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Streptococcus mutans

Streptococcus mutans is a Gram-positive, facultative anaerobic bacterium that serves as a primary etiological agent of dental caries, the most common chronic infectious disease affecting humans worldwide.^[1] It predominantly inhabits the human oral cavity, where it colonizes tooth surfaces and integrates into multispecies biofilms known as dental plaque.^[1] Classified within the phylum Firmicutes and genus Streptococcus, it is serologically grouped into types c, e, f, and k based on cell-surface polysaccharides, with serotype c being the most prevalent (approximately 75% of isolates).^[1] The bacterium's genome typically spans about 2.0 megabases, encoding around 2,000 genes that enable its adaptation to the oral environment.^[1] Key virulence factors of S. mutans include its acidogenic and aciduric properties, allowing it to metabolize dietary carbohydrates—particularly sucrose—into lactic acid, which lowers the local pH and promotes enamel demineralization.^[1] Through glucosyltransferases, it synthesizes extracellular polysaccharides that facilitate robust biofilm formation, enhancing its persistence and dominance in plaque communities.^[1] Additionally, S. mutans exhibits stress tolerance to acidic, oxidative, and osmotic conditions, as well as quorum sensing mechanisms that regulate genetic competence and biofilm dynamics.^[1] Beyond dental caries, emerging research highlights S. mutans's potential contributions to systemic health issues, including infective endocarditis, cerebral microbleeds, IgA nephropathy, and cardiovascular diseases, particularly through strains expressing adhesins like Cnm that enable bloodstream invasion and tissue adherence.^[2] For instance, Cnm-positive isolates, found in about 15% of clinical samples, have been associated with increased risks of hemorrhagic stroke and renal pathology via proinflammatory pathways involving cytokines such as TNF-α and IL-6.^[2] These findings underscore S. mutans as a multifaceted pathogen with implications extending from oral to extraintestinal health.^[2]

Taxonomy and Characteristics

Classification and Etymology

Streptococcus mutans is a species of bacterium classified within the domain Bacteria, phylum Bacillota, class Bacilli, order Lactobacillales, family Streptococcaceae, genus Streptococcus, and species mutans.^[3] The species was first described in 1924 by James Kilian Clarke, who isolated it from human carious dentine and identified it as a causative agent in dental caries.^[4] ^[1] The genus name Streptococcus derives from the Greek words streptos (twisted or pliant) and kokkos (berry or grain), referring to the chain-forming, spherical morphology of the bacteria observed under microscopy.^[5] The specific epithet mutans comes from the Latin participle mutans (changing), chosen by Clarke due to the pleomorphic, oval-shaped forms he observed, which he interpreted as mutant variants of typical streptococci.^[6] ^[1] Strains of S. mutans are further classified into serotypes based on the composition of cell wall-associated polysaccharides, primarily rhamnose-glucose polymers, with the four recognized serotypes being c, e, f, and k; serotype c is the most prevalent in human isolates associated with caries.^[7] ^[8]

Morphology and Physiology

Streptococcus mutans is a Gram-positive coccus characterized by its spherical shape, with cells typically measuring 0.5 to 0.75 μm in diameter, and commonly arranged in pairs (diplococci) or short chains.^[9] In the presence of sucrose, cells may elongate into short rods measuring 0.5 to 1.0 μm in length, while longer chains form in broth cultures.^[9] As a member of the family Streptococcaceae, it exhibits these morphological traits that facilitate its identification under microscopic examination.^[1] This bacterium is a facultative anaerobe, capable of growth in both aerobic and anaerobic conditions, with optimal proliferation occurring at 37°C and in atmospheres enriched with 5-10% CO₂.^[10] Growth is favored at pH levels ranging from 5 to 7, reflecting its adaptation to the mildly acidic oral environment, though it demonstrates tolerance to lower pH values during metabolic activity.^[11] Metabolically, S. mutans relies on glycolysis for energy production as a lactic acid bacterium, fermenting carbohydrates such as glucose, fructose, and sucrose through homolactic fermentation.^[1] This process yields primarily L-lactic acid, accounting for approximately 90% of the end products under anaerobic conditions, with minor amounts of other acids like acetate and formate.^[12] Biochemically, S. mutans is catalase-negative, which contributes to its sensitivity to oxidative stress, and it is resistant to optochin while testing negative for bile-esculin hydrolysis, aiding in its differentiation from other streptococcal species.^[13] Under specific environmental conditions, it produces low levels of hydrogen peroxide via NADH oxidase activity and bacteriocins known as mutacins, which serve as antimicrobial agents against competing microbes.^[14]^[15]

Ecology and Habitat

Oral Cavity Residence

Streptococcus mutans primarily inhabits the human oral cavity, where it resides in dental plaque biofilms formed on tooth surfaces, particularly in pits, fissures, and approximal sites.^[1] These biofilms represent the bacterium's natural niche, enabling persistent colonization on enamel.^[16] The prevalence of S. mutans in dental plaque is notably high among caries-active individuals. Colonization typically occurs early in life, often within months after the eruption of primary teeth, establishing a foundation for long-term presence in the oral microbiome.^[17] S. mutans forms robust biofilms, known as dental plaque, through sucrose-dependent adhesion to enamel surfaces. This process involves the secretion of glucosyltransferases (Gtfs) that polymerize sucrose into adhesive glucans, creating a structural matrix that anchors the bacterium and facilitates accumulation.^[1] Transmission of S. mutans occurs mainly via vertical routes from mother to child during infancy, often through close contact and saliva sharing, with additional horizontal spread possible via saliva exchange among individuals.^[18] The bacterium preferentially occupies niches within plaque that feature low-pH microenvironments, which arise from the metabolism of fermentable sugars. As a facultative anaerobe, S. mutans adapts to the fluctuating oxygen conditions in these oral biofilms while leveraging its aciduricity to dominate such acidic habitats.^[1]

