Gene Phenotypes: The Role Can't Be Ignored in Etiology of Dental Caries

https://doi.org/10.1016/j.ebiom.2017.12.009 2352-3964/© 2017 The Authors. Published by Elsevier B.V Etiology of dental caries is crucial for disease prevention and cure. The traditional concept of dental caries is an imbalance in saliva defense, microbial load and life style habits like sugar consumption. Distinctions have been revealed between dental caries and caries-free microbiomes in terms of microbial community structure by DNA sequencing to elucidate andmonitor supragingival plaque bacterial diversity in the primary dentition of young children (Aas et al., 2008; Xu et al., 2014; Teng et al., 2015). Xu et al. have found that caries-related genera included Streptococcus and Veillonella; while Leptotrichia, Fusobacterium, and Porphyromonas were more related to the caries-free samples. Interactions between the microbiome and sugar intake frequency were also found (Moynihan and Kelly, 2014; Tian et al., 2015). The bacterial community richness, diversity, structure, and relative abundance of bacterial taxa were significantly different between different levels of sugar consumption groups, and patients in the dental caries relapse group had higher sugar intake frequencies than those in the relapse-free group during follow-up. Also, distinct adhesion biotypes of Streptococcus mutanswith increased cariogenicity were defined in a sample of Swedish adolescents (Esberg et al., 2017). Thus, both microbiome and clonal bacterial structures seems to be involved in plaque cariogenicity. In EBioMedicine, Strömberg et al. combined specific human genotypes with susceptibility of dental caries, revealing the evidence of variation in specific human genes (Strömberg et al., 2017). PRH1 and PRH2 variation and adhesion of indigenous and cariogenic (S. mutans) model bacteria were measured in 452 12-year-old Swedish children along with traditional risk factors and related to caries at baseline and after 5-years. The childrenwere grouped into low-to-moderate and high susceptibility phenotypes for caries based on allelic PRH1, PRH2 variation. The high susceptibility phenotype (Db, PIF, PRP12) suggests an autoimmune-like condition. Children had more caries despite receiving extra prevention and irrespective of eating sugar or bad oral hygiene or S. mutans infection, developing 3.9-fold more caries than P1 children from plaque accumulation in general when treated with orthodontic