When dentinal tubules first become exposed, patients note that those areas become more sensitive to tactile, evaporative, and osmotic stimuli. However, over time, especially with poor plaque control, those areas become progressively truly hypersensitive. There are a number of mechanisms responsible for hypersensitivity including localized pulpal inflammation, sprouting of pulpal nerves, and expression of “inflammatory” sodium channels. Often such hypersensitivity spontaneously disappears. These protective mechanisms will be reviewed. The problem arises for patients whose exposed dentin becomes hypersensitive and whose endogenous protective mechanism fails to correct the hypersensitivity.
