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Isolation and analysis of complement activating aggregates from synovial fluid of patients with rheumatoid arthritis using monoclonal anti-C3d antibodies.

The complement activating aggregates in synovial fluids of patients with rheumatoid arthritis (RA) have been isolated using monoclonal IgM anti-C3d antibodies attached to solid phases, and the content of the material bound has been analysed. High levels of aggregated IgG bearing C3d were found in RA synovial fluids, and IgG was the major immunoglobulin bound from such synovial fluids by anti-C3d Sepharose. A strong correlation was shown between levels of aggregated IgG bearing C3d and complement activation, as judged by C3d levels. Significant (but less strong) relationships were also observed between C3d levels and both complement consuming and C1q binding activity. C3d levels and levels of aggregated IgG bearing C3d were both significantly associated with the numbers of polymorphonuclear leucocytes (PMNs) found in RA synovial fluids. From these results it is concluded that the aggregated immunoglobulins bearing C3d (particularly IgG) isolated from RA synovial fluids are responsible for activating complement and attracting PMNs into the joint space. Radioimmunoassay showed no correlation, however, between levels of aggregated IgG (or IgM) bearing C3d and rheumatoid factor (RF) activity bound by anti-C3d. In addition, the material bound by anti-C3d Sepharose from most synovial fluid polyethylene glycol precipitates did not contain either IgM or IgG RF. Thus both techniques show that the majority of complexes bearing C3d do not contain RF. As the complement fixing aggregates apparently contain only immunoglobulin and complement components the results raise the problem of how the aggregates are formed. It is suggested that RA IgG may remain aggregated after either antigen or antibody (RF) has dissociated from the complex.

Antibodies, Monoclonal↗

Peptide hormones and histamine in plasma and synovial fluid of patients with rheumatoid arthritis and osteoarthrosis.

OBJECTIVES: Hormones other than adrenal and gonadal steroids may play also a significant role in the pathogenesis of rheumatoid arthritis. The aim of this study was to investigate the levels of selected peptide hormones and histamine in synovial fluid of knee joints and in plasma of patients with rheumatoid arthritis and with osteoarthrosis. METHODS: The concentrations of insulin, C-peptide, prolactin, growth hormone, free triiodothyronine (FT3), thyrotropin (TSH), and histamine were determined in synovial fluid and plasma of 27 patients with rheumatoid arthritis (RA) and in 12 patients with osteoarthrosis (OA). RESULTS: The presence of peptide hormones in synovial fluid was demonstrated. The levels of TSH and growth hormone were lower in synovial fluid than in plasma in both groups, while those of prolactin were comparable in synovial fluid and in plasma. The levels of C-peptide (p < 0.05), insulin and FT3 were higher in synovial fluid than in plasma of OA patients, but lower in synovial fluid of RA patients as compared to their levels in plasma. Significant positive correlations between the levels in plasma and synovial fluid were observed in prolactin (p < 0.001, r = 0.741) and TSH (p < 0.05, r = 0.88) only. After age adjustment, no significant differences in synovial fluid and in plasma levels of all hormones were found between OA and RA patients. The levels of histamine in plasma were similar in RA and OA patients, in synovial fluid of both groups histamine was found in almost undetectable amounts. CONCLUSIONS: The selected peptide hormones, e.g. insulin, C-peptide, prolactin, growth hormone, FT3 and TSH, are present in synovial fluid of RA and OA patients, some of them in the concentrations comparable to these in plasma. The role of the locally present hormones in pathogenesis of RA has to be investigated in further studies and analyses.

Arthritis, Rheumatoid↗

Correlation of anti-cytoskeleton antibody activities in synovial fluid with interleukin-6 in patients with osteoarthritis and inflammatory joint disease.

Synovial fluids and sera from patients with rheumatoid arthritis, psoriatic arthritis, yersinia arthritis, Behçet's syndrome, Crohn's disease, and osteoarthritis were tested for antinuclear antibodies and antibodies to five cytoskeletal components in sensitive enzyme-linked immunosorbent assay (ELISA) systems and for IL-6 concentrations in a proliferation assay (IL-6 dependent hybridoma cell line B13.29, subclone B9). Statistically significant correlations between antibody activities and IL-6 levels were found for vimentin antibodies (r = 0.56; p less than 0.05) and actin antibodies (r = 0.44; p less than 0.05). In patients with chronic and active disease like rheumatoid arthritis and psoriatic arthritis, optical densities measured by vimentin- and actin-ELISA were significantly different from those measured in patients with osteoarthritis. To date only a few reports exist concerning the incidence of antibodies in synovial fluids. We have shown to our knowledge for the first time that IL-6 seems to induce synovial fluid antibody activities restricted to cytoskeletal components of synoviocytes (i.e., vimentin and actin). Synovial fluid antibody activities against vimentin and actin appear to be markers of activity in patients with inflammatory joint disease.

