Alli will be heading off to dental school soon enough. One way she has made a difference at our college is working as a student mentor. I know Alli has lots of valuable student insight to share, and I'm sure her mentees would agree. Last year, Alli did an experiment on whether the use of mouthwash changed the microbiota of our mouth and had some interesting findings. If you get the chance, ask her about it!
Chances are, you have probably had a cavity at some point in your life. Dental caries [cavities] are one of the most prevalent non-contagious infectious diseases in humans. There are many options to help prevent cavities, such as flossing, brushing one’s teeth twice a day, mouthwash, regular six-month checkups with the dentist, and many more. However, many people still end up with cavities. How could it be that we have so many tools to help prevent cavities, and yet it is still the most prevalent non-contagious infectious disease in humans? Perhaps genetics could play a role.
The prevalence of caries is known to be influenced by numerous environmental factors, including the normal bacteria living in one’s oral cavity (microbial flora), how much saliva one produces, and what it is made of, fluoride exposure, and many other environmental factors. As our knowledge base and resources expand, more studies are beginning to investigate the role that genetics plays in caries.
In twin studies conducted in 2005 in the Journal of Dental Research, a genetic component in sugar preference has been proposed to play a role in caries susceptibility. In experiments with mice, a 2004 study by the Department of Pediatric Dentistry in Japan showed that chromosomal loci, possibly correlated with salivary composition and immunity are associated with caries susceptibility. The impact of genetic factors has been acknowledged for a long time, with heritability being estimated to be between 40% and 60%.
A study completed in 2012 by Graduate School of Public Health investigated the role of genetics on two classes of tooth surfaces, pit and fissure surfaces (PFS), which are in the grooves of the teeth and smooth surfaces (SMS), which are the smooth edges or sides of the teeth, in more than 2,600 subjects from 740 families. The genetic correlations between the two surface type caries were calculated to assess the degree to which traits occur due to common genetic effects such as gene sequences, mutations, proteins, and pathways in the body.
To test whether caries and genetics are correlated or just occur due to random chance, a p-value was used, which is a value based on statistical calculations. If the p-value is < 0.01, the data is considered significant, meaning that something other than random chance is playing a role in caries formation. Overall, the heritability of caries scores were similar for PFS (h2 = 19–53%; p < 0.001) and SMS (h2 = 17–42%; p < 0.001). Here, note that the p-value fits the criteria listed above, so this data suggests that genetics is playing a role in caries formation for both smooth surfaces (SMS) as well as pit and fissure surfaces (PFS). Genetic correlation for the primary dentition dfs (decay + filled surfaces) was significantly less than 100% (p < 0.001), indicating that genetic factors may exert differential effects on caries risk in PFS versus SMS in the primary dentition. Simply put, this 2012 study showed that based on statistical calculations, genetics are playing various roles in caries formation in both smooth surfaces and pit and fissure surfaces.
A study completed in London in 2012 conducted the first genome-wide association study to identify genes affecting susceptibility to caries in adults using over 7,000 participants. For each subject, dental caries were assessed and genetic markers (single nucleotide polymorphisms, SNPs) were genotyped or imputed across the entire genome.
The researchers performed three meta-analyses to combine results for: (i) the comparatively younger, Appalachian cohorts (N = 1483) with well-assessed caries phenotype [physical characteristics/appearances] (ii) the comparatively older, non-Appalachian cohorts (N = 5960) with inferior caries phenotypes, and (iii) all five cohorts (N = 7443). The results identified several suggestive loci (P-value ≤ 10E-05) within or near genes with plausible biological roles for dental caries, including RPS6KA2 and PTK2B, involved in p38-dependent MAPK signaling, and RHOU and FZD1, involved in the Wnt signaling cascade, both of which are signaling pathways or mechanisms known to be involved in dental caries formation. These results provided useful data for future, specific research to gain a better understanding of cariogenesis to improve prevention/treatment for caries.
These studies support the notion that individuals can be genetically predisposed to caries. Future research would include focusing on specific genes that are the main causation of caries and then developing vaccines or treatments targeted to those specific genes. The best prevention mechanisms for caries include good oral hygiene—brushing and flossing at least twice a day with a fluoride-containing toothpaste—and maintaining a healthy, balanced diet while avoiding sticky, sugary foods that tend to stick on teeth.
For treatment, individuals must visit their dentist regularly for professional cleanings and oral exams to maintain good oral health and receive treatment for existing caries. Check out the infographic below for use as a quick reference guide. Stay healthy, and remember, keep on flossing!
Thanks for reading!
Figure 1: Caries Infographic. To be used as a quick reference guide to the information provided in the blog post as well as treatment and prevention options for dental caries.
Great blog post Alli, and thanks for the reminder to book my dental checkup!