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At least 217 records · Page 12Linked to original sources
PubMed1988

Bone resorbing activity in synovial fluids in destructive osteoarthritis and rheumatoid arthritis.

The synovial fluids of patients with a destructive form of osteoarthritis (DOA) were shown to contain high levels of bone resorbing activity as judged by the ability of the fluid to stimulate the release of 45Ca from labelled cultured mouse calvariae. The activity was lost on extended storage of the synovial fluids and was dependent for its effect on cellular activity in bone. Bone resorbing activity was present in most synovial fluids from patients with DOA and rheumatoid arthritis (RA) but occurred at higher levels in the former. In contrast, interleukin 1 (IL1) activity, measured by the mouse thymocytes costimulation assay, was higher in RA than DOA synovial fluids. Little or no bone resorbing or IL1 activity was detected in synovial fluids from patients with pseudogout or non-destructive osteoarthritis. These results suggest that most DOA synovial fluids contain a bone resorbing factor other than IL1. It is considered that the factor may be produced by synovial cells stimulated by hydroxyapatite crystals.

Adult↗
PubMed1988

Integrated plasma and synovial fluid pharmacokinetics of tenoxicam in patients with rheumatoid arthritis and osteoarthritis: factors determining the synovial fluid/plasma distribution ratio.

Single oral doses of 40 mg of the nonsteroidal antiinflammatory drug, tenoxicam, were given to four patients (three with rheumatoid arthritis, one with osteoarthritis). The concentrations of the drug in synovial fluid and plasma were measured by a specific high-performance liquid chromatography method. The unbound fractions of the drug in both fluids were determined at pH 7.4 and 37 degrees C by equilibrium dialysis. The possible influence of the pH on the protein binding was also assessed. The total concentration time curves in plasma and synovial fluid were fitted to linear oral 1 and 2 compartment body models with an additional synovial fluid compartment connected to the central compartment. The unbound fractions of drug in synovial fluid and plasma were on average 0.015 and 0.011, respectively: not significantly different from each other. The protein binding of tenoxicam was pH dependent with increased free fractions at pH values less than 7.4. The average peak concentrations of tenoxicam in plasma and synovial fluid were 4.3 and 1.4 micrograms/ml, respectively. The mean ratio of the areas under the total concentration time curves in synovial fluid and plasma was 0.42, which corresponded to the steady state of equilibrium ratio of the total drug concentrations in the two body fluids. Two hypotheses were tested: hypothesis I assuming that equilibration across the synovial tissue takes place between the unbound, unionized tenoxicam molecules; hypothesis II assuming that equilibration across the synovial tissue is established between the unbound (unionized + ionized) tenoxicam molecules. Based on the available evidence hypothesis II was rejected.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1985

Plasma and synovial fluid concentrations of sulphasalazine and two of its metabolites in rheumatoid arthritis.

A study was made of plasma and synovial fluid levels of sulphasalazine, one of its dissociation products--sulphapyridine and a metabolite of the latter--acetyl sulphapyridine in patients with rheumatoid arthritis (RA) who were in a steady state on sulphasalazine therapy. Combined sulphapyridine levels were significantly higher than those of sulphasalazine both in plasma and synovial fluid. Synovial fluid levels of both drugs correlated with their plasma levels and were generally slightly lower. Some patients accumulated sulphasalazine and sulphapyridine in the synovial fluid and the mean concentration of sulphasalazine was higher in the fluid than in the plasma. The explanation for this is uncertain. The concentration of combined sulphapyridine in synovial fluid was related to local joint inflammation and more active systemic disease. No consistent association was found between sulphasalazine levels and local or systemic activity. The higher sulphapyridine levels in synovial fluid found in this study suggest the possibility that this moiety could play a more active role in RA than it does in inflammatory bowel disease.

Adult↗
PubMed1987

[Catalase activity of synovial fluid leukocytes in rheumatoid arthritis].

Catalase activity of rheumatoid synovial fluid measured by a gasometry was higher than that of osteoarthritic fluids, suggesting a possible origin of the catalase activity from synovial fluid leukocytes. Isoelectric focusing polyacrylamide gel electrophoresis of the extract from polymorphonuclear leukocytes (PMN) of rheumatoid synovial fluid exhibited two to four achromatic bands and one dark band of catalase activity. Catalase staining of synovial fluid cells with diaminobenzidine revealed a marked activity in PMN, no or weak activity in monocytes and negative activity in lymphocytes. Catalase scores of the PMN in rheumatoid synovial fluid were lower than those of osteoarthritic fluid and of normal peripheral blood PMN. Ultrastructural localization of catalase activity in leukocytes of rheumatoid synovial fluid was examined by diaminobenzidine staining. Electron dense deposits were observed in granules, probably peroxisomes and in cytoplasm of the PMN and also in microperoxisomes of the monocyte.

