Role of sucrose in the fitness of Streptococcus mutans.
BACKGROUND
Dental caries has been closely linked to fermentable carbohydrates as key environmental factors. Sucrose has been identified as the most cariogenic carbohydrate. Streptococcus mutans, considered to be the primary pathogen causing dental caries, is able to utilize sucrose as a nutrient source, partially for the production of intracellular storage components and for the production of extracellular glucans via the glucosyltransferases GtfB, GtfC, and GtfD. The following study explores the competitiveness and fitness of S. mutans when grown with different concentrations of sucrose.


METHODS
Growth competition with oral streptococci and antimicrobial susceptibility in static biofilm models grown without sucrose or with 0.1% or 0.5% sucrose were investigated using confocal laser scanning microscopy. The numbers of surviving S. mutans of both wild-type and an isogenic Gtf-negative mutant after antimicrobial treatment were determined as colony-forming units.


RESULTS
S. mutans was able to establish microcolonies with increasing sucrose concentration in the presence of other streptococcal competitors during biofilm development. The antimicrobial susceptibility decreased when sucrose was available as substrate and was dependent on the presence of the Gtfs.


CONCLUSIONS
The increased resistance against antimicrobial treatment was associated with the availability of sucrose, but was not influenced much by the concentration used during this study. The resistance was strongly associated with the Gtf activity, excluding any intracellular metabolic effect of sucrose in the resistance mechanism.
Kreth
J
J
School of Dentistry, University of Minnesota, Minneapolis, MN 55455, USA. kreth001@umn.edu
Zhu
L
L
Merritt
J
J
Shi
W
W
Qi
F
F
D000891:Anti-Infective Agents, Local / Q000008:administration & dosage / Q000494:pharmacology; D018441:Biofilms / Q000187:drug effects / Q000254:growth & development; D002326:Cariogenic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D002710:Chlorhexidine / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology; D015169:Colony Count, Microbial; D004338:Drug Combinations; D005964:Glucosyltransferases / Q000235:genetics; D006801:Humans; D008667:Metalloproteins / Q000008:administration & dosage / Q000494:pharmacology; D008826:Microbial Sensitivity Tests; D018613:Microscopy, Confocal; D009055:Mouth / Q000382:microbiology; D009154:Mutation / Q000235:genetics; D012459:Salicylates / Q000008:administration & dosage / Q000494:pharmacology; D054773:Streptococcus gordonii / Q000187:drug effects / Q000254:growth & development; D034361:Streptococcus mitis / Q000187:drug effects / Q000254:growth & development; D013295:Streptococcus mutans / Q000187:drug effects / Q000201:enzymology / Q000254:growth & development*; D019533:Streptococcus oralis / Q000187:drug effects / Q000254:growth & development; D016986:Streptococcus sobrinus / Q000187:drug effects / Q000254:growth & development; D013395:Sucrose / Q000008:administration & dosage / Q000494:pharmacology*; D013729:Terpenes / Q000008:administration & dosage / Q000494:pharmacology
D000891:Anti-Infective Agents, Local; D002326:Cariogenic Agents; D004338:Drug Combinations; D008667:Metalloproteins; C090220:Perioguard; D012459:Salicylates; D013729:Terpenes; C057473:Listerine; D013395:Sucrose; C036655:1,3-alpha-D-glucan synthase; D005964:Glucosyltransferases; C110463:glucosyltransferase C; C113848:glucosyltransferase D; C010882:chlorhexidine gluconate; D002710:Chlorhexidine