No abstract

Dental pathology is commonly described among patients with systemic sclerosis (SSc), a multisystem autoimmune disorder, and assumed to be multifactorial. We aimed to evaluate the periodontal status and to identify potential relation with SSc-specific parameters as well as serum lipid profile in a cross-sectional study on consecutive SSc. Standard assessments comprised dual, rheumatologic (disease subtype, clinical spectrum, inflammatory, immunological, lipid metabolism - total cholesterol and fractions, triglycerides), and dental evaluation (plaque index, bleeding on probing, pocket depth, clinical attachment level). 70.96% SSc developed oral manifestations, 51.61% periodontal disease, while one third severe aggressive periodontitis, particularly in diffuse SSc (p[0.05). Abnormal lipid pattern (low serum HDL- and high LDL-cholesterol, increased serum triglycerides, without significant modification in total cholesterol level) significantly correlated with diffuse SSc and skin involvement, disease duration, anti-topoisomerase 1 positivity, SSc activity and severity, as well as periodontitis (p[0.05). Our results clearly define an association between the presence and severity of periodontal disease and lipid anomalies in SSc, suggesting a potential link with early atherosclerosis via gingival inflammation and altered lipid metabolism.

Nine dual-fluorescence combinations were used to enumerate T-cell subsets in 112 human immunodeficiency virus type 1-infected patients. Two blood samples were analyzed, with a 6-month interval between the tests, in 53 of these 112 patients. The alteration in CD4 over this period of time correlated with the change in CD8 and CD8S6F1 (P < 0.02 and P < 0.01), irrespective of the disease stage. Two groups of patients were defined by the CD8S6F1 subset at the first normal levels. Changes in numbers of CD4, CD4CD45RA, and CD4CD29 were significantly higher in group B than in group A patients. The absolute count of CD8S6F1 could thus serve as an indicator of the ensuing depletion of the CD4 population, as well as the CD4 subsets.

Recent advances in understanding the multifaceted pathobiology of rheumatoid arthritis have highlighted the pivotal role and continuing crosstalk between activated immune cells, pro-inlammatory cytokines, and matrix-degrading mediators, promoting chronic inlammation as well as irreversible tissue damage within an autoimmune background.B cells are widely recognized as leading players in immune-mediated pathology based on their ability to produce not only diferent paterns of autoantibodies and driving cyto-