Pain and the rate of dentinal fluid flow produced by hydrostatic pressure stimulation of exposed dentine in man

Charoenlarp, Panta; Wanachantararak, Sitthichai; Vongsavan, Noppakun; Matthews, Bruce

doi:10.1016/j.archoralbio.2006.12.014

Cited by 62 publications

(45 citation statements)

References 19 publications

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“…In this context, movements of the dentinal fluid (acting as hydraulic links) filling the upper part of tubules down to odontoblasts tip could be assumed as the earliest step of signal induction. Efflux of dentinal fluid flow within tubules at exposed dentine has been carefully analyzed in vivo and in vitro (Linden and Brännstrom, '67;Vongsavan and Matthews, '91;Pashley, '96;Charoenlarp et al, 2007;Chidchuangchai et al, 2007;Linsuwanont et al, 2008). Taken together, these findings have clearly demonstrated the relationship between dentine permeability and dentine sensitivity and support the widely accepted hydrodynamic theory of dentine sensitivity (Brännstrom and Astrom,'72).…”

Section: Odontoblast Process and Dentinal Fluidmentioning

confidence: 56%

Odontoblast: a mechano‐sensory cell

et al. 2008

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Odontoblasts are organized as a single layer of specialized cells responsible for dentine formation and presumably for playing a role in tooth pain transmission. Each cell has an extension running into a dentinal tubule and bathing in the dentinal fluid. A dense network of sensory unmyelinated nerve fibers surrounds the cell bodies and processes. Thus, dentinal tubules subjected to external stimuli causing dentinal fluid movements and odontoblasts/nerve complex response may represent a unique mechano-sensory system giving to dentine-forming cells a pivotal role in signal transduction. Mediators of mechano-transduction identified in odontoblast include mechano-sensitive ion channels (high conductance calcium-activated potassium channel--K(Ca)--and a 2P domain potassium channel--TREK-1) and primary cilium. In many tissues, the latter is essential for microenvironment sensing but its role in the control of odontoblast behavior remains to be elucidated. Recent evidence for excitable properties and the concentration of key channels to the terminal web suggest that odontoblasts may operate as sensor cells.

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Section: Odontoblast Process and Dentinal Fluidmentioning

confidence: 56%

Odontoblast: a mechano‐sensory cell

et al. 2008

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“…The most largely accepted theory to explain activation of the pulpal afferents is the hydrodynamic theory, in which tooth stimulation causes fluid movement within dentinal tubules, activating sensory afferents located in or near the dentinal tubules. Indeed, it was shown that application of a noxious cold stimulation (0 °C) on teeth induces dentinal tubule fluid movements and neuronal activation 31,32 . In our experimental condition, the stimulation applied on the tooth was certainly cold enough (Frigi-dent −50 °C out of the can) to induce dentinal tubule fluid movements that would then mechanically activate pulpal sensory afferents activating central pain pathways evidenced by c-Fos upregulation in the trigeminal nucleus.…”

Section: Discussionmentioning

confidence: 99%

TRPM8 and TRPA1 do not contribute to dental pulp sensitivity to cold

Michot

Lee

Gibbs

2018

Sci Rep

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Sensory neurons innervating the dental pulp have unique morphological and functional characteristics compared to neurons innervating other tissues. Stimulation of dental pulp afferents whatever the modality or intensity of the stimulus, even light mechanical stimulation that would not activate nociceptors in other tissues, produces an intense pain. These specific sensory characteristics could involve receptors of the Transient Receptor Potential channels (TRP) family. In this study, we compared the expression of the cold sensitive receptors TRPM8 and TRPA1 in trigeminal ganglion neurons innervating the dental pulp, the skin of the cheek or the buccal mucosa and we evaluated the involvement of these receptors in dental pulp sensitivity to cold. We showed a similar expression of TRPM8, TRPA1 and CGRP in sensory neurons innervating the dental pulp, the skin or the mucosa. Moreover, we demonstrated that noxious cold stimulation of the tooth induced an overexpression of cFos in the trigeminal nucleus that was not prevented by the genetic deletion of TRPM8 or the administration of the TRPA1 antagonist HC030031. These data suggest that the unique sensory characteristics of the dental pulp are independent to TRPM8 and TRPA1 receptors expression and functionality.

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“…Fluid movements in dentin tubules were shown to induce action potentials of sensory nerves associated with the exposed dentin and cause transient pain. [11][12][13] For fluid movement to occur inside the dentin tubules, the latter must be patent, with one end open to the dentin surface and the other to the pulp. Imaging studies of human dentin showed that the tubules are larger in size and greater in number in sensitive areas than in non-sensitive areas of dentin, 14,15 further substantiating the role of open dentin tubules in the aetiology of dentin sensitivity.…”

mentioning

confidence: 99%