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At least 289 records · Page 16Linked to original sources
PubMed2001

Bacterial DNA in synovial fluid cells of patients with juvenile onset spondyloarthropathies.

OBJECTIVE: To identify bacterial DNA in synovial fluid cells of patients with active juvenile onset spondyloarthropathy (SpA). METHODS: The main group of study constituted 22 patients with juvenile onset SpA. In addition, five patients with adult onset SpA and nine with rheumatoid arthritis (RA) were studied. Polymerase chain reaction (PCR) with either genus- or species-specific primers was performed on synovial fluid cells to detect DNA sequences of Chlamydia trachomatis, Yersinia enterocolitica, Salmonella sp., Shigella sp., Campylobacter sp. and Mycobacterium tuberculosis. The presence of antibacterial antibodies in sera and synovial fluid was also determined by enzyme-linked immunoassay. RESULTS: The synovial fluid of nine patients with juvenile onset SpA, three with adult onset SpA and one with RA contained bacterial DNA. Five juvenile onset SpA samples had DNA of one single bacterium; two juvenile onset SpA and three adult onset SpA had DNA of two bacteria and two juvenile onset SpA had DNA of three bacteria. Overall, Salmonella sp. DNA was detected in seven synovial fluid samples, Shigella sp., Campylobacter sp. and M. tuberculosis were found in four samples each, and C. trachomatis was found in two. The bacterial DNA findings correlated with neither diagnosis nor disease duration. One RA synovial fluid had DNA of Campylobacter sp. Neither serum nor synovial fluid antibacterial antibodies correlated with DNA findings or clinical diagnosis. CONCLUSION: In this study, single and several combinations of bacterial DNA were identified in the synovial fluid of patients with long-term undifferentiated and definite juvenile onset SpA and adult onset SpA. Of relevance is that bacterial DNA corresponds to bacteria producing endemic disease in our population.

Adolescent↗
PubMedDate not supplied

Comparisons of the oscillatory shear viscoelasticity and composition of pathological synovial fluids.

Rheological and compositional properties of pathological synovial fluids were measured and compared in order to reveal differences between disease states. The cases include degenerative joint disease, rheumatoid arthritis, mixed connective tissue disease, and pseudogout. Using an oscillatory flow capillary instrument, measurements were made of both the frequency and shear rate dependence of the complex viscoelasticity. The fluid types differ most in their elasticity, with the degenerative joint disease fluids having the greatest average viscosity, elasticity and intrinsic viscosity, followed by the rheumatoid arthritis fluids, and the fluids from cases of mixed connective tissue disease. Differences in the hyaluronate and protein concentrations are not as great as those between rheological variables. The viscoelasticity of synovial fluid appears more strongly dependent on the degree of polymerization of hyaluronate than on its concentration. These synovial fluids conform well to a model of relaxation process truncation. Distinct types of elastic stress-strain behavior reveal the nature of the dynamic fluid structure.

Arthritis, Rheumatoid↗
PubMed1990

Cytolytic activity in T cell clones derived from human synovial rheumatoid membrane: inhibition by synovial fluid.

A panel of T cell clones was derived from the synovial membrane of a patient with rheumatoid arthritis (RA). We investigated whether T cell clones with cytolytic properties were present and whether T cell cytotoxicity was influenced by the presence of synovial fluid. These issues were studied using anti-CD3 and lectin-induced cytotoxicity assays. The majority of the T cell clones derived from the synovial membrane showed cytotoxic properties although non-cytotoxic clones were also found. Three clones (N11, N6 and N15) showed strong cytotoxicity (more than 40% lysis at an effector-to-target cell ratio of 10:1) whereas three clones (N16, N4 and N14) were non-cytotoxic (less than 20% lysis at an effector-to-target cell ratio of 10:1). The induction of cytotoxicity in the anti-CD3-driven system was shown to be dependent on the dose of anti-CD3 present. When synovial fluid was added to these assays a strong inhibition of cytotoxicity was found. This inhibition of cytotoxicity was found with synovial fluid samples of RA patients, as well as with non-RA synovial fluids. Both anti-CD3 and lectin-dependent cytotoxicity assays were strongly inhibited. In conclusion, T cell clones with cytotoxic activity can be isolated from rheumatoid synovial membrane. In the presence of synovial fluid these cytotoxic cells are inhibited to exert their cytotoxic function.

