[Blastogenesis of peripheral blood lymphocytes by autologous synovial fluid lymphocytes and synovial fluid from patients with rheumatoid arthritis (author's transl)].
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Adolescent↗
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Results for “SYNOVIAL FLUID”
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Hydroxypyridinium collagen crosslinks in serum, urine, synovial fluid and synovial tissue in patients with rheumatoid arthritis compared with osteoarthritis.
OBJECTIVE: To investigate the relationship between inflammation markers and content of pyridinium crosslinks in hydrolysates of synovial tissue and to specify the significance of urinary excreted pyridinoline, released primarily from collagen I and II of bone and cartilage, and deoxypyridinoline released especially from collagen I of bone and dentin, dependent on disease activity in rheumatoid arthritis (RA). METHODS: Synovial tissue and fluid from knee endoprosthesis surgery, as well as simultaneously obtained serum and urine, were collected from 12 patients with inactive RA or RA with low disease activity [iRA: C-reactive protein (CRP) <28 mg/l], 10 with active RA (aRA: CRP > or =28 mg/l) and 21 with OA. After preparation of the synovial tissue, including hydrolysis, completely released synovial pyridinoline and deoxypyridinoline crosslinks as well as those from synovial fluid, serum and urine were investigated using a gradient ion-paired reversed-phase HPLC method. Crosslink levels in synovial tissue are expressed as mol/mol collagen, assuming 300 residues of hydroxyproline per collagen molecule, also measured by HPLC. RESULTS: In the synovial tissue of aRA patients we found significantly elevated total pyridinoline concentrations and pyridinoline/deoxypyridinoline (Pyr/Dpyr) quotients compared with the iRA and OA controls, indicating an elevated crosslinking density of mature synovial tissue collagen with increased activity of RA. Pyridinoline levels and the Pyr/Dpyr ratio were correlated with those of urine and with acute-phase reactants in RA patients. Compared with serum crosslink levels, which were unrelated to disease activity, the urinary concentration of pyridinoline was increased by a factor of 2 and showed a simultaneous increase with increasing synovitis. CONCLUSION: Both crosslinking density and degradation of mature collagen from synovial tissue depend on the disease activity in RA. Urinary excretion of associated crosslinks, expressed as the Pyr/Dpyr ratio, correlates with those in synovial tissue and may be confirmed as a marker of synovial tissue collagen degradation. We suggest that increased crosslinking of mature collagen in the synovial tissue of RA is related to an inflammation-dependent regulation of collagen synthesis in activated synovial fibroblasts, in which lysyl oxidase represents the final enzymatic step for crosslinking.
Adult↗
Immunoelectrophoretic assay for synovial fluid C3 with correction for synovial fluid globulin.
Synovial fluid C3 was measured by electroimmunoassay. When C3 was expressed as mg/ml, the amounts found in Reiter's disease, psoriatic arthritis, gout, and systemic lupus erythematosus were significantly different from degenerative arthritis. When C3 was corrected for total protein, the levels for rheumatoid arthritis, Reiter's disease, psoriatic arthritis, and systemic lupus were significantly different from degenerative arthritis. When C3 was corrected for synovial fluid globulin, only rheumatoid arthritis and systemic lupus were significantly different from degenerative arthritis. Correction of C3 for globulin increases the difference between rheumatoid arthritis and degenerative arthritis. A proportion of gouty fluids with a relative decrease in C3 is demonstrated. It is argued that correction of C3 for globulin is more meaningful than correction for total protein. While many nonrheumatoid inflammatory effusions demonstrate split products of C3, the majority of fluids from patients with systemic lupus have none.
Arthritis↗
Detection of Borrelia burgdorferi by species-specific and broad-range PCR of synovial fluid and synovial tissue of Lyme arthritis patients before and after antibiotic treatment.
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Anti-Bacterial Agents↗
[Morphological activity estimation of rheumatoid arthritis: a comparative study of synovial fluid and synovial membrane].
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Arthritis, Rheumatoid↗
Hydroxyproline metabolism in serum, synovial fluid ans synovial membrane in joint diseases.
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Adolescent↗
Physiopathologic aspects of fibrinolytic system in knee joint--fibrinolytic system of synovial fluid and synovial membrane--.
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Fibrinolysis↗
Inhibitors of interleukin 1 activity in synovial fluids and in cultured synovial fluid mononuclear cells.
