Streptococcus mutans és un bacteri gram-positiu anaeròbic facultatiu que es troba normalment en la cavitat oral dels humansi contribueix significativament a la càries dental.[1][2] Aquest microbi va ser descrit per Clarke el 1924.[3]
Els colonitzadors primerencs de la superfície de les dent són principalment bacteris del grup Neisseria i streptococus, incloent S. mutans. El metabolisme de creixement d'aquests microorganismes canvia el medi ambient local i permet que microorganismes pitjors colonitzin després d'ells, formant la placa dental.[4] Junt amb S. sobrinus, S. mutans juga un paper principal en la càries, metabolitzant la sacarosa a àcid làctic[2] usant l'enzim Glucansacarasa.[5] L'ambient àcid que creen mineralitza l'esmalt dental i la fa vulnerable a la càries.
La sacarosa és l'únic sucre que S. mutans pot fer servir.
Molts altres sucres com;glucosa, fructosa, lactosa— poden ser digerits per S. mutans, però aquests produeixen àcid làctic com producte final. És la combinació entre la placa i l'àcid que fa la càries.[6] S'ha intentat fer una vacuna contra l'acció de S. mutans però encara sense èxit en humans.[7] Recentment s'ha descobert que les proteïnes induïdes per la colonització de S. mutans fan anticossos que inhibeixen el procés de la càries.[8]
Streptococcus mutans és un bacteri gram-positiu anaeròbic facultatiu que es troba normalment en la cavitat oral dels humansi contribueix significativament a la càries dental. Aquest microbi va ser descrit per Clarke el 1924.
Streptococcus mutans je druh bakterie, která obvykle žije v ústní dutině člověka. Tato bakterie se přichycuje na zubech a vylučuje žíravou kyselinu. Toto přichycení umožňuje sacharidový polymer, který tvoří hlavní součást zubního plaku. Bakterie Streptococcus mutans se obvykle přenášejí z dospělých na děti a po přesunu se v ústech usadí a napadají nově se vytvářející zuby. Bakterie Streptococcus mutans se množí při teplotě 18–40 stupňů Celsia.
Streptococcus mutans ist eine Bakterienart aus der Gattung der Streptokokken (Streptococcus). S. mutans ist der Leitorganismus der Zahnkaries und bei fast jedem Menschen im Speichel vorhanden. Die Höhe der Konzentration von S. mutans im Speichel korreliert eng mit dem Kariesrisiko.[2]
S. mutans hat etwa kugel- bis eiförmige Zellen („Kokken“), die zu zweit oder in Ketten angeordnet sind und bewegt sich nicht aktiv. Das Bakterium ist grampositiv, fakultativ anaerob, hat oxidativen und fermentativen Energiestoffwechsel und bildet keine Sporen. Auf Gelnährmedien mit komplexen Nährstoffen bildet S. mutans rundliche, konvexe (gewölbte) Kolonien mit granulierter (gekörnter) Oberfläche. Die meisten Stämme wirken α-hämolytisch (grünliche Verfärbung um die Bakterien herum auf einem bluthaltigen Nährboden).[3] Bei drei Stämmen wurde aber auch eine β-Hämolyse (vollständige Auflösung der Erythrozyten und Abbau des Hämoglobins) nachgewiesen.[4]
Streptococcus mutans gilt als wichtigster Verursacher der Karies. Der Erreger besitzt eine Reihe spezieller Eigenschaften (Virulenzfaktoren), die ihm eine Hauptrolle bei der Entstehung des bakteriellen Zahnbelags zuweisen:
Streptococcus mutans ist eine Bakterienart aus der Gattung der Streptokokken (Streptococcus). S. mutans ist der Leitorganismus der Zahnkaries und bei fast jedem Menschen im Speichel vorhanden. Die Höhe der Konzentration von S. mutans im Speichel korreliert eng mit dem Kariesrisiko.
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.[1][2] 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.[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. Therefore, for clinical purposes they are often considered together as a group, called the mutans streptococci.[4] This grouping of similar bacteria with similar tropism can also be seen in the viridans streptococci, another group of Streptococcus species.
