Abstract
able. Histological observations are still subject to alternative explanations. Studies have indicated that acid forma tion might be concerned indirectly with pigmentation of the lesion and that decal cification might be a necessary precursor to depolymerization and lysis of the organic matrix. Careful in vitro decalcification has produced many of the phenomena observed in beginning caries. Beginning carious lesions stained with alizarin red S and lesions produced in vitro by acid and subsequently stained with alizarin red S have been shown to be very similar. In bacterial examination of early caries le sions, the majority of organisms were found to be acidogenic. The cumulative evidence to date is strongly indicative that acid is the initiating factor in enamel caries. Much of the difficulty in arriving at positive conclusions as to the mechanism of caries initiation is due to the present inability to study very early lesions com pletely. Neither decalcified nor ground sections permit study of all the essential components. Direct sectioning of carious material is possible only after deminer alization has proceeded to a substantial degree. Scott and Albright have suggested that investigation of changes on the enamel surface by replica technic would be a promising approach. It would seem that study of the very earliest manifestations of structural alteration is necessary to establish the mechanism of caries initia tion. A full appreciation of this process would aid substantially in an understand ing of the complete etiology of the disease and provide a rational basis for preven tion.
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