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J Dent Res 83(Spec Iss C):C35-C38, 2004
© 2004 International and American Associations for Dental Research


PROCEEDINGS
Clinical

What Constitutes Dental Caries? Histopathology of Carious Enamel and Dentin Related to the Action of Cariogenic Biofilms

E.A.M. Kidd*, and O. Fejerskov

GKT Dental Institute, Floor 25, Guy’s Tower, London Bridge, London SE1 9RT, England; and Royal Dental College, Faculty of Health Sciences, University of Aarhus, Vennelyst Boulevard, DK-8000 Aarhus C, Denmark;

* corresponding author, edwina.kidd{at}kcl.ac.uk

Substantial pH fluctuations within the biofilm on the tooth surface are a ubiquitous and natural phenomenon, taking place at any time during the day and night. The result may be recordable in the dental tissues at only a chemical and/or ultrastructural level (subclinical level). Alternatively, a net loss of mineral leading to dissolution of dental hard tissues may result in a caries lesion that can be seen clinically. Thus, the appearance of the lesion may vary from an initial loss of mineral, seen only in the very surface layers at the ultrastructural level, to total tooth destruction. Regular removal of the biofilm, preferably with a toothpaste containing fluoride, delays or even arrests lesion progression. This can occur at any stage of lesion progression, because it is the biofilm at the tooth or cavity surface that drives the caries process. Active enamel lesions involve surface erosion and subsurface porosity. Inactive or arrested lesions have an abraded surface, but subsurface mineral loss remains, and a true subsurface remineralization is rarely achievable, because the surface zone acts as a diffusion barrier. The dentin reacts to the stimulus in the biofilm by tubular sclerosis and reactionary dentin.

KEY WORDS: caries process • caries lesion • active lesions • arrested lesions




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