Adult↗
PubMedDate not supplied

Synovial fluid tests. What should be ordered?

To determine which synovial fluid tests are most useful, we prospectively analyzed the synovial fluid test results of 100 consecutive patients undergoing diagnostic arthrocentesis. Each patient's diagnosis was established independently of synovial fluid laboratory test results; in 69 patients a definite inflammatory or noninflammatory categorization could be made. Sensitivity and specificity were estimated for synovial fluid white blood cell count (sensitivity, 0.84; specificity, 0.84), percentage of polymorphonuclear cells (sensitivity, 0.75; specificity, 0.92), glucose (sensitivity, 0.20; specificity, 0.84), protein (sensitivity, 0.52; specificity, 0.56), and lactate dehydrogenase (sensitivity, 0.83; specificity 0.71). Receiver operating characteristic regression analysis indicated that both white blood cell count and percentage of polymorphonuclear cells were found to contribute independent diagnostic information but lactate dehydrogenase did not. In a separate, retrospective analysis of 19 patients with definite septic arthritis, similar results were observed. We conclude that synovial fluid white blood cell count and percentage of polymorphonuclear cells perform well as discriminators between inflammatory and noninflammatory disease. Ordering chemistry studies of synovial fluid should be discouraged because they are likely to provide misleading or redundant information.

Arthritis, Infectious↗
PubMed1981

Reciprocal relationship of synovial fluid volume and oxygen tension.

To investigate the impact of synovial fluid volume on oxygen tension (PO2) and other metabolic correlates, 24 specimens of synovial fluid from the knees of 22 patients were analyzed for volume, number of leukocytes (WBC), pH, PO2, PCO2, glucose, protein, and complement (CH50) levels. Concurrent arterial blood samples were obtained in 21 instances. Synovial fluid PO2 values varied inversely with volumes of synovial fluid (r = -0.54, P less than 0.01), but when patients with rheumatoid arthritis were excluded, the correlation was more significant (r = -0.76, P less than 0.001). When synovial fluid PO2 dropped below 45 mm Hg, intraarticular acidosis resulted. The decrease in pH (r = 0.93, P less than 0.001), the lowering of glucose values (r = 0.89, P less than 0.001), and the rise in PCO2 (r = -0.79, P less than 0.01) can be explained by a shift toward anaerobic metabolism coupled with the impaired elimination of its products. Systemic acidosis and hypoxia were not found. Intraarticular hypoxia most likely represents circulatory imbalance at the level of the synovial membrane, although an inverse relationship of synovial fluid PO2 and WBC was also noted. Complement and protein levels had no correlation with volume, pH, or respiratory gas tensions of synovial fluids. Our data support the importance of the effective blood flow to the joint in maintaining homeostasis. The volume of synovial effusion and the compliance of the joint capsule appear to be important determinants of the articular blood supply.

Adult↗
PubMed1998

Elevated nerve growth factor levels in the synovial fluid of patients with inflammatory joint disease.

A novel pH shock extraction procedure was used to measure nerve growth factor (NGF) levels in both normal and inflamed synovial fluids using a sensitive and specific two-site enzyme linked immunosorbant assay. To date no data is available on NGF levels in normal synovial fluids. Synovial fluids were taken from 5 normal volunteers, 12 patients with rheumatoid arthritis and 10 patients with other inflammatory arthropathies. The mean +/- SEM NGF concentration in normal synovial fluids was 95 +/- 33.2 pg/ml (range 39.1-143.1 pg/ml), whereas the mean NGF concentration in the synovial fluids taken from patients with rheumatoid arthritis was 532.5 +/- 123.8 pg/ml (range 152-1686 pg/ml). The mean NGF concentration in patients with other inflammatory arthropathies was also raised (430.6 +/- 90 pg/ml; range 89-1071 pg/ml). The NGF concentrations were significantly higher in the synovial fluids from both inflamed groups (ANOVA p < 0.05) compared to normals. Raised levels of NGF in synovial fluid may contribute directly to joint inflammation via activation of inflammatory cells.

Arthritis↗
PubMed1984

B cell differentiation factor in synovial fluid of patients with rheumatoid arthritis.

