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PubMed1987

Mononuclear cells in synovial fluid of rheumatoid arthritis patients undergoing joint surgery.

Analysis of synovial fluid from patients with rheumatoid arthritis (RA) and a long history of RA, who were undergoing synovectomy and joint surgery, revealed that 71 +/- 15% of the mononuclear cells in the synovial fluid were lymphocytes. 3 +/- 2% lymphoid blast cells, and 26 +/- 15% of monocytes/macrophages. The lymphocyte population consisted mainly of T cells, and 72 +/- 15% of lymphocytes were OKT11-positive. OKT8-positive cells (48 +/- 9%) dominated over OKT4-positive (32 +/- 8%) cells with a mean OKT4/OKT8 ratio of 0.69. On the basis of Ia- and Tac-markers, very few of the lymphocytes were activated. Few B cells (12 +/- 7%) and no plasma cells were seen. The results are discussed in relation to previous reports.

Antibodies, Monoclonal↗
PubMed1996

Absolute identification of muramic acid, at trace levels, in human septic synovial fluids in vivo and absence in aseptic fluids.

This is the first report of a study employing the state-of-the-art technique of gas chromatography-tandem mass spectrometry for absolute identification of muramic acid (a marker for peptidoglycan) at trace levels in a human or animal body fluid or tissue. Daughter mass spectra of synovial fluid muramic acid peaks (> or = 30 ng/ml) were identical to those of pure muramic acid. Absolute chemical identification at this level represents a 1,000-fold increase in sensitivity over previous gas chromatography-mass spectrometry identifications. Muramic acid was positively identified in synovial fluids during infection and was eliminated over time but was absent from aseptic fluids.

Arthritis, Infectious↗
PubMed1981

Investigation of blood platelets in synovial fluid from patients with rheumatoid arthritis.

Synovial fluid (SF) aspirated from inflamed knee joints from each of 13 patients with adult rheumatoid arthritis (RA) was mixed with ACD in the ratio SF/ACD=9:1 with subsequent addition of an equivalent amount of an edta-tris buffer. The mixture was centrifuged to obtain a platelet-rich supernatant. The platelets were washed three times and counted. The same procedure was performed with SF from non-inflamed knee-joints from 3 patients with osteoarthrosis (OA). Direct immunofluorescence (IF) studies were performed with aliquots of platelet suspensions from each SF. In most RA specimens observed under the microscope before separation of platelets, a few small platelet aggregates were observed and platelets were seen in contact with lymphocytes. In all instances, the platelet count appeared to be positively correlated to the total number of white blood cells. In the OA specimens, relatively few platelets were detected, a few lymphocytes were seen in contact with platelets, but no platelet aggregates or correlation between platelets and white blood cell counts were found. Results of the IF studies of RA specimens provide evidence that IgG, IgM and C3 are located on the platelet surface. On the surface of OA platelets, however, only IgG and C3 were detected. Identical staining results were found with washed peripheral platelets from 3 of the RA and 1 of the OA patients. Neither medical treatment nor Waaler serology influenced the staining results. In inflamed SF from RA patients, both IgG aggregates, immune complexes, collagen, and prostaglandins can induce a platelet release reaction with liberation of vasoactive compounds, chemotactic substances and enzymes which can destroy connective tissue, cartilage and bone structures. Interpretations and the significance of the different results are discussed.

Adult↗
PubMed1997

Routine synovial fluid culture: is it necessary? Lessons from an audit.

An estimated third of rheumatologists send aspirated synovial fluid samples for culture routinely during the course of management of their patients irrespective of the underlying diagnosis. This is done apparently even when sepsis is not suspected. This audit of 507 synovial fluid culture requests revealed that positive bacterial growth was rare even when sepsis was queried on the request forms but none was positive in any of the routine samples. Our findings throw doubt on the value of routine synovial fluid culture. We recommend that such cultures are undertaken when infection is a possibility and in immuno-compromised patients. An average health district would save pounds 3000 per annum if such a policy was adopted, but across the National Health Service as a whole the total expenditure saved on this unnecessary investigation would be considerable.

