Tooth mineral surfaces and Streptococcus mutans biofilms

The 'Tooth mineral surfaces and Streptococcus mutans biofilms' target represents the complex pathological interface where cariogenic bacteria, primarily Streptococcus mutans, colonize the hydroxyapatite-rich enamel of human teeth [1]. S. mutans utilizes glucosyltransferases to synthesize extracellular polysaccharides (glucans) from dietary sucrose, which facilitates firm adherence and the formation of a protective biofilm matrix [1, 3]. Within this biofilm, the bacteria ferment carbohydrates to produce organic acids, which lower the local pH and drive the dissolution of tooth mineral, a process known as demineralization [3, 4]. Therapeutic interventions targeting this system focus on reducing the bacterial load, disrupting the biofilm architecture, or altering the mineral chemistry to favor remineralization [2, 4]. Fluoride is the most prominent agent, acting by incorporating into the mineral lattice to form acid-resistant fluorapatite and interfering with bacterial metabolic enzymes [4]. Other agents, such as chlorhexidine, target the biofilm directly by disrupting bacterial cell membranes [3].

Other names

Dental plaqueCariogenic biofilmTooth-biofilm interfaceHydroxyapatite-biofilm complex

The mechanisms include the inhibition of bacterial metabolic enzymes (such as enolase) by fluoride, the disruption of microbial cell membranes by cationic agents like chlorhexidine, and the promotion of mineral remineralization through the formation of acid-resistant fluorapatite [3, 4].