Studies have shown that dental caries may or may not be associated with tertiary dentin formation in the pulp. On the basis of histological examinations of 69 clinical well-defined caries lesions, a hypothesis is proposed on the dynamics of the hard-tissue responses of the pulp to caries. In active non-cavitated lesions, the formation of tertiary dentin seems to be initiated by primary odontoblast cells that subsequently result in atubular dentin/fibrodentinogenesis, whereas, in similarly aged but more rapidly progressing cavitated enamel lesions, no tertiary dentin is laid down by primary odontoblast cells. In all old-dentin exposed lesions, a so-called closed lesion environment was defined with subjacent atubular dentin formation. As these lesions progress, a shift from a closed to a more large and open lesion environment may develop in the very old lesions, and a new tubular dentinal matrix is noted on the top of the fibrodentin, also defined as reparative dentinogenesis. In very old slowly progressing lesions, a relatively small open lesion environment is also observed, with tubular tertiary dentin resembling the primary dentin being strictly tubular. It is suggested that the absence of tertiary dentinogenesis can be expected in very rapid caries lesions, whereas a variety of tertiary dentin is observed in older dentin cavitated lesions guided by a changing external lesion environment over time.
The role of transforming growth factor beta in tertiary dentinogenesis
