The Role of Ion Channels in Dentine Hypersensitivity

Abstract

OBJECTIVES

Dentin hypersensitivity (DH) is a common condition caused by exposure of dentinal tubules to the oral environment. This results in sharp pain in response to mechanical, thermal, chemical, and osmotic stimuli.

This review examined the roles of various ion channels in DH, focusing on how they contribute to pain perception and intercellular communication between odontoblasts and afferent sensory neurons.

METHODS

A comprehensive review of literature on ion channels involved in DH was conducted, with emphasis on transient receptor potential (TRP) channels, Piezo channels, acid-sensing ion channels (ASICs), and voltage-gated ion channels. Special focus was placed on the physiological function of these channels, their response to stimuli, and their role in DH-related pain pathways.

RESULTS

(If applicable) Ion channels such as TRPV1, TRPA1, and ASICs are activated by pressure, heat, acidic environments, and chemical irritants, all of which contribute to DH pain. Activation of ion channels located on odontoblasts triggers the release of adenosine triphosphate and glutamate from odontoblasts. These neurotransmitters bind to purinergic and glutamate receptors, respectively, on sensory neurons. This interaction causes depolarization and generates action potentials that relay pain signals to the brain. In addition, voltage-gated sodium channels such as NaV1.7 amplify neuronal excitability, promoting rapid pain signal transmission in response to DH stimuli.

CONCLUSIONS

The presence of diverse ion channels in odontoblasts and trigeminal ganglion-associated sensory neurons provides an intricate system for detecting and relaying DH-associated pain signals. Activation of these ion channels converts external stimuli into electrical signals that the central nervous system interprets as pain.

IMPLICATIONS

Although ion channels are crucial for pain perception, it is challenging to target them directly for DH management. Most of these channels are expressed in tissues other than the dental pulp, raising the risk of off-target systemic effects and adverse outcomes. Because of the essential roles of these channels in general physiological processes, approaches that desensitize dentinal tubules to prevent fluid movement appears to be safer and more effective for managing DH pain.