Microbial Interactions

Streptococcus mutans engages in complex interactions with other oral microorganisms, influencing biofilm dynamics and community structure within the dental plaque. A notable synergy occurs with Candida albicans, where S. mutans extracellular membrane vesicles (EMVs) promote cross-kingdom biofilm formation by regulating ubiquitin modification in C. albicans. Specifically, S. mutans EMVs modulate the ubiquitination of superoxide dismutase 3 (SOD3) in C. albicans, leading to reduced reactive oxygen species (ROS) levels and enhanced fungal growth and virulence.^[19] This interaction facilitates denser dual-species biofilms, as S. mutans MVs carrying glucosyltransferases stimulate exopolysaccharide production that augments C. albicans adhesion and hyphal development.^[20] In contrast, S. mutans exhibits competitive antagonism against commensal streptococci, such as Streptococcus sanguinis, primarily through resource competition for adhesion sites on tooth surfaces and the production of bacteriocins known as mutacins. Mutacins I, II, III, and IV, along with others like mutacin K8 and Smb, inhibit the growth of S. sanguinis by disrupting cell membranes and metabolic processes, allowing S. mutans to dominate early plaque formation.^[21]^[22] This competition is exacerbated in sucrose-rich environments, where S. mutans outcompetes S. sanguinis for binding to salivary pellicle components, thereby shifting the microbial balance toward cariogenic species.^[23] S. mutans also participates in co-aggregation with other bacteria, enhancing plaque complexity and stability. It forms physical associations with Actinomyces naeslundii, where cell surface receptors mediate adherence that supports multilayered biofilm architecture in mixed cultures.^[24] Similarly, co-culturing with Veillonella parvula or Veillonella dispar results in increased sucrose-dependent biofilm biomass, up to 150% greater than monocultures, due to metabolic exchanges like lactate utilization by Veillonella that promotes S. mutans proliferation. These interactions contribute to heterogeneous plaque communities.^[25] Recent studies from 2024 and 2025 highlight S. mutans's role in polymicrobial communities driving caries progression, where interspecies synergies amplify virulence in mixed biofilms. For instance, systematic reviews confirm that S. mutans-Veillonella interactions enhance acid production and biofilm resilience, correlating with higher caries risk in clinical samples.^[26] These findings emphasize how S. mutans interactions foster community-level adaptations that sustain cariogenic environments.^[27]

Pathogenesis

Dental Caries Mechanisms

Streptococcus mutans initiates dental caries by adhering to the saliva-coated enamel surface of teeth, primarily through its surface antigen I/II (Ag I/II) protein, a multifunctional adhesin that binds to salivary glycoproteins such as amylase and mucins.^[28] This adhesion is crucial for colonization, as mutants lacking Ag I/II exhibit significantly reduced binding to experimental salivary pellicles under flow conditions, mimicking oral shear forces.^[29] Once attached, S. mutans forms a biofilm, leveraging its ability to metabolize dietary sucrose via extracellular enzymes. Sucrose metabolism by S. mutans drives biofilm matrix formation through glucosyltransferases (Gtfs), including GtfB, GtfC, and GtfD, which cleave sucrose to synthesize water-insoluble and soluble glucans rich in α-1,3 and α-1,6 linkages.^[30] GtfB primarily produces insoluble glucans with mainly α-1,3 linkages that anchor cells to surfaces and promote adherence, while GtfD yields soluble glucans with α-1,6 linkages that act as primers and energy reserves; GtfC produces both insoluble and soluble forms, enhancing biofilm architecture and accumulation.^[31] Fructosyltransferases further contribute by generating fructans such as levans (β-2,6-linked polymers) from sucrose, which support biofilm stability.^[1] Within this biofilm, S. mutans exhibits acidogenesis by fermenting available sugars, predominantly to lactic acid, rapidly lowering the local pH below 5.5—the critical threshold for enamel demineralization.^[32] This acidification dissolves hydroxyapatite crystals in enamel, represented as \ce{Ca10(PO4)6(OH)2}, releasing calcium and phosphate ions and initiating subsurface lesions.^[33] The process is exacerbated by frequent sugar exposure, as S. mutans efficiently converts carbohydrates via glycolysis, favoring the lactate dehydrogenase pathway to produce lactic acid as the primary end product.^[34] To persist in this acidic environment, S. mutans demonstrates aciduricity, tolerating pH as low as 4.5 through mechanisms such as the F-ATPase, which extrudes protons using ATP hydrolysis to maintain cytoplasmic pH homeostasis.^[35] The F-ATPase operon is upregulated under acidic conditions, with its lower pH optimum enabling survival compared to less acid-tolerant streptococci.^[36] Additionally, stress response genes, including those encoding chaperones like GroEL and DnaK, protect proteins from denaturation, further enhancing acid adaptation.^[32] In children, S. mutans colonization poses a heightened risk for early childhood caries (ECC), particularly with frequent sugar consumption that fuels acid production and biofilm growth.^[37] Maternal transmission is a key factor, as vertical transfer of S. mutans occurs through saliva during close contact, such as kissing or sharing utensils, with higher maternal caries experience correlating to earlier and denser child colonization.^[38] This early establishment, often by age 2-3, amplifies caries risk when combined with dietary sugars, leading to rapid enamel breakdown in primary teeth.^[39]

