The viability of the cast-off menstrual endometrium

Cron, Roland S.; Gey, George O.

doi:10.1016/s0002-9378(27)90487-6

Cited by 48 publications

(9 citation statements)

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“…Sampson (1,11,201) proposed retrograde menstruation as the cause of cystic ovarian endometriosis. Retrograde menstruation is an attractive hypothesis because menstrual fluid contains living cells, demonstrated already in 1927 (202), with implantation and growth potential as demonstrated in 1958 by means of subcutaneous injection (203) and by growth in vitro and on the chicken allantoic membrane (204). For the latter, tissue integrity is important (204).…”

Section: The Pathogenesis Of Endometriosis: the Genetic/epigenetic Thmentioning

confidence: 99%

Pathogenesis of endometriosis: the genetic/epigenetic theory

Koninckx

Ussia

Adamyan

et al. 2019

Fertility and Sterility

303

187

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Objective: To study the pathophysiology of endometriosis. Design: Overview of observations on endometriosis. Setting: Not applicable. Patient(s): None. Interventions(s): None. Main Outcome Measure(s): The hypothesis is compatible with all observations. Result(s): Endometriosis, endometrium-like tissue outside the uterus, has a variable macroscopic appearance and a poorly understood natural history. It is a hereditary and heterogeneous disease with many biochemical changes in the lesions, which are clonal in origin. It is associated with pain, infertility, adenomyosis, and changes in the junctional zone, placentation, immunology, plasma, peritoneal fluid, and chronic inflammation of the peritoneal cavity. The Sampson hypothesis of implanted endometrial cells following retrograde menstruation, angiogenic spread, lymphogenic spread, or the metaplasia theory cannot explain all observations if metaplasia is defined as cells with reversible changes and an abnormal behavior/morphology due to the abnormal environment. We propose a polygenetic/polyepigenetic mechanism. The set of genetic and epigenetic incidents transmitted at birth could explain the hereditary aspects, the predisposition, and the endometriosis-associated changes in the endometrium, immunology, and placentation. To develop typical, cystic ovarian or deep endometriosis lesions, a variable series of additional transmissible genetic and epigenetic incidents are required to occur in a cell which may vary from endometrial to stem cells. Subtle lesions are viewed as endometrium in a different environment until additional incidents occur. Typical cystic ovarian or deep endometriosis lesions are heterogeneous and represent three different diseases. Conclusion(s): The genetic epigenetic theory is compatible with all observations on endometriosis. Implications for treatment and prevention are discussed. (Fertil Steril Ò 2019;111:327-40. Ó2018 by American Society for Reproductive Medicine.) El resumen está disponible en Español al final del artículo.

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Section: The Pathogenesis Of Endometriosis: the Genetic/epigenetic Thmentioning

confidence: 99%

Pathogenesis of endometriosis: the genetic/epigenetic theory

Koninckx

Ussia

Adamyan

et al. 2019

Fertility and Sterility

303

187

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“…The endometrium is the candidate because shredded menstrual endometrium is viable, was demonstrated in 1927 (113) and has implantation potential as demonstrated by subcutaneous injection (114) as early as 1958. For development on the chicken allantoic membrane, tissue integrity is important (115).…”

Section: Development Of (Deep) Endometriosis: What Is the Original Cell?mentioning

confidence: 99%

Pathogenesis of deep endometriosis

Gordts

Koninckx²,

Brosens

2017

Fertility and Sterility

187

115

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“…It was known since the beginning of this century that menstrual endometrium contains viable cells [7][8][9]. After it became evident that retrograde menstruation is a frequent phenomenon [10], it was no surprise that peritoneal fluid contains viable endometrial cells [11,12], which have the capacity to implant [13], to grow, and to infiltrate superficially [14].…”

Section: Introductionmentioning

confidence: 99%

Implantation versus Infiltration: The Sampson versus the Endometriotic Disease Theory

Koninckx

Barlow

Kennedy

1999

Gynecol Obstet Invest

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It has been assumed that endometriosis is a progressive disease, with growth and development of lesions being inevitable once the disease has started. The implantation and the metaplasia theories describe the mechanism of initiation of endometriotic lesions, but do not explain the different clinical manifestations of endometriosis. To explain the variable expression, growth and development of lesions into severe disease, a new endometriotic disease theory is proposed. This theory suggests that progression of endometriosis to endometriotic disease is considered similar to the onset and progression of a benign tumour. In this theory, the most important factor in the development of endometriotic disease is not the initial implantation/metaplasia, but cellular changes such as mutations. According to this theory, endometriotic disease develops from endometriotic cells that have ‘escaped’ the influence of protective and regulatory factors in the peritoneal fluid.

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The viability of the cast-off menstrual endometrium

Cited by 48 publications

References 0 publications

Pathogenesis of endometriosis: the genetic/epigenetic theory

Pathogenesis of endometriosis: the genetic/epigenetic theory

Pathogenesis of deep endometriosis

Implantation versus Infiltration: The Sampson versus the Endometriotic Disease Theory

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