Endometriosis and Mechanisms of Pelvic Pain
Abstract
Endometriosis remains an enigmatic disorder in that the cause, the natural history, and the precise mechanisms by which it causes pain are not completely understood. The pain symptoms most commonly attributed to endometriosis are dysmenorrhea, dyspareunia, and chronic pelvic pain. Pain may be due to nociceptive, inflammatory, or neuropathic mechanisms, and there is evidence that all 3 of these mechanisms are relevant to endometriosis-associated pelvic pain. It is proposed that the clinically observed inconsistencies of the relationships of endometriosis severity and the presence or severity of pain are likely due to variable roles of different pain mechanisms in endometriosis. A better understanding of the roles of nociceptive, inflammatory, and neuropathic pain in endometriosis is likely to improve the treatment of women with endometriosis-associated pelvic pain.
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Among women undergoing laparoscopy, endometriosis is found in one-third of those having surgery for chronic pelvic pain, compared with 5% of those without infertility or chronic pelvic pain.
“among women who undergo laparoscopy, endometriosis is found in one-third who undergo surgery for CPP, compared with only 5% of those who do not have infertility or CPP”
From Chronic pelvic pain and endometriosis: translational evidence of the relationship and implications (2011) · cites this paper as Howard, 2009
The pathophysiology of pain in rectovaginal endometriosis is multifactorial and not determined solely by anatomical involvement.
“The pathophysiology of pain in RVE is multifactorial and not determined solely by anatomical involvement.”
From Pain and functional outcomes after surgical versus hormonal treatment in rectovaginal endometriosis: a retrospective cohort study (2026) · cites this paper as [8]
Lesion removal does not necessarily eliminate the biological processes that sustain pain.
“However, lesion removal does not necessarily eliminate the biological processes that sustain pain [8, 16, 24, 26].”
From Pain and functional outcomes after surgical versus hormonal treatment in rectovaginal endometriosis: a retrospective cohort study (2026) · cites this paper as [8]
The ectopic growth's own innervation is a major contributor to the maintenance and modulation of pain in established endometriosis.
“This discovery suggests that, rather than the growths alone, it is the ectopic growth's own innervation that is a major contributor to the maintenance and modulation of pain in established endometriosis [12].”
From Sprouted Innervation into Uterine Transplants Contributes to the Development of Hyperalgesia in a Rat Model of Endometriosis (2012) · cites this paper as [12]
Endometriosis-associated pain is often difficult to alleviate without hormonal treatments that produce often-intolerable side effects of hypoestrogenicity or surgery that frequently fails to help.
“Symptoms include dysmenorrhea, dyspareunia (vaginal hyperalgesia), chronic pelvic/abdominal musculoskeletal and other types of severe pain that are often difficult to alleviate without resorting either to hormonal treatments that produce often-intolerable side effects of hypoestrogenicity or to surgery that frequently fails to help [16,21,27,16,48].”
From Endocannabinoid involvement in endometriosis. (2010) · cites this paper as [21]
Findings from the rat model and clinical studies strongly support the conclusion that this innervation contributes to endometriosis-associated pain.
“Findings from the rat model and clinical studies strongly support the conclusion that this innervation contributes to endometriosis-associated pain [21,45,48].”
From Endocannabinoid involvement in endometriosis. (2010) · cites this paper as [21]
Progress in developing new treatment strategies for endometriosis-associated pain is impeded by a poor understanding of how the growths contribute to the pains.
“Although it is recognized that both inflammatory and neuropathic mechanisms contribute to endometriosis-associated pains, progress in developing new treatment strategies is impeded by a poor understanding of how the growths, which do not correlate with the pains, contribute to them [16,21,27,48].”
From Endocannabinoid involvement in endometriosis. (2010) · cites this paper as [21]
The growths do not correlate with the pains.
“Although it is recognized that both inflammatory and neuropathic mechanisms contribute to endometriosis-associated pains, progress in developing new treatment strategies is impeded by a poor understanding of how the growths, which do not correlate with the pains, contribute to them [16,21,27,48].”
From Endocannabinoid involvement in endometriosis. (2010) · cites this paper as [21]
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- Authors
- Howard, F. M.
- Affiliations
- University of Rochester Medicine (US)
- Corresponding author
- Howard, Fred M.
- Venue
- Journal of Minimally Invasive Gynecology
- Publisher
- Elsevier BV
- Published
- 2009-09
- Volume
- 16
- Issue
- 5
- Pages
- 540-550
- ISSN
- 1553-4650 (ISSN-L)
- OpenAlex
- W2085922363
- Cited by
- 218
- References
- 90
- Citations by year
- 2026: 4 · 2025: 15 · 2024: 14 · 2023: 18 · 2022: 8 · 2021: 12 · 2020: 20 · 2019: 18 · 2018: 11 · 2017: 15 · 2016: 11 · 2015: 15 · 2014: 12 · 2013: 11 · 2012: 12
- FWCI
- 1.60
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Minimally Invasive Gynecology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
- Health Sciences › Medicine › Obstetrics and Gynecology › Gynecological conditions and treatments
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Menstrual Health and Disorders
- Keywords
- endometriosis, chronic pelvic pain, dysmenorrhea, dyspareunia, nociceptive pain, inflammatory pain, neuropathic pain, pain mechanisms, endometriosis severity, pain management
- MeSH terms
- Animals, Chronic Disease, Disease Models, Animal, Endometriosis, Endometrium, Female, Humans, Interleukins, Mast Cells, Nerve Growth Factors, Pelvic Pain, Chemokine CCL2, Tumor Necrosis Factors, Pain, Referred, Referred Pain
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