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.[5] 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%).[6]
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.[7]
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.[8] Its presence in the biofilm promotes higher levels of S. mutans when looking at early childhood caries.[8] It stimulates the formation of S. mutans microcolonies.[8] This is achieved through low concentrations of cross-kingdom metabolites, such as farnesol, derived from the biofilm.[8] It has been suggested that when both microbes are present, more biofilm matrix is produced, with a greater density.[8] When farnesol is in high concentration, it inhibits the growth of both S. mutans and C. albicans.[8] This decreases the biofilm pathogenesis, and therefore its caries promoting potential.[8] This offers the potential for an anti-fungal to be used in the prevention of dental caries.[8]
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.[9] Along with S. sobrinus, S. mutans plays a major role in tooth decay, metabolizing sucrose to lactic acid.[2][10] 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:
Sucrose is the only sugar that bacteria can use to form this sticky polysaccharide.[1]
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.[11] 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.[12] Recently, proteins involved in the colonization of teeth by S. mutans have been shown to produce antibodies that inhibit the cariogenic process.[13] 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.[14]
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.[15][16]
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.[17] 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.[17]
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.[18] 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.[19]
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 [20]. 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.[18] Streptococcus mutans is a bacterium which is prevalent within the oral environment [21] and is thought to be a vital microorganism that contributes to this initiation.[22] S. mutans thrives in acidic conditions, becoming the main bacterium in cultures with permanently reduced pH [23]. 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.[18]
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.[24] In young children, the pain from a carious lesion can be quite distressing and restorative treatment can cause an early dental anxiety to develop.[25] 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.[26] 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.[27]
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.[28]
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.[29][30]
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.[31] Streptococcus sanguinis, closely related to S. mutans and also found in the oral cavity, has been shown to cause Infective Endocarditis.[32]
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.[33]
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.[34]
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.[35] 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.[36] 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 less acid produced during the bacterial glycolysis.[37] Therefore, fluoride mouthwashes, toothpastes, gels and varnishes can help to reduce the prevalence of caries.[38] However, findings from investigations into the effect of fluoride-containing varnish, on the level of Streptococcus mutans in the oral environment in children suggest that the reduction of caries cannot be explained by a reduction in the level of Streptococcus mutans in saliva or dental plaque.[39] Fluoride varnish treatment with or without prior dental hygiene has no significant effect on the plaque and salivary levels of S. mutans.[40]
S. mutans secretes Glucosyltransferase on its cell wall, which allows the bacteria to produce polysaccharides from sucrose. These sticky polysaccharides are responsible for the bacteria's ability to aggregate with one another and adhere to tooth enamel, i.e. to form biofilms. 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. Studies have shown that Anti-CA-gtf IgY is able to effectively and specifically suppress S. mutans in the oral cavity.[41]
Other common preventative measures center on reducing sugar intake. One way this is done is with sugar replacements such as xylitol or erythritol which cannot be metabolized into sugars which normally enhance S. mutans growth. The molecule xylitol, a 5 carbon sugar, disrupts the energy production of S.mutans by forming a toxic intermediate during glycolysis.[42][43] Various other natural remedies have been suggested or studied to a degree, including deglycyrrhizinated licorice root extract,[44][45] tea tree oil,[46] macelignan (found in nutmeg),[47] curcuminoids (the main components of turmeric),[48] and eugenol (found in bay leaves, cinnamon leaves and cloves). Additionally various teas have been tested for activity against S. mutans and other dental benefits.[49][50][51][52][53] However, none of these remedies have been subject to clinical trials or are recommended by mainstream dental health groups to treat S. mutans.
The addition of bioactive glass beads to dental composites reduces penetration of Streptococcus mutans into the marginal gaps between tooth and composite.[54] They have antimicrobial properties, reducing bacterial penetration.[54] This decreases the risk of secondary caries developing, a common reason for failure of dental restorations.[54] This means that the longevity and efficacy of composite restorations may be improved.[54]
Conditions in the oral cavity are diverse and complex, frequently changing from one extreme to another. Thus, to survive in the oral cavity, S. mutans must tolerate rapidly harsh environmental fluctuations and exposure to various antimicrobial agents to survive.[17] Transformation is a bacterial adaptation involving the transfer of DNA from one bacterium to another through the surrounding medium. Transformation is a primitive form of sexual reproduction. For a bacterium to bind, take up, and recombine exogenous DNA into its chromosome, it must enter a special physiological state termed "competence". In S. mutans, a peptide pheromone quorum-sensing signaling system controls genetic competence.[55] This system functions optimally when the S. mutans cells are in crowded biofilms.[56] S. mutans cells growing in a biofilm are transformed at a rate 10- to 600-fold higher than single cells growing under uncrowded conditions (planktonic cells).[55] Induction of competence appears to be an adaptation for repairing DNA damage caused by crowded, stressful conditions.[57]
Knowing about quorum-sensing gives rise to the potential development of drugs and therapies. Quorum-sensing peptides can be manipulated to cause target suicide. Furthermore, quenching quorum-sensing can lead to prevention of antibiotic resistance.[58]
Three key traits have evolved in S. mutans and increased its virulence by enhancing its adaptability to the oral cavity: increased organic acid production, the capacity to form biofilms on the hard surfaces of teeth, and the ability to survive and thrive in a low pH environment.[59]
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.[60] 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.[61] It is thought that the trait evolved in S. mutans via lateral gene transfer with another bacterial species present in the oral cavity. There are several genes, SMU.438 and SMU.1561, involved in carbohydrate metabolism that are up-regulated in S. mutans. These genes possibly originated from Lactococcus lactis and S. gallolyticus, respectively.[60]
Another instance of lateral gene transfer is responsible for S. mutans' acquisition of the glucosyltransferase (GTF) gene. The GTF genes found in S. mutans most likely are derived from other anaerobic bacteria found in the oral cavity, such as Lactobacillus or Leuconostoc. Additionally, the GTF genes in S. mutans display homology with similar genes found in Lactobacillus and Leuconostoc. The common ancestral gene is believed to have been used for hydrolysis and linkage of carbohydrates.[14]
The third trait that evolved in S. mutans is its ability to not only survive, but also thrive in acidic conditions. This trait gives S. mutans a selective advantage over other members of the oral microbiota. 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.[61] Natural selection is most likely the primary evolutionary mechanisms responsible for this trait.
