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Hypothetical roadmap towards endometriosis: prenatal endocrine-disrupting chemical pollutant exposure,anogenital distance,gut-genital microbiota and subclinical infections

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dc.contributor.authorGarcía Peñarrubia, María del Pilar
dc.contributor.authorRuiz Alcaraz, Antonio José
dc.contributor.authorMartínez-Esparza Alvargonzález, María Concepción
dc.contributor.authorMarín Sánchez, Pilar
dc.contributor.authorMachado Linde, Francisco
dc.contributor.departmentBioquímica y Biología Molecular B e Inmunología
dc.contributor.otherFacultad de Biología
dc.date.accessioned2026-01-12T12:38:12Z
dc.date.available2026-01-12T12:38:12Z
dc.date.copyright© The Author(s) 2020
dc.date.issued2020-02-28
dc.description.abstractBACKGROUND Endometriosis is a gynaecological hormone-dependent disorder that is defined by histological lesions generated by the growth of endometrial-like tissue out of the uterus cavity, most commonly engrafted within the peritoneal cavity, although these lesions can also be located in distant organs. Endometriosis affects ~10% of women of reproductive age, frequently producing severe and, sometimes, incapacitating symptoms, including chronic pelvic pain, dysmenorrhea and dyspareunia, among others. Furthermore, endometriosis causes infertility in ~30% of affected women. Despite intense research on the mechanisms involved in the initial development and later progression of endometriosis, many questions remain unanswered and its aetiology remains unknown. Recent studies have demonstrated the critical role played by the relationship between the microbiome and mucosal immunology in preventing sexually transmitted diseases (HIV), infertility and several gynaecologic diseases. OBJECTIVE AND RATIONALE In this review, we sought to respond to the main research question related to the aetiology of endometriosis. We provide a model pointing out several risk factors that could explain the development of endometriosis. The hypothesis arises from bringing together current findings from large distinct areas, linking high prenatal exposure to environmental endocrine-disrupting chemicals with a short anogenital distance, female genital tract contamination with the faecal microbiota and the active role of genital subclinical microbial infections in the development and clinical progression of endometriosis. SEARCH METHODS We performed a search of the scientific literature published until 2019 in the PubMed database. The search strategy included the following keywords in various combinations: endometriosis, anogenital distance, chemical pollutants, endocrine-disrupting chemicals, prenatal exposure to endocrine-disrupting chemicals, the microbiome of the female reproductive tract, microbiota and genital tract, bacterial vaginosis, endometritis, oestrogens and microbiota and microbiota–immune system interactions. OUTCOMES On searching the corresponding bibliography, we found frequent associations between environmental endocrine-disrupting chemicals and endometriosis risk. Likewise, recent evidence and hypotheses have suggested the active role of genital subclinical microbial infections in the development and clinical progression of endometriosis. Hence, we can envisage a direct relationship between higher prenatal exposure to oestrogens or estrogenic endocrine-disrupting compounds (phthalates, bisphenols, organochlorine pesticides and others) and a shorter anogenital distance, which could favour frequent postnatal episodes of faecal microbiota contamination of the vulva and vagina, producing cervicovaginal microbiota dysbiosis. This relationship would disrupt local antimicrobial defences, subverting the homeostasis state and inducing a subclinical inflammatory response that could evolve into a sustained immune dysregulation, closing the vicious cycle responsible for the development of endometriosis. WIDER IMPLICATIONS Determining the aetiology of endometriosis is a challenging issue. Posing a new hypothesis on this subject provides the initial tool necessary to design future experimental, clinical and epidemiological research that could allow for a better understanding of the origin of this disease. Furthermore, advances in the understanding of its aetiology would allow the identification of new therapeutics and preventive actions.
dc.formatapplication/pdf
dc.format.extent33
dc.identifier.citationHuman Reproduction Update, Volume 26, Issue 2, March-April 2020, Pages 214–246
dc.identifier.doihttps://doi.org/10.1093/humupd/dmz044
dc.identifier.eissn1460-2369
dc.identifier.issn1355-4786
dc.identifier.urihttp://hdl.handle.net/10201/185829
dc.languageeng
dc.publisherOxford University Press
dc.relationSupport to the Precipita crowdfunding (PR200; Endometriosis). financial support from the association ‘Endomequé’, founded by Lucia Arnaiz García to provide supportto scientific endometriosis research.
dc.relation.publisherversionhttps://academic.oup.com/humupd/article/26/2/214/5765414
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectAnogenital distance
dc.subjectChemical pollutants
dc.subjectPrenatal exposure to endocrine-disrupting chemicals
dc.subjectFemale genital microbiome
dc.subjectMicrobiota-immune system interactions
dc.subjectEndometriosis
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleHypothetical roadmap towards endometriosis: prenatal endocrine-disrupting chemical pollutant exposure,anogenital distance,gut-genital microbiota and subclinical infections
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
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