Abstract

Periodontitis is a chronic inflammation that destroys periodontal tissues caused by the accumulation of bacterial biofilms that can be affected by environmental factors. This report describes an association study to evaluate the relationship of environmental factors to the expression of periodontitis using the National Health and Nutrition Examination Study (NHANES) from 1999–2004. A wide range of environmental variables (156) were assessed in patients categorized for periodontitis (n = 8884). Multiple statistical approaches were used to explore this dataset and identify environmental variable patterns that enhanced or lowered the prevalence of periodontitis. Our findings indicate an array of environmental variables were different in periodontitis in smokers, former smokers, or non-smokers, with a subset of specific environmental variables identified in each population subset. Discriminating environmental factors included blood levels of lead, phthalates, selected nutrients, and PCBs. Importantly, these factors were found to be coupled with more classical risk factors (i.e. age, gender, race/ethnicity) to create a model that indicated an increased disease prevalence of 2–4 fold across the sample population. Targeted environmental factors are statistically associated with the prevalence of periodontitis. Existing evidence suggests that these may contribute to altered gene expression and biologic processes that enhance inflammatory tissue destruction.

Highlights

  • Despite increasing awareness and improvement in oral health, periodontitis, together with dental caries, remain major health concerns across the lifespan in the United States[1]

  • When the periodontitis group defined by National Health and Nutrition Examination Survey (NHANES) measures was compared to the subset of subjects considered periodontally healthy, individuals with periodontal disease were more likely to be male, older than 30 years of age, Mexican American, non-Hispanic black or Hispanic and current smoker compared to Non-Hispanic white and non-smoker (p < 0.001) (Tables 1 and 3)

  • The current paradigm of periodontitis is that it represents a dysregulation of the host response to a dysbiotic microbiome that occurs in a large portion of the global population

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Summary

Introduction

Despite increasing awareness and improvement in oral health, periodontitis, together with dental caries, remain major health concerns across the lifespan in the United States[1]. It is anticipated that 80% of the risk for periodontal tissue damage is a result of dysregulated host responses against the chronic bacterial insult[2,3,4] This interaction can progress to destroy the periodontal tissues and bone, and eventually is the major basis of tooth loss in adults with edentulous individuals having difficulty eating, swallowing, and speaking properly[5,6,7]. Emphasis has been placed on the need for more effective management of these modifiable risk factors to impact this global disease[18], albeit, non-modifiable factors including age, genetics and the existence of various systemic diseases are clearly more challenging to address across the population[18,19,20,21] In this regard, various studies of this chronic disease have provided some support attributing disease expression and severity to genetic predisposition regulating the characteristics of the host response to the oral microbial challenge. This report describes the use of various epidemiologic and statistical tools to conduct an association study with periodontitis in the U.S adult population

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