Virulence Factors

Streptococcus mutans employs several key virulence factors that contribute to its pathogenicity in the oral cavity and beyond. These include surface adhesins for host tissue attachment, regulators of biofilm formation, genes enhancing acid tolerance, and bacteriocins for interspecies competition. These molecular elements enable the bacterium to colonize surfaces, withstand environmental stresses, and outcompete other microbes, thereby promoting dental caries and potential systemic infections.^[1] Surface adhesins play a critical role in initial attachment and invasion. The SpaP protein, also known as antigen I/II (Ag I/II), facilitates binding to salivary components, particularly glycoprotein-340 in the salivary pellicle on tooth surfaces, promoting adherence and coaggregation with other oral bacteria. SpaP's N-terminal region interacts specifically with salivary agglutinin, enhancing S. mutans colonization of the oral environment. Additionally, collagen-binding proteins such as Cnm enable adherence to extracellular matrix components like collagen types I-IV and laminin, supporting invasion of host tissues and contributing to systemic dissemination, including associations with cardiovascular and renal complications. Cnm-positive strains exhibit increased endothelial cell invasion, facilitating spread from the oral cavity.^[40]^[41]^[42]^[43] Biofilm formation is regulated by two-component systems that coordinate matrix production and community behaviors. The VicRK system modulates exopolysaccharide synthesis and cell wall biogenesis, promoting robust biofilm architecture through regulation of genes like gtfB/C for glucan production and gbpB for glucan binding, which are essential for the structural integrity of dental plaque. VicRK mutants show reduced biofilm biomass and altered matrix composition, underscoring its role in virulence. Similarly, the ComDE quorum-sensing system senses cell density via competence-stimulating peptide, activating density-dependent gene expression that enhances biofilm development and competence for genetic transformation, thereby amplifying virulence traits like acid production in mature communities.^[44]^[45]^[46]^[47] Acid tolerance mechanisms allow S. mutans to survive in the low-pH environment of plaque. The atpD gene encodes the beta subunit of the F-ATPase, a proton-pumping enzyme that extrudes H⁺ ions from the cytoplasm, maintaining intracellular pH homeostasis during acid challenges; inhibition of F-ATPase significantly reduces survival at pH 5.0 or lower. The relA gene mediates the stringent response by synthesizing alarmone (p)ppGpp, which reprograms metabolism under nutrient stress and acid exposure, upregulating adaptive genes for enhanced tolerance and persistence in cariogenic biofilms. RelA mutants exhibit diminished acid adaptation and reduced virulence in caries models.^[48]^[49]^[50]^[51] Bacteriocin production provides a competitive advantage in the oral microbiome. S. mutans produces mutacins I-IV, ribosomally synthesized antimicrobial peptides that inhibit closely related streptococci and other oral pathogens. Mutacin I is a lantibiotic active against Gram-positive bacteria, while mutacin IV targets a broader range including non-mutans streptococci, aiding in niche dominance without affecting S. mutans itself. These mutacins are regulated by quorum sensing and contribute to monospecific plaque formation.^[21]^[22]^[52]

Disease Associations

Oral Health Impacts

Streptococcus mutans is recognized as the primary etiologic agent of dental caries, a prevalent oral disease characterized by the demineralization of tooth enamel due to acid production from bacterial metabolism of dietary carbohydrates.^[27] This bacterium's acidogenic and aciduric properties enable it to thrive in low-pH environments, particularly in individuals consuming high-sugar diets where frequent carbohydrate exposure amplifies acid attacks on tooth surfaces.^[53] In such conditions, S. mutans dominates the cariogenic biofilm, leading to enamel breakdown and cavity formation.^[54] In early childhood caries (ECC), a severe form affecting primary teeth in young children, S. mutans plays a prominent role, with high levels observed in affected lesions. Studies indicate its detection at high prevalence in ECC cases, often exacerbated by prolonged bottle-feeding with sugary liquids that promote bacterial colonization and acid production.^[37] This early acquisition, typically from maternal transmission, correlates with rapid caries progression in preschoolers.^[55] S. mutans contributes indirectly to periodontal conditions like gingivitis through its role in plaque maturation, where biofilm formation creates a complex microbial community that harbors pathogens and irritates gingival tissues. High salivary levels of S. mutans are associated with increased periodontal disease severity, as the accumulated plaque fosters inflammation and tissue damage.^[56]^[57] Assessment of cariogenic potential often involves measuring mutans streptococci (MS) counts in saliva, where levels exceeding 10^5 colony-forming units (CFU) per milliliter signal high caries risk, guiding clinical interventions.^[58] In adults, S. mutans is implicated in recurrent decay around restorations, where microleakage at margins allows bacterial ingress and acid production beneath fillings, leading to secondary caries.^[59] Among the elderly, it is strongly associated with root caries, as exposed root surfaces—due to gingival recession—provide susceptible sites for colonization, with mutans streptococci detected more frequently in carious root plaques than healthy ones.^[60] This vulnerability increases with age-related factors like reduced saliva flow and dietary changes.^[61]

Systemic Disease Links

Streptococcus mutans, primarily recognized as an oral pathogen, has been implicated in various systemic diseases through mechanisms involving bacteremia and tissue invasion, particularly by strains expressing the collagen-binding protein Cnm.^[43] In cardiovascular disease, Cnm-positive S. mutans strains promote adhesion to cardiac tissues and endothelial cells, contributing to infective endocarditis (IE) and atherosclerosis. The Cnm protein facilitates bacterial binding to collagen types I, II, III, and IV, as well as laminin, enhancing invasion of human coronary artery endothelial cells and retention on damaged heart valves, which is critical for vegetation formation in IE.^[43] S. mutans has been detected in 68.6% of extirpated heart valve specimens from IE patients and 74.1% of atheromatous plaque specimens from atherosclerosis patients, indicating a significant prevalence in cardiovascular lesions.^[62] Additionally, Cnm-expressing strains induce platelet aggregation in the presence of fibrinogen, acting as a bridging molecule, which exacerbates thrombus formation and vascular damage.^[63] Recent studies from 2024 and 2025 have linked Cnm-positive S. mutans strains to immunoglobulin A nephropathy (IgAN), a leading cause of glomerulonephritis. These strains, via bacteremia or immune complex formation, trigger glomerular inflammation and mesangial IgA deposition, mimicking IgAN pathology in rat models where recombinant Cnm administration induced nephritis-like lesions.^[64] Oral carriage of such strains correlates with elevated urinary protein levels and galactose-deficient IgA1 production in IgAN patients, suggesting a role in disease progression through tonsillar immune responses.^[65]^[66] S. mutans also contributes to nonalcoholic fatty liver disease (NAFLD), where oral translocation leads to hepatic inflammation and steatosis exacerbation in mouse models. Intravenous administration of specific S. mutans strains, particularly those expressing Cnm, aggravates nonalcoholic steatohepatitis (NASH) by promoting inflammatory cell infiltration and adipocyte deposition in the liver, with histopathological changes observed as early as 8 weeks post-infection.^[67] Cnm-positive strains further intensify fibrosis in NAFLD models, linking oral infection to systemic hepatic pathology.^[68] Other potential associations include rheumatoid arthritis, where molecular mimicry between S. mutans surface antigens (e.g., antigen I/II or SR) and human proteins may elicit cross-reactive autoantibodies in rheumatic diseases.^[69] In rare cases of bacteremia, S. mutans has been isolated from brain abscesses, often originating from odontogenic sources and leading to pyogenic intracranial infections.^[70] The primary mechanisms underlying these systemic links involve bacteremia arising from oral mucosal breaches during dental procedures or periodontitis, allowing S. mutans entry into the bloodstream.^[71] Collagen-binding via Cnm aids in tissue invasion and dissemination to distant organs, amplifying virulence in susceptible hosts.^[43]

