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PubMed1984

Protective factors against oxygen free radicals and hydrogen peroxide in rheumatoid arthritis synovial fluid.

Oxygen free radicals are probably involved in the pathogenesis of rheumatoid arthritis (RA). The enzymes involved in protection against oxygen free radicals and H2O2 (superoxide dismutase, catalase, and glutathione peroxidase) were measured. Superoxide dismutase was not increased, glutathione peroxidase was slightly and catalase was strongly elevated in RA synovial fluid (SF) compared with control SF. Although these enzymes are present in SF, the activities are insufficient to protect against oxygen free radicals and H2O2. In contrast to transferrin, ferritin was increased in RA synovial fluid. Ceruloplasmin was also elevated. When rat liver microsomes were used as a target for oxygen free radicals, serum and SF were both protective. Gel filtration experiments showed that the fraction pattern in which there was maximal protective potential against lipid peroxidation corresponded closely to the level of ceruloplasmin. After removal of ceruloplasmin from serum or SF, about 70% of the protective capacity disappeared. It is concluded that ceruloplasmin is an important protector against oxygen free radicals.

Arthritis, Rheumatoid↗
PubMed1999

Neither nociceptin nor its receptor are present in human synovial fluid or tissue.

Our aim was to identify the nociceptin receptor and its endogenous ligand, nociceptin, in human peripheral tissue. Synovial tissue was obtained from 11 patients (ASA I-III, 66-84 yr) undergoing elective total knee replacement. Synovial fluid was obtained from another 10 patients (ASA I-III, 57-81 yr). Fluid was mixed with trifluoroacetic acid and the tissue with isopentone before freezing at -70 degrees C. Nociceptin receptor identification was performed using a [3H]nociceptin binding assay and nociceptin detection by radioimmunoassay. There was no specific [3H]nociceptin binding to knee synovial tissue and radioimmunoassay did not detect nociceptin. Neither the nociceptin receptor nor nociceptin was found in human synovial tissue or fluid.

Aged↗
PubMed1998

Intra-articular injection of hyaluronic acid reduces total amounts of leukotriene C4, 6-keto-prostaglandin F1alpha, prostaglandin F2alpha and interleukin-1beta in synovial fluid of patients with internal derangement in disorders of the temporomandibular joint.

This prospective randomised study was designed to assess the effect of an intra-articular injection of sodium hyarulonate on internal derangement in disorders of the temporomandibular joint. Fifteen patients (4 men, 11 women, mean (SEM) age 33(3) years) with unilateral internal derangement of the temporomandibular joint without radiographic evidence of the condylar degeneration who were randomly allocated to have arachidonic acid metabolites (n = 9) or cytokines (n = 6) measured in synovial fluid. The preauricular area was disinfected and anaesthetised locally with 1% lignocaine hydrochloride. Synovial fluid was collected by rinsing the joint with saline 5 ml. Sodium hyaluronate 1 ml (10 mg) was then injected into the superior compartment of the temporomandibular joint. The treatment was repeated after two weeks. The effects of sodium hyaluronate on total amounts of arachidonic acid metabolites and cytokines and on symptoms was measured. Injection of sodium hyaluronate caused significant reductions in the mean (SEM) of total amounts of leukotriene C4 (4.68 (2.27) to 0.48 (0.24) ng/joint), 6-keto-prostaglandin F1alpha (12.12 (2.78) to 5.19 (1.90) ng/joint), prostaglandin F2alpha (12.63 (5.51) to 4.21 (2.20) ng/joint), and interleukin-1beta (100.5 (14.2) to 50.8 (13.9) pg/joint), respectively (P<0.05 in each case). The mean (SEM) pain score was significantly reduced from 2.56 (0.18) to 0.89 (0.26) (P<0.01), the noise score from 2.18 (0.23) to 1.18 (0.18) (P<0.05), and degree of mouth opening from 28.2 (2.5) to 34.9 (2.0) mm (P<0.01). However, no improvement in symptoms was recorded in 1/9, 5/11, and 1/9 patients, respectively. These findings suggest that inflammation plays a part in internal derangement of the temporomandibular joint, and injection of an anti-inflammatory substance may be beneficial to such patients.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Helper (OKT4)/suppressor (OKT8) ratios in the peripheral blood and synovial fluid of patients with rheumatoid arthritis.