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. As humans evolved anthropologically, the bacteria evolved biologically. 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. Agriculture introduced fermented foods, as well as more carbohydrate-rich foods, into the diets of historic human populations. These new foods introduced new bacteria to the oral cavity and created new environmental conditions. For example, Lactobacillus or Leuconostoc are typically found in foods such as yogurt and wine. Also, consuming more carbohydrates increased the amount of sugars available to S. mutans for metabolism and lowered the pH of the oral cavity. This new acidic habitat would select for those bacteria that could survive and reproduce at a lower pH.[60]
Another significant change to the oral environment occurred during the Industrial Revolution. More efficient refinement and manufacturing of foodstuffs increased the availability and amount of sucrose consumed by humans. This provided S. mutans with more energy resources, and thus exacerbated an already rising rate of dental caries.[14] Refined sugar is pure sucrose, the only sugar that can be converted to sticky glucans, allowing bacteria to form a thick, strongly adhering plaque.[62]
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.
Streptococcus mutans es una bacteria Gram positiva, anaerobia facultativa que se encuentra normalmente en la cavidad bucal humana, formando parte de la placa dental o biofilm dental. Se asocia al inicio y desarrollo de la caries dental y es la que más tiene influencia en el desarrollo de dicha enfermedad. Es neutrofilo porque vive en medio con pH neutro, acidúrico por sintetizar ácidos a pesar de encontrarse en un medio de tales condiciones. Metaboliza la sacarosa para producir polisacáridos extracelulares (sustancia laxa que facilita su adhesión a las caras libres de las piezas dentarias) e intracelulares (metabolismo energético). En estado de salud, un recuento de estas bacterias en boca será de menos de 100.000 UFC.
Streptococcus mutans bakterio Gram positiboa da, estreptokokoen viridans taldean sailkatzen dena, eta txantxarraren eragile nagusia. J. K. Clarkek mikrobioa deskribatu zuen lehenbizikoz 1924an.
Bakterio horren habitat ohikoena ahoa da. Bakterioak polisakarido oso itsaskorra ekoizten du, hortz-esmaltean atxikitzen dena [1]. Hortzetan itsasita, bakterioak glukosa hartzitzen du, azido laktikoa sortuz. Azido horrek hortza kaltetzen du, txantxarra agertuz.
Txantxarra oso ohikoa da herrialde garatuetan, eta askoz gutxiago Hirugarren Munduko herrialdeetan. Lehenengoetan sakarosaren kontsumoa oso hedatuta dago. Sakarosa da Streptococcus mutansek erabiltzen duen azukrea polisakarido itsaskorra sortzeko, eta beraz sakarosa da txantxarraren eragile nagusietako bat.
Streptococcus mutans pertsona gehienen ahoan dago, kasu askotan txantxarra eragin gabe. Txantxarrarekiko norberaren joera fisiologiko eta genetikoak, dietak eta sakarosaren kontsumoak baldintzatuko dute gaitzaren agerpena.
Txantxarraren aurkako txerto baten ikerketa egiten ari da azken urteotan, oraingoz emaitzarik gabe [2].
Streptococcus mutans bakterio Gram positiboa da, estreptokokoen viridans taldean sailkatzen dena, eta txantxarraren eragile nagusia. J. K. Clarkek mikrobioa deskribatu zuen lehenbizikoz 1924an.
Bakterio horren habitat ohikoena ahoa da. Bakterioak polisakarido oso itsaskorra ekoizten du, hortz-esmaltean atxikitzen dena . Hortzetan itsasita, bakterioak glukosa hartzitzen du, azido laktikoa sortuz. Azido horrek hortza kaltetzen du, txantxarra agertuz.
Txantxarra oso ohikoa da herrialde garatuetan, eta askoz gutxiago Hirugarren Munduko herrialdeetan. Lehenengoetan sakarosaren kontsumoa oso hedatuta dago. Sakarosa da Streptococcus mutansek erabiltzen duen azukrea polisakarido itsaskorra sortzeko, eta beraz sakarosa da txantxarraren eragile nagusietako bat.
Streptococcus mutans pertsona gehienen ahoan dago, kasu askotan txantxarra eragin gabe. Txantxarrarekiko norberaren joera fisiologiko eta genetikoak, dietak eta sakarosaren kontsumoak baldintzatuko dute gaitzaren agerpena.
Txantxarraren aurkako txerto baten ikerketa egiten ari da azken urteotan, oraingoz emaitzarik gabe .
Streptococcus mutans est une bactérie cocci de type Gram positif. Elle fait partie de la flore commensale de la cavité buccale, elle intègre les streptocoques oraux (ou viridans), et plus précisément le groupe des streptocoques mutants.
