Evidence map›Paper›PMID 22922120›Full record

ArticleNeuroscience2012

Ectopic uterine tissue as a chronic pain generator.

P Alvarez, X Chen, J Hendrich, J C Irwin, P G Green, L C Giudice, J D Levine

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.1field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Modelling Endometriosis Using In Vitro and In Vivo Systems.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. EPScientific reports · 2017
    Article
  10. Research Priorities for Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2017
    Article
  11. Article
  12. Article
  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

7 authors at 2 institutions in 1 country.

P AlvarezDepartment of Oral and Maxillofacial Surgery, University of California San Francisco, San Francisco, CA, USA.
X Chen
J Hendrich
J C Irwin
P G Green
L C Giudice
J D Levine
University of California, San Francisco · USReproductive Science Center · US

Funding

Acute-to-Chronic Transition in Ergonomic Muscle Pain: Nociceptor MechanismsR01AR063312 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEVINE, JON DAVID · 2013 to 2022
$6.5M
Receptors and Second Messengers for Pain and AnalgesiaP01NS053709 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEVINE, JON DAVID · 2007 to 2011
$5.0M
Mechanisms and Risk Factors in Musculoskeletal PainR01AR054635 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEVINE, JON DAVID · 2007 to 2011
$1.6M
NIAMS NIH HHS R01 AR054635NIAMS NIH HHS R01 AR063312NINDS NIH HHS P01 NS053709
6 · The paper itself

Abstract

While chronic pain is a main symptom in endometriosis, the underlying mechanisms and effective therapy remain elusive. We developed an animal model enabling the exploration of ectopic endometrium as a source of endometriosis pain. Rats were surgically implanted with autologous uterus in the gastrocnemius muscle. Within two weeks, visual inspection revealed the presence of a reddish-brown fluid-filled cystic structure at the implant site. Histology demonstrated cystic glandular structures with stromal invasion of the muscle. Immunohistochemical studies of these lesions revealed the presence of markers for nociceptor nerve fibers and neuronal sprouting. Fourteen days after surgery rats exhibited persistent mechanical hyperalgesia at the site of the ectopic endometrial lesion. Intralesional, but not contralateral, injection of progesterone was dose-dependently antihyperalgesic. Systemic administration of leuprolide also produced antihyperalgesia. In vivo electrophysiological recordings from sensory neurons innervating the lesion revealed a significant increase in their response to sustained mechanical stimulation. These results are consistent with clinical and pathological findings observed in patients with endometriosis, compatible with the ectopic endometrium as a source of pain. This model of endometriosis allows mechanistic exploration at the lesion site facilitating our understanding of endometriosis pain.

Indexed as

4-AminopyridineAction PotentialsAmifampridineAnimalsAntineoplastic Agents, HormonalBiophysicsCalcitonin Gene-Related PeptideCells, CulturedChronic PainDisease Models, AnimalDose-Response Relationship, DrugElectric StimulationEndometriosisEndometriumEstrous CycleFemale4-AminopyridineAmifampridineAntineoplastic Agents, HormonalCalcitonin Gene-Related PeptideGAP-43 ProteinLectinsLeuprolidePotassium Channel BlockersProgesteroneProgestinsTetraethylammonium

Identifiers

PMID22922120
PMCPMC3479308
OpenAlexW2064456534

What OpenQuestion holds

Textmetadata
LicenceTDM
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.