Lymphocyte subsets in the peripheral blood of 10 patients with RA were studied using monoclonal antibodies. The mean percentages of total T, T helper, T suppressor and TAR in the peripheral blood of RA patients were not different from those observed in normal controls. In the synovial fluid the mean percentages of T suppressor cells were present in increased numbers associated with a decreased number of autorosette T cells. We conclude that patients with rheumatoid arthritis present distinct immunoregulatory abnormalities in the synovial fluid not present in the peripheral blood. These changes may be related to the immune abnormalities present and related to the etiology of RA.

Antibodies, Monoclonal↗
PubMed1978

Immunological and functional characteristics of peripheral blood and synovial fluid lymphocytes from patients with rheumatoid arthritis.

Spontaneous (SCMC) and antibody dependent cellular cytotoxicity (ADCC); mitogenic responsiveness (PHA, Con A, PPD, dextran and pokeweed) as well as lymphocyte subpopulations (E-, EA-, EAC-rosettes, S-Ig) were studied simultaneously in peripheral blood (PBL) and synovial fluid lymphocytes (SFL) of fifteen patients with rheumatoid arthritis. Marked differences were observed in the cytotoxic activity of SFL and PBL. Whereas SCMC activity of SFL was always significantly elevated above the cytotoxic levels of PBL, the reverse was true for the ADCC reaction; here, 50% of the patients showed a decreased cytotoxicity of SFL compared to PBL. Synovial fluid neutrophils (SFN) were found to be inactive in both cytotoxic assays. No differences were found in ADCC activity of PBL between normal controls and RA patients. In SCMC assays a significantly increased activity of control PBL was only observed at L/T ratios of 100:1. Overnight incubation of PBL from RA patients and normal controls resulted in a marked decrease in SCMC and, to a smaller extent, in ADCC activity. SFL from three out of four patients lost less SCMC activity after overnight incubation than the corresponding PBL. In one patient even an increased activity in both cytotoxic systems was obtained. Regarding lymphocyte populations, T-cells were significantly decreased in PBL of RA patients. With the exception of a significantly lowered percentage of C3 receptor positive cells in SFL, no significant differences were recorded in the lymphocyte distribution between the patients' PBL and SFL. In the RA patients, the response to T-cell mitogens was significantly depressed in SFL while PPD and pokeweed reactivity was equal to that of PBL.

Adult↗
PubMed1996

Leflunomide, a novel immunomodulating drug, inhibits homotypic adhesion of peripheral blood and synovial fluid mononuclear cells in rheumatoid arthritis.

OBJECTIVE AND DESIGN: A novel immunomodulating drug, leflunomide has been shown recently to be effective and well tolerated in patients suffering from rheumatoid arthritis (RA). The present study evaluated the effect of the drug on cell adhesion in RA. MATERIAL AND TREATMENT: Peripheral blood and synovial fluid mononuclear cells were obtained from a clinical trial, undertaken primarily to evaluate the efficacy and pharmacokinetic profile of multiple-dose pulsing leflunomide therapy in RA patients. PB MNC and corresponding synovial fluid (SF) MNC for in vitro homotypic aggregation (HA) assay were obtained from healthy volunteers and RA patients with active disease not treated with leflunomide in vivo. METHODS: Expression of activation antigens (CD25, CD54, CD69, CD71, HLA-DR) on peripheral blood mononuclear cells (PB MNC), as well as ex vivo ability of cells to aggregate spontaneously were determined in patients before entering into the clinical trial and at the end of 6 months treatment. HA was measured by aggregation in vitro. Data were compared by Student's t-test. RESULTS: There was a decreased expression of activation antigens and decreased spontaneous MNC clustering after leflunomide therapy. We found in the in vitro study that HA of PB and SF MNC was mainly mediated through beta 2-integrin molecules. The active metabolite of leflunomide, A77 1726, effectively suppressed both spontaneous and phorbol-ester (PMA)-induced HA. Disruption of cell aggregates by A77 1726 was dose-dependent and, most likely, unrelated to the quantitative modulation of integrin receptors. CONCLUSIONS: Results from this study support the idea that leflunomide elicits its immunomodulatory action, at least partially, by modulating the adhesion process.

Adjuvants, Immunologic↗
PubMedDate not supplied

[Cefotaxime levels in synovial fluid following intravenous administration].

