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PubMed1985

Characterization of extracellular phospholipase A2 in rheumatoid synovial fluid.

Phospholipase A2 (PLA2) activity has now been identified in rheumatoid synovial fluids. This PLA2 is a calcium-requiring protein of MW 11,000 with a neutral pH optimum. Its activity was inhibited by high concentrations of Mg2+, and by the active site-directed histidine reagent p-bromophenacyl bromide. Ionic and nonionic detergents, or the sulfhydryl reagent dithiothreitol caused loss of enzyme activity. Synovial fluid PLA2 did not interact with sulphated mucopolysaccharides such as heparin or chondroitin sulphate. Release and sequestration of PLA2 in the joint space may contribute to the characteristic rheumatoid inflammatory changes.

Acetophenones↗
PubMed1975

Effect of intra-articular 90Y resin treatment on the chemical properties of synovial fluid in rheumatoid arthritis.

Lyaluronic acid and total protein concentrations in synovial fluid of the knee joint obtained from 48 patients with classical or definite rheumatoid arthritis were determined before, and 1 week, 1 month and 6 months after intra-articular injection of 90Y resin colloid. The concentration ratio of total protein to hyaluronic acid, which is a sensitive index of the abnormality of the synovial fluid, was worse a week after the injection in each group as regards the clinical effect of the 90Y resin injection, but was better 1 month and 6 months after the injection only in the remission group.

Adolescent↗
PubMed1993

Total and free plasma and total synovial fluid piroxicam concentrations: relationship to antiinflammatory effect in patients with reactive arthritis and other arthritides.

Twenty-five patients (14 males, 11 females), sixteen with reactive arthritis and 9 with other arthritides were treated with piroxicam, 40 mg at day 1 and 20 mg daily the following 9 days. Both local knee joint and general disease activity were assessed at day 0 and day 10. At day 10, plasma and synovial fluid were drawn. Total and free (determined after equilibrium dialysis) plasma concentrations and total synovial fluid concentrations were measured by HPLC. Total plasma piroxicam concentrations (micrograms/ml) were 4.1 (0.5-8.3) [median (range)], free piroxicam plasma concentrations were 0.051 (0.012-0.118), total synovial fluid concentrations were 2.2 (0.3-4.6) and ratios total synovial to total plasma concentration were 0.51 (0.39-0.90). The effect of piroxicam treatment varied among the patients. We found no relationship between drug concentration and change in any of the disease activity parameters nor any correlation between the ratio of synovial fluid to plasma piroxicam concentration and the local knee joint disease activity parameters.

Adult↗
PubMed1984

Concentrations of lonazolac in serum and synovial fluid of patients with inflammatory or degenerate joint disease.

In 15 patients with inflammatory and degenerative joint disease the concentrations of lonazolac were measured in serum and synovial fluid at steady state conditions. The mean concentration in the synovial fluid in 14 patients was 0.275 microgram/ml, which was 48% of that in the serum. For the patients with inflammatory joint disease, the synovial fluid concentration of lonazolac was 61% of that in the serum whereas in degenerative joint disease it reached only 39%.

Adult↗
PubMed2001

Measurement of the bioactivity of interleukin and tumour necrosis factor in synovial fluid of Kashin-Beck disease.

We studied the bioactivity of interleukin (IL-1) and tumour necrosis factor (TNF) in the synovial fluid of 12 patients with Kashin-Beck disease (KBD), 8 patients with osteoarthritis (OA) and 8 normal controls. C57 female mouse T cell proliferation method was used to test the bioactivity of IL-1, and lethality method with L929 cells to test the bioactivity of TNF. The bioactivities of IL-1 and TNF in the synovial fluid from patients with KBD were higher than those in the synovial fluid of osteoarthritis and normal controls, indicating the participation of IL-1 and TNF in the pathogenesis of KBD.

Adult↗
PubMed1983

Synovial fluid lactic acid in septic and nonseptic arthritis.