Antibodies, Monoclonal↗
PubMed1983

Direct activation of neutrophil chemiluminescence by rheumatoid sera and synovial fluid.

The majority of paired sera and synovial fluids from 21 patients with rheumatoid arthritis produced a rapid chemiluminescent response when incubated with human neutrophils. Synovial fluid gave considerably higher responses than the paired serum specimen. In contrast little or no response was found with paired sera and joint fluid taken from patients with gout, psoriasis, and osteoarthritis and with sera from healthy donors. A similar chemiluminescent response was observed when neutrophils were preincubated with large aggregates of heated human gammaglobulin (HAGG), which were used as a model of immune complexes. Smaller nonreactive aggregates of gammaglobulin became reactive after preincubation with a purified monoclonal rheumatoid factor (mRF) which had a high avidity for aggregated IgG. The addition of this monoclonal rheumatoid factor also caused enhancement of chemiluminescence by rheumatoid sera. Further evidence suggesting that the active material found in these rheumatoid specimens contained complexed immunoglobulin was obtained by indirect immunofluorescence. Neutrophils developed intracellular immunoglobulin inclusions after preincubation in reactive rheumatoid sera but not with nonreactive or normal sera. However, activation of neutrophil chemiluminescence by rheumatoid specimens did not correlate significantly with levels of rheumatoid factor or immune complexes suggesting that the activating complexes were of a particular type. In conclusion we have shown the direct activation of neutrophil chemiluminescence by rheumatoid sera synovial fluid and suggest that the activation is caused by large IgG-containing immune complexes. It is possible that this activation may have important implications in the immunopathogenesis of the rheumatoid inflammatory process.

Arthritis, Rheumatoid↗
PubMed1995

Coagulant proteins and thrombin generation in synovial fluid: a model for extravascular coagulation.

The coagulant content and thrombin generating potential of synovial fluid from patients with osteoarthritis were studied as a model of extravascular coagulation. The concentrations of individual coagulant proteins were partially correlated with their molecular weight. The levels of the very large coagulants factor V, factor VIII and von Willebrand factor antigen (vWF:ag) are less than 1% of the activities found in a normal pooled reference plasma while smaller coagulants including factors IX, XI and prothrombin range between 9 and 30%. The protease inhibitors antithrombin-III (AT-III) and Alpha-2 macroglobulin in synovial fluid were present at levels of 74% and 13% of plasma, higher than expected based on their molecular weights. Prothrombin was more rapidly activated by tissue thromboplastin than by aPTT reagent. The thrombin activity formed in synovial fluid decreased more rapidly than that formed in dilute plasma. The addition of recombinant factor VIII or bovine factor V to synovial fluid accelerated the thrombin production by APTT but not by tissue thromboplastin. Indicating that the low levels of factor VIII and factor V did limit the rate of thrombin production. The addition of specific antibodies to factor VIII or factor V strongly inhibited thrombin production by aPTT. These data confirm a roughly inverse relationship between the concentrations of coagulation proteins and their molecular weight in synovial fluid and indicate that thrombin can be generated in synovial fluid. The inactivation of thrombin in synovial fluid may be more dependent on antithrombin-III than in plasma because of the increased AT-III/alpha-2 macroglobulin ratio seen in synovial fluid.

Animals↗
PubMed1993

Soluble tumor necrosis factor receptors in human inflammatory synovial fluids.

OBJECTIVE: To test synovial fluid (SF) for the presence of soluble fragments originating from distinct tumor necrosis factor receptors (TNF-sR55 and TNF-sR75) which bind to TNF and inhibit its biologic activity. METHODS: TNF-sR55 and TNF-sR75 were measured in 62 SF samples by specific immunoassays using monoclonal antibodies. RESULTS: Both TNF-sR were present in all of the SF tested. Their concentrations were higher in SF from patients with seropositive rheumatoid arthritis than in patients with other inflammatory arthritides. The relative amount of TNF-sR75, as compared with TNF-sR55, was higher in seropositive RA SF than in other SF. CONCLUSION: The balance between TNF and its specific inhibitors may be critical to the biologic outcome mediated by this cytokine.

Humans↗
PubMed1984

Demonstration of a helper factor(s) with T-cell-replacing activity in synovial fluid.

