{"paper_id":"121f9c59-c6c5-4630-a5fe-b44cdd3736c3","body_text":"vv\nJournal of \nGynecological Research and Obstetrics\nClinical, Surgery and \nMedicine\n001\nCitation: Lins VC, Lins G, Vanderlei L, Ferreira MB, Azevedo L, Cavalcanti V, et al. Dysbiosis as a Risk Factor for Endometriosis: A Synt hesis of Systematic Reviews \nand Meta-analyses. J Gynecol Res Obstet. 2025;11(1):001-005. Available from: https://dx.doi.org/10.17352/jgro.000131\nhttps://dx.doi.org/10.17352/jgroDOI: 2581-5288ISSN: \nAbstract\nIntroduction: Endometriosis is a chronic inﬂ ammation that represents one of the most common benign gynecological diseases. It is a condition in which endometrial-\nlike tissue grows outside the uterine cavity, implanting itself in tissues and organs, causing pelvic pain, dysmenorrhea and in fertility. The increase in Escherichia coli and \nbacterial endotoxins are associated with the proliferation of endometriotic lesions by activating inﬂ ammatory factors. In the cervicovaginal microbiome, the dominance of \nLactobacillus is associated with gynecological and reproductive health. \nObjective: To perform a synthesis of systematic reviews and meta-analyses published on the association of dysbiosis with the development of endometriosis . \nMethodology: Systematic literature search in the PubMed, BVS, Scielo and Cochrane library platforms, using the descriptors Dysbiosis OR “mic robiota imbalance” \nOR “vaginal microbiome” OR “gut microbiota” AND Bacterial Vaginosis OR “bacterial vaginosis” OR “Gardnerella vaginalis” OR “vaginal dysbiosis” AND Endometriosis OR \n“endometriotic lesions” OR “chronic pelvic pain” OR “ectopic endometrium” and their combinations. \nResults: A total of 383 productions were found in the searched platforms, after selection stages, two articles were selected, both of w hich are systematic reviews \nor meta-analyses  that met the eligibility criteria. \nConclusion: The association between endometriosis and the presence of dysbiosis in samples collected from the intestine, vagina and periton eal ﬂ uid of patients \nwith endometriosis was shown to be signiﬁ cant.\nResearch Article\nDysbiosis as a Risk Factor for \nEndometriosis: A Synthesis of \nSystematic Reviews and Meta-\nanalyses\nViviane Cavalcanti Lins1*, Gilvandro Lins2, Leticia Vanderlei1, \nMaria Beatriz Ferreira1, Larissa Azevedo1, Virginia Cavalcanti3 \nand Carolina Bandeira1\n1Paraiba School of Public Health, Executive Secretariat of Health, Brazil\n2Federal University of Paraiba, Brazil\n3Afya Faculty of Medical Sciences of Paraiba, João Pessoa/PB, Brazil \nReceived: 07 March, 2025\nAccepted: 31 March, 2025\nPublished: 01 April, 2025\n*Corresponding author: Viviane Cavalcanti Lins, \nParaiba School of Public Health, Executive Secretariat \nof Health, Avenida Dom Pedro II, nº 1826, Torre, João \nPessoa/PB Zip Code: 58040-440, Brazil, \nE-mail: vivianembc@gmail.com\nORCiD: https://orcid.org/0009-0006-6237-3410\nKeywords: Dysbiosis; Bacterial vaginosis; \nEndometriosis; Vaginal microbiome\nCopyright License: © 2025: Lins VC, et al. This is an \nopen-access article distributed under the terms of the \nCreative Commons Attribution License, which permits \nunrestricted use, distribution, and reproduction in any \nmedium, provided the original author and source are \ncredited.\nhttps://www.clinsurggroup.us\nIntroduction\nEndometriosis is a chronic, steroid-dependent condition \nand one of the most prevalent benign gynecological diseases. \nIt is characterized by the ectopic growth of tissue similar to \nthe endometrium—composed of glands and stroma—outside \nthe uterine cavity. These implants can establish themselves \nin structures such as the fallopian tubes, ovaries, peritoneum, \ncolon, rectovaginal area, and bladder [1], triggering symptoms \nsuch as pelvic pain, dysmenorrhea, and infertility, affecting \napproximately 40% of women with pelvic pain and 50% of \nthose with infertility, although 16% may remain asymptomatic \n[2,3].