Genomics and Evolution

Genome Structure

The genome of Streptococcus mutans consists of a single circular chromosome, with sizes ranging from approximately 2.0 to 2.4 Mb across strains. The reference strain UA159 features a 2,030,921 bp chromosome encoding 1,960 predicted protein-coding genes, representing a compact genome typical of low-GC Gram-positive bacteria. The overall GC content is around 37%, which contributes to the bacterium's metabolic efficiency in the nutrient-limited oral environment.^[72] Some strains harbor small plasmids, such as those carrying bacteriocin production genes (e.g., pUA159-like elements), which facilitate antimicrobial competition within biofilms, though the reference UA159 lacks native plasmids.^[73] Key genomic operons include gtfBCD, which encodes glucosyltransferases essential for extracellular polysaccharide synthesis and biofilm formation. Another notable cluster, smu_759-761, encompasses genes related to collagen-binding proteins like Cnm, enabling adhesion to host tissues in certain strains. These operons are tightly regulated and integral to virulence. Mobile genetic elements are prominent, including a CRISPR-Cas system comprising type I-C and type II-A arrays that provide adaptive immunity against phages and plasmids by targeting foreign DNA. Integrases associated with integrative and conjugative elements (ICEs), such as TnSmu1, promote horizontal gene transfer, allowing acquisition of adaptive traits like antibiotic resistance. Recent metagenomic analyses reveal significant strain variability, with the accessory genome comprising 20-30% of the pan-genome and often including virulence islands that enhance cariogenic potential. A 2025 study resequencing genomes from individuals with high and low caries risk identified differences in virulence-related genes, further highlighting genomic diversity linked to pathogenicity.^[74]

Phylogenetic Development

Streptococcus mutans is believed to have co-evolved with the human oral microbiome, with its origins tracing back to approximately 100,000 to 200,000 years ago, aligning with the dispersal of modern humans out of Africa.^[75] This bacterium is human-specific, distinguishing it from related streptococci found in other primates, and its phylogenetic history reflects a close association with human migration patterns. Phylogenetic analyses place S. mutans within the Streptococcus mutans group, which diverged from other oral streptococci through a series of genomic rearrangements and acquisitions that enhanced its cariogenic potential.^[76] A key event in the phylogenetic development of S. mutans was the acquisition of glucosyltransferase (gtf) genes via horizontal gene transfer from lactic acid bacteria, particularly species within the genus Lactobacillus. These genes, encoding enzymes that synthesize adhesive glucans from sucrose, were likely transferred during interactions in the oral niche, enabling S. mutans to form robust biofilms on tooth surfaces and marking a pivotal adaptation for cariogenicity. Phylogenetic reconstruction of glycosyl hydrolase family 70 enzymes supports this transfer, showing that streptococcal gtf variants cluster closely with those from Lactobacillus and Leuconostoc, predating the diversification of the S. mutans lineage.^[77]^[78] Additional lateral gene transfers, including those contributing to competence and bacteriocin production, have been inferred from comparative genomics, facilitating genetic diversity and competitiveness within streptococcal populations.^[79] Population genomic studies from 2012 to 2024 reveal a clonal expansion of S. mutans in modern human populations, characterized by remarkably low genetic diversity indicative of a recent bottleneck followed by rapid proliferation. Analysis of 57 global isolates supports an African origin for the species, with subsequent dispersal mirroring human migrations out of Africa and into the Americas around 10,000–6,500 years ago, coinciding with the Neolithic agricultural revolution and increased dietary carbohydrates. This expansion is evidenced by a star-like phylogeny in core genome alignments, where most variation arises from recombination rather than mutation, underscoring the role of natural transformation in its evolution.^[80]^[81] Later studies confirm this low diversity pattern across continents, with strains from indigenous populations showing deeper branching consistent with ancient African roots.^[82] Adaptations to the human oral environment have driven selective pressures on S. mutans phylogeny, including the loss of certain galactose metabolism genes in some lineages, which may have streamlined carbohydrate utilization toward sucrose-dominant diets. This gene loss, observed in comparative analyses with non-human streptococci, reflects specialization for acidogenic niches. Conversely, gains in acid tolerance have occurred through gene duplication events, notably of atpD encoding the F1F0 ATPase beta subunit, enhancing proton extrusion and survival in low-pH biofilms. Genome-wide scans identify these duplications, along with positively selected loci in adhesion and exopolysaccharide pathways, as hallmarks of adaptation post-human colonization.^[81]^[76] Recent insights from 2025 highlight cross-kingdom evolutionary dynamics, where interactions with Candida albicans modulate S. mutans virulence gene expression via the LiaS two-component system. This regulatory pathway promotes hyphal invasion and biofilm synergy, suggesting co-evolutionary pressures from fungal partners that amplify cariogenic and candidal pathologies in the oral microbiome. Such mechanisms underscore ongoing phylogenetic interplay in polymicrobial communities.^[83]

Prevention and Control

Hygiene and Dietary Strategies

Maintaining rigorous oral hygiene practices is essential for minimizing Streptococcus mutans colonization and biofilm formation on tooth surfaces. Brushing twice daily with fluoride toothpaste effectively removes dental plaque and reduces caries risk when performed correctly for two minutes each time, thereby limiting the substrate available for S. mutans proliferation.^[84] Complementing brushing, daily flossing disrupts interdental biofilms where S. mutans thrives, mechanically dislodging bacterial aggregates and preventing their maturation into acid-producing structures.^[85] These mechanical interventions, when combined, significantly lower salivary and plaque levels of S. mutans, promoting a less cariogenic oral environment.^[86] Dietary modifications play a critical role in curbing S. mutans activity by restricting its primary energy sources. The World Health Organization recommends limiting free sugars, including sucrose—a key fermentable carbohydrate—to less than 5% of total energy intake to prevent dental caries, as higher consumption fuels S. mutans acid production and enamel demineralization.^[87] Chewing gum sweetened with xylitol, a non-fermentable sugar alcohol, inhibits S. mutans growth through competitive inhibition of bacterial metabolism and reduced adhesion to teeth, without contributing to acidogenesis.^[88] Fluoride, incorporated via toothpaste or mouth rinses, enhances these efforts by promoting enamel remineralization and forming fluorapatite [Ca₅(PO₄)₃F], a mineral phase more resistant to acid dissolution at pH levels above 4.5 compared to native hydroxyapatite.^[89] Preventive strategies targeting vertical transmission from mother to child are vital during early childhood. Maternal use of chlorhexidine rinses, particularly in the prenatal and postnatal periods, can reduce S. mutans levels in the mother's oral cavity and delay subsequent transmission to infants, lowering early caries risk.^[90] On a public health scale, community water fluoridation at optimal levels (0.7 mg/L) decreases caries incidence by about 25% across populations, providing systemic and topical benefits that inhibit S. mutans-driven demineralization.^[91] Guidelines from organizations such as the American Academy of Pediatric Dentistry recommend limiting added sugars to prevent early childhood caries, advising caregivers to minimize added sugars in children's intake to align with overall oral health promotion.^[92]

