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PubMed1997

Pain and synovial fluid concentration of serotonin in arthritic temporomandibular joints.

The aim of this study was to investigate the relation between serotonin in the synovial fluid (SF-5-HT) and pain of arthritic temporomandibular joints (TMJ). The study comprised 1 male and 10 female patients (22 TM joints) with bilateral TMJ pain or tenderness and a mean age of 42 years. The patients were studied regarding pain from the TMJ at rest and during mandibular movements as well as regarding pressure pain thresholds and tolerance levels over the TMJ. TMJ samples, obtained by saline washing of the joint, and blood serum samples were taken for measurement of the 5-HT content. There was a positive correlation between SF-5-HT and pain in the TMJ upon movement. Maximum voluntary mouth opening ability was negatively correlated to SF-5-HT. In conclusion, the results of this study indicate that 5-HT in the TMJ synovial fluid is related to pain perceived upon movement of the joint and to decreased mandibular mobility.

Adult↗
PubMed1993

Quantitation of substance-P and its metabolites in plasma and synovial fluid from patients with arthritis.

Substance-P (SP) and its metabolites, SP-(1-7) and SP-(5-11), were quantitated in arthritic synovial fluids and plasma using a validated procedure. This process involved collection into appropriate enzyme inhibitors, extraction with acid-acetone, high pressure liquid chromatography, and RIA using region-specific antisera. Our results demonstrate that the levels of authentic SP in these fluids are less than 3.5 pmol/L, which is 50- to 10,000-fold less than those previously reported by others. These discrepant findings were not attributable to degradation, because added SP was recovered in good yield, and the measured levels of the metabolites SP-(1-7) and SP-(5-11) were also extremely low. In search of an explanation, we noted that many of the earlier reports involved direct assay of these fluids (without extraction and chromatography). Further work indicated that proteolytic enzymes (e.g. protease 24.11) present in these unextracted fluids can give rise to artifactually high SP measurements. We conclude that if SP is released within the joint space and if it participates in the inflammatory reaction and/or healing process, it most likely does so in a local fashion, which would not involve its accumulation in synovial fluid or plasma.

Adult↗
PubMedDate not supplied

[(Fab')2-antiglobulins in serum and synovial fluid in patients with chronic polyarthritis].

In addition to the well-known rheumatoid factors or antiglobulins belonging to different immunoglobulin classes, a new type of antiglobulin has been found in serum and synovial fluid from patients with rheumatoid arthritis. 15/20 sera and 6/6 synovial fluids contained serologically active material with a molecular weight of approximately 95.000 Daltons. Using chromatographic and affinity chromatographic methods as well as specific precipitation techniques, the (Fab')2 character of these antiglobulins could be ascertained. These antiglobulins may arise through enzymatic degradation of IgG or monomeric IgM antiglobulins, or may be the product of partial intracellular degradation of phagocytosed immune complexes with subsequent extrusion of such material. An in vitro blocking effect of (Fab')2 type antiglobulins on SCMC or ADCC reactions was not found.

Adult↗
PubMed1996

Augmented plasma and tissue kallikrein like activity in synovial fluid of patients with inflammatory articular diseases.

We studied some of the components of the kininogen-kallikrein-kinin system, simultaneously, in plasma and synovial effusions of patients with inflammatory articular diseases. Plasma and tissue kallikrein like activity and kininogen levels were evaluated. Active plasma and tissue kallikreins in plasma and synovial fluid were detected by their amidase activity upon specific chromogenic substrates. Kininogen levels were determined by a bioassay. Both specific amidase activity of plasma and tissue kallikreins were augmented in synovial effusions in relation to their own plasma activity. Kininogen levels in synovial fluid tended to be diminished in relation to plasma, however statistical significance was not reached. The consumption of kininogen is probably related to kinin production. This finding together with increased activities of plasma and tissue kallikreins reinforce the involvement of kinins in pathogenesis of inflammatory articular diseases.

