New Understanding of Diagnosis, Treatment and Prevention of Endometriosis

Abstract

For 100 years, pelvic endometriosis has been considered to originate from the implantation of endometrial cells following retrograde menstruation or metaplasia. Since some observations, such as the clonal aspect, the biochemical variability of lesions and endometriosis in women without endometrium, the genetic-epigenetic (G-E) theory describes that endometriosis only begins after a series of cumulative G-E cellular changes. This explains that the endometriotic may originate from any pluripotent cell apart from the endometrium, that ‘endometrium-like cells’ can harbour important G-E differences, and that the risk is higher in predisposed women with more inherited incidents. A consequence is a high risk after puberty which decreases progressively thereafter. Considering a 10-year delay between initiation and performing a laparoscopy, this was observed in the United Arab Emirates, Belgium, France and USA. The subsequent growth varies with the G-E changes and the environment but is self-limiting probably because of the immunologic reaction and fibrosis. That each lesion has a different set of G-E incidents explains the variability of pain and the response to hormonal treatment. New lesions may develop, but recurrences after surgical excision are rare. The fibrosis around endometriosis belongs to the body and does not need to be removed. This suggests conservative excision or minimal bowel without safety margins and superficial treatment of ovarian endometriosis. This G-E concept also suggests prevention by decreasing oxidative stress from retrograde menstruation or the peritoneal microbiome. This suggests the prevention of vaginal infections and changes in the gastrointestinal microbiota through food intake and exercise. In conclusion, a higher risk of initiating endometriosis during adolescence was observed in UAE, France, Belgium and USA. This new understanding and the limited growth opens perspectives for earlier diagnosis and better treatment.

Endometrial Inflammation and Impaired Spontaneous Decidualization: Insights into the Pathogenesis of Adenomyosis

“…Helicobacter pylori-induced inflammation contributes to neoplastic transformation via oxidative stress, DNA damage, epigenetic modifications, and genetic alterations [ 124 ]. Recently, the oxidative stress induced by retrograde menstruation and changes in the pelvic microbiota was deemed likely to promote endometriosis development [ 125 ]. Similarly, a minority of women with pre-existing inflammation in the endometrium may be more likely to develop adenomyosis.…”

The connection between epigenetics and gut microbiota‐current perspective

“…GM and epigenetic factors are studied to be involved in the pathogenesis of Vogt–Koyanagi–Harada disease syndrome, experimental autoimmune uveitis, 37 pelvic endometriosis, 38 and schizophrenia 39 . ncRNA, histone modifications, and DNA methylation in insulin resistance (IR) are associated with tumorigenesis of various types of cancer.…”

“…34 Through the persistence of inflammation by inducing epigenetic changes, GM is studied to promote the HCC 35 while reverses some other forms of cancers. 36 GM and epigenetic factors are studied to be involved in the pathogenesis of Vogt-Koyanagi-Harada disease syndrome, experimental autoimmune uveitis, 37 pelvic endometriosis, 38 and schizophrenia. 39 ncRNA, histone modifications, and DNA methylation in insulin resistance (IR) are associated with tumorigenesis of various types of cancer.…”

Higher Prevalence of Chronic Endometritis in Women with Cesarean Scar Defect: A Retrospective Study Using Propensity Score Matching

“…Hysteroscopy combined with three-dimensional ultrasound was used to diagnose uterine abnormalities [ 34 , 35 ]. Endometriosis was diagnosed via ultrasound and laparoscopy [ 36 ].…”