Antimicrobial Approaches

Antimicrobial approaches targeting Streptococcus mutans primarily involve antibiotics, bacteriophages, vaccines, natural compounds, and emerging targeted therapies, aimed at disrupting bacterial growth, biofilm formation, and virulence in the oral cavity.^[93] These strategies address the pathogen's role in dental caries and potential systemic infections, with a focus on overcoming resistance and minimizing disruption to the oral microbiome.^[94] Traditional antibiotics such as penicillin and ampicillin remain effective against most S. mutans isolates, with minimal inhibitory concentrations (MICs) typically below 0.08 μg/ml for susceptible strains.^[93] However, emerging resistance has been observed, particularly to amoxicillin (a penicillin derivative), where MICs of 16 μg/ml or higher were detected in isolates from approximately 4% of subjects in a study of dental plaque samples.^[95] In cases of infective endocarditis associated with viridans group streptococci, including S. mutans, penicillin G or ceftriaxone combined with gentamicin is the first-line regimen, but alternatives like clindamycin are considered for penicillin-allergic patients to ensure effective treatment.^[96] Clindamycin's utility stems from its activity against streptococci, though its use is guided by susceptibility testing to avoid broader resistance issues.^[97] Bacteriophages offer a targeted alternative by specifically lysing S. mutans cells without affecting commensal oral bacteria. For instance, the temperate phage φAPCM01 has demonstrated broad lytic activity against clinical S. mutans isolates in vitro, reducing biofilm formation and promoting clearance in experimental models.^[98] Similarly, the newly isolated phage SMHBZ8 exhibits potent antibacterial effects against S. mutans, inhibiting growth and biofilm development, positioning it as a candidate for caries prevention therapies.^[99] Recent studies highlight phages' potential in oral applications, with in vivo models showing significant plaque reduction through selective bacterial elimination.^[100] Vaccine development focuses on key S. mutans antigens to elicit protective immunity against caries. Subunit vaccines targeting glucosyltransferase B (GtfB), which catalyzes extracellular polysaccharide synthesis, have shown promise in preclinical animal models by reducing bacterial adhesion and biofilm accumulation.^[101] Antigen I/II (AgI/II), a surface adhesin, is another primary target; immunization with recombinant AgI/II fragments induces salivary IgA responses that inhibit S. mutans colonization in rodent studies.^[102] Despite these advances, challenges persist, including oral tolerance, where repeated mucosal exposure may dampen immune responses, necessitating adjuvants or alternative delivery routes like nasal immunization to enhance efficacy.^[103] Natural antimicrobials provide non-antibiotic options for biofilm disruption. Probiotics such as Streptococcus salivarius K12 compete effectively with S. mutans for adhesion sites and produce bacteriocins that inhibit its growth, with co-culture experiments demonstrating up to 90% reduction in S. mutans viability and biofilm formation.^[104] Clinical trials support this, showing sustained suppression of S. mutans levels in saliva after 60 days of probiotic lozenge use.^[105] Essential oils, particularly thymol from thyme, exhibit strong anti-biofilm activity by inducing autolysis and membrane damage in S. mutans, with MICs as low as 0.016% v/v preventing acid production and adherence in vitro.^[106] Thymol's efficacy is enhanced in combinations, reducing biofilm biomass by over 50% without cytotoxicity at therapeutic doses.^[107] Targeted therapies exploit S. mutans signaling pathways for precision intervention. Quorum-sensing inhibitors, such as analogs of autoinducer-2 (AI-2), disrupt LuxS-dependent communication, thereby attenuating biofilm formation and virulence gene expression without killing the bacteria.^[108] For example, synthetic CSP analogs derived from related streptococci suppress S. mutans competence and biofilm development by interfering with ComDE signaling.^[109] CRISPR-based antimicrobials represent a cutting-edge approach; in 2024 studies, CRISPR-Cas9 systems from S. mutans itself were repurposed to edit essential genes like those for biofilm synthesis, achieving targeted killing in preclinical models while preserving microbiome diversity.^[110] These tools, including SmutCas9 variants, enable precise gene inactivation, offering potential for caries prevention with minimal off-target effects.^[111]

