Cellular and molecular mechanisms of dental nociception.

Abstract

Due, in part, to the unique structure of the tooth, dental pain is initiated via distinct mechanisms. Here we review recent advances in our understanding of inflammatory tooth pain and discuss 3 hypotheses proposed to explain dentinal hypersensitivity: The first hypothesis, supported by functional expression of temperature-sensitive transient receptor potential channels, emphasizes the direct transduction of noxious temperatures by dental primary afferent neurons. The second hypothesis, known as hydrodynamic theory, attributes dental pain to fluid movement within dentinal tubules, and we discuss several candidate cellular mechanical transducers for the detection of fluid movement. The third hypothesis focuses on the potential sensory function of odontoblasts in the detection of thermal or mechanical stimuli, and we discuss the accumulating evidence that supports their excitability. We also briefly update on a novel strategy for local nociceptive anesthesia via nociceptive transducer molecules in dental primary afferents with the potential to specifically silence pain fibers during dental treatment. Further understanding of the molecular mechanisms of dental pain would greatly enhance the development of therapeutics that target dental pain.

• Authors: G Chung, S J Jung, S B Oh
• Journal: Journal of dental research (J Dent Res) Vol. 92 Issue 11 Pg. 948-55 (Nov 2013) ISSN: 1544-0591 [Electronic] United States
• PMID: 23955160 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Topics

• Dentin (innervation)
• Dentin Sensitivity (physiopathology)
• Dentinal Fluid (physiology)
• Humans
• Mechanoreceptors (physiology)
• Mechanotransduction, Cellular (physiology)
• Nerve Endings (physiology)
• Neurons, Afferent (physiology)
• Nociception (physiology)
• Nociceptors (physiology)
• Odontoblasts (physiology)
• Thermoreceptors (physiology)
• Toothache (physiopathology)