Streptococcus mutans
Streptococcus mutans is a facultatively anaerobic, gram-positive coccus commonly found in the human oral cavity and is a significant contributor to tooth decay.
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 – of which Streptococcus mutans is itself also a member.
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.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 and adhere sufficiently to the dental hard tissues. The growth and metabolism of these pioneer species changes local environmental conditions, 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 glucosyltransferase enzymes to convert the glucosyl moiety of sucrose into a sticky, extracellular, dextran-like polysaccharide that allows them to cohere, forming plaque: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.
It is believed that Streptococcus mutans acquired the gene that enables it to produce biofilms through horizontal gene transfer with other lactic acid bacterial species, such as Lactobacillus.
Life in the oral cavity
Surviving in the oral cavity, S. mutans is the primary causal agent and the pathogenic species responsible for dental caries specifically in the initiation and development stages.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 adheres to the teeth and consists of bacterial cells, while plaque is the biofilm on the surfaces of the teeth. Dental plaque and S. mutans is frequently exposed to "toxic compounds" from oral healthcare products, food additives, and tobacco.
While S. mutans grows in the biofilm, cells maintain a balance of metabolism that involves production and detoxification. Biofilm is an aggregate of microorganisms in which cells adhere to each other or a surface. Bacteria in the biofilm community can actually generate various toxic compounds that interfere with the growth of other competing bacteria.
S. mutans has over time developed strategies to successfully colonize and maintain a dominant presence in the oral cavity. The oral biofilm is continuously challenged by changes in the environmental conditions. In response to such changes, the bacterial community evolved with individual members and their specific functions to survive in the oral cavity. S. mutans has been able to evolve from nutrition-limiting conditions to protect itself in extreme conditions. Streptococci represent 20% of the oral bacteria and actually determine the development of the biofilms. Although S. mutans can be antagonized by pioneer colonizers, once they become dominant in oral biofilms, dental caries can develop and thrive.
Cariogenic potential
The causative agent of dental caries is associated with its ability to metabolize various sugars, form a robust biofilm, produce an abundant amount of lactic acid, and thrive in the acid environment it generates. A study into pH of plaque said that the critical pH for increased demineralisation of dental hard tissues is 5.5. The Stephan curve illustrates how quickly the plaque pH can fall below 5.5 after a snack or meal.Dental caries is a dental biofilm-related oral disease associated with increased consumption of dietary sugar and fermentable carbohydrates. When dental biofilms remain on tooth surfaces, along with frequent exposure to sugars, acidogenic bacteria will metabolize the sugars to organic acids. Untreated dental caries is the most common disease affecting humans worldwide . 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. The low-pH environment in the biofilm matrix erodes the surface of the teeth and begins the "initiation" of the dental caries. Streptococcus mutans is a bacterium which is prevalent within the oral environment and is thought to be a vital microorganism that contributes to this initiation. S. mutans thrives in acidic conditions, becoming the main bacterium in cultures with permanently reduced pH . If the adherence of S. mutans to the surface of teeth or the physiological ability of S. mutans in dental biofilms can be reduced or eliminated, the acidification potential of dental biofilms and later cavity formations can be decreased.
Ideally, the early various lesion is prevented via treatment from developing beyond the white spot stage. Once beyond here, the enamel surface is irreversibly damaged and cannot be biologically repaired. In young children, the pain from a carious lesion can be quite distressing and restorative treatment can cause an early dental anxiety to develop. Dental anxiety has knock-on effects for both dental professionals and patients. Treatment planning and therefore treatment success can be compromised. The dental staff can become stressed and frustrated when working with anxious children. This can compromise their relationship with the child and their parents. Studies have shown a cycle to exist, whereby dentally anxious patients avoid caring for the health of their oral tissues. They can sometimes avoid oral hygiene and will try to avoid seeking dental care until the pain is unbearable.
Susceptibility to disease varies between individuals and immunological mechanisms have been proposed to confer protection or susceptibility to the disease. 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. Immunological tolerance to S. mutans at the mucosal surface may make individuals more prone to colonisation with S. mutans'' and therefore increase susceptibility to dental caries.