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PubMed1994

Expression of a developmentally regulated epitope on fibronectins from the synovial fluid of patients with rheumatic disease.

OBJECTIVE: To determine if differential glycosylation of fibronectin (Fn) in inflammatory synovial fluid (SF) included expression of an oncofetal epitope (Onf Fn) heretofore detected only on Fn derived from embryonal or neoplastic tissue. METHODS: Fn were purified from plasma, SF and synoviocyte conditioned medium by affinity chromatography and were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting utilizing a monoclonal antibody (FDC-6) specifically recognizing the Onf Fn. RESULTS: The Onf Fn was not expressed on Fn isolated from normal or RA plasma but was strongly expressed on Fn from rheumatoid arthritis (RA) SF and to a lesser extent osteoarthritis SF. Onf Fn was also detected on Fn secreted by cultured RA synoviocytes. CONCLUSION: Fn present in the SF but not plasma of patients with rheumatic disease contains an epitope previously thought to be restricted to Fn produced by embryonal or malignant tissue.

Antibodies, Monoclonal↗
PubMed1995

Discrepancy in T cell clonal expansions in synovial fluid and peripheral blood from rheumatoid arthritis patients.

Rheumatoid arthritis (RA) is an autoimmune disease involving the synovial membrane of peripheral joints. T cells specific for self antigens may play a critical role. Identification of T cell receptors (TCR) of such specific T cell clones is very important for treatment, prevention and identification of relevant autoantigens. To identify specific T cells, TCR V beta family repertoire and the clonal expansion of T cells were analyzed in this study. The percentage of V beta 5+ or V beta 8+ cells in the synovial fluid mononuclear cells (SFMCs) was similar to that in the peripheral blood mononuclear cells (PBMCs). However, the percentage of DR+ T cells in the SFMCs was higher (p < 0.01). Analyzing the clonality of T cells in 8 V beta families (V beta 1, V beta 5, V beta 8, V beta 14, V beta 16, V beta 17, V beta 18, V beta 20), clonal expansions in CD8+ T cells from the SFMCs were found more frequently than in the PBMCs. The patterns of clonal expansions were discrepant between the SFMCs and the PBMCs even in the same patient, which suggests several inflamed tissue specific T cell clonal expansions in the SFMCs. These T cell clones might be activated by autoantigens which are not identified yet and responsible for the RA pathogenesis.

Arthritis, Rheumatoid↗
PubMed1998

Quality control of synovial fluid crystal identification.

OBJECTIVE: To establish a quality assessment programme for the diagnosis of crystal arthropathies by synovial fluid (SF) microscopy. METHODS: Three or four cytocentrifuge slides prepared from suitable patient SF specimens were distributed to 25-47 predominantly Finnish clinical laboratories once a year. Sodium urate crystals were included in every survey. RESULTS: Returns for the years 1989-1996 were reviewed. Laboratories that participated in > four surveys made on an average one error a year (range 0.25-2). The error rate for specimens containing abundant crystals was acceptable but it increased considerably for specimens showing few crystals per microscope field. No laboratory characteristic predictive of successful performance was found. CONCLUSION: Errors in quality assessment results for crystal identification were much more frequent than in the fields of, for example, clinical chemistry or microbiology. Despite efforts to provide educational feedback, no improvement was seen during the study period. Because of the dearth of data from other parts of the world it is not known for certain whether this study has merely pinpointed a local problem or if the same trend applies elsewhere.

Arthritis↗
PubMedDate not supplied

Increased native chemiluminescence in granulocytes isolated from synovial fluid and peripheral blood of patients with rheumatoid arthritis.

Polymorphonuclear leukocytes (PMNs) isolated from peripheral blood and synovial fluid of patients with rheumatoid arthritis and from peripheral blood of volunteers were stimulated with 12-phorbol-13-myristate acetate (PMA). No significant differences in luminol-amplified chemiluminescence were found between different patients and control groups. However, two distinct patterns of native chemiluminescence were observed. Type I showed no, or only a small, increase in native chemiluminescence with integral counts over 30 min less than 3 x 10(5) cpm, and the majority of samples from volunteers were of this type. Type II was characterized by a burst of native chemiluminescence starting 8 to 15 min after cell stimulation. It was found in most PMN samples from patients with rheumatoid arthritis. Integral counts over 30 min were always higher than 10(6) cpm and as high as 10(8) cpm in some cases. A strong inhibition of the Type II native chemiluminescence was caused by desferal, catalase, thiourea, and glutathione. However, the luminol-amplified chemiluminescence remained unchanged or was only slightly decreased under the same experimental conditions. Sodium azide strongly inhibited both kinds of luminescence. Hydroxyl radicals, formed in a Fenton reaction, may be important intermediates in the Type II native chemiluminescence.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Evaluation of amplicor chlamydia PCR and LCX chlamydia LCR to detect Chlamydia trachomatis in synovial fluid.