\nVarious theories have been proposed to explain the origin \nand dissemination of endometriotic implants. The theory of \nretrograde menstruation, ﬁ rst described by Sampson, et al. \nin 1927, is the most widely accepted; however, considering \nthat more than 90% of women of reproductive age experience \nretrograde menstruation without developing the disease, \nit is plausible that additional factors—such as genetic \npredisposition, immunological alterations, and environmental \ninﬂ uences - play a crucial role in its pathogenesis [4].\n\n002\nhttps://www.clinsurggroup.us/journals/journal-of-gynecological-research-and-obstetrics\nCitation: Lins VC, Lins G, Vanderlei L, Ferreira MB, Azevedo L, Cavalcanti V, et al. Dysbiosis as a Risk Factor for Endometriosis: A Synt hesis of Systematic Reviews \nand Meta-analyses. J Gynecol Res Obstet. 2025;11(1):001-005. Available from: https://dx.doi.org/10.17352/jgro.000131\nThe development of endometriosis is intrinsically linked to \nan intense inﬂ ammatory process. Cytokines such as IL-1, IL-6, \nIL-8, and Tumor Necrosis Factor (TNF) promote the inﬁ ltration \nof peritoneal leukocytes and facilitate both the implantation \nand progression of endometriotic lesions [5]. Studies have \nshown that affected tissues exhibit an increased expression \nof the enzyme cyclooxygenase-2 (COX-2), whose activity is \nassociated with various pathologies of the reproductive tract \n-including carcinomas, menorrhagia, and dysmenorrhea—and \nplays a central role in both the in ﬂ ammatory and tumorigenic \nprocesses [6].\nFurthermore, endometrial samples from women with \nendometriosis reveal a higher expression of the COX-2 gene \ncompared to tissues from women without the disease. This \nincrease may promote cellular proliferation, inhibit apoptosis, \nenhance tissue invasion, and stimulate angiogenesis as well as \naromatase activity, resulting in elevated estrogen levels—a key \nfactor in the development and maintenance of endometriosis \n[7].\nIt is also observed that women with endometriosis exhibit \nhigher quantities of Escherichia coli and elevated levels of \nbacterial endotoxin in menstrual blood compared to control \ngroups. These elements may stimulate lesion proliferation \nthrough the activation of Toll-like receptor 4 (TLR-4), while \ngram-negative bacteria, by activating nuclear factor kappa B \n(NF-κB) and COX-2, contribute to the maintenance of a highly \ninﬂ ammatory environment [8].\nAlterations in the microbiome also play a signi ﬁ cant \nrole in the pathogenesis of endometriosis. In the gut, for \ninstance, estrogen deconjugation — mediated by the enzyme \nβ-glucuronidase present in bacteria such as Escherichia coli , \nBacteroides fragilis , and Streptococcus agalactiae — allows the \nreabsorption of active estrogen, creating an in ﬂ ammatory \nenvironment that may disrupt circulating estrogen levels and \npredispose to the development of the disease through the \npromotion of in ﬂ ammation, cellular proliferation, inhibition \nof apoptosis, increased oxidative stress, and angiogenesis [9].\nIn the cervicovaginal microbiome, the predominance of \nLactobacillus is essential for maintaining gynecological health, \nas these microorganisms produce lactic acid, reducing the \nvaginal pH to 4.5 or lower and inhibiting pathogen growth. \nAdditionally, Lactobacillus spp . contribute to homeostasis by \npreventing colonization by pathogenic agents and stimulating \nthe production of anti-in ﬂ ammatory cytokines, as well as \nstrengthening the epithelial barrier. In contrast, bacterial \nvaginosis (BV)—characterized by a reduction in Lactobacillus \nand an overgrowth of anaerobic bacteria—has been associated \nwith endometriosis, as it favors the formation of resistant \npolymicrobial bioﬁ lms in the cervicovaginal epithelium.\nComparative studies of the endometrial microbiota indicate \nthat, in women with endometriosis, there is an increase in \ngenera such as Streptococcus, Gardnerella, Escherichia, Shigella, \nand Ureaplasma, along with an absence of Atopobium, compared \nto control groups. These ﬁ ndings support the hypothesis that a \nreduction in Lactobacillus within the cervicovaginal microbiome \nmay be associated with the presence of microorganisms \ncommonly related to BV [9]. Similarly, analyses of the peritoneal \nﬂ uid microbiota, collected during laparoscopic surgeries, have \nshown an enrichment of Prevotella, Veillonellaceae, Atopobium, \nand Comamonas in women with endometriosis, suggesting that \ndysbiotic bacteria may ascend to the upper genital tract and \ncontribute to the development of the disease.