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Polymorphisms and oral diseases in Thailand

The taste buds in our tongues contain receptor cells that detect food particles dissolved in saliva.  G-protein coupled receptors on the surface of those receptor cells have been identified that respond to sweet, savory, or bitter tasting chemicals.  Twenty-five different G-protein coupled bitter taste receptors have been identified in humans.  When these bitter receptors are activated on the tongue, we sense a bitter taste that promotes rejection of the food we are eating.  It turns out that bitter taste receptors are not just in the taste buds of the tongue, however.  Bitter taste receptors are also found in the epithelium of the nasal cavity, trachea, gut, urethra and other tissues.  The bitter taste receptors in tissues outside the taste buds do not play a role in taste perception.  Instead, these receptors detect chemicals released by pathogens.  Activation of the bitter receptors in these other tissues trigger host-defense and immune responses that help protect against disease.

BMC LogoAt the University of Washington, we identified one type of bitter taste receptor (T2R38) in gingival epithelial cells of the gums.  There are three important single nucleotide polymorphisms (genetic differences) in the TAS2R38 bitter taste receptor gene, which codes for the T2R38 receptor.  These polymorphisms result in two common genetic haplotypes, which are labeled PAV (Proline, Alanine, Valine) and AVI (Alanine, Valine, Isoleucine) based on the amino acid substitutions that result at positions 49, 262, and 296 of the receptor.  People inherit two haplotypes, one from their father and the other from their mother, resulting in a genetic diplotype.  People who have PAV/PAV or PAV/AVI genetic diplotypes perceive thiourea-containing compounds as bitter tasting, whereas those with the AVI/AVI genotype find these compounds to be almost taste-less.  In our work at University of Washington, we found that gingival epithelial cells with PAV/PAV and AVI/AVI diplotypes responded differently to the bacteria involved in dental caries and periodontal disease.  Gingival epithelial cells with PAV/PAV genotype responded more to S. mutans (a pathogen involved in caries), whereas gingival epithelial cells with the AVI/AVI genotype responded more to P. gingivalis (a pathogen involved in periodontal disease).

Previous studies have shown a protective effect against caries for those with the PAV haplotype of TAS2R38.  The previous laboratory work at University of Washington led us to believe that the AVI haplotype might be protective against periodontal disease.  We conducted a cross-sectional study at Khon Kaen University in Thailand to learn more about genetic differences in the T2R38 bitter taste receptor among Thai people.  We also examined the association of genetic differences with measures of caries (decayed-missing-filled teeth) and periodontal disease (defined as one site with probing depth greater than 5 mm).  In the study, we genotyped 250 patients seeking care at Khon Kaen University Dental Hospital.  Of those patients, 46% were PAV/PAV genotype, 42% were PAV/AVI, and 12% were AVI/AVI.  These distributions are similar to that seen in other studies of Asian populations.  As we expected based on the prior laboratory work at University of Washington, those patients with an AVI haplotype had less periodontal disease than those with the PAV/PAV genotype.  However, trends for differences in decayed-missing-filled teeth did not reach statistical significance in our study.  This study provides evidence of the importance of the T2R38 bitter taste receptor in maintaining oral health.

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