OBJECTIVES: PCR has been successfully used in research for the detection of C. trachomatis DNA in synovial samples. However, each research laboratory has developed its own PCR, making inter-laboratory comparisons difficult. To allow for standardization we evaluated two commercially available amplification systems originally designed for the examination of urogenital samples (Roche Amplicor Chlamydia PCR and Abbott LCX Chlamydia LCR), using them to analyse spiked and clinical synovial fluid (SF) samples from reactive arthritis (ReA), undifferentiated arthritis (UA), and rheumatoid arthritis (RA) patients. We compared their sensitivity in assays of clinical SF samples with our in-house developed C. trachomatis specific nested PCR. METHODS: SF was spiked with purified C. trachomatis elementary bodies (EB) and analyzed by the commercial assays. Clinical SF samplesfrom ReA (n=21), UA (n=79) and RA (n=50) patients were examined by the two commercial assays and our in-house PCR. RESULTS: Using SF samples spiked with defined numbers of C. trachomatis EB, the sensitivity of the commercial tests was high and similar to published PCR sensitivity. In clinical SF specimens the commercial assays was also able to detect CT; however, the in-house PCR was more sensitive. Out of 10 PCR-positive SF samples Amplicor tested positive in only 4/10 and LCX in only 3/10. The in-house PCR detected chlamydial DNA in synovialfluidfrom 5/21 ReA (24%), 5/79 UA (6%) and in none of the 50 RA patients. CONCLUSION: Commercial amplification assays allow the detection of C. trachomatis in clinical specimens, although with a lower sensitivity than optimized PCR. Potential explanations are discussed.

Adult↗
PubMed1990

[The occurrence and clinical significance of antibodies to type II collagen in sera and synovial fluid of Chinese patients with rheumatoid arthritis].

Antibodies to type II collagen (Col II) in sera and synovial fluid (SF) were measured with an enzyme linked immunosorbent assay (ELISA) using a solid phase sandwich method. The subjects included: 42 patients with rheumatoid arthritis (RA); 31 cases of osteoarthritis (OA); 10 cases of gouty arthritis; 4 cases of ankylosing spondylitis (AS); 5 cases of systemic lupus erythematosus (SLE); and 44 normal controls. The antigens used to detect antibodies against Col II were in native and heat-treated denatured forms, both of which were purified from chicken sternal cartilage by limited enzyme digestion and differential precipitation with salt. The reactivity to native type II collagen was generally higher than the reaction to the denatured collagen. In sera, significant higher levels of Col II were detected in the different arthritis groups when compared with the normal control group, with the exception of AS. In SF, the Col II was significantly higher in RA than it was in OA (p less than 0.001), while no difference was present between gout and OA (p less than 0.05). When native Col II was simultaneously measured in sera and SF among arthritics, positive rates were both higher among RA (65% and 58%, respectively). Positive rates were only higher in sera among OA (59% in sera and 3% in SF) and were both lower among gouty arthritis. The above findings show that the measurement of Col II is more important in SF than in sera.

Arthritis, Rheumatoid↗
PubMed1997

Differences in synovial fluid cytokine levels between juvenile and adult rheumatoid arthritis.

OBJECTIVE: To evaluate quantitative or qualitative differences in synovial fluid (SF) cytokine levels among patients with systemic juvenile rheumatoid arthritis (JRA), antinuclear antibody positive pauciarticular JRA, or adult RA. METHODS: SF levels of interleukin 1alpha (IL-1alpha), IL-1beta, IL-1 receptor antagonist (IL-1Ra) IL-11, tumor necrosis factor-alpha (TNF-alpha), soluble TNF receptor 1 (sTNFR1), leukemia inhibitory factor (LIF), all measured by immunoassays, and of IL-6, measured with a bioassay using B9 cells, were evaluated in 11 patients with systemic JRA, 24 with pauciarticular JRA, and 22 adult patients with RA. RESULTS: SF IL-6 levels were significantly higher in patients with systemic JRA than patients with pauciarticular JRA (p = 0.003) or RA (p = 0.002). IL-1alpha was detectable in 12/24 SF samples from pauciarticular JRA, in 2/22 SF from RA, and in no sample from systemic JRA (p = 0.004 vs RA; p = 0.005 vs systemic JRA). SF IL-11 levels were significantly higher in patients with RA than patients with systemic JRA (p = 0.012) or pauciarticular JRA (p = 0.005). We found no significant differences in SF levels of IL-1beta, IL-1Ra, TNF-alpha, sTNFR1, or LIF. CONCLUSION: In systemic JRA, SF levels of IL-6 are significantly higher than in pauciarticular JRA or in RA; IL-1alpha is present in a significant proportion of patients with pauciarticular JRA, but not in those with RA or systemic JRA.