Measurement of interleukin 1 (IL-1) in synovial fluids (SF) yielded variable results and implied the presence of an inhibitory activity. As peripheral blood monocytes produce an IL-1 receptor antagonist (IL-1ra), we investigated whether SF mononuclear cells (SFMC) also secreted such inhibitory activity. MC isolated from inflammatory SF produced, in addition to variable levels of IL-1, a specific IL-1 inhibitor of approximately 23 kDa which blocked both IL-1 biological activity and binding to its receptor. Western blot, using a polyclonal antibody to rhIL-1ra, indicated that SFMC secreted material that shared immunological crossreactivity with the cloned IL-1ra. IL-1 inhibitory activity was also detected in SF but not formally demonstrated to be related to IL-1ra. In conclusion, SFMC could produce IL-1ra and an imbalance between IL-1 and its specific antagonist may be relevant to the severity of joint destruction.
Blotting, Western↗
Connective tissue activation by synovial fluids and synovial-tissue extracts of rheumatoid arthritis patients.
Prompted by Castor's investigations (4) on a connective-tissue-activating peptide (CTAP) we investigated the stimulative effect of synovial fluids and synovial-tissue extracts on the synthesis of collagen by incubated embryonic-chick tendon cells. The stimulative effect was greater with synovial-tissue extracts from more severe cases than with samples from patients having milder forms of the disease. There was no correlation between the stimulation by synovial fluids and synovial-tissue extracts from the same patient. The stimulative activity was lost at dialysis. A slight stimulation in the incorporation of glucosamine was also observed. Treatment of the patients with gold, chloroquine or steroids decreased the stimulating capacity. These effects seem to depend on factors different from those described by Castor. The differerences in the stimulant activity of samples from various groups cannot be entirely due to glutamine, which is one of the limiting nutrients of the embryonic-chick tendon cells.
Animals↗
Peripheral blood and synovial fluid monocyte activation in inflammatory arthritis. II. Low levels of synovial fluid and synovial tissue interferon suggest that gamma-interferon is not the primary macrophage activating factor.
Because synovial fluid monocytes (SFM) in patients with inflammatory arthritis bear an activated phenotype (i.e., high expression of HLA-DR and low expression of the monocyte differentiation antigen Mo2), we assessed the role of gamma-interferon (gamma-IFN) in the activation of these cells. Sensitive and specific radioimmunoassays detected only 0.40 +/- 0.20 units/ml of gamma-IFN in the SF of patients with rheumatoid arthritis (RA) and 0.61 +/- 0.67 units/ml of gamma-IFN in the SF of patients with other forms of chronic inflammatory arthritis. There was no detectable alpha-IFN in any SF studied by radioimmunoassay. Bioassays failed to detect nonimmunoreactive IFN. Synovial tissue (ST) explants produced very little gamma-IFN (0.14 +/- 0.091 units/ml), and production was not increased by the presence of indomethacin in the cultures or by removal of adherent cells. However, gamma-IFN was produced if ST was cultivated in the presence of phytohemagglutinin. In SF and ST supernatants, gamma-IFN-mediated induction of HLA-DR on monocytes was inhibited, even though the amount of immunoreactive IFN was not affected. Prostaglandin E2 was shown to be one possible inhibitor. We demonstrated that a factor that induces HLA-DR on some individuals' peripheral blood monocytes, and cannot be neutralized by monoclonal anti-gamma-IFN antibody, is present in SF and ST supernatants. These data suggest that activation of SFM may occur by mechanisms other than gamma-IFN.
Absorption↗
Boundary conditions at the cartilage-synovial fluid interface for joint lubrication and theoretical verifications.
The objective of this study is to establish and verify the set of boundary conditions at the interface between a biphasic mixture (articular cartilage) and a Newtonian or non-Newtonian fluid (synovial fluid) such that a set of well-posed mathematical problems may be formulated to investigate joint lubrication problems. A "pseudo-no-slip" kinematic boundary condition is proposed based upon the principle that the conditions at the interface between mixtures or mixtures and fluids must reduce to those boundary conditions in single phase continuum mechanics. From this proposed kinematic boundary condition, and balances of mass, momentum and energy, the boundary conditions at the interface between a biphasic mixture and a Newtonian or non-Newtonian fluid are mathematically derived. Based upon these general results, the appropriate boundary conditions needed in modeling the cartilage-synovial fluid-cartilage lubrication problem are deduced. For two simple cases where a Newtonian viscous fluid is forced to flow (with imposed Couette or Poiseuille flow conditions) over a porous-permeable biphasic material of relatively low permeability, the well known empirical Taylor slip condition may be derived using matched asymptotic analysis of the boundary layer at the interface.