Adolescent↗
PubMed1983

Effect of stimulated neutrophils from the synovial fluid of patients with rheumatoid arthritis on lymphocytes--a possible role of increased oxygen radicals generated by the neutrophils.

Neutrophils from the synovial fluid (SFN) of 10 patients with active rheumatoid arthritis (RA) were investigated to determine the generation of oxygen intermediates (OI) (O2-, H2O2, OH .), chemiluminescence, and lysosomal enzymes (lysozyme and beta-glucuronidase). Lymphocytes from healthy individuals were cocultured at 37 degrees C for 17 hr with SFN from the patients and the number of OKT4+, OKT8+, and OKT3+ cells and the response to mitogens were determined. A markedly increased OI and slightly elevated lysosomal enzyme levels were observed in SFN from patients. Coculture of lymphocytes with SFN resulted in a decreased number of OKT4+ and OKT8+ cells and a greatly reduced response to Con A and mildly diminished response to PHA, while OKT3+ cells were not affected. The simultaneous addition of superoxide dismutase and catalase restored the impairment of monoclonal antibody reaction and lymphocyte responsiveness almost to control levels. It is suggested that the disturbed immunoreactivity of synovial fluid lymphocytes from RA patients may be due to increased OI generated by stimulated neutrophils.

Antibodies, Monoclonal↗
PubMedDate not supplied

[The cellular immune reaction in synovial fluid lymphocytes to Ureaplasma antigens in patients with Reiter's syndrome].

INTRODUCTION: Reiter's syndrome (RS) is an seronegative arthritis that occurs after urogenital or enteric infection which in addition with occular and/or mucocutaneous manifestations presents complete form of disease. According to previous understanding arthritis in the RS is the reactive one, which means that it is impossible to isolate its causative agent. However, there are the more and more authors suggesting that arthritis in the urogenital form of disease is caused by the infective agent in the affected joint. This suggestion is based on numerous studies on the presence of Chlamydia trachomatis and Ureaplasma urealyticum in the inflamed joint by using new diagnostic methods in molecular biology published in the recent literature [1-3]. Besides, numerous studies of the humoral and cell-mediated immune response to "triggering" bacteria in the affected joint have supported previous suggestions [4-7]. Aim of the study was to determine whether synovial fluid T-cells specifically recognize the "triggering" bacteria presumably responsible for the Reiter's syndrome. METHOD: The 3H-thymidine uptake procedure for measuring lymphocyte responses was applied to lymphocytes derived concurrently from synovial fluid (SF) and from peripheral blood (PB) [8]. Ureaplasma antigen and mitogen PHA stimulated lymphocytes in 24 RS patients (24 PB samples, 9 SF samples) and the results were compared with those found in 10 patients with rheumatoid arthritis (RA) (10 PB samples, 5 SF samples). Preparation of ureaplasma antigen. Ureaplasma was cultured on cell-free liquid medium [9]. Sample of 8 ml was heat-inactivated for 15 minutes at 601C and permanently stirred with magnetic mixer. The sample was centrifuged at 2000 x g for 40 minutes and than deposits carefully carried to other sterile glass tubes (Corex) and recentrifuged at 9000 x g for 30 minutes. The deposit was washed 3 times in sterile 0.9% NaCl, and final sediment was resuspended in 1.2 ml sterile 0.9% NaCl. BACTERIOLOGY: Chlamydia trachomatis was isolated by cell culture using cycloheximide-treated McCoy cells [10], while Ureaplasma urealyticum was identified according to its biochemical properties grown on cell-free liquid medium [9]. RESULTS: Proliferative response of the PB lymphocytes to stimulation by mitogen and ureaplasma antigen did not differ between RS and RA patients. Also, there was no difference in proliferative response of SF lymphocytes to mitogen stimulation between RS and RA patients (Figure 1). However, proliferation of SF lymphocytes stimulated by ureaplasma antigen was significantly elevated in RS patients compared with the control group. This difference is statistically significant (p < 0.05) (Figure 2). Difference in proliferative response of the PB and SF lymphocytes stimulated by the ureaplasma antigen was not found in RS patients. DISCUSSION: It was found that SF lymphocytes of RS patients showed significantly elevated proliferative response to stimulation by the ureaplasma antigen compared with SF lymphocytes of the control group. There was no difference when the lymphocytes were stimulated by the mitogen. Our findings suggest that elevated proliferative response of lymphocytes is the sign of stimulation cell-mediated immunity to antigen present in inflamed joint. Hence, the main immune response to Ureaplasma is on the cell-mediated level in the affected joint. This confirms the earlier finding reported by Ford et al. who concluded that synovial rather than peripheral blood lymphocytes indicate the microbiological cause of arthritis [11, 12]. Horowitz et al. demonstrated the correlation between clinical remission after antibiotic therapy and eradication of Ureaplasma, together with a decrease in cellular immune response synovial fluid lymphocytes to ureaplasma antigen stimulation [13]. In that study Horowitz did not find statistically significant difference of ureaplasma proliferative response between PB and SF lymphocytes in patients with RS. We obtained the same results. Than we concluded that sensibilization of immune system exist in the presence of foreign antigen in RS patients. The other authors demonstrated higher stimulation indices than the ones we found in our patients [11-15]. This difference may be the result of different preparation of antigens, in other words selection of serotype of Ureaplasma for antigen preparation different conditions of lymphocyte cultivation. We concluded that the presence of antigen, antigen-specific T cells and efficient antigen-presenting cells (CD4+ T cells) in the joint of RS patients strongly suggests that a T-cell-mediated response to bacteria has the central role in the pathogenesis of Reiter's syndrome.