Cell-free synovial fluid (SF) obtained from patients with rheumatoid arthritis contains a helper factor(s) capable of augmenting the generation of plaque-forming cells (PFC) in pokeweed mitogen (PWM)-stimulated normal peripheral blood mononuclear cells (PBMC). This helper factor behaves like a polyclonal B-cell activator, in that it triggers the formation of IgM, IgG, and IgA PFC. However, SF has little or no effect on the proliferation of PWM-activated PBMC. Furthermore, SF was capable of replacing T cells for PWM-induced differentiation but not proliferation of enriched human blood B lymphocytes. No helper factor or T-cell-replacing activity was found in SF from patients with traumatic synovitis. Fractionation of SF containing helper activity on staphylococcal protein A column indicated that the activity is induced by biologically active molecules distinct from materials that preferentially bind to protein A such as IgG immune complexes. We conclude that the present activity has striking similarities to the recently described B-cell differentiation factor that is produced by specifically activated T-cell lines in vitro.

Arthritis, Rheumatoid↗
PubMed1984

[Cytofluorometric study of the cell cycle and various lymphocyte differentiation membrane antigens in the synovial fluid in rheumatoid polyarthritis].

Synovial fluid lymphocytes were studied by cytofluorometry in 11 patients with classical or definite rheumatoid arthritis. This method allowed the study of the cellular cycle after acridine orange staining and of membrane antigens, expressed by normal and/or activated lymphocytes, which were demonstrated by using various monoclonal antibodies (OKT3, OKT4, OKT8, OKIa1, OKT10). The OKT4/OKT8 ratio was decreased in 4 out of 5 cases and the percentage of HLA DR + cells was clearly increased. In 6 out of the 11 patients, the percentage of dividing cells varied from 2.2 to 7.2 and was less than 1 in the others as in normal blood lymphocytes. Increase in cellular RNA content characterized the non dividing cells. The most elevated values of the cellular RNA content were observed in patients who had the smallest percentage of dividing cells, suggesting that the cellular cycle was stopped between the G1 and S phases. Study of the cellular cycle may reveal a lymphocyte activation parameter which could be unrelated to the expression of differentiation membrane antigens.

Adolescent↗
PubMed2003

Functional characterization of adherent synovial fluid cells in rheumatoid arthritis: destructive potential in vitro and in vivo.

OBJECTIVE: To characterize the morphologic and immunologic features of adherent synovial fluid cells derived from patients with rheumatoid arthritis (RA), and to explore their potential function in vitro and in vivo by focusing on cartilage destruction. METHODS: Synovial fluid adherent cells obtained from patients with RA and from control subjects were characterized by immunohistochemistry, flow cytometry, and electron microscopy. In vitro, these cells were cultured in the presence of cartilage particles. Cartilage destruction was monitored by the release of sulfated glycosaminoglycans (sGAG) into the medium, and the level of matrix metalloproteinase 1 (MMP-1) in the cell culture supernatant was measured by enzyme-linked immunosorbent assay. To inhibit cartilage destruction in vitro, the MMP inhibitor marimastat was tested in this system. In vivo, in the SCID mouse coimplantation model, RA synovial fluid adherent cells and RA synovial fibroblasts (as positive controls) were coimplanted with human cartilage under the kidney capsule and maintained there for 60 days. RESULTS: In vitro, the synovial fluid adherent cells consisted of 2 subpopulations, large round-shaped macrophage-like cells (CD68+) and spindle-shaped fibroblast-like cells (Thy-1+). When passaged, the latter cells proliferated and organized themselves into 3-dimensional formations. This allowed them to reach collagen particles fixed with agarose. Fibroblasts derived from synovial tissues could not be used in this assay because they grew only in monolayers and not on agarose. The majority (>90%) of passaged RA synovial fluid adherent cells expressed the Thy-1+,CD45-,CD68-,CD86- phenotype. Electron microscopy did not reveal important morphologic differences between the 2 types of fibroblasts, those from synovial tissue or those from synovial fluid. However, synovial fluid adherent cells expressed lower levels of adhesion molecules, including CD54 and galectin 3, as well as the complement-regulatory molecule CD55. The in vitro release of sGAG associated with cell activity was 2.5-fold higher from RA synovial fluid adherent cells in comparison with that from negative control cells. The release of sGAG correlated with the concentration of MMP-1 and was inhibited by the broad-range MMP inhibitor marimastat in a dose-dependent manner. RA synovial fluid adherent cells coimplanted with cartilage in SCID mice showed the same invasive behavior as that displayed by tissue-derived RA synovial fibroblasts. CONCLUSION: Similar to tissue-derived RA synovial fibroblasts, RA synovial fluid adherent cells, which contain "floating" anchorage-independent fibroblast-like cells, mediate cartilage destruction independent of the hyperplastic synovial tissue.

