Sensory transduction mechanisms responsible for pain caused by cold stimulation of dentine in man

Chidchuangchai, W.; Vongsavan, Noppakun; Matthews, Bruce

doi:10.1016/j.archoralbio.2006.09.009

Cited by 70 publications

(60 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Thus, intradental afferents are thought to be activated by a mechanism detecting changes in movement, not temperature (Chidchuangchai et al, 2007). However, previous evidence suggests that, in the case of cold stimulation, alternative mechanisms may also be in play (Chidchuangchai et al, 2007). Combining in vivo pain ratings in humans and in vitro measurements of tubule fluid flow, Chidchuangchai et al (2007) demonstrated that exposure of dentinal tubules increased cold pain, but conversely decreased fluid movement (Chidchuangchai et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…Strong experimental evidence suggests that sensory afferents innervating the dentin are activated via hydrodynamic receptors detecting fluid movement through dentinal tubules, a process termed the dentinal hydrodynamic theory (Matthews, 1977;Byers and Narhi, 2002;Park et al, 2006;Chidchuangchai et al, 2007). Thus, intradental afferents are thought to be activated by a mechanism detecting changes in movement, not temperature (Chidchuangchai et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…Combining in vivo pain ratings in humans and in vitro measurements of tubule fluid flow, Chidchuangchai et al (2007) demonstrated that exposure of dentinal tubules increased cold pain, but conversely decreased fluid movement (Chidchuangchai et al, 2007). This conflicts with the hydrodynamic theory and predicts that the greatest cold-evoked afferent discharge occurs when fluid flow rates are at their lowest, prompting the authors to suggest that cold-pain involves other transduction mechanisms such as cold receptors (Chidchuangchai et al, 2007). Our observation of Trpm8 GFP fibers in dentine supports this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Diversity in the Neural Circuitry of Cold Sensing Revealed by Genetic Axonal Labeling of Transient Receptor Potential Melastatin 8 Neurons

Takashima¹,

Daniels²,

Knowlton³

et al. 2007

J. Neurosci.

195

214

View full text Add to dashboard Cite

Sensory nerves detect an extensive array of somatosensory stimuli, including environmental temperatures. Despite activating only a small cohort of sensory neurons, cold temperatures generate a variety of distinct sensations that range from pleasantly cool to painfully aching, prickling, and burning. Psychophysical and functional data show that cold responses are mediated by both C-and A␦-fibers with separate peripheral receptive zones, each of which likely provides one or more of these distinct cold sensations. With this diversity in the neural basis for cold, it is remarkable that the majority of cold responses in vivo are dependent on the cold and menthol receptor transient receptor potential melastatin 8 (TRPM8). TRPM8-null mice are deficient in temperature discrimination, detection of noxious cold temperatures, injury-evoked hypersensitivity to cold, and nocifensive responses to cooling compounds. To determine how TRPM8 plays such a critical yet diverse role in cold signaling, we generated mice expressing a genetically encoded axonal tracer in TRPM8 neurons. Based on tracer expression, we show that TRPM8 neurons bear the neurochemical hallmarks of both C-and A␦-fibers, and presumptive nociceptors and non-nociceptors. More strikingly, TRPM8 axons diffusely innervate the skin and oral cavity, terminating in peripheral zones that contain nerve endings mediating distinct perceptions of innocuous cool, noxious cold, and first-and second-cold pain. These results further demonstrate that the peripheral neural circuitry of cold sensing is cellularly and anatomically complex, yet suggests that cold fibers, caused by the diverse neuronal context of TRPM8 expression, use a single molecular sensor to convey a wide range of cold sensations.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Diversity in the Neural Circuitry of Cold Sensing Revealed by Genetic Axonal Labeling of Transient Receptor Potential Melastatin 8 Neurons

Takashima¹,

Daniels²,

Knowlton³

et al. 2007

J. Neurosci.

195

214

View full text Add to dashboard Cite

show abstract

“…Several theories have been presented to characterize Dentin Hypersensitivity After Treatment With Desensitizing Agents: A Randomized, Double-Blind, Split-Mouth Clinical Trial dentin hypersensitivity, but the hydrodynamic theory proposed by Brännström is the most widely accepted (4)(5)(6). According to its principles, the fluid movement inside the dentin tubules leads to sensorial activation of the nerve cells in the pulp, thus causing pain (7).…”

Section: Introductionmentioning

confidence: 99%

Dentin hypersensitivity after treatment with desensitizing agents: a randomized, double-blind, split-mouth clinical trial

et al. 2011

View full text Add to dashboard Cite

The aim of this study was to evaluate the efficacy of two desensitizing agents in the reduction of dentin hypersensitivity in a randomized, double-blind, split-mouth clinical trial. Seventy-seven teeth from 13 patients that presented some degree of sensitivity to probing and/ or air stimulation were treated with one of the following desensitizing agents: Oxa-Gel (G1), Sensi Kill (G2) and placebo gel (G3 -control). According to paired t-test, all treatments, even the placebo gel, were capable of reducing sensitivity scores for both stimuli.Analysis of data by ANOVA and Tukey's test (α=0.05) showed that the sensitivity scores were significantly lower only for Sensi Kill in comparison to the other products (Oxa-Gel and placebo), when air stimulus was applied. It may be concluded that treatment with Sensi Kill presented a slightly better performance in reducing dentin hypersensitivity when compared to the other desensitizing agent.

show abstract

“…Todavia o estímulo que mais comumente incomoda é o frio quando da ingestão de alimentos gelados (GILAM et al, 2001;CHIDCHUANGCHAI;VONGSAVAN;MATTHEWS, 2007) ou da própria respiração, quando esta ocorre pela boca. Devido a essas características, a HD é considerada uma desordem crônica manifestada através de uma dor aguda (HOLLAND et al, 1997), não vinculada a um processo patológico real.…”

Section: Introductionunclassified

Análise quantitativa e qualitativa da condutividade hidráulica da dentina após tratamento com diferentes agentes dessensibilizantes. Estudo in vitro

Dantas¹

View full text Add to dashboard Cite

Sensory transduction mechanisms responsible for pain caused by cold stimulation of dentine in man

Cited by 70 publications

References 21 publications

Diversity in the Neural Circuitry of Cold Sensing Revealed by Genetic Axonal Labeling of Transient Receptor Potential Melastatin 8 Neurons

Diversity in the Neural Circuitry of Cold Sensing Revealed by Genetic Axonal Labeling of Transient Receptor Potential Melastatin 8 Neurons

Dentin hypersensitivity after treatment with desensitizing agents: a randomized, double-blind, split-mouth clinical trial

Análise quantitativa e qualitativa da condutividade hidráulica da dentina após tratamento com diferentes agentes dessensibilizantes. Estudo in vitro

Contact Info

Product

Resources

About