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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