial fluid metabolites, glucose and lactate, as biomarkers in a canine model of osteonecrosis. METHODS: Osteonecrosis was cryosurgically induced in the right femoral head while the left hip served as control (n = 31). Animals either underwent no further intervention (n = 10), vascular endothelial growth factor (VEGF) injections (n = 4), placement of a vascularized bone graft (n = 6), a combination of VEGF microinjection and vascularized graft placement (n = 5), or treatment with daily oral alendronate (n = 6). After 12 weeks, synovial fluid from each hip joint was obtained for glucose and lactate concentrations. RESULTS: Joints with surgically induced osteonecrosis demonstrated decreased synovial fluid concentrations of glucose (P < 0.05) and elevated concentrations of lactate (P < 0.05) relative to contralateral control hips. When animals were treated with VEGF, the vascularized graft placement, or vascularized graft and VEGF, there were no differences in the synovial fluid concentrations of these metabolites between cryoablated and control hips. In contrast, alendronate did not normalize the concentration of these synovial fluid metabolites in the cryoablated hips. CONCLUSIONS: Osteonecrosis of the femoral head is associated with alterations in synovial fluid glucose and lactate, reflecting anaerobic metabolism. These metabolites may serve as useful tools for monitoring response to revascularization therapies.

Animals↗
PubMed1981

Plasma and synovial fluid as solvents for monosodium urate.

In-vitro differences in monosodium urate (MSU) crystal dissolution in paired plasma and synovial fluid samples from patients with various arthritides were studied. Plasma was a significantly better solvent for MSU than synovial fluid (overall difference 6.3 mg/dl (0.37 mmol/l); significant at P less than 0.001). Attempts to correlate the solubility differentials with the principal compositional differences between the 2 fluids were only partially successful. (1) A tendency towards higher MSU solubility at higher protein levels was observed, but it was too slight to reach statistical significance. (2) Hyaluronidase treatment of synovial fluid significantly enhanced its ability to dissolve MSU (overall difference 2.2 mg/dl (0.13 mmol/l); significant at P less than 0.01) but not sufficiently to explain wholly the plasma-synovial fluid differential.

Arthritis↗
PubMed2005

Aggrecanase analysis of synovial fluid of temporomandibular joint disorders.

OBJECTIVES: To determine whether or not aggrecanase in synovial fluid can be used as a biochemical marker in the diagnosis of temporomandibular joint disorder (TMJD). MATERIALS AND METHODS: Forty-four samples of synovial fluid were obtained from 35 patients with internal derangement or osteoarthritis and 15 control samples from 10 asymptomatic volunteers. Aggrecanase in the synovial fluid was examined by immunoblotting. RESULT: The incidence of aggrecanase expression in TMJD group were significantly higher than that in the normal control group (P < 0.05). Those with severe OA and anterior disc displacement without reduction showed significantly high expression of aggrecanase compared with other disease subgroups (P < 0.05). CONCLUSION: These findings suggested that aggrecanase could be a potential biochemical marker for cartilage degeneration in the TMJD.

Adolescent↗
PubMed1986

Superoxide dismutase isoenzymes of the synovial fluid in rheumatoid arthritis and in reactive arthritides.

The activity of superoxide dismutase isoenzymes was determined in knee joint synovial fluid from 21 patients with rheumatoid arthritis, nine patients with reactive arthritides, and from 17 patients before arthroscopy or arthrotomy for suspected meniscal or ligament injury (controls). Extracellular superoxide dismutase was the major isoenzyme and accounted for about 80% of the total superoxide dismutase activity in the controls. The pattern of the superoxide dismutase isoenzymes was significantly different in rheumatoid arthritis, extracellular (EC) superoxide dismutase being half, CuZn superoxide dismutase double, and the total superoxide dismutase activity a third lower than the activity in the synovial fluid of the controls. The superoxide dismutase activities were similar in synovial fluid from the controls and from the patients with reactive arthritides. The total superoxide dismutase activity was almost three times higher in control synovial fluid than in normal human plasma, but 300 times lower than in human tissues.

Arthritis↗
PubMed1979

T lymphocyte subpopulations in synovial fluid of patients with rheumatic disease.

The proportion of T lymphocytes with receptors for the Fc portion of IgG (TG cells) of IgM (TM cells) was determined in synovial fluid and blood of 16 patients with various rheumatic diseases including rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. The percentage of TG cells was low in all synovial fluid samples, whereas in the patients' blood the percentage was higher than or equal to the level found in the blood of healthy subjects. Eight patients also had a lower level of TM cells in synovial fluid as compared to the percentage found in the blood of healthy donors. In the patients' blood the percentage of TM cells was usually within the normal range. Thus the proportion of T cells lacking either receptor (Tnull cells) was higher in synovial fluid than in blood. This pattern of low TG cell and high Tnull cell percentages was found in the synovial fluid of patients with various rheumatic diseases and thus seems to be a general feature of chronic inflammatory joint exudates.

