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A new component has been detected in synovial fluid by the agar double-diffusion technique. This component is closely related immunologically to the proteinpolysaccharides of cartilage, and is the first probable degradation product of the cartilage matrix to be consistently identified in human synovial fluid.
One case of arthritis complicating leukemia is described in which leukemic cells were identified in synovial fluid by light microscopy. Although arthritis is a well-known manifestation of leukemia with an incidence of 13.5%, the pathogenesis often is unclear, and the direct demonstration of leukemic cells in synovial fluid has been very uncommon. A 16 year-old male patient was admitted due to left elbow joint pain and swelling. Synovial fluid examination revealed blast cells and this finding has directed to a final diagnosis of acute lymphoblastic leukemia.
Deposition of intra-articular calcium pyrophosphate is associated with both aging and arthropathy; increased concentrations of free pyrophosphate (PPi) may contribute to such deposition. Free pyrophosphate and nucleoside triphosphate pyrophosphatase (NTPase) were estimated in synovial fluids from 50 subjects with normal knees and from 44 patients with rheumatoid arthritis, 61 with pyrophosphate arthropathy, and 59 with osteoarthritis. For arthropathic knees clinically assessed inflammation was classified as active or inactive using a summated score of six clinical features. The order of PPi (mumol/l) and NTPase (mumol PPi/30 min/mg protein) was pyrophosphate arthropathy greater than osteoarthritis greater than rheumatoid arthritis (median PPi, NTPase respectively: for pyrophosphate arthropathy 15.9, 0.45; for osteoarthritis 9.3, 0.25; for rheumatoid arthritis 4.4, 0.18), with significant differences between all groups. In pyrophosphate arthropathy both PPi (mumol/l) and NTPase (mumol PPi/30 min/mg protein) were higher than normal (15.9, 0.45 v 8.6, 0.2 respectively), but findings in osteoarthritis did not differ from normal. The inflammatory state of the knee had a distinct but variable effect on synovial fluid findings in rheumatoid arthritis and pyrophosphate arthropathy, but not in osteoarthritis. There was no correlation of either PPi or NTPase with age, or between PPi and NTPase in any group. This study provides in vivo data for synovial fluid PPi and NTPase. It suggests that factors other than PPi need to be considered in a study of crystal associated arthropathy. Clinical inflammation, as well as diagnosis, is important in synovial fluid studies.
Synovial fluid cells obtained from a carrageenan-induced chronic arthritis in the juvenile dog knee were allowed to adhere and proliferate in culture flasks. After twelve days secondary cultures were made and either 10(-8)M leukotriene B4 (LTB4), 25 microM 15-hydroxy-eicosatetraenoic acid (15-HETE), or both, were added and the cells were cultured for another 6 days. LTB4 is generated via the 5-lipoxygenase pathway of arachidonic acid metabolism and stimulates a number of phagocyte functions. Compared to control cells LTB4 increased proliferation in 9 out of 10 cell cultures (p less than 0.05). The 15-lipoxygenase product, 15-HETE, is not proinflammatory and is an endogenous inhibitor of 5-lipoxygenase. Addition of 15-HETE decreased proliferation of cell cultures by 23% (p less than 0.01). It is speculated that LTB4 in addition to its effect on phagocytes may play a role in synovial hyperproliferation observed in arthritis.
Serial samples of synovial fluid aspirated from two patients with septic arthritis were assayed for proteinases and proteinase inhibitors. Active metalloproteinases but no proteinase inhibitors were present in all samples taken prior to treatment. The levels of active metalloproteinases fell with time although proenzyme forms were still present in the fluids. Both alpha 2-macroglobulin and the tissue inhibitor of metalloproteinases were found in the septic synovial fluids after treatment commenced. It is proposed that the lack of inhibitors and the presence of active proteinases capable of digesting collagen, gelatin and proteoglycan accounts for the rapid loss of cartilage found in septic arthritis.
Sera and synovial fluid (SF) from rheumatoid arthritis (RA) patients were evaluated for anti-HLA class II beta-chain antibodies using single and two-dimensional immunoblots. The antibodies from RA sera and SFs which reacted with class II beta-chain determinants were predominantly IgM and IgA with minimal IgG. This reactivity was also present in SFs from other rheumatic diseases. Anti-class II beta-chain antibodies were also shown to be present simultaneously in RA sera and SF.
