Pre- and perinatal exposures associated with molar incisor hypomineralization: Birth cohort, Brazil.

OBJECTIVE: To analyze prenatal and perinatal stressors associated with molar incisor hypomineralization (MIH) in adolescents. METHODS: Prospective cohort study collected prenatal (socioeconomic status, maternal age, number of prenatal visits, smoking, obesity during pregnancy, abortion history, gestational hypertension) and perinatal stressors (type of delivery, gestational age, birth weight, intensive care unit-ICU at birth). The outcome was MIH at 18-19 years follow-up (n = 590). MIH was defined according to the Ghanim criteria - Model I. We performed a sensitivity analysis, including opacities demarcated in index tooth, incisive or molars, Model II. Through structural equation modeling, we analyzed direct and mediating pathways between multiple stressors with outcomes. RESULTS: MIH was observed in 15.25% (n = 90), and opacities demarcated in any index tooth were observed in 22.8% of adolescents (n = 135). In Model I, no stressor explained MIH significantly, although we watched high standardized coefficients (SC) for low birth weight (SC = 0.223, p = 0.147), lower gestational age (SC = 0.351; p = 0.254), and ICU admission (SC = 0.447, p = 0.254). In Model II, advanced maternal age (SC = 0.148; p < 0.05) and not undergoing prenatal care (SC = 0.384, p < 0.03) explained opacities demarcated in incisors or molars. CONCLUSION: Advanced maternal age and not undergoing prenatal care were associated with MIH lesion-like in incisors or molars.

Precursors of insulin resistance underlying periodontitis in adolescents aged 17-18 years.

OBJECTIVE: To investigate the association between insulin resistance markers and periodontitis in adolescents, analyzing confounder variables and the adiposity as a mediator. METHODS: This is population-based study is representative of adolescents aged 17-18 years from public schools in São Luís, Brazil (n = 405). Insulin resistance was assessed using the Model of Assessment of the Homeostasis of the Insulin Resistance Index (HOMA-IR) and its percussor triglycerides/HDL-cholesterol ratio (TG/HDL-c). The outcome was Initial Periodontitis, a latent variable estimated by the common variance shared among bleeding on probing, probing depth ≥ 4 mm, and clinical attachment loss ≥ 4 mm. The association between insulin resistance and Initial Periodontitis was modeled via pathways triggered by socioeconomic status, smoking, alcohol, and Adiposity, using structural equation modeling. RESULTS: Higher TG/HDL-c was directly associated with higher Initial Periodontitis (standardized coefficient [SC] = 0.130, p < 0.001). HOMA-IR was not associated with periodontal outcome (SC = 0.023, p = 0.075), but it was with Adiposity (SC = 0.495, p < 0.001). Higher TG/HDL-c was associated with Adiposity (SC = 0.202, p < 0.001). CONCLUSION: The insulin resistance markers were associated with early signs of periodontal breakdown among adolescents, suggesting a possible relationship between diabetes and periodontitis commences early in life.

Higher sugar intake is associated with periodontal disease in adolescents.

OBJECTIVES: Analyze the association between higher added sugar exposure and periodontal disease in adolescents (18-19 years old). MATERIALS AND METHODS: This was a cross-sectional study nested to RPS Cohorts Consortium, São Luís, Brazil (n = 2515). The exposure was percentage of daily calories from added sugar (≥ 10%), estimated from a quantitative food frequency. The outcome was periodontal disease estimated by the number of teeth affected by bleeding on probing, periodontal probing depth ≥ 4 mm, and clinical attachment level ≥ 4 mm at the same site. A theoretical model was depicted in a directed acyclic graph to identify the minimal sufficient adjustment set: household income, adolescent's educational level, sex, alcohol use, and smoking. Periodontal disease was categorized into < 2 teeth affected, 2 to 3 teeth affected, and ≥ 4 teeth affected to estimate prevalence ratios (PR) by multinomial logistic regression. To test for consistency, means ratio (MR) were estimated using zero-inflated Poisson. RESULTS: High sugar intake was associated with ≥ 4 teeth affected by periodontal disease (PR = 1.42; 95% confidence interval (CI) = 1.03-1.94; p = 0.030); consistency Poisson analysis reinforced these results (MR = 1.15; 95% CI = 1.03-1.29; p = 0.011). CONCLUSION: High level of added sugar intake was associated with greater extent of periodontal disease in adolescents. CLINICAL RELEVANCE: High sugar intake was associated with periodontal disease in adolescents, supporting the integrated hypothesis of dental caries and periodontal disease and giving impetus to future clinical investigation on the effect of restriction of added sugar consumption in periodontal parameters, which potentially may change traditional treatment protocols of periodontal disease.

Streptococcus mutans in Mother-Child Dyads and Early Childhood Caries: Examining Factors Underlying Bacterial Colonization.

This study investigated the association between colonization of mother-child dyads with Streptococcus mutans (SM) and early childhood caries (ECC), with consideration of the mediator and confounders, using a theoretical model. Four hundred mothers and their children from São Luís, Brazil, were included in the study. A diagram based on directed acyclic graphs was elaborated to analyze the association between SM colonization of the mother, mediated by child SM, and ECC. Other maternal (socioeconomic, waist circumference, sugar consumption, DMFT index, and visible plaque) and child factors (sugar consumption, visible plaque, and child age) composed the theoretical model. A total effect model (maternal SM on ECC) and a direct effect model, adjusted by the mediation effect of child SM (maternal SM via child SM) on ECC, were analyzed. The outcome of interest in this study was ECC (number of teeth with caries experience, dmft), which was analyzed as a discrete variable by Poisson regression. The Paramed test was used to analyze mediation. The following variables were associated with ECC in the total effect model: maternal SM, maternal waist circumference ≥80 cm, DMFT, maternal visible plaque, child age ≥4 years, and increased sugar consumption of the child (>3 times/day). In the direct effect model, high maternal SM levels remained associated with ECC, while moderate and high colonization of the child with SM was also associated with ECC. Child SM colonization just partially mediated the effect of maternal SM on ECC (33%). Thus, factors other than the mechanism of bacterial colonization should be considered in mother-child dyads, including eating habits, oral hygiene practices, and a family history of caries.