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Background: The interfacial membrane between bone and implant has been shown to be a key tissue in the process of aseptic loosening of total hip arthroplasty. The cells within the interfacial membrane produce numerous inflammatory mediators which, through complex mechanisms, cause periprosthetic osteolysis and aseptic loosening. Both epidermal growth factor (EGF) and transforming growth factor alpha (TGFalpha) have similar biological functions. They have been found to stimulate bone resorption.Objective: To investigate the presence, cellular localisation, and extent of expression of EGF and TGFalpha in interfacial membrane retrieved from revision total hip arthroplasty and compare it with that in synovial membrane from primary total hip arthroplasty.Methods: Ten interfacial membranes and 10 synovial membranes were stained with avidin-biotin-peroxidase complex for EGF and TGFalpha. The staining process was done using the Lab Vision Autostainer. The results were measured by a semiautomatic VIDAS image analysis system.Results: Immunoreactivity for both EGF and TGFalpha was found in the endothelial cells of blood vessels, macrophages, and fibroblasts, both in interfacial membranes and synovial membranes. However, the number of EGF (980 (370)) and TGFalpha (1070 (360)) positive cells per mm(2) was greater in interfacial membranes than in the synovial membranes (220 (200), 270 (100); p<0.01).Conclusion: It is suggested that owing to their increased expression in interfacial membrane, EGF and TGFalpha may have an important pathogenetic role in stimulating periprosthetic bone resorption in aseptic loosening of total hip arthroplasty. [ABSTRACT FROM AUTHOR]

Type A synovial lining cells have been shown to contain lysozyme in their lysosomes. This might be phagocytosed because synovial fluid contains lysozyme originating from tissue macrophages and articular cartilage but in arthritides, in particular, from neutrophils. In situ hybridisation with 35S labelled cDNA was used to detect mRNA for lysozyme over synovial lining in patients with rheumatoid arthritis. No hybridisation was found with lactoferrin cDNA, which was used as a negative control. Computer search against the EMBL gene bank (release 14) did not show any significant cross hybridisation to a known sequence. In cytological specimens 35S-cDNA:mRNA hybrids were observed in positive but not in negative control cells. The presence of lysozyme and its mRNA suggests that type A synovial lining cells are of mononuclear phagocyte lineage. [ABSTRACT FROM PUBLISHER]

High performance liquid chromatography (HPLC) with a size exclusion column and ultraviolet monitoring was used to study the effect of synovial fluid hyaluronate concentration and degree of polymerisation on viscosity and mucin clot formation. Rotational viscometry measurements showed an exponential relation between the synovial fluid hyaluronate concentration and relative viscosity, the viscosity increasing particularly steeply with hyaluronate concentrations exceeding 2-2.5 mg/ml. The scattering of individual values observed around the expected curve was eliminated when both the hyaluronate concentration and its degree of polymerisation were taken into account. Hyaluronate concentration and degree of polymerisation also correlated with the quality of mucin clot, though only HPLC provided more detailed quantitative information about this association. Because HPLC allows reproducible and rapid simultaneous analysis of the synovial fluid hyaluronate concentration and the degree of polymerisation in small volumes of unprocessed samples it can be used in well equipped rheumatological units to replace other methods used previously. [ABSTRACT FROM PUBLISHER]

Zinc and copper have important effects on T cell mediated immunity and on neutrophil function, but it is not known how the causes or effects, of low serum zinc and high serum copper relate to the clinical picture of rheumatoid arthritis (RA). In this study serum zinc and copper determined by flame atomic absorption spectrometry and 30 other clinical, immunological, and laboratory parameters in 60 patients with RA were analysed by stepwise multiple linear regression analysis. Joint score index, rheumatoid factor titre, seropositivity, haemoglobin, and C reactive protein (CRP) were among the nine independent variables which together predicted 73% of the serum zinc variation. This suggests that there is an association between the immune-inflammatory rheumatoid process and the serum zinc concentration. CRP alone had only a 3% independent predicting value for serum zinc, however. This suggests that metallothionein mediated sequestration in the liver, induced by interleukin 1, is not an important explanatory factor in a cross sectional study of chronic inflammation. Furthermore, serum zinc did not have any predictive value at all for serum copper concentration. This does not support the hypothesis suggesting that serum zinc deficiency leads to high serum copper by inducing gastrointestinal metallothionein and high caeruloplasmin. [ABSTRACT FROM PUBLISHER]

