Endometriose und Adenomyose

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Uterine hyperperistalsis, driven by endometrial estrogen's interference with ovarian control, facilitates endometrial fragment implantation in the peritoneum (endometriosis) and myometrium (adenomyosis), leading to infertility.

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This paper reviews uterine peristaltic activity in the non-pregnant uterus and proposes a causal framework linking hyperperistalsis to the development of endometriosis and adenomyosis, drawing on prior evidence about menstrual transport and sperm transport. It argues that hyperperistalsis detaches fragments of basal endometrium during menstruation, increasing their implantation potential in the peritoneal cavity for pelvic endometriosis, and simultaneously drives proliferation of basal endometrium into myometrial dehiscences, producing adenomyosis with a reported prevalence of about 90% among those with endometriosis. It further links adenomyosis to impaired directed sperm transport and thus infertility, and posits an underlying archimetral hyperestrogenism that interferes with ovary-controlled cyclical mechanisms regulating uterine peristalsis. The paper explicitly frames fertile minimal endometriosis, endometriosis with adenomyosis in infertile women, and peri/postmenopausal adenomyosis as phenotypes of a pathophysiological continuum centered on uterine peristalsis. This paper is centrally about endometriosis and adenomyosis—specifically uterine peristalsis/hyperperistalsis as a unifying mechanism and sterility-related outcome.

