The Physiological Basis of Dentin Hypersensitivity

Sensations of pain resulting from dentin stimulation can occur in response to a variety of innocuous stimuli. The physiological mechanisms responsible for these pain sensations have been studied from the perspective of both nerve function and the specific environment of those nerves—the dentin tubules. Since the sensitive outer portion of the dentin is not innervated, odontoblasts have long been suspected as playing an important role in this sensory process. The nerve cells mediating dentin hypersensitivity (DH) pain appear to have unique features when compared to nociceptors innervating other parts of the body. These cells respond directly to various stimuli and become activated by dentin fluid shifts that are induced by many pain-provoking actions, for example, probing or air blasting the dentin surface. Dental pathologies that result in dentin hypersensitivity can alter both the dentin structure and the function of intradental nerves. Conversely, healing processes within the tooth and desensitizing therapies can target both dentin and nerve function, with the goal of reducing stimulus-evoked activation. By approaching the problem from the anatomic, physiological, and molecular perspective, we hope to facilitate efforts to offer patients reliable preventive strategies and therapies for dentin hypersensitivity.