Endometriosis is driven by relatively low levels of prenatal and postnatal testosterone. Testosterone affects the developing hypothalamic–pituitary–ovarian (HPO) axis, and at low levels, it can result in an altered trajectory of reproductive and physiological phenotypes that can mediate the symptoms of endometriosis. Women with endometriosis exhibit, relative to controls: have shorter AGDs, indicative of lower prenatal testosterone (2) lower LH relative to FSH, (3) higher SHBG, (4) higher serum oxytocin, (5) lower ovarian and serum testosterone, (6) lower AMH, (7) lower WHR and BMI, (8) lower β-endorphin and (9) a wider endometrial-myometrial junction (JZ zone).
The endometrial-myometrial junctional zone (JZ), is related to peristaltic-like movements in the non-pregnant uterus. Hyperperistalsis and dysperistalsis of uterus underlie many important disorders such as dysmenorrhea, infertility, endometriosis, implantation failure. The maximum thickness of JZ in patients with endometriosis is significantly greater than in patients without endometriosis (6.5 ± 1.9 mmvs 4.8 ± 1.0 mm.
The major proteins for uterine contraction of the non-pregnant uterus are Oxytocin (OT) and the oxytocin receptor (OTR). The expression level of OTR in the fundus region is positively associated with the severity of dysmenorrhea in endometriosis group (r = 0.870, p < 0.05). Comparing to normal uteri, the expression of OTR in the secretory phase was significantly higher in the endometriosis uteri (p < 0.05). In the fundus of endometriosis uteri, OTR expression was significantly higher in both the proliferative and secretory phases (p = 0.045 and 0.028, respectively).1
The pathogenic hypothesis of endometriosis supported by the most robust evidence is based on the so-called retrograde menstruation phenomenon. Viable endometrial fragments are driven through the fallopian tubes, possibly by a pressure gradient originating from dyssynergic uterine contractions. Once they reach the peritoneal cavity, they can implant, grow and invade onto pelvic structures.
In normal couples, fecundity is in the range of 0.15 to 0.20 per month and decreases with age. Women with endometriosis tend to have a lower monthly fecundity of about 0.02–0.1 per month. In addition, endometriosis is associated with a lower live birth rate.
Preterm delivery appears to be the biggest issue linked to endometriosis during pregnancy. Oxytocin mediated changes in the uterine wall from a state of rest to a state of activity during labor is believed to be the catalyst in endometriosis-related pregnancy complications.