Adolescent↗
PubMed1997

CR1, CD35 in synovial fluid from patients with inflammatory joint diseases.

OBJECTIVE: To investigate synovial fluid (SF) for the presence of CR1 and to study its relationship to SF leukocytes and to serum levels of soluble CR1 (sCR1) in patients with rheumatic diseases. METHODS: Synovial fluids were collected from 35 patients with rheumatoid arthritis (RA) and 26 patients with other inflammatory joint diseases. Total CR1 in the SF and serum were measured with a sandwich enzyme-linked immunosorbent assay (ELISA) that recognized both soluble and transmembrane forms of CR1. The characteristics of CR1 in SF were analyzed by ultracentrifugation and by a second ELISA specific for transmembrane CR1. RESULTS: CR1 was found in all SF samples tested (range 5-281 ng/ml). SF CR1 was higher in patients with RA (mean +/- SD 81 +/- 66 ng/ml) than in those with other inflammatory joint diseases (31.8 +/- 23.8 ng/ml) (P < 0.001). Serum sCR1 was not significantly increased in the patients compared with the normal subjects. There was no correlation between serum sCR1 and SF CR1. In 44% of the patients, the SF CR1 level was higher than the serum sCR1 level. A fraction (30-80%) of SF CR1 was pelleted by ultracentrifugation and, unlike serum sCR1, it reacted in an ELISA specific for transmembrane CR1. Thus, SF contained 2 forms of CR1: a membrane-associated and a soluble form, which was confirmed by sucrose density-gradient ultracentrifugation. SF CR1 levels correlated directly with the number of SF total leukocytes and polymorphonuclear leukocytes (PMN). These 2 forms of CR1 were also found in the supernatant of in vitro-activated PMN from normal subjects. SF CR1 exhibited the capacity to act as a cofactor for the factor I degradation of C3b. CONCLUSION: CR1 is found in the SF of patients with joint inflammation. The data suggest that SF CR1 originates from the infiltrating leukocytes, which shed both a soluble and a membrane-associated form. Whether SF CR1 participates in the local regulation of complement activation remains to be examined.

Arthritis↗
PubMed2003

Synovial fluid nitric oxide levels in patients with knee osteoarthritis.

Nitric oxide (NO) has an important role in the inflammatory arthropathies. This study investigated NO levels in the synovial fluid and plasma of patients with primary osteoarthritis (OA) of the knee. Twenty-seven cases with primary knee OA and 13 controls were recruited for the study. Nitrate/nitrite levels of synovial fluid and plasma were measured by Griess reaction, and interleukin-1 beta (IL-1 beta) levels were measured quantitatively by a sandwich immunoassay technique. We found a significant increase in the synovial fluid nitrate/nitrite levels in cases with primary OA of the knee compared to controls (50.26+/-23.63 microg/l vs 32.49+/-10.05 microg/l, p=0.002) as well as increased plasma nitrate/nitrite levels (57.06+/-23.32 microg/l vs 39.98+/-16.36 microg/l, p=0.012). There was no difference in plasma and synovial fluid IL-1 beta concentrations between the study and control groups. These results may be considered as supporting evidence that NO might be one of the factors responsible for cartilage destruction in primary osteoarthritis of the knee.

Adolescent↗
PubMed1978

[Proliferation of synovial fluid cells (author's transl)].

Investigations with labelled thymidine indicated that the mononuclear cells of the synovial fluid only rarely proliferateunder physiological conditions. Even in cases of rheumatoid arthritis no elevated proliferation rate was found. Cytophotometric investigations on Feulgen-stained nuclei is another way to determine cellular proliferation. To answer the question if the relative content of neutrophilic granulocytes in synovial fluids influences the proliferation of mononuclear cells, the DNA content of these cells was determined after Feulgen-staining with respect to the number of neutrophilic granulocytes. It was observed that nearly all mononuclear round cells exhibit diploid nuclear DNA content. No effect of the intensity of inflammation (as expressed by the content of neutrophilic granulocytes) was observed. From these results it is concluded that mononuclear cell proliferation is not influenced by the intensity of the inflammation. On the other hand it can be assumed that there is no immunological stimulus for an increassed proliferation of the synovial fluid in rheumatoid arthritis.

