Team:Northwestern/problem

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Summary of Problem

Oral health is one of the most overlooked aspects of health care in the world. According to the World Health Organization, 60-90% of children worldwide have dental cavities, while they are present in nearly 100% of adults.

Tooth decay and cavity development are a direct result of the plaque that accumulates in the mouth after meals. The plaque is a biofilm composed of a number of different types of bacteria native to the oral biome. In particular, a bacteria called Streptococcus mutans metabolizes sucrose from our meals. An enzyme called glucosyl transferase on S. mutans converts sucrose into dextran polymers or glucan. Glucan facilitates S. mutans and others bacteria to stick to each other and on the tooth surface. This chunk of bacteria that is attached to our teeth is commonly called as plaque. Below is a detailed picture of this process.

Figure 1. For Streptococcus mutans, the main causative agent of dental caries, the main virulence factor is the production of acid as part of the bacterial biofilm that constitutes dental plaque.

S. mutans inside the placque metabolizes sugars from our meals to lactic acid as a metabolic byproduct from glycolysis. Since the plaque traps the lactic acid on the surface of the teeth this pH drop takes place in direct contact with the tooth enamel at a significant concentration. The threshold pH at which enamel or dentin demineralization occurs is 5.5. This pH drop is most prevalent directly following mealtimes. The figure below shows that the surface of the enamel can spend nearly 5 hours a day exposed to pH below the demineralization threshold, thus this is a serious problem that provides motivation for this research.

Figure 2: The Stephan Curve4, depicting pH fluctuation in the mouth over 24 hours.

Project References

  1. World Health Organization . 2012 April. Oral health [Internet]. [cited 2013 Jul 2] . Available from: http://www.who.int/mediacentre/factsheets/fs318/en/
  2. Zijnge V, van Leeuwen MB, Degener JE, Abbas F, Thurnheer T, Gmur R, Harmsen HJ. 2010. Oral biofilm architecture on natural teeth. NCBI [Internet]. [cited 2013 Jul 8] 5(2):e9321. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20195365
  3. Selwitz RH, Ismail AI, Pitts NB. 2007. Dental caries. The Lancet [Internet]. [cited 2013 Jul 15] 369(9555):51-59. Available from: http://www.sciencedirect.com/science/article/pii/S0140673607600312
  4. Stephan RM &Miller BF. The Effect of Synthetic Detergents on pH Changes in Dental Plaques. J DENT RES Feb 1943 22: 53-61
  5. Tucker DL, Tucker N, Conway T. 2002. Gene Expression Profiling of the pH Response in Escherichia coli. Journal of Bacteriology [Internet]. [cited 2013 Jul 19] 184(23):6551-6558. Available from: http://jb.asm.org/content/184/23/6551.full
  6. de Boer HA, Comstock LJ, Vasser M. 1983. The tac promoter: a functional hybrid derived from the trp and lac promoters. NCBI [Internet]. [cited 2013 Jul 22] 80(1):21-5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/6337371
  7. Inouye S, Inouye M. 1985. Up-promoter mutations in the lpp gene of Escherichia coli. Nucleic Acids Research [Internet]. [cited 2013 Jul 22] 13(9):3101-3110. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC341223/
  8. Figure 1: Mitchell J, Timonthy 2003 The pathogenesis of streptococcus infections: from Tooth decay to meningitus. Nature Reviews Microbiology [Interent]. [cited 2013 Sept. 25] 1:219-230. Available from http://www.nature.com.turing.library.northwestern.edu/nrmicro/journal/v1/n3/full/nrmicro771.html

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