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At least 145 records · Page 8Linked to original sources
PubMed1994

Expression of L-selectin, CD43, and CD44 in synovial fluid neutrophils from patients with inflammatory joint diseases. Evidence for a soluble form of L-selectin in synovial fluid.

OBJECTIVE: To study the expression of L-selectin, CD43, and CD44 on peripheral blood (PB) and synovial fluid (SF) neutrophils from patients with inflammatory joint diseases, and to investigate the presence of soluble L-selectin in both SF and plasma from patients with acute and chronic arthritis. METHODS: PB and SF neutrophils were isolated from 13 patients with rheumatoid arthritis (RA) and 17 patients with various inflammatory joint diseases other than RA. Expression of L-selectin, CD43, CD44, CD11a, and CD11b was determined in both unstimulated and in vitro-activated cells by immunofluorescence flow cytometry. Soluble L-selectin levels were estimated in SF and plasma by a semiquantitative radioimmunoassay. RESULTS: Neutrophils from SF showed diminished expression of L-selectin compared with PB neutrophils; CD43 expression and CD44 expression were decreased in SF neutrophils from most patients. In contrast, SF neutrophils exhibited significantly increased expression of CD11b, to an extent similar to that seen with in vitro-activated PB neutrophils. Soluble L-selectin was detected at similar levels in SF and PB. CONCLUSION: The phenotypic profile of SF neutrophils (low levels of L-selectin, CD43, and CD44, and high levels of CD11b) from most patients with RA or other inflammatory joint conditions resembles that observed in in vitro-activated neutrophils. Our results suggest that SF neutrophils are activated to a similar degree in inflammatory joint diseases with different pathogenic mechanisms.

Acute Disease↗
PubMed1999

Synovial fluid CD146 (MUC18), a marker for synovial membrane angiogenesis in rheumatoid arthritis.

OBJECTIVE: CD146 (MUC18/MCAM/S-Endo) is a marker of tumor progression and metastasis formation in human melanoma. This molecule has also been identified in smooth muscle, endothelial cells, and activated T lymphocytes. We measured the synovial fluid levels of soluble CD146 in various human joint diseases, including rheumatoid arthritis (RA). In addition, we studied the distribution of CD146 in normal and RA synovial tissues. METHODS: CD146 was isolated from MEL-OH melanoma cells and characterized by Coomassie blue staining and Western blotting. Soluble CD146 was measured by competitive enzyme-linked immunosorbent assay in synovial fluids of 3 healthy individuals and 7 cadavers (controls), as wells as in patients with traumatic joint injury (n = 10), osteoarthritis (OA; n = 10), psoriatic arthritis (PsA; n = 10), other non-RA polyarthritis (NRAP; n = 10), and RA (n = 31). Immunohistochemistry was performed on 3 normal and 3 RA synovial tissues. Flow cytometric, reverse transcription-polymerase chain reaction, and Western blot analyses were performed on enzymatically separated RA synovial tissue cells. RESULTS: Compared with controls (mean +/- SD 10 +/- 2 ng/ml), significantly elevated synovial fluid levels of soluble CD146 were detected in patients with OA, PsA, and RA (17 +/- 7, 21 +/- 11, and 39 +/- 16 ng/ml, respectively; P < 0.02-0.001), but not in patients with traumatic joint injury or NRAP. Patients with early RA (<1 year after diagnosis) revealed the highest levels (51 +/- 15 ng/ml, n = 10; P < 0.001 versus controls). In RA, soluble CD146 correlated significantly with morning stiffness (P < 0.001), the number of tender joints (P < 0.02), and the number of swollen joints (P < 0.005), but not with the erythrocyte sedimentation rate (P = 0.07) or the C-reactive protein level (P = 0.57). CONCLUSION: Since CD146 is expressed almost exclusively by vascular endothelium, high levels of soluble CD146 found in RA synovial fluid, particularly in patients with early disease, could reflect increased activity of endothelial cells and angiogenesis.

Adult↗
PubMed1975

Demonstration of antibodies to collagen and of collagen-anticollagen immune complexes in rheumatoid arthritis synovial fluids.

Twenty-nine synovial fluids from patients with rheumatoid arthritis (RA) and 10 synovial fluids from patients with other joint diseases were investigated with regard to the presence of antibodies to denatured human collagen and of collagen-anticollagen immune complexes. 12 of the 29 RA synovial fluids showed anticollagen titres from 1:16 to 1:512 in passive haemagglutination. Only one patient in the group with no arthritis had a significant anticollagen titre of 1:32. Digestion of the synovial fluids with bacterial collagenase resulted in an anticollagen titre increase from two to four dilution steps in 9 of the RA fluids, while 6 previously negative RA synovial fluids showed anticollagen titres from 1:32 to 1:28 after digestion with collagenase. These results indicate the existence of collagen-anticollagen immune complexes in 15 of the 29 RA synovial fluids investigated.

