Endometriosis UK
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Correcting a very common myth - Endometriosis does NOT bleed and shed!

Hi all,

I thought I would share this and hope some of you find it interesting - I did!

As I'm sure you are all aware there are just soooo many myths about Endo especially online. This particular one about endometriosis being exactly the same as endometrium (the lining of the womb) and bleeding during your cycle etc, is used in many places to describe what the condition Endometrisosis is - when it actually isn't even factually correct!

This article was written by Endometriosis Researcher Libby Hopton (who is the Director of Research and Evidence Based Medicine at Vital Health Institute) Libby has collaborated with World renowned Endometriosis specialist Dr David Redwine on several projects including their great informative website endopaedia.info/

"Does endometriosis bleed and shed?

Endometriosis is not the same as endometrium (the tissue that lines the uterus). While endometriosis is more similar to endometrium than any other tissue in the body, they are both different in many ways. One difference is that while endometrium has a basement membrane with a blood supply allowing it to bleed and shed each month, endometriosis does not and therefore can neither bleed nor shed. The chemicals released by the endometriotic glands seen in endometriosis can cause changes in the surrounding tissue. One such change is the growth of new blood vessels in the tissue surrounding the endometriosis (angiogenesis). This does not however happen in all cases and does not actually innervate the endometriotic tissue. Another change that may happen as a result of the chemicals released is that the surrounding blood vessels may rupture and bleed. The pattern of bleeding may change with fluctuations in hormone levels although not necessarily in a strict predictable fashion. This is because endometriotic tissue contains hormone receptors but these receptors do not respond in the same predictable fashion as the hormone receptors in native endometrium.

So..... endometriosis does not bleed and does not shed and disease is not spread from one site to another. But, the glands in this tissue do secrete chemicals that trigger an immune response causing inflammation. Inflammation is a process whereby the blood supply to the site of disease increases. The blood vessels surrounding the lesions of endometriosis become engorged and vasodilate (they get bigger). This can cause little blood vessels to haemorrhage (rupture) and bleeding occurs. Not all lesions are associated with bleeding.

What you'll find in a lot of info on-line is that the author mistakenly assumes that endometriosis is exactly the same as endometrium and therefore their thought process logically brings them to the idea that endometriosis also behaves exactly like endometrium... i.e. that it has a blood supply, that it bleeds and sheds each month and that at menopause the tissue always atrophies and no longer causes any problems. But this is not the case and we know this based on numerous scientific articles identifying differences between endometrium and endometriosis and documenting symptoms of endometriosis and histological findings in women in natural, surgical and medical menopause."

4 Replies

I think it is now well understood that endometriotic tissue is different from normal endometrium in various ways to include local expression of aromatase to enable it to produce oestrogen within its own cells and different expressions of oestrogen and progesterone receptors to favour progesterone resistance. This is clearly what has ruled our Sampson's theory as the cause of endometriosis as it has the claims that endometriosis has been found in fetuses. These references to 'endometriosis' refer to misplaced 'normal' endometrium and in the case of fetuses to tissue that is even less differentiated. However, both sources of ectopic tissue appear to provide the potential for transformation into endometriosis with the required immune trigger taking place at some time in the woman's life that is yet to be understood. Research suggests that retrograde menstruation might be a source of peritoneal endometriosis and Mullerian tissue a source for nodular endometriosis and possibly adenomyosis but this is yet to be proven.

It cannot be said that endometriosis does not bleed and shed as this assumes that all endometriosis is the same and the pathogenesis of the different subtypes of endometriosis is far from understood. It is established that peritoneal and deep nodular lesions are very different with with nodular endo having a basalis component and peritoneal lesions lacking it, leading some researchers to have at times considered them to perhaps be separate diseases. My personal view is that they are both endometriosis with most likely different origins. Endometriomas represent yet another different manifestation of the disease. Certainly we know that endometriomas bleed which is very evident upon rupture but the pathogenesis of endometriomas is still unknown.

It is well understood that the growth of new blood vessels is required for endometriotic cells to proliferate and invade the peritoneal membrane in order for lesions to become established, in a similar way to tumour metastases. Angiogenesis is thought to play an important role in the pathogenesis of endometriosis and vascular endothelial growth factor (VEGF) has been consistently detected in high concentration in peritoneal fluid from women with endometriosis, and the level appears to correlate with stage of disease.

The article on Endometropolis does not seem to reflect the latest research that has found that early peritoneal lesions do bleed and shed (remodel), which supports a view that peritoneal endometriosis probably has its origin in retrograde menstruation with the early red vesicular lesions representing the first partial transformation. Evidence supports the progression of peritoneal endometriosis through stages of phenotype starting with red vesicular, black powder-burn through to fibrotic lesions. Red vesicular lesions have been defined as a cluster of communicating glands that are more biochemically active than black powder-burn lesions and appear to be more responsive to cyclic sex hormones than other lesion subtypes. Laparoscopy timed to menstruation has observed these lesions to bleed in response to progesterone withdrawal. Furthermore MMPs (Matrix metalloproteinases implicated in normal cyclic endometrial turnover and menstruation) is expressed focally in red peritoneal lesions but not in black peritoneal lesions and this, along with the absence of progesterone receptors in adjacent epithelial cells, is thought to be involved in the tissue remodeling and bleeding of these early endometriotic lesions.


Clearly not well understood:


patient.info/health/endomet... (several of us have been in consultations where GP's use this site....)



Just to name a few!


Is this the same for adenomyosis?

Or does the fact that it's uterine mean it is endometriotic tissue that has infiltrated the deeper muscle layer (as us the accepted belief)?

If it'ss the latter, then menopause could give relief, right (since the endometrium is regulated by hormones) I've heard that adenomyomas can produce their own oestrogen but if there are lower levels to kick-start the process surely the adenomyoma is less likely to react.

I recently spoke to a highly respected endo specialist in Spain who said menopause would end my misery. And yet I know that others say otherwise (Dr Redwine's take was that insome cases menopause helps).

Does anyone know the science behind to help me understand and make a more informed decision?

Adenomyosis is definitely endo's poor relation; so little info and I think it's because there's the idea that hyster will solve all problems!


Hi janeingirona - Sorry I'm unsure about Adenomyosis as you say there is so little information about it available too, extremely frustrating for sufferers.


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