Mild or moderate endometriosis and infertility

Severe endometriosis can distort the tubes and ovaries so much that it’s not hard to imagine why fertility fails. With more moderate endometriosis, though, the tubes and ovaries are usually completely normal. What’s going wrong?

Recent speculations center on two things. First, there are wandering cells about the body called macrophages, which surround and ingest all sorts of debris that one way or another gets into the body. There are many macrophages in the peritoneal cavity (probably because in women the peritoneal cavity, via the tubes, the uterus and the vagina, is open to the outside environment). Macrophages, for example, ultimately dispose of sperm cells that get into the body.

In endometriosis, these macrophages are known to be particularly aggressive -- we call them activated macrophages. Activated macrophages may get into the fallopian tubes and dispose of sperm before they’ve had a chance of getting to the egg. This is one way endometriosis probably works in decreasing fertility -- especially in a woman whose husband has a low sperm count or low sperm motility (see chapter 9).

Activated macrophages also produce a variety of chemicals (called cytokines) that have been shown, at least in the laboratory, to interfere with sperm motility and also with the survival of embryos.

Cytokines are also capable of causing normal tissues to bleed, perhaps explaining the premenstrual spotting that endometriosis so often causes.

Second -- and this is still speculative -- we know that the endometriosis that’s associated with infertility is located very superficially in the peritoneal cavity, just on the peritoneal surface, the serosa. According to Dr I.A. Brosens and his colleagues at the Gasthuisberg University Hospital in Leuven, Belgium, this is different to endometriosis that's causing pain, which is more likely to be several millimeters deep, growing into the underlying tissues.

We also know that superficial endometriosis has glands that secrete mucus, just like the endometrium in the uterus secretes mucus in the second half of the menstrual cycle. This mucus, if it were to specially adhere to the fimbrial ends of the tubes (responsible for attracting the mucus-surrounded egg, which you may remember is called the cumulus), could stop the egg from entering the tube, with the egg more likely either to remain within the follicle or to float into oblivion in the abdomen.

What’s the evidence that this might be taking place?

Researchers have been working on endometriosis in hamsters. Hamsters are rodents, like mice and rats. Rodents don’t develop endometriosis naturally but they can be made to develop it by grafting endometrial tissue into their peritoneal cavity.

The hamsters with endometriosis induced this way (but not normal hamsters) have shown a mucus-coating over the surface of the fimbrial ends of their fallopian tubes when looked at with great magnification using scanning electron microscopy.

This is just what one might expect if secretion of mucus from the endometriosis were to be getting in the way of ovulating eggs at the ends of the tubes.

We also know from extensive experience among women with endometriosis that when we put lots of sperm directly into the tube (getting around a low sperm count), and we also put three or so eggs directly into the tube (getting around any possible problem with egg pick-up by the tube’s fimbrial end), we have a very high chance of the woman getting pregnant. (This is the procedure of gamete intrafallopian transfer, or GIFT, discussed on WebPage 20.)