Mesenchymal stem cells (MSC) have the potential to differentiate into distinct mesenchymal tissues including cartilage, which suggest these cells as an attractive cell source for cartilage tissue engineering approaches. Our objective was to study the effects of TGF-beta1, hyaluronic acid and synovial fluid on chondrogenic differentiation of equine MSC. For that, bone marrow was aspirated from the tibia of one 18-month-old horse (Haflinger) and MSC were isolated using percoll-density centrifugation. To promote chondrogenesis, MSC were centrifuged to form a micromass and were cultured in a medium containing 10 ng/ml TGF-beta1 or 0.1mg/ml hyaluronic acid (Hylartil, Ostenil) or either 5%, 10% or 50% autologous synovial fluid as the chondrogenesis inducing factor. Differentiation along the chondrogenic lineage was documented by type II collagen and proteoglycan expression. MSC induced by TGF-beta1 alone showed the highest proteoglycan expression. Combining TGF-beta1 with hyaluronic acid could not increase the proteoglycan expression. Cultures stimulated by autologous synovial fluid (independent of concentration) and hyaluronic acid demonstrated a pronounced, but lower proteoglycan expression than cultures stimulated by TGF-beta1. The expression of cartilage-specific type II collagen was high and about the same in all stimulated cultures. In summary, hyaluronic acid and autologous synovial fluid induces chondrogenesis of equine mesenchymal stem cells, which encourage tissue engineering applications of MSC in chondral defects, as the natural environment in the joint is favorable for chondrogenic differentiation.
Sialic acids, derivatives of neuraminic acid, are present as structural components of mucoprotein mainly in the alpha 1 and alpha 2-globulin regions, and they are known to change in diseases associated with acute inflammation or tissue necrosis. The present study was performed to clarify the significance of measurements of sialic acids in the serum and synovial fluid of patients with diseases in the field of orthopaedic surgery. 1. Serum sialic acids were markedly high in cases of acute pyogenic diseases and showed moderately high values in stage 2 or 3 of rheumatoid arthritis (RA). There was a close correlation with ESR in RA cases and with CRP in cases of acute pyogenic diseases. Differences in the correlation with ESR and CRP were seen in proportion to the severity of the inflammation. 2. Synovial fluid sialic acids were high in cases of RA, and within the normal range in cases of osteoarthritis. The values changed within this range in accordance with treatment. In RA cases, there was a significant correlation with monocytes in the synovial fluid. 3. Serum sialic acids appeared to be sufficiently useful as a parameter of inflammation independent of ESR and CRP, and synovial fluid sialic acids were also considered to be useful for differentiation between RA and OA.
Specimens of synovial fluid taken from patients with rheumatoid arthritis were tested for the presence of mycoplasmas and mycoplasmic antigens. In 30% of cases the direct inoculation into cell-free media permitted the detection of mycoplasma-like agents which could not be subcultured on solid media for identification. Mycoplasmic antigens were detected in the tested material with the same frequency by means of the immunofluorescence test. The use of cell cultures made it possible to isolate and identify mycoplasmas. M. arthritidis and M. fermentans, as well as their association, were identified in the immunofluorescence test and in cell cultures.
The synovial fluids (SF) of patients with rheumatoid arthritis (RA) were investigated for their effects on thymocytes of C3H/HeJ mice. Of the 20 SF tested, 17 (85%) showed an augmentation of the phytohaemagglutinin (PHA) induced thymocyte stimulation. Out of 16 SF of patients with osteoarthrosis, such an activity was detected in only one (6.25%). Further characterisation of the amplification factor revealed that (1) the SF of RA patients augmented both the PHA and the Concanavalin A response of the thymocytes (2) in the absence of mitogens, SF-treated thymocytes showed an increased uptake of 3H-thymidine, (3) the SF did not propagate the growth of an interleukin 2 dependent ovalbumin specific T cell clone, but (4) the SF were found to be required for optimal interleukin 2 release by spleen cells stimulated with suboptimal doses of lectin. Based on these biological effects the factor in the SF of RA patients is suggested to represent an interleukin 1 (IL-1). IL-1 produced in cultures by activated macrophages has been shown to stimulate T and B cell functions and to induce the production of collagenase and prostaglandins by cultured synovial cells. Both properties of IL-1 could be relevant in the pathogenesis of RA.