Actins↗

Phagocytosis and intracellular killing of Staphylococcus aureus by polymorphonuclear cells from synovial fluid of patients with rheumatoid arthritis.

The phagocytosis and intracellular killing by synovial fluid (SF) polymorphonuclear cells (PMN) of 10 patients with rheumatoid arthritis was studied. PMN phagocytosis was assessed by morphologic and microbiologic methods and intracellular killing was measured independently of continuous phagocytosis of Staphylococcus aureus. Phagocytosis of S aureus by SF PMN or peripheral blood (PB) PMN was as effective in the presence of synovial fluid as in the presence of serum. On average, SF PMN ingested S aureus opsonized with synovial fluid and serum more efficiently than patient or donor PB PMN did. Enhanced ingestion of S aureus was associated with increased expression of C3 receptors on the membrane of SF PMN. In the presence of heat-inactivated synovial fluid, the capacity of SF PMN to ingest S aureus was greater than that of patient or donor PB PMN. Under these conditions, phagocytic activity was correlated with Fc receptor expression. SF PMN was found to be as active in killing S aureus as PB PMN from healthy donors.

Analysis of Variance↗

Measurement of soluble pyrophosphate in plasma and synovial fluid of patients with various rheumatic diseases.

Soluble pyrophosphate was measured in the plasma and synovial fluid of various groups of patients and in the plasma of two control groups. The two control groups consisted of 13 healthy subjects and 19 patients suffering from benign lumbar back pain. The other group of patients had rheumatoid arthritis (RA) (14 plasma and 19 synovial fluid examinations), osteoarthrosis (OA) (19 plasma and 26 synovial fluids) and articular chondrocalcinosis (ACC) (27 plasma and 43 synovial fluids). The level of soluble pyrophosphate in the plasma was 3.5 mumol/l in healthy subjects, 4.0 mumol/l in patients with lumbar back pain, 4.1 mumol/l in individuals having OA and 3.5 mumol/l in the group suffering from RA as well as for those with ACC. The differences between these values are not significant statistically. In the synovial fluid the values were 4.6 mumol/l for the group with RA, 12.7 mumol/l for those with OA and 34.2 mumol/l in the group having ACC. If a normal distribution of these values is assumed and the average values and standard deviations recalculated for each group after elimination of cases more than 3 standard deviations above the mean, then we obtain 9.8 mumol/l for the group with OA and 23.8 mumol/l for those with ACC. The difference between the group with RA and that with OA is highly significant (p greater than 0.0001). Even more significant is the difference between the group with RA and ACC (p less than 0.0005). The difference between the OA and the ACC is also highly significant (p less than 0.001). On the basis of these observations various mechanisms leading to the pyrophosphage crystal deposition disease are discussed.

Arthritis↗

Synovial fluid cytokines and eicosanoids as markers of joint disease in horses.