We determined lactic acid levels by the lactic dehydrogenase method in synovial fluid of 41 patients with various rheumatic diseases, to test the concept that significantly elevated values were diagnostic of septic arthritis. Nine patients had septic arthritis, 15 rheumatoid arthritis (RA), and the remainder miscellaneous conditions. In another 9 patients with different rheumatic diseases, including 1 with septic arthritis, synovial fluid lactic acid was determined by both the lactic dehydrogenase and gas-liquid chromatography methods. There was a wide scatter of values among patients with septic and nonseptic inflammatory arthritis, and much overlap occurred. We could not differentiate septic arthritis from RA on the basis of synovial fluid lactic acid levels. Results were similar with both procedures for determining lactic acid levels.

Arthritis, Infectious↗
PubMed1977

Levels of immunoglobulin E (IgE) in paired examinations of serum and synovial fluid in rheumatoid arthritis and reactive synovitis of local origin.

Levels of IgE were examined in pairs of serum and synovial fluid of the knee joint in a series of 78 patients with rheumatoid arthritis (RA), reactive synovitis during osteoarthrosis, and after injury. The IgE levels in synovial fluid were significantly lower (p less than 0.05) in all groups; in RA, they were in significant correlation (r=0.6208, p less than 0.0001) and in direct linear regression to the levels in serum. In 5 patients of the whole series, however, the IgE levels in serum were lower by one order of magnitude as compared with synovial fluid. Serum levels of IgE in RA were in significant correlation and in direct linear regression to the titres of rheumatoid factors according to the latex-fixation test (r=0.3688, p=0.0249) and the haemagglutination test with sheep red cells (r=0.3721, p=0.0235).

Adult↗
PubMed1979

[Scanning electron microscopic observations of calcium pyrophosphate crystals of joint tissues and synovial fluid (author's transl)].

The deposition and ultrastructure of calcium pyrophosphate (CPPD) crystals in joint tissues of pseudogout patients and cadavers were studied. Nine calcified menisci, 2 articular cartilages and 6 samples of synovial fluid were examined by scanning electron microscopy (SEM). Some of them were examined by analytical electron microscopy (EMMA). In the samples of menisci and cartilages, the findings were compared with those in the soft X-ray examinations and polarized light microscopy. The results are summarized as follows: 1) SEM observation of the cut surfaces of calcified menisci and cartilages showed a three-dimensional ultrastructure for the CPPD crystals. The crystals in the synovial fluid taken from pseudogout knees were also clearly demonstrated by this method. The EMMA analysis provided the possibility to examine the structure and content of the crystals simultaneously. 2) Crystal deposition in the meniscus varied with the depth of the tissues; it was diffuse in the collagen framework of the superficial layer, but showed accumulation in the deep layer where a clear line of demarcation between the collagen framework and crystals was seen. 3) The crystals in the meniscus were rod, granular or rectangular in shape, and 0.2-6.5 micro by 0.2-3.5 micro in size. Crystals from the articular cartilage were granular or rod-like in shape, and 0.2-3.5 micro by 0.2-1.0 micro in size. Most of the crystals found in the synovial fluid were rod-shaped. 4) X-ray microanalysis of the meniscus crystals by EMMA showed the same pattern of PK alpha, CaK alpha, and CaK beta content as that of CPPD crystals commercially available. The P/Ca ratio was about 0.7. 5) SEM and EMMA examination can be very useful for accurate identification of the form and content of the tiny crystals in joint tissues and synovial fluid. This can also be useful in proving a diagnosis of crystal-induced synovitis.

Calcinosis↗
PubMed2001

Comparison of UHMWPE particles in synovial fluid and tissues from failed THA.

The size and morphology of ultra high molecular weight polyethylene (UHMWPE) wear particles isolated from synovial fluid and periprosthetic tissues from three failed total hip arthroplasties were evaluated. Hip capsule, femoral canal tissue, and synovial fluid were collected at the time of revision surgery. The polyethylene wear particles were isolated and then imaged using a scanning electron microscope. The size and morphology of the particles were quantified using an image analysis protocol. Five shape descriptors were defined for each particle: equivalent circle diameter (ECD, a measure of size having units of length), aspect ratio (AR), elongation (E), roundness (R), and form factor (FF). The size and shape of the polyethylene particles differed depending on the source. Femoral tissue particles had the lowest equivalent circle diameter (0.697 +/- 0.009 mm), aspect ratio (1.577 +/- 0.016), and elongation (1.912 +/- 0.030), but the highest values for roundness (0.715 +/- 0.005) and form factor (0.874 +/- 0.003). Hip capsule particles had the highest equivalent circle diameter (0.914 +/- 0.019 mm), aspect ratio (1.764 +/- 0.025), and elongation (2.488 +/- 0.053), but the lowest values for roundness (0.642 +/- 0.006) and form factor (0.803 +/- 0.005). The size and shape descriptors for synovial fluid particles (equivalent circle diameter: 0.763 +/- 0.012 mm; aspect ratio: 1.700 +/- 0.029; elongation: 2.212 +/- 0.054; roundness: 0.681 +/- 0.006; and form factor: 0.841 +/- 0.004) were intermediate among the femoral tissue and hip capsule particles. These data suggest that larger particles may become lodged in the hip capsule, while smaller particles may migrate to more distant tissues and subsequently cause aseptic loosening and osteolysis.

