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Article © Center for Endometriosis Care/Ken Sinervo MD, MSc, FRCSC. All rights reserved. No reproduction permitted without written permission. Current version as of 2023. No external funding was utilized in the creation of this material. The Center for Endometriosis Care neither endorses nor has affiliation with any resources cited herein. The following material is for informational purposes only and does not constitute medical advice.

By Dr Jose Eugenio-Colon | June 19, 2023
With contributions from Dr Ken Sinervo & Cassara Cook, CRA, Clinical Research Coordinator, WUSTL Division of Clinical Research & President, Midwest Endometriosis Society.

The June 14, 2023 article published in Science Translational Medicine1 suggesting bacterial involvement in the pathogenesis of endometriosis has caused quite a stir in the endometriosis community. However, the resulting uproar is not due to the potential positive effect the authors anticipated. Rather, it is a result of frustration with the ongoing lack of understanding of this complex disease by researchers and physicians.

This article has several fatal flaws, the first of which is evident in the author’s first sentence. Retrograde menstruation is no longer believed to be a significant causative factor in the pathogenesis of endometriosis.2  Research that Dr. David Redwine published in 1988 presented the best-fit model of endometriosis pathogenesis, in which some cells that will make up the reproductive organs fail to make their way to their proper place during embryogenesis.3 This is the model that endometriosis experts believe is most likely. This is also the only theory which explains the finding of endometriosis lesions in far-reaching locations such as the brain, as well as lesions found in infants4 and those assigned male at birth. The theory of retrograde menstruation, referred to by Dr. Redwine as “the most dangerous theory in the history of medicine,” does not explain these situations. It has been over 100 years since Dr. John Sampson coined the idea of retrograde menstruation,5 and since that time the medical and research communities have been mired down in the sludge of incorrect information and lack of willingness to question this theory.

The researchers also failed to utilize the correct definition of endometriosis, and thus used tissue that does not represent endometriosis. In this study, the researchers transplanted endometrial lining into mice.1 However, it is widely known that endometriotic (endometriosis tissue) and the endometrial lining are distinctly different. Utilizing endometrial lining rather than endometriotic tissue fails to account for these differences. The ultimate result of this is that the information the authors gleaned from their data cannot be extrapolated and applied to endometriosis. The finding of bacteria in the “endometriosis lesions” in the mice does not necessarily indicate that the bacteria are responsible for the growth of the lesions.

Fusobacterium nucleatum is commonly found in the mouth and intestinal flora of humans.6 It is possible that the finding of the bacteria was caused simply by poor aseptic technique. One of the most vital rules of research is that correlation does not equal causation. The theory the authors present - that Fusobacteria plays a role in endometriosis - is not supported by pathological findings in patients. When patients undergo excision of endometriosis - which is the gold standard treatment - samples of the excised tissue are sent for pathological analysis. To date, there has been no data to support the presence of bacteria in these tissues. If the correlation is as strong as the authors suggest, one would expect that the pathologic analysis of endometriosis lesions would support that finding. This is not the case. Unfortunately for the nearly 200 million people with endometriosis, the possibility that endometriosis could be cured by simply taking antibiotics is merely wishful thinking.

Endometriosis is now, and has always been, a surgical disease. A surgical disease necessitates surgical treatment. Hippocrates understood this, writing between 400-500 BCE, “the diseases which medicines cannot cure, the knife [excision] cures…”7 Quick fixes rarely, if ever, work. Endometriosis patients are not hoping for science to provide a ‘quick fix’ for the disease, but for the medical and research communities to embrace what the endometriosis community has understood for decades: retrograde menstruation is not the cause, GnRH drugs and birth control are not curative treatment, and excision is the gold standard.



1. Muraoka A, Suzuki M, Hamaguchi T, Watanabe S, Iijima K, Murofushi Y, Shinjo K, Osuka S, Hariyama Y, Ito M, Ohno K, Kiyono T, Kyo S, Iwase A, Kikkawa F, Kajiyama H, Kondo Y. Fusobacterium infection facilitates the development of endometriosis through the phenotypic transition of endometrial fibroblasts. Sci Transl Med. 2023 Jun 14;15(700):eadd1531.
2. Vinatier D, Cosson M, Dufour P. Is endometriosis an endometrial disease? Eur J Obstet Gynecol Reprod Biol. 2000 Aug;91(2):113-25.
3. Redwine DB. Mülleriosis: the single best-fit model of the origin of endometriosis. J Reprod Med. 1988;33(11):915–920.
4.  Signorile PG, Baldi F, Bussani R, Viceconte R, Bulzomi P, D'Armiento M, D'Avino A, Baldi A. Embryologic origin of endometriosis: analysis of 101 human female fetuses. J Cell Physiol. 2012 Apr;227(4):1653-6.
5. Sampson JA. Heterotopic or misplaced endometrial tissue. American Journal of Obstetrics and Gynecology, Volume 10, Issue 5, 1925.
6. Citron DM. Update on the taxonomy and clinical aspects of the genus fusobacterium. Clin Infect Dis. 2002 Sep 1;35(Suppl 1):S22-7.
7. The Aphorisms of Hippocrates: with a translation into Latin and English. Translation by Thomas Coar. Published by A.J. Valpy, London, 1822. Digitized, page 235. Web: https://tinyurl.com/bde8xubv.