Abstract

Mutated sub-strains of Str. mutans were prepared from strain 10449 (human type) and strain RC-20 (rat type) with the nitrogen mustard mutation method. The mutant which produced a great deal of insoluble glucans was named phase I, and the mutant which failed to form insoluble glucans was named phase III. Four mutants (10449-phase I, III and RC-20-phase I, III) were examined for cariogenicity with an experimental caries model using rats.At weaning, the rats were given 200 μg/ml streptomycin-sulfate water during two days. The rats were divided into four groups and were challenged with the 4 mutants of Str. mutans once a day for eiyht days. All animals were fed with the cariogenic diet (6PMV) and distilled water for 30 days after weaning. During this period, the residual Str. mutans in the mouth of the rats was examined. The upper and lower jaws with teeth and the blood were taken from sacri ficed animals. There was more Str. mutans remaining in the rats' mouth in the phase I sub-strain than in the phase HI sub-strain of both 10449 and RC-20 strains. Although there was no significant difference between the amount of Str. mutans 10449-phase I and RC-20-phase I remaining, significantly more carious lesions were discovered on the molars of the rats in the RC-20-phase I group. The rats of the 10449-phase I group had many more carious lesions than the 10449-phase III group. However, the RC-20-phase I group had a caries score nearly equal to that of the RC-20-phase III group. During the experimental period, a rat-type strain of Str. mutans, which seemed to be an indigenous organism within the rats' mouth, was detected in the RC-20-phase III group. It seemed that the poor ability of the RC-20-phase III strain to become established induced the prevalence of indigenous Str. mutans, and carious lesions developed from these indigenous organisms.The serum collected from the rats in the four groups had a similar level of agglutinating titer against RC-20 or 10449 whole cell antigen.

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