En 1924, le Dr J. Kilian Clarke l'identifie et la désigne comme bactérie responsable de la carie dentaire[1]. Malgré ces travaux, S. mutans ne fut reconnue en corrélation que dans les années 1960.
Cependant depuis 2005, des études montrent que l'abondance de S. mutans n'implique pas nécessairement l'apparition de caries. Celles-ci seraient la conséquence du régime alimentaire, principalement le saccharose, qui engendre une acidité ainsi qu'une production de glucanes insolubles dans l'eau (par la présence de S. mutans), puis fragilise l'émail dentaire avec la formation d'un biofilm, entraînant une virulence des streptocoques mutants[2]. Les caries dentaires résultent de l'action de Streptococcus mutans qui transforme le sucre en acide lactique, et ce dernier attaque l'émail dentaire[3].
Des travaux faits par le Dr Jeffrey D. Hillman, de l'université de Floride, ont permis d'éliminer de S. mutans le gène responsable du codage de l'enzyme permettant la transformation du sucre en acide lactique (lactate déshydrogénase). Appliquée sur les dents de rats, la souche génétiquement modifiée (BCS3-L1) de S. mutans permet une réduction très significative du nombre de caries[4]. Il reste toutefois à poursuivre les travaux sur l'homme; ce qui pourrait poser des problèmes éthiques.
Cette bactérie modifiée BCS3-L1 peut également produire un lantibiotique, la mutacine 1140 (en) (MU1140)[5].
Comme Streptococcus sanguinis, S. mutans ne s’installe dans la bouche qu'après la naissance des dents. Avec Streptococcus sobrinus, en plus de causer la formation de caries, elles sont associées aux endocardites (bien que S. sanguinis et S. oralis en soient les principales) et autres infections du cœur[2].
Streptococcus mutans est une bactérie cocci de type Gram positif. Elle fait partie de la flore commensale de la cavité buccale, elle intègre les streptocoques oraux (ou viridans), et plus précisément le groupe des streptocoques mutants.
En 1924, le Dr J. Kilian Clarke l'identifie et la désigne comme bactérie responsable de la carie dentaire. Malgré ces travaux, S. mutans ne fut reconnue en corrélation que dans les années 1960.
Cependant depuis 2005, des études montrent que l'abondance de S. mutans n'implique pas nécessairement l'apparition de caries. Celles-ci seraient la conséquence du régime alimentaire, principalement le saccharose, qui engendre une acidité ainsi qu'une production de glucanes insolubles dans l'eau (par la présence de S. mutans), puis fragilise l'émail dentaire avec la formation d'un biofilm, entraînant une virulence des streptocoques mutants. Les caries dentaires résultent de l'action de Streptococcus mutans qui transforme le sucre en acide lactique, et ce dernier attaque l'émail dentaire.
Des travaux faits par le Dr Jeffrey D. Hillman, de l'université de Floride, ont permis d'éliminer de S. mutans le gène responsable du codage de l'enzyme permettant la transformation du sucre en acide lactique (lactate déshydrogénase). Appliquée sur les dents de rats, la souche génétiquement modifiée (BCS3-L1) de S. mutans permet une réduction très significative du nombre de caries. Il reste toutefois à poursuivre les travaux sur l'homme; ce qui pourrait poser des problèmes éthiques.
Cette bactérie modifiée BCS3-L1 peut également produire un lantibiotique, la mutacine 1140 (en) (MU1140).
Comme Streptococcus sanguinis, S. mutans ne s’installe dans la bouche qu'après la naissance des dents. Avec Streptococcus sobrinus, en plus de causer la formation de caries, elles sont associées aux endocardites (bien que S. sanguinis et S. oralis en soient les principales) et autres infections du cœur.
Streptococcus mutans adalah kokus (bakteri berbentuk bulat) anaerob fakultatif gram-positif yang biasa ditemukan dalam rongga mulut manusia dan merupakan kontributor yang signifikan untuk kerusakan gigi.[1][2] Bakteri ini adalah bagian dari "streptococci" (jamak, tidak miring, huruf kecil), nama umum informal untuk semua spesies dalam genus Streptococcus. Mikroba ini pertama kali dijelaskan oleh J Kilian Clarke pada tahun 1924.[3]
Bakteri ini, bersama dengan spesies yang terkait erat Streptococcus sobrinus, dapat hidup bersama di mulut: Keduanya berkontribusi terhadap penyakit mulut, dan biaya untuk membedakan mereka dalam pengujian laboratorium seringkali tidak diperlukan secara klinis. Oleh karena itu, untuk tujuan klinis mereka sering dianggap bersama-sama sebagai sebuah kelompok, yang disebut mutans streptococci (jamak, tidak miring karena itu adalah nama kelompok informal).[4] Pengelompokan dari bakteri yang sama dengan tropisme yang sama juga dapat dilihat di viridans streptococci, kelompok lain dari spesies Streptococcus.
