Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SYNOVIAL FLUID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,747 records · Page 97Linked to original sources
PubMed1977

Cyclic AMP response to prostaglandin E1 in mononuclear cells from peripheral blood and synovial fluid of patients with rheumatoid arthritis.

The cyclic AMP response to prostaglandin E1 (PGE1) was studied in peripheral blood (PB) and synovial fluid (SF) mononuclear cells from patients with rheumatoid arthritis (RA). The PGE1 induced accumulation of cyclic AMP was consistently (7 of 8 patients) less in cell suspensions derived from SF than in suspensions of equivalent numbers of mononuclear cells obtained simultaneously from PB. The high PB/SF cyclic AMP ratio was seen most clearly at the lowest concentration (10(-6)M) of PGE1 tested. There was no correlation between the patients' therapy and cyclic AMP response to PGE1. The high PB/SF cyclic AMP ratio was not accounted for by the presence of platelets in PB cell suspensions.

Arthritis, Rheumatoid↗
PubMed2006

Osteogenic protein 1 in synovial fluid from patients with rheumatoid arthritis or osteoarthritis: relationship with disease and levels of hyaluronan and antigenic keratan sulfate.

The measurement of body fluid levels of biochemical markers in joint tissues has begun to provide clinically useful information. Synovial fluid (SF) plays an important role in articular joint lubrication, nutrition, and metabolism of cartilage and other connective tissues within the joint. The purpose of our study was to identify and characterize osteogenic protein 1 (OP-1) in SF from patients with rheumatoid arthritis (RA) or with osteoarthritis (OA) and to correlate levels of OP-1 with those of hyaluronan (HA) and antigenic keratan sulfate (AgKS). SF was aspirated from the knees of patients with either RA or OA and from the knees of asymptomatic organ donors with no documented history of joint disease. The presence of detectable OP-1 in SF was demonstrated by western blots with specific anti-pro-OP-1 and anti-mature OP-1 antibodies. Measurement of levels of OP-1, HA and AgKS was performed using ELISAs. OP-1 was identified in human SF in two forms, pro-OP-1 and active (mature) OP-1--mature OP-1 being detected only in SF from OA patients and RA patients. Levels of OP-1 and HA were higher in RA patients than in OA patients and asymptomatic donors, while the level of AgKS was highest in SF from asymptomatic donors. Statistically significant differences were found between SF levels of OP-1 in RA and OA patients and between SF levels of AgKS among the three groups tested. The SF content of OP-1 tended to correlate positively with HA levels, but negatively with AgKS concentrations. In conclusion, the results of this study suggest that measurement of OP-1 in joint fluid may have value in the clinical evaluation of joint disease processes.

Arthritis, Rheumatoid↗
PubMed1975

[Capacity for in vitro growth and the character of synovial fluid cell transformation in rheumatoid arthritis patients].

Investigations carried out permitted to detect the in vitro growth of cells in the synovial fluid of patients suffering from rheumatoid arthritis. Five types of cells (macrophages, polykariocytes, fibroblast-like cells histiocytes and lymphocytes) appeared during transformation. It was revealed that the intensity of the cell growth in the culture depended on the activity of the disease; there was also a significant decrease of this intensity (P less than 0.01) in the treatment of the patients. The growth of the fibroblast-like cells up to the formation of colonies pointed to their possible participation in the genesis of inflammatory processes and sclerosing of the vessels. The observed phenomenon of the cytopathic interaction of the lymphocytes and of the fibroblast-like cells served as an index of an autoimmune conflict in the joint and, possibly, one of the mechanisms of automaintenance of the autoimmune process.

Arthritis, Rheumatoid↗
PubMed2005

Evaluation of the speciation status of aluminium(III) ions in isolated osteoarthritic knee-joint synovial fluid.

High field 1H NMR spectroscopy demonstrated that the equilibration of added Al(III) ions in osteoarthritic (OA) knee-joint synovial fluid (SF) resulted in its complexation by citrate and, to a much lesser extent, tyrosine and histidine. The ability of these ligands, together with inorganic phosphate, to compete for the available Al(III) in terms of (1) thermodynamic equilibrium constants for the formation of their complexes and (2) their SF concentrations was probed through the use of computer speciation calculations, which considered low-molecular-mass binary and ternary Al(III) species, the predominant Al(III) plasma transport protein transferrin, and also relevant hydrolysis and precipitation processes. It was found that, at relatively low added Al(III) concentrations, citrate species were more favoured, whilst phosphate species became dominant at higher levels. The significance of these findings with regard to the in vivo corrosion of aluminium-containing metal alloy joint prostheses (e.g., TiAlV alloys) is discussed.