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Roles of Streptococcus mutans in human health: beyond dental caries
Dec 18, 2024 · Streptococcus mutans (S. mutans) is the main pathogenic bacterium causing dental caries, and the modes in which its traits, such as acid production, acid ...Missing: etymology | Show results with:etymology
[24]
The changing faces of Streptococcus antigen I/II polypeptide family ...
The AgI/II protein (also named P1, SpaP, AgB or PAc) is a major surface protein that functions as an adhesin, attaching S. mutans to the saliva-coated tooth ...
[25]
Functional Variation of the Antigen I/II Surface Protein in ... - NIH
By using isogenic mutants, we show that the antigen I/II in S. mutans, but not in S. intermedius, was involved in adhesion to a salivary film under flowing ...Adhesion To Matrix Proteins · Results · Binding To Salivary Film
[26]
Molecular mechanisms of inhibiting glucosyltransferases for biofilm ...
Sep 30, 2021 · Glucosyltransferases (Gtfs) play critical roles in the etiology and pathogenesis of Streptococcus mutans (S. mutans)- mediated dental caries ...
[27]
The catalytic domains of Streptococcus mutans glucosyltransferases
May 5, 2023 · GtfC synthesizes both soluble and insoluble glucans (α-1,3 and α-1,6 glycosidic linkages), while GtfB and GtfD only synthesize insoluble glucans ...
[28]
Exopolysaccharides Produced by Streptococcus mutans ...
Results of previous studies have shown that sucrose induces the expression of gtfB and gtfC by S. mutans in single-species biofilms (22, 29, 41), directly ...
[29]
Acid tolerance mechanisms utilized by Streptococcus mutans - PMC
The capacity of S. mutans to initiate caries via acid production from the metabolism of dietary carbohydrates [12] would be suicidal if not for its remarkable ...
[30]
Evaluation of bacteria-induced enamel demineralization using ...
Streptococcus mutans is considered a major causative of tooth decay due to it's ability to rapidly metabolize carbohydrates such as sucrose.Materials And Methods · Lactic Acid Induced... · Citric Acid Induced...
[31]
Bacterial Acid Production | Caries Process, Prevention, and ...
mutans favors the lactate dehydrogenase pathway to produce lactic acid, which significantly lowers the pH in the immediate environment of the tooth. This drop ...
[32]
Acid-adaptive mechanisms of Streptococcus mutans–the more we ...
The F-ATPase of S. mutans has a lower optimal pH than that of many other oral microbes and is also significantly upregulated during growth in acidic conditions, ...
[33]
The F-ATPase Operon Promoter of Streptococcus mutans Is ...
Streptococcus mutans F-ATPase, the major component of the acid-adaptive response of the organism, is transcriptionally upregulated at low pH.
[34]
Early Childhood Caries: Prevalence, Risk Factors, and Prevention
Jul 17, 2017 · Poor maternal oral hygiene maintenance and frequent snacking and sugar exposure increase the chances of transmission of the infection to child ( ...
[35]
Early Childhood Caries - StatPearls - NCBI Bookshelf - NIH
Aug 8, 2023 · Direct Transmission of Infection The vertical transmission of Streptococcus mutans from the mother to the child occurs through infected saliva ...
[36]
Streptococcus mutans in Mother-Child Dyads and Early Childhood ...
Oct 21, 2017 · This study investigated the association between colonization of mother-child dyads with Streptococcus mutans (SM) and early childhood caries ...
[37]
Diversity of SpaP in genetic and salivary agglutinin mediated ...
Dec 27, 2019 · SpaP is also named P1, Antigen I/II or Pac. It mediates the adherence of S. mutans to the saliva-coated tooth surface by interacting ...
[38]
The Multifaceted Nature of Streptococcal Antigen I/II Proteins in ...
mutans SpaP knockout to bind human laminin but as the difference was not significant, the authors concluded that SpaP did not contribute to laminin binding ( ...
[39]
The Collagen Binding Proteins of Streptococcus mutans and ...
The ability of Streptococcus mutans to interact with collagen through the expression of collagen-binding proteins (CBPs) bestows this oral pathogen with an ...Missing: spread | Show results with:spread
[40]
Role of Streptococcus mutans adhesin Cnm in systemic disease - NIH
Cnm has been shown to promote attachment to extracellular matrix (ECM) proteins collagen (types I, II, III and IV) and laminin, and to facilitate invasion of ...Missing: AbpB spread
[41]
The vicK gene of Streptococcus mutans mediates its cariogenicity ...
Dec 16, 2021 · Our report demonstrates that vicK gene enhances biofilm formation and subsequent caries development. And this may due to its regulations on EPS metabolism.
[42]
CovR and VicRK Regulate Cell Surface Biogenesis Genes ...
The two-component system VicRK and the orphan regulator CovR of Streptococcus mutans co-regulate a group of virulence genes associated with the synthesis of ...
[43]
Quorum Sensing in Streptococcus mutans Regulates Production of ...
We found that S. mutans uses a quorum-sensing system to regulate production of a novel posttranslationally modified peptide capable of inhibiting growth of ...
[44]
Death and survival in Streptococcus mutans: differing outcomes of a ...
Recent studies have shown that S. mutans uses a canonical Gram-positive two-component quorum-sensing (QS) system to regulate expression of genes controlling ...
[45]
Proton-pumping F-ATPase plays an important role in Streptococcus ...
May 15, 2019 · mutans is highly sensitive to F-ATPase inhibitors under acidic conditions and that F-ATPase plays an important role in acid tolerance of this ...Missing: atpD | Show results with:atpD
[46]
The F-ATPase Operon Promoter of Streptococcus mutans Is ...
Streptococcus mutans F-ATPase, the major component of the acid-adaptive response of the organism, is transcriptionally upregulated at low pH.
[47]
Role of RelA of Streptococcus mutans in Global Control of Gene ...
RelA is the major (p)ppGpp synthase controlling the stringent response in S. mutans, and it coordinates the expression of genes and phenotypes.
[48]
An Essential Role for (p)ppGpp in the Integration of Stress Tolerance ...
Conformational antagonism between opposing active sites in a bifunctional RelA/SpoT homolog modulates (p)ppGpp metabolism during the stringent response.
[49]
Mutacins from Streptococcus mutans UA159 Are Active against ...
Our results suggest that mutacin IV and mutacin V may act synergistically to inhibit various organisms. Bacteriocins are ribosomally synthesized small ...
[50]
Contribution of collagen-binding protein Cnm of Streptococcus ...
Sep 14, 2024 · In the present study, we focused on the ability of Cnm on S. mutans to cause IgAN-like nephritis in rats using Cnm-deficient mutant strains and recombinant Cnm ...
[51]
The Biology of Streptococcus mutans | Microbiology Spectrum
