The exposure of cervical dentine has a multifactorial aetiology and pain may frequently be elicited by a number of stimuli. Management of the condition, dentine hypersensitivity, tends to be empirical because of the lack of knowledge concerning the mechanism of pain transmission through dentine. The pulpal changes associated with the condition and any modulating effect on symptoms are by no means clearly established. Evidence suggests that exposed dentine which is sensitive exhibits patent tubules. The question of how pain is initiated across the dentine has received considerable attention but still remains somewhat debatable. The literature reviewed indicates that, at most, nerve fibres only penetrate a limited distance along some dentinal tubules. The theories that either the odontoblasts and their processes act as dentinal receptors or the nerves in the pulp are the pain receptors, are discussed. Evidence for the stimulation of pulp nerve fibres by a hydrodynamic mechanism would appear the most likely mechanism. Nevertheless, whichever theory proves to be correct, occlusion of dentinal tubules would appear an essential prerequisite for an effective desensitising agent.