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Mycoplasma colonies were found on culture of synovial fluid in 14 of 18 cases of rheumatoid arthritis. It was possible to demonstrate the colonies in primary culture medium only by the method of hot water fixation and Giemsa staining. The organisms grown on solid medium were also observed electron-microscopically.
OBJECTIVE: We have previously reported that the anti-6C2 monoclonal antibody (mAb) defines a subset of human CD4+ memory T cells. The present study sought to determine the nature of the 6C2 molecule and the function associated with 6C2+ T cells, and to examine whether this T cell subset is involved in the pathophysiology of rheumatoid arthritis (RA). METHODS: Cytofluorographic analysis was performed for identification of T cell surface molecules displaying a distribution similar to that of the 6C2 molecule. T cells in the synovial fluid of RA patients were examined for expression of the 6C2 molecule. Transendothelial migratory activity was assessed by assay using monolayers of human endothelial cells. Specific reactivity of the anti-6C2 mAb was determined by immunoblotting on gangliosides separated by thin-layer chromatography, and flow cytometric analysis of the cells transfected with complementary DNA (cDNA) was performed for determination of the glycosyltransferases involved in biosynthesis of the gangliosides. RESULTS: On human peripheral T cells, the 6C2 molecule was distributed, by and large, in a pattern similar to that of CDw60, or O-acetyl-GD3. The majority (>70%) of synovial fluid T cells from patients with RA were found to be 6C2 positive, and those 6C2+ T cells exhibited a transendothelial migratory capacity that was inhibited by pretreatment of T cells with anti-6C2 mAb. Moreover, treatment of T cells with neuraminidase resulted in a loss of 6C2 expression as well as a reduction in the transendothelial migratory activity. Anti-6C2 mAb reacted specifically with GD3, but not with O-acetyl-GD3. The reactivity of anti-6C2 mAb was induced on the cell surface only by transfection with cDNA for GD3 synthase. CONCLUSION: The 6C2 molecule is a disialoganglioside, GD3, and is present on a subset of T cells with transendothelial migratory capacity. The 6C2/GD3 molecules, as well as 6C2/GD3+ T cells, appear to play a role in T cell migration and in the inflammation of RA.
Interleukin-6 (IL-6) was detected at low levels in plasma [0.014 +/- 0.006 ng/ml (mean +/- SEM] and in high amounts in synovial fluid [SF; 2.6 +/- 2.2 ng/ml (mean +/- SEM)] of patients with rheumatoid arthritis. No correlation of IL-6 levels in plasma or SF with the ESR (n = 15) or with histological parameters of acute local synovitis (n = 10) was observed. In contrast, SF IL-6 was positively correlated with histological characteristics of chronic synovitis (n = 10; P < or = 0.01) and elevated plasma IgG concentrations (n = 15; P < or = 0.05). In vitro concentrations of IL-6 comparable to those detected in SF increased the production of both IgG and IgM by synovial membrane mononuclear cells. The present results contribute to the view that high local IL-6 concentrations in SF promote chronic synovitis in RA.
Objective was to study the significance and the mechanism of action of elastase from polymorphonuclear leukocyte (PMN elastase) in patients with rheumatoid arthritis (RA). The experiments conducted consisted of two phases. Firstly, articular cartilage and synovia from 8 patients with RA undergoing total knee replacement were obtained, and the gelatinolytic enzyme activity was extracted with 2M guanidine hydrochloride. The gelatinolytic activity of each tissue was measured to confirm that the activity was due to PMN elastase by using an antihuman leukocyte elastase antibody. Secondly, the levels of PMN elastase-alpha 1 proteinase inhibitor complex (EIC) in the blood and synovial fluid of 170 patients with RA were measured by immunoassay. The results were as follows: 1. Gelatinolytic activity was shown to be mainly due to PMN elastase, and found to be highest in cartilage and synovia in RA joints. 2. The EIC levels in plasma of RA patients were significantly higher than those in gout and osteoarthritis (OA), and the EIC levels increased according to the stage of articular cartilage destruction. Moreover, the EIC levels in synovial fluid of RA patients were higher compared to those of OA patients. The activity of PMN elastase was elevated in destructive joints of RA. With the progression of articular cartilage destruction, EIC levels in plasma of RA patients increased as well. We suggest that PMN elastase may play a significant role in RA disease.
