Abstract
In 1944, Hunt, Hoppert, and Erwin1 de veloped two inbred strains of rats of d if ferent caries-susceptibility. Animals of the caries-susceptible strain, if placed on a cariogenic diet at the age o f 35 days, de velop the first clinically visible carious lesions at the age o f 70 days. Animals of the resistant strain under the same condi tions are found free of caries until 400 to 500 days o f age. Mechanisms underlying the different caries-susceptibility o f these two strains have been sought in the struc ture o f the enamel, in the bacterial flora and in the salivary secretion. Nakfoor, Hunt and Hoppert2 showed «that when the rats were 60 days o f age, the lower molars o f the resistant strain fractured less readily than those in ani mals o f the susceptible strain. This was not thought to be an important factor in the initiation of dental caries, since few spontaneous fractures had occurred in the molar teeth o f the susceptible rats at a time when caries had appeared in nearly half o f these animals. Further more, the relative weakness of the molars in the susceptible rats may have been in fluenced by incipient decay. Jay3 re covered lactobacilli more frequently and in greater numbers in the susceptible than in the resistant rats. Jay’s observa tion was confirmed in later studies by Rosen and others,4 who further stated that Streptococcus salivarius was found more often in the caries-susceptible ani mals. Their data, however, do not permit an estimate of the quantitative difference in the flora of the two strains. Cheyne5’ 6 has shown that in the rat a considerable increase in caries incidence occurs when the submaxillary and parot id glands are extirpated. This observa tion makes it seem that the presence of saliva has a caries-preventing effect. A similar conclusion for the human being had been reached by Weinmann7 in 1936,
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