title: 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.
authors.affiliation: Department of Obstetrics and Gynecology, Klinikum Darmstadt, 64283 Darmstadt, Germany. gerhard.leyendecker@t-online.de
authors.forename: Gerhard
authors.initials: G
authors.lastname: Leyendecker
authors.forename: Georg
authors.initials: G
authors.lastname: Kunz
authors.forename: Mark
authors.initials: M
authors.lastname: Herbertz
authors.forename: Dolores
authors.initials: D
authors.lastname: Beil
authors.forename: Peter
authors.initials: P
authors.lastname: Huppert
authors.forename: Gerhard
authors.initials: G
authors.lastname: Mall
authors.forename: Stephan
authors.initials: S
authors.lastname: Kissler
authors.forename: Marion
authors.initials: M
authors.lastname: Noe
authors.forename: Ludwig
authors.initials: L
authors.lastname: Wildt
mesh_terms: D004715:Endometriosis / Q000209:etiology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D014590:Uterine Contraction / Q000502:physiology*; D014599:Uterus / Q000502:physiology*