Streptococcus sobrinus is known to possess cariogenic properties in vitro. It can produce acid in large amounts and it has the capacity to adhere to enamel and other surfaces. However, most studies on cariogenicity have been performed with laboratory strains that have been subcultured over long periods of time. Therefore, the cariogenicity and acidogenicity of 9 fresh isolates of both S. sobrinus and Streptococcus mutans from human dental plaque were compared. The bacteria were inoculated into the oral cavity of rats. The rats were fed diet SSP 20/5, containing 20% sucrose and 5% glucose. After the experimental period of 42 days, the amount of caries was assessed and bacterial counts were determined using monoclonal antibodies. Four out of 9 S. sobrinus strains and 3 out of 9 S. mutans strains did not colonize the rats. Colonizing strains constituted 39–78% of the total anaerobic cultivable microflora. The numbers of advanced dentinal lesions in the fissures of the rats colonized with S. mutans were significantly lower than those colonized with S. sobrinus (p < 0.05). S. sobrinus produced acid more rapidly than S. mutans in a pH-stat system at pH values between 6.5 and 5.0 (p < 0.01). The results indicate that fresh isolates of S. sobrinus are more cariogenic in rats than fresh isolates of S. mutans. This is possibly due to differences in glycolytic properties of these two species.

The aim of this investigation was to study the effect of an in vitro acquired, stable, fluoride-resistant strain of Streptococcus mutans on dental caries in rats. Three groups (P0, P5 and P10) of SPF Osborne-Mendel rats were inoculated with the fluoride-sensitive S. mutans C180–2. Three other groups (FR0, FR5 and FR10) were inoculated with cultures of the fluoride-resistant S. mutans C180–2FR. Diet SSP 20/5 and tap water ( < 0.2 ppm fluoride) were available ad libitum to all groups. The drinking water of groups P5 and FR5 was supplemented with 5 mg F-/l and the drinking water of groups P10 and FR10 with 10 mg F-/l. At the end of the caries experiment (days 58/59) there were no significant differences in the percentages and in the numbers of S. mutans in the total maxillary plaques of groups P0 to P10 and of groups FR0 to FR10, respectively. The fluoride tolerance of S. mutans cells re-isolated from rats, inoculated with the fluoride-sensitive strain, showed an unstable decrease compared to before inoculation. S. mutans cells re-isolated from rats, inoculated with the fluoride-resistant strain, showed both unstable and stable adaptation towards fluoride sensitivity. The animals superinfected with the fluoride-resistant strain developed less dentinal/fissure caries. Fluoride given in the drinking water at concentrations of 5 and 10 mg/l was effective in reducing caries irrespective of whether the animals were superinfected with the fluoride-sensitive or the fluoride-resistant strain. The data suggest that adaptation of S. mutans to fluoride in dental plaque, if occurring, will not reduce the effect of waterborne fluoride, but does reduce the cariogenicity of the plaque.

Fluoride-resistant strains of mutans streptococci have been found to be less cariogenic than their parent strains in the rat model system. Therefore, it is important to determine whether the use of fluorides in vivo will increase the fluoride resistance of mutans streptococci and thereby possibly decrease their cariogenic potential. We studied (1) the fluoride resistance of Streptococcus mutans C180-2 in rat dental plaque exposed to various fluoride treatments (experiment 1), (2) the cariogenic potential of the exposed plaque after transmission to other animals (experiment 2), and (3) whether the fluoride treatments favoured the establishment of in vitro induced fluoride-resistant S. mutans in competition with a fluoride-sensitive strain in rat dental plaque (experiment 3). In all experiments, specific pathogen-free Osborne-Mendel rats were used, and all animals received diet SSP 20/5, containing 20% (w/w) sucrose and 5% (w/w) glucose, and tap water ad libitum. In experiment 1, the rats were inoculated with S. mutans C180-2. For an experimental period of 44 days, the rats either received no F treatment or received NaF mixed in the diet and drinking water (20 or 60 ppm F) or were brushed 6 days per week with an aqueous NaF solution containing either 0.1% (w/v) or 1% (w/v) F, respectively. Bacteriological analyses at the end of the experiment revealed that none of the fluoride treatments had caused a detectable increase in the inherent fluoride resistance of S. mutans C180-2. In experiment 2, the rats were inoculated with pooled plaque samples collected from animals of the control group, the group that received 60 ppm F, or the group treated with 1% F in experiment 1, respectively. After an experimental period of 35 days, no significant differences were observed in amount or severity of fissure caries in the mandibular molars of animals inoculated with one of the pooled plaque samples or with the original S. mutans C180–2. In experiment 3, rats were inoculated with a mixture of equal numbers of colony-forming units of a fluoride-sensitive (C180-2SR) and a fluoride-resistant (C180-2FR) S. mutans strain and subjected to one of the F treatments described in experiment 1. The results showed that the fluoride-resistant strain had not emerged in rat dental plaque by day 14 after inoculation, irrespective of the F treatments. The fluoride-resistant strain did establish when inoculated separately. The results of the studies described here indicate that growth adaptation to fluoride resistance by S. mutans is not likely to occur in vivo, that fluoride does not induce a prolonged reduction in the cariogenicity of dental plaque, and that fluoride resistance impairs establishment of S. mutans when competing with fluoride-sensitive strains.