title: Elevated incidence of dental caries in a mouse model of cystic fibrosis.
abstract: BACKGROUND
  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 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.
  
  
  RESULTS
  We 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
  Considering 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.
authors.affiliation: Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York, United States of America.
authors.forename: Marcelo A
authors.initials: MA
authors.lastname: Catalán
authors.forename: Kathleen
authors.initials: K
authors.lastname: Scott-Anne
authors.forename: Marlise I
authors.initials: MI
authors.lastname: Klein
authors.forename: Hyun
authors.initials: H
authors.lastname: Koo
authors.forename: William H
authors.initials: WH
authors.lastname: Bowen
authors.forename: James E
authors.initials: JE
authors.lastname: Melvin
mesh_terms: D000818:Animals; D001639:Bicarbonates / Q000032:analysis / Q000494:pharmacology; D050260:Carbohydrate Metabolism; D003550:Cystic Fibrosis / Q000150:complications*; D003731:Dental Caries / Q000209:etiology* / Q000382:microbiology; D004195:Disease Models, Animal; D006863:Hydrogen-Ion Concentration; D015994:Incidence; D051379:Mice; D012463:Saliva / Q000737:chemistry; D013295:Streptococcus mutans
chemical_list: D001639:Bicarbonates