Streptococcus mutans (S. mutans) is generally regarded as a major contributor to dental caries because of its ability to synthesize extracellular polysaccharides (EPS) that aid in the formation of plaque biofilm. The VicRKX system of S. mutans plays an important role in biofilm formation. The aim of this study was to investigate the effects of vicK gene on specific characteristics of EPS in S. mutans biofilm. We constructed single-species biofilms formed by different mutants of vicK gene. Production and distribution of EPS were detected through atomic force microscopy, scanning electron microscopy and confocal laser scanning microscopy. Microcosmic structures of EPS were analyzed by gel permeation chromatography and gas chromatography-mass spectrometry. Cariogenicity of the vicK mutant was assessed in a specific pathogen-free rat model. Transcriptional levels of cariogenicity-associated genes were confirmed by quantitative real-time polymerase chain reaction. The results showed that deletion of vicK gene suppressed biofilm formation as well as EPS production, and EPS were synthesized mostly around the cells. Molecular weight and monosaccharide components underwent evident alterations. Biofilms formed in vivo were sparse and contributed a decreased degree of caries. Moreover, expressional levels of genes related to EPS synthesis were down-regulated, except for gtfB. Our report demonstrates that vicK gene enhances biofilm formation and subsequent caries development. And this may due to its regulations on EPS metabolism, like synthesis or microcosmic features of EPS. This study suggests that vicK gene and EPS can be considered as promising targets to modulate dental caries.

变形链球菌( S. mutans ) 通常被认为是导致龋齿的主要原因，因为它能够合成有助于牙菌斑生物膜形成的细胞外多糖 (EPS)。变形链球菌的 VicRKX 系统在生物膜形成中起着重要作用。本研究的目的是研究vicK基因对变形链球菌生物膜中 EPS 特定特征的影响。我们构建了由vicK的不同突变体形成的单一物种生物膜基因。通过原子力显微镜、扫描电子显微镜和共聚焦激光扫描显微镜检测 EPS 的产生和分布。通过凝胶渗透色谱和气相色谱-质谱法分析了 EPS 的微观结构。在特定的无病原体大鼠模型中评估了vicK突变体的致龋性。致龋性相关基因的转录水平通过定量实时聚合酶链反应确认。结果表明，删除vicK基因抑制生物膜的形成以及 EPS 的产生，EPS 主要在细胞周围合成。分子量和单糖成分发生了明显的变化。体内形成的生物膜稀疏，有助于降低龋齿程度。此外，除gtfB外，与 EPS 合成相关的基因表达水平下调。我们的报告表明vicK基因增强了生物膜的形成和随后的龋齿发展。这可能是由于其对EPS代谢的调节，如EPS的合成或微观特征。这项研究表明，vicK基因和 EPS 可被视为调节龋齿的有希望的目标。