The corresponding levels of cefotaxime in serum and synovial fluid were investigated in patients undergoing surgery under perioperative antibiotic medication. By investigating 32 samples a concentration band over 4 hours could be established. Clinically relevant levels of the drug could be found from 10 minutes after start of the intravenous dose with an increase up to 30 minutes. Between 30 and 90 minutes the average concentration was about 40 micrograms/ml. After 90 minutes a decrease of the concentration was found and the median lines for synovial and serum concentrations crossed at about 105 minutes. Even after 4 hours we found synovial titers of 10 to 20 micrograms/ml having therapeutical relevance. From the results we can conclude, that cefotaxime infusion of 2 g produced over hours therapeutical synovial levels being significantly over the break point of 16 micrograms/ml for bacteria susceptible to this antibiotic agent. On the other hand we strongly recommend not to wait too long with surgical intervention when a joint infection does not improve significantly in 48 hours under systemic antibiotic treatment.

Adolescent↗
PubMed1996

Fibrin degradation in the synovial fluid of rheumatoid arthritis patients: a model for extravascular fibrinolysis.

The patterns of degradation and the influence of factor XIII polymerization on fibrin stability were examined in vitro following incubation with leukocyte elastase. In vivo experiments, various factor XIII-polymerized fibrin clots were implanted subcutaneously in mice to evaluate the stability of clots in the extravascular space. Both in vitro and in vivo lysis proceeded faster with nonpolymerized fibrin and was not influenced by the presence of cross-linked alpha 2-plasmin inhibitor. In vivo lysis of implanted clots was prevented by elastatinal, powerful elastase inhibitor, suggesting that granulocyte elastase is chiefly responsible for clot lysis in the extravascular space. To further extend investigations on the mechanisms of fibrinolysis in tissues, we evaluated fibrin and its degradation products in the synovial space. Expression of factor XIII in synovial cells and activities of coagulation factors, fibrinolytic enzymes, and inhibitors were investigated in the synovial fluid of rheumatoid arthritis patients. Immunohistochemical analysis showed deposits of insoluble fibrin on synovial membranes and pannus to an extent related to the progression of the disease. Factor XIII was expressed by fibroblasts and macrophages in the early stages of the disease, whereas in advanced stages factor XIII staining was associated with fibrin. The reduction of certain coagulation factors and high level of thrombin-antithrombin complexes in synovial fluid show a steady activation of the coagulation cascade. The evaluation of fibrinogen degradation products and the pattern of degradation of synovial fibrin(ogen) suggest the participation of leukocyte elastase in fibrin(ogen) lysis in synovial tissue of rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1985

[Leukocyte agglomeration in synovial fluid].

The agglomeration of leucocytes serves as evidence of leucocytic activation. In rheumatoid arthritis it can be used as a very sensitive criterion of activity. Patients with rheumatoid arthritis with joint effusions showed a high agglomeration of leucocytes in 97%, i.e. a clear activation of leucocytes. In 74.3% the number of punctate leucocyte agglomerated increased. Punctates with a proof of a spontaneous agglomeration of leucocytes showed the most intensive inclination to agglomeration also after incubation. By synovial fluid normal but also leucergic granulocytes could be stimulated to increased agglomeration to leucocytes. In the synovial fluid also factors stimulating the agglomeration of leucocytes are found. They probably come from punctate granulocytes and stimulate also the chemotaxis and activation of the blood granulocytes. Since granulocytes essentially participate in the inflammatory reaction of the rheumatoid arthritis and in the joint destruction evoked by it, the therapeutic aspect should be directed also to the inhibition of such leucocyte-activating factors in the synovia.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Synovial fluid analysis by ferrography.

Ferrography is a technique for magnetically harvesting and separating metallic particles from aqueous and non-aqueous suspensions. We have adapted this method of analysis to the study of cartilaginous and osseous wear particles, as well as fragments of soft tissue, found in the synovial fluid of human joints. As ferrography employes magnetism to harvest particles and arrange them in an orderly fashion, it is first necessary to impart a positive magnetic susceptibility to the biological materials. The trivalent paramagnetic cation of the rare earth element erbium is used for this purpose. Based on this principle, a method for the ferrographic analysis of synovial fluid has been devised, which is presently being employed in the study of human joint disease. Using this technique, improved diagnosis of arthritis may be possible. In addition, it may lead to a deeper understanding of the aetiology and pathogenesis of degenerative arthritis and other destructive joint diseases.