OBJECTIVE: To evaluate the value of various synovial fluid cytokines and eicosanoids to diagnose joint disease or categories of joint disease. STUDY DESIGN: Prospective acquisition of clinicopathologic data. ANIMALS OR SAMPLE POPULATION: Client-owned or donated horses: 50 joints with no evidence of disease; 28 joints with acute disease; 32 joints with chronic disease; 9 joints with cartilage damage and no other signs of joint disease. METHODS: Concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), prostaglandin E(2) (PGE(2)), thromboxane B(2) (TXB(2)), prostaglandin F1-alpha (PGF(1)-alpha), and leukotriene B(4) (LTB(4)), were measured in equine synovial fluid by immunoassay and categorized according to duration and degree of joint disease. Any test value for a given category that was different from normal was further analyzed for sensitivity (S), specificity (Sp), and operating point (most valid test cutoff value). Likelihood ratios and predictive values were calculated at the operating point. Mediator concentrations were correlated to synovial fluid white blood cell count. Tests were reported as poor, fair, good, or excellent based on predictive values of <.25,.25-.5,.5-.75, or >.75, respectively. RESULTS: TNF synovial fluid concentration as a predictor of joint disease was good, and the value of TNF (maximum S and Sp) indicating joint disease was >36 pg/mL. IL-1beta as a predictor of joint disease was good, and the value of IL-1beta indicating joint disease was >4.5 pg/mL. IL-6 concentration was an excellent predictor of joint disease. Any IL-6 in synovial fluid indicated joint disease and correlated highly with synovial fluid white blood cell count (P <.0001). PGE(2) was a good-excellent predictor of disease (positive predictive value [PPV] = 0.75), and the concentration indicating joint disease was >22.5 pg/mL. The diagnostic PGF(1)-alpha concentration indicating severe chronic joint disease was identified to be >16.5 pg/mL with very high sensitivity (S = 1) and specificity (Sp =.89). PGF(1)-alpha concentrations > 9.5 pg/mL had a good PPV (.69) and NPV (.6) for any joint disease. TBX(2) concentrations below 31.5 pg/mL (S =.57; Sp =.61) were a very good predictor of joint disease (PPV =.72). LTB(4) concentration appeared to be greater in severe acute joint disease than normal joints; this was not significant (P =.15) and correlated highly with synovial fluid white blood cell count (P =.0001). CONCLUSIONS: The ability of a single value from a joint in an adult horse predicting the presence of joint disease was often good (.5-.75), and was excellent (> or =.75) for IL-6 and PGE(2). TNF-alpha and IL-1beta were no more effective than white blood cell count in screening for joint disease. IL-6 was the most sensitive and specific for joint disease and could be an excellent screening test for the presence of joint disease when lameness is difficult to identify or is intermittent. PGE(2) would be a functional screening test for the presence of any joint disease and offers a differentiating feature because values were not influenced by white blood cell count. PGF(1)-alpha values > 16.5 pg/mL identified chronic severe joint disease and may be clinically useful when there are minimal radiographic changes but substantial articular cartilage degradation.

Acute Disease↗

Alpha-tocopherol, lipids and lipoproteins in knee-joint synovial fluid and serum from patients with inflammatory joint disease.

1. We have determined the antioxidant status of synovial fluid and serum of patients with inflammatory joint disease in terms of the biologically active lipid-soluble antioxidant, alpha-tocopherol. Synovial fluid concentrations of alpha-tocopherol were significantly lower relative to those of paired serum samples (P < 0.001). Serum levels of alpha-tocopherol in these patients did not differ significantly from those in control serum. 2. Lower concentrations of cholesterol, triacylglycerol and low-density lipoprotein were also observed in patients' synovial fluid compared with matched serum samples. However, multiple regression analysis of the data indicated that there remained a significant depletion of alpha-tocopherol, which was largely independent of these co-variables, in inflammatory synovial fluid. These findings are consistent with the consumption of alpha-tocopherol within the inflamed joint via its role in terminating the process of lipid peroxidation. 3. Nuclear magnetic resonance spectroscopic analysis of matched inflammatory synovial fluid and serum confirmed lower concentrations of triacylglycerol in synovial fluid together with evidence of a shortened mean triacylglycerol chain length. The latter metabolic difference suggests an increased utilization of triacylglycerols for energy within the inflamed joint.

Arthritis↗

Serum and synovial fluid concentrations of endothelin-1 in patients with rheumatoid arthritis.

To determine the endothelin-1 (ET-1) concentrations in synovial fluid and serum of rheumatoid arthritis (RA) patients, this study was designed to examine if serum ET-1 concentration of control subjects has any correlation either with the ET-1 concentration of synovial fluid or ET-1 concentration of serum from RA patients. Twenty-eight patients were studied of whom eight males and twenty females with confirmed rheumatoid arthritis. Twenty-eight healthy volunteers were also included as controls. The immunoreactive concentration of ET-1 was measured using commercially available radioimmunoassay (RIA) kits (Peninsula Laboratories, Belmont CA) specific for ET-1. All the samples were performed in duplicate and after plotting % B/Bo for each standard directly on Y axis and endothelin concentrations on the X axis, the "best fit" curve was drawn and the amount of ET-1 was calculated. Mean ET-1 level in synovial fluid was 15.53 +/- 2.82 pg/me. In serum samples from RA patients, the mean ET-1 level was detected as 16.42 +/- 3.07 pg/ml (n = 28). Sera from twenty-eight healthy volunteers were analyzed as controls and mean ET-1 concentration was 8.68 +/- 1.96 pg/ml. A significant difference (P < 0.001) was found between ET-1 level of sera from RA patients and ET-1 levels from control sera. Highly significant difference (P < 0.001) was also detected between synovial fluid ET-1 and control ET-1 levels. However, no significant difference was found between ET-1 levels of synovial fluid and serum ET-1 levels of RA patients. Results of this study confirmed the presence of elevated levels of ET-1 concentration in synovial fluid and serum samples of patients with RA. The clinical significance and physiological role of endothelin in synovial fluids and sera of patients suffering from a variety of pathophysiological conditions of arthritis deserves further studies.