As a major etiological agent of human dental caries, Streptococcus mutans resides primarily in biofilms that form on the tooth surfaces, also known as dental ...
[52]
Streptococcus mutans and Caries: A Systematic Review and Meta ...
Feb 2, 2025 · The collected evidence based on microbiome studies suggests a strong association between the prevalence and abundance of S. mutans and caries experience.
[53]
Oral colonization by Streptococcus mutans and its association with ...
High S. mutans levels appear directly co-associated with increased severity of periodontal disease at older ages in untreated patients.
[54]
Assessment of Streptococcus mutans in healthy versus gingivitis ...
Increased colonization of Streptococcus mutans was seen in chronic periodontitis subjects both in saliva and sub-gingival plaque samples.
[55]
The Effect of Probiotics Use on Salivary Cariogenic Bacteria ... - MDPI
Aug 4, 2022 · Density of 105 CFU or more of lactobacilli and mutans streptococci per ml saliva indicated a high caries risk. The evaluation chart was recoded ...
[56]
A microbiological study of recurrent dentinal caries - PubMed
A cross-sectional microbiological study of recurrent (secondary) dentinal caries was conducted. Freshly extracted human teeth containing amalgam ...
[57]
Bacterial Profiles of Root Caries in Elderly Patients - PMC - NIH
Mutans streptococci alone or in combination with lactobacilli were detected more frequently in plaque overlying carious surfaces than on healthy root surfaces.
[58]
A Co-Association of Streptococcus mutans and Veillonella parvula ...
Sep 21, 2022 · Root caries in geriatric patients is a growing problem as more people are maintaining their natural teeth into advanced age.
[59]
Detection of Cariogenic Streptococcus mutans in Extirpated Heart ...
Streptococcus mutans was frequently detected in the heart valve (69%) and atheromatous plaque (74%) specimens, while other bacterial species, including those ...
[60]
Contribution of Streptococcus mutans Strains with Collagen-Binding ...
Nov 17, 2017 · CBP (especially Cbm)-positive S. mutans strains also possess properties of binding to and aggregation with fibrinogen, which acts as a bridging ...
[61]
Cnm-Positive Streptococcus mutans Is Specifically Associated with ...
We previously reported an association between the presence of cnm-positive Streptococcus mutans in the oral cavity and IgA nephropathy (IgAN).
[62]
cnm-positive Streptococcus mutans, a major pathogen in dental ...
cnm-positive Streptococcus mutans, a major pathogen in dental caries, may exacerbate IgA nephropathy via the tonsils. Clin Exp Nephrol. 2025 Oct;29(10):1400 ...Missing: 2024 | Show results with:2024<|control11|><|separator|>
[63]
Longitudinal comparison of Streptococcus mutans-induced ...
Conclusion: These results suggest that intravenous administration of a specific S. mutans strain aggravates NASH in a time-dependent manner in the mice in ...
[64]
Contributions of Streptococcus mutans Cnm and PA antigens to ...
Nov 11, 2016 · One study found that a Cnm+/PA+ strain of S. mutans contributed to the aggravation of non-alcoholic steatohepatitis (NASH) in mice but that ...
[65]
Anti-IgG antibodies in rheumatic diseases cross-react with ...
Anti-IgG antibodies in rheumatic diseases cross-react with Streptococcus mutans SR antigen. · Abstract · Full text · Images in this article · Selected References.
[66]
Pyogenic Brain and Lung Abscesses Due to Streptococcus ...
Sep 4, 2013 · Streptococcus mutans · Hydrocephalus. REFERENCES. Khatib R, Ramanathan J ... Brain abscess. Clin Infect Dis. 1997;25(4):763–779. quiz 780 ...Pyogenic Brain And Lung... · Explore Related Subjects · Author Information
[67]
Streptococcus mutans and cardiovascular diseases - ScienceDirect
Streptococcus mutans, a pathogen of dental caries, is known to be associated with bacteremia and infective endocarditis (IE).
[68]
Streptococcus mutans UA159 genome assembly ASM746v2 - NCBI
Assembly statistics ; Contig L50, 1, 1 ; GC percent, 37, 37 ; Genome coverage, 1x ; Assembly level, Complete Genome, Complete Genome.Missing: structure | Show results with:structure
[69]
Population Structure of Plasmid-Containing Strains of Streptococcus ...
Genome sequence of Streptococcus mutans UA159, a cariogenic dental pathogen. ... Distinct bacteriocin groups correlate with different groups of Streptococcus ...Missing: pUA159 | Show results with:pUA159
[70]
Pangenome evaluation of gene essentiality in Streptococcus ...
Jul 16, 2024 · Across four genetic backgrounds and nine phenotypic conditions, 355 genes were essential for survival, corresponding to ~24% of the core genome.
[71]
Tooth Decay Analysis Supports 'Out Of Africa' Theory Of Human ...
Mar 16, 2007 · The team discovered that Streptoccocus mutans, a bacterium associated with dental caries, has evolved along with its human hosts in a clear line ...<|separator|>
[72]
Phylogenomics and the Dynamic Genome Evolution of the Genus ...
Mar 12, 2014 · Here, we make use of 46 Streptococcus genome sequences (44 distinct species), including eight species for which genome sequences were previously ...
[73]
Evolution of Cariogenic Character in Streptococcus mutans - Nature
Jul 18, 2012 · We found that streptococcal GTFs were derived from other lactic acid bacteria such as Lactobacillus and Leuconostoc, and propose the following ...
[74]
Evolution of Cariogenic Character in Streptococcus mutans
Jul 18, 2012 · The genus Streptococcus acquired the gtf gene via horizontal gene transfer when it encountered lactic acid bacteria, such as Lactobacillus ...
[75]
Comparative genomic analyses of Streptococcus mutans provide ...
Aug 5, 2009 · The average GC content is 36.85%, which is similar to that of UA159. ... Genome sequence of Streptococcus mutans UA159, a cariogenic dental ...Putative Bacitracin... · Crispr Associated Regions · Genome Sequencing And...
[76]
Evolutionary and Population Genomics of the Cavity Causing ...
Dec 10, 2012 · In this study, we generated genome sequences of 57 S. mutans isolates, as well as representative strains of the most closely related species to ...
[77]
Evolutionary and Population Genomics of the Cavity Causing ... - NIH
Streptococcus mutans is known to be one of the most prevalent bacteria in human oral flora and is widely recognized as a key etiological agent of human dental ...<|control11|><|separator|>
[78]
Metagenomics of the modern and historical human oral microbiome ...
Oct 5, 2020 · Finally, we examine the population genomic structures of Streptococcus mutans and Streptococcus sobrinus, which are associated with dental ...
[79]
Streptococcus mutans LiaS gene regulates its cross-kingdom ...
Feb 13, 2025 · Streptococcus mutans LiaS gene regulates its cross-kingdom interactions with Candida albicans to promote oral candidiasis. View ORCID Profile ...