Adolescent↗
PubMed1998

Comparative study of serum and synovial fluid interleukin-11 levels in patients with various arthritides.

OBJECTIVE: To determine the levels of serum and synovial fluid (SF) interleukin (IL)-11 in patients with various arthritides and estimate the contribution of IL-11 to acute phase response (APR). DESIGN AND METHODS: Serum and SF IL-11 were measured by ELISA in patients with rheumatoid arthritis (RA, n = 31), seronegative spondyloarthritis (SSA, n = 23), gout (GT, n = 14) and osteoarthritis (OA, n = 20) and were correlated with ESR and acute phase proteins as well as with cytokines IL-1 alpha, IL-1 beta, IL-6, and TNF alpha. RESULTS: IL-11 was detected in both serum and SF in each group, with IL-11 being statistically higher in SF than serum in all groups, suggesting reduced catabolism or increased synthesis of IL-11 intra-articularly. Median SF IL-11 levels were higher in OA patients than in other groups and in the treated than in the untreated RA subgroup. Moreover, serum and SF IL-11 were correlated significantly with each other, and moderately with the other cytokines examined in RA, SSA, and GT, but not in OA patients, while a significant negative correlation was found with a few of the inflammatory markers examined in each group. CONCLUSIONS: Our findings provide evidence of extensive intra-articular expression of IL-11 in arthritides, especially in OA and treated RA patients, suggesting a protective role for IL-11 in joints, probably through the induction of tissue inhibitor of metalloproteinases.

Acute-Phase Proteins↗
PubMed1997

Concentrations and origins of soluble interleukin 6 receptor-alpha in serum and synovial fluid.

OBJECTIVE: To determine levels of soluble interleukin 6 receptor-alpha (sIL-6R alpha) in synovial fluid (SF) and serum from patients with different rheumatic diseases, and to analyze its cellular origin compared to IL-6. METHODS: IL-6 and sIL-6R alpha concentrations were measured in sera, SF, and culture supernatants of different cells types using specific sandwich ELISA. RESULTS: IL-6 levels were significantly higher (30 to 1000-fold) in SF than in sera, and higher in inflammatory arthropathies such as rheumatoid arthritis (RA), chondrocalcinosis, and gout than in osteoarthritis (OA). sIL-6R alpha levels in SF from patients with RA, gout, and chondrocalcinosis were also higher (24.7 +/- 7.5, 23.2 +/- 9.1, and 19.5 +/- 7.4 ng/ml, respectively) than in patients with OA (10.1 +/- 5 ng/ml), although the difference was distinctly smaller. In contrast, sIL-6R alpha concentrations did not differ significantly between the sera of healthy donors and patients. sIL-6R alpha levels were similar in SF and sera from inflammatory arthropathies, but lower in all osteoarthritic SF, compared to their corresponding serum. In contrast to IL-6, sIL-6R alpha was produced in high amounts by hepatocytes but not by structural cells of the joint (chondrocytes, synoviocytes, fibroblasts, and endothelial cells). Polymorphonuclear cells and mononuclear cells released intermediate levels. A significant correlation between sIL-6R alpha concentration and total number of leukocytes was observed in SF. CONCLUSION: Elevated levels of sIL-6R alpha were found in serum, likely to result from a marked release by hepatocytes in vitro. That levels are higher in inflammatory SF may be due in part to release by inflammatory cells in situ.

Antigens, CD↗
PubMedDate not supplied

Impaired glutathione reductase activity and levels of collagenase and elastase in synovial fluid in rheumatoid arthritis.

