Abstract
Streptococcus mutans is a well-known cause of dental caries, due to its acidogenicity, aciduricity, and ability to synthesize exopolysaccharides in dental plaques. Intriguingly, not all children who carry S. mutans manifest caries, even with similar characteristics in oral hygiene, diet, and other environmental factors. This phenomenon suggests that host susceptibility potentially plays a role in the development of dental caries; however, the association between host genetics, S. mutans, and dental caries remains unclear. Therefore, this study examined the influence of host gene-by-S. mutans interaction on dental caries. Genome-wide association analyses were conducted in 709 US children (<13 years old), using the dbGap database acquired from the center for oral health research in appalachia (COHRA) and the Iowa Head Start programmes (GEIRS). A generalized estimating equation was used to examine the gene-by-S. mutans interaction effects on the outcomes (decayed and missing/filled primary teeth due to caries). Sequentially, the COHRA and GEIRS data were used to identify potential interactions and replicate the findings. Three loci at the genes interleukin 32 (IL32), galactokinase 2 (GALK2), and CUGBP, Elav-like family member 4 (CELF4) were linked to S. mutans carriage, and there was a severity of caries at a suggestive significance level among COHRA children (P < 9 × 10−5), and at a nominal significance level among GEIRS children (P = 0.047–0.001). The genetic risk score that combined the three loci also significantly interacted with S. mutans (P < 0.000 1). Functional analyses indicated that the identified genes are involved in the host immune response, galactose carbohydrate metabolism, and food-rewarding system, which could potentially be used to identify children at high risk for caries and to develop personalized caries prevention strategies.
Highlights
Largely preventable, dental caries remains the single most common chronic childhood disease, with nearly 1.8 billion new cases per year globally.[1,2,3] Dental caries is a chronic infectious disease initiated from the virulent dental biofilms/plaque formed on tooth surfaces.[4]
Studies have identified a group of children who are colonized by S. mutans but do not manifest the disease, even with similar social–demographic–hygiene behavior characteristics compared with those of their counterparts.[12]
Participants’ characteristics Genome-wide association analyses were conducted in 709 US children (
Summary
Dental caries remains the single most common chronic childhood disease, with nearly 1.8 billion new cases per year globally.[1,2,3] Dental caries is a chronic infectious disease initiated from the virulent dental biofilms/plaque formed on tooth surfaces.[4]. Traditional microbial risk markers for caries include Streptococcus mutans, a well-known culprit for dental caries, due to its acidogenicity, aciduricity, and capability of synthesizing dental plaque extracellular matrix.[7,8,9,10,11] In theory, higher S. mutans carriage indicates higher caries risk. Studies have identified a group of children who are colonized by S. mutans but do not manifest the disease, even with similar social–demographic–hygiene behavior characteristics compared with those of their counterparts.[12] This phenomenon suggests that host susceptibility potentially plays a role in modulating the risk of S. mutans on the development of dental caries. Elucidating the interaction between host susceptibility, S. mutans carriage and their impact on caries onset could help identify high-risk child populations, and develop personalized precision dental caries prevention strategies
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