Adolescent↗

Synovial fluid cells in juvenile arthritis: evidence of selective T cell migration to inflamed tissue.

The perpetuation of chronic synovitis in juvenile arthritis (JA) is a complex interaction of local and systemic regulatory mechanism. We examined the cell surface phenotype of synovial fluid cells and peripheral blood lymphocytes from 15 patients with JA to better understand the mechanism of local inflammation. Synovial fluid and peripheral blood mononuclear cells were analysed for cell surface expression of CD2, CD3, CD4, CD8, CD19, CD25, CD29, CD45R and Ia using flow cytometry. We found a very low percentage of B cells with a concomitant increase of T cells in synovial fluid as compared with peripheral blood. A large percentage of the synovial fluid T cells were HLA-DR+, or activated T cells, and there was a relative decrease in CD4+ cells in synovial fluid as compared with peripheral blood. There was only a minimal increase in CD25+ synovial fluid cells. The synovial fluid CD4+ cells were mainly of the CD2high, CD29+, CD45RO phenotype. This CD4 phenotype found on synovial fluid cells from patients with JA and in particular the CD29 cell surface marker, which recognizes a common beta-chain of adhesion molecules, is associated with binding to extracellular matrix proteins and is also associated with 'primed' T cells. Our results demonstrated the presence of T cells which either selectively migrate to synovium and synovial fluid or are activated in situ in the joint.

Adolescent↗

Cartilage oligomeric matrix protein and hyaluronan levels in synovial fluid from horses with osteoarthritis of the tarsometatarsal joint compared to a control population.

REASONS FOR PERFORMING STUDY: Quantification of cartilage oligomeric matrix protein (COMP) levels within synovial fluid from the tarsometatarsal joint has not previously been reported and an effective synovial fluid marker would allow monitoring of disease progression and treatment. OBJECTIVES: To quantify levels of COMP and hyaluronan (HA) in synovial fluid from the tarsometatarsal joint, identify differences in levels from horses with osteoarthritis (OA) of the tarsometatarsal joint compared to a control population and to correlate levels with radiographic changes in horses with OA. METHODS: Synovial fluid was collected from the tarsometatarsal joint of 25 horses without hindlimb lameness (controls) and 25 lame horses, subjected to analgesia of the joint. COMP concentrations were measured using a homologous inhibition ELISA. Immunoblots of synovial fluid from 3 lame horses and 3 controls were performed to identify fragmentation of COMP. Hyaluronan (HA) concentration in synovial fluid was determined using a competition ELISA. Radiographs of the lame horses with OA were scored and correlated with levels of COMP and HA. RESULTS: Concentrations of COMP in OA of the tarsometatarsal joint were significantly lower than in the control samples. An additional fragment band of COMP (approximately 30 kDa) was identified on the immunoblots of the horses with OA and this fragment was not identified in controls. No significant difference was identified in the HA or HA:COMP ratio between lame and control horses. There was no correlation between levels of synovial fluid COMP and HA, and radiographic changes. CONCLUSIONS AND POTENTIAL RELEVANCE: Lowered levels of COMP in synovial fluid of tarsometatarsal joints correlates with the presence of osteoarthritis. However, a single value cannot be used to stage the disease process. Levels of HA may not be a useful marker for this disease. Decreased, rather than increased COMP levels, may reflect significant loss of cartilage in established osteoarthritis. A specific assay for the COMP fragment generated with osteoarthritis may allow the earlier detection of clinical cases.

Animals↗

Elevation of a collagenase generated type II collagen neoepitope and proteoglycan epitopes in synovial fluid following induction of joint instability in the dog.