In this paper we have summarized our findings on immune activity in patients with Rheumatoid Arthritis. RA is characterized not only by the formation of various autoantibodies but also of a hyperreactivity of the B cell system, shown as an increased DNA synthetic rate of blood non-T, non-monocytic lymphocytes as well as an increased number of actively antibody secreting cells both in the blood and the synovial fluid. Synovial fluid contains biological activity which synergizes with PWM for the induction of Ig-secreting cells in blood from healthy controls. The factor can also substitute for T cells in the PWM-induced antibody synthesis in vitro. This activity fits well with the finding that SF contains a factor which induces increased formation of IgG in LPS-pretreated mouse cell cultures. Experiments show that the factor leads to a preferential increase in the production of IgG2b antibody secreting cells. Therefore, we conclude that synovial fluid contains a B cell differentiating factor with a selective effect on the induction of a particular IgG subclass.

Antibody Formation↗
PubMed2001

Correlation of acoustic velocity of synovial fluid with markers of inflammation in arthritic patients.

Analysis of synovial fluid is important in the evaluation and treatment of arthritic conditions. This study measured the acoustic velocity of synovial fluids in patients with degenerative joint diseases, crystal arthropathy, and other inflammatory arthropathies using the ultrasonic pulse-echo method. The measured acoustic velocities of these bio-fluids were then correlated with clinical parameters including the synovial white blood cell count (WBC), clarity, viscosity, string test, erythrocyte sedimentation rate (ESR), and serum C-reactive protein (CRP). Results showed that the acoustic velocities were correlated with ESR (p = 0.0016) and CRP (p = 0.0001). The mean acoustic velocity of inflammatory synovial fluids, defined as synovial fluids with WBCs of more than 2000/mm3, was greater than that of synovial fluids with WBCs of less than 2000/mm3 (1550 +/- 4.5 m/s vs 1544 +/- 1.5 m/s, p = 0.007). This study demonstrated that the acoustic velocity of synovial fluid correlates well with severity of inflammation. These findings suggest that measurement of acoustic velocity may be useful in the clinical evaluation and management of arthritic conditions.

Arthritis↗
PubMed1989

[A study on lymphocyte subsets of peripheral blood and synovial fluid using monoclonal antibodies in patients with rheumatoid arthritis].

Synovial fluid lymphocytes and paired peripheral blood lymphocytes from 29 patients with rheumatoid arthritis (RA) were analyzed using two-dimensional flow cytometry. The lymphocytes of peripheral blood from 20 normal subjects were served as control. In the RA patients, the composition of the lymphocyte population was different in the synovial fluid and peripheral blood. Compared with the peripheral blood, the synovial fluid contained higher populations of Ia+ (Leu 4 + Leu HLA-DR+) T cells, especially Leu 2a + Leu HLA-DR+ (activated suppressor/cytotoxic) T cells, and of Leu 2a + Leu 15- (cytotoxic T) cells and Leu 3a + Leu 8- (helper T) cells. Contrary, the synovial fluid contained lower populations of Leu 2a + Leu 15+ (suppressor T) cells and Leu 3a + Leu 8+ (inducer T) cells. Compared with the lymphocytes of the normal peripheral blood, the RA patients had an elevated ratio of helper T/suppressor T cells (Th/Ts) in both the synovial fluid and peripheral blood, incidentally the former group showed striking elevation. The ratio of Th/Ts in the synovial fluid showed considerable variation, with a significant inverse correlation with the disease activity (Lansbury index). These findings suggest that patients with rheumatoid arthritis show more specific changes in their synovial fluid lymphocytes than in their peripheral blood lymphocytes.

Adult↗
PubMed1997

Molecular abnormalities of human plasminogen isolated from synovial fluid of rheumatoid arthritis patients.

Plasminogen (Pg) in the synovial fluid of patients with acute inflammatory disease, including rheumatoid arthritis, osteoarthritis, and gout, was purified by affinity chromatography techniques. The Pg isolated from patients with osteoarthritis and gout has affinities for L-lysine Sepharose and structural properties similar to those of normal plasma Pg. However, Pg from rheumatoid synovial fluids is abnormal in that it does not bind to L-lysine Sepharose. Analyses of rheumatoid synovial fluid Pg purified by immunoaffinity chromatography indicate that the molecule has size and folding properties similar to those of normal plasma Pg. However, we detected abnormalities in the molecule using two different criteria. First, isolated kringles 1-3 fragments are unable to bind L-lysine Sepharose. Second, reactivity toward a monoclonal antibody against a region in kringles 1-3 is decreased. In addition, rheumatoid synovial fluid Pg competes with normal plasma Pg for binding to the receptor on rheumatoid synovial fibroblasts but not on normal synovial fibroblasts. We also found that binding and activation of rheumatoid synovial fluid derived Pg on the surface of rheumatoid synovial fibroblasts elicits a rise in the concentration of cytosolic free Ca2+ similar to that of normal plasma Pg. Our data suggest that the inability of rheumatoid synovial fluid Pg to bind to L-lysine Sepharose is due to minor structural changes in kringle 1-3. These changes do not affect the physiological properties or the binding ability of synovial fluid Pg to cellular receptors on cells obtained from rheumatoid synovial tissue.