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Abstract

Peristaltic activity of the non-pregnant uterus serves fundamental functions in the early process of reproduction. 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 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 about 90%. Adenomyosis results in impaired directed sperm transport and thus constitutes an important cause of sterility in women with endometriosis. 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. Minimal endometriosis of the fertile women, endometriosis and adenomyosis of the infertile women and adenomyosis of the parous peri- and postmenopausal women are considered as phenotypes of a pathophysiological continuum with uterine peristalsis playing a prominent role.
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Subscribe to RSS DOI: 10.1055/s-2005-836885 © Georg Thieme Verlag Stuttgart · New York Endometriose und Adenomyose Neue Sichtweisen der Uterus(patho)physiologie Endometriosis and adenomyosisNew insight into uterine (patho)physiologyPublication History Publication Date: 29 September 2005 (online) Zusammenfassung Die uterine Peristaltik ist von fundamentaler Bedeutung im frühen Prozess der Reproduktion. Gleichzeitig ist sie mit der Entwicklung des Krankheitsbildes von Endometriose/Adenomyose kausal verbunden. Eine Endometriose ist mit einer Hyperperistaltik assoziiert. Sie führt zur Desquamation von Fragmenten basalen Endometriums, die vermehrt durch retrograde Menstruation in die Peritonealhöhle gelangen, wo sie Endometrioseherde bilden. Gleichzeitig fördert die Hyperperistaltik die Bildung von myometrialen Dehiszenzen, in die basales Endometrium infiltriert und eine Adenomyose bildet. Die Prävalenz der Adenomyose bei Endometriose beträgt bis zu 90 %. Die Adenomyose ist wesentlich an der Endometriose-assoziierten Sterilität kausal beteiligt. Es liegen Hinweise dafür vor, dass ursächlich für die Hyperperistalsis, also für die Pathogenes von Endometriose und Adenomyose, ein archimetraler Hyperestrogenismus verantwortlich ist, der mit der ovariellen Steuerung der peristaltischen Aktivität interferiert. Die Minimalendrometriose der fertilen Frau, Endometriose und Adenomyose der Sterilitätspatientin sowie die perimenopausale Adenomyose werden als ein pathophysiologisches Kontinuum mit einer prinzipiell gemeinsamen Pathogenese betrachtet. Abstract Peristaltic activity of the non-pregnant uterus serves fundamental functions in the early process of reproduction. 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 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 about 90 %. Adenomyosis results in impaired directed sperm transport and thus constitutes an important cause of sterility in women with endometriosis. 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. Minimal endometriosis of the fertile women, endometriosis and adenomyosis of the infertile women and adenomyosis of the parous peri- and postmenopausal women are considered as phenotypes of a pathophysiological continuum with uterine peristalsis playing a prominent role. Schlüsselwörter Endometriose - Adenomyose - Hyperperistaltik - archimetraler Hyperestrogenismus - Sterilität Key words adenomyosis - endometriosis - uterine peristalsis and hyperperistalsis - archimetral hyperestrogenism - infertiliy Literatur - 1 Absenger Y, Hess-Stumpp H, Kreft B, Kratzschmar J, Haendler B, Schutze N, Regidor P A, Winterhager E. Cyr61, a deregulated gene in endometriosis. Mol Hum Reprod. 2004; 10 399-407 - 2 Cullen T S. The distribution of adenomyoma containing uterine mucosa. Arch Surgery. 1920; 1 215-283 - 3 De Snoo K. Das Problem der Menschwerdung im Lichte der Vergleichenden Geburthilfe. Gustav Fischer, Jena 1942 - 4 Einer-Jensen N. Countercurrent transfer in the ovarian pedicle and its physiological implications. Oxford Rev Reprod Biol. 1988; 10 348-381 - 5 Hull M E, Moghissi K S, Magyar D F, Hayes M F. Comparison of different treatment modalities of endometriosis in infertile women. Fertil Steril. 1987; 47 40-44 - 6 Kunz G, Beil D, Deininger H, Wildt L, Leyendecker G. The dynamics of rapid sperm transport through the female genital tract. Evidence from vaginal sonography of uterine peristalsis (VSUP) and hysterosalpingoscintigraphy (HSSG). Hum Reprod. 1996; 11 627-632 - 7 Kunz G, Noe M, Herbertz M, Leyendecker G. Uterine peristalsis during the follicular phase of the menstrual cycle. Effects of oestrogen, antioestrogen and oxytocin. Hum Reprod Update. 1998; 4 647-654 - 8 Kunz G, Herbertz M, Noe M, Leyendecker G. Sonographic evidence of a direct impact of the ovarian dominant structure on uterine function during the menstrual cycle. Hum Reprod Update. 1998; 4 667-672 - 9 Kunz G, Beil D, Huppert P, Leyendecker G. Structural abnormalities of the uterine wall in women with endometriosis and infertility visualized by vaginal sonography and magnetic resonance imaging. Hum Reprod. 2000; 15 76-82 - 10 Kunz G, Beil D, Huppert P, Noe M, Kissler S, Leyendecker G. Adenomyosis in endometriosis - prevalence and impact on fertility. Evidence from magnetic resonance imaging. Hum Reprod.. 2005; 20 2309-2316 - 11 Leiva M C, Hasty L A, Lyttle C R. Inflammatory changes of the endometrium in patients with minimal-to-moderate endometriosis. Fertil Steril. 1994; 62 967-972 - 12 Leyendecker G, Kunz G, Wildt L, Beil D, Deininger H. Uterine hyperperistalsis and dysperistalsis as dysfunctions of the mechanism of rapid sperm transport in patients with endometriosis and infertility. Hum Reprod. 1996; 11 1542-1551 - 13 Leyendecker G, Kunz G, Noe M, Herbertz M, Mall G. Endometriosis: A dysfunction and disease of the archimetra. Hum Reprod Update. 1998; 4 752-762 - 14 Leyendecker G. Endometriosis is an entity with extreme pleiomorphism. Hum Reprod. 2000; 15 4-7 - 15 Leyendecker G, Herbertz M, Kunz G, Mall G. Endometriosis results from the dislocation of basal endometrium. Hum Reprod. 2002; 17 2725-2736 - 16 Leyendecker G, Kunz G, Herbertz M, Beil D, Huppert P, Mall G, Kissler S, Noe M, Wildt L. Uterine peristaltic activity and the development of endometriosis. Ann NY Acad Sci. 2004; 1034 338-355 - 17 Marcoux S, Maheux R, Berube S. Laparoscopic surgery in infertile women with minimal or mild endometriosis. Canadian Collaborative Group on Endometriosis. N Engl J Med. 1997; 337 217-222 - 18 Meyer R. Über den Stand der Frage der Adenomyositis und Adenome im Allgemeinen und insbesondere über Adenomyositis seroepithelialis und Adenomyometritis sarcomatosa. Zbl Gynäkol. 1919; 43 745-750 - 19 Noe M, Kunz G, Herbertz M, Mall G, Leyendecker G. The cyclic pattern of the immunocytochemical expression of oestrogen and progesterone receptors in human myometrial and endometrial layers: Characterisation of the endometrial-subendometrial unit. Hum Reprod. 1999; 14 101-110 - 20 Parazzini F, Vercellini P, Panazza S, Chatenoud L, Oldani S, Crosignani P G. Risk factors for adenomyosis. Hum Reprod. 1997; 12 1275-1279 - 21 Ridley J H. The histogenesis of endometriosis. Obste Gynec Surv. 1968; 23 1-35 - 22 Sampson J A. Peritoneal endometriosis due to the menstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynaecol. 1927; 14 422-429 - 23 Takahashi K, Nagata H, Kitao M. Clinical usefulness of determination of estradiol levels in the menstrual blood for patients with endometriosis. Acta Obstet Gynecol Jpn. 1989; 41 1849-1850 - 24 Werth R, Grusdew W. Untersuchungen über die Entwicklung und Morphologie der menschlichen Uterusmuskulatur. Arch Gynäkol. 1898; 55 325-409 Prof. Dr. med. G. Leyendecker Frauenklinik des Klinikum Darmstadt · Akademisches Lehrkrankenhaus der Universitäten Frankfurt und Heidelberg/Mannheim Grafenstr. 9 64283 Darmstadt Phone: +49/61 51/1 07 61 50 Email: [email protected]

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Condition tags

endometriosisadenomyosis

MeSH descriptors

Endometriosis Uterus Uterus Endometriosis Endometriosis Endometriosis Estrogens Estrogens Female Humans Uterus

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