The composition and lipid profiles of the following tissues of the human knee joint were determined: articular cartilage, meniscus, ligaments, synovial fluid, synovium, intra-articular fat pad and bone marrow. The tissues were obtained from fresh cadavers and from surgical specimens. The lipid profiles of articular cartilage, meniscus and ligaments were similar to reported analyses of other tissues that are also rich in collagen. The lipid profiles for the remaining tissues were more like the profiles found in the fat depots and fatty tissues of the human body. Both the phospholipid and fatty acid patterns of these tissues were similar within statistical deviation. These results suggest that the per cent compositions of fatty acids and the phospholipid family profile ratios have limited range variability in the "normal" tissues of the human knee. On the other hand, the per cent neutral lipid compositions and their individual profiles showed great variations among the different tissue tissues of the knee.
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Indices of fibrinolytic blood and synovial fluid activity were investigated in 75 and 25 patients with proved sero-positive rheumatoid arthritis (RA) with systemic manifestations. Changes in the parameters of the fibrinolytic system in the patients suffering from RA with systemic manifestations were regarded as symptoms of the chronic intravascular coagulation syndrome. They could play a pathogenetic role in the time course and progression of rheumatoid inflammation.
The distribution of molecular forms of serum IgA rheumatoid factor (IgA-RF) in 42 patients with rheumatoid arthritis was examined by solid-phase radioimmunoassay following fractionation by gel chromatography or ultracentrifugation in acidic buffer. Analysis of the fractions using phosphate buffered saline indicated that the IgA-RF in each serum was mainly polymeric. However, monomeric IgA-RF was detected in sera from approximately two-thirds of the patients, after dilution of chromatographic or ultracentrifugal fractions in diluent containing mouse monoclonal anti-human alpha chain antibody. The levels of monomeric IgA-RF (mean +/- SD 38 +/- 86 micrograms/ml) and the ratios of monomeric to polymeric IgA-RF (mean +/- SD 0.29 +/- 0.41) varied over a wide range. Paired synovial fluids from 9 of the patients were also examined. Monomeric IgA-RF was detected in each, although 2 samples demonstrated only minimal quantities. Neither form of IgA-RF was detected in serum from healthy adults when analyzed under the same conditions. Thus, both monomeric and polymeric IgA-RF can occur in serum and synovial fluid from patients with rheumatoid arthritis, and their proportions vary widely among patients.
OBJECTIVE: To understand the regulation of rheumatoid factor (RF) production in rheumatoid arthritis (RA), we studied IgM-RF production by B cells isolated from the synovial fluid (SF). METHODS: Highly purified SF and peripheral blood (PB) B cells were isolated by negative selection in a fluorescence-activated cell sorter (FACS) and then cultured with either L cells, CD40 ligand (CD40L)-transfected L cells, or type B synoviocytes in the presence or absence of interleukin-2 (IL-2), IL-4, or IL-10. Total IgM and IgM-RF were detected after 14 days by enzyme-linked immunosorbent assay. Enzyme-linked immunospot assays were performed to detect cells that spontaneously produced immunoglobulin. SF B cells were also phenotypically characterized by FACS analysis. RESULTS: Terminally differentiated CD20-,CD38+ synovial plasma cells (PC) present in the SF of RA patients secreted IgM-RF in the absence of a stimulus. IgM-RF production markedly increased when SF B cells were cultured in the presence of type B RA synoviocytes together with IL-10, but independently of CD40-CD40L interaction. Although CD20-,CD38+ PC could also be demonstrated in SF B cells from patients with other forms of arthritis, IgM-RF production was restricted to the SF B cell cultures of patients with seropositive RA. The frequency of IgM-RF-producing cells among IgM-producing PC in patients with seropositive RA was estimated to be as much as 50%. CONCLUSION: These data demonstrate that terminally differentiated CD20-,CD38+ IgM-RF-producing B cells are specifically present in the inflamed joints of patients with seropositive RA. There is evidence that the local environment in the rheumatoid joint favors RF production. The relatively high frequency of IgM-RF PC in the SF B cell population provides evidence of a dominant RA-specific antigen-driven response in the development of the synovial PC repertoire.
