Dental composite materials and renal function in children.

OBJECTIVE: To examine whether greater exposure to resin-based composite materials, which may intra-orally release bisphenol A (BPA), is associated with worse renal function outcomes in children. DESIGN: Prospective multi-centre study. SETTING: Community health dental clinics in Boston and Maine from 1997-2005.Subjects and methods Five hundred and thirty-four New England Children's Amalgam Trial participants aged six to ten years were randomised to treatment with amalgam or resin-based composite restorations over five years of follow-up. INTERVENTIONS: Restorations were placed according to treatment arm, and sealants placed per standard of care. Cumulative composite exposure was calculated using surface-years (each treated surface weighted by number years present). MAIN OUTCOME MEASURES: Urinary excretion of albumin, gamma-glutamyl transpeptidase (gamma-GT), and N-acetyl-ß-D-glucosaminidase (NAG) were available for 417 children. RESULTS: Analysis of covariance showed no association between exposure to dental composites, polyacid-modified compomer, or flowable composite dental sealants and preventative resin restorations with levels of renal function. There was no association between composite materials and thresholds indicating renal damage in logistic regression models. CONCLUSIONS: This study found no harmful associations between dental composite materials and renal function in children. Therefore, concerns about renal function need not be a consideration in the choice of dental restoration material or placement of preventative dental sealants.

Dental composites and amalgam and physical development in children.

Resin-based composite dental restoration materials may release bisphenol-A, an endocrine-disrupting chemical. Using secondary analysis of a randomized clinical safety trial of amalgam vs. composites, we tested the hypothesis that dental restoration materials affect children's growth. Children (N = 218 boys, N = 256 girls) aged 6 to 10 yrs at baseline with ≥ 2 decayed posterior teeth were randomized to amalgam or composites (bisphenol-A-diglycidyl-dimethacrylate composite for permanent teeth, urethane-dimethacrylate compomer for primary teeth) for treatment of posterior caries throughout follow-up. Primary outcomes for this analysis were 5-year changes in BMI-for-age z-scores, body fat percentage (BF%), and height velocity; exploratory analyses (n = 113) examined age at menarche. Results showed no significant differences between treatment assignment and changes in physical development in boys [(composites vs. amalgam) BF%, 4.9 vs. 5.7, p = 0.49; (BMI-z-score) 0.13 vs. 0.25, p = 0.36] or girls (8.8 vs. 7.7, p = 0.95; 0.36 vs. 0.21, p = 0.49). Children with more treatment on primary teeth had greater increases in BF% regardless of material type. Girls assigned to composites had lower risk of menarche during follow-up (hazard ratio = 0.57, 95% CI 0.35-0.95). Overall, there were no significant differences in physical development over 5 years in children treated with composites or amalgam. Additional studies examining these restoration materials in relation to age at menarche are warranted (clinicaltrials.gov number NCT00065988).

Insulin resistance influences the association of adiponectin levels with diabetes incidence in two population-based cohorts: the Cooperative Health Research in the Region of Augsburg (KORA) S4/F4 study and the Framingham Offspring Study.

AIMS/HYPOTHESIS: Lower adiponectin levels are associated with higher risk of incident type 2 diabetes. Most analyses have been adjusted for confounding factors, but few have taken into account insulin resistance per se. We tested the hypothesis that the association of adiponectin levels with incident type 2 diabetes differs between insulin-resistant and insulin-sensitive individuals. METHODS: We studied two prospective cohorts: the Framingham Offspring Study (n = 2,023) and the Cooperative Health Research in the Region of Augsburg (KORA) S4/F4 study (n = 887) cohorts. Insulin resistance was estimated by HOMA-insulin resistance (HOMA-IR). We used logistic regression analysis to test the association between adiponectin and incident type 2 diabetes overall and in insulin-resistant vs insulin-sensitive individuals (defined by ≥ vs <75th percentile of HOMA-IR). RESULTS: At baseline, Framingham's participants were 60 ± 9 years old and 56% were women; KORA's participants were 63 ± 5 years old and 49% were women. Type 2 diabetes incidence was 5.4% over 6.5 years (n = 109) in Framingham and 10.5% over 8 years (n = 93) in KORA. Lower adiponectin levels were associated with type 2 diabetes incidence in both cohorts. In insulin-resistant individuals, lower adiponectin levels were associated with higher risk of type 2 diabetes incidence (OR 1.60 [95% CI 1.10-2.31] per SD decrease in Framingham, p = 0.01; and OR 2.34 [95% CI 1.16-4.73] in KORA, p = 0.02); while this was not observed in insulin-sensitive individuals (OR 1.10 [95% CI 0.73-1.67] in Framingham, p = 0.64; and OR 1.34 [95%CI: 0.88-2.03] in KORA, p = 0.18). CONCLUSIONS/INTERPRETATION: We conclude that lower adiponectin levels are associated with higher risk of type 2 diabetes in insulin-resistant but not in insulin-sensitive individuals. This suggests that some level of insulin resistance is needed to see deleterious effects of low adiponectin.

Circulating IL-18 and the risk of type 2 diabetes in women.

AIMS/HYPOTHESIS: The pathophysiology of type 2 diabetes involves pro-inflammatory pathways. We tested the hypothesis that IL-18 predicts future diabetes cases. METHODS: We used a nested case-control design based in the Nurses' Health Study. Baseline blood samples were collected between 1989 and 1990. Questionnaires to assess body weight, lifestyle (physical activity, diet, smoking) and diabetes diagnosis were sent out and assessed biennially (follow-up until 2002). Cases (n = 1,012) were defined as women developing type 2 diabetes at least 1 year after blood sampling. Control women (n = 1,081) were matched to cases by age, date of blood draw, fasting status and race. We calculated the RR (95% CI) of type 2 diabetes in quintiles of IL-18 using conditional logistic regression with the first quintile as referent; adjustments included matching factors, diabetes risk factors, BMI, adipokine levels (adiponectin, resistin) and inflammatory proteins (C-reactive protein, tumour necrosis factor receptor 2 (TNFalpha-R2) and IL-6). RESULTS: Higher IL-18 levels were associated with increased risk of developing diabetes, even after adjustment for matching factors and multiple diabetes risk factors: being in the highest quintile of IL-18 was associated with a RR of 1.75 (1.41-2.18) for diabetes relative to the first quintile (p < 0.0001 for trend). Significant trends in association were still observed after adjustment for BMI (RR 1.44 [1.15-1.80], p < 0.0001 for trend) and adiponectin levels (RR 1.28 [1.02-1.60], p = 0.006 for trend). Further adjustment for inflammatory markers in a sub-sample did not significantly change the results. CONCLUSIONS/INTERPRETATION: Elevated IL-18 levels are associated with higher risk of diabetes. This association is independent of usual risk factors, including BMI and adipokine levels.