CLINICAL RELEVANCE: Measurement of markers of cartilage pathology in synovial fluid may provide clinical rheumatologists and osteoarthritis (OA) researchers important information for early diagnosis of OA as well as a method for monitoring disease progression and response to treatment. This study demonstrates the value of this approach in an established model of OA (cranial cruciate ligament rupture) at a point distant enough from the original surgical manipulation so as to have little to no effect on the marker concentrations. OBJECTIVE: The objective of this study was to determine whether measurement of markers of cartilage collagen cleavage and proteoglycan turnover in synovial fluid from a canine model could be used to detect cartilage changes following the onset of joint instability during the development of OA. DESIGN: A model of joint instability that develops OA was created in 18 mature dogs using monopolar radiofrequency energy (MRFE). MRFE was arthroscopically applied to one cranial cruciate ligament (CCL) while the contralateral CCL was sham treated. The treated CCLs ruptured approximately 8 weeks (55 +/- 1.6 days) after MRFE treatment. Synovial fluid was collected at time zero prior to MRFE treatment, 4 weeks after MRFE treatment, and at 4, 8, and 16 weeks after CCL rupture. Synovial fluid concentrations of the neoepitope COL2-3/4C long (type II collagen cleavage by collagenase) and epitopes 3B3(-) (proteoglycan aggrecan sulfation) and 846 (associated with aggrecan synthesis) were analyzed. RESULTS: Compared to sham treated joints, the synovial fluid concentrations of COL2-3/4C long and 3B3(-) were significantly increased 2.2 fold and 2.9 fold, respectively, in joints with MRFE treated CCLs following CCL rupture. Concentrations of the 846 epitope in synovial fluid showed a trend toward an increase, which was not significant, after CCL rupture. CONCLUSIONS: Concentrations of the collagenase-cleaved type II collagen neoepitope and 3B3(-) epitope in synovial fluid were significantly increased by 4 weeks and remained elevated for at least 16 weeks after CCL rupture. This suggests that in dogs the COL2-3/4C long neoepitope and 3B3(-) epitope are sensitive markers for changes in joint cartilage turnover in joints that are developing OA.

Animals↗

Studies of rheumatoid synovial fluid lymphocytes. III. Phenotypic and functional analysis of natural killer-like cells.

Synovial fluid and peripheral blood lymphocytes from patients with rheumatoid arthritis have been compared in terms of phenotypic and functional expression of natural killer (NK) activity. Following pretreatment with the monoclonal antibodies anti-HNK-1 (anti-Leu-7) or anti-Leu-11b and complement, NK activity against K562 cells was assessed in 4-hr chromium release assays. Rheumatoid peripheral blood lymphocytes resembled those of normal individuals, in that complement-mediated lysis of Leu-11b+ cells virtually eliminated all NK activity. Complement-mediated lysis of Leu-7+ cells resulted in only a modest reduction in NK activity. Rheumatoid synovial fluid lymphocytes differed from autologous peripheral blood lymphocytes: the overall cytotoxicity was generally less and only a fraction of the NK-like activity appeared to be mediated by Leu-11b+ cells. This apparent lack of Leu-11b expression by rheumatoid synovial fluid NK-like cells could not be accounted for by blockage or alteration of the Leu-11b antigen by factors present in synovial fluid. These observations support and extend previous data showing a discordance of phenotype and function of lymphocytes in rheumatoid synovial fluid possibly representing activation of such cells within the rheumatoid joint.

Arthritis, Rheumatoid↗

Plasma and synovial fluid endothelin-1 and nitric oxide concentrations in horses with and without joint disease.

