Background
Dental caries is the most prevalent chronic bacterial infectious disease of the mouth and an aggravating or triggering systemic disease. As teeth decay continues to be so prevalent, dental caries is now a worldwide public health problem. It is a progressive invasive disease of the dental hard tissues caused by multiple causes: microbes, host, environment and time. The main cause of caries is adherence of oral microbes to tooth surfaces as biofilms that generate and adapt to acid. The ecological plaque hypothesis suggests that dental plaque is a dynamically evolving system, and caries develops when the microbial ecological balance in plaque is disrupted. This disruption leads to a shift toward acid-producing and acid-tolerating bacteria, resulting in decreased environmental pH, reduced microbial diversity, and weakened antagonistic effects. Streptococcus mutans (an acid-generating and acid-tolerant organism) is capable of quickly dissolving carbohydrates, and is a big manufacturer of extracellular matrix. It is involved in the onset and progression of caries in the teeth, and it is the main cariogenic bacteria.
Initial adhesion to host surfaces by Streptococcus mutans is a prime step in biofilm formation. Bacterial adhesion has two types — reversible and irreversible adhesion. Unreversible adhesion is mainly based on non-specific interactions such as van der Waals interactions, electrostatic (double layer) interactions, hydrophobic and hydrophilic interactions, and osmotic influences. During the irreversible adhesion phase, surface adhesion proteins secreted by bacteria, such as Ag I/II, SpaP, and SrtA, specifically recognize glycoproteins and glycolipids on the bacterial surface, leading to specific adhesion involving pili and flagella. As irreversible forces gradually strengthen, bacteria sense signal molecules and activate biofilm regulatory gene expression through signal transduction pathways. This means bacteria can change their physiological characteristics quickly in response to environmental stimuli.
Once adhesive, bacteria synthesise the extracellular matrix (EPS, water-insoluble exopolysaccharides, proteins) by enzymes such as alamine racemase (Alr), adhesins and glycosyltransferases. EPS serves as the primary component of biofilms. Proteins in biofilms can be categorized into surface matrix proteins and secreted extracellular protein components. Surface matrix proteins include bacterial surface appendages such as flagella, type IV pili, and functional amyloid proteins. These surface appendages regulate bacterial adhesion, mechanical stability, and quorum sensing by influencing bacterial movement and surface attachment. The extracellular proteins include the glucan binding protein (Gbp) family, which regulates biofilm elasticity. S. mutans Gbp proteins control bacterial adhesion forces and promote biofilm elasticity. Proteinase K can degrade Gbp proteins, disrupting the three-dimensional structure of biofilms. The combination of EPS and extracellular protein matrix provides a scaffold for biofilm growth and maintains structural stability.
Figure 1. Streptococcus mutans virulence is related to sugars
(Source: Kawada-Matsuo M, et al. 2016)
Alternative Names
Anti-Streptococcus mutans Polyclonal antibody
References
- 1. Baker JL, et al. Acid-adaptive mechanisms of Streptococcus mutans-the more we know, the more we don't. Mol Oral Microbiol. 2017 Apr;32(2):107-117.
- 2. Kawada-Matsuo M, et al. Sugar Allocation to Metabolic Pathways is Tightly Regulated and Affects the Virulence of Streptococcus mutans. Genes (Basel). 2016 Dec 28;8(1):11.