Clinical overview
Endometriosis is the presence of endometrial-like glands and stroma outside the uterine cavity. It affects approximately 10% of reproductive-aged women and accounts for a substantial fraction of dysmenorrhoea, Chronic pelvic pain, deep dyspareunia, and infertility. Adenomyosis is the same tissue but inside the myometrium — endometrial glands and stroma surrounded by hypertrophied smooth muscle. The two diseases are conceptually similar (ectopic endometrial tissue) but clinically distinct (pelvic vs uterine, surgical lesions vs uterine bulk).
Pathophysiology matters because it shapes management: a disease driven by oestrogen-dependent inflammation responds to hormonal suppression; a disease maintained by ongoing peritoneal seeding from retrograde menstruation argues for menstrual suppression as a long-term strategy; a disease with deep nerve-fibre infiltration requires excisional surgery to relieve pain. Each of these mechanisms is supported by evidence.
A registrar should be able to (1) explain why ectopic endometrium causes pain and infertility; (2) describe the three classical phenotypes (superficial peritoneal, ovarian endometrioma, deep infiltrating); (3) outline mechanisms in adenomyosis; (4) discuss how hormonal therapy, surgery, and fertility treatment each address a different mechanism.
Core knowledge
Theories of origin
Retrograde menstrual fragments can reflux through the tubes and implant on pelvic peritoneum, ovary and the pouch of Douglas.
No single theory accounts for all cases. The four major theories:
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Sampson's retrograde menstruation theory (1927) — viable endometrial fragments reflux through the fallopian tubes during menses, implant on pelvic peritoneum, and grow. Supported by: anatomical distribution (more posterior than anterior, more left than right because the sigmoid traps tissue), more disease in women with outflow tract obstruction, the absence of disease beyond the reach of refluxed material in most cases.
- Limitations: retrograde menstruation occurs in ~90% of women but only ~10% develop endometriosis — there must be additional factors (immune clearance failure, susceptible peritoneum, hormonal milieu).
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Coelomic metaplasia theory (Meyer) — peritoneal cells transform under oestrogen and inflammatory stimuli into endometrial-like cells. Supported by: endometriosis in prepubertal girls, in men on oestrogen therapy, and in remote sites (pleura, brain) impossible to reach by reflux.
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Lymphovascular embolisation (Halban) — fragments seeded via lymphatic and vascular channels. Explains distant disease (lung, brain, umbilicus).
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Stem cell theory — endometrial stem cells migrate and implant. Supported by recent identification of endometrial mesenchymal stem cells.
The current synthesis: retrograde menstruation provides the substrate; immune surveillance fails to clear it; ectopic implants develop their own pathology including local oestrogen synthesis (aromatase expression), inflammation, and neurogenesis.
Histopathology
Diagnostic histopathological criteria require both:
- Endometrial glands.
- Endometrial stroma.