IntroductionCalprotectin, a heterodimeric complex of S100A8/9 (MRP8/14), has been proposed as an important serum biomarker that reflects disease activity and structural joint damage in rheumatoid arthritis (RA). The objective of this cross-sectional study was to test the hypothesis that calprotectin is associated with clinical and ultrasound-determined disease activity in patients with RA.MethodsA total of 37 patients with RA (including 24 females, a mean disease duration of 20 months) underwent a clinical examination and 7-joint ultrasound score (German US-7) of the clinically dominant hand and foot to assess synovitis by grey-scale (GS) and synovial vascularity by power Doppler (PD) ultrasound using semiquantitative 0–3 grading. The levels of serum calprotectin and C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were determined at the time of the ultrasound assessment. We analysed the relationship between serum calprotectin level, traditional inflammatory markers, and ultrasound-determined synovitis.ResultsThe levels of serum calprotectin were significantly correlated with swollen joint count (r = 0.465, p < 0.005), DAS28-ESR (r = 0.430, p < 0.01), ESR (r = 0.370, p < 0.05) and, in particular, CRP (r = 0.629, p < 0.001). Calprotectin was significantly associated with GS (r = 0.359, p < 0.05) and PD synovitis scores (r = 0.497, p < 0.005). Using multivariate regression analysis, calprotectin, adjusted for age and sex, was a better predictor of PD synovitis score (R2 = 0.765, p < 0.001) than CRP (R2 = 0.496, p < 0.001).ConclusionsThe serum levels of calprotectin are significantly associated with clinical, laboratory and ultrasound assessments of RA disease activity. These results suggest that calprotectin might be superior to CRP for monitoring ultrasound-determined synovial inflammation in RA patients.
This is the first study to show that the levels of the S100A4 protein are correlated with RA disease activity. Furthermore, only the bioactive form, but not the total amount of S100A4, decreases after successful TNF-alpha blocking therapy in patients with RA. These data support an important role for the S100A4 multimer in the pathogenesis of RA.
Interactions of the foreign material of implant and the living tissue on the cell level can cause prolonged healing or, worse, loss of the implant. The cell response to the presence of some implant materials was studied under in vitro conditions. The influence of physicochemical surface parameters on the response of the cells in the immediate vicinity of implants, namely on adhesion, proliferation and synthetic activity of fibroblasts, and on the blood coagulation were compared. The direct contact of tested materials (titanium and Ti6Al4V alloy with various surface treatments, Cr Co Mo alloy, hydroxyapatite-coated titanium, zirconium oxide ceramics, polyethylene and carbon composite) on cell spreading was monitored and the presence of TNF-alpha and IL-8 was evaluated in the cultivation medium. The formation of blood clots was investigated on samples immersed in a well with freshly drawn whole rabbit blood using a scanning electron microscope. The surface free energy was estimated using the measurement of static contact angle. Both the advancing and receding contact angles were measured by the dynamic Wilhemy plate method. Two main groups with extremes in cell viability were established. In the first group the increased polar component of surface free energy, the highest cell density, the lowest inflammatory cytokine production, but no fibres in the clotting blood were found. On the contrary, the second group of materials with a very low polar component of the surface free energy showed distinctly higher expression of inflammatory mediators, low cell proliferation, but faster formation of fibres in the blood coagulum.
HA is increased in patients with erosive HOA and could be proposed as a surrogate marker with a predictive value for further radiographic progression of HOA in general. Further investigation is necessary to confirm these results.
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