Arthritis, Rheumatoid↗
PubMed1988

Inflammatory synovial fluid and absorbable suture strength.

The effect of inflammatory synovial fluid upon several absorbable sutures commonly used for meniscus repair was studied by implanting lengths of these sutures into unstable, arthritic rabbit knees and, after varying lengths of time (1-6 weeks), testing their breaking strength. Both polyglactin-910 (Vicryl) and polyglycolic-acid (Dexon) sutures retained only minimal breaking strength 3 weeks after implantation. Chromic gut sutures demonstrated a steady reduction in breaking strength until they retained only 6% of their original strength at 5 weeks and none at 6 weeks. Polydioxanone (PDS) sutures began to lose breaking strength at 2 weeks and retained only 40% of their original strength 5 weeks after implantation. The rate of loss in polydioxanone breaking strength was faster in inflammatory synovial fluid than previously reported in the normal synovial joint. Braided polyester sutures (Mersiline) showed no loss of breaking strength over the duration of this test. While the choice of suture is only one variable influencing the outcome of a meniscus repair, this study demonstrates that only polydioxanone and green braided polyester sutures retain any strength 6 weeks after implantation (the time of immobilization commonly recommended for meniscal repairs). Complete meniscal healing can require several months. In the absence of compelling evidence to the contrary, the use of nonabsorbable suture materials for meniscal repair seems the most appropriate choice.

Absorption↗
PubMed2003

Zymographic analysis of latent and activated forms of matrix metalloproteinase-2 and -9 in synovial fluid: correlation to polymorphonuclear leukocyte infiltration and in response to infection.

BACKGROUND: Matrix metalloproteinase-2 and-9 (MMP-2, MMP-9), and gelatinase A and B participate in the degradation of the extracellular matrix proteins in a variety of inflammatory connective tissue diseases including arthritis. METHODS: Synovial fluid was collected by aseptic aspiration from patients with rheumatoid arthritis (RA), osteoarthritis (OA), gout, infected joint, septic arthritis, and systemic lupus erythematosus (SLE). Synovial fluid was subjected to cell count with polymorphonuclear leukocyte (PMN) differential, Gram staining and culture as necessary. MMP-2 and -9 were characterized by substrate gel electrophoresis (gelatin zymography) to resolve latent and activated 'partially proteolyzed' forms. RESULTS: Gelatin zymography revealed that MMP-9 (92, 130, 225 kDa) in synovial fluid was associated with extent of white blood cell infiltration specifically PMNs. In contrast, fibroblast MMP-2 (72 kDa) was present in all synovial fluids irrespective of PMN count. No MMP-9 was detected in the osteoarthritic specimen with low PMN count. Higher PMN count was associated with the presence of activated MMPs, especially in specimens that were confirmed culture positive. Activated synovial fluid MMPs persisted despite resolution of infection. DISCUSSION: Latent and activated MMP-2 and MMP-9 in synovial fluids fluctuate in proportion to PMN infiltration and specifically in response to infection. The presence of activated MMPs post-therapy would suggest that use of specific MMP inhibitors be indicated to eliminate activated MMPs that apparently persist post-infection.

Adult↗
PubMed1969

Collagenases in human synovial fluid.

An enzyme which degrades native collagen at neutral pH has been isolated from cultures of rheumatoid synovium in vitro, but little or no collagenolytic activity has been found in homogenates of fresh rheumatoid synovium. Similar to most other mammalian collagenases this synovial enzyme is readily inhibited by serum proteins. Proteins of synovial fluid are derived largely from serum and synovial fluid from noninflamed joints was found to inhibit synovial collagenase; the inhibitor was destroyed by trypsin, but not by hyaluronidase. Inhibitory activity was reduced in approximately one-half of the fluids from patients with rheumatoid arthritis. In a total of nine synovial fluids, collagenolytic activity was detectable. This activity was not present in constant amounts in synovial fluids aspirated at different times from the same patient and tended to vary inversely with the titer of inhibitory proteins. The collagenolytic activity in the synovial fluids from different patients was variably inhibited by serum proteins. Two distinct collagenases were detected in some rheumatoid synovial fluids and separated by gel filtration. One, labeled "B" enzyme, with an estimated molecular weight 20,000-25,000 resembled the collagenase obtained from synovial cultures. The other, labeled "A" enzyme degraded collagen fibrils as well as collagen in solution. Disc electrophoresis on acrylamide gels and electron microscopy of segment long spacing (SLS) aggregates of reaction products of the enzymes at 27 degrees C demonstrated that both "A" and "B" enzymes cleaved collagen molecules at a point three-quarters from the amino terminal end of the molecule. Thus collagen degradation in rheumatoid arthritis could result from the operation of these two collagenases.

Arthritis, Rheumatoid↗