Uterine peristaltic activity and the development of endometriosis
Abstract
Peristaltic activity of the nonpregnant uterus serves fundamental functions in the early process of reproduction, such as directed transport of spermatozoa into the tube ipsilateral to the dominant follicle, high fundal implantation of the embryo, and, possibly, retrograde menstruation. Hyperperistalsis of the uterus is significantly associated with the development of endometriosis and adenomyosis. In women with hyperperistalsis, fragments of basal endometrium are detached during menstruation and transported into the peritoneal cavity. Fragments of basal endometrium have, because of their equipment with estrogen and progesterone receptors and because of their ability to produce estrogen, an increased potential of implantation and proliferation, resulting in pelvic endometriosis. In addition, hyperperistalsis induces the proliferation of basal endometrium into myometrial dehiscencies. This results in endometriosis-associated adenomyosis with a prevalence of approximately 90%. Adenomyosis results in impaired directed sperm transport and thus constitutes an important cause of sterility in women with endometriosis. Our own date and that from the literature strongly suggest that the principal mechanism of endometriosis/adenomyosis is the paracrine interference of endometrial estrogen with the cyclical endocrine control of archimyometrial peristalsis exerted by the ovary, thus resulting in hyperperistalsis.
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Serum oxytocin and uterine peristalsis are elevated in women with endometriosis relative to controls.
“Serum oxytocin and uterine peristalsis are elevated in women with endometriosis relative to controls (He et al., 2016; Leyendecker et al., 2004).”
From Endometriosis and polycystic ovary syndrome are diametric disorders (2021) · cites this paper as Leyendecker et al., 2004
Uterine hyperperistalsis/dysperistalsis may result from archimetral hyperestrogenism.
“Third, uterine hyperperistalsis/dysperistalsis may be a result of archimetral hyperestrogenism [38,47].”
From The Pathogenesis of Adenomyosis vis-à-vis Endometriosis (2020) · cites this paper as [47]
Auto-traumatization of the uterus constitutes the critical factor in the development of endometriosis and adenomyosis.
“On the basis of the data presented above we had suggested that auto-traumatization of the uterus would constitute the critical factor in the development of endometriosis and adenomyosis [3, 4, 33].”
From The pathophysiology of endometriosis and adenomyosis, tissue injury and repair (2009) · cites this paper as [33]
Uterine dysfunction in women with endometriosis and adenomyosis is a result of archimetral hyperestrogenism.
“It was suggested that this uterine dysfunction in women with endometriosis and adenomyosis is a result of archimetral hyperestrogenism [3, 4, 29, 33].”
From The pathophysiology of endometriosis and adenomyosis, tissue injury and repair (2009) · cites this paper as [33]
The basal endometrium in women with endometriosis is twice as thick as in healthy women.
“The basal endometrium in women with endometriosis is twice as thick as in healthy women [21, 33].”
From The pathophysiology of endometriosis and adenomyosis, tissue injury and repair (2009) · cites this paper as [33]
Hyperperistalsis causes overt uterine auto-traumatization, detachment of fragments of basal endometrium, and their transtubal dislocation into the peritoneal cavity as well as infiltrative growth of basal endometrium into the underlying myometrium, resulting in pelvic endometriosis and uterine adenomyosis.
“As outlined previously, hyperperistalsis causes overt uterine auto-traumatization, detachment of fragments of basal endometrium, and their transtubal dislocation into the peritoneal cavity as well as infiltrative growth of basal endometrium into the underlying myometrium resulting in pelvic endometriosis and uterine adenomyosis, respectively [3, 33].”
From The pathophysiology of endometriosis and adenomyosis, tissue injury and repair (2009) · cites this paper as [33]
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- Authors
- LEYENDECKER, G., KUNZ, G., HERBERTZ, M., BEIL, D., HUPPERT, P., MALL, G., KISSLER, S., NOE, M., & WILDT, L.
- Affiliations
- Klinikum Darmstadt (DE)
- Goethe University Frankfurt (DE)
- University of Vienna (AT)
- Innsbruck Medical University (AT)
- Corresponding author
- LEYENDECKER, GERHARD
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2004-12
- Volume
- 1034
- Issue
- 1
- Pages
- 338-355
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- OpenAlex
- W2021228825
- Cited by
- 162
- References
- 42
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 12 · 2023: 5 · 2022: 8 · 2021: 10 · 2020: 16 · 2019: 7 · 2018: 4 · 2017: 11 · 2016: 4 · 2015: 7 · 2014: 8 · 2013: 6 · 2012: 7
- FWCI
- 1.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of the New York Academy of Sciences (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
- uterine peristalsis, endometriosis, adenomyosis, retrograde menstruation, sperm transport, female infertility, estrogen, paracrine signaling, endometrial implantation
- MeSH terms
- Endometriosis, Female, Humans, Uterine Contraction, Uterus
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