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Endometriosis Excision Specialist in San Francisco Bay Area, California


How Does Endometriosis Occur?

Endometriosis develops when endometrial-like mucosal cells normally found in the endometrial lining of the uterus begin growing (or otherwise become activated through metaplastic transformation) and functioning in other areas or organs of the body. Under the microscope, endometriosis almost always contains mutated versions of the glands and stroma of normal endometrial-like cells found in the uterus. These mutated endometrial-like cells share some similarities with normal glands and stroma, but ultimately act and appear very differently. That’s why it’s important to always refer to endometriosis has having cells that are endometrial-like, but not actually true endometrial-like tissue.

Despite these microscopic differences, endometriotic growths can usually respond to the monthly fluctuations of female sex hormones, in a similar but still aberrant fashion as normal uterine endometrial-like cells do in reproductive-aged women and girls. Because of this, endometriosis growths may bleed, shed, and proliferate in concert with a woman’s monthly menstrual and/or ovulatory cycle. This is why the pain usually becomes most acute around menstruation and/or ovulation, though up to 30-40% of endometriosis sufferers experience pain all the time, acyclic pain, or sometimes even no pain symptoms.

In the broadest terms, many researchers hypothesize that the body’s immune system recognizes that these endometriotic growths are not growing where they should and therefore launches an immune response in order to destroy them. (Others believe that the immune system does not recognize them until it’s too late). As a result of this continued battle between endometriosis and your body’s immune system, the cytokine-prostaglandin response, inflammation, and other immune system factors appear to become chronically dysregulated.

It’s a classic vicious cycle. Partially as a result of this immune response and other factors, severe pain with menstruation, chronic pain independent of menstruation, inflammation, subfertility, infertility, tissue necrosis, and scar tissue (adhesions) can develop. In severe cases, endometriosis causes such extensive damage that serious complications ensue, like life-threatening bowel obstruction, bladder dysregulation, kidney dysfunction, silent loss of kidney (Ureteral endometriosis), collapsed lungs, and destruction of the ovaries and fallopian tubes. Meanwhile, scar tissue formation also damages organs by encasing them together in abnormal ways -in a sense strangling them – which, in severe cases, leads to the so-called frozen pelvis which can cause chronic pain and even loss of organ function.

Like the aberrant agents of destruction that they are, it appears that endometriotic growths can also reprogram genetic pathways, allowing them to continue to become activated possibly from existing cells that have undergone metaplastic transformation.

Whatever the etiology, the end result is that newly activated cells can transform into endometriotic lesions that begin producing their own hormones, nerves, and blood supply. It’s as if endometriosis is determined to live and will do anything to ensure its own survival. In this sense, endometriosis appears to behave in some similar ways as some cancers, even though endometriosis is not cancer and is classified as a benign condition. (Endometriosis is, however, associated with an increased risk of certain cancers).

A combination of genetic predisposition, epigenetic mutations, stem cell dysregulation, immune system dysfunction, and environmental triggers have all been proposed as potential factors in the pathogenesis of endometriosis.

Through all of these potential pathways, endometriosis can be a progressive disease; that is, it can continue to grow or become activated in new places throughout the body and become worse, despite medical and/or surgical interventions and even if the uterus and ovaries have been surgically removed. (This is not to suggest that these growths move or travel; rather, it may be that these cells are in place from birth and are activated through certain environmental, epigenetic, immune, stem cell, or other unknown factors. However, there is no scientific consensus on the etiology, so these are still under the category of hypothesis).

Did you know?

Did you know that teenage girls can develop endometriosis as soon as they start menstruating?

Please email us at for your questions about Endometriosis.

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