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A correlated microradiographic-transmission electron microscopic study examined incipient caries in human enamel from the enamel surface through the body of the lesion. In sections parallel to enamel prisms in the body of the lesion, cross-striations are accentuated as 3–4 μm wide, light and dark bands. In the more radiolucent striations, crystals are reduced in number as well as in length with some showing longitudinal splitting. In sections with prisms cut in cross-section, most crystals exhibit central dissolution except for isometric hexagonal crystals bordering a gap at the prism periphery. Eventually a complete loss of crystals from prism cores occurs. Asymmetric widening of the gap at the prism borders may be associated with the striae of Retzius. Possible causes for differences in the rate of crystal dissolution in alternating striations are discussed.

Ameloblastic disturbances are correlated with defects in enamel. Experimental disturbances created by tetracyclines, fluorides, and antimitotic drugs are emphasized. Cellular alterations are shown to interfere with both matrix production and secretion. Defects in enamel formation are characterized by abnormal crystal size and distribution. Further research in normal and particularly abnormal enamel development is needed to establish: 1. exact mode of matrix secretion and its relation to crystal nucleation and orientation 2. function of maturative ameloblast and its relation to the stratum intermedium and papillary layer during that phase 3. cause for lack of mineralization of matrix, particularly in ectopic areas.