Evidence map›Paper›PMID 19329451›Full record

ReviewJournal of dental research2009

Emerging peripheral receptor targets for deep-tissue craniofacial pain therapies.

R Ambalavanar, D Dessem

Open access · greenAbstract readReview
In one paragraph

Review in Journal of dental research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Peripheral role of glutamate in orofacial pain.Frontiers in neuroscience · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
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  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

R AmbalavanarDepartment of Neural and Pain Sciences and Program in Neuroscience, University of Maryland, Baltimore, MD 21201, USA.
D Dessem
University of Maryland, Baltimore · US

Funding

TOOTH MERCHANORECEPTORS IN JAW MOVEMENTR01DE010132 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI DESSEM, DEAN A · 1991 to 2006
$2.0M
Neuronal Plasticity Related to TMD and FibromyalgiaR01DE015386 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI DESSEM, DEAN A · 2003 to 2006
$1.2M
Neural Mechanisms of Chronic Muscle Pain DisordersR03DE016795 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI AMBALAVANAR, RANJINIDEVI · 2005 to 2007
$217k
NIDCR NIH HHS R01 DE010132NIDCR NIH HHS R01 DE015386NIDCR NIH HHS R01DE10132NIDCR NIH HHS R01DE15386NIDCR NIH HHS R03 DE016795NIDCR NIH HHS R03DE016795
6 · The paper itself

Abstract

While effective therapies are available for some types of craniofacial pain, treatments for deep-tissue craniofacial pain such as temporomandibular disorders are less efficacious. Several ion channels and receptors which are prominent in craniofacial nociceptive mechanisms have been identified on trigeminal primary afferent neurons. Many of these receptors and channels exhibit unusual distributions compared with extracranial regions. For example, expression of the ATP receptor P2X(3) is strongly implicated in nociception and is more abundant on trigeminal primary afferent neurons than analogous extracranial neurons, making them potentially productive targets specifically for craniofacial pain therapies. The initial part of this review therefore focuses on P2X(3) as a potential therapeutic target to treat deep-tissue craniofacial pain. In the trigeminal ganglion, P2X(3) receptors are often co-expressed with the nociceptive neuropeptides CGRP and SP. Therefore, we discuss the role of CGRP and SP in deep-tissue craniofacial pain and suggest that neuropeptide antagonists, which have shown promise for the treatment of migraine, may have wider therapeutic potential, including the treatment of deep-tissue craniofacial pain. P2X(3), TRPV1, and ASIC3 are often co-expressed in trigeminal neurons, implying the formation of functional complexes that allow craniofacial nociceptive neurons to respond synergistically to altered ATP and pH in pain. Future therapeutics for craniofacial pain thus might be more efficacious if targeted at combinations of P2X(3), CGRP, TRPV1, and ASIC3.

Indexed as

Purinergic P2 Receptor AntagonistsAcid Sensing Ion ChannelsCalcitonin Gene-Related PeptideFacial PainHumansNeurons, AfferentNeuropeptidesNociceptorsReceptors, Purinergic P2Receptors, Purinergic P2X3Sodium Channel BlockersSodium ChannelsSubstance PTrigeminal NerveTRPV Cation ChannelsAcid Sensing Ion ChannelsASIC3 protein, humanCalcitonin Gene-Related PeptideNeuropeptidesP2RX3 protein, humanPurinergic P2 Receptor AntagonistsReceptors, Purinergic P2Receptors, Purinergic P2X3Sodium Channel BlockersSodium ChannelsSubstance PTRPV1 protein, humanTRPV Cation Channels

Identifiers

PMID19329451
PMCPMC3317937
OpenAlexW1995376992

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.