Dislozierung basalen Endometriums

Zusammenfassung Endometriose und Adenomyose beruhen auf der Dislozierung basalen Endometriums durch Autotraumatisierung des Uterus infolge Hyper- und Dysperistaltik als physiologische uterine Funktionen des gerichteten Spermientransportes sowie infolge eines erhöhten intrauterinen Drucks. Die Endometriose entsteht durch die transtubare Dissemination von Fragmenten der Basalis während der Menstruation und die Adenomyose durch die unmittelbare Infiltration von basalem Endometrium in das Myometrium. Dislozierte Fragmente basalen Endometriums entwickeln Organstammzellcharakter und formen alle morphologischen Elemente des primordialen Uterus oder der Archimetra. Auch die peristromale Muskulatur der Adenomyoseherde beruht auf dem paramesonephrischen Potenzial der Basalis zur Bildung von glatten Muskefasern. Die Endometrioseherde können daher als ektope "Miniaturuteri" angesehen werden, die wie der Uterus selbst der zyklischen Kontrolle des Ovars ausgesetzt sind. Hierzu gehören strukturelle, zellbiochemische sowie immunologische Veränderungen, die auf der Ebene des Uterus seine normalen archimetralen Funktionen ermöglichen, auf der Ebene der ektopen Herde jedoch den Krankheitscharakter ausmachen. Es liegen Hinweise vor, dass eine Erhöhung der in der Basalis lokal produzierten Östrogene, die parakrine Wirkungen entfalten, in der Kausalkette der Pathogenese von Endometriose und Adenomyose zu den initialen Veränderungen gehört. Abstract Like adenomyosis, endometriosis is primarily a disease of the archimetra. There is strong circumstantial evidence that both are derived from the basal layer of the endometrium. Furthermore, we propose that dislocated basal endometrium has stem cell character and is capable of resuming embryonic growth potential and resulting in the ectopic formation of all archimetrial components such as epithelium, stroma, and paramesonephric smooth muscle cells. In women with early-onset endometriosis and adenomyosis, dislocation of the basal endometrium most probably results from autotraumatization by uterine hyperperistalsis as a dysfunction of the uterine mechanism of rapid sperm transport. There is some evidence that, in the pathogenesis of endometriosis and adenomyosis, locally increased production of endometrial estrogen might have a prominent role in the chain of events leading to uterine hyperperistalsis. The biological mechanisms that govern normo- and hyperperistalsis, however, remain to be elucidated in detail. Similar content being viewed by others Literatur Anaf V, Simon P, Fayt I, Noel J (2000) Smooth muscles are frequent components of endometriotic lesions. Hum Reprod 15: 767–771 Attia GR, Zeitoun K, Edwards D, Johns A, Carr BR, Bulun SE (2000) Progesterone receptor isoform A but not B is expressed in endometriosis. 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J Clin Endocrinol Metab 83: 4474–4480 Author information Authors and Affiliations Corresponding author Rights and permissions About this article Cite this article Leyendecker, G., Mall, G., Noe, M. et al. Dislozierung basalen Endometriums. Reproduktionsmedizin 19, 181–188 (2003). https://doi.org/10.1007/s00444-003-0413-3 Issue date: DOI: https://doi.org/10.1007/s00444-003-0413-3 Schlüsselwörter - Endometriose - Adenomyose - Archimetra - Gerichteter Spermientransport - Hyperperistaltik und Dysperistaltik - Basalis