\nIn summary, endometriosis is associated with dysbiosis \ncharacterized by a reduction in bene ﬁ cial microorganisms \nand an increase in pathogens, resulting in an in ﬂ ammatory \nenvironment and compromised immune response. This \ndysregulation favors the elevation of pro-in ﬂ ammatory \ncytokines and the progression of endometriotic implants, \nhighlighting the central role of in ﬂ ammation in the disease’s \npathogenesis [10].\nGiven this scenario, the present study proposes a synthesis \nof published systematic reviews and meta-analyses, aiming to \nelucidate the underlying mechanisms linking dysbiosis to the \nonset of endometriosis.\nMethodology\nA systematic literature search was conducted to evaluate \nthe presence of dysbiosis in the microbiome of women with \nendometriosis and its relationship with the development of the \ndisease. A systematic review involves identifying, selecting, \ncritically appraising, compiling, and presenting published \nevidence on topics relevant to population health. To ensure \nmethodological transparency and reproducibility , this study \nfollowed the Preferred Reporting Items for Systematic Reviews \nand Meta-Analyses (PRISMA) protocol.\nThe search strategy included the following descriptors and \ntheir combinations: Dysbiosis OR “microbiota imbalance” \nOR “vaginal microbiome” OR “gut microbiota”; Bacterial \nVaginosis OR “bacterial vaginosis” OR “Gardnerella vaginalis” \nOR “vaginal dysbiosis” AND Endometriosis OR “endometriotic \nlesions” OR “chronic pelvic pain” OR “ectopic endometrium”.\nThese terms were applied to the databases PubMed, BVS, \nSciELO, and Cochrane Library, as shown in Table 1 . The \nselection and analysis of articles were conducted independently \nby two researchers, and compiled the results for analysis. \nTable 1: Search Strategy.\nPlatform Descriptors Filters Results\nLilacs\nhttps://bvsalud.org/ Dysbiosis AND Endometriosis No ﬁ lters 23 \narticles\nPubmed\nhttps://pubmed.ncbi.\nnlm.nih.gov/\nDysbiosis AND Endometriosis \nOR \"endometriotic lesions\" OR \n\"chronic pelvic pain\" OR \"ectopic \nendometrium\"\nSystematic \nReview, Meta-\nanalysis\n360 \narticles\nScielo\nhttps://www.scielo.\norg/\nDisbiose/Dysbiosis AND \nEndometriose/ Endometriosis No ﬁ lters No \narticles\nCochrane library\nhttps://www.\ncochranelibrary.com/\nDysbiosis AND Endometriosis No ﬁ lters No \narticles\n\n003\nhttps://www.clinsurggroup.us/journals/journal-of-gynecological-research-and-obstetrics\nCitation: Lins VC, Lins G, Vanderlei L, Ferreira MB, Azevedo L, Cavalcanti V, et al. Dysbiosis as a Risk Factor for Endometriosis: A Synt hesis of Systematic Reviews \nand Meta-analyses. J Gynecol Res Obstet. 2025;11(1):001-005. Available from: https://dx.doi.org/10.17352/jgro.000131\nResults\nStudies included in the review focused on women over 18 \nyears of age diagnosed with endometriosis and, additionally, \nwith bacterial vaginosis con ﬁ rmed either by microscopic \nevaluation (using the Nugent score or Amsel/Spiegel criteria) \nor by gene sequencing analysis. Only studies published in \nPortuguese or English from 2014 to 2024 were considered .\nAn initial search yielded 383 records , of which 15 duplicates \nwere excluded, leaving 368 publications. Subsequently, a \nscreening of titles and abstracts led to the exclusion of 356 \nrecords that were not related to the topic, leaving 12 studies \nfor full-text evaluation. After a complete review of these texts, \n3 studies were initially deemed eligible; however, following \na thorough analysis, 2 articles were ultimately selected, both \nbeing systematic reviews or meta-analyses based exclusively \non  human samples (Figure 1, Table 2).\nDiscussion\nEndometriosis is a complex condition involving physical \nand emotional symptoms, signiﬁ cantly impacting the personal \nand professional lives of those affected, as well as leading to \nconsiderable ﬁ nancial and economic implications—estimated \nto incur a global economic burden exceeding 80 million USD.  \nAs a public health issue, it is essential that clinical decisions are \nbased on robust, evidence-based studies.