Arthritis, Rheumatoid↗
PubMed1988

Synovial fluid osmolality in osteoarthritis and rheumatoid arthritis.

The osmolality of synovial fluid aspirated from the knees of 15 rheumatoid and 15 osteoarthritic patients was observed concurrently with the same measurement on blood serum. The group averages were compared to a group of 13 with identical apparati. Synovial fluid osmolality in rheumatoid arthritics (280 +/- 7.7 mmol/kg) was significantly different from that in osteoarthritics (297 +/- 16.9 mmol/kg), and both group averages were significantly different from normal (404 +/- 57 mmol/kg). Blood serum osmolality also differed between the normal and the two arthritic groups. The potential application of vapor pressure osmometry techniques in the diagnosis and management of joint disease is discussed.

Aged↗
PubMed2005

Effect of synovial fluid, phosphate-buffered saline solution, and water on the dissolution and corrosion properties of CoCrMo alloys as used in orthopedic implants.

The corrosion and dissolution of high- and low-carbon CoCrMo alloys, as used in orthopedic joint replacements, were studied by immersing samples in phosphate-buffered saline (PBS), water, and synovial fluid at 37 degrees C for up to 35 days. Bulk properties were analyzed with a fine ion beam microscope. Surface analyses by X-ray photoelectron spectroscopy and Auger electron spectroscopy showed surprisingly that synovial fluid produced a thin oxide/hydroxide layer. Release of ions into solution from the alloy also followed an unexpected pattern where synovial fluid, of all the samples, had the highest Cr concentration but the lowest Co concentration. The presence of carbide inclusions in the alloy did not affect the corrosion or the dissolution mechanisms, although the carbides were a significant feature on the metal surface. Only one mechanism was recognized as controlling the thickness of the oxide/hydroxide interface. The analysis of the dissolved metal showed two mechanisms at work: (1) a protein film caused ligand-induced dissolution, increasing the Cr concentration in synovial fluid, and was explained by the equilibrium constants; (2) corrosion at the interface increased the Co in PBS. The effect of prepassivating the samples (ASTM F-86-01) did not always have the desired effect of reducing dissolution. The release of Cr into PBS increased after prepassivation. The metal-synovial fluid interface did not contain calcium phosphate as a deposit, typically found where samples are exposed to calcium rich bodily fluids.

Biocompatible Materials↗
PubMed2003

Tunnel enlargement and changes in synovial fluid cytokine profile following anterior cruciate ligament reconstruction with patellar tendon and hamstring tendon autografts.

There is growing evidence that cytokines such as tumor necrosis factor (TNF) alpha, interleukin (IL) 1beta, IL-6, bone morphogenetic proteins (BMP), and nitric oxide (NO) play an important role in the pathogenesis of bone tunnel enlargement following anterior cruciate ligament (ACL) reconstruction. Furthermore, the release of these mediators has been considered a possible reason for the higher incidence of bone tunnel enlargement following hamstring tendon (HST) than following patellar tendon (PT) ACL reconstruction observed in several studies. In this investigation synovial fluid samples from 13 patients were collected immediately before (24+/-7 days after ACL rupture) and 7 days after ACL surgery and values of TNF-alpha, IL-1beta, IL-6, NO, and BMP-2 were analyzed. Furthermore, the incidence of bone tunnel enlargement was assessed using radiographs 38+/-7 weeks after surgery. Six patients underwent autologous HST ACL reconstruction, and in seven patients an PT autograft was used. In the overall patient population there were significantly higher synovial fluid concentrations of IL-6 and BMP-2 postoperatively than preoperatively; TNF-alpha showed a trend towards lower postoperative levels while IL-1beta and NO remained unchanged. The concentrations of NO, TNF-alpha, and IL-6 found in the present study were clearly higher than normal values given in the literature. Assessment of bone tunnel enlargement revealed an average increase in tibial tunnel width of 28.4+/-3.1% with comparable values for HST and PT ACL reconstructions. There was no significant correlation between bone tunnel enlargement and postoperative synovial fluid concentrations of TNF-alpha, IL-1beta, IL-6, NO, and BMP-2. However, all patients with bone tunnel enlargement had higher postoperative concentrations of TNF-alpha, IL-6, and NO in the synovial fluid. There were no significant differences in concentrations between HST and PT groups. In conclusion, we observed an association between tibial bone tunnel enlargement and elevated synovial fluid concentrations of IL-6, TNF-alpha, and NO 7 days after ACL surgery indicating the potential involvement of these biological mediators in the pathogenesis of bone tunnel enlargement. However, there was no difference between HST and PT ACL reconstructions regarding synovial fluid contents of IL-6, TNF-alpha, IL-1beta, NO, and BMP-2, suggesting a comparable biological response between these autografts following their use in ACL reconstruction.

