In Utero and Early-Life

In: Endometriosis and Adenomyosis · 2022 · pp. 145–154 · doi:10.1007/978-3-030-97236-3_11 · W4285291131
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Congenital endometriosis may arise from displaced Müllerian duct epithelium or embryonic rests, with mesenchymal stem cells and progenitor cells potentially involved in pathophysiology.

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This chapter examines how ectopic endometrial foci and congenital endometriosis might originate during fetal life by considering mechanisms of reproductive tract embryogenesis, displaced Müllerian epithelium, and congenital genital anomalies that can be associated with variable teen incidence (reported 11%–40%, higher with outflow obstruction). It highlights uncertainty about which developmental pathways are most relevant, including coelomic metaplasia, embryonic Müllerian rests, persistence of embryonic endometriosis, and the potential role of mesenchymal stem/progenitor cells in establishing endometriosis outside the peritoneal cavity. It also proposes that progenitor cells could contribute to premenarcheal and adolescent endometriosis, potentially seeded by retrograde neonatal uterine bleeding. This paper is centrally about endometriosis — fetal and early-life mechanisms for ectopic endometrial foci and congenital/early-onset endometriosis are discussed, with adenomyosis mentioned only indirectly as part of the developmental context.

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Abstract

Information on the development of ectopic endometrial foci during fetal life be deduced from the embryogenesis of the reproductive tract. It is possible that fragments of the Müllerian duct epithelium become displaced to adjacent sites, giving rise to ectopic foci. Congenital endometriosis also remains a possibility. The reported incidence of endometriosis in teenagers with genital tract anomalies varies between 11% and 40%. The incidence appears to be higher in anomalies associated with genital tract outflow obstruction. There is still considerable uncertainty about whether mechanisms such as coelomic metaplasia, embryonic Müllerian rests, or persistence of other forms of embryonic endometriosis are relevant to endometriosis. Mesenchymal stem cells may be the principal source of endometriosis outside the peritoneal cavity. It is possible that progenitor cells play a role also in the pathophysiology of premenarcheal and adolescent endometriosis, since they may originate and implant into the peritoneum as a consequence of retrograde neonatal uterine bleeding. Access this chapter Tax calculation will be finalised at checkout Purchases are for personal use only Similar content being viewed by others

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Kalu E, McAuley W, Richardson R. Teenagers, adolescents, endometriosis and recurrence: a retrospective analysis of recurrence following primary operative laparoscopy. Gynecol Surg. 2008;5:209–12. Author information Authors and Affiliations Corresponding author Editor information Editors and Affiliations Rights and permissions Copyright information © 2022 The Author(s), under exclusive license to Springer Nature Switzerland AG About this chapter Cite this chapter Habiba, M., Benagiano, G. (2022). In Utero and Early-Life. In: Oral, E. (eds) Endometriosis and Adenomyosis. Springer, Cham. https://doi.org/10.1007/978-3-030-97236-3_11 Download citation DOI: https://doi.org/10.1007/978-3-030-97236-3_11 Published: Publisher Name: Springer, Cham Print ISBN: 978-3-030-97235-6 Online ISBN: 978-3-030-97236-3 eBook Packages: MedicineMedicine (R0)

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