The authors of this paper published in the journal Minerva Ginecologica frame the problem:

“Endometriosis is classically described as the presence of both endometrial glandular and stromal cells outside the uterine cavity, mainly in the pelvis. The pathogenesis of this enigmatic disorder still remains controversial despite extensive research. Although multiple theories have been put forth to explain the pathophysiology and pathogenesis of endometriosis, the retrograde menstruation theory of Sampson is the most widely accepted. However, since retrograde menstruation occurs in most of the reproductive age women, it is clear that there must be other factors which may contribute to the implantation of endometrial cells and their subsequent development into endometriotic disease.”

The authors argue that immune dysfunction must be playing an important role:

“There is substantial evidence to support that the alterations in both cell-mediated and humoral immunity contribute to the pathogenesis of endometriosis.

They note that immune dysregulation is associated with inadequate removal of ectopic endometrial cells from the peritoneal cavity.

“Moreover, increased levels of several cytokines and growth factors which are secreted by either immune and endometrial cells seem to promote implantation and growth of ectopic endometrium by inducing proliferation and angiogenesis.”

Finally, they make important observation:

“Endometriosis has also been considered to be an autoimmune disease, since it is often associated with the presence of autoantibodies, other autoimmune diseases, and possibly with recurrent immune-mediated abortion.”

This review published recently in the journal Reproduction concentrates on the role of inflammation:

“It is well recognised that many physiological reproductive events such as ovulation, menstruation, implantation and onset of labour display hallmark signs of inflammation. …Moreover, initiation and maintenance of inflammatory pathways are the key components of many pathologies of the reproductive tract and elsewhere in the body. The onset of reproductive disorders or disease may be the result of exacerbated activation and maintenance of inflammatory pathways or their dysregulated resolution.”

Specifically in regard to endometriosis they observe:

“Recent reports suggest that dysregulation of inflammatory factors play a role in endometriosis-associated reproductive failure…The concentration of inflammatory cytokines (IL1B and TNF) and PGs (PGE2 and PGF2{alpha}) produced by peritoneal macrophages and pro-inflammatory chemokines for monocyte/macrophages and for granulocytes is elevated in women with endometriosis…”

What other evidence might we find of inflammatory and autoimmune phenomena in endometriosis? This paper published in the journal Gynecological Endocrinology begins by noting how common a problem this is:

“Endometriosis affects 10–20% of women during reproductive age and is a common cause of infertility and pain leading to work absenteeism and reduced quality of life.”

The authors studied the correlation of the cytokines interleukin-8 (IL-8), tumor necrosis factor alpha (TNF-α), glycodelin and other factors in the peritoneal fluid with pain reported by patients undergoing laparoscopy, and pain during menstruation and intercourse. The presence of endometriosis was histologically confirmed (microscopic examination of the cellular structure).

What did their data show?

“TNF-α and glycodelin correlated positively with the level of menstrual pain…Patients with severe dysmenorrhoea had increased PF cytokine and marker levels; the difference was significant for TNF-α and glycodelin…TNF-α and glycodelin may thus play a role in endometriosis and the severity of menstrual pain.”

If you are treating or you suffer from endometriosis (or severe dysmenorrhea without a diagnosis of endometriosis), is it important to investigate the autoimmune inflammatory components? This and other evidence indicates that it is.