Aged↗
PubMed1991

Candida arthritis: cellular immune responses of synovial fluid and peripheral blood lymphocytes to Candida albicans.

A case of septic Candida albicans arthritis of the knee in a patient with systemic candidiasis is presented. Systemic and intra-articular cellular immune responses to C albicans and various bacterial antigens were monitored for 15 weeks. It is shown that the candida induced blastogenesis of synovial fluid lymphocytes was much more stimulated than that of peripheral blood lymphocytes, and that the proportion of activated cells expressing HLA class II antigens was markedly increased in the synovial fluid. Strong cellular immune responses to Candida albicans could still be shown many weeks after the synovial fluid aspirates had become sterile. For the first time synovial fluid derived, CD4 positive T lymphocyte clones with specificity for candida antigens were characterised and further propagated in vitro.

Antibodies, Monoclonal↗
PubMedDate not supplied

The anticytokine neuropeptide alpha-melanocyte-stimulating hormone in synovial fluid of patients with rheumatic diseases: comparisons with other anticytokine molecules.

The aim of this study was to determine if the anticytokine neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) occurs, along with interleukin 1 receptor antagonist (IL-1ra) and soluble tumor necrosis factor receptor (sTNFr), in synovial fluid of patients with rheumatoid arthritis (RA), juvenile chronic arthritis (JCA), or osteoarthritis. The data show that alpha-MSH does occur in the synovial fluid and its concentrations are greater in patients with RA than in those with osteoarthritis. Synovial fluid concentrations of IL-1ra and sTNFr were likewise greater in RA. Further, concentrations of alpha-MSH, IL-1-ra, and sTNFr were greater in patients with polyarticular/systemic-onset JCA than in those with pauciarticular disease, that is in patients with greater joint inflammation. Concentrations of alpha-MSH were greater in synovial fluid than in plasma in a substantial proportion of patients, suggesting local production of the peptide; this is the first indication that the anticytokine molecule alpha-MSH is produced within a site of inflammation. Further, it appears that local production of alpha-MSH is induced particularly in those arthritic joints that have more intense inflammatory reactions. This finding, combined with previous evidence of the marked anti-inflammatory activity of alpha-MSH, suggests that the peptide acts locally to modulate proinflammatory influences in rheumatic diseases.

Arthritis, Rheumatoid↗
PubMed1999

Pharmacokinetics of carprofen enantiomers in equine plasma and synovial fluid - a comparison with ketoprofen.

Carprofen is a Non Steroidal Anti-Inflammatory Drug (NSAID) which is widely used for the treatment of musculoskeletal disorders in horses. The commercial preparation is a racemic mixture of two enantiomers (R and S carprofen). We used HPLC to measure plasma and synovial fluid R and S carprofen concentrations following a single intravenous (i.v.) dose, and computer modelling to determine the pharmacokinetic parameters of the enantiomers in these two body fluids. A comparison was made with results from an identical experiment using ketoprofen. The plasma elimination half lives of R and S carprofen were 20 and 16 times longer than those of R and S ketoprofen, and clearance was considerably slower for carprofen than ketoprofen. Plasma R carprofen concentrations were higher than S carprofen concentrations throughout the 48-h period. Ketoprofen was no longer detectable in synovial fluid after 5 h (S enantiomer) or 12 h (R enantiomer), whereas synovial fluid carprofen concentrations did not peak until 12 h and were still detectable at 48 h. Synovial fluid concentrations of both carprofen enantiomers were significantly lower than plasma concentrations, probably due to high plasma protein binding which could limit transfer through the synovial membrane. Our results indicate significant differences between carprofen and ketoprofen and between the two carprofen enantiomers.