Animals↗
PubMed1996

Identification and characterization of insulin-like growth factors (IGFs), IGF-binding proteins (IGFBPs), and IGFBP proteases in human synovial fluid.

The insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) in human synovial fluid play an important role in maintaining articular cartilage metabolism. In this study we measured the concentrations of IGF-I, IGF-II, and IGFBP-3 in normal human synovial fluid by RIA and characterized the IGFBPs by Western ligand blot (WLB), Western immunoblot, and immunoprecipitation. We also extended the study and compared normal synovial fluid to synovial fluids from patients with osteoarthritis (OA) and rheumatoid arthritis (RA). The concentrations of IGF-I, IGF-II, and IGFBP-3 in normal synovial fluid were 19 +/- 3 (mean +/- SE), 194 +/- 14, and 349 +/- 65 ng/mL, respectively. In synovial fluid of patients with OA, IGF-I levels were elevated, whereas IGF-II was decreased, and the IGFBP-3 level was similar to the control value. In patients with RA, both IGF-I and IGFBP-3 were elevated, whereas IGF-II remained unchanged. WLB and immunoprecipitation of normal synovial fluid revealed IGFBP-1 (26-29 kDa), IGFBP-2 (32 kDa), IGFBP-3 (42- to 39-kDa doublet), and IGFBP-4 (24 kDa); the IGFBP-3 doublet was very faint. In RA synovial fluid, all IGFBPs were dramatically increased, whereas little change was seen in the synovial fluid of OA. Western immunoblot against IGFBP-3 revealed a prominent 30-kDa immunoreactive fragment of IGFBP-3 in synovial fluids of normal adults as well as in those of RA and OA patients. This was concurrent with detectable IGFBP-3 protease activity, which was characterized to be of the metallo- and serine protease family. Thus, in normal synovial fluid, there is a balance of circulating IGF, IGFBP, and proteases to modulate the bioactivity of IGF. In pathological states, the increased IGF-I concentrations were accompanied by an increase in IGFBP-I concentrations were accompanied by an increase in IGFBP-3 levels in synovial fluid. These findings suggest that alteration of the IGF and IGFBP axis in pathological states may be important for understanding the underlying pathophysiology of disordered articular growth and metabolism.

Adult↗
PubMed1987

Kallikrein in synovial fluid with rheumatoid arthritis.

The levels of kallikrein and collagenase in synovial fluid from rheumatoid arthritis (RA) patients were examined and the role of kallikrein in procollagenase activation is discussed. Both prekallikrein and active kallikrein in synovial fluid from patients with RA were significantly elevated when compared to synovial fluid from patients with osteoarthritis (OA). In RA synovial fluid, the ratio of the active form to total kallikrein was also higher than that in OA synovial fluid. Both active collagenase and the alpha 2-macroglobulin (alpha 2M)-collagenase complex in RA synovial fluid were higher than in OA synovial fluid. A partial correlation (r = 0.58) between active kallikrein and total collagenase (active and alpha 2M-collagenase complex) was observed in RA synovial fluid. These observations indicate that both kallikrein and collagenase are associated with the destruction of cartilage, but the role of kallikrein in procollagenase activation was not fully clarified.

Adult↗
PubMed1984

The lubricating activity of human synovial fluids.

The lubricating abilities of human synovial fluids were measured using a rotating cartilage-on-glass apparatus. A total of 247 human fluids were lubrication-tested. Of these, 20 of the 180 knee fluids from patients with degenerative/traumatic joint disease lubricated less well than normal bovine synovial fluid. The remainder of the fluids from the knee and other joints were equivalent to normal bovine synovial fluid in their lubricating properties. The concentrations of hyaluronic acid, protein, and sialic acid and the relative viscosity of 117 human fluid samples were determined, but no relationships between the gross composition and the lubricating abilities were apparent.

Glycoproteins↗
PubMed1980

[Viscosity of synovial fluid and possible artificial lubricants (author's transl)].