Animals↗
PubMed1995

The role of synovial fluid filtration by cartilage in lubrication of synovial joints--III. Squeeze-film lubrication: axial symmetry under low loading conditions.

A mixture model of synovial fluid filtration and synovial gel formation at normal approach of cartilage surfaces in the human synovial joints loaded by a compressive force has been recently presented in Parts I and II of this paper (Hlavácek, 1993, J. Biomechanics 26, 1145-1150; 1151-1160). In the model synovial fluid is taken as a mixture of two incompressible fluids (ideal and Newtonian viscous), while the biphasic model of Mow et al. (1980, J. Biomech. Engng 102, 73-84) is used for cartilage. A system of partial differential equations for the normal approach of axially symmetric cartilage surfaces in the human hip joint obtained in Part II is solved numerically for low loads. A shallow pocket-type configuration of the synovial film is formed shortly after the load application at time t = 0. For constant loads the fluid film pressure profile follows very closely that in a dry frictionless contact. To this approximation and with the exception of a close vicinity of the squeeze-film edge the flux of the ideal fluid across the synovial fluid-cartilage interface varies quadratically with the radial distance r and decreases as t-1/2 with time. The ideal fluid is forced into cartilage at the central region and out of cartilage at the low-pressure periphery of the squeezed synovial film. The maximum gel-forming concentration (the 20-fold of the original value) of the hyaluronic acid-protein macromolecular complex of the synovial fluid is reached at the film centre first, then the gel film starts spreading quickly sideways. Later, the process slows down approaching the value r/2 1/2 where r is the radius of a dry frictionless contact. The final gel-film thickness decreases very slowly with the increasing r for 0 < or = r < r/2 1/2.

Biomechanical Phenomena↗
PubMed2002

Another look at synovial fluid leukocytosis and infection.

Synovial fluid white blood cell counts are considered to be useful in diagnosing infectious arthritis, however, considerable overlap exists between infectious and noninfectious types of inflammatory arthritis. We undertook this review of synovial fluid studies at our institution to better define this degree of overlap and characterize the features of infectious arthritis in relationship to synovial fluid white cell counts. The records of 202 consecutive patients with synovial fluid white blood cell counts >2000/mm were reviewed. Infectious arthritis was diagnosed in 77% (10/13) of patients with counts >100,000, 47% (8/17) in the 50,000-100,000 range, and 5% (9/172) with counts <50,000. Crystal-induced arthritis and rheumatoid arthritis made up 81% of patients in the 15,000-50,000 range. Overall, 10 of 27 (37%) cases of infectious arthritis had white cell counts >100,000, and 18 of 27 (67%) had counts >50,000. A majority of these infections (14/18) were related to Staphylococcus aureus, while 5 of 7 infections associated with counts <20,000 were associated with atypical organisms. This study confirms that a majority of patients with very high synovial fluid white blood cell counts have infectious arthritis, and that the likelihood of infection is markedly reduced, but certainly not excluded, below this level. The presence of atypical infections in a small percentage of patients with low counts emphasizes the importance of clinical judgment in evaluating all patients with inflammatory arthritis, regardless of synovial fluid white cell counts.

Journal Article↗
PubMedDate not supplied

Clinical pathology of synovial fluid.

Examination of synovial fluid should be performed in a systematic manner so as to derive the maximum of information. Synovial fluids should be divided into (1) non-inflammatory, (2) inflammatory, (3) purulent and (4) hemorrhagic types. In addition to general description, analysis should include mucin clot test, fibrin clog formation, microscopic examination for cell count and differential cell count, microscopic examination for crystals of gout and pseudogout and microgiological examination. Chemical examination should include estimation of glucose and uric acid. Immunochemical examination may include determination of immunoglobulins, antinuclear factor and LE factor.

Antibodies, Antinuclear↗
PubMed1985

Partial characterization of synovial fluid nucleotide pyrophosphohydrolase.

Synovial fluid adenosine triphosphate pyrophosphohydrolase, an enzyme which manifests increased activity in chondrocalcinosis and osteoarthritis, was partially characterized in synovial fluids from 41 patients who had a variety of arthropathies. Activity was found to be a soluble, heat labile, and divalent cation-dependent nonspecific nucleotide pyrophosphohydrolase with pH optimum 9.0-9.5.