Animals↗
PubMed2006

Matrix metalloproteinase and tissue inhibitor of metalloproteinase in serum and synovial fluid of osteoarthritic dogs.

To better understand the mechanisms responsible for the pathological processes of osteoarthritis (OA) and to potentially identify a profile of changes that could be predictive of early OA, matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of matrix metalloproteinase-2 (TIMP-2) in the synovial fluid and serum of normal and osteoarthritic dogs were examined. The concentration of MMP-1 in the synovial fluid of osteoarthritic dogs (0.62 +/- 0.16), as measured by densitometry, was significantly higher than that found in control dogs (0.42 +/- 0.19) (P = 0.03). The concentration of MMP-1 in the serum of osteoarthritic dogs (0.74 +/- 0.16) was significantly less than that found in control dogs (0.87 +/- 0.08) (P = 0.05). The concentration of TIMP-2 in the synovial fluid of osteoarthritic dogs (46.2 +/- 21.9 ng/ml) was significantly less than that of control dogs (122.0 +/- 66.5 ng/ml) (P = 0.009). The concentration of TIMP-2 in the serum of osteoarthritic dogs (116.2 +/- 43.1 ng/ml) was not significantly different than that of control dogs (95.1 +/- 94.4 ng/ml) (P = 0.554). In addition, a phospho-tyrosine immunoprecipitation and mass spectrometry were used to isolate and identify interferon-alpha in canine synovial fluid.

Animals↗
PubMed2006

Prevalence of anti-3-nitrotyrosine antibodies in the joint synovial fluid of patients with rheumatoid arthritis, osteoarthritis and systemic lupus erythematosus.

BACKGROUND: Increased reactive nitrogen species (RNS) production has been suggested in the pathogenesis of rheumatoid arthritis (RA), osteoarthritis (OA) as well as in systemic lupus erythematosus (SLE). They are known to have direct toxicity to cells. High concentrations of serum nitrite/nitrate and elevated urinary nitrate:creatine ratio has been found in patients with RA, OA and SLE. Reactive nitrogen species play a role in the chronicity of inflammatory reaction such as cartilage and bone destruction seen in patients with RA and OA. Arthritis is also associated with increased intra-articular formation of 3-nitrotyrosine (3-NT), which may contribute to joint damage. There is growing evidence that nitrative injury plays an important role in oxidative stress in the etiology and pathogenesis of SLE. 3-nitrotyrosine is thought to be a relatively specific marker of nitrosative damage mediated by nitric oxide (NO) and its by-products. METHODS: Commercially available poly l-tyrosine was exposed to nitrating species resulting in the formation of 3-nitrotyrosine. Antibodies present in synovial fluid and sera of 30 patients with rheumatoid arthritis, 15 patients with osteoarthritis and 15 patients with SLE were studied for their recognition of 3-NT by direct binding ELISA. RESULTS: IgG from the synovial fluid (SF) of RA and OA patients, purified on protein A-Sepharose matrix, exhibited increased recognition of 3-NT, than the IgG isolated from the sera of RA and OA patients in competitive ELISA, whereas IgG isolated from the sera of SLE patients exhibited increased recognition of 3-NT, than the IgG isolated from the synovial fluid. There was a higher prevalence of antibodies against 3-NT in the synovial fluid than in the sera of patients with RA and OA. Higher level of anti-3-NT antibodies were found in the synovial fluid in the later stages of SLE when compared to the early stages but was not more than that found in the sera. CONCLUSION: The RNS may be produced within the inflamed joints of RA and OA patients but not in SLE patients. The 3-NT levels also correlated directly with disease activity.

Arthritis, Rheumatoid↗
PubMed1989

Multiple forms of phospholipase A2 in arthritic synovial fluid.

