Almost all research on the process of dental caries supports the chemoparasitic theory
proposed by W. D. Miller in 1890. This is now more commonly known as the
acidogenic theory of caries aetiology. The main features of the caries process are:
(1) fermentation of carbohydrate to organic acids by micro-organisms in plaque on the
tooth surface;
(2) rapid acid formation, which lowers the pH at the enamel surface below the level
(the critical pH) at which enamel will dissolve;
(3) when carbohydrate is no longer available to the plaque micro-organisms, the pH
within plaque will rise due to the outward diffusion of acids and their metabolism and
neutralization in plaque, so that remineralization of enamel can occur; and
(4) dental caries progresses only when demineralization is greater than
remineralization. The realization that demineralization and remineralization is an
equilibrium is key to understanding the dynamics of the carious lesion and its
prevention.
One of the interesting features of an early carious lesion of the enamel is that the
lesion is subsurface; that is, most of the mineral loss occurs beneath a relatively intact
enamel surface. This contrasts strongly with the histological appearance of enamel
after a clean tooth surface has been exposed to acid, where the surface is etched and
there is no subsurface lesion. This dissolution of the surface of enamel, or etching, is a
feature of enamel erosion caused, among other things, by dietary acids. The
explanation for the intact surface layer in enamel caries seems to lie in diffusion
dynamics: the layer of dental plaque on the tooth surface acting as a partial barrier to
diffusion. Further erosion occurs at much lower pHs (<4) than caries.
Dental plaque forms on uncleaned tooth surfaces and is readily apparent if
toothbrushing is stopped for 2-3 days. Contrary to popular opinion, plaque does not
consist of food debris, but comprises 70% micro-organisms⎯about 100 million
organisms per milligram of plaque. When plaque is young, cocci predominate but as
plaque ages the proportions of filamentous organisms and veillonellae increase. Diet
influences the composition of the plaque flora considerably, with mutans streptococci
much more numerous when the diet is rich in sugar and other carbohydrates, and
these organisms are particularly good at metabolizing sugars to acids.
Knowledge of the dental caries process increased considerably with the development
of pH electrodes, particularly microelectrodes that could be inserted into plaque
before, during, and after the ingestion of various foods. The pioneer of this area of
research was Robert Stephan, and the plot of plaque pH against time (208HFig. 6.1) has
become known as the Stephan curve. Within 2-3 min of eating sugar or rinsing with a
sugar solution, plaque pH falls from an average of about 6.8 to near pH 5, taking
about 40 min to return to its original value. Below pH 5.5 demineralization of the
enamel occurs, this is known as the critical pH.
The clinical appearance of these early lesions is now well recognized (209HFigs. 6.2, 210H6.3,
211H6.4, and 212H6.5). They appear as a white area that coincides with the distribution of
plaque. This might be around the gingival margin, as in 213HFig. 6.2, or between the teeth,
as in 214HFig. 6.3. A histological section through a lesion such as that shown in 215HFig. 6.3
would look like 216HFig. 6.4 and a microradiograph like 217HFig. 6.5⎯in both the subsurface