Approximately 44% of patients develop osteoarthritis (OA) following rupture of the anterior cruciate ligament (ACL) if the injury is left unrepaired. Restoring knee stability through reconstruction, while providing symptomatic relief, has not been shown to reduce the incidence of degenerative changes. In fact, recent studies have shown that 50%-60% of ACL-reconstructed patients go on to develop degenerative changes or frank osteoarthritis. In light of these data, our group suggests that the cause of post-traumatic osteoarthritis is not biomechanical but biochemical. To test this hypothesis, we measured levels of nine cytokines which are important in modulating physiological and pathophysiological metabolism of cartilage in knee joint synovial fluid following ACL rupture. Our patient population contained both acute and chronic ACL ruptures. A total of 84 samples were collected and analyzed by enzyme-linked immunosorbent assay. On the basis of the data collected, we were able to identify subgroups of patients who, on the basis of their synovial fluid cytokine profile, may be at greater or lesser risk of developing post-traumatic OA. In general, patients displayed concentrations of interleukin-1 alpha (IL-1 alpha), basic fibroblastic growth factor (bFGF), transforming growth factor-beta (TGF-beta), granulocyte/macrophage-colony stimulating factor (GM-CSF), IL-6, and IL-8 that we interpreted as being consistent with an inflammatory reaction. Of great interest is the fact that the levels of these cytokines were very similar in patients 4 weeks after injury and in chronic patients, leading us to hypothesize that a chronic smoldering inflammatory reaction persists after resolution of the acute effusion.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: Difficulties in detecting Chlamydia trachomatis in human joints by polymerase chain reaction (PCR) may be related to whether synovial tissue or synovial fluid (SF) is used as the source of DNA in PCR amplification. In this study, a new PCR assay was developed and used to compare chlamydial DNA in paired samples of SF and synovial tissue from patients with arthritis. METHODS: The PCR assay targeted the ribosomal RNA operons, which are present in 2 copies on the C trachomatis chromosome. DNA from several relevant bacteria and chlamydial serovars was used for testing this screening system. The detection of chlamydial DNA in nucleic acid preparations from matched samples of SF and synovial tissue was compared by PCR assay. Samples were obtained from 55 patients, including patients with reactive arthritis, Reiter's syndrome, and other arthropathies. RESULTS: Testing of the PCR screening system confirmed it to be highly specific and sensitive. Use of this assay to screen DNA from SF and synovial tissue samples showed that 29 (53%) of 55 synovial tissue preparations were positive for chlamydial DNA, but only 16 (29%) of the matched SF samples from these 29 patients were similarly positive. Five (9%) of 55 SF samples, but not their tissue counterparts, were positive for chlamydial DNA by PCR. CONCLUSION: Detection of chlamydial DNA in the joints of patients by PCR gives positive results more often when synovial tissue rather than SF is the source of target nucleic acids. Although synovial tissue is the source of choice for the most reliable determination of chlamydia in the joint, both synovial tissue and SF should be assayed if possible.
Thirty-six synovial fluid samples of temporomandibular joints were obtained from 33 patients with pain and anterior disk displacement (closed lock) in the joints. DNAs were prepared from the samples and amplified by a PCR-based assay specific for Mycoplasma salivarium or Mycoplasma fermentans. Of the 36 samples, five (14%), three (8%), and 19 (53%) were positive for M. salivarium, M. fermentans and both, respectively.
An erroneous identification of sodium urate and calcium pyrophosphate crystals in synovial fluid may occur when utilizing compensated polarized microscopy with a dual-viewing-head teaching microscope. This is due to alteration of the observed image orientation with respect to the actual orientation of the crystal in space. By viewing a simple geometric figure through each microscope head, two basic types of image alterations are identified: a 180-degree rotation and a mirror-image transformation. Combinations of these two may also occur. This problem is clarified and illustrated and suggestions are offered to avoid erroneous crystal identification.
A simple method for measuring synovial fluid (SF) volume is described. The degree of dilution of SF albumin after intraarticular injection of a defined volume of saline was used to calculate residual SF volume. Good correlation between calculated and aspirated SF volume was found for knee joint exudates. The method is simple, requires no radioactive tracer and should be useful in quantitative studies involving SF pathophysiology. Interestingly, the major portion of the SF could be directly aspirated, since residual volumes were small in comparison.
Since the presence of Chlamydia nucleic acids has been shown in synovial fluid (SF) from some patients with Chlamydia reactive arthritis, we investigated whether commercially available tests, developed to detect Chlamydia nucleic acids in urogenital samples, could also be used for their detection in SF samples. We therefore tested SF samples, found positive with at least two different systems of DNA amplification in a previous study, with three commercially available kits. No positive results were obtained. It is concluded that the commercially available tests Gen-Probe PACE 2, Amplicor (developed by Roche Molecular Systems) and LCx (developed by Abbott Laboratories) do not have sufficient sensitivity to detect reliably Chlamydia RNA or DNA in SF.
We studied the subsets of synovial fluid (SF) lymphocytes and their activation states in 4 subtypes of juvenile rheumatoid arthritis. The expression of lymphocyte differentiation antigens and activation markers (Ia and Tac) appeared to be similar in these subgroups. Tac + DNA-synthesizing T blasts represented, at most, 5% of all SF mononuclear cells. This finding was in clear contrast to the high proportion of Ia-positive SF mononuclear cells. There were no differences in Ia and Tac expression or DNA synthesis among the different juvenile rheumatoid arthritis subgroups. This finding suggests that the cell-mediated immune response may represent secondary features of the disease that are involved as a final common pathogenetic pathway.