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1 University of Missouri at Kansas City, School of Dentistry, Kansas City, Missouri, and the University of Texas Dental Branch, Houston, Texas
Forty-eight extracted teeth (unerupted third molars) were mounted individually in plastic tubes in such a manner as to permit the study of the effects of the diffusion of microbial growth factors on the development of in vitro carious lesions. Intact teeth were exposed for 12 weeks to the growth of L. arabinosus in various culture media, and drilled teeth were exposed 12 weeks to either the growth of L. arabinosus or the growth of S. faecalis in various culture media.
L-tryptophan, niacin, pantothenate, and folic acid diffused, alone and in combination, from the pulp sides to the crown sides of teeth in sufficient amounts to support the growth of microorganisms on tooth surfaces.
In vitro carious lesions were produced in intact teeth and varied in extent from enamel etchings in some teeth to lesions extending into dentin in others. In vitro carious lesions produced in drilled teeth often extended to the pulp chamber.
When bacterial growth was dependent on the diffusion of growth factors from within the tooth, in vitro carious lesions were produced that simulated natural caries: discrete, deep penetrating lesions with microbial invasion of dentinal tubules. In contrast, when the roots of teeth were immersed in distilled water and the crowns were covered with either a complete medium or a deficient medium to which growth factors were added at intervals to simulate diffusion, the in vitro lesions produced did not simulate natural caries. There appeared diffuse, shallow lesions without microbial invasion of dentinal tubules.
The tooth itself did not support the growth of the test organisms, and no visible lesions were observed when the crowns of teeth were covered with a medium deficient in a single growth factor and the roots were immersed in distilled water.
Microscopic observations revealed that enamel lamellae may provide a specific pathway for demineralizing solutions on the coronal surface to reach the dentin as well as to provide a specific pathway for microbial invasion of the dentin.
Submitted on March 22, 1965
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