dentin. Usually, the demineralized areas within a well-developed dentin caries lesion precede the bacterially infected areas. Among the histological techniques used to investigate enamel and dentin caries lesions, light microscopy can be used to reveal different zones within enamel and dentin caries that correspond to different pore volumes and size distribution of such porosities. Microradiographic techniques are able to analyze exactly the mineral content as a function of lesion depth. Scanning electron microscopy shows changes at the enamel surface at early lesion states and within a lesion at the enamel prism level, while transmission electron microscopy provides insight into changes at the crystal level. Even when a caries lesion progresses, demineralization is interrupted by phases of remineralization. Net remineralization can be achieved only when the biological and chemical conditions at the surface of such a lesion change toward a less cariogenic environment. Clinically, this means successful regular plaque removal and administration of fluoride. Under these conditions, the caries process can come to halt and remineralization of the outer layers of enamel or exposed dentin is possible. However, the result of lesion remineralization can be considered to be a “scar,” because complete remineralization in the sense of a “restitutio ad integrum” does not occur. Remineralization of deeper lesions most likely leaves behind a less mineralized area. Both caries and erosion cause loss of mineral from a tooth, but the etiology and the histology are considerably different. Erosion is not caused by bacteria, but by the direct dissolution of enamel and dentin due to acids that originate from the nutrition, the stomach, or other environmental sources. Erosion leads to immediate irreversible loss of calcium and phosphate from the enamel or dentin surface and creates only a shallow softening of the surface. This softened surface is prone to abrasive loss, but may be remineralized when left mechanically undisturbed for some time.
Acknowledgments. The author would like to thank Prof. Dr. Hans Ulrich Luder, University of Zurich, Center for Dentistry, Institute for Oral Biology for kindly providing Figs. 3.9, 3.10, 3.13, 3.16, 3.17, and 3.18 and for numerous valuable discussions. I also would like to thank Dr. Hao Yu for preparation and imaging of Figs. 3.3, 3.4, and 3.14 and PD Dr. Áine M. Lennon for providing Fig. 3.21.
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