\nResearch investigating the association between dysbiosis \nand endometriosis has relied on experimental results \nsupporting the in ﬂ ammatory pathophysiology of the disease \n. The advancement in understanding the human microbiome \nhas led to the emergence of a new hypothesis proposing \nan infectious origin for endometriosis. According to this \nhypothesis, alterations in the healthy microbiota—whether \nfrom the gut, oral cavity, or female genital tract—could \ncontribute to the risk of developing the disease, possibly \nFigure 1: PRISMA study selection ﬂ owchart.\nTable 2: Summary of studies found.\nAuthor Quing, et al. Colonetti, et al.\nANO 2024 2023\nDatabase\nEmbase, PubMed, Cochrane, \nMEDLINE, BIOSIS, China National \nKnowledge, Infrastructure and \nWanfang\nPubMed, Embase, Web \nof Science  and Google \nScholar \nNumber of \nPrimary Studies 8 studies 16 studies\nKanoko Akyama, 2019\nBaris Ata, 2019\nXiaopei Chao, 2021\nAllison R. Perrotta, 2020\nRasheed M. Salah, 2013\nBryan A. Wee, 2017\nWeixia Wei, 2020\nJanet D. Wilson, 2002\nAkiyama, 2019\nAta, 2019\nChang, 2022\nHernandes, 2020\nHuang, 2021\nKhan, 2014\nKhan, 2016\nKhan, 2021\nLee, 2021\nNabiel, 2020\nPerrotta, 2020\nShan, 2021\nSvensson, 2021\nWang, 2018\nWei, 2020\nYuan, 2022\nTypes of\nstudies\n2 cohort\n3 case-control\n3 transversal\n1 cohort \n14 case-control\n1 transversal\nParticipants 1036 women \n(300 endometriosis/763 control)\n1151 women\n(556 endometriosis/595 \ncontrol)\nDiagnosis of \nvaginosis\n6 (rRNA)\n2 (Spiegel) todas rRNA\nSample location vaginal\ncervical\nendometrial\nperitoneal ﬂ uid\nMost signiﬁ cant \nmicrobiota\nEnterobacterias\nStreptococcus\nLactobacillus\nGardnerella\nClostridium\nAlloscardovia\nVeillonella\nUreaplasma\nPrevotella\nActinobacteria\nAcinetobacter\nAtopobium\nBacteroidetes\nEnterobacteriaceae\nEscherichia\nEubacterium\nFaecalibacterium\nFirmicutes\nFusobacterium\nGardnerella\nLactobacillus\nMobiluncus\nPrevotella\nProteobacteria\nPseudomonas\nRuminococcus\nStaphylococcus\nStreptococcus\nVeillonella\nMethodological \nquality\nPRISMA- yes\nPROSPERO - no\nPRISMA – Yes\nPROSPERO - Yes\nPublication bias \nassessment\nNeucastle-Ottawa Scale (NOS) 6.5\n(moderate quality)\nNeucastle-Ottawa Scale \n(NOS) 7.0\n(high quality)\n\n004\nhttps://www.clinsurggroup.us/journals/journal-of-gynecological-research-and-obstetrics\nCitation: Lins VC, Lins G, Vanderlei L, Ferreira MB, Azevedo L, Cavalcanti V, et al. Dysbiosis as a Risk Factor for Endometriosis: A Synt hesis of Systematic Reviews \nand Meta-analyses. J Gynecol Res Obstet. 2025;11(1):001-005. Available from: https://dx.doi.org/10.17352/jgro.000131\nas a result of a compromised immune response, leading \nto subclinical in ﬂ ammation conducive to the formation of \nendometriotic implants [10]. \nAdditionally, the bacterial contamination hypothesis \nsuggests that the increased endotoxins produced by bacteria, \nin conjunction with tubal retrograde menstruation, could \ntrigger in ﬂ ammatory processes in the pelvic environment, \npromoting the growth and progression of endometriosis \nthrough the activation of in ﬂ ammatory receptors. In this \ncontext, lipopolysaccharide (LPS), a component of the outer \nmembrane of gram-negative bacteria, may act as an initiating \nfactor, either alone or in combination with ovarian steroids, \ncontributing to the development of the disease [11]. \nExperimental studies in murine models have shown \npromising results. Protocols using Letrozole-a cytochrome \nP450 aromatase inhibitor—combined with Alpha-Linolenic \nAcid (ALA) supplementation have demonstrated a signi ﬁ cant \nreduction in both the number and size of surgically induced \nendometriotic lesions. These treatments have been associated \nwith decreased cellular proliferation , increased apoptosis, \ndecreased angiogenesis, and improved gut microbiota \ncomposition. This resulted in a stronger intestinal barrier and \nreduced macrophage aggregation within the intestinal walls, \nmitigating the local inﬂ ammatory process [12-14]. \nGiven the multifactorial nature of endometriosis, this \nsystematic review and meta-analysis aimed to gather evidence \non the association