Arthritis↗
PubMed1997

Synovial fluid concentrations of the C-propeptide of type II collagen correlate with body mass index in primary knee osteoarthritis.

OBJECTIVE: To explore in a cross sectional study in patients with primary knee osteoarthritis (OA) the relations between body mass index (BMI), disease stage, and the concentrations of a putative joint fluid marker of type II collagen synthesis, procollagen II C-propeptide. PATIENTS AND METHODS: The study included 142 patients with knee OA (median age 68, median BMI 24.1). OA was staged radiologically. The concentrations in synovial fluid of procollagen II C-propeptide were measured by a sandwich enzyme immunoassay. RESULTS: Joint fluid concentrations of procollagen II C-propeptide were increased in knees with OA (median 3.7 ng/ml), compared with published reference values for knees in healthy adult volunteers (median 1.3 ng/ml). The concentrations of procollagen II C-propeptide were independently related to both OA stage and BMI (r = 0.343, p < 0.0001 and r, = 0.253, p = 0.002, respectively). CONCLUSIONS: Joint fluid concentrations of this putative marker of collagen II synthesis are high in early and mid-stage OA, but decrease in end stage disease. In addition and for the first time it was shown that the concentrations in synovial fluid of procollagen II C-propeptide increase with increasing BMI in primary knee OA. The increased joint fluid values of this marker in patients with primary knee OA and a high BMI, may reflect increased rates of collagen synthesis in their joint cartilage and could relate to the previously shown increased risk for disease progression in such patients.

Adult↗
PubMed1984

The correlation of clinical assessment of synovial fluid with its measured viscosity.

The viscosity of 10 specimens of rheumatoid synovial fluid was assessed using side-room tests as well as being measured in a viscometer. All of the tests, and particularly the 'mucin clot', correlated well with measured viscosity. We conclude that the mucin clot test does indeed reflect viscosity and can demonstrate the presence of inflammatory joint disease.

Arthritis, Rheumatoid↗
PubMed1988

Evaluation of immune complexes and collagen type-specific antibodies in sera and synovial fluids of horses with secondary osteoarthritis.

Thirty-one horses with secondary osteoarthritis as a sequel of trauma (chip fractures) or osteochondritis dissecans were screened for immune complexes (IC) and anticollagen antibodies. Eighty-two percent of horses with joint disease had circulating C1q-binding IC; 77% of those horses had IC in synovial fluids of affected joints. Although only a few horses had anticollagen type-II antibodies, anticollagen type-I antibodies were found in sera of 25% of the horses and in 41% of their synovial fluids. This correlated well with the clinical data and suggested that antibodies might have been elicited by antigens derived from detached intra-articular osteochondral fragments. Immunologic reactivity is a new concept in equine secondary osteoarthritis and might be involved in the mechanisms of chronic inflammation and progressive collagen destruction in degenerative joint disease.

Animals↗
PubMed1991

Limiting dilution analysis of proliferative T cell responses to mycobacterial 65-kDa heat-shock protein fails to show significant frequency differences between synovial fluid and peripheral blood of patients with rheumatoid arthritis.

Recent evidence has pointed to the mycobacterial 65-kDa heat-shock protein (hsp 65) as an antigen that may be important in the pathogenesis of rheumatoid arthritis (RA). Using limiting dilution analysis the frequency of purified protein derivative of tuberculin (PPD) and hsp 65-responsive T cells was measured in paired peripheral blood and synovial fluid samples of patients with RA. There was no increase in the anti-PPD or anti-hsp 65 frequency in synovial fluid compared with peripheral blood. In addition, no difference was found between peripheral blood of RA patients and healthy controls. These results do not support the idea of an important pathogenic role of T cells responding to hsp 65, or a cross-reacting antigen, in RA.

Antigens, Bacterial↗
PubMed2006

Synovial fluid cell counts and total protein concentration in clinically normal fetlock joints of young dromedarian camels.