Adenosine Triphosphatases↗
PubMed1984

Cytokines and the chronic inflammation of rheumatic disease. II. The presence of interleukin-2 in synovial fluids.

Sera and synovial fluids from patients with a variety of rheumatic diseases were assayed for interleukin-2 (IL-2) activity in a system utilizing the proliferative response of cultured human phytohaemagglutinin (PHA) T cell blasts. The synovial fluids from 14 rheumatoid arthritis, eight ankylosing spondylitis, three psoriatic arthritis and 11 osteoarthritis patients, all showed IL-2 activity. The amounts of IL-2 present in the fluids from different diseases were compared and ranged from 4.2 to 140.0 units/ml.

Arthritis, Rheumatoid↗
PubMed1983

[Pharmacokinetics of ketoprofen in the synovial fluid].

Serum and synovial fluid concentrations of ketoprofen were studied after administration of 50 or 100 mg in a single oral dose to patients with rheumatoid arthritis. Results show that ketoprofen is rapidly absorbed. Serum concentrations are similar in patients and healthy subjects. During the initial phase, plasma half-life, which averaged 1.5 to 2 hours in study patients, was similar to that recorded in controls. Significant accumulation of ketoprofen in synovial fluid of patients was demonstrated.

Administration, Oral↗
PubMed1995

Klebsiella pneumoniae-reactive T cells in blood and synovial fluid of patients with ankylosing spondylitis. Comparison with HLA-B27+ healthy control subjects in a limiting dilution study and determination of the specificity of synovial fluid T cell clones.

OBJECTIVE: To study the frequency of Klebsiella pneumoniae-responsive T cells in the peripheral blood (PB) of ankylosing spondylitis (AS) patients compared with that in healthy HLA-B27+ donors, and to examine T lymphocyte clones (TLC) derived from AS patient synovial fluid (SF) for the presence of Klebsiella reactivity. METHODS: Limiting dilution analysis of PB T cells in 8 patients with active AS and in 8 HLA-B27+ healthy subjects was used to determine the frequency of PB T cells responsive to K pneumoniae and Escherichia coli GroEL. SF T cells from a patient with active AS were cloned, and 125 TLC were characterized in proliferation assays. RESULTS: There were fewer T cells in the PB of AS patients that reacted with K pneumoniae than in the PB of healthy HLA-B27+ subjects. The frequencies of E coli GroEL-responsive T cells were approximately 5-10 times lower in all subjects tested (healthy donors and AS patients), but without significant differences between the 2 groups. Two CD4+ TLC that recognized K pneumoniae (1 cross-reactive with E coli) as well as 3 TLC that recognized GroEL (2 CD4+, 1 T cell receptor gamma/delta+) were isolated from the SF of a patient with actige AS. CONCLUSION: Our results indicate that there is a quantitative reduction of K pneumoniae-responsive T cells in the PB of AS patients as compared with healthy controls. This may reflect a defective peripheral T cell defense in the immune response to Klebsiella and may allow bacterial antigens to reach the synovium, where they initiate specific T cell responses.

Adult↗
PubMed1984

[Leukocyte migration inhibitory factor of synovial fluid lymphocytes in rheumatoid arthritis].

Synovial fluid lymphocytes from patients with rheumatoid arthritis were examined for the presence of leukocyte migration inhibitory factor by the agarose technique of Clausen. T and B lymphocytes were stimulated with phytohemagglutinin, concanavalin A, and pokeweed mitogen, and the culture supernatants were used for the migration inhibitory test. Migration index of the culture supernatants of T cells from rheumatoid synovial fluids was significantly greater than those of peripheral blood from rheumatoid patients and healthy controls. The results indicated that the production of leukocyte migration inhibitory factor following stimulation by mitogens was decreased in the T cells of rheumatoid synovial fluid. In the rheumatoid synovial fluid there was a positive correlation between the migration index and polymorphonuclear leukocyte counts. A similar result was also obtained in the study of B cells from rheumatoid synovial fluid. These results suggest that the rheumatoid synovial lymphocytes have been already activated in the synovial fluid. On the other hand, the supernatants of rheumatoid synovial fluid showed an elevated migration index, exceeded 1.0 and higher than those of osteoarthritic synovial fluid. This suggests that chemotactic factors play an important part in the rheumatoid synovial fluid, though the leukocyte migration inhibitory factor is present in the rheumatoid fluid.

Adult↗
PubMed1986

Knee arthrography: effects of various contrast media and epinephrine on synovial fluid.

