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 (approximately equal to 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 lesions depth and demineralization period are denoted by df and t, lesion progress can be described by: dfp = alpha t + c, where alpha and c are constants with 1 less than or equal to p less than or equal to 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 = 1. 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 liquid phase (FL) between the enamel crystallites. Under acidic conditions (plaque), we have, due to an influx of fluoride from the saliva or plaque as FL, an aqueous phase in the enamel supersaturated with respect to the mineral for a small distance (x*) only.(ABSTRACT TRUNCATED AT 400 WORDS)