Evidence map›Paper›PMID 27422858›Full record

ReviewJournal of dental research2016

Pain Mechanisms and Centralized Pain in Temporomandibular Disorders.

D E Harper, A Schrepf, D J Clauw

Registry-linked trialAbstract 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. It is linked to trial NCT07598994 (Topical Capsaicin Versus Diclofenac for Chronic Temporomandibular Joint-Related Pain), which is not on this map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
9.6field-weighted citation impact, top 1% 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.

NCT07598994 nacompletednot on this mapstarted 2025, after this paper: background citation

Topical Capsaicin Versus Diclofenac for Chronic Temporomandibular Joint-Related Pain: A Randomized, Prospective, Single-Blind Clinical Trial

TypeinterventionalSponsorIstanbul UniversityRan2025 to 2026Enrolled50ConditionsTemporomandibular Disorders (TMD), Temporomandibular PainArmsCapsaicin Topical Cream, Diclofenac 1% Topical
3 · Its place in the literature

Who cites it

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 166 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  6. Review
  7. CD4The journal of headache and pain · 2026
    Article
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  9. Observational
  10. Review
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  16. Review
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  18. Observational
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  20. Article

5 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

D E HarperChronic Pain and Fatigue Research Center, Department of Anesthesiology, School of Medicine, University of Michigan, Ann Arbor, MI, USA harperd@med.umich.edu.
A SchrepfChronic Pain and Fatigue Research Center, Department of Anesthesiology, School of Medicine, University of Michigan, Ann Arbor, MI, USA.
D J ClauwChronic Pain and Fatigue Research Center, Department of Anesthesiology, School of Medicine, University of Michigan, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · US

Funding

University of Michigan's TMJD and Orofacial Pain Interdisciplinary ConsortiumK12DE023574 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CLAUW, DANIEL J, KAPILA, SUNIL D · 2013 to 2017
$1.8M
NIDCR NIH HHS K12 DE023574
6 · The paper itself

Abstract

Until recently, most clinicians and scientists believed that the experience of pain is perceptually proportional to the amount of incoming peripheral nociceptive drive due to injury or inflammation in the area perceived to be painful. However, many cases of chronic pain have defied this logic, leaving clinicians perplexed as to how patients are experiencing pain with no obvious signs of injury in the periphery. Conversely, there are patients who have a peripheral injury and/or inflammation but little or no pain. What makes some individuals experience intense pain with minimal peripheral nociceptive stimulation and others experience minimal pain with serious injury? It is increasingly well accepted in the scientific community that pain can be generated and maintained or, through other mechanisms, suppressed by changes in the central nervous system, creating a complete mismatch between peripheral nociceptive drive and perceived pain. In fact, there is no known chronic pain condition where the observed extent of peripheral damage reproducibly engenders the same level of pain across individuals. Temporomandibular disorders (TMDs) are no exception. This review focuses on the idea that TMD patients range on a continuum-from those whose pain is generated peripherally to those whose pain is centralized (i.e., generated, exacerbated, and/or maintained by central nervous system mechanisms). This article uses other centralized chronic pain conditions as a guide, and it suggests that the mechanistic variability in TMD pain etiology has prevented us from adequately treating many individuals who are diagnosed with the condition. As the field moves forward, it will be imperative to understand each person's pain from its own mechanistic standpoint, which will enable clinicians to deliver personalized medicine to TMD patients and eventually provide relief in even the most recalcitrant cases.

Indexed as

Central Nervous System SensitizationChronic PainEvidence-Based DentistryFacial PainHumansPain PerceptionTemporomandibular Joint Disordersevidence-based dentistry/health caremultisensory perceptionneuroscience/ neurobiologyorofacial pain/TMDpsychosocial factorstreatment planning

Identifiers

PMID27422858
PMCPMC5004242
OpenAlexW2473982039

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.