Streptococcus mutans is a facultatively anaerobic, gram-positive coccus (round bacterium) commonly found in the human oral cavity and is a significant contributor to tooth decay. It is part of the "streptococci", an informal general name for all species in the genus Streptococcus. The microbe was first described by James Kilian Clarke in 1924.
This bacterium, along with the closely related species Streptococcus sobrinus, can cohabit the mouth: Both contribute to oral disease, and the expense of differentiating them in laboratory testing is often not clinically necessary. Therefore, for clinical purposes they are often considered together as a group, called the mutans streptococci. This grouping of similar bacteria with similar tropism can also be seen in the viridans streptococci, another group of Streptococcus species.
Ecology
S. mutans is naturally present in the human oral microbiota, along with at least 25 other species of oral streptococci. The taxonomy of these bacteria remains tentative. Different areas of the oral cavity present different ecological niches, and each species has specific properties for colonizing different oral sites. S. mutans is most prevalent on the pits and fissures, constituting 39% of the total streptococci in the oral cavity. Fewer S. mutans bacteria are found on the buccal surface (2–9%).
Bacterial-fungal co-coaggregation can help to increase the cariogenic potential of S. mutans. A symbiotic relationship with S. mutans and Candida albicans leads to increased glucan production and increased biofilm formation. This therefore amplifies the cariogenic effect of S. mutans.
Oral streptococci comprise both harmless and harmful bacteria. However, under special conditions commensal streptococci can become opportunistic pathogens, initiating disease and damaging the host. Imbalances in the microbial biota can initiate oral diseases.
C. albicans is an opportunistic pathogenic yeast that can be found within the oral cavity. Its presence in the biofilm promotes higher levels of S. mutans when looking at early childhood caries. It stimulates the formation of S. mutans microcolonies. This is achieved through low concentrations of cross-kingdom metabolites, such as farnesol, derived from the biofilm. It has been suggested that when both microbes are present, more biofilm matrix is produced, with a greater density. When farnesol is in high concentration, it inhibits the growth of both S. mutans and C. albicans. This decreases the biofilm pathogenesis, and therefore its caries promoting potential. This offers the potential for an anti-fungal to be used in the prevention of dental caries.
Role in disease
Tooth decay
Early colonizers of the tooth surface are mainly Neisseria spp. and streptococci, including S. mutans. They must withstand the oral cleansing forces (e.g. saliva and the tongue movements) and adhere sufficiently to the dental hard tissues. The growth and metabolism of these pioneer species changes local environmental conditions (e.g., Eh, pH, coaggregation, and substrate availability), thereby enabling more fastidious organisms to further colonize after them, forming dental plaque. Along with S. sobrinus, S. mutans plays a major role in tooth decay, metabolizing sucrose to lactic acid. The acidic environment created in the mouth by this process is what causes the highly mineralized tooth enamel to be vulnerable to decay. S. mutans is one of a few specialized organisms equipped with receptors that improve adhesion to the surface of teeth. S. mutans uses the enzyme glucansucrase to convert sucrose into a sticky, extracellular, dextran-based polysaccharide that allows them to cohere, forming plaque. S. mutans produces dextran via the enzyme dextransucrase (a hexosyltransferase) using sucrose as a substrate in the following reaction:
n sucrose → (glucose)n + n fructose
Sucrose is the only sugar that bacteria can use to form this sticky polysaccharide.
However, other sugars—glucose, fructose, lactose—can also be digested by S. mutans, but they produce lactic acid as an end product. The combination of plaque and acid leads to dental decay. Due to the role S. mutans plays in tooth decay, many attempts have been made to create a vaccine for the organism. So far, such vaccines have not been successful in humans. Recently, proteins involved in the colonization of teeth by S. mutans have been shown to produce antibodies that inhibit the cariogenic process. A molecule recently synthesized at Yale University and the University of Chile, called Keep 32, is supposed to be able to kill S. mutans. Another candidate is a peptide called C16G2, synthesised at UCLA.