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.

[3] 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.

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.

[2][11] 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 uses the enzyme glucansucrase to convert sucrose into a sticky, extracellular, dextran-based polysaccharide that allows them to cohere, forming plaque.

[13] Recently, proteins involved in the colonization of teeth by S. mutans have been shown to produce antibodies that inhibit the cariogenic process.

[16][17] Dental plaque, typically the precursor to tooth decay, contains more than 600 different microorganisms, contributing to the oral cavity's overall dynamic environment that frequently undergoes rapid changes in pH, nutrient availability, and oxygen tension.

Dental plaque and S. mutans is frequently exposed to "toxic compounds" from oral healthcare products, food additives, and tobacco.

[citation needed] While S. mutans grows in the biofilm, cells maintain a balance of metabolism that involves production and detoxification.

[citation needed] S. mutans has over time developed strategies to successfully colonize and maintain a dominant presence in the oral cavity.

In response to such changes, the bacterial community evolved with individual members and their specific functions to survive in the oral cavity.

Persistence of this acidic condition encourages the proliferation of acidogenic and aciduric bacteria as a result of their ability to survive at a low-pH environment.

[25] In young children, the pain from a carious lesion can be quite distressing and restorative treatment can cause an early dental anxiety to develop.

[27] Studies have shown a cycle to exist, whereby dentally anxious patients avoid caring for the health of their oral tissues.

These mechanisms have yet to be fully elucidated but it seems that while antigen presenting cells are activated by S. mutans in vitro, they fail to respond in vivo.

[30][31] S. mutans is implicated in the pathogenesis of certain cardiovascular diseases, and is the most prevalent bacterial species detected in extirpated heart valve tissues, as well as in atheromatous plaques, with an incidence of 68.6% and 74.1%, respectively.

[32] Streptococcus sanguinis, closely related to S. mutans and also found in the oral cavity, has been shown to cause Infective Endocarditis.

For example, serotype k initially found in blood isolates has a large reduction of glucose side chains attached to the rhamnose backbone.

The results demonstrate that the virulence of infective endocarditis caused by S. mutans is linked to the specific cell surface components present.

These include fluoride, which has a direct inhibitory effect on the enolase enzyme, as well as chlorhexidine, which works presumably by interfering with bacterial adherence.

Use of Anti Cell-Associated Glucosyltransferase (Anti-CA-gtf) Immunoglobulin Y disrupts S. mutans' ability to adhere to the teeth enamel, thus preventing it from reproducing.

Phages have shown promise in reducing S. mutans in lab settings, potentially offering a targeted approach to caries prevention without harming the mouth's natural microbiome.

[71] During its evolution, S. mutans acquired the ability to increase the amount of carbohydrates it could metabolize, and consequently more organic acid was produced as a byproduct.

[72] This is significant in the formation of dental caries because increased acidity in the oral cavity amplifies the rate of demineralization of the tooth, which leads to carious lesions.

[73] It is thought that the trait evolved in S. mutans via lateral gene transfer with another bacterial species present in the oral cavity.

As a result, S. mutans could outcompete other species, and occupy additional regions of the mouth, such as advanced dental plaques, which can be as acidic as pH 4.0.

[citation needed] In discussing the evolution of S. mutans, it is imperative to include the role humans have played and the co-evolution that has occurred between the two species.

It is widely accepted that the advent of agriculture in early human populations provided the conditions S. mutans needed to evolve into the virulent bacterium it is today.

Also, consuming more carbohydrates increased the amount of sugars available to S. mutans for metabolism and lowered the pH of the oral cavity.