The viscosity of "normal" post mortem synovial fluid, and synovial fluid samples of knee joints affected by various joint diseases (inflammatory and non inflammatory) was investigated and compared with flow curves of Hyaluronic acid and Polyacrylamide solutions. The viscoelastic behaviours of synovial fluid seems to be of great importance for the lubrication mechanism of the joints. Differing results of the viscoelastic properties could be determined in different joint diseases. As a result of these changes the lubrication mechanism is impaired and this leads to cartilage wear. Solutions of Polyacrylamide and Hyaluronic acid have been investigated as model-substances, the former showing rheological properties similar to normal synovial fluid. Their application as an artificial lubricant has been investigated.

Acrylic Resins↗
PubMed1994

Substance P-, neurokinin A-, calcitonin gene-related peptide- and neuropeptide Y-like immunoreactivity (-LI) in rat knee joint synovial fluid during acute monoarthritis is not correlated with concentrations of neuropeptide-LI in cerebrospinal fluid and plasma.

In a recent study we have shown a bilateral release of substance P (SP)-, neurokinin A (NKA)-, calcitonin gene-related peptide (CGRP)- and neuropeptide Y (NPY)-like immunoreactivity (-LI) in rat synovial fluid during acute monoarthritis. In order to elucidate the mechanisms underlying these phenomena, we examined the correlation between neuropeptide-LI in rat cerebrospinal fluid (CSF) and synovial fluid and between plasma and synovial fluid following the intra-articular injection of equal volumes (0.05 ml) of either Freund's adjuvans, carrageenan 2%, substance P 10(-5) M or human recombinant interleukin-1 alpha. Control rats were given saline intra-articularly. CSF, plasma and synovial fluid from the knee joints were obtained at 2, 6 and 24 h after injection and were analysed by specific radioimmunoassays. The intra-articular injection of pro-inflammatory substances induced changes in neuropeptide-LI in synovial fluid, CSF and plasma. However, there was no correlation between neuropeptide-LI in synovial fluid and plasma or between synovial fluid and CSF. The results of the present study does not support the hypothesis that the bilateral changes in neuropeptide-LI in synovial fluid were due to a release of neuropeptides from the inflamed joint into the systemic circulation. However, in carrageenan induced inflammation there was a tendency towards a correlation in SP-LI between CSF and synovial fluid suggesting that central neurogenic mechanisms should be studied in order to explain the bilateral changes seen.

Acute Disease↗
PubMed1997

Chondroitin sulfate isomers in synovial fluid of healthy and diseased human temporomandibular joints.

Synovial fluid was collected from the superior articular cavity of the temporomandibular joint in patients with unilateral internal derangement and joint pain whose contralateral joint was healthy. Glycosaminoglycans were liberated by digestion with pronase E, and precipitated with cetylpyridinium chloride and ethanol. Unsaturated disaccharide isomers of chondroitin sulfate, obtained following chondroitinase ACII digestion, were analyzed by high-performance liquid chromatography. Analytic data indicated that deltaDi-0S and deltaDi-6S were often found in chondroitin sulfate from the fluid of the diseased joints. The amounts of deltaDi-0S and deltaDi-6S differed significantly between synovial fluid samples from the diseased and healthy joints. Comparison of the relative proportions of the unsaturated disaccharides in the synovial fluid with previously reported values for several tissues, indicated that the chondroitin sulfate originated from articular cartilage, with possibly some contributions from soft connective tissues and serum present in the synovial fluid. These results suggest that chondroitin sulfate in the synovial fluid provides a useful indicator of the degree of internal derangement of the temporomandibular joint.

Adult↗
PubMed1992

Lipoxygenase products in inflammatory synovial fluids and other exudates.

Forty six synovial fluid samples from 42 patients with inflammatory joint disease were analysed by reversed phase high performance liquid chromatography to determine 5-lipoxygenase products, specifically dihydroxyeicosatetraenoic acids (diHETEs). Twenty eight per cent of the fluids which were assayed had one or more products of 5-lipoxygenase activation. Seven fluids contained leukotriene B4 (0.1-28.1 ng/ml); three fluids had low concentrations of 20 carboxy/hydroxy-leukotriene B4 (0.01-0.05 ng/ml); three samples had leukotriene B4 isomers (1.5-2.4 ng/ml); and four fluids contained 5,15-diHETE (2.3-16.4 ng/ml). There was a poor correlation between synovial fluid white blood cell counts and evidence of 5-lipoxygenase activation. Several fluids contained unidentified compounds with spectra similar in shape to that of trienes, but the lambda max values of these unidentified compounds were different from those of known leukotrienes. A septic peritoneal exudate and a septic pleural fluid had concentrations of leukotriene B4 and leukotriene B4 isomers and metabolites in a range similar to those found in synovial fluids.

Arachidonate 5-Lipoxygenase↗