Aluminum↗
PubMed1991

Concentration of substance P, neurokinin A, calcitonin gene-related peptide, neuropeptide Y and vasoactive intestinal polypeptide in synovial fluid from knee joints in patients suffering from rheumatoid arthritis.

We have studied the presence of five neuropeptides in knee joint synovial fluid from either patients suffering from rheumatoid arthritis and pain (n = 18) or being subjected to arthroscopy due to meniscal/cruciate ligament injuries (n = 13). Radioimmunoassay technique was used for peptide analysis using antisera SP2 against substance P (SP), K12 against neurokinin A (NKA), CGRPR8 against calcitonin gene-related peptide (CGRP), NPY1 against neuropeptide Y (NPY) and VIP2 against vasoactive intestinal polypeptide (VIP). No SP could be detected, and lower levels of NKA was found in arthritic joints vs controls. CGRP and NPY was found in higher concentrations in arthritic patients vs controls. VIP was found sporadically in both arthritis and control patients. Our data show some quantitative differences between patients suffering rheumatoid arthritis and pain, and patients with non-inflamed joints without pain; indicating an involvement of peptidergic fibers in arthritis in humans.

Adult↗
PubMed1988

Measurement of oxygen and carbon dioxide partial pressures in synovial fluid after tonometry.

A commercially available gas analyser was used to measure tension of oxygen (PO2) and carbon dioxide (PCO2) in synovial fluid samples after tonometry. Measured values of PCO2 were close to the expected (median difference 0.2 kPa, range -0.4 to 0.4) within the analysed concentration range of 4-10 kPa. No consistent difference between measured and expected values of PO2 were found for oxygen in the range 3-11 kPa (median difference 0.1 kPa, range -0.3 to 1.2). For oxygen tensions below 3 kPa, however, the measured values invariably overestimated the actual PO2, the errors ranging from 0.3 to 1.9 kPa, median 1.1. The importance of proper handling of samples was investigated and storage for 1 h at 0 degrees C in plastic syringes resulted in elevation of the PO2 levels measured (range of elevation 0.2 to 3.6 kPa, median 1.15), whilst no significant differences were found when stored in glass syringes. Within the limits stated, commercially available gas analysers may thus be used to investigate these parameters related to local tissue metabolism in effusive joint conditions.

Carbon Dioxide↗
PubMed2000

Humoral autoreactivity directed against surfactant protein-A (SP-A) in rheumatoid arthritis synovial fluids.

SP-A is found principally in the lung, and has been associated with lamellar bodies also found in the synovial joint. Both SP-A and C1q contain collagen-like regions, and SP-A and C1q have some structural similarities, both having a globular head region and a collagen-like tail. Here we are able to show that (i) autoreactivity to SP-A, as expressed by IgG and IgM autoantibodies, is present in synovial fluid (SF) isolated from patients with rheumatoid arthritis (RA); (ii) in absorption experiments only a limited degree of cross-reactivity between autoantibodies reactive with C1q and SP-A is observed; (iii) there is no cross-reactivity between autoantibodies reactive with type II collagen (CII) and those reactive with SP-A or C1q; (iv) autoantibodies react with polymeric (dimers and larger) SP-A, but not with monomeric SP-A subunits, indicating that a degree of quaternary structure is required for antibody binding. Unlike CII, which not accessible in the normal joint, both SP-A and C1q are available within the SF in patients with RA and may therefore provide antigens driving an autoimmune response directed against collagen-like structures.

Animals↗
PubMed1988

Amino acid composition and NH2-terminal amino acid sequence of human phospholipase A2 purified from rheumatoid synovial fluid.

