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This study used data from the 1982 Pelotas Birth Cohort Study, Brazil, to estimate the controlled direct effect of early-life socioeconomic position (SEP) on periodontitis at age 31 years, controlling for adulthood income and education, smoking, and dental hygiene. Sex was included as a covariate. Early-life SEP was measured at participant birth based on income, health services payment mode, maternal education, height, and skin color (lower versus middle/higher SEP). Periodontitis was assessed through clinical examination at age 31 years (healthy, mild periodontitis, or moderate-to-severe disease). Adulthood behaviors (smoking, dental hygiene) were the mediators, and adulthood SEP (education and income) represented the exposure-induced mediator-outcome confounders. A regression-based approach was used to assess the controlled direct effect of early-life SEP on periodontitis. Multinomial regression models were used to estimate risk ratios and their 95% confidence intervals. The prevalences of mild and moderate-to-severe periodontitis were 23.0% and 14.3%, respectively (n = 539). Individuals from the lowest early-life SEP had a higher risk of moderate-to-severe periodontitis controlled for mediators and exposure-induced mediator-outcome confounders: risk ratio = 1.85 (95% confidence interval: 1.06, 3.24), E value 3.1. We found that early-life SEP was associated with the development of periodontitis in adulthood that was not mediated by adulthood SEP and behaviors. [ABSTRACT FROM AUTHOR]

Objective. Complete deficiency of Complement C4 component is a strong genetic risk factor for SLE. C4 is encoded by two different genes, C4A and C4B, which show considerable gene copy number (GCN) variation. This study investigates the association of total C4, C4A and C4B GCN with JSLE. Methods. Ninety JSLE patients, 170 adult-onset SLE (aSLE) patients and 200 healthy individuals were evaluated for C4A and C4B GCN by quantitative real-time PCR. Results. JSLE patients had lower GCN for C4A (mean = 1.7; 95% CI: 1.5, 1.9) and C4B (mean = 1.5; 95% CI: 1.3, 1.6) compared with healthy individuals (mean C4A = 2.3; 95% CI: 2.2, 2.5, P< 0.001; C4B = 2.0; 95% CI: 1.8, 2.1; P<0.001) or with aSLE patients (mean C4A = 1.9; 95% CI: 1.8, 2.1, P = 0.006; mean C4B = 1.8; 95% CI: 1.7, 1.9, P< 0.001). Low total C4 GCN (<4 copies) was more frequent in JSLE than in healthy individuals (59% vs 28%; P< 0.001). The same was observed for low C4A (≤1 copy) (52% vs 18%; P < 0.001) and for low C4B (60% vs 31 %; P < 0.001). JSLE had a stronger association with low total C4 (OR = 3.68, 95% CI: 2.19, 6.20), C4A (OR = 4.98, 95% CI: 2.88, 8.62) and C4B (OR = 3.26; 95% CI: 1.95, 5.47) than aSLE (C4 OR = 2.03; 95% CI: 1.32, 3.13; C4A OR = 2.36; 95% CI: 1.46, 3.81; C4B OR = 1.13; 95% CI: 0.73, 1.74). In addition, pericarditis in JSLE patients was associated with low C4 (OR=4.13; 95% CI: 1.02, 16.68; P = 0.047) and low C4A (OR = 5.54; 95% CI: 1.37, 22.32; P = 0.016). Conclusion. Low total C4, C4A and C4B GCN were associated with a stronger risk for developing JSLE than aSLE. Additionally, low total C4 and C4A GCN are risk factors for pericarditis in JSLE. [ABSTRACT FROM AUTHOR]