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ObjectiveThe objective of this case–control study was to quantify the immune responsiveness in individuals with type 2 diabetes (T2D) as compared with patients without diabetes (NT2D) diagnosed with periodontitis.Research Design and MethodsPeripheral blood was collected from 20 patients with moderate-to-severe chronic periodontitis (10 T2D, 10 NT2D). Blood samples were stimulated with ultrapure Porphyromonas gingivalis and Escherichia coli lipopolysaccharide (LPS) for 24 hours. 14 cytokines/chemokines were quantified in culture supernatants using multiplex technology.ResultsT2D individuals demonstrated higher unstimulated levels of interleukin 6 (IL-6), IL-1β, tumor necrosis factor α, interferon γ, IL-10, IL-8, macrophage inflammatory protein 1α (MIP1α), and 1β (MIP1β), and higher stimulated levels of IL-6, IL-8, IL-10, MIP1α and MIP1β, along with lower unstimulated and stimulated levels of granulocyte-macrophage colony-stimulating factor (GM-CSF) when compared with NT2D (p<0.05). Importantly, the LPS-induced levels of IL-6, IL-8, IL-10 and MIP1α strongly correlated with severity of disease, measured by pocket depths (PD), within the T2D group (r2≥0.7, p<0.05), but not within NT2D.ConclusionsAmong patients with chronic periodontitis, patients with T2D seem to have an enhanced LPS-induced immune responsiveness than individuals without diabetes, which correlates with periodontal disease severity, concomitant with a less robust GM-CSF response. This data may in part explain the higher predisposition to periodontitis in this population.

BackgroundThere is a controversy about the association between vitamin D and cardiovascular diseases (CVDs). The effect of serum 25-OH-vitD on the risk of CVDs was evaluated.MethodsMajor electronic databases including Scopus, Science Direct, and PubMed were searched. All prospective cohort studies on the relationship between vitamin D status and CVDs conducted between April 2000 and September 2017 were included, regardless language. The study participants were evaluated regardless of their age, sex, and ethnicity. The Newcastle-Ottawa Scale was used to assess the quality of the studies. Two investigators independently selected the studies and extracted the data. The designated effects were risk ratio (RR) and hazard ratio (HR). The random effects model was used to combine the results.ResultsA meta-analysis of 25 studies with 10,099 cases of CVDs was performed. In general, a decrease in the level of vitamin D was associated with a higher relative risk of CVDs (incidence-mortality combined) (RR = 1.44, 95% CI: 1.24–1.69). This accounts for 54% of CVDs mortality rate (RR = 1.54, 95% CI: 1.29–1.84(. However, no significant relationship was observed between the vitamin D status and incidence of CVDs (RR = 1.18, 95% CI: 1–1.39). In general, low serum vitamin D level increased the risk of CVD by 44% (RR = 1.44, 95% CI: 1.24–1.69). It also increased the risk of CVD mortality (RR = 1.54, 95% CI: 1.29–1.84) and incidence rates (RR = 1.18, 95% CI: 1–1.39).ConclusionsThe findings showed that vitamin D deficiency increases the CVDs mortality rate. Due to the limited number of studies on patients of the both genders, further research is suggested to separately evaluate the effect of vitamin D status on CVD in men and women.