Cartilage, Articular↗
Biologically active thrombomodulin is synthesized by adherent synovial fluid cells and is elevated in synovial fluid of patients with rheumatoid arthritis.
Thrombomodulin (TM) is a transmembrane glycoprotein that interacts with thrombin, thereby serving as a cofactor in the activation of protein C, a major physiologically relevant natural anticoagulant. Although initially described as a vascular endothelial cell receptor, TM has also been reported to be synthesized by several cells, including megakaryocytes, platelets, monocytes, neutrophils (PMN), mesothelial cells, and synovial lining cells. A prominent feature of rheumatoid arthritis (RA) is infiltration of PMN into the joint space. To determine whether TM might play a role in the inflammatory process, we examined synovial fluid for the presence of TM in 10 patients with RA and five patients with osteoarthritis (OA). We determined that the mean synovial fluid and plasma TM levels in the OA group were 23.5 ng/mL and 24.2 ng/mL, respectively, whereas those with RA had a significantly elevated mean synovial fluid TM level of 136.2 ng/mL as compared with the plasma TM concentration of 43.9 ng/mL (P < .05). Synovial fluid TM levels did not correlate with PMN counts (r = .261). Purified TM from synovial fluid was identical in molecular weight to plasma-derived TM and was biologically functional with respect to protein C cofactor activity. Using direct immunofluorescence, we determined that adherent cultured synovial fluid cells that are not monocytoid in origin express surface and cytoplasmic TM, thereby providing an alternative source of the protein. Biologic activity of the cell-surface TM was confirmed by acceleration of thrombin-dependent protein C activation. Northern analysis of RNA extracted from the cultured cells indicated that TM messenger RNA was present, suggesting local synthesis. Our results indicate that in RA-associated synovial effusions, biologically active TM is increased, the source of which may be from plasma, PMN, and/or synovial lining cells. TM may play a regulatory role either in fibrin deposition in the inflamed joint and/or in the progression of the inflammatory process.
Arthritis, Rheumatoid↗
Induction of a lymphotoxin-like mediator in peripheral blood and synovial fluid lymphocytes by incubation with synovial fluid from patients with rheumatoid arthritis.
A significantly increased spontaneous cell-mediated cytotoxicity (SCMC) has been reported in synovial fluid lymphocytes (SFL) as compared to peripheral blood lymphocytes (PBL) of patients with rheumatoid arthritis (RA) and that of normal controls [1-3]. To determine whether this increased SCMC activity is due to the production of a lymphokine and related to the production of a lymphotoxin(LT)-like mediator, PBL from normal controls and PBL and SFL from RA patients were incubated either with a human melanoma cell line (IGR 3) or with cell-free synovial fluid (SF) from RA patients. The SF and the cell-free supernatants of the different cultures were tested for LT activity by estimation of inhibition of DNA synthesis of HeLa cell monolayers and they were added to a SCMC assay system using normal PBL and IGR 3 as target. In the supernatants from cocultures of either PBL from controls or PBL and SFL from RA patients with IGR 3 cells, there was no significant difference in LT activity. An LT-like mediator was observed in the supernatants of all lymphocytes cocultured with SF, whereas SF alone and supernatants of lymphocytes alone exhibited little or no LT activity. In a control experiment, LT induction was not observed when normal lymphocytes were cultured with the serum of RA patients. Absorption of the culture supernatants with an insolubilised goat anti-human Ig did not remove LT activity. The demonstrated release of an LT-like mediator from lymphocytes incubated with SF might be one contributing mechanism to the inflammatory joint reaction in RA patients.
Arthritis, Rheumatoid↗
Superoxide generation by synovial fluid neutrophils enhanced by immune complexes and suppressed by rheumatoid factor in synovial fluid.
Synovial fluid (SF) from patients with rheumatoid arthritis (RA) enhanced superoxide generation by neutrophils isolated from RA SF, in contrast to SF from patients with osteoarthritis. These superoxide generation-enhancing substances may be intermediate-sized immune complexes and a complement C5-derived fragment. Rheumatoid factor (RF) isolated from RA SF suppressed superoxide generation-enhancing activity of aggregated IgG. Therefore, biologically active RF may block the interaction of the immune complexes with neutrophils accumulating in RA SF, and protect the joint tissue from the effects of oxygen radicals or proteases.
