Vitamin D as a candidate host susceptibility factor in sugar-driven oral dysbiosis

Sugar-sweetened beverages (SSBs) represent a modifiable dietary factor that promotes oral dysbiosis by supplying fermentable sugars and generating low-pH conditions that favor acidogenic and acid-tolerant biofilms. Vitamin D plays a biologically significant role in oral host defense through regulation of the epithelial barrier, induction of antimicrobial peptides, immune modulation, inflammatory control, and mineral metabolism. However, the extent to which vitamin D modifies the SSB -oral microbiome -disease pathway in humans remains unclear.

This narrative-conceptual review employed structured evidence mapping. Relevant literature was identified through PubMed/MEDLINE, Scopus, and Web of Science Core Collection, with additional sources obtained via citation and hand searching. Evidence was categorized into predefined domains: SSB/free-sugar exposure and oral outcomes; sugar exposure and oral microbiome characteristics; vitamin D status and oral health outcomes; vitamin D-related host-defense mechanisms; vitamin D and human oral microbiome evidence; and proposed SSB × vitamin D interaction pathways. A PRISMA-ScR-style flow diagram documented the process of evidence identification and selection, resulting in the inclusion of 90 sources. Evidence interpretation followed a tiered approach.

The most robust evidence indicates an association between frequent SSB/free-sugar exposure and caries-related outcomes. Human microbiome studies suggest that high sugar intake may be linked to dysbiotic shifts, although results differ depending on sampling site, study design, and analytical methods. Evidence connecting vitamin D to caries and periodontal outcomes is suggestive but remains heterogeneous. Direct human evidence relating 25(OH)D status to oral microbiome trajectories or SSB × vitamin D interaction models is limited. Mechanistic studies support biological plausibility but do not establish causality in humans.

Vitamin D should be considered a candidate susceptibility factor and a potential proxy marker for broader behavioral, socioeconomic, metabolic, and inflammatory risk environments. Future longitudinal studies are needed to jointly assess SSB exposure, standardized 25(OH)D levels, plaque-site microbiome trajectories, confounders, and incident oral outcomes. Current practice recommendations continue to emphasize reducing SSB consumption, encouraging non-sugary alternatives, promoting fluoride use, maintaining oral hygiene, and supporting preventive dental care.