Adolescent↗
PubMed1982

[Mononucleated phagocytes from rheumatoid synovial fluid. Synthesis of prostanoids and first pharmacological applications].

An original and easily reproducible technique for isolating and culturating mononucleated phagocytes from rheumatoid synovial fluid was used by the authors to study the synthesis of PGE2, PGF alpha 2 and TxB2 by macrophages taken from 16 patients with rheumatoid arthritis. The functional importance of these macrophages was evaluated by comparing their ratios of prostaglandin synthesis. PGE2 and TxB2 are released in large quantities and are increased after stimulation with zymosan. Two distinct cell populations having different biochemical characteristics were identified from these macrophages based on their capacity to synthesize prostaglandins. Prostaglandin synthesis was correlated with the clinical progression of rheumatoid arthritic disease as evaluated by Lee's index and the time required to loosen up morning joint stiffness in these patients. No correlation was found between prostaglandin synthesis and the quantity of synovial fluid in the affected joint. The first results of a pharmacological study evaluating the activity of non steroid anti-inflammatory drugs using this experimental model are presented here. The addition of indomethacin to culture medium produces dose-dependent inhibition of prostaglandin synthesis.

Adult↗
PubMed2005

Analysis of inflammatory mediators in temporomandibular joint synovial fluid lavage samples of symptomatic patients and asymptomatic controls.

PURPOSE: It was our purpose to study IgA, IgG, and beta-glucuronidase levels in temporomandibular joint fluid lavage samples in order to find a correlation between biochemical markers and joint pathology. MATERIALS AND METHODS: Our patient population included 20 patients (18 female and 2 male) with severe pain and limitation of mandibular movement that failed to improve with at least 3 months of a full course of nonsurgical therapy. After institutional review board approval, 13 control subjects (6 female and 7 male), with no history of temporomandibular joint pain/dysfunction, were obtained. Arthroscopic examination of the patient and control groups involved classification of joints for osteoarthritis and synovitis using a visual grading system. All synovial fluid samples were analyzed for beta-glucuronidase, IgA, and IgG using fluorometric assay and enzyme-linked immunosorbent assay. RESULTS: beta-Glucuronidase was significantly elevated (P<.05, t test) in the patient group compared with the control group (4.13+/-8.30 versus 0.9+/-0.83 [mean+/-SD]). The difference in the IgG level was also statistically significant (31,638+/-70,714 versus 4,407+/-1,324) (P<.05, t test). IgA level showed a similar trend between the patient and control groups (6,315+/-19,037 versus 425+/-192) (P=.10, t test). CONCLUSIONS: Quantitative synovial fluid analysis of beta-glucuronidase, IgA, and IgG demonstrates elevated levels of inflammatory mediators in diseased joints compared with asymptomatic nondiseased joints. We hypothesize that high levels of IgA, IgG, and beta-glucuronidase in the TMJ synovial fluids are due to infiltration from the sera and chronic inflammatory cells residing in the synovium. High levels of immunoglobulins in a closed joint space can elicit strong inflammatory reaction and cause destruction to the joint tissues via complement activation and immune complex deposition. Complement activation increases blood vessel permeability to enable recruitment of neutrophilic leukocytes, which then liberate various lysosomal enzymes and damage the articular cartilage.