Phospholipase A2 (PLA2) has been purified to homogeneity from human arthritic synovial fluid. The activity resolved into multiple peaks by preparative HPLC. The most abundant peak (A) was present in synovial fluid from patients with rheumatoid arthritis, osteoarthritis, and psoriatic arthritis. A second major peak (B) was variable and lower in relative abundance, but was distinguishable from peak A by its stimulated activity in the presence of either 0.5 M Tris or 0.1% sodium deoxycholate (DOC), in addition to its longer HPLC column retention time. Both peaks required Ca2+ and showed optimal activity in DOC/phosphatidylcholine (PC) mixed micelle assays between pH 8.0 and 9.0. Both peaks showed higher activity with PC as substrate than with PI, however peak A exhibited higher activity with PE than PC. Upon preparative SDS-polyacrylamide gel electrophoresis, both peaks of PLA2 activity were resolved as proteins of approximately 14,000 Da. The N-terminal sequence obtained from purified peak A material matched that of a recent similar isolate (Hara et al. (1988) J. Biochem. 104, 326-328).

Animals↗
PubMed1985

Lymphocyte activation in rheumatoid arthritis synovial fluid in vivo.

Monoclonal antibodies were used in avidin-biotin-peroxidase complex staining for activation marker analysis of rheumatoid synovial fluid cells. Although Ia expression indicates T cell activation, cells displaying receptors for interleukin 2 (Tac)-and transferrin receptor (T9)- positive proliferating cells were relatively few. Similarly, activated terminal effector cells of suppressor/cytotoxic nature were scarce in rheumatoid synovial fluid, as suggested by a low expression of Tac and 4F2 markers. The in vivo situation in the rheumatoid arthritic (RA) joint does not seem to be due to the inability of synovial fluid lymphocytes to become activated, because mitogen stimulation in vitro, in spite of a low proliferative response, induced expression of all the activation markers studied. The relevance of the present observations to the down-regulation of the active, inflammatory-immune response in situ is speculative, but the data show that in spite of T-cell activation and Ia expression, activated terminal effector cells of suppressor/cytotoxic nature are few in the RA joint in vivo.

Antibodies, Monoclonal↗
PubMed1997

Comparison of synovial fluid cartilage marker concentrations and chondral damage assessed arthroscopically in acute knee injury.

OBJECTIVE: To examine the correlation between synovial fluid cartilage markers and degree of cartilage damage determined by arthroscopic evaluation in subjects with acute knee injury. DESIGN: Chondral damage was quantified using a validated arthroscopic scoring system in 20 subjects with effusive acute knee injuries of less then 4 months duration and no history or radiographic evidence of joint pathology. Levels of synovial fluid 3B3(-) neoepitope, 3B3(+) chondroitinase generated epitope of proteoglycan, keratan sulfate (KS) and hyaluronic acid (HA) were measured by competitive enzyme-linked immunosorbent assays using monoclonal antibodies 3B3 and 5D4. Total sulfated glycosaminoglycan (GAG) was measured by 1,9-dimethylmethylene blue colorimetric dye-binding assay. RESULTS: We found a dramatic decrease in levels of 3B3(-) (rs = -0.62, P = 0.004), and GAG (rs = -0.49, P = 0.03) with increasing chondral damage score; but no correlation of damage score with 3B3(+), KS or HA levels. CONCLUSION: These data reveal a change in cartilage metabolism within the first 4 months of symptomatic knee injury evinced by a significant inverse correlation of 3B3(-) and GAG levels to chondral lesion severity. These results suggest that serial measurement of these synovial fluid markers in the setting of acute knee injury could predict chondral lesion severity and aid in the decision to intervene surgically.

Acute Disease↗
PubMed1991

Enkephalinase: a physiologic neuroimmunomodulator detected in the synovial fluid.

Enkephalinase (endopeptidase 24.11) is a metallopeptidase that is able to cleave not only neuropeptides and hormones but also immune mediators. The enzyme was quantified in synovial fluid obtained from 36 swollen joints. Its concentration correlated with the synovial fluid cell count, mainly the polymorphonuclear cells and lymphocytes, and with the erythrocyte sedimentation rate. No statistically significant difference in enkephalinase levels was demonstrated between the groups of patients with rheumatoid arthritis, seronegative spondylarthropathy, microcrystalline arthritis, or osteoarthritis. The presence of enkephalinase in the synovial fluid could reflect the intensity of the inflammatory process, or it could represent a physiologic regulator of inflammation and pain within the joint.

Arthritis↗