Adult↗
PubMed1993

Calcitonin gene-related peptide II, substance P and vasoactive intestinal peptide in plasma and synovial fluid from patients with inflammatory joint disease.

Immunoreactive plasma and synovial fluid concentrations of calcitonin gene-related peptide II (CGRP II), substance P and vasoactive intestinal peptide (VIP) were measured in patients with osteoarthritis, gout and rheumatoid arthritis. Significantly higher levels of CGRP II and substance P-like immunoreactivity levels in synovial fluid were found in gout as well as CGRP II, substance P and VIP-like immunoreactivities in rheumatoid arthritis when compared to those in osteoarthritis. Plasma CGRP II, substance P and VIP-like immunoreactivity levels showed no significant differences among patients in the three different groups of arthritis. Our results suggest that these neuropeptides released from peripheral nerve endings into the synovial cavity probably play a pathogenic role in human joint inflammation.

Adult↗
PubMedDate not supplied

Correlation between osteoarthritic cartilage damage and levels of proteinases and proteinase inhibitors in synovial fluid from the knee joint.

Matrix metalloproteinases (MMPs) in the synovial fluid are responsible for collagen breakdown during physiologic cartilage turnover and the pathologic destruction of the cartilage. We measured the levels of MMPs, specific tissue inhibitors of metalloproteinases (TIMPs), and interleukin-6 (IL-6) in synovial fluid from the knees of 36 patients with cartilage lesions subdivided according to severity based on arthroscopic findings. Lesions were classified as mild (group 1, edema with no disruption of the surface), moderate (group 2, open lesions without exposure of subchondral bone), or severe (group 3, exposure of subchondral bone). Zymography (gel electrophoresis in the presence of hydrolizable substrates) showed a 60-kd band in all samples. A second band (94-kd) was found exclusively in specimens from groups 2 and 3, and a third band (110-kd) was present only in group 3. Concentrations of 2 of the most important modulators of MMP activity, TIMP-1 and IL-6, were measured. TIMP-1 levels did not vary significantly with the severity of cartilage damage. Linear regression analysis revealed a significant positive correlation between TIMP-1 and IL-6 in groups 1 and 2. These data indicate that the severity of the cartilage damage corresponds with MMP activity. The correlation between IL-6 and TIMP-1 in groups with mild and moderate damage suggests a regulating mechanism that is absent in severe lesions.

Adult↗
PubMed2006

The utility of measuring C-terminal telopeptides of collagen type II (CTX-II) in serum and synovial fluid samples for estimation of articular cartilage status in experimental models of destructive joint diseases.

