Adherence Inhibition of
            <i>Streptococcus mutans:</i>
            an Assay Reflecting a Possible Role of Antibody in Dental Caries Prophylaxis

Olson, Gerald A.; Bleiweis, Arnold S.; Small, Parker A.

doi:10.1128/iai.5.4.419-427.1972

Cited by 91 publications

(46 citation statements)

References 22 publications

(16 reference statements)

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“…For this establishment, adhesive and aggregative abilities of S. mutans cells should be involved [11,30,31,33]. These Table 5.…”

Section: Discussionmentioning

confidence: 99%

“…The ability to produce sticky polysaccharides has been suggested as one of the virulent factors of Streptococcus mutans, an organism which causes dental caries in experimental animals as well as humans [9,14,40]. The extracellular polysaccharides synthesized by S. mutans in the presence of sucrose are responsible for the adherence ability of S. mutans cells on smooth surfaces including extracted or artificial teeth, glass and wire surfaces [21, [29][30][31]33]. This property of S. mutans explains in part its plaque-forming potential which will result in the development of dental caries.…”

mentioning

confidence: 99%

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Inhibition of Rat Dental Caries by Dextranase from a Strain of Spicaria violacea

Hamada

Ooshima

Masuda

et al. 1976

Japanese Journal of Microbiology

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Dextranase AD 17 obtained from a culture liquor of a strain of Spicaria violacea was assessed for its ability to inhibit the development of dental caries in conventional Sprague-Dawley rats which had been infected with one of the Streptococcus mutans strains, MT6R (serotype c), OMZ 176R (d), or MT-703R (e). These experiments showed that caries was significantly inhibited when rats were given cariogenic diet #2000 and drinking water containing AD17 at a concentration of 10 units/g, as compared to control rats not given dextranase.The inhibitory effects of AD17 were more prominent in smooth surface caries than in total caries. AD17 had a tendency to retard both the establishment of inoculated S. mutans and plaque deposition on tooth surfaces. However, S. mutans could be implanted in the rat oral cavity after repeated inoculation of the bacteria, even in the presence of AD 17. These results suggest that the anticaries activity of AD17 is due to not only inhibition of adherence of S. mutans cells on tooth surfaces but also to physicochemical changes of dental plaque formed under the enzymatic action of AD 17. Preliminary histopathological examination showed that AD17 had no significant toxicity in rats.

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“…For this establishment, adhesive and aggregative abilities of S. mutans cells should be involved [11,30,31,33]. These Table 5.…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Inhibition of Rat Dental Caries by Dextranase from a Strain of Spicaria violacea

Hamada

Ooshima

Masuda

et al. 1976

Japanese Journal of Microbiology

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“…An assay measuring biofilm formation on a glass wall was performed as described previously (Olson et al, 1972) with some modifications. BHI broth supplemented with 5% sucrose (3 mL) in a glass tube was inoculated with an 18-24-h streptococcal culture (final A 620 nm = 0.01).…”

Section: Biofilm Assaysmentioning

confidence: 99%

Identification of theStreptococcus gordonii glmMgene encoding phosphoglucosamine mutase and its role in bacterial cell morphology, biofilm formation, and sensitivity to antibiotics

Shimazu¹,

Takahashi²,

Uchikawa³

et al. 2008

FEMS Immunol Med Microbiol

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Phosphoglucosamine mutase (EC 5.4.2.10) catalyzes the interconversion of glucosamine-6-phosphate into glucosamine-1-phosphate, an essential step in the biosynthetic pathway leading to the formation of peptidoglycan precursor uridine 5'-diphospho-N-acetylglucosamine. The gene (glmM) of Escherichia coli encoding the enzyme has been identified previously. We have now identified a glmM homolog in Streptococcus gordonii, an early colonizer on the human tooth and an important cause of infective endocarditis, and have confirmed that the gene encodes phosphoglucosamine mutase by assaying the enzymatic activity of the recombinant GlmM protein. Insertional glmM mutant of S. gordonii did not produce GlmM, and had a growth rate that was approximately half that of the wild type. Morphological analyses clearly indicated that the glmM mutation causes marked elongation of the streptococcal chains, enlargement of bacterial cells, and increased roughness of the bacterial cell surface. Furthermore, the glmM mutation reduces biofilm formation and increases sensitivity to penicillins relative to wild type. All of these phenotypic changes were also observed in a glmM deletion mutant, and were restored by the complementation with plasmid-borne glmM. These results suggest that, in S. gordonii, mutations in glmM appear to influence bacterial cell growth and morphology, biofilm formation, and sensitivity to penicillins.

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“…The glucosyltransferases on the cell surface of Streptococcus mutans have been reported to be responsible for the adherence of the cells to a smooth surface (16,17,19), leading to the initiation and development of smooth surface dental caries (3,6,25). The extracellular enzymes of S. mutans HS6 (serotype a) (10, IS) are able to bind to heat-treated cells and subsequently synthesize water-insoluble glucan from sucrose, resulting in the adherence of cells (10,16).…”

mentioning

confidence: 99%

Synthesis of Glucan on the Cell Surface of Streptococcus mutans: Chemical and Scanning Electron Microscopic Studies

Tsumori

Mukasa

Zinnaka

1982

Microbiology and Immunology

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The appearance and continuing growth of extracellular material on Streptococcus mutans HS6 cells in sucrose-containing Merthiolated buffer was observed in a scanning electron microscope and was found to be related to the glucan synthesis on the cell and to adherence of the cell to a smooth surface. Cells grown in broth completely deprived of sucrose by invertase (HS6-IV) had a characteristic, slightly rugged surface structure. On incubation of HS6-IV in the sucrosecontaining buffer, a few small globular particles appeared on the surface and grew to an irregular shape (globular to fibrilar) after several hours. The increase in the total glucan content of the cells paralleled the growth of the globular material, to which ferritin-conjugated anti-dextran globulin was found to bind. On the cell surface of cells harvested from conventional broth, both small globular and irregular structures, which possibly formed from sucrose in the broth, existed originally and continued to grow during incubation, along with the material newly appearing on the surface. The accumulation of glucan on the cells resulted in their adherence to a glass surface. The inhibition of growth of the extracellular material on the cells by trypsin, dextranase or anti-glucosyltransferase corresponded to the decrease in glucan synthesis and the loss of adhering ability. These results indicated that the material growing on the cell surface was glucan synthesized by glucosyltransferases.

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Adherence Inhibition of Streptococcus mutans: an Assay Reflecting a Possible Role of Antibody in Dental Caries Prophylaxis

Cited by 91 publications

References 22 publications

Inhibition of Rat Dental Caries by Dextranase from a Strain of Spicaria violacea

Inhibition of Rat Dental Caries by Dextranase from a Strain of Spicaria violacea

Identification of theStreptococcus gordonii glmMgene encoding phosphoglucosamine mutase and its role in bacterial cell morphology, biofilm formation, and sensitivity to antibiotics

Synthesis of Glucan on the Cell Surface of Streptococcus mutans: Chemical and Scanning Electron Microscopic Studies

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