Evidence map›Paper›PMID 27307050›Full record

ReviewJournal of dental research2016

Role of Oxidized Lipids and TRP Channels in Orofacial Pain and Inflammation.

K M Hargreaves, S Ruparel

Abstract readReview
In one paragraph

Review in Journal of dental research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Diabesity and Oral Immunity: Exploring the Interconnection.Advances in experimental medicine and biology · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. The anatomy, neurophysiology, and cellular mechanisms of intradental sensation.Frontiers in pain research (Lausanne, Switzerland) · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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.

K M HargreavesDepartment of Endodontics, University of Texas Health Science Center at San Antonio, TX, USA Hargreaves@uthscsa.edu.
S RuparelDepartment of Endodontics, University of Texas Health Science Center at San Antonio, TX, USA.
The University of Texas Health Science Center at San Antonio · US

Funding

Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR001120 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2013 to 2017
$16.5M
Scaffolding the Transition to Chronic PainR01NS082746 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JESKE, NATHANIEL AARON · 2013 to 2017
$1.7M
NCATS NIH HHS UL1 TR001120NINDS NIH HHS R01 NS082746
6 · The paper itself

Abstract

Acute or chronic inflammation comprises a highly prevalent type of orofacial pain and is mediated by the generation of endogenous agonists that activate numerous receptors expressed on terminals of trigeminal (TG) nociceptive afferent neurons. One such studied receptor is transient receptor potential vanilloid subtype 1 (TRPV1). TRPV1 is a ligand-gated cation channel that is expressed on a major subclass of nociceptors and is found in many orofacial tissues, including dental pulp. Antagonists to TRPV1 reveal an important role for this channel in mediating hypersensitivity in preclinical models of inflammatory or neuropathic pain. Recent studies have demonstrated that endogenous TRPV1 agonists are generated by oxidation of omega-6 polyunsaturated fatty acids, including both linoleic acid and arachidonic acid. A major mechanism triggering the release of oxidative linoleic acid metabolites (OLAMs) and oxidative arachidonic acid metabolites (OAAMs) is the action of oxidative enzymes. Oxidative enzymes such as cytochrome P450 isozymes are rapidly upregulated in TG neurons after orofacial inflammation and increase the capacity of TG neurons to generate OLAMs. Cytochrome P450 isozymes are also increased in immune cells in irreversibly inflamed human dental pulp, and extracts of this tissue have significantly increased capacity to generate OLAMs. Together, these studies point to a novel pain mechanism involving the enzymatic generation of endogenous OLAM and OAAM agonists of TRPV1. This finding provides a rationale for an entirely new class of analgesics by inhibition of oxidative enzyme activity.

Indexed as

Cytochrome P-450 Enzyme SystemEnzyme InhibitorsFacial PainFatty Acids, Omega-6HumansHyperalgesiaInflammationIsoenzymesNociceptorsOxidation-ReductionTRPV Cation ChannelsCytochrome P-450 Enzyme SystemEnzyme InhibitorsFatty Acids, Omega-6IsoenzymesTRPV1 receptorTRPV Cation Channelsarachidonic acidcapsaicincytochrome P450linoleic acidpulpitisTRPV1

Identifiers

PMID27307050
PMCPMC5004240
OpenAlexW2440783555

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.