It is well known that cytokines are highly involved in the disease process of rheumatoid arthritis (RA). Recently, targeting of neuropeptides has been suggested to have potential therapeutic effects in RA. The aim of this study was to investigate possible interrelations between five neuropeptides (bombesin/gastrin-releasing peptide (BN/GRP), substance P (SP), vasoactive intestinal peptide, calcitonin-gene-related peptide, and neuropeptide Y) and the three cytokines tumour necrosis factor (TNF)-alpha, IL-6, and monocyte chemoattractant protein-1 in synovial fluid of patients with RA. We also investigated possible interrelations between these neuropeptides and soluble TNF receptor 1 in serum from RA patients. Synovial fluid and sera were collected and assayed with ELISA or RIA. The most interesting findings were correlations between BN/GRP and SP and the cytokines. Thus, in synovial fluid, the concentrations of BN/GRP and SP grouped together with IL-6, and SP also grouped together with TNF-alpha and monocyte chemoattractant protein-1. BN/GRP and SP concentrations in synovial fluid also grouped together with the erythrocyte sedimentation rate. In the sera, BN/GRP concentrations and soluble TNF receptor 1 concentrations were correlated. These results are of interest because blocking of SP effects has long been discussed in relation to RA treatment and because BN/GRP is known to have trophic and growth-promoting effects and to play a role in inflammation and wound healing. Furthermore, the observations strengthen a suggestion that combination treatment with agents interfering with neuropeptides and cytokines would be efficacious in the treatment of RA. In conclusion, BN/GRP and SP are involved together with cytokines in the neuroimmunomodulation that occurs in the arthritic joint.
We studied the relationship between osteoprotegerin (OPG)/osteoclastogenesis inhibitory factor (OCIF) concentration in synovial fluid from individuals with osteoarthritis (OA) of the knee and the severity of this condition. The study population included 111 Japanese women with knee OA (153 knees) and 23 normal controls. Osteoarthritic changes were graded according to the system of Kellgren and Lawrence. The concentration of OPG/OCIF in synovial fluid increased with severity of knee OA and was significantly higher in individuals with OA of grade IV than in those with OA of grade 0 or grade 1. It has been shown in a previous study that administration of OPG/OCIF prevents cartilage destruction in adjuvant-induced arthritis in rats. The increase in the concentration OPG/OCIF in synovial fluid of individuals with knee OA might thus reflect a compensatory response to degeneration of articular cartilage and serve to protect cartilage rather than be a cause of OA.
OBJECTIVE: To evaluate simultaneous serum and synovial fluid (SF) urate levels in various inflammatory and noninflammatory joint disorders and to correlate SF white blood cell (WBC) counts with serum and joint fluid urate levels. METHODS: Sixty-three paired samples of sera and SF from 58 patients including 25 patients with inflammatory arthropathies, 18 patients with gout and 15 patients with noninflammatory joint disorders, were measured for urate concentrations by a UV enzymatic method. RESULTS: In inflammatory arthropathies other than gout, urate concentrations in SF were significantly lower than in paired sera (p < 0.0001). There was no difference between the SF and serum urate levels in noninflammatory arthropathies and in gout. In gout, however, SF urate occasionally were found to be considerably higher than in sera. This phenomenon was observed in fluids with massive amounts of monosodium urate crystals. There was no correlation between SF WBC counts and serum of SF urate levels in any of the disease groups studied. CONCLUSIONS: Serum and synovial fluid levels vary more than previously recognized. SF urate levels tend to reflect serum levels in gout and noninflammatory arthropathies but not in inflammatory joint disorders. Disturbed purine metabolism in inflammatory arthropathies may reflect a component in the pathophysiology of inflammation. The elevations of SF urate levels seen in gout are unique for this disease and most likely reflect crystal dissolution in joints.
OBJECTIVE: To evaluate the relation between synovial fluid (SF) concentrations of interleukin-6 (IL-6) and other mediators of inflammation which are responsible for joint degradation in rheumatoid arthritis (RA). METHODS: We measured IL-6, IL-1 beta, tumour necrosis factor alpha (TNF alpha), granulocyte macrophage colony stimulating factor, IL-8, and polymorphonuclear leucocyte (PMNL) chemotaxis and degranulation in SF from patients with RA (n = 30) in the early phase of the disease. RESULTS: In a cross-sectional study IL-6 concentrations correlated with those of IL-1 beta, IL-8 and with PMNL activation as reflected by lactoferrin concentrations. In a longitudinal study, changes in IL-6 concentrations correlated with changes in TNF alpha, IL-8 and lactoferrin concentrations. CONCLUSION: IL-6 in SF appears to reflect the local proinflammatory, potentially erosive activity in RA. This supports the use of acute phase proteins, which are mainly induced by IL-6, as variables to monitor the course of RA.
