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Objective: Untreated periodontal disease seems to cause low grade systemic inflammation and blood lipid alteration leading to increased cardiovascular disease risk. To start testing this hypothesis in Colombian patients, a multicentre study was conducted including the three main state capitals: Bogotá, Medellín and Cali. Methods: In this study 192 (28.4%) advanced and 256 (37.8%) moderate periodontitis patients were investigated for socio-demographic variables, city of precedence, periodontal parameters, smoking, red complex periodontopathic bacteria, serum antibodies against Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans and blood lipids including total cholesterol, HDL, LDL and triglycerides (TG). Those parameters were compared to 229 (33.8%) controls having periodontal health or gingivitis. Results: Advanced periodontitis had worst periodontal indexes, than moderate periodontitis and controls. Interestingly, higher HDL and TG levels were present in periodontitis. BMI > 30 and smoking were associated with increased HDL, HDL-35, LDL and TG, while glycemia >100 mg/dL associated with HDL, HDL-35 and TG. Tannerella forsythia showed a significant association with HDL-35 in bivariate analysis and serum IgG1 against P. gingivalis associated with HDL-35 and serum IgG1 against T. forsythia associated with TG and serum IgG2 against A. actinomycetemcomitans correlated with levels of HDL y HDL-35. In logistic regression the periodontitis patients from Cali presented reduced HDL levels as compared to Bogota and Medellín patients. Presence of IgG1 antibodies against P. gingivalis and A. actinomycetemcomitans correlated with reduced HDL levels. Conclusion: This study confirmed that untreated periodontitis generates alteration in serum lipid levels and systemic bacterial exposure against important periodontopathic bacteria could to be the biological link. [ABSTRACT FROM AUTHOR]

Objective The common promoter –675 4G/5G insertion/deletion polymorphism (indel) in the plasminogen activator inhibitor-1 ( PAI-1) gene has been associated with quantitative components of the metabolic syndrome. We hypothesized that this polymorphism is associated with precocious pubarche (PP), a population known to be at risk for hyperinsulinaemic hyperandrogenism. Design A cross-sectional, hospital-based study. Patients A total of 115 control and 182 PP Catalan girls and young women. Measurements Subjects were genotyped for the –675 4G/5G indel in the PAI-1 gene. Insulin resistance and insulin secretion were estimated by the homeostasis model assessment. Results Genotype frequencies for the PAI-1–675 4G/5G indel (4G4G, 4G5G and 5G5G) were similar in control and PP subjects (24% vs. 27%, 50% vs. 47%, and 26% vs. 26%, respectively; P = 0·85) and these frequencies were in Hardy–Weinberg equilibrium. The 5G allele, however, was associated with insulin resistance in both postmenarcheal control and PP subjects ( P < 0·01 for pooled postmenarcheal subjects, N = 122). The coexistence with the at-risk genotype of both a low birthweight (standard deviation score, SDS < –1·0) and a high body mass index (BMI) at time of the study (SDS > +1·0) resulted in a noteworthy increase ( P < 0·001) in insulin resistance. Conclusion The common promoter –675 4G/5G indel of the PAI-1 gene is not associated with PP but, in Catalan young women, the 5G allele enhances the risk for insulin resistance imposed by the sequence of a low birth weight (LBW) and a high BMI. [ABSTRACT FROM AUTHOR]