OBJECTIVE: To characterize and validate a novel, enzyme-linked immunoassay for measuring cross-linked dimer forms of C-terminal telopeptides of type II collagen (CTX-II) in serum and synovial fluid of rodents, and investigate whether CTX-II measurements can reflect joint status in two established animal models of destructive joint diseases. METHODS: Firstly, the specificity, in vivo validity, antigen recovery, and reproducibility of the assay were investigated. Secondly, we induced arthritis in rats using either bovine collagen type II or mono-iodoacetate. CTX-II levels were measured in the serum and synovial fluid of the affected femoro-tibial joint and correlated with microscopic severity of joint lesions as determined by validated scoring systems. RESULTS: The F4601 monoclonal antibody (mAb) is highly specific for the EKGPDP sequence at the CTX-II. Strong CTX-II signals were detected during enzymatic degradation of articular cartilage explants by matrix metalloproteinase (MMP)-9 or MMP-13. The assay presented a good degree of precision and reproducibility (inter- and intra-assay CVs< 8.0%). In the collagen-induced arthritis (CIA) model, the assay indicated markedly increased levels of CTX-II in both the synovial fluid and the serum. Furthermore, CTX-II levels in both the synovial fluid (r = 0.76; P < 0.0001) and the serum (r = 0.85; P < 0.0001) showed strong correlations with the microscopic severity scores of joint lesions at Day 22. In the mono-iodoacetate-induced arthritis (MIA) model, CTX-II concentration in the synovial fluid (r = 0.53; P < 0.0001), but not in the serum, correlated with the microscopic severity score. CONCLUSIONS: The Preclinical CTX-II assay could provide a useful supplement to currently available methods for the non-invasive assessment of cartilage status. The utility of serum CTX-II to reflect joint status appeared to be limited to systemic forms of destructive joint diseases.

Animals↗
PubMed1988

Quantification of leukotriene B4 in synovial fluid by gas chromatography/tandem mass spectrometry.

A procedure for the quantification of leukotriene B4 (LTB4) in synovial fluid has been developed using gas chromatography/tandem mass spectrometry based on selected reaction monitoring of the elimination of t-butyldimethylsilanol from the ions of m/z 431 and 438 in the negative ion chemical ionization mass spectra of the di-t-butyldimethylsilyl/pentafluorobenzyl derivatives of leukotriene B4 and the internal standard (2H8)leukotriene B4. The detection limit (approximately 10 pg ml-1) is sufficiently low to permit determination of LTB4 concentration in the synovial fluid of patients with various arthropathies. Single-stage mass spectrometry was found not to be selective enough to permit quantification of LTB4 in synovial fluid.

Arthritis, Rheumatoid↗
PubMed1992

An altered repertoire of T cell receptor V gene expression by rheumatoid synovial fluid T lymphocytes.

The pattern of T cell receptor V gene expression by lymphocytes from rheumatoid synovial fluid and paired peripheral blood samples was compared using a polymerase chain reaction (PCR)-based assay. Eight rheumatoid arthritis (RA) patients who had varying durations of disease (from 2 to 20 years) were studied. In all patients there was evidence of a different pattern of V gene expression between the two compartments. Significantly increased expression of at least one V alpha or V beta gene family by synovial fluid T cells was observed in all the patients studied. Three different V alpha (V alpha 10, 15 and 18) and three V beta (V beta 4, 5 and 13) families were commonly elevated. Sequencing of synovial V beta transcripts demonstrated that the basis of increased expression of selected V gene families in the synovial fluid was due to the presence of dominant clonotypes within those families, which constituted up to 53% of the sequences isolated from one particular synovial V gene family. There were considerable differences in the NDJ sequences found in synovial and peripheral blood T cell receptor (TCR) transcripts of the same V beta gene family. These data suggest that the TCR repertoire in the two compartments differs, and that antigen-driven expansion of particular synovial T cell populations is a component of rheumatoid synovitis, and is present in all stages of the disease.

Arthritis, Rheumatoid↗
PubMed2000

Temporomandibular joint pain: relationship to internal derangement type, osteoarthrosis, and synovial fluid mediator level of tumor necrosis factor-alpha.