Bradykinin has been implicated in the pathogenesis of inflammatory arthritis by virtue of the potent pro-inflammatory properties. The purpose of this study is to investigate the expression of bradykinin in patients with internal derangement of the temporomandibular joint (TMJ). We examined 33 TMJ synovial biopsy specimens from 31 patients with internal derangement of the TMJ by an immunohistochemical technique using specific antibodies. We also determined the concentration of bradykinin in 20 synovial fluids from 18 patients with TMJ internal derangement by enzyme-linked immunosorbent assay. These data were compared with those of the control subjects. Bradykinin was predominantly localized in the synovial lining cell layer of TMJ samples obtained from patients with TMJ internal derangement. Bradykinin was also detected in 19 patients' TMJ synovial fluids and the average of bradykinin concentration in the synovial fluids of patients was higher than that of the healthy controls. Although a statistically significant correlation was not observed, these findings support the hypothesis that bradykinin may also be involved in the pathogenesis of TMJ pain and synovitis.
Five acid lysosome hydrolases were studied in 20 patients with rheumatoid arthritis (RA), active stage in serum (S) and synovial fluid (SF) in parallel, obtained from the knee joint. The enzyme activity was fluorimetrically determined, making use of substrates specific for each enzyme, derivatives of 4-methyl-umbelliferone. The serum lysosome activity of the patients with RA, compared with that of a referent group of healthy subjects, showed a significant increase in three of the hydrolases studied. With the juxtaposition of enzyme activity between SF and serum of the patients with RA, the activity of all acid hydrolases in the synovial fluid studied proved to be several times higher and with high statistical significance (p less than 0.01-0.001). Our data support the valuable informative value of the study on acid lysosome hydrolases in the synovial fluid. A sensitive indicator of the activity of the joint process in RA is the coefficient of lysosome enzymatic activity SF/S, substantially surpassing 1.0.
OBJECTIVE: To study CD69+ synovial fluid (SF) T cells and the mechanisms regulating CD69 expression in rheumatoid arthritis (RA). METHODS: One or 2 color flow cytometry was used to determine CD69 and other surface markers. Cultures of SF T cells alone or mixed with autologous SF non-T cells were used for CD69 maintenance assays. RESULTS: SF T cells were enriched in CD69+. These cells were mainly CD3+, CD8+ and CD25-. CD69 was maintained on SF T cells cultured with SF non-T cells but not when the former were cultured alone or in the presence of different supernatants from RA SF T and non-T cells cultures with sustained CD69 expression. Pretreatment of T and non-T cells with anti-CD18 monoclonal antibody inhibited CD69 expression, while paraformaldehyde-"fixed" non-T cells effectively maintained it. CONCLUSION: SF T cells exhibit a phenotype with evidence of past and recent activation. Our studies demonstrate that most of the recently activated SF T cells are CD8+. We also found that continuous cell-to-cell interaction between T and non-T cells are responsible for the maintenance of this particular state of activation of SF T cells.
OBJECTIVES: To investigate the hypothesis that synovial fluid (SF) from patients with osteoarthritis (OA) may contain calcium phosphate crystals that are either too small, or too few in number to be identified by conventional light microscopy techniques. METHODS: Twelve SF from 11 patients with established knee OA, five SF from patients with rheumatoid arthritis (RA), and two control samples of SF from patients with pseudogout were subjected to an enzyme/hypochlorite extraction procedure. The patients with OA and RA had no radiographic evidence of chondrocalcinosis, or SF crystals on polarised light microscopy. Extracted material was examined and analysed by analytical electron microscopy (AEM) and x ray powder diffraction (XRD). RESULTS: Mineral was found in 11 of 12 OA samples, ranging from 2-120 micrograms/ml SF. Analytical electron microscopy revealed calcium pyrophosphate dihydrate (CPPD) crystals in five (confirmed by XRD in three) and basic calcium phosphates (BCP) in eight (five on XRD). Two samples with confirmed CPPD contained some rods with a mean length below 100 nm. The majority of BCP clusters were also less than 100 nm in diameter. BCP was detected in 1/5 RA samples. Control samples contained CPPD crystals of the expected size range of 0.42-17.9 microns. CONCLUSIONS: The data indicate that many OA SF may contain CPPD or BCP crystals which are too small or too few in number to be identified by conventional techniques. Crystal deposition is not an 'on-off' phenomenon in OA.