[80]
Diet and Nutrition to Prevent Dental Problems - StatPearls - NCBI - NIH
Jul 10, 2023 · Sucrose is the most common dietary sugar and is considered the most cariogenic carbohydrate. Frequent consumption of carbohydrates in the form ...
[81]
Accumulation and removal of Streptococcus mutans biofilm on ... - NIH
Interdental aids such as interdental brushes, dental floss or water flossers are recommended as supplements to remove biofilm from interproximal and subgingival ...
[82]
Short-term effect of mechanical plaque control on salivary mutans ...
Conclusion: Meticulous and continuous plaque control with toothbrush and dental floss can decrease the mutans streptococci level in preschool children.Missing: brushing reduces
[83]
WHO calls on countries to reduce sugars intake among adults and ...
Mar 4, 2015 · This new updated WHO guideline calls for further reduction of free sugars intake to less than 5% of total energy intake if possible.
[84]
The effect of xylitol on dental caries and oral flora - PMC - NIH
Thus, xylitol inhibits S. mutans growth essentially by starving the bacteria. Xylitol can inhibit the growth of harmful oral bacteria such as S. mutans, but its ...
[85]
Fluoride | Caries Process, Prevention and Management
While demineralization of hydroxyapatite typically begins at a pH of around 5.5, fluorapatite resists acid dissolution until the pH drops closer to 4.5.Missing: Ca5( PO4) 3F
[86]
Caries prevention during pregnancy: results of a 30-month study
The results show that treatment significantly reduced salivary mutans streptococci levels in mothers and delayed the colonization of bacteria in their children ...Missing: maternal | Show results with:maternal
[87]
CDC Scientific Statement on Community Water Fluoridation
May 15, 2024 · CDC promotes the safety and benefits of community water fluoridation as an effective, cost-efficient method for preventing tooth decay and improving overall ...
[88]
Caries Risk Assessment and Management
Jul 18, 2023 · Patients should limit sugary snacks between meals15 and eat a healthy diet that limits added sugars and high-acid foods that can affect ...<|control11|><|separator|>
[89]
Antimicrobial Susceptibility of Streptococcus mutans Isolated ... - NIH
Most of the strains were very susceptible to ampicillin, penicillin, and erythromycin, with most strains having minimal inhibitory concentrations of 0.08 μg/ml ...
[90]
Antimicrobial Susceptibility of Streptococcus mutans Isolated from ...
Most of the strains were also susceptible to cephalothin, methicillin, chloramphenicol, tetracycline, and vancomycin. Gentamicin was the most effective ...Missing: clindamycin treatment
[91]
Amoxicillin-resistant oral streptococci identified in dental plaque ...
Seven strains with an MIC of AMPC of 16 μg/mL or more were isolated from 5 subjects. The bacterial species were confirmed by sequence analysis of 16S rRNA from ...
[92]
Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy ...
A 2-week treatment regimen that includes gentamicin is reasonable in patients with uncomplicated IE, rapid response to therapy, and no underlying renal disease ...
[93]
[PDF] infective-endocarditis-in-adults-diagnosis-antimicrobial-therapy-and ...
Oct 16, 2018 · Clindamycin therapy of Staphylococcus aureus endocarditis: clinical relapse and development of resistance to clindamy- cin, lincomycin and ...
[94]
Phage Targeting Streptococcus mutans In Vitro and In Vivo as ... - NIH
Aug 21, 2021 · Various studies have showed its efficacy in reducing plaque accumulation, but it also causes colorization of teeth and exhibits a cytotoxic ...
[95]
Isolation and Characterization of Streptococcus mutans Phage as a ...
Oct 15, 2025 · The isolation and characterization of SMHBZ8 may be the first step towards developing a potential phage therapy for dental caries.Missing: P235 | Show results with:P235
[96]
The potential use of bacteriophages as antibacterial agents in dental ...
Oct 18, 2024 · This review summarizes the current antibacterial properties of phages used to treat a variety of dental infections.Antibiotic Resident In... · Bacteriophages In Dental... · Advantages And DisadvantagesMissing: P235 | Show results with:P235
[97]
Immunogenic and Protective Potential of Mutans Streptococcal ... - NIH
Abstract. Mutans streptococcal glucosyltransferases (GTF) have been demonstrated to be effective components of dental caries vaccines.Missing: GtfB tolerance
[98]
Alterations in Immunodominance of Streptococcus mutans AgI/II
Streptococcus mutans Antigen I/II (AgI/II) has been widely studied as a candidate vaccine antigen against human dental caries. In this report we follow up on ...Missing: GtfB preclinical
[99]
The scientific and public-health imperative for a vaccine against ...
May 26, 2006 · One of the main groups of oral microorganisms, the mutans streptococci, has been associated with the aetiology of dental caries, and preclinical ...
[100]
Antimicrobial effect of probiotic bacteriocins on Streptococcus ... - NIH
Jan 28, 2024 · Co-cultivation of S. mutans and S. salivarius K12 and/or S. salivarius M18 led to the inhibition of S. mutans viability, thereby, preventing its ...
[101]
The Effect of Dental Probiotic Use on the Inhibition of Streptococcus ...
Conclusion: The daily administration of dental probiotics for 60 days sufficiently suppressed the level of oral S.mutans and suppression continued for 30 more ...
[102]
Thymol and carvacrol induce autolysis, stress, growth inhibition and ...
Feb 23, 2017 · Thymol and carvacrol induce autolysis, stress, growth inhibition and reduce the biofilm formation by Streptococcus mutans. Shams Tabrez Khan ...
[103]
Antimicrobial Activity of Essential Oils against Streptococcus mutans ...
This study aimed to evaluate the activity of essential oils (EOs) against Streptococcus mutans biofilm by chemically characterizing their fractions responsible ...
[104]
Mutation of luxS Affects Biofilm Formation in Streptococcus mutans
In this study, we report for the first time that luxS-dependent quorum sensing is involved in biofilm formation of Streptococcus mutans.
[105]
Exploiting Conserved Quorum Sensing Signals in Streptococcus ...
S. mutans uses multiple Quorum Sensing (QS) systems to interact with other bacterial species in the oral cavity and to regulate biofilm formation, acid ...
[106]
CRISPR/Cas‑mediated targeted gene editing of Streptococcus mutans
May 8, 2025 · CRISPR enables the precise genetic targeting of Streptococcus mutans and other cariogenic bacteria, potentially reducing resistance development and microbiome ...
[107]
Insight into crRNA Processing in Streptococcus mutans P42S and ...
Feb 25, 2025 · In this study, we assessed the potential of Cas9 from Streptococcus mutans strain P42S (SmutCas9) in gene editing.