Antigen-Antibody Complex↗
Survey of synovial fluid cryoprecipitates.
Synovial fluid cryoproteins from various inflammatory and noninflammatory arthritides were examined for the presence of immunoglobulin, fibrinogen, antiglobulin activity, and third component of complement and correlated with the synovial fluid leucocyte count. The majority of rheumatoid synovial fluid cryoproteins contained either IgG-IgM complexes or IgG alone. Contrary to previous reports, many synovial fluid cryoproteins from psoriasis, Reiter's syndrome, nonspecific acute polyarthritis, gout, and gonococcal arthritis also contained IgG and occasionally IgG-IgM complexes. Noninflammatory synovial fluids were less likely to contain any immunoglobulin. The highest concentration of cryoprotein was found in Reiter's syndrome. There was a significant (P < 0.05) correlation between the presence of immunoglobulin and the concentration of the synovial fluid cryoprotein with the synovial fluid leucocyte count. Since synovial fluid cryoproteins containing immunoglobulin are present in the synovial fluids of many diverse rheumatic diseases not postulated to be immune complex mediated, they may be a nonspecific phenomenon related to the degree of inflammation.
Arthritis↗
The role of synovial fluid filtration by cartilage in lubrication of synovial joints--I. Mixture model of synovial fluid.
A mathematical model of lubrication of human synovial joints under squeeze-film conditions is presented in this several-part paper. Squeeze-film action leads to a concentration of hyaluronic-acid-protein macromolecular complex in the synovial fluid between the approaching cartilage surfaces as a result of the diffusion of water and low molecular weight substances through the cartilage surfaces or along the gap. Increasing viscosity of synovial fluid delays the approach of these surfaces and the formation of stable gels then protects cartilage, if sliding motion ensues, before fluid film lubrication is restored. In Part I of the present paper synovial fluid is considered as a mixture of two incompressible fluids. The material parameters of this mixture of fluids are found using previously published experimental results. Squeeze-film analysis is carried out for the axially symmetric synovial film.
Cartilage, Articular↗
The basis of the synovial fluid analysis.
Synovial fluid fills the spaces in the joint cavities. Many diseases can affect the joints and frequently only a direct examination of the tissue or synovial fluid will yield the correct diagnosis. The article presents the basis of the synovial fluid analysis and a relevant decision-making scheme. The reliability and applicability of synovial fluid tests are commented upon. The synovial fluid analysis undoubtedly plays an important role in the management of patients with joint diseases. Due to a lack of interlaboratory comparisons, and therefore expert opinions on the interpretation of results, this knowledge and the acquisition of relevant experience should be encouraged to enable evaluation of the clinical applicability of recent discoveries in synovial fluid pathology.
Gentian Violet↗
Epstein-Barr virus infection in peripheral blood mononuclear cells, synovial fluid cells, and synovial membranes of patients with rheumatoid arthritis.
OBJECTIVE: Different infectious agents have been proposed to be involved in the pathogenesis of rheumatoid arthritis (RA). We investigated the role of latent Epstein-Barr virus (EBV) infection in patients with RA. METHODS: Sera of 55 patients with RA and 60 age and sex matched healthy controls were examined for antibodies against EBV encoded antigens (EBNA-1, VCA, and EA) by ELISA. The presence of viral DNA was analyzed by polymerase chain amplification of DNA isolated from peripheral blood mononuclear cells (PBMC) of these samples and from cells of synovial fluid (SF) specimens. Paraffin sections of synovial membranes from 25 patients were subjected to in situ hybridization analysis for the EBV encoded small RNA EBER1 and EBER2. RESULTS: Two-fold increased values of IgG antibodies against EBNA-1 were found in patients with RA in comparison to healthy controls (p = 0.029). No statistically significant difference could be observed for antibody levels against EBV-VCA. Fourteen (24.1%) of 55 patients with RA had serological evidence of reactivated EBV infection in comparison to none of the control group (p = 0.028). In PBMC, EBV DNA was detected in a significantly higher proportion in the patient group (50.9 vs. 30%; p = 0.02). In addition, SF cells harbored the viral DNA in 30% of RA cases compared to 16.6% of control cases (p = 0.02). However, EBER1/2 transcripts could only be found within synovial membranes of 2 (8%) of 25 patients with RA. CONCLUSION: These findings support the hypothesis that EBV infection may be involved in the pathogenesis of RA. Further studies may define the precise pathogenetic mechanisms of viral infection for the development of inflammatory arthritis.
Adolescent↗