IADR Abstract Archives
The Exposome and Periodontal Disease: Epidemiologic Evaluation of NHANES
Objectives: Periodontal disease is an immunoinflammatory disease with individual variation in disease processes regulated by the exposome, which extends beyond the individual’s microbiome and may fundamentally impact the epigenome, with modulated responses to the microbiome. This report documented an Environment Wide Association Study (EWAS) of the exposome to the expression of periodontitis in smoking and non-smoking patients using data from the NHANES from 1999-2004.
Methods: Environmental variables (n=156) were assessed in blood/urine and periodontitis patients categorized in a final cohort of 10,278 individuals. Multiple statistical approaches were used to explore this dataset (Logistic Regression, Classification and Regression Tree, Random Forests) and identify patterns of the environmental variables that significantly enhanced the risk for expression of periodontitis.
Results: Overall there were 47 environmental factors (cotinine, 5 heavy metals, 7 nutrients, 8 hydrocarbons, 2 phthalates, 1 dioxin, 20 PCBs and 3 volatile compounds) that resulted in a statistically significant odds ratio for disease versus health in this NHANES cohort. When data was stratified by the smoking status 18 environmental factors (2 heavy metals, 1 nutrient, 2 phthalates, 1 phytoestrogens, 2 dioxins, 1 furans dibenzofuran, 8 PCBs, and 1 pesticide) in current smokers, 15 factors (acrylamide, 1 heavy metal, 2 pesticide, 1 phthalates and 10 PCBs) in former smokers, and 10 factors (2 heavy metals, 1 nutrient, 1 phthalates, 1 dioxin, 1 diakyl and 4 PCBs) in non-smokers were identified. These factors were found to be coupled with more classical risk factors (ie. age, gender, race/ethnicity) to create a model that predicted an increased disease likelihood of 3-4 fold across the population.
Conclusions: The results support an association of targeted environmental factors with the risk of periodontitis, and may contribute altered gene expression and subsequent biologic processes enhancing the inflammatory tissue destruction. Supported by the Center for Oral Health Research and UL1 TR0001988.
Methods: Environmental variables (n=156) were assessed in blood/urine and periodontitis patients categorized in a final cohort of 10,278 individuals. Multiple statistical approaches were used to explore this dataset (Logistic Regression, Classification and Regression Tree, Random Forests) and identify patterns of the environmental variables that significantly enhanced the risk for expression of periodontitis.
Results: Overall there were 47 environmental factors (cotinine, 5 heavy metals, 7 nutrients, 8 hydrocarbons, 2 phthalates, 1 dioxin, 20 PCBs and 3 volatile compounds) that resulted in a statistically significant odds ratio for disease versus health in this NHANES cohort. When data was stratified by the smoking status 18 environmental factors (2 heavy metals, 1 nutrient, 2 phthalates, 1 phytoestrogens, 2 dioxins, 1 furans dibenzofuran, 8 PCBs, and 1 pesticide) in current smokers, 15 factors (acrylamide, 1 heavy metal, 2 pesticide, 1 phthalates and 10 PCBs) in former smokers, and 10 factors (2 heavy metals, 1 nutrient, 1 phthalates, 1 dioxin, 1 diakyl and 4 PCBs) in non-smokers were identified. These factors were found to be coupled with more classical risk factors (ie. age, gender, race/ethnicity) to create a model that predicted an increased disease likelihood of 3-4 fold across the population.
Conclusions: The results support an association of targeted environmental factors with the risk of periodontitis, and may contribute altered gene expression and subsequent biologic processes enhancing the inflammatory tissue destruction. Supported by the Center for Oral Health Research and UL1 TR0001988.