Adult↗
PubMed1978

Markedly raised synovial fluid leucocyte counts not associated with infectious arthritis in children.

Synovial fluid leucocyte counts greater than 50 000 cells/mm3 (50 X 10(9)/1) are usually associated with infectious arthritis. Six children, 3 of whom meet the criteria for juvenile rheumatoid arthritis (JRA), are described with synovial fluid white blood cell counts greater than 88 000 cells/mm3 (88 X 10(9)/1). Two had synovial fluid leucocyte counts greater than 100 000 cells/mm3 (100 X 10(9)/1). The diagnosis of infectious arthritis was unlikely in these 6 children since the synovial fluid smears and cultures for infectious agents were negative and their histories atypical for infection. While in most instances such markedly raised synovial fluid leucocyte counts indicate infection, this finding is not diagnostic of septic arthritis.

Adolescent↗
PubMed1979

Plasma and synovial fluid cAMP in patients with rheumatoid arthritis.

cAMP was measured in plasma and synovial fluid from 11 patients suffering from rheumatoid arthritis with a specific protein-binding assay. Plasma and synovial fluid values were 17.0 +/- 6.8 pmol/ml and 8.3 +/- 3.7 pmol/ml, range 5-28 pmol/ml and 5-16 pmol/ml, respectively. No correlation could be established between plasma and synovial fluid levels, plasma and disease activity, or synovial fluid and disease activity, as judged by Lansbury's index. It is concluded that it seems unlikely that synovial fluid cAMP is derived solely from plasma and that no simple relation exists between cAMP in plasma and synovial fluid and total disease activity.

Adult↗
PubMed1992

Predictive value of synovial fluid analysis in juvenile chronic arthritis.

To investigate the value of synovial fluid analysis in predicting the articular evolution of juvenile chronic arthritis, synovial fluid from 29 patients with oligoarticular onset juvenile chronic arthritis were examined prospectively. The patients were subsequently classified after a three year period of observation as having polyarticular (10 patients) or pauciarticular (19 patients) disease. The synovial fluid samples were analysed for total and differential white blood cell count, total protein, beta 2 microglobulin, and total complement activity. For comparison, synovial fluid samples from 95 patients with adult onset rheumatoid arthritis were also analysed. In patients with polyarticular disease polymorphonuclear cells and beta 2 microglobulin concentrations were higher than in the patients with pauciarticular disease (80 (29.2) v 58.1 (25.3), and 3.6 (1.2) v 2.2 (0.5) mg/l, respectively), but there was no significant difference from the patients with rheumatoid arthritis. Synovial fluid analysis may be useful in predicting the evolution of juvenile chronic arthritis and improve definition of its subtypes.

Arthritis, Juvenile↗
PubMed1979

Plasma and synovial fluid lysozyme activity in horses with experimental cartilage defects.

Cartilaginous defects were created in the radiocarpal joints of 12 horses. Synovial fluid cytologic features, lysozyme activity, and beta-glucuronidase activity were monitored for 16 days. A comparison was made of plasma lysozyme and beta-glucuronidase activity and of synovial fluid lysozyme, beta-glucuronidase, and leukocyte concentrations. Plasma lysozyme was found to be independent of synovial fluid lysozyme activity. Synovial fluid lysozyme was significantly increased (P less than 0.001) in all joints with surgically induced defects (group I) compared with controls (arthrocentesis done; group III). However, there was no significant difference in lysozyme activity in group I joints and sham-operated controls (cartilage exposed only; group II). Increased lysozyme concentration was found to be positively correlated with increased numbers of leukocytes in the synovial fluid. Parallel changes were noted in synovial fluid beta-glucuronidase activity, indicating that much of the observed synovial fluid lysozyme activity was of lysosomal origin and not from cartilage destruction. Lysozyme activity in synovial fluid was found to be a very sensitive indicator of acute joint injury or inflammation (or both).

