Genetic- and Lifestyle-dependent Dental Caries Defined by the Acidic Proline-rich Protein Genes PRH1 and PRH2

Abstract

Dental caries is a chronic infectious disease that affects billions of people with large individual differences in activity. We investigated whether PRH1 and PRH2 polymorphisms in saliva acidic proline-rich protein (PRP) receptors for indigenous bacteria match and predict individual differences in the development of caries. PRH1 and PRH2 variation and adhesion of indigenous and cariogenic (Streptococcus 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 children grouped into low-to-moderate and high susceptibility phenotypes for caries based on allelic PRH1, PRH2 variation. The low-to-moderate susceptibility children (P1 and P4a−) experienced caries from eating sugar or bad oral hygiene or infection by S. mutans. The high susceptibility P4a (Db, PIF, PRP12) children had more caries despite receiving extra prevention and irrespective of eating sugar or bad oral hygiene or S. mutans-infection. They instead developed 3.9-fold more caries than P1 children from plaque accumulation in general when treated with orthodontic multibrackets; and had basic PRP polymorphisms and low DMBT1-mediated S. mutans adhesion as additional susceptibility traits. The present findings thus suggest genetic autoimmune-like (P4a) and traditional life style (P1) caries, providing a rationale for individualized oral care.

Enamel and Dentin Caries Risk Factors of Adolescents in the Context of the International Caries Detection and Assessment System (ICDAS): A Longitudinal Study

“…The failure of oral hygiene in prediction among this population could due to their genetic background. Strömberg et al indicated that individuals with a specific genetic background may develop more caries from bad oral hygiene than individuals with other genetic backgrounds (54). Hence, variables such as PlI and tooth brushing frequency could still be predictable in other populations with different genetic backgrounds.…”

Nutritional impact on Immunological maturation during Childhood in relation to the Environment (NICE): a prospective birth cohort in northern Sweden

“… 17 These high-caries cases derive from an immune deficiency or carriage of high virulence strains of Streptococcus mutans , consistent with their non-responder behaviour. 18 19 By contrast, the low-to-moderate risk children develop caries as expected from eating and oral hygiene habits. 18 Therefore, the NICE study aims to evaluate the oral health of all participating children in order to better understand the link between impaired immune maturation and the risk for caries development.…”

“… 18 19 By contrast, the low-to-moderate risk children develop caries as expected from eating and oral hygiene habits. 18 Therefore, the NICE study aims to evaluate the oral health of all participating children in order to better understand the link between impaired immune maturation and the risk for caries development.…”

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

“…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.…”

“…As present etiological studies of dental caries focus on correlations between microbial load and life style habits, few studies have been done on the correlations between specific host genotypes, microbial load and caries, which is the highlight of this study by Strömberg et al (2017) . Host genotypes, microbiomes, life style, oral hygiene, and disease process may as independent influential factors have great potential to correlate with each other, contributing to the complex etiological network of dental caries.…”