INTRODUCTION:Traditional cardiovascular risk factors such as central obesity, high blood pressure and insulin resistance, all constituents of metabolic syndrome, have been associated with increased levels of C-reactive protein (CRP). Therefore, this marker of low-grade inflammation may play a major role in the pathogenesis of cardiovascular diseases. In this study, data from a representative sample of urban adults was used to evaluate the association between CRP and metabolic syndrome, accounting for the type and number of its constituents. METHODS: Using random digit dialing, 1022 participants, aged 18-92 y, were selected. All participants completed a structured questionnaire comprising of information on social, demographic, behavioral and clinical aspects. Anthropometrics and blood pressure were recorded and a fasting blood sample collected. Metabolic syndrome was defined, according to the Third Report of the Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults, as the presence of three or more of the following characteristics: waist circumference greater than 102 cm in men and 88 cm in women; triglyceride levels Z150 mg/dl; high-density lipoprotein cholesterol levels o40 mg/dl in men and o50 mg/dl in women; blood pressure Z130/ 85 mm Hg; and serum glucose Z110 mg/dl. High-sensitivity CRP was assessed by immunonephelometric assay. After excluding 65 participants with CRP Z10 mg/l, 957 subjects (599 women and 358 men) remained for analysis. Geometric means were compared after adjustment for age, sex, alcohol consumption and smoking. RESULTS: Higher mean levels of CRP (2.34 vs 1.36, Po0.001) were observed when metabolic syndrome was present. Also, mean CRP levels were significantly higher in the presence of central obesity (2.45 vs 1.24, Po0.001), high blood pressure (1.76 vs 1.12, Po0.001), hypertriglyceridemia (2.17 vs 1.32, Po0.001) and high fasting glucose (1.96 vs 1.46, P ¼ 0.032). We found a significant increasing trend (Po0.001) in mean levels of CRP as the number of features of metabolic syndrome increased. The major contributing features for high CRP levels were central obesity and high blood pressure. CONCLUSIONS: Present data show that increasing severity of metabolic syndrome is associated with increasing CRP. Additionally, we found that central obesity and high blood pressure are the most important determinants of the low-grade chronic inflammation present in metabolic syndrome.

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Although a number of inflammatory cytokines have been shown to be associated with periodontal pathogenesis, it is important to investigate further whether these biomarkers are associated with the degree of success in nonsurgical treatment of chronic periodontitis. The aim of the present study was to quantify the total levels of interleukin (IL)-1α, -1β, -6, -10 and tumour necrosis factor (TNF)-α in gingival crevicular fluid (GCF) of chronic periodontitis patients prior to and following nonsurgical periodontal therapy. In total, 52 GCF samples from disease sites of patients with chronic periodontitis, prior to and following periodontal therapy, and ten non-disease sites from non-periodontitis subjects, were collected and cytokine concentrations were determined using a multiplex method. Periodontal parameters, including bleeding on probing, probing pocket depth and the clinical attachment level, in all the sites were recorded. Untreated disease sites exhibited higher cytokine levels in the GCF when compared with the non-disease sites. Nonsurgical periodontal therapy resulted in a statistically significant decrease in the total levels of IL-1α, -1β and -6 in the GCF, but not in IL-10 or TNF-α. The results support the hypothesis that proinflammatory cytokines, including IL-1α, IL-1β and IL-6, are likely to be involved in the pathogenesis of periodontitis and are good markers to evaluate the success of nonsurgical therapy in disease sites of patients with periodontitis.