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

Michot, B.; Lee, Caroline Sunyong; Gibbs, Jennifer L.

doi:10.1038/s41598-018-31487-2

Cited by 24 publications

(24 citation statements)

References 40 publications

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“…The trigeminal ganglion was examined as cell bodies of the primary afferent neurons that innervate the dental pulp reside there 16 . We chose to assess the Toll-like Receptor 4 (Tlr4), transient receptor potential channels vanilloid 1 and ankyrin 1 (Trpv1 and Trpa1), and the mas-related G protein coupled receptor D (Mrgprd), because all are found in neurons that innervate the dental pulp 7,[17][18][19][20][21] and could be involved in the development of either spontaneous or mechanical pain in the context of infection and injury. In particular, TLR4 is part of a larger class of receptors that recognize pathogen-and damage-associated molecular patterns (PAMPs and DAMPs) 22 , and has known interactions with both TRPV1 and TRPA1 in the context of dental injury 19,21,23,24 .…”

Section: Morphological and Gene Expression Changes Twenty-four Hours mentioning

confidence: 99%

Evoked and spontaneous pain assessment during tooth pulp injury

Rossi

See

Foster

et al. 2020

Sci Rep

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injury of the tooth pulp is excruciatingly painful and yet the receptors and neural circuit mechanisms that transmit this form of pain remain poorly defined in both the clinic and preclinical rodent models. Easily quantifiable behavioral assessment in the mouse orofacial area remains a major bottleneck in uncovering molecular mechanisms that govern inflammatory pain in the tooth. In this study we sought to address this problem using the Mouse Grimace Scale and a novel approach to the application of mechanical Von frey hair stimuli. We use a dental pulp injury model that exposes the pulp to the outside environment, a procedure we have previously shown produces inflammation. Using RNAscope technology, we demonstrate an upregulation of genes that contribute to the pain state in the trigeminal ganglia of injured mice. We found that mice with dental pulp injury have greater Mouse Grimace Scores than sham within 24 hours of injury, suggestive of spontaneous pain. We developed a scoring system of mouse refusal to determine thresholds for mechanical stimulation of the face with Von Frey filaments. This method revealed that mice with a unilateral dental injury develop bilateral mechanical allodynia that is delayed relative to the onset of spontaneous pain. This work demonstrates that tooth pain can be quantified in freely behaving mice using approaches common for other types of pain assessment. Harnessing these assays in the orofacial area during gene manipulation should assist in uncovering mechanisms for tooth pulp inflammatory pain and other forms of trigeminal pain.

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Section: Morphological and Gene Expression Changes Twenty-four Hours mentioning

confidence: 99%

Evoked and spontaneous pain assessment during tooth pulp injury

Rossi

See

Foster

et al. 2020

Sci Rep

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“…TRPM8 is expressed in rat DPAs in the TG [137,138,176]. By immunohistochemistry, Park et al observed that 13% of rat DPAs expressed TRPM8 [138].…”

Section: Trp Channels and Their Presence In Dental Tissuesmentioning

confidence: 99%

“…In one study, TRPM8 mRNA expression was detected in 58% of rat DPAs [137]. However, Michot et al detected TRPM8 expression in only 5.7% of mouse DPAs, similar to that in afferent neurons innervating the facial skin and the buccal mucosa [176].…”

Section: Trp Channels and Their Presence In Dental Tissuesmentioning

confidence: 99%

“…TRPA1 protein in the rat TG was increased following experimental exposure of the dental pulp, implicating the protein in hyperalgesia and allodynia following tooth injury [194]. In the mouse, TRPA1 was detected in 18.9% of DPAs, lower than in neurons innervating the buccal mucosa (43%) or the facial skin (24.6%) [176]. In the same study, noxious cold stimulation of the tooth increased the expression of c-Fos (a marker of neuronal excitation) in the brainstem trigeminal nucleus; however, this increase was not blocked by systemic administration of a TRPA1 antagonist [176].…”

