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Throughout my early specialist gynaecology training I compared the pathogenesis of endometriosis to one of my Otago University Dunedin flats. My bedroom in this flat had a serious case of ‘mouldy roof’. If I neglected to ‘mop the roof’ every few months, things got way out of control.

At the time this seemed a fitting analogy to the pathogenesis of endometriosis. The development of endometriosis reflected ‘parasitic endometrial glands and tissue’ that had refluxed through the fallopian tubes and then found a suitable place to grow1. If this tissue (or ‘mould’) was not ‘mopped up’ every few years, things were liable to become seriously problematic.

With experience, further training, and a more complex understanding of endometriosis, I began to appreciate that the theory of ‘retrograde menstruation’ could not be the only pathogenic mechanism.

If this were the case simply clipping or removing the fallopian tubes would be curative. While still not completely understood, we now understand that the development of endometriosis is related to multiple and complex overlapping mechanisms.

Retrograde menstruation appears to somehow trigger a change in the underlying peritoneal mesothelial cells. Given that 90% of women will have retrograde menstruation, the peritoneal mesothelial cells must be susceptible to ‘change’2. Deficient immune and inflammatory systems may contribute to endometriosis development as menstrual debris evade clearance3. Genetic or hereditary factors may play a role in each of these mechanisms. If a first-degree relative has endometriosis the individual has a seven percent chance of developing endometriosis. This is compared to one percent background risk4.

Emerging evidence shows that genetic and environmental factors may enhance the ability of refluxed endometrial tissue to development in ectopic sites. Micro RNAs (miRNA) are epigenetic modifiers of gene expression, and differential regulated miRNAs have been found in eutopic and ectopic endometrium5. This area of research is interesting as it may lead to miRNA-based therapies of endometrial disorders such as endometriosis.

A better understanding of the pathogenesis also challenges us to review our understanding of endometriosis ‘recurrence’. Does endometriosis truly recur? Or, is it reemergence of abnormal peritoneal mesothelial cells that have not been surgically removed?

‘Parasitic’ endometriosis would continue to develop until the source (uterus) is removed or fallopian tubes blocked. Women would require laparoscopy every few years to keep things ‘under control’. Then hysterectomy once childbearing is complete. Certainly this has been the approach in the past.

In many patients ‘recurrence’ of endometriosis reflects endometriotic tissue that was incompletely removed at initial surgery6. We know that ablation or cauterisation of endometriosis has higher rates of recurrence7. This likely occurs because the tissue was never completely removed. Full excision of disease with wide and clear margins should lead to more women having a solitary laparoscopy or a very limited number of procedures. Unfortunately endometriosis can be challenging to remove in entirety; the more severe disease the higher the risk of residual endometriosis. Progressive development of residual disease will continue to be a problem. Repeat endometriosis surgery is also challenging due to adhesions. Endometriosis and adhesions can be difficult to differentiate.

The idea that endometriosis develops like a parasite is incorrect. Retrograde menstruation plays a role in the development of endometriosis but is not the only mechanism. Endometriosis surgeons should focus on performing ‘one excellent operation’ and avoid ablation or partial resection. This may mean women with unexpected severe disease have a short ‘planning laparoscopy’ with no attempt to ‘make a start’. Clinicians should endeavour to avoid performing multiple laparoscopies on the same woman.

References

  1. Olive D, Henderson D. Endometriosis and mullerian anomalies. Obstet Gynecol 1987; 69(3): 412
  2. Vercellini P, Vigano P, Somigliana E et al. Endometriosis: pathogenesis and treatment. Nat Rev Endocrinol 2014; 10(5): 261-75
  3. Steele R, Dmowski W, Marmer D. Immunologic aspects of human endometriosis. Am J Rep Im 1984; 6(1): 33-36
  4. Simpson J, Elias S, Malinak L et al. Heritable aspects of endometriosis. I. Genetic studies. Am J Obstet Gynecol 1980; 137(3): 327
  5. Hull L, Nisenblat V. Tissue and circulating microRNA influence reproductive function in endometrial disease. Reprod Biomed Online 2013; 27; 515-529
  6. Rizk B, Fischer A, Lotfy H et al. Recurrence of endometriosis after hysterectomy. Facts Views Vis Obgyn 2014; 6(4): 219-227
  7. Wood C, Maher P. Peritoneal surgery in the treatment of endometriosis – excision or thermal ablation? Aus N Z J Obstet Gynaecol 1996; 36(2): 190-

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