. Streptococcus mutans adalah kokus (bakteri berbentuk bulat) anaerob fakultatif gram-positif yang biasa ditemukan dalam rongga mulut manusia dan merupakan kontributor yang signifikan untuk kerusakan gigi. Bakteri ini adalah bagian dari "streptococci" (jamak, tidak miring, huruf kecil), nama umum informal untuk semua spesies dalam genus Streptococcus. Mikroba ini pertama kali dijelaskan oleh J Kilian Clarke pada tahun 1924.
Bakteri ini, bersama dengan spesies yang terkait erat Streptococcus sobrinus, dapat hidup bersama di mulut: Keduanya berkontribusi terhadap penyakit mulut, dan biaya untuk membedakan mereka dalam pengujian laboratorium seringkali tidak diperlukan secara klinis. Oleh karena itu, untuk tujuan klinis mereka sering dianggap bersama-sama sebagai sebuah kelompok, yang disebut mutans streptococci (jamak, tidak miring karena itu adalah nama kelompok informal). Pengelompokan dari bakteri yang sama dengan tropisme yang sama juga dapat dilihat di viridans streptococci, kelompok lain dari spesies Streptococcus.
Lo Streptococcus mutans è un batterio gram positivo ed anaerobio facoltativo, gruppo Lancefield E, che comunemente si trova nella cavità orale umana. Descritto per la prima volta da Clarke nel 1924, è uno dei principali responsabili della carie dentaria.
Lo Streptococcus mutans è uno dei principali batteri coinvolti nel metabolismo del saccarosio, lo zucchero più cariogeno per l'uomo, in quanto ridotto ad acido lattico. Metabolizza anche altri zuccheri ma con minore cariogenicità.
Streptococcus mutans is een gram-positieve, facultatief anaerobe bacterie. De bacterie is acidogeen, waardoor de bacterie in de tandplak een van de voornaamste veroorzakers van cariës is.
Streptococcus mutans is een gram-positieve, facultatief anaerobe bacterie. De bacterie is acidogeen, waardoor de bacterie in de tandplak een van de voornaamste veroorzakers van cariës is.
Multimedia w Wikimedia Commons Streptococcus mutans – bakteria gram dodatnia, będąca fakultatywnym beztlenowcem. Należy do paciorkowców γ-hemolizujących i jest zaliczana do Streptococcus viridans. Po raz pierwszy została opisana przez Clare w 1924 roku.
Fizjologicznie występuje w jamie ustnej człowieka, wchodząc tam w skład naturalnej flory bakteryjnej (ok. 2%) . Streptococcus mutans i inne bakterie stanowią główny czynnik etiologiczny powstawania próchnicy zębów[1] (wraz z L. acidophilus). Podczas zapalenia dziąseł może przejść przez uszkodzone błony śluzowe do krwiobiegu, powodując przejściową bakteriemię oraz infekcyjne zapalenie wsierdzia.
Mogą mieć zmniejszoną wrażliwość na penicyliny, dlatego w zakażeniach uogólnionych penicyliny powinno kojarzyć się z aminoglikozydami.
Mikrobiolodzy z UCLA School of Dentistry w listopadzie 2011 ogłosili, iż opracowali płukankę do ust zawierającą STAMP (ang. specifically targeted anti-microbial peptides) o symbolu C16G2, dobrze rokującą jeśli chodzi o eliminację S. mutans (bez wpływu na bakterie saprofityczne) i zapobieganie próchnicy[1]. Jest to pierwsze tego typu celowane działanie na świecie[1].
Streptococcus mutans – bakteria gram dodatnia, będąca fakultatywnym beztlenowcem. Należy do paciorkowców γ-hemolizujących i jest zaliczana do Streptococcus viridans. Po raz pierwszy została opisana przez Clare w 1924 roku.
Fizjologicznie występuje w jamie ustnej człowieka, wchodząc tam w skład naturalnej flory bakteryjnej (ok. 2%) . Streptococcus mutans i inne bakterie stanowią główny czynnik etiologiczny powstawania próchnicy zębów (wraz z L. acidophilus). Podczas zapalenia dziąseł może przejść przez uszkodzone błony śluzowe do krwiobiegu, powodując przejściową bakteriemię oraz infekcyjne zapalenie wsierdzia.
Streptococcus mutans é uma espécie de bactérias Gram-positivas com morfologia de coco, pertencentes ao género Streptococcus, do grupo A de Lancefield.[1]
Esta bactéria é vulgar na boca do Homem e é o principal fator do desenvolvimento de cáries devido a sua capacidade acidogênica e acidúrica.
Logo ao nascimento, as crianças adquirem uma série de microrganismos que vão compor a microbiota bocal . Estes são transmitidos através da saliva, por indivíduos com os quais as crianças mantêm contato. Diversas técnicas foram desenvolvidas para rastrear cepas de S. mutans adquiridas pelas crianças durante a fase de aquisição inicial destes microrganismo. Este rasteamento é feito a partir do princípio de que cepas da mesma espécie de S. mutans diferem entre si características únicas que nos permitem ser diferenciados dos outros, como por exemplo as impressões digitais, também as cepas de S. mutans têm características únicas, podendo ser rastreadas. Técnicas para se obter a "impressão digital" de cada cepa de S. mutans consistem da obtenção de padrões da sequência do cromossomo. Cada padrão genético indica um genótipo distinto. É possível rastrear de onde foram transmitidos os clones adquiridos por uma criança, através da identificação do padrão genótipo das cepas de S. mutans. Diversos estudos indicam que as crianças são colonizadas por clones presentes na cavidade bucal das mães, sendo estas a principal fonte de infecção. Outros indivíduos da família, como pais, irmão mais velhos e avós, são potenciais transmissores de S. mutans para crianças, embora na maioria dos casos, transmitam SM com menor freqüência do que as mães. Raramente, uma criança é colonizada por um clone de SM presente em outro indivíduo que não seja da mesma família.