Section: Trp Channels and Their Presence In Dental Tissuesmentioning

confidence: 99%

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The Role of Transient Receptor Potential (TRP) Channels in the Transduction of Dental Pain

Hossain

Bakri

Yahya

et al. 2019

IJMS

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Dental pain is a common health problem that negatively impacts the activities of daily living. Dentine hypersensitivity and pulpitis-associated pain are among the most common types of dental pain. Patients with these conditions feel pain upon exposure of the affected tooth to various external stimuli. However, the molecular mechanisms underlying dental pain, especially the transduction of external stimuli to electrical signals in the nerve, remain unclear. Numerous ion channels and receptors localized in the dental primary afferent neurons (DPAs) and odontoblasts have been implicated in the transduction of dental pain, and functional expression of various polymodal transient receptor potential (TRP) channels has been detected in DPAs and odontoblasts. External stimuli-induced dentinal tubular fluid movement can activate TRP channels on DPAs and odontoblasts. The odontoblasts can in turn activate the DPAs by paracrine signaling through ATP and glutamate release. In pulpitis, inflammatory mediators may sensitize the DPAs. They could also induce post-translational modifications of TRP channels, increase trafficking of these channels to nerve terminals, and increase the sensitivity of these channels to stimuli. Additionally, in caries-induced pulpitis, bacterial products can directly activate TRP channels on DPAs. In this review, we provide an overview of the TRP channels expressed in the various tooth structures, and we discuss their involvement in the development of dental pain.

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“…The cell bodies of the primary afferent neurons that innervate the dental pulp reside in the trigeminal ganglion 24 . We chose to assess the Toll-like Receptor 4 (Tlr4), transient receptor potential channels vanilloid 1 and ankyrin 1 (Trpv1 and Trpa1), and the mas-related G protein coupled receptor D (Mrgprd), because all are found in neurons that innervate the dental pulp 7,20,22,25-27 and could be involved in the development of either spontaneous or mechanical pain in the context of infection and injury. In particular, TLR4 is part of a larger class of receptors that recognize pathogen- and damage-associated molecular patterns (PAMPs and DAMPs) 19 , and has known interactions with both TRPV1 and TRPA1 in the context of dental injury 20-23 .…”

Section: Resultsmentioning

confidence: 99%

Evoked and spontaneous pain assessment during tooth pulp injury

Rossi

See

Foster

et al. 2019

Preprint

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Injury of the tooth pulp is excruciatingly painful and yet the receptors and neural circuit mechanisms that transmit this form of pain remain poorly defined in both the clinic and preclinical rodent models. Easily quantifiable behavioral assessment in the rodent orofacial area remains a major bottleneck in uncovering molecular mechanisms that govern inflammatory pain in the tooth. Here we use a dental pulp injury model in the mouse and expose the tooth pulp to the outside environment, a procedure we have previously shown produces pulpal inflammation. We demonstrate here with RNAscope technology in the trigeminal ganglion of injured mice, an upregulation of genes that contribute to the inflammatory pain state. Using both evoked and spontaneous measures of pain in the orofacial area, including application of von Frey Hair filaments and pain feature detection with the mouse grimace scale, we reveal a differential timeline of induction of spontaneous pain versus mechanical allodynia following pulpal injury. This work demonstrates that tooth pain can be easily assessed in freely behaving mice using approaches common for other types of pain assessment. Harnessing these assays in the orofacial area during gene manipulation should assist in uncovering mechanisms for tooth pulp inflammation and other forms of trigeminal pain. 11, eaal2171,

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

Cited by 24 publications

References 40 publications

Evoked and spontaneous pain assessment during tooth pulp injury

Evoked and spontaneous pain assessment during tooth pulp injury

The Role of Transient Receptor Potential (TRP) Channels in the Transduction of Dental Pain

Evoked and spontaneous pain assessment during tooth pulp injury

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