OBJECTIVE: To test the activity of elastase, collagenase and glutathione reductase in the synovial fluid (SF) of patients with rheumatoid arthritis (RA) and in patients with osteoarthritis (OA); to correlate the elastase and collagenase activity with the glutathione reductase activity, which is important for the inactivation of oxygen free radicals. METHODS: 24 patients affected by osteoarthrosis and 24 patients affected by rheumatoid arthritis took part in the study. We measured elastase activity towards the substrate metoxysuccinyl-alanyl-alanyl-prolyl-valyl-p-nitroanilide (MeOSuc-ala-ala-proval-p-NA) which is highly specific for elastase, and insensitive to the other serine proteases, such as cathepsin G; collagenase activity was measured using [14C]-acetylated collagen as the substrate. Glutathione reductase activity was measured following the oxidation of nicotinamide adenine dinucleotide phosphate reduced (NADPH) in the presence of oxidized glutathione (GSSG). RESULTS: The concentrations of elastase, collagenase and glutathione reductase were statistically higher in patients with RA than in patients with OA. Moreover, in the SF of patients with RA we found positive correlation between enzyme activity levels. CONCLUSION: These results confirm a high activity of collagenase and elastase in the SF of patients with RA, which is about 30 times higher than that found in the SF of patients with OA. These data underline the synergic action of these enzymes in the pathogenesis of joint damage. RA patients also exhibit higher levels of glutathione reductase, which is important for the detoxification pathway of oxygen free radicals. However, compared with findings for collagenase and elastase, the increase in glutathione reductase is only three times higher than level found in the SF of OA patients. The limited increase in glutathione reductase activity during the inflammatory process might lead to an insufficient protective effect at the joint level in rheumatoid arthritis.

Adult↗
PubMed1995

Naproxen concentrations in plasma and synovial fluid and effects on prostanoid concentrations.

OBJECTIVE: To test the hypothesis that unbound concentrations of naproxen in synovial fluid (SF) and plasma (P) are equal over a drug dosage interval at steady state or after a single dose of drug. The relationship between plasma and SF concentrations of naproxen, respectively, and prostaglandin concentrations were also examined. METHODS: Paired, sequential, total, and unbound naproxen concentrations were determined in plasma and SF in 2 groups of 6 patients. A single dose group was given naproxen 500 mg. The chronic dose group was given 500 mg bd for 7 days before collection of blood and SF samples. The effect of naproxen on prostanoid production by clotting whole blood (thromboxane B2, TXB2) and in SF (PGE2, 6-keto-PGF1 alpha) was determined by radioimmunoassay. RESULTS: Average area under the curve (AUC) of unbound (U) naproxen concentrations against time in plasma and SF were the same over a dosage interval at steady state (ratio AUCU,SF/AUCU,P, 1.12 +/- 0.18; p = 0.108), but not after a single acute dose (AUCU,SF/AUCU,P, 1.34 +/- 0.32; p = 0.044). Data from the single dose study revealed that the mean (+/- SD) of the concentrations required for 50% inhibition (EC50) of platelet derived TXB2 by total naproxen was 7.7 +/- 4.4 micrograms/ml (n = 5) and for unbound drug 25.4 +/- 22.0 ng/ml (n = 5). SF prostanoid concentrations after both acute and chronic dosing were low, as expected, but temporal and dose relationships of prostanoid concentrations with SF naproxen could not be discerned. However, this may reflect study design. CONCLUSIONS: The AUC of unbound naproxen in SF and plasma were similar at steady state. Plasma concentrations correlated with inhibition of TXB2 generation by platelets. There was sustained depression of PG concentrations in SF beyond the time suggested by plasma drug concentrations.

Adult↗
PubMedDate not supplied

The effects on synovial permeability and synovial fluid leukocyte counts in symptomatic osteoarthritis after intraarticular corticosteroid administration.

The mode of action of intraarticularly administered corticosteroids was studied. Fifteen patients with osteoarthritis and painful effusions had one knee injected with normal saline, triamcinolone hexacetonide 20 mg or prednisolone tebuate 20 mg. Fifteen millicuries of 99mTc-labeled albumin was given intravenously before and at various time intervals after the injection of the depot corticosteroid or saline. Whole blood and synovial fluid (SF) samples were used for blood to SF count rate ratio determinations. SF white blood cell counts (WBC) were also performed. The results indicated that intraarticular depot corticosteroids decreased synovial permeability and caused increases in the SF WBC. Moreover, decreases in pain and knee swelling correlated better with a decrease in vascular permeability, as assessed by the count ratio, than with SF leukocytosis.

Adrenal Cortex Hormones↗
PubMed1999

[Pathologic study on synovial fluid after intra-articular corticosteroid therapy in temporomandibular joint disorders].

OBJECTIVE: To study what happens after intra-articular injection of corticosteroid. METHODS: Synovial fluid after intra-articular corticosteroid therapy in temporomandibular joint disorders (TMD) was studied by hematoxylin-eosin, PAS, and Atcian blue staining. RESULTS: The results were that broken synovial membrane and articular cartilage, lots of synovial lining cells, macrophagocytes, inflammatory cells and free cartilage matrix could be found in the lavage fluid. CONCLUSION: The results suggest that drug synovectomy may be one mechanism about intra-articular corticosteroid therapy in TMD, and this therapy could lead to progressive degradation and destruction of the articular cartilage. Arthrocentesis and lavage are needed three to five days after this therapy.