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Streptococcus mutans é uma espécie de bactérias Gram-positivas com morfologia de coco, pertencentes ao género Streptococcus, do grupo A de Lancefield.
Streptococcus mutans är en bakterie som är världens ledande orsak till karies. Den hör till släktet streptokocker, är sfärisk till formen och grampositiv.
Denna bakterie hittas i människans mun, främst på tandytan[1].
Streptococcus mutans upptäcktes först av J. K. Clarke år 1924 i kariesskador på tänder, men uppmärksammades inte särskilt mycket förrän under 1960-talet då forskare ordentligt började studera karies[1].
S. mutans tillhör släktet streptokocker, som är ett väldigt brett släkte med bakterier som många skapar sjukdomar av väldigt olika slag. Gemensamt för streptokocker är att de växer i par eller i långa kedjor som liknar pärlhalsband[2].
Specifikt för S. mutans är att den är en icke-mobil bakterie som genom att producera en polysackarid som kallas dextran kan fästa vid t.ex. tandens emalj eller andra bakterier. S. mutans trivs bäst i en miljö med en temperatur på 18-40°C. Den är en fakultativ anaerob, vilket betyder att den kan leva både i syresatta och syrefria miljöer[3]. Bakterien är också speciell på så vis att den klarar av att leva i miljöer med lågt pH, den kan anpassa sig till så låga pH-värden som 3,0[4]. Bakterien har alltså en stor överlevnadsförmåga i sura miljöer om man jämför med andra bakterier som oftast bara klara sig i spannet pH 5-9. Detta är av betydelse eftersom S. mutans producerar syror vid nedbrytning av sockerarter[3].
S. mutans återfinns främst hos människor, och verkar inte vara särskilt utbredd bland vilda djur.[5] Forskare har dock hittat bakterien hos råttor,[6] husarapor och en art av fladdermöss.[7]
Man har hittat sju olika serotyper av S. mutans. Hos människor har serotyp c och d hittats överallt i världen, medan de andra serotyperna verkar vara mindre utbredda.[8] Serotyp c står vanligtvis för 80 % av den S. mutans man kan finna på mänskliga tänder angripna av plack.[5]
I princip alla världens invånare bär alltså på S. mutans i sin mun. Bakterien sätter sig på utsidan av tänderna och livnär sig på flera olika sorters kolhydrater. S. mutans kan syntetisera extracellulära polysackarider. Den kan ur sackaros bilda olika sorters glukaner och fruktaner. Speciellt glukaner bidrar sedan till bildandet av plack på tänderna. Men sackaros används inte bara vid syntes av polysackarider utan används även som energikälla under bakteriens tillväxt[5].
Clarke upptäckte att S. mutans som återfanns i kariesangrepp kunde fermentera ämnen som glukos, laktos, raffinos, mannitol, inulin och salicin och bilda syra[9]. Då glukoshalten i munnen är hög, bryter S.mutans ner glukos till laktat som i sin tur kan bilda mjölksyra. Glukosen kommer bland annat från nedbrytningen av sackaros. Om tillgången på glukos är begränsad tillverkas även formiatjoner (som bildar myrsyra) och acetatjoner (som bildar ättiksyra) [10]. Syrorna som bildas gör att man får karies och hål i tänderna[11].
S. mutans är dock inte den enda bakterien i munnen av släktet Streptokocker som orsakar karies, utan även många andra microber växer på tänderna och kan orsaka karies om man inte sköter munhygienen ordentligt. Några av dessa andra bakterier är Streptococcus sanguis, S. mitior, S. salivarius och S. milleri. S. mutans är dock den av streptokockerna i munnen som använder sackaros snabbast och därmed bildar mer glukos, som i sin tur blir till laktat som orsakar karies[5].
Streptococcus mutans är en bakterie som är världens ledande orsak till karies. Den hör till släktet streptokocker, är sfärisk till formen och grampositiv.
Denna bakterie hittas i människans mun, främst på tandytan.
