FACTORS INFLUENCING DENTAL CARIES 269 



Other findings in coincidence with these include those of Zipkin et 

 al (1960) and of Larson and Zipkin (1961). 



By the use of bacterially depressed or similar noninfected animals 

 it is possible to show that caries is related to an infectious agent 

 which can be passed from cagemate to cagemate and from mother 

 to young. The disease can also be induced by inoculating either 

 feces or carious dentin and plaque into the mouth of a noninfected 

 young animal. The point has been emphasized that because the ali- 

 mentary canal microbiota with its cariogenic components is not 

 stable but varies with different experimental diets and conditions, 

 it is difficult to design and interpret many caries studies in animals. 

 For example, many attempts have been made to correlate caries 

 susceptibility with prenatal diets and those consumed during the 

 early stages of tooth formation. The mechanisms whereby protein- 

 carbohydrate ratios, ash and salt mixtures, dietary deficiencies, etc., 

 influence susceptibility of the host cannot be detennined if the diet 

 induces unrecognized changes in the alimentary canal microflora of 

 mother animals, who then transmit their altered flora to the young. 



It has also been pointed out that in hamsters the dietary history 

 of the mother and her own caries experience may be independent 

 of the susceptibihty to caries of her offspring (Keyes, 1960Z?). A 

 susceptible and infected female will not develop caries unless main- 

 tained on a cariogenic diet; but since she harbors a pathogenic flora, 

 her offspring will develop caries if a suitable diet is provided while 

 the animals are young. It has also been reported (Keyes and Fitz- 

 gerald, 1962 ) that a female can harbor cariogenic bacteria and con- 

 sume a caries-conducive ration, and still be caries-inactive for various 

 reasons, e.g. maturation factors, etc. Yet such an animal can transmit 

 the flora to her offspring, who will develop the disease. Since the 

 entire alimentary canal microbiota is involved and not the mouth 

 alone, one would not expect to find offspring from females whose 

 teeth had been extracted to be appreciably different from animals 

 whose dams were allowed to develop the disease in retained teeth. 

 This possibility, as postulated by Shaw et al. (1962), would seem 

 unlikely. Indeed, animals in which caries activity has been sup- 

 pressed by fluoride continue to harbor pathogenic organisms and to 

 produce infected offspring (Keyes et al., 1962), and even though the 