Animals↗
PubMed1981

Detection and quantitation of fibronectin in synovial fluid from patients with rheumatic disease.

Fibronectin, a high molecular weight glycoprotein that binds to glycosaminoglycans, fibrinogen or fibrin, and collagen, was identified and quantitated in synovial fluid from patients with various rheumatic diseases. Fibronectin concentration was significantly higher in synovial fluids from patients with rheumatoid arthritis (RA) (697 microgram/ml) than in other synovial fluids. In RA, synovial fluid fibronectin concentration exceeded that in plasma and did not directly correlate with synovial fluid concentrations of albumin, total protein, or fibrinogen. Synovial fluid fibronectin concentration correlated directly with synovial fluid white blood cell count (r = 0.50, P less than 0.005). Fibronectin was present in cryoprotein formed from four rheumatoid synovial fluids.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Fat droplets and synovial fluid leukocytosis in traumatic arthritis.

The presence of fat droplets in synovial fluid signifies major or minor joint trauma with damage to the bones or adjacent supporting structures. Synovial fluids aspirated after traumatic hemorrhage usually have a low white blood cell count. In this report 2 patients with hemorrhagic effusions had synovial fluid leukocytosis, presumably secondary to lipid droplet phagocytosis. Lipid globules intra- and extracellulalary in the synovial fluid and a top fatty layer in the hematocrit spin of the hemorrhagic synovial fluid are indications of the traumatic etiology of this inflammatory arthritis.

Adult↗
PubMed1989

A defect in immunoregulatory synovial fluid T cells in Behçet's syndrome.

Synovial fluid mononuclear cells from 5 patients with active Behçet's syndrome who were receiving no treatment were observed to have: decreased proportions of CD4+ and CD8+ cells, decreased proliferative responses of T cells in AMLR, poor capacity of non-T cells to stimulate in AMLR, decreased production of IL-2 upon PHA stimulation as compared both to their own peripheral blood mononuclear cells and to synovial fluid and peripheral blood mononuclear cells from 6 patients with RA and 6 patients with synovial effusions due to noninflammatory conditions. These findings provide further evidence of an immunoregulatory disturbance in Behçet's syndrome and indicate that synovial fluid, may be an important site where this derangement occurs in the active stage of the disease.

Adult↗
PubMed1982

The penetration of metronidazole into synovial fluid.

Six patients with non-infected synovial effusions, associated either with inflammatory or degenerative arthropathy and requiring diagnostic or therapeutic aspiration, were given a short course of 400 mg metronidazole (Flagyl) 8-hourly for 3 doses. Serum and synovial fluid (SF) were sampled frequently during this time, and assayed for metronidazole by a specific high pressure liquid-chromatographic method. It was found that concentrations of metronidazole in SF reached those in serum after a short time-lag, and thereafter approximated to the serum concentration. With this regimen, metronidazole concentrations were readily achieved in synovial fluid, above the minimum inhibitory concentrations for most susceptible anaerobes. These results indicate that the drug freely enters the synovial fluid and suggests that metronidazole would prove effective in the treatment of septic arthritis due to anaerobic bacteria.

Administration, Oral↗
PubMed1990

Oxidative response of polymorphonuclear leucocytes to synovial fluids from patients with rheumatoid arthritis.

Only a minority (7/35, 20%) of synovial fluids from patients with rheumatoid arthritis (RA) and none from patients with other arthritides stimulated the oxidative response of polymorphonuclear leucocytes (PMNs). Superoxide anion generation was measured by superoxide dismutase inhibitable reduction of cytochrome c. The same synovial fluids stimulated superoxide release by PMNs regardless of their source, though they elicited a greater response from RA synovial fluid PMNs than from either RA blood PMNs or blood PMNs from normal subjects. The remaining synovial fluids failed to stimulate any of the PMNs, though some (2/10) stimulated PMNs pretreated with cytochalasin B. The stimulatory activity was removed from RA synovial fluids by protein A-Sepharose and eluted with the void volume on gel chromatography. It is considered that immunoglobulin aggregates in some RA synovial fluids may stimulate the oxidative response of PMNs in the joint space but that most do not because these fluids contain either a specific inhibitor or immunoglobulin aggregates of an inappropriate type, or both.

Arthritis, Rheumatoid↗