Abstract

Dental caries is one of the most prevalent and costly biofilm-associated infectious diseases affecting most of the world’s population. In particular, dental caries is driven by dysbiosis of the dental biofilm adherent to the enamel surface. Specific types of acid-producing bacteria, especially Streptococcus mutans, colonize the dental surface and cause damage to the hard tooth structure in the presence of fermentable carbohydrates. Streptococcus mutans has been established as the major cariogenic pathogen responsible for human dental caries, with a high ability to form biofilms. The exopolysaccharide (EPS) matrix, mainly contributed by S. mutans, has been considered as a virulence determinant of cariogenic biofilm. As EPS is an important virulence factor, targeting EPS metabolism could be useful in preventing cariogenic biofilm formation. This review summarizes plausible strategies targeting S. mutans biofilms by degrading EPS structure, inhibiting EPS production, and disturbing the EPS metabolism-related gene expression and regulatory systems.

摘要

龋齿是影响世界大多数人口的最普遍和最昂贵的生物膜相关传染病之一。特别是，龋齿是由附着在牙釉质表面的牙齿生物膜的生态失调引起的。特定类型的产酸细菌，尤其是变形链球菌，在可发酵碳水化合物存在的情况下，定植于牙齿表面并对坚硬的牙齿结构造成损害。变形链球菌已被确定为导致人类龋齿的主要致龋病原体，具有形成生物膜的高能力。胞外多糖 (EPS) 基质，主要由变形链球菌贡献，已被认为是致龋生物膜的毒力决定因素。由于 EPS 是一种重要的毒力因子，靶向 EPS 代谢可能有助于防止生龋生物膜的形成。本综述总结了通过降解 EPS 结构、抑制 EPS 产生和扰乱 EPS 代谢相关基因表达和调节系统来针对变形链球菌生物膜的合理策略。