Abstract

BackgroundDental caries is the single most prevalent and costly infectious disease worldwide, affecting more than 90% of the population in the U.S. The development of dental cavities requires the colonization of the tooth surface by acid-producing bacteria, such as Streptococcus mutans. Saliva bicarbonate constitutes the main buffering system which neutralizes the pH fall generated by the plaque bacteria during sugar metabolism. We found that the saliva pH is severely decreased in a mouse model of cystic fibrosis disease (CF). Given the close relationship between pH and caries development, we hypothesized that caries incidence might be elevated in the mouse CF model.Methodology/Principal FindingsWe induced carious lesions in CF and wildtype mice by infecting their oral cavity with S. mutans, a well-studied cariogenic bacterium. After infection, the mice were fed a high-sucrose diet for 5 weeks (diet 2000). The mice were then euthanized and their jaws removed for caries scoring and bacterial counting. A dramatic increase in caries and severity of lesions scores were apparent in CF mice compared to their wildtype littermates. The elevated incidence of carious lesions correlated with a striking increase in the S. mutans viable population in dental plaque (20-fold increase in CF vs. wildtype mice; p value<0.003; t test). We also found that the pilocarpine-stimulated saliva bicarbonate concentration was significantly reduced in CF mice (16±2 mM vs. 31±2 mM, CF and wildtype mice, respectively; p value<0.01; t test).Conclusions/SignificanceConsidering that bicarbonate is the most important pH buffering system in saliva, and the adherence and survival of aciduric bacteria such as S. mutans are enhanced at low pH values, we speculate that the decrease in the bicarbonate content and pH buffering of the saliva is at least partially responsible for the increased severity of lesions observed in the CF mouse.

Highlights

  • Dental caries is the single most prevalent and costly infectious disease worldwide, affecting more than 90% of the population in the U.S [1]

  • To directly test the association between cystic fibrosis disease (CF) and dental caries we used the DF508 mouse CF model, which reproduces many of the defects observed in human disease [25]

  • Using the DF508 mouse cystic fibrosis model, we previously found that the CFTR channel mediates Cl2 reabsorption by salivary gland ducts [11]

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Summary

Introduction

Dental caries is the single most prevalent and costly infectious disease worldwide, affecting more than 90% of the population in the U.S [1]. CFTR is highly expressed in salivary glands [11,12,13,14,15], but the reported effects of CF on salivary gland function [6,7,8,16,17] and the incidence of dental cavities are inconsistent [16,17,18,19,20,21] The basis for these discrepancies is unknown, but many of these studies were performed before it was routine to determine the nature of the CF mutation, which relates to the severity of disease, and when patients rarely survived to adulthood because the treatment of CF was largely ineffective. Dental caries is the single most prevalent and costly infectious disease worldwide, affecting more than 90% of the population in the U.S The development of dental cavities requires the colonization of the tooth surface by acidproducing bacteria, such as Streptococcus mutans. Given the close relationship between pH and caries development, we hypothesized that caries incidence might be elevated in the mouse CF model

Methods
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