Changes in synovial fluid leukocytes, total protein, and total complement were studied in 58 patients after they underwent single contrast material-enhanced knee arthrography with ionic (sodium iothalamate, sodium meglumine diatrizoate, meglumine iothalamate) and nonionic (iopamidol, iohexol) contrast media. In 30 of 58 cases, 0.3 mg epinephrine was also injected. In patients examined without epinephrine, a significant increase in the number of leukocytes was observed when sodium iothalamate and sodium meglumine diatrizoate were used. When administered with epinephrine all ionic compounds produced significant leukocytosis; articular reactions were most evident in patients examined with sodium salts. No inflammatory changes in the synovial fluid were observed when nonionic compounds were used. These data suggest that sodium-containing compounds produce a greater reaction in the joint compared with other contrast media, nonionic compounds are better tolerated by the joint, and epinephrine increases the articular reaction to ionic contrast media.

Adolescent↗
PubMed1994

The effect of a single intraperitoneal dose of hrIL-1 alpha on substance P-, neurokinin A-, calcitonin gene-related peptide- and neuropeptide Y-like immunoreactivity in cerebrospinal fluid, plasma and knee joint synovial fluid in the rat.

Substance P (SP)-, neurokinin A (NKA)-, calcitonin gene-related peptide (CGRP)- and neuropeptide Y (NPY)-like immunoreactivity (-LI) was studied in rats' cerebrospinal fluid (CSF), plasma and synovial fluid (SF) from both knee joints at 2 and 24 h following an intraperitoneal administration of 0.05 ml human recombinant interleukin-1 alpha (i.p. hrIL-1 alpha) or saline. Increased or decreased levels of SP-, NKA and CGRP-LI were detected in CSF and plasma, whereas NPY-LI was unaffected. In SF only CGRP-LI increased bilaterally. There was a correlation in CGRP-LI content between plasma and CSF following i.p. hrIL-1 alpha but not between plasma and SF or CSF and SF. It can be concluded that (1) i.p. hrIL-1 alpha activates somatosensory afferents thereby increasing SP- and CGRP-LI content in CSF and plasma and NKA-LI in CSF; 2) i.p. hrIL-1 alpha induces a bilateral increase of CGRP-LI in SF which is not mediated through systemic circulation and is possibly a part of the general host defensive reaction.

Animals↗
PubMed1997

Matrix metalloproteinases 2 and 9 in equine synovial fluids.

Matrix metalloproteinases (MMPs) may be important in the destruction of cartilage seen in equine osteoarthritis and may be detectable in synovial fluid. Synovial fluids were obtained from normal equine joints and from joints of horses with aseptic and septic joint diseases. The total MMP gelatinase enzyme activities were measured by gelatin zymography and image analysis of the gels. The bioactivity of gelatinase in synovial fluid was determined by a gelatin degradation ELISA. Potential MMP-2 & MMP-9 monomer enzyme activities were significantly elevated in both septic and aseptic joint disease synovial fluids in comparison to fluids from normal joints. The dimer form of MMP-9 enzyme activity was significantly elevated in fluids from septic joint disease cases in comparison to fluids form normal joints, but not fluids from horses with aseptic joint diseases. MMP-9 monomer and dimer levels in synovial fluids correlated with the synovial fluid white blood cell count. Using the gelatin degradation ELISA to measure net active gelatinases, significant increases in gelatinase bioactivities were seen in synovial fluids from both aseptic and septic joint disease cases. The enzymes in equine joint diseases were present in a bioactive form, in that they were present in the activated form and present in excess of inhibitors, and could therefore be important in the degradation of articular cartilage in joint disease.

Animals↗
PubMed1992

Inhibition of interleukin-1 activity by equine synovial fluid.

The presence, in equine synovial fluid, of inhibitors of interleukin-1 (IL-1) activity has been investigated by means of an assay involving IL-1-mediated production of PGE2 by synovial cells. Inhibitors of IL-1 alpha and IL-1 beta were identified in normal synovial fluid and synovial fluid from two horses with early joint disease. Inhibitors of IL-1 alpha were also present in synovial fluid from two horses with long-standing joint disease. However, IL-1 beta inhibitory activity was not present in fluid from the horses with more chronic joint disease. The effect appeared to be specific for IL-1, and not a direct action on PGE2 production, as synovial fluid had no effect on lipopolysaccharide-mediated PGE2 production. It is suggested that the inhibitory activity may be involved physiologically in the control of IL-1 activity in the joint, and the loss of IL-1 inhibition may be at least as important biologically as increased production of IL-1.

Animals↗