We have constructed a panel of mutants of S. mutans V403 which are def
ective in one or more of the glucosyltransferase genes (gtfB,C or D) o
r the fructosyltransferase gene (ftf). These strains have been tested
for virulence in a gnotobiotic rat caries model with reference to both
buccal (smooth surface) and sulcal (pit and fissure) carious lesions.
Our data suggest differing roles for degradable and non-degradable po
lymers at buccal and sulcal sites. Non-degradable polymers (made by pr
oducts of the gtfB and C genes) contributed significantly to the sever
ity of smooth surface lesions. However, our studies suggested their ro
le in pit and fissure lesions was not as important as the role of degr
adable polymers. Specifically, a mutant deficient in the major insolub
le glucan synthesizing activity (product of the gtfB gene) was 25% mor
e cariogenic on sulcal surfaces than was the wild-type V403 strain. We
propose that extracellular glucosyltransferases and fructosyltransfer
ase compete for sucrose and that this competition influences pathogeni
city at differing tooth sites.