Adult↗
PubMed1996

The association between tumour necrosis factor-alpha, interleukin-6 and microbiological findings in the synovial fluid of aborted and neonatal calves.

Tumour necrosis factor-alpha (TNF alpha) and interleukin-6 (IL-6) were detected in the intra-carpal synovial fluids collected from aborted and recently dead young calves. Five out of seven TNF-alpha positive joint fluids were bacteriologically positive and two were sterile. Only one out of 20 TNF-alpha negative joint aspirates was infected (P = 0.0014). Sixteen of the synovial fluid samples were examined for the presence of IL-6. In 12 samples IL-6 was detected, six of which were bacteriologically contaminated. Four out of the 16 samples were IL-6 negative. These findings indicated the possible association between TNF-alpha and the intra-articular inflammatory processes in young calves, which in the present study were either found in combination with or without IL-6.

Abortion, Veterinary↗
PubMed1992

Occurrence of (E)-4-hydroxy-2-nonenal in plasma and synovial fluid of patients with rheumatoid arthritis and osteoarthritis.

(E)-4-Hydroxy-2-nonenal (HNE), a cytotoxic propagation product of lipid peroxidation, is present in the synovial fluid (0.54 (0.19) mumol/l; mean (SE), n = 9) and plasma (0.34 (0.09) mumol/l, n = 9) of patients with rheumatoid arthritis. This compound was also found in the synovial fluid (0.24 (0.19) mumol/l, n = 9) and plasma (0.09 (0.03) mumol/l, n = 9) of patients with osteoarthritis. The concentration of HNE in the plasma of patients with rheumatoid arthritis was significantly greater than in patients with osteoarthritis.

Aldehydes↗
PubMed1998

Osteoarthritic synovial fluid and synovium supernatants up-regulate tumor necrosis factor receptors on human articular chondrocytes.

OBJECTIVE: To determine whether the up-regulation of chondrocyte tumor necrosis factor receptor (TNF-R) expression in osteoarthritis (OA) is due to molecules released within the OA knee joint. DESIGN: Non-arthritic (NA) human articular chondrocytes were incubated with normal serum, OA synovial fluid, or supernatants from either cultured NA or OA synovium, and TNF-R expression measured by flow cytometry. RESULTS: OA synovial fluid, but not normal serum, significantly up-regulated the proportion of chondrocytes expressing p55 TNF-R as well as the number of p55 TNF-R/chondrocyte. Similarly, supernatants from OA, but not NA, synovia significantly up-regulated chondrocyte p55 TNF-R expression. Chondrocyte p75 TNF-R expression was also significantly increased by some of the OA supernatants but not others, and overall no significant increase was seen. OA synovium supernatants contained higher concentrations of interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) than NA synovium supernatants and neutralizing antibodies to these cytokines either partially or totally abrogated the ability of the OA supernatants to increase chondrocyte p55 TNF-R expression. Finally, various concentrations of recombinant human (rh)IL-1 beta and rhIL-6 up-regulated chondrocyte p55 TNF-R expression. CONCLUSION: These results suggest that IL-1 and IL-6 produced by OA synovium contribute to the progression of the disease by rendering chondrocytes more susceptible to stimulation by catabolic cytokines.

