Microstructure of Active and Arrested Dentinal Caries

¹ Department of Pedodontics, University of Illinois College of Dentistry, Chicago, Illinois

An electron microscopic study was made of active and arrested carious lesions in human dentin. Samples were taken from each characteristic layer in each type of lesion. Most of the specimens were fixed in alcohol (70 per cent) and were either left undecalcified or were decalcified in EDTA, pH 7.2. They were imbedded in epoxy resin, and ultrathin sections were observed under the electron microscope. The photographs were processed using the logetronic printing technique. The major findings of the study follow.

Active lesions.-(1) The infected (bacteria-rich) zone lay within the deep portion of the necrotic layer and the upper portion of the decalcified layer. (2) The deeper portion of the decalcified layer was free of bacteria and contained many large crystals presumably formed by reprecipitation of apatite dissolved by the bacterial acids above. (3) Sclerosis began early, at the junction between the decalcified layer and the normal dentin. (4) The deeper layers were also bacteria-free.

Arrested lesions.-(1) In the superficial bacteria-rich zone of the arrested lesion, most of the intratubular bacterial bodies had disintegrated and coalesced. (2) The intertubular zone appeared to have become more mineralized. (3) In the deeper layers the intratubular contents were hyper-mineralized and obliterated (sclerosed). The calcification appeared to be continuous with the peritubular zone. This entire area was bacteria-free.

This study again emphasizes the differentiation of two distinct layers in the active lesion—the bacteria-rich layer (infected zone) and the practically bacteria-free layer underneath (affected zone). The hypothesis that the pigmentation of the arrested lesion may be related to degenerative changes in the bacteria is suggested.

Future studies are proposed using multiple disciplines and co-ordination of findings in order to achieve a more complete understanding of dentinal reactions to injury.