The amino acid composition and partial NH2-terminal amino acid sequence of an extracellular phospholipase A2 in human rheumatoid synovial fluid were determined. The predominant amino acids in the phospholipase A2 were cysteine, glycine, arginine, and lysine, suggesting that it is a basic one. The NH2-terminal 34 amino acids were found to be as follows: Asn-Leu-Val-Asn-Phe-His-Arg-Met-Ile-Lys-Leu-Thr-Thr-Gly-Lys-Glu-Ala-Ala-Leu- Ser-Tyr-Gly-Phe-Tyr-Gly-Cys-X-Cys-Gly-Val-Gly-Gly-Arg-Gly The enzyme contains Phe-5, Met-8, Ile-9, Tyr-24, Gly-25, Cys-26, Cys-28, Gly-29, Gly-31, Gly-32, and Gly-34 residues, all of which are conserved in most of the sequenced phospholipase A2. The remarkable feature of this enzyme was the absence of Cys-11, which is conserved in the "Group I" enzyme family. This is the first report concerning partial amino acid sequences of human non-pancreatic phospholipase A2.

Amino Acid Sequence↗
PubMed1992

Detection of Mycobacterium tuberculosis antigen in synovial fluid of patients with rheumatoid arthritis.

By use of antimycobacterial saline extract antibodies, Mycobacterium tuberculosis (MT) antigens have been detected in synovial fluid (SF) of patients with rheumatoid arthritis (RA) by a highly specific and sensitive double-antibody sandwich enzyme-linked immunosorbent assay (ELISA). Absorbance for 15 gout, 14 osteoarthritis (OA) patients, 12 patients with spondylarthropathies (SA) and eight patients with other inflammatory disorders (OID) ranged from 0.001 to 0.025 with the mean values of 0.0086 +/- 0.0078, 0.0077 +/- 0.0051, 0.0069 +/- 0.0059 and 0.0113 +/- 0.0059, respectively. Among 65 SF of patients with RA examined, 34 were found to be negative for MT antigen with absorbance ranging from 0.002 to 0.024 and a mean value of 0.0114 +/- 0.0070. For 31 (47.7%) MT antigen-positive specimens of RA, optical density ranged from 0.052 to 2.446 with a mean value of 0.5564 +/- 0.7354. Significant statistical difference (P less than 0.05) was found when MT antigen positives were compared with MT antigen negatives, gout, OA, SA and OID groups. Our results indicate that MT may be relevant to the pathogenesis of RA.

Analysis of Variance↗
PubMed1997

Systematic detection of mycoplasmas by culture and polymerase chain reaction (PCR) procedures in 209 synovial fluid samples.

The objective was to investigate the presence of mycoplasmas in rheumatoid arthritis (RA) and other chronic arthritides. Samples of synovial fluid (SF) were systematically collected from all patients presenting with an articular effusion. Each sample was divided into three parts. The first was kept for cytological count and culture on standard media for pyogens and mycobacteria, the second was cultivated on specific media for mycoplasmas and the third frozen for subsequent study by polymerase chain reaction (PCR). A total of 209 samples were studied. Half of the patients had inflammatory rheumatic diseases: RA (27), spondyloarthropathy (28), connective tissue disease (5), unclassified arthritis (45). The remaining suffered from other conditions, including osteoarthritis (60), gouty arthritis (19), haemarthrosis (5), post-traumatic effusion (2). Eight samples were positive by culture, two for Mycoplasma hominis; three for M. fermentans, one for M. salivarium, one for M. orale and one for Ureaplasma urealyticum. All the patients concerned had an inflammatory rheumatic disease: five had RA, one had psoriatic arthritis and two had unclassified arthritis. These results were confirmed by PCR in two cases (one M. fermentans, one U. urealyticum). The lack of sensitivity of the conventional PCR assay on SF is discussed. Mycoplasmas were mainly detected in SF of RA patients. These results raise the question of the possible role of mycoplasmas in the triggering and maintenance of inflammatory rheumatic diseases, especially RA.

Adult↗
PubMed2003

Development of a solid-phase assay for measurement of sulfated glycosaminoglycan concentrations in equine synovial fluid.

