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Objective. Recent findings suggest that interferon regulatory factor 5 (IRF-5) may play a crucial role in several cellular processes, including the transcription of genes for inflammatory cytokines. Two genetic variants of the IRF5 gene (rs2004640 in exon 1 and rs2280714 in the 3-untranslated region) have been shown to exert functional modifications affecting IRF5 messenger RNA splicing and expression, and have been associated with genetic predisposition to systemic lupus erythematosus (SLE). The aim of this study was to analyze the possible contribution of the IRF5 gene to the predisposition to rheumatoid arthritis (RA).Methods. Three case-control cohorts from Spain (724 RA patients and 542 healthy controls), Sweden (281 RA patients 474 healthy controls), and Argentina (284 RA patients and 286 healthy controls) were independently analyzed. Genotyping for IRF5 rs2004640 and rs2280714 was performed using a TaqMan 5 allele-discrimination assay.Results. In the 3 cohorts studied, no statistically significant differences in allele or genotype frequencies of the rs2004640 and rs2280714 IRF5 polymorphisms were observed between RA patients and controls. Accordingly, haplotype analysis revealed that none of the IRF5 haplotypes was associated with genetic predisposition to RA.Conclusion. Our results suggest that the IRF5 functional polymorphisms analyzed do not seem to be implicated in genetic susceptibility to RA.The type I interferon (IFN) family, which includes multiple subtypes of IFN␣ and the single IFN␤, is one of the most important classes of cytokines. These mediators have a broad range of biologic activities, playing a crucial role in the innate and adaptive immune responses, as well as in the altered mechanisms that lead to autoimmune diseases (1). In this regard, evidence has established a pivotal role of IFN␣ in the pathogenesis of systemic lupus erythematosus (SLE) (2,3). Although less is known about the implication of type I IFNs (IFN␣/␤) in the pathophysiologic mechanisms of rheumatoid arthritis (RA), evidence suggests that type I and type II (IFN␥) interferons may be implicated in the pathogenesis of autoimmune diseases, including RA (1,4).A family of transcription factors bearing a helixturn-helix DNA-binding motif, termed IFN regulatory factors (IRFs) are the most important regulators of type I IFN gene expression (5). Among the 9 identified

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Artículo de publicación ISIThe aim of this prospective, blind, and randomized clinical trial was to assess the effectiveness of repair of localized clinical defects in amalgam restorations that were initially scheduled for replacement. A cohort of 20 patients with 40 (Class I and Class II) amalgam restorations that presented one or more clinical features that deviated from the ideal (Bravo or Charlie) according to US Public Health Service criteria, were randomly assigned to either the repair or the replacement group—A: repair, n = 19; and B: replacement, n = 21. Two examiners who had calibration expertise evaluated the restorations at baseline and 10 years after according to seven parameters: marginal occlusal adaptation, anatomic form, surface roughness, marginal staining, contact, secondary caries, and luster. After 10 years, 30 restorations (75%) were evaluated (Group A: n = 17; Group B: n = 13). Repaired and replaced amalgam restorations showed similar survival outcomes regarding marginal defects and secondary caries in patients with low and medium caries risk, and most of the restorations were considered clinically acceptable after 10 years. Repair treatment increased the potential for tooth longevity, using a minimally interventional procedure. All restorations trend to downgrade over time