streptococcus mutans streptococcus mutans 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" (plural, non-italic lowercase), an informal general name for all species in the genus streptococcus. the microbe was first described by james kilian clarke in 1924. streptococcus mutans stain of s. mutans in thioglycollate broth culture. scientific classification domain: bacteria phylum: bacillota class: bacilli order: lactobacillales family: streptococcaceae genus: streptococcus species: s. mutans binomial name streptococcus mutansclarke 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 (plural, non-italic due to its being an informal group name). 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. 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 (tooth decay or cavities) 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 (enamel and dentine) 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 (members of dental biofilms) 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 (acidogenity and aciduricity) 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, we can stop the early various lesion 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. in children s. mutans is often acquired in the oral cavity subsequent to tooth eruption, but has also been detected in the oral cavity of predentate children. it is generally, but not exclusively, transmitted via vertical transmission from caregiver (generally the mother) to child. this can also commonly happen when the parent puts their lips to the child's bottle to taste it, or to clean the child's pacifier, then puts it into the child's mouth. cardiovascular disease 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. streptococcus sanguinis, closely related to s. mutans and also found in the oral cavity, has been shown to cause infective endocarditis. streptococcus mutans has been associated with bacteraemia and infective endocarditis (ie). ie is divided into acute and subacute forms, and the bacterium is isolated in subacute cases. the common symptoms are: fever, chills, sweats, anorexia, weight loss, and malaise. s. mutans has been classified into four serotypes; c, e, f, and k. the classification of the serotypes is devised from the chemical composition of the serotype-specific rhamnose-glucose polymers. for example, serotype k initially found in blood isolates has a large reduction of glucose side chains attached to the rhamnose backbone. s. mutans has the following surface protein antigens: glucosyltransferases, protein antigen and glucan-binding proteins. if these surface protein antigens are not present, then the bacteria is a protein antigen-defective mutant with the least susceptibility to phagocytosis therefore causing the least harm to cells. furthermore, rat experiments showed that infection with such defective streptococcus mutants (s. mutans strains without glucosyltransferases isolated from a destroyed heart valve of an infective endocarditis patient) resulted in a longer duration of bacteraemia. the results demonstrate that the virulence of infective endocarditis caused by s. mutans is linked to the specific cell surface components present. in addition, s. mutans dna has been found in cardiovascular specimens at a higher ratio than other periodontal bacteria. this highlights its possible involvement in a variety of types of cardiovascular diseases, not just confined to bacteraemia and infective endocarditis. prevention and treatment practice of good oral hygiene including daily brushing, flossing and the use of appropriate mouthwash can significantly reduce the number of oral bacteria, including s. mutans and inhibit their proliferation. s. mutans often live in dental plaque, hence mechanical removal of plaque is an effective way of getting rid of them. the best toothbrushing technique to reduce plaque build up, decreasing caries risk, is the modified bass technique. brushing twice daily can help decrease the caries risk. however, there are some remedies used in the treatment of oral bacterial infection, in conjunction with mechanical cleaning. 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. furthermore, fluoride ions can be detrimental to bacterial cell metabolism. fluoride directly inhibits glycolytic enzymes and h+atpases. fluoride ions also lower the ph of the cytoplasm. this means there will be