Adolescent↗
PubMed1992

Estimated synovial fluid leukocyte numbers on wet drop preparations as a potential substitute for actual leukocyte counts.

Leukocyte counts on synovial fluid are widely used in classification of joint disease as inflammatory or "noninflammatory." We have evaluated estimates of leukocytes (WBC) per high power field (HPF) on wet drop preparations to see if they might be suitable substitutes in some situations. If there was a mean WBC of 0-2/field on 10 HPF, all leukocyte counts were less than 1,300/mm3. Thus, in such fluids expense might be reduced by eliminating the actual leukocyte count. Estimates also roughly correlated with WBC counts at higher counts but were less consistent.

Arthritis↗
PubMed2000

Synovial fluid induced nuclear factor-kappaB DNA binding in a monocytic cell line.

OBJECTIVE: To determine the effects of synovial fluids (SF) on DNA binding activity of transcription factor nuclear factor-kappaB (NF-kappaB) in the Mono Mac 6 monocytic/macrophage cell line as a model for the interaction between SF and synovial tissue macrophages in arthritis. METHODS: Mono Mac 6 cells were incubated with SF from the knee joints of human subjects with rheumatoid arthritis (RA), undifferentiated seronegative oligoarthritis, and osteoarthritis (OA). Nuclear extracts prepared from the Mono Mac 6 cells and RA synovial tissue were analyzed by electrophoretic mobility shift analysis (EMSA) for NF-kappaB DNA binding proteins. RESULTS: Induction of NF-kappaB DNA binding by the p65(RelA)/p50 heterodimer was observed in response to incubation of Mono Mac 6 cells with SF (20% in culture medium) from 5 of 8 subjects with RA, 4 of 5 with OA, and none of 3 with undifferentiated seronegative oligoarthritis. Incubation of SF with neutralizing antibodies against tumor necrosis factor-alpha (TNF-alpha), but not antibodies against interleukin 6 (IL-6), significantly reduced the induction of p65/p50 binding activity in SF from subjects with RA and OA. Unexpectedly, a slowly migrating SF inducible NF-kappaB-binding complex was observed in EMSA of Mono Mac 6 cells after incubation with SF from 5 of 8 RA and 2 of 5 OA subjects. The induction of this complex by SF was not affected by neutralization of TNF-alpha or IL-6 in SF, and the complex was not inducible by TNF-alpha, IL-1beta, TNF-alpha/IL-1beta, IL-6, platelet derived growth factor, lipopolysaccharide, or tetradecanoyl phorbol acetate. The slowly migrating complex could not be supershifted with antibodies against NF-kappaB, Jun, or the transcriptional coactivators p300 or CBP. A NF-kappaB-binding complex with similar slow mobility was observed in nuclear extracts prepared from fresh human RA synovial tissue. CONCLUSION: Biological activity of TNF-alpha in SF from RA and OA subjects is capable of inducing p65/p50 NF-kappaB DNA binding activity in macrophages. A property of SF that is independent of TNF-alpha and other cytokines is responsible for the induction of a novel slowly migrating NF-kappaB-binding complex. Soluble mediators in SF of subjects with RA and OA can therefore modulate binding of nuclear proteins to the NF-kappaB binding site in macrophages and may play a role in inflammatory gene expression in arthritis.

Adult↗
PubMed1994

Induction of increased levels of proteoglycan fragments in synovial fluid (SF) and increased levels of stromelysin in cartilage, synovium and SF by intraarticular injection of canine monocyte conditioned medium into dogs.

OBJECTIVE: To study the effects of the intraarticular injection of canine monocyte conditioned medium (cMCM) into dogs on proteoglycan fragment and stromelysin levels in the joint. METHODS: cMCM was injected intraarticularly into dogs, and the levels of proteoglycan fragments in synovial fluid (SF) as well as stromelysin levels in cartilage, synovium, and SF were assessed after 12 h. RESULTS: There was a 4-fold increase of proteoglycan fragment levels and a 6-fold increase in stromelysin levels in SF, and a 4.4-fold increase in stromelysin levels in cartilage extracts. Elevated mRNA levels were detected in both synovium and cartilage. By immunofluorescence staining, stromelysin was localized in chondrocytes throughout the cartilage and in synovial cells. CONCLUSION: Intraarticular injection of cMCM stimulated the expression of stromelysin mRNA and protein in cartilage and synovium and caused marked increases in stromelysin protein and proteoglycan fragment levels in SF.

Animals↗