Streptococcus mutans çoğunlukla insan ağız boşluğunda bulunan gram-pozitif, fakültatif anaerobik bir bakteridir ve diş çürüğünün oluşumunda önemli bir etkendir.[1][2] Mikroorganizma ilk kez 1924'te Clarke tarafından tanımlanmıştır.[3]
Gram pozitif bakteriler Gram boyamasında koyu mavi veya mor renkte boyanmaktadır. Bu durum, gram negatif bakterilerinin hücre duvarlarının mor boya kristallerinin tutamamasının tersine gram-pozitif bakterilerin hücre duvarlarının bu fiziksel özelliği taşımasına bağlıdır.[4] Streptokok lar, Firmicutes bölümüne ve laktik asit bakteri grubuna bağlı olan halka şekilli bir gram-pozitif bakteri cinsidir.[5] İnsan ağız florasının bir öğesi olan S. mutans, büyük oranda diş çürüğünün ana etyolojik etkeni olarak kabul edilmektedir. Ağız boşluğu içindeki şartlar uç noktalarda hareket edecek kadar çok değişken ve karmaşıktır. Bu nedenden dolayı, ağız boşluğunda yaşamaya devam edebilmek için, S. mutans, çok keskin çevresel değişimlere ve farklı toksik maddelere karşı dayanabilmelidir.[6] Ne var ki, çürük yapıcı bu patojenin hayatta kalabildiği ve böylesi uç çevresel şartlar altında çoğalmaya devam edebildiği mekanizmalar bu konuyla ilgili çok az araştırma yapıldığı için büyük oranda bilinmemektedir.
Oral streptokok ların 25 türü ağız boşluğunda yaşamaktadır. Her tür, farklı ağız bölgesinde koloni kurmak, rekabet içinde olduğu bakterilerle değişen koşullarda mücadele edebilmek ve dış saldırılar karşısında hayatta kalmak için farklı özgün özellikler geliştirmiştir. Mikrobik biotadaki dengesizlikler ağız hastalıklarına neden olabilir.Özel şartlar altında, komensal streptokoklar hastalık yapan ve konakçıya zarar veren fırsatçı patojenlere dönüşebilir. Ağızdaki streptokoklar arasında hem zararsız hem de zararlı bakteriler vardır. Streptococcus mutans diş çürüğüne eşlik eden en önemli bakteridir. Bu karmaşık bakterinin taksonomisi henüz deneme aşamasındadır.[7] 1970 yılında yapılan bir çalışmada ağız boşluğundaki toplam streptokokların % 39'unu oluşturan s.mutans'ın çoğunlukla dişteki çürük alanlarında ve çatlaklarda olduğu bulgulandı. Daha az sayıda S.mutans'ın ise yanak yüzeyinde (% 2-9)olduğu gösterildi.[8]
Diş yüzeyinin ilk yerleşimcileri en yüksek oranda Neisseria spp. ve S. mutans'ı da içeren Streptokoklardır. Bu öncü türlerin sayısının artması ve metabolizmaları, diş bakteri plağını oluşturacak daha etkili organizmaların onlardan sonra buraya yerleşmesine neden olacak şekilde ortamın şartlarını (Ör:pH, birlikte kümelenme,substrat varlığı vb.) değiştirmektedir.[9] S. mutans, S. sobrinus ile sukroz'u Glukansükraz enzimi ile [10] laktik aside dönüştürerek diş çürüğünde büyük bir rol oynar.[2] Bu süreç ile ağız içinde oluşan bu asidik ortam, çürük için elverişli olan yüksek düzeyde mineralize olmuş diş minesinin meydana gelmesinin nedenidir.
Streptococcus mutans çoğunlukla insan ağız boşluğunda bulunan gram-pozitif, fakültatif anaerobik bir bakteridir ve diş çürüğünün oluşumunda önemli bir etkendir. Mikroorganizma ilk kez 1924'te Clarke tarafından tanımlanmıştır.
Gram pozitif bakteriler Gram boyamasında koyu mavi veya mor renkte boyanmaktadır. Bu durum, gram negatif bakterilerinin hücre duvarlarının mor boya kristallerinin tutamamasının tersine gram-pozitif bakterilerin hücre duvarlarının bu fiziksel özelliği taşımasına bağlıdır. Streptokok lar, Firmicutes bölümüne ve laktik asit bakteri grubuna bağlı olan halka şekilli bir gram-pozitif bakteri cinsidir. İnsan ağız florasının bir öğesi olan S. mutans, büyük oranda diş çürüğünün ana etyolojik etkeni olarak kabul edilmektedir. Ağız boşluğu içindeki şartlar uç noktalarda hareket edecek kadar çok değişken ve karmaşıktır. Bu nedenden dolayı, ağız boşluğunda yaşamaya devam edebilmek için, S. mutans, çok keskin çevresel değişimlere ve farklı toksik maddelere karşı dayanabilmelidir. Ne var ki, çürük yapıcı bu patojenin hayatta kalabildiği ve böylesi uç çevresel şartlar altında çoğalmaya devam edebildiği mekanizmalar bu konuyla ilgili çok az araştırma yapıldığı için büyük oranda bilinmemektedir.
Streptococcus mutans Clarke 1924
Streptococcus mutans (лат.) — вид грамположительных, факультативно анаэробных бактерий рода стрептококков, обычно обнаруживаемая в ротовой полости человека, вносит существенный вклад в возникновение кариеса[1][2]. Микроорганизм первоначально был описан Д. К. Клэрком в 1924 году[3]. Передача бактерии может происходить от родителей к ребёнку, а также, от одного ребёнка к другому через бытовые контакты (посуда, соломки для питья и пр.).
