Uterine Peristalsis and the Development of Endometriosis and Adenomyosis

G. Leyendecker, L. Wildt
In: Endometriosis · 2011 · pp. 200–211 · doi:10.1002/9781444398519.ch20 · W2113038670
other OA: closed CC0 ⤵ 4 in-corpus citations
View on OpenAlex View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

This paper proposes that uterine hyperperistalsis causes microtraumatization and subsequent estrogen production, driving the development and self-perpetuation of endometriosis and adenomyosis through a tissue injury and repair mechanism.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Pelvic endometriosis, deeply infiltrating endometriosis, and uterine adenomyosis share a common pathophysiology and may be integrated into the physiological mechanism and new nosological concept of “tissue injury and repair” and may, in this context, represent the extreme of a basically physiological, estrogen-related mechanism, that is pathologically exaggerated in an extremely estrogen-sensitive, reproductive organ. Endometriosis and adenomyosis are caused by trauma. In the spontaneously developing disease, chronic uterine peristaltic activity or phases of hyperperistalsis induce, at the endometrial–myometrial interface near the fundocornual raphe, microtraumatizations with activation of the tissue injury and repair mechanism. This inflammatory process results in the local production of estrogen. With ongoing trauma, such sites might accumulate and the estrogens thus increasingly produced interfere in a paracrine fashion with the ovarian control over uterine peristaltic activity, resulting in permanent hyperperistalsis and self-perpetuation of the disease process. Overt autotraumatization of the uterus with dislocation of fragments of basal endometrium into the peritoneal cavity and infiltration of basal endometrium into the depth of the myometrial wall ensues. In most cases of endometriosis/adenomyosis, a causal event early in the reproductive period of life must be postulated leading rapidly to archimetral hyperestrogenism and uterine hyperperistalsis. In late premenopausal adenomyosis, such an event might not have occurred. However, as indicated by the high prevalence of the disease, it appears to be unavoidable that, with time, chronic normoperistalsis throughout the reproductive period of life accumulates to the same extent of microtraumatization. With the activation of the tissue injury and repair mechanism followed by chronic inflammation and infiltrative growth, endometriosis/adenomyosis of the younger woman and premenopausal adenomyosis share in principle the same pathophysiology.

My notes (saved in your browser only)

Condition tags

endometriosisadenomyosis

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (96)

Cited by (4)

Source provenance

openalex
last seen: 2026-06-04T00:00:01.174412+00:00
License: CC0 · commercial use OK