between dysbiosis and the development of \nthe disease. Quing, et al. [15] performed a systematic review \nthat identi ﬁ ed a potential positive association between \ndysbiosis and endometriosis (OR 1.17 [0.81–1.70]), although \nwithout statistical signi ﬁ cance. In contrast, the analysis of \nthe relationship between a normal vaginal microbiota and \nendometriosis incidence revealed an inverse association (OR \n0.90 [0.55–1.46]), suggesting a protective effect from a healthy \nvaginal microbiota, even though this association also did not \nreach statistical signi ﬁ cance. The authors further highlighted \nthe relationship between the absence of Lactobacillus and \nthe proliferation of bacteria linked to bacterial vaginosis \nin the cervicovaginal microbiota and the association with \nendometriosis and infertility [15]. \nIn line with this, Colonetti, et al. [16] reviewed 16 studies \ninvestigating dysbiosis in various samples—including material \nfrom the intestinal tract, vagina, and peritoneal ﬂ uid—and its \nassociation with endometriosis. Although the group of women \nwith endometriosis showed higher levels of certain markers, no \nanalysis achieved statistical signiﬁ cance. In one of the studies, \nit was observed that in more severe cases of endometriosis, \nthe vaginal and cervical microbiota displayed an absence of \nAtopobium (Actinobacteria) and increased levels of Gardnerella, \nStreptococcus, Escherichia, Shigella, and Ureaplasma, potentially \npathogenic organisms [16].\n The studies analyzed indicated the prevalence of some genera \nsuch as Enterobacter, Streptococcus, Lactobacillus, Gardnerella, \nVeillonella and Prevotella in patients with endometriosis, \nhighlighting the need for more speci ﬁ c investigations, \nfocused on the identi ﬁ cation of genera and species that may \nbe implicated in the pathogenesis of endometriosis, and that \ntrigger inﬂ ammatory changes arising from dysregulated states \nof the intestinal ﬂ ora, allowing translocation of pathogenic \nmicrobial metabolites .\nExperimental analyses have explored emerging therapies \nfor endometriosis, such as antibiotics , Lactobacillus \nsupplementation and microbial transplantation; preliminary \nresults demonstrate a reduction in endometriotic lesions \nin animal models . And the use of probiotics, for oral \nsupplementation of Lactobacillus , can alleviate pain and \nimprove the quality of life of patients with endometriosis, \nalbeit to a limited extent [17,18]. Such ﬁ ndings may contribute \nto more targeted and effective clinical management  of these \npatients. \nFinally, it is important to recognize that the microbiome \nis inﬂ uenced by a variety of factors—including demographics, \nlifestyle, age, race/ethnicity, diet, medical history, pregnancy, \nchildbirth, sexual and hygiene practices, genetic variation, \ncultural habits, menstrual cycle, hormone levels, and the \ngeneral environment—thus making more accurate analyses of \nthis study difﬁ cult. Therefore, standardizing sample collection \nmethods and matching clinical factors, such as menstrual cycle \nphase and technique used, are essential to ensure consistency \nof results and correct interpretation of data.\nConclusion\nAlthough current data do not demonstrate a statistically \nsigniﬁ cant association between endometriosis and the presence \nof dysbiosis in intestinal, vaginal, and peritoneal ﬂ uid samples, \nconsiderable heterogeneity among the populations studied \nhighlights the need  for further investigations. \nFuture studies should investigate the most prevalent \nbacterial taxa  in women with endometriosis and apply \nstandardized methodologies for more robust and generalizable \nﬁ ndings  in order to validate these ﬁ ndings and enhance our \nunderstanding  of the underlying mechanisms of the disease.\nReferences\n1. Giudice LC, Kao LC. Endometriosis. Lancet. 2004;1789–99. Available from: \nhttps://doi.org/10.1016/s0140-6736(04)17403-5 \n2. Missmer AS, Cramer DW. 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Front Med. 2022. \nAvailable from: https://doi.org/10.3389/fmed.2022.831115 \n \n \n \nhttps:/ /www.peertechzpublications.org/submission","source_license":"CC0","license_restricted":false}