Aged↗
PubMedDate not supplied

Des-Lys58-beta 2m and native beta 2m in rheumatoid arthritis serum and synovial fluid.

OBJECTIVE: Levels of beta 2-microglobulin and modified beta 2-microglobulin (Des-Lys58-beta 2m) were measured in serum and synovial fluids from patients with rheumatoid arthritis (RA) and other inflammatory joint disorders using rabbit antisera prepared against the beta 2m peptide VEHSDLSFS encompassing residues 49-57 and absorbed with the C-terminal beta 2m peptide (87-97) LSQPKIVKWDR: These antisera which did not react with native beta 2m were employed to quantitate Des-Lys58-beta 2m in serum and SF. Native beta 2m was measured using a direct ELISA method. RESULTS: Removal of serum rheumatoid factor by adsorption to monomeric IgG columns did not change serum levels of beta 2m or Des-Lys58-beta 2m. Native beta 2m was found in all of 20 RA sera, but only rarely in SLE sera. No serum beta 2m was found in 20 patients with ankylosing spondylitis or 25 normal controls. Significant elevations of Des-Lys58-beta 2m were found in 80% of 21 SF from RA patients and in 43% of 41 SF from other subjects with various forms of inflammatory arthritis. In RA and other disorders such as gout or pseudogout, levels of Des-Lys58-beta 2m were higher in synovial fluid than in serum during an acute episode of synovitis. Both native beta 2m and Des-Lys58-beta 2m showed minimal neutrophil and T cell chemotactic activity. CONCLUSION: Des-Lys58-beta 2m present in many inflammatory SF may contribute to the inflammatory reaction in many forms of connective tissue disease by its known amplification of T cell cytotoxicity.

Amino Acid Sequence↗
PubMed2001

Dynamic changes in cytokine levels in serum and synovial fluid following filtration leukocytapheresis therapy in patients with rheumatoid arthritis.

We attempted to determine whether various cytokine levels in the serum and synovial fluid (SF) of rheumatoid arthritis (RA) patients are influenced by the performance of filtration leukocytapheresis (LCP). The filtration LCP procedure that used a Cellsorba column (LCP group: n=22; responder subgroup: n=17, non-responder subgroup: n=5) or sham apheresis (control group; n=7) was repeated three times at 1-week intervals. Serum (LCP group, n=22; control group, n=7) and SF (LCP group, n=6; control group, n=3) samples were collected before and after LCP. Levels of tumor necrosis factor alpha (TNFalpha), interleukins (IL-1 beta, IL-2, IL-6, IL-8, IL-10, and IL-15), granulocyte-macrophage colony-stimulating factor (GM-CSF), monocyte chemoattractant protein-1 (MCP-1), RANTES were measured by an enzyme-linked immunosorbent assay. Serum TNF alpha, IL-15, and RANTES were significantly reduced only in the LCP group. Serum IL-10 significantly increased only in the LCP group. In the LCP subgroup, serum IL-15, GM-CSF, and RANTES levels were reduced significantly, while serum IL-10 levels increased significantly only in the responder group after treatment. Serum TNF alpha levels were reduced significantly in both subgroups. Changes in serum IL-10 correlated positively with the improvement of patient's assessment of pain and global severity, and physician's assessment of global severity. These results indicate that the removal of leukocytes from the peripheral blood of RA patients provokes dynamic changes in some cytokine levels in the serum and/or synovial fluid. These changes may explain some of the mechanisms by which the articular symptoms are improved by filtration LCP.

Adult↗
PubMed1978

[Study of C3 and C4 complement components of synovial fluids in connective tissue diseases (author's transl)].

C3 and C4 levels and the relative concentration of C3 degradation products were measured in fifty pairs of synovial fluids and sera of patients who suffered from different connective tissue diseases. Inverse correlation between C4 level and C3 breakdown products were found in synovial fluids of different groups. Compared to the other groups of patients, the highest increase of C3 degradation was found in RA. patients and it occurred in the SF all of these patients. In arthrosis cases we failed to find any degradation of C3. Of the seven investigated ankylosing spondylitis only two showed some degree of activation of C3 in the SF. Our results suggest that the occurrence and degree of degradation of C3 complement component is a valuable laboratory parameter in the study of connective tissue diseases.

