Crowns of human molars were exposed to lactate buffers, pH 5.0, with or without diphosphonate (MHDP) for periods of 1 h to 10 days. The changes in the enamel surface appearance were observed by scanning electron microscope (SEM) at up to × 40,000, and lesion progress was assessed by chemical analysis and polarized light microscopy. In both model systems subsurface caries-like demineralization was produced. The SEM observations showed that the opening up of the intercrystalline spaces by acid over the entire exposed enamel surface appears to be the initiating stage during the first few minutes or hours of caries attack in both systems. These intercrystalline pathways provide the route for subsequent mineral loss during carious lesion progression prior to establishment of the classical subsurface lesion