OBJECTIVE: To compare plasma and synovial fluid endothelin-1 (ET-1) and nitric oxide (NO) concentrations in clinically normal horses and horses with joint disease. ANIMALS: 36 horses with joint disease, and 15 horses without joint disease. PROCEDURE: Horses with joint disease were assigned to 1 of the 3 groups (ie, synovitis, degenerative joint disease [DJD], or joint sepsis groups) on the basis of findings on clinical and radiographic examination and synovial fluid analysis. Endothelin-1 and NO concentrations were measured in plasma from blood samples, collected from the jugular vein and ipsilateral cephalic or saphenous vein of the limb with an affected or unaffected joint, as well as in synovial fluid samples obtained via arthrocentesis from the involved joint. RESULTS: Plasma ET-1 concentrations between affected and unaffected groups were not significantly different. Median concentration and concentration range of ET-1 in synovial fluid obtained from the joint sepsis group (35.830 pg/mL, 7926 to 86.614 pg/mL; n = 7) were significantly greater than values from the synovitis (17.531 pg/mL, 0.01 to 46.908 pg/mL; 18), DJD (22.858 pg/mL, 0.01 to 49.990 pg/mL; 10), and unaffected (10.547 pg/mL, 0.01 to 35.927 pg/mL; 10) groups. Plasma and synovial fluid NO concentrations between affected and unaffected groups were not significantly different. CONCLUSIONS AND CLINICAL RELEVANCE: Endothelin-1 is locally synthesized in the joints of horses with various types of joint disease. Synovial fluid concentrations of ET-1 varied among horses with joint disease, with concentrations significantly higher in the synovial fluid of horses with joint sepsis. These results indicate that ET-1 may play a role in the pathophysiologic mechanism of joint disease in horses.

Animals↗

Increased release of bone sialoprotein into synovial fluid reflects tissue destruction in rheumatoid arthritis.

OBJECTIVE: Bone sialoprotein (BSP) was quantified in synovial fluids and sera from rheumatoid arthritis (RA) patients to elucidate whether its release from bone relates to the degree of joint tissue destruction. Osteocalcin was assayed for comparison. METHODS: BSP and osteocalcin levels were determined by immunoassays of knee synovial fluids and of sera from RA patients who were selected on the basis of radiographic knee joint tissue damage. RESULTS: Synovial fluid concentrations of BSP increased with increasing degrees of knee joint damage (rs = 0.6848, P < 0.001). Synovial fluid concentrations of osteocalcin did not relate to the degree of joint damage. Serum concentrations of BSP were increased, but did not relate to the degree of joint damage. Serum concentrations of osteocalcin were normal, but increased within the range of normal during progression of joint destruction (rs = 0.4567, P < 0.001). CONCLUSION: Quantification of BSP in synovial fluid holds promise as a useful means of assessing the degree of tissue damage at the molecular level in patients with RA.

Adult↗

Increment of CD8S6F1 cells in synovial fluid from patients with rheumatoid arthritis.

OBJECTIVE: To investigate the role of CD8 cell subsets in the pathogenesis of rheumatoid arthritis (RA) and the phenotypes of T cells adherent or non-adherent to the target cells (endothelial cells and synovial cells) pre-treated with IL-1 beta. METHODS: The expression of S6F1 on CD8 cells and that of an activation marker on CD8 cells and CD8 cell subsets was evaluated in specimens of peripheral blood and synovial fluid obtained from 15 patients with RA and 10 with osteoarthritis (OA) using a two- or three-colour immunofluorescence method for analysis. RESULTS: The percentage of CD8S6F1 cells among CD8 cells in synovial fluid was significantly greater than that of peripheral blood. Synovial fluid from RA patients had a greater percentage of CD8S6F1 cells compared with either peripheral blood of matched patients or synovial fluid of OA patients. The percentage of CD8HLA-DR cells in synovial fluid was markedly greater than that in paired samples of peripheral blood in patients with RA. In the CD8S6F1 cells from both groups of patients, synovial fluid showed an increased percentage of HLA-DR cells compared with peripheral blood. Similar results were observed in CD8 cells lacking S6F1 expression (CD8S6F1-) from both groups of patients. There was no significant difference in the percentage of HLA-DR cells between CD8S6F1 and CD8S6F1- cell populations in peripheral blood. In contrast with peripheral blood, in synovial fluid of RA patients the percentage of HLA-DR cells in the CD8S6F1 cell population was markedly greater than that in the CD8S6F1- population. However, the percentage of HLA-DR cells in both cell populations was similar in synovial fluid of OA patients. In both the endothelial and the synovial cell adhesion assays, the percentage of CD8S6F1 among CD8 cells and the mean fluorescence intensity of S6F1 antigen on CD8S6F1 cells were significantly greater in the adherent T cell population than that in the non-adherent T cell population. CONCLUSION: These results suggest that increased expression of S6F1 antigen and the increased percentage of HLA-DR cells on CD8 cells in synovial fluid may be responsible for the migration of these cells into inflamed synovial tissues, and for cellular interactions between these cells and synovial cells or the extracellular matrix.

Adult↗

[The normal and pathological proteic, immunological and cytoimmunological features of synovial fluid (author's transl)].