OBJECTIVE: To develop a new 1,9-dimethylmethylene blue (DMMB) assay for measurement of sulfated glycosaminoglycan (sGAG) concentrations in equine synovial fluid (SF) by use of membrane technology and to compare the assay's ability to measure sGAG concentrations with that of 2 other established DMMB assays. SAMPLE POPULATION: 25 samples of SF collected from affected joints of 14 horses and 13 samples of SF collected from nonaffected (control) joints of 4 horses. PROCEDURE: A solid-phase DMMB assay was developed to measure sGAG concentrations in SE Results for the assay were then compared with results obtained by use of the direct spectrophotometric method (ie, Famdale method) and microplate DMMB assay. RESULTS: The solid-phase assay and direct spectrophotometric assay measured the same sGAG concentrations in identical equine SF, but those concentrations differed significantly from results obtained by use of the microplate DMMB assay. All other aspects of the solid-phase DMMB assay were comparable to both the direct spectrophotometric and microplate DMMB assays. CONCLUSIONS AND CLINICAL RELEVANCE: The new solid-phase assay can be used interchangeably with the direct spectrophotometric method to measure sGAG concentrations in equine SF samples, but it cannot be interchanged with the microplate DMMB assay. Results can be rapidly obtained with the solid-phase assay. Also, the solid-phase assay can detect nanogram quantities of sGAGs in SF, circumvent the problem of premature precipitation of sGAG-dye complexes, and provide quantitative or qualitative results. The solid-phase assay may replace other DMMB assays for measuring sGAG concentrations in SF obtained from horses.

Animals↗
PubMed1994

Concentration and molecular weight distribution of hyaluronate in synovial fluid from clinically normal horses and horses with diseased joints.

High molecular weight (MW) hyaluronate (HA) is an integral part of synovial fluid (SF), regulating many important physiologic and pathophysiologic mechanisms. Many of its effects depend on, or are reflected in, the concentration and MW of HA. High-performance liquid chromatography was used to assess simultaneously the concentration and MW of HA in SF obtained from horses with various arthritides: acute traumatic arthritis; chronic traumatic arthritis, including degenerative joint disease (DJD); and infectious arthritis. The size-exclusion column was calibrated, using appropriate HA concentration and MW standards, before the high-performance liquid chromatographic assays of the SF samples. Calibration of the column disclosed that the maximal limit for MW estimation of HA was around 3 million. In control joints, MW of HA ranged from 2 to 3 x 10(6) (mean 2.5 x 10(6)) and did not differ significantly from MW of HA in SF from horses with acute or chronic traumatic arthritis (mean 2 x 10(6); range 1.5 to 3 x 10(6)). Interestingly, a small amount of HA of moderately high MW (approx 1 to 1.5 x 10(6)) was detected in chromatograms of SF from infected joints. This degree of polymerization of SF HA was significantly (P < 0.01) lower, compared with that for control joints. There was no difference in mean (+/- SD) concentration of HA between control joints and joints with acute or chronic traumatic arthritis (0.33 +/- 0.12 g/L vs 0.18 +/- 0.03 g/L or 0.23 +/- 0.12 g/L), indicating that SF HA concentration probably should not be used as a diagnostic marker for the condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed2000

Cyclosporin A inhibits CD69 expression induced on synovial fluid and peripheral blood lymphocytes by interleukin 15.

OBJECTIVE: To study the modulation of CD69 expression on peripheral blood (PB) and synovial fluid (SF) lymphocytes by interleukin 15 (IL-15) and several other cytokines and chemokines widely detected in the rheumatoid microenvironment. The effect of cyclosporin A (CSA) or methotrexate (MTX) in the cytokine mediated regulation of CD69 was analyzed. METHODS: CD69 expression on lymphocytes was assessed by flow cytometry after incubation with different cytokines, chemokines, phorbol myristate acetate, or calcium ionophore in the presence or absence of CSA, MTX, or both. The effect of IL-15 and SF supernatants in maintaining CD69 expression on SF lymphocytes was also assessed. IL-15 levels in SF supernatants were measured by ELISA. RESULTS: IL-15 induced the greatest upregulation of CD69 expression on PB lymphocytes in a time and dose dependent manner. IL-15 was able to maintain a high CD69 expression on SF lymphocytes. SF supernatants from rheumatoid arthritis (RA), which contain significant amounts of IL-15, also reversed the CD69 downregulation of SF lymphocytes in culture. CSA, but not MTX, inhibited the CD69 upregulation mediated by IL-15 both in PB and SF lymphocytes. CONCLUSION: IL-15 appears to be responsible, at least in part, for the high CD69 expression on lymphocytes from the rheumatoid microenvironment. Consistent with the virtual absence of lymphocyte derived cytokines in RA synovium, the prevention of IL-15 mediated CD69 upregulation on lymphocytes may explain the effect of CSA in the treatment of RA.

Antigens, CD↗
PubMed1995

Peripheral blood and synovial fluid mononuclear cell phenotypes in lentivirus induced arthritis.