Twenty-seven 9-12 months old healthy male dromedarian camels were used to determine total nucleated leucocyte count (TNCC), absolute and percentages of polymorphonuclear (PMN) and mononuclear leucocytes, and total protein (TP) concentration in synovial fluid from grossly and radiographically normal fetlock joints. Arthrocentesis was performed bilaterally from the fetlock joints of the forelimbs and hindlimbs. Blood contaminated samples and samples obtained from grossly or radiographically abnormal joints were excluded. The mean +/- SD of TNCC in 108 samples of fetlock joint synovial fluids was 500 +/- 400 cells/microl. Monocytes/macrophages were the predominant cell type. There were no significant differences in mean TNCC, absolute numbers and percentages of various leucocytes and TP concentrations between the right and left fetlock joints of the forelimbs and hindlimbs or between the fetlock joints of the forelimbs and hindlimbs. The mean +/- SD of absolute numbers and percentages of various cell types were: PMN leucocytes 1 +/- 2 cells/microl (2%), lymphocytes 116 +/- 167 cells/microl (26%), and monocytes/macrophages 383 +/- 323 cells/microl (72%). The mean +/- SD of TP concentration was 2 +/- 1 g/dl.

Animals↗
PubMed1998

Synovial fluid cytokines in patients with rheumatoid arthritis or other arthritic lesions.

The synovial fluid (SF) of rheumatoid arthritis (RA) patients contains a mixture of inflammatory mediators. In order to determine whether certain cytokine patterns locally in the joint are specifically related to the chronic inflammation in RA, the concentrations of interleukin (IL)-1alpha, IL-1beta, IL-6, IL-10, transforming growth factor-beta (TGF-beta), tumour necrosis factor-alpha (TNF-alpha) and IgG2b-inducing factor (IgG2bIF) were measured in SF from 22 patients with RA and 22 patients with other types of arthritic lesions. High levels of IL-10, latent and active TGF-beta and the presence of IgG2bIF are significantly correlated with RA when corrected for age. As these factors have the capacity to promote antibody production, they might contribute to the maintenance of local antibody production in RA synovial tissues. All RA-SF samples contained detectable levels of IL-10 and all except one contained IL-1beta, while concentrations in several non-RA-SF samples were below detection limits. IL-6 and TGF-beta were present in all SF samples from both RA and non-RA patients. The presence of IgG2bIF was strongly correlated with high levels of IL-10 and IL-1beta in SF. However, no distinct cytokine profile specific for the chronic inflammation characteristic of RA was found.

Adult↗
PubMed1978

Influence of proquazone (Biarison) on the levels of complement components (C3 and C4) in synovial fluid and on IgM in serum in patients with active rheumatoid arthritis. A preliminary report.

Four patients with erosive rheumatoid arthritis and one with psoriasis arthropathy were treated with 600-900 mg/day proquazone for 4-7 weeks. All patients had acute knee effusions. The complement components C3 and C4, as well as IgG, IgA, IgM and total protein, were measured in both the synovial fluid and serum before and after treatment. In the 4 patients with rheumatoid arthritis, a marked increase in C3 and/or C4 levels in the synovial fluid was found, correlating in 3 cases with a good clinical response. However, no corresponding changes in complement levels were recorded in the serum. The patient with psoriasis arthropathy did not show any reaction. These preliminary results suggest that proquazone may influence the immunological processes in rheumatoid arthritis.

Adult↗
PubMed1986

Mini-plasminogen-like fragments of plasminogen in synovial fluid in acute inflammatory arthritis.

Neutrophil elastase digests plasminogen to yield a fragment, mini-plasminogen, which is activatable to a mini-plasmin capable of escaping the action of the primary plasmin inhibitor. Such a molecule may play a role in joint destruction, either directly or by activation of procollagenase to collagenase. Synovial fluid samples from 34 acute joint effusions were examined by lysine-Sepharose chromatography and fibrinolytic assay of the fall-through (non-lysine-binding) fractions in presence of urokinase. Fragments similar to mini-plasminogen were found in 20 of 23 inflammatory effusions (cell count greater than 0.5 X 10(3)/microliter) and in none of 11 non-inflammatory (traumatic and osteoarthritic) effusions (cell count less than 0.5 X 10(3)/microliter) (p less than 0.001). Analysis of four inflammatory fluids by gel filtration on Bio-Gel P 100 and enzyme-linked immunoassay for plasminogen antigen revealed plasminogen fragments with molecular weight similar to mini-plasminogen (34,000 daltons) in three, and larger plasminogen fragments (or complexes of mini-plasminogen with other synovial fluid macromolecules) in all four. Fibrinolytic activity was demonstrable in fractions containing plasminogen fragments after treatment with tissue type plasminogen activator. In contrast with non-inflammatory effusions, inflammatory joint fluids contain plasminogen fragments with the properties of mini-plasminogen, suggesting their possible role in inflammatory joint destruction.

Acute Disease↗