Invited Review Article

Since 1935, various mechanisms have been suggested for the formation of subsurface lesions and, in particular, the surface layer covering enamel lesions. The relatively intact mineral-rich and porous surface layer is most likely caused by kinetic events. The suggested mineral-rich outer layer in sound enamel, the organic matrix, the pellicle, or a non-uniform ion distribution have all been shown to be non-essential for surface layer formation; they may, however, influence the rate of surface layer formation. Models based on outer surface protection by adsorbed agents, the dissolution-precipitation mechanism, and combinations of these two models, as well as models based on porosity or solubility gradients, are discussed in this paper together with their advantages and disadvantages. Most models have not explained some important recent experimental observations on initial in vivo caries lesion formation: e.g., initial enamel lesions formed in vivo do not have a surface layer initially but develop this mineral-rich layer later on; and the fact that the F- level in the solid sound enamel is not determining the subsurface lesion formation. Furthermore, the observations that in vitro fluoride ions in the liquid at very low levels (~ 0.02 ppm) determine surface layer formation are difficult to explain. A new kinetic model for subsurface lesion formation is described, in which inhibitors such as F- or proteins play an important role. The model predicts that if lesion depth and demineralization period are denoted by d f and t, lesion progress can be described by: d f p = αt + c, where a and c are constants with 1 ≤ p ≤ 3, depending on the lesion formation conditions. If lesion progress is entirely diffusion-controlled, p = 3, corresponding to low inhibitor concentrations; if the inhibitor content is so high that the progress is controlled by processes at the crystallite surface, p = I. A kinetic mechanism for surface layer formation in vivo is proposed, based on the assumption that F- is a main inhibitor in the plaque-covered acidic in vivo situation. The inhibiting fluoride, adsorbed onto the crystallite surfaces at OH- vacancies, originates from the so-called fluoride in the ljquid phase (F L ) between the enamel crystallites. Under acidic conditions (plaque), we have, due to an influx of fluoride from the saliva or plaque as F L , an aqueous phase in the enamel supersaturated with respect to the mineral for a small distance (x*) only. Deep in the lesion the solution is undersaturated. For d x*, enamel dissolution. The surface layer thickness, about x*, depends on F L level, on pH, and on time. The results described indicate that the surface layer is formed after a considerable period if a fluoride gradient has been established in initially surface-softened enamel. The combination of this F L gradient and pH dependency of the inhibitor effectiveness results in two regions in the enamel: (1) a small surface region where, due to inhibitor action, no dissolution takes place (and possible mineral redeposition occurs), and (2) a subsurface region where dissolution takes place. The mechanism of surface layer formation is based mainly on the information available for one inhibitor: fluoride. Other inhibitors, such as proteins, can have a similar effect. The kinetic model for subsurface lesion formation can, in contrast to thermodynamic models, explain the facts that: (a) the initial lesions do not show a surface layer; (b) the thickness of the surface layer, once formed, appears to be roughly constant; (c) the fluoride level in the saliva is the main reason for the surface layer to develop; and (d) the fluoride level in the solid sound enamel does not materially influence the surface layer formation.