OBJECTIVE: To identify the phenotypes and activation status of peripheral blood (PB) and synovial fluid (SF) mononuclear cells associated with caprine arthritis encephalitis virus (CAEV) induced arthritis in goats. METHODS: PB and SF mononuclear cells from 8 goats chronically infected with CAEV and 2 mock-infected goats were phenotyped by single immunofluorescence flow cytometry using a panel of monoclonal antibodies (Mab) to caprine leukocyte differentiation molecules. The activation status of mononuclear cell subsets was evaluated by dual immunofluorescence flow cytometry using Mab to major histocompatibility complex (MHC) class II molecules and the interleukin 2 receptor (IL-2R). RESULTS: Three CAEV infected goats had chronic progressive arthritis, clinically evident by periarticular swelling of carpal joints with excessive SF containing inflammatory cells and radiographic changes indicating soft tissue swelling and erosion of articular surfaces. The other 5 infected goats and 2 mock-infected control goats did not exhibit criteria of arthritis. The composition of PB mononuclear cells (11.3 +/- 5.0% monocytes, 21.1 +/- 4.7% B cells, 29.6 +/- 5.4% CD4+ cells, 15.2 +/- 6.1% CD8+ cells, and 9.7 +/- 3.9% gamma delta T cells) was not significantly different between mock-infected and CAEV infected goats. In contrast, cells within the SF of arthritic carpal joints consisted of 71.9 +/- 7.9% CD8+ T cells, 13.3 +/- 5.9% CD4+ T cells and < 2% B cells. The proportions of SF macrophages (7.8 +/- 5.2%) and gamma delta T cells (6.5 +/- 1.3%) were not significantly different from PB. All SF mononuclear cells were activated with respect to class II determinants orthologous to HLA-DR, DP and DQ. IL-2R expression by CD4+ and CD8+ T lymphocytes in SF was reduced compared to PB. CONCLUSION: Lymphocytes infiltrating the SF of arthritic carpal joints of CAEV infected goats consisted of a predominant subset of class II activated CD8+ T lymphocytes and a minority population of CD4+ T lymphocytes, both of which express very little IL-2R. These results parallel previous reports of the phenotypes and activation status of mononuclear cells in rheumatoid SF. A potential connection between T lymphocyte subset reactivity to CAEV and immunopathogenesis of arthritis is suggested.

Animals↗
PubMed1983

Molecular weight distribution of hyaluronic acid of human synovial fluid in rheumatic diseases.

New methods to isolate and characterize the molecular weight distribution of hyaluronic acid have been applied to human synovial fluids from arthritic patients. Considerable variations in molecular weight distribution were found between the individual fluids. These methods facilitate a detailed characterization of hyaluronic acid--a prerequisite for understanding the role of hyaluronic acid for normal joint function and to evaluate the therapeutic use of local application in joint diseases.

Adult↗
PubMed1992

Influence of rheumatoid synovial fluid and cells on proteoglycans in human cartilage explants. Modulation by piroxicam.

We have studied the effects of cell-free rheumatoid synovial fluid (RASF) and the conditioned medium (CM) from these cells on the proteoglycans (PGs) of normal human cartilage and the influence which piroxicam might have on these processes. Both RASF and the CM from RASF cells enhanced the PG release from the cartilage explants. The effects of the above mentioned fluids on the cartilage PG content depended on the metabolic state of the cartilage i.e. correlated inversely with the PG synthesis. Whether this was due to the presence of anabolic and catabolic factors in these fluids is discussed. Piroxicam had no adverse effect on the PGs of human cartilage in vitro. Piroxicam prevented the cartilage PG depletion when it was induced by the CM from RASF cells.

Adult↗
PubMed1993

Pharmacokinetics and pharmacodynamics of non steroidal anti-inflammatory drugs in synovial fluid.

Since the joint is the target organ of non steroidal anti-inflammatory drugs (NSAIDs) in rheumatic diseases, the concentration in the synovial fluid (SF) is an important determinant of clinical response to these agents. Present data indicate that in the SF pharmacokinetic behaviour of NSAIDs depends on their plasma elimination half-life. Moreover, some chiral drugs exhibit stereoselective distribution properties. Finally, pharmacodynamic investigations suggest that inhibition of prostaglandin synthesis in the synovial compartment is the dominant mechanism of action for most, if not all, NSAIDs.

Anti-Inflammatory Agents, Non-Steroidal↗