Local lymphoplasmacytoid infiltration of the diseased exocrine glands is a cardinal sign of Sjögren's syndrome (SS). The state of T lymphocyte activation present in these local infiltrations was studied by three different techniques: determination of interleukin 2 (IL2) receptor (Tac) on cell surface membrane; autoradiography combined with immunoperoxidase staining of T cell epitopes; and electron microscopic analysis of the lymphoblast subclasses. Although 64 (SEM 4)% of the local inflammatory cells expressed Ia antigen, only 4 (SEM 1)% of them displayed the T cell activation antigen Tac. Autoradiography-immunoperoxidase double labelling showed that less than 1% of all T cells in situ were [3H]thymidine incorporating blasts. This finding suggests that although T lymphocyte is the dominant cell in situ, only a few of these cells have passed the G0/G1 interphase, and even fewer have been pushed to the S phase of the cell cycle by IL2. Transmission electron microscopy showed that few T blasts were present, even though there were many plasma cells. This result further confirms the impression that only a minor T cell subpopulation in situ is blast transformed despite the fact that many of the local T lymphocytes in the diseased salivary glands in SS are Ia positive. [ABSTRACT FROM PUBLISHER]

Synovial fluid cells in Reiter's syndrome were studied by cell subset specific monoclonal antibodies and avidin-biotin-peroxidase complex staining. Mean leucocyte count was 9842/mm3 (9.842 X 10(9)/l), and 71% of all cells were polymorphonuclear leucocytes. 26 +/- 11 (SEM)% and 47 +/- 5% of all mononuclear cells in synovial fluid were M1+ monocytes and Ia+ cells, respectively. T11+ T lymphocyte was the predominant synovial fluid mononuclear cell (61 +/- 8%) but, in contrast to the inflammatory joint effusions in rheumatoid arthritis, T4+ cells clearly outnumbered T8+ cells in Reiter's syndrome. Thus the synovial fluid in Reiter's syndrome contains the immunocompetent and accessory cells required for immune response, which in fact is activated as suggested by lymphocyte Ia expression. Furthermore, in contrast with rheumatoid arthritis inducer/helper cells with T4 phenotype seem to be involved preferentially in the local pathogenetic mechanisms in Reiter's syndrome. [ABSTRACT FROM PUBLISHER]

Cellular inflammation in rheumatoid arthritis (RA) synovial membrane was studied in biopsy specimens taken at different stages of synovitis and disease. Patients were classified into three subgroups: acute RA, subacute RA, and chronic RA. Inflammatory cells were characterised by a histochemical esterase method and immunohistochemical peroxidase-antiperoxidase (PAP) and avidin-biotin-peroxidase (ABC) staining. The amounts and distribution of inflammatory cells were different in various stages of the synovitis. In acute onset RA monocytes and granulocytes predominated, suggesting that the beginning of rheumatoid inflammation is similar to inflammatory reaction in general. The presence of T cells and also of plasma cells in subacute RA suggests underlying subclinical changes also in apparently healthy joints in RA. The most typical feature of prolonged synovitis in chronic RA was its intensity, characterised by the presence of large T cell and plasma cell infiltrates. Our findings suggest that the immunological mechanisms are secondary to the tissue damage caused by the initial inflammatory events of unknown cause. However, the immunological mechanisms may still play a central role in the aetiopathogenesis, because findings in chronic RA suggest a defective down-regulation of the immune response. [ABSTRACT FROM PUBLISHER]