The A. describes the normal pathological proteic, immunological and cito-immunological features of synovial fluid. According to these features, the synovial fluid have been classified into 3 groups: a) non-inflammatory, animmune fluids (without pathological immunitary features); b) inflammatory, normoimmune fluids (having immunological features with normal physiopathological reactions); c) inflammatory, iperimmune-disimmune fluids (with complex and abnormal immunological features). Histologically, they correspond to: a) non flogistic artrosynovitis (synoviosis, simple synovitis); b) inflammatory arthrosynovitis without tipical features (they are also described as cronic aspecific arthorosynovitis) or characterized by pathohomonic features (tubercolar synovitis, gouty synovitis. ecc.); c) rheumatoid arthrosynovitis (and inflammatory arthrosinovitis rheumatoid like). There is a generical correlation between histological aspects of groups a) and b) and humoral values of synovial fluid. Tipical correlations have been found between histological features of RA and humoral values of synovial fluid. These are expression of individual immunological reactivity of tissues in presence of rheumatoid factors. The tissutal reactivity can subiecy even to endogenous or exogenous causes.

Blood Proteins↗

Relationship between antinuclear antibodies and differential cell counts in synovial fluid of patients with rheumatoid arthritis.

Presence and titres of organ non-specific and granulocyte-specific antinuclear antibodies (ON-ANA and GS-ANA) were studied in 100 samples of synovial fluids taken from 95 patients with seropositive rheumatoid arthritis and in corresponding sera. At the same time the white cell count as well as the percentage of granulocytes and granulocytes with pycnotic or fragmented nuclei (PGS and FGS, respectively) were evaluated in the synovial fluid sediment. Twenty six percent of synovial fluid samples were positive for ON-ANA and the same percentage of samples were positive for GS-ANA. Titres of GS-ANA showed a clear inverse correlation with the number of granulocytes. The rate of PGS as well as of FGS increased with the titer of both types of studied ANA, however, a significant correlation was observed only between the percentage of these cells and GS-ANA. Differences in specificity and titres of ANA were demonstrated in samples of synovial fluids taken at the same time from both knee joints of 5 patients under study. The differences were also noticed when the specificity and titer of ANA present in synovial fluid and serum samples were compared. A case of rheumatoid arthritis showing sudden appearance of numerous plasma cells in the synovial fluid in course of the disease is presented. This patient initially had no ANA in the synovial fluid or in serum, but ANA were detected at the time of synovial fluid plasmacytosis. These data indicate that a local production of ANA is likely to take place in ANA positive rheumatoid arthritis.

Adult↗

Gentamicin concentrations in synovial fluid obtained from the tarsocrural joints of horses after implantation of gentamicin-impregnated collagen sponges.

OBJECTIVE: To determine synovial fluid gentamicin concentrations and evaluate adverse effects on the synovial membrane and articular cartilage of tarsocrural joints after implantation of a gentamicin-impregnated collagen sponge. ANIMALS: 6 healthy adult mares. PROCEDURES: A purified bovine type I collagen sponge impregnated with 130 mg of gentamicin was implanted in the plantarolateral pouch of 1 tarsocrural joint of each horse, with the contralateral joint used as a sham-operated control joint. Gentamicin concentrations in synovial fluid and serum were determined for 120 hours after implantation by use of a fluorescence polarization immunoassay. Synovial membrane and cartilage specimens were collected 120 hours after implantation and evaluated histologically. RESULTS: Median peak synovial fluid gentamicin concentration of 168.9 microg/mL (range, 115.6 to 332 microg/mL) was achieved 3 hours after implantation. Synovial fluid gentamicin concentrations were < 4 microg/mL by 48 hours. Major histologic differences were not observed in the synovial membrane between control joints and joints implanted with gentamicin-impregnated sponges. Safranin-O fast green stain was not reduced in cartilage specimens obtained from treated joints, compared with those from control joints. CONCLUSIONS AND CLINICAL RELEVANCE: Implantation of a gentamicin-impregnated collagen sponge in the tarsocrural joint of horses resulted in rapid release of gentamicin, with peak concentrations > 20 times the minimum inhibitory concentration reported for common pathogens that infect horses. A rapid decrease in synovial fluid gentamicin concentrations was detected. The purified bovine type I collagen sponges did not elicit substantial inflammation in the synovial membrane or cause mechanical trauma to the articular cartilage.

Animals↗