Наряду с Streptococcus sobrinus, Streptococcus mutans играет главную роль в разрушении зубов, переводя сахарозу в молочную кислоту[2]. Кислая среда, создаваемая во рту этим процессом является причиной того, что высоко минерализованная зубная эмаль испещряется и становится уязвимой для разрушения. Streptococcus mutans — один из нескольких специализированных организмов, снабжённых рецепторами для прилипания к поверхности зубов. Сахароза используется Streptococcus mutans, чтобы произвести липкий внеклеточный полисахарид на основе декстрана, который позволяет им связываться между собой, формируя зубной налёт. Streptococcus mutans производит декстран при помощи фермента декстрансахаразы, используя сахарозу как субстрат. Сахароза — единственный сахар, который Streptococcus mutans может использовать, чтобы образовывать этот полисахарид[1].
Метаболизирует другие сахара, такие как: глюкоза, фруктоза, лактоза и сахарозу в молочную кислоту в качестве конечного продукта. Эта комбинация зубного камня и кислоты ведёт к разрушению зуба[4].
Возрастание роли Streptococcus mutans в возникновении кариеса связано с переходом цивилизации к земледелию 10 тыс. лет назад. Увеличение доли зерновых продуктов содержащих крахмал в диете человека создало благоприятные условия для жизни бактерий. Значительно увеличивается доминирование бактерии после промышленной революции 1850-х годов с увеличением рафинированных сахаров в диете[5].
Некоторые штаммы Streptococcus mutans образуют протеазы, деактивирующие содержащиеся в слюне антитела IgA, ослабляя тем самым иммунную защиту. Некоторые штаммы Streptococcus mutans способны выделять бактериоцины, при помощи которых ведётся борьба за среду обитания.
Это заготовка статьи по бактериологии. Вы можете помочь проекту, дополнив её. Streptococcus mutans (лат.) — вид грамположительных, факультативно анаэробных бактерий рода стрептококков, обычно обнаруживаемая в ротовой полости человека, вносит существенный вклад в возникновение кариеса. Микроорганизм первоначально был описан Д. К. Клэрком в 1924 году. Передача бактерии может происходить от родителей к ребёнку, а также, от одного ребёнка к другому через бытовые контакты (посуда, соломки для питья и пр.).
ストレプトコッカス・ミュータンス（英語: Streptococcus mutans）は、グラム陽性で通性嫌気性のレンサ球菌の一種である。ヒトの口腔内にも存在し、う蝕（虫歯）の原因菌のひとつである。1924年にJ Kilian Clarkeによって発見された。
ストレプトコッカス・ミュータンスは最初からヒトの口腔内に存在しているのではなく、口移しや食器の共有などによって、感染者の唾液が口に入ることによって感染する。なお、同属にストレプトコッカス・ソブリヌス（Streptococcus sobrinus）などがあるが、それら全てがストレプトコッカス・ミュータンスと考えられていた。しかし、DNAによる同定法などが確立してきたために、それらが別の菌であることが分かった。
標準菌と異なる糖鎖を持つグルコースの側鎖を持たない菌株は高病原性株と呼ばれ、白血球に貪食されにくく、血液中に菌が存在する菌血症状態となり、全身に病原性をもたらす。現在では、脳出血や潰瘍性大腸炎への関与が疑われている。
高病原性株TW295 への感染は、潰瘍性大腸炎の発症リスクを高めているとの日経メディカルは報じている[1][2]。
ミュータンス群は7菌種に分類されているが、ヒトの口腔内に存在するのはストレプトコッカス・ミュータンスとストレプトコッカス・ソブリヌスで、ともにう蝕に関与している。ストレプトコッカス・ミュータンスは、菌体内に保持する酵素群により以下に示すようなう蝕過程の反応を活性化させる。
この項目は、歯学に関連した書きかけの項目です。この項目を加筆・訂正などしてくださる協力者を求めています（プロジェクト:歯学／Portal:医学と医療）。 
この項目は、真正細菌（バクテリア）に関連した書きかけの項目です。この項目を加筆・訂正などしてくださる協力者を求めています（Portal:生き物と自然／ウィキプロジェクト 生物）。 ストレプトコッカス・ミュータンス（英語: Streptococcus mutans）は、グラム陽性で通性嫌気性のレンサ球菌の一種である。ヒトの口腔内にも存在し、う蝕（虫歯）の原因菌のひとつである。1924年にJ Kilian Clarkeによって発見された。
충치균(蟲齒菌)은 연쇄상구균의 일종이다. 학명은 스트렙토코쿠스 뮤탄스(Streptococcus mutans). 락토바실러스와 함께 충치의 주 원인균으로 지목된 바 있다. 그러나 현재까지 알려진 바로는 뮤탄스는 치아를 검은색으로 변색시켜 썩게 만들며 락토바실러스 같은 경우 색이 변하는 것과는 무관하지만 치아를 썩게 만든다.