Arthritis↗
PubMed1975

High synovial fluid white blood cell counts in pseudogout; Possible confusion with septic arthritis.

During a 12-month period, we have treated five patients with acute inflammatory arthritis and synovial fluid leukocyte counts of 65,000 to 100,00/cu mm with 93% to 100% polymorphonuclear cells, calcium pyrophosphate dihydrate crystals in the synovial fluid, and negative cultures. Four of these five were origingally treated for septic joints. We would like to emphasize this relatively uncommon, but important manifestation of pseudogout.

Arthritis, Infectious↗
PubMed2001

The thixotropic effect of the synovial fluid in squeeze-film lubrication of the human hip joint.

The thixotropic (shear-thinning) effect of the synovial fluid in squeeze-film lubrication of the human hip joint is evaluated, taking into account filtration of the squeezed synovial film by biphasic articular cartilage. A porous, homogeneous, elastic cartilage matrix filled with the interstitial ideal fluid, with the intact superficial zone (of lower permeability and stiffness in compression) already disrupted or worn away, models an early stage of arthritis. Due to a high viscosity of the normal synovial fluid at very low shear rates, the squeezed synovial film at a fixed time after the application of a steady load is found to be much thicker in a small central part of the lubricated contact area. In the remaining part, the film is thin as it corresponds to the Newtonian fluid with the same high-shear-rate viscosity. Filtration is lower for the normal cartilage with the intact superficial zone due to its lower permeability and compression stiffness. But even in the fictitious case of zero filtration, calculations show that the effect of thixotropy on the increase of the minimum synovial film thickness would manifest itself as late as after several tens of seconds since the physiologic load application. At that time, this thickness would be as low as about 0.3 microm. It follows that thixotropy of the normal synovial fluid (and so much more of the inflammatory fluid) is irrelevant in squeeze-film lubrication of both the normal and arthritic human hip joints.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Predominance of T-lymphocytes with a high-affinity receptor for sheep red blood cells in the synovial fluid of patients with rheumatoid arthritis. A short communication.

Using different modifications of the spontaneous rosette-forming assay, T-lymphocytes were determined in the synovial fluid and the peripheral blood of patients with rheumatoid arthritis (RA). It was shown that a T-lymphocyte subpopulation, forming E-rosettes by a high affinity receptor for SRBC was enriched in the synovial fluid as compared to the peripheral blood.

Animals↗
PubMed1991

Hydroxyapatite crystals are a frequent finding in osteoarthritic synovial fluid, but are not related to increased concentrations of keratan sulfate or interleukin 1 beta.

Synovial fluid (SF) was obtained from 40 patients with varying grades of osteoarthritis (OA) of the knee and examined by transmission electron microscopy to ascertain how frequently hydroxyapatite crystals (HA) were present and whether they were related to disease severity or putative markers or promoters of cartilage resorption. HA crystals were conspicuous and abundant in specimens from 21 of the 40 patients studied. Patients in whom HA was present had significantly larger effusions (13.0 +/- 8.9 vs 8.7 +/- 6.1 ml, p less than 0.05). They also tended to have radiologically more severe disease (radiological grade: 2.91 +/- 0.92 vs 2.39 +/- 0.85, p = 0.056). No difference in keratan sulfate (KS) concentrations was observed. Moreover, despite the presence in some specimens of numerous free histiocytes which were actively phagocytosing HA aggregates, the concentrations of interleukin 1 beta (IL-1 beta), a monocyte product with cartilage and bone resorbing activity, were below the limit of detection (20 pg/ml). Our results confirm that HA crystals are a common finding in patients with OA of the knee and show that HA is associated with larger effusions, but not increased SF concentrations of cartilage proteoglycan substituents (KS) or IL-1 beta.

Aged↗