OBJECTIVES: The purpose of this study was to investigate whether patients with temporomandibular joint (TMJ)-related pain classified as capsulitis/synovitis may be linked to magnetic resonance imaging (MRI) findings of internal derangement, osteoarthrosis, or the synovial fluid aspirate findings of tumor necrosis factor-alpha (TNF-alpha) level. STUDY DESIGN: The study comprised 23 patients with temporomandibular disorders (TMD), who had nonchronic pain (pain onset < or =6 months) and a unilateral TMJ-related diagnosis of capsulitis/synovitis. Bilateral sagittal and coronal magnetic resonance images were obtained to establish the presence or absence of internal derangement, osteoarthrosis, or both. TMJ synovial fluid aspirates were obtained from the pain and contralateral nonpain sides to determine the TNF-alpha level. RESULTS: Comparison of the TMJ side-related data showed a significant relationship between the clinical TMD diagnosis of capsulitis/synovitis and the MRI diagnoses of TMJ internal derangement (P =.002) and of TMJ internal derangement type (P =.04). The mean TNF-alpha level in synovial fluid aspirates from TMJs assigned a clinical TMD diagnosis of capsulitis/synovitis was significantly higher than in those obtained from contralateral nonpain sides (P =.001). There was no correlation between the clinical diagnosis of capsulitis/synovitis and the MRI diagnosis of TMJ osteoarthrosis (P =.13) or between the MRI diagnosis of TMJ osteoarthrosis and that of TMJ internal derangement (P =.70) or TMJ internal derangement type (P =.33). CONCLUSIONS: The results suggest that the TMJ pain condition of capsulitis/synovitis is related to TMJ-side specific MRI diagnoses of internal derangement and internal derangement type, and synovial fluid aspirate findings of TNF-alpha level. The data confirm the concept of elevated mediator level as a diagnostic approach for patients presenting with TMJ-related pain. MRI and synovial fluid aspirates may be used as diagnostic methods for evaluating TMJ-related pain conditions.

Adolescent↗
PubMedDate not supplied

von Willebrand factor in synovial fluid.

Von Willebrand factor (vWf), an endothelial product that arises in plasma in conditions associated with vascular damage and acute phase reaction, was evaluated in paired samples of plasma and synovial fluid obtained from 54 patients with inflammatory joint effusion, 19 patients with osteoarthritis, and from the plasma of 19 controls. Synovial fluid levels of vWf were detected in 36 of the patients. The mean value of vWf in the inflammatory joint effusion group was 18.27 +/- 3.03%, significantly higher than the mean value of 7.7 +/- 4.4% found in the osteoarthritis group (p less than 0.01). The significant difference between these groups was maintained when vWf was expressed as a ratio of albumin. vWf was correlated with synovial fluid levels of alpha-1-antitrypsin (r = 0.83, p less than 0.01) and with the white cell count (r = 0.74, p less than 0.01), but not with the levels of immunoglobulins or C3. vWf in the synovial fluid may reflect the local degree of inflammation.

Adult↗
PubMed2006

Expression of matrix metalloproteinases and aggrecanase in the synovial fluids of patients with symptomatic temporomandibular disorders.

OBJECTIVE: To investigate whether matrix metalloproteinases (MMPs) and/or aggrecanase in synovial fluid can be used as biochemical markers in the diagnosis of internal derangement (ID) of the temporomandibular joint (TMJ). STUDY DESIGN: Forty-four samples of synovial fluid were obtained from 35 patients with ID and osteoarthritis (OA) and 15 normal samples from 10 asymptomatic volunteers. MMP-2, -9, and aggrecanase in the synovial fluid were examined by immunoblotting. RESULTS: The incidences of MMP-2, -9, and aggrecanase expression in the ID and OA group were significantly higher than those in the normal group (P < .05). Those with anterior disc displacement without reduction and severe OA showed significantly high expression of MMP-9 compared with other disease subgroups (P < .05). Conversely, comparatively high expression of MMP-2 and aggrecanase was shown in the early-stage OA group. However, there was no significant difference in expression of MMP-2 and aggrecanase among disease subgroups. CONCLUSIONS: These findings suggested that expression of aggrecanase could be a potential biochemical marker for articular cartilage degradation in ID of the TMJ.

Adolescent↗