Endometriosis is a chronic, estrogen-dependent condition characterized by the presence of endometrial-like tissue outside the uterine cavity – on the peritoneum, ovaries, uterosacral ligaments, bladder, bowel and other pelvic structures. These ectopic implants respond to hormonal cycles, generating recurrent inflammation, scarring and pain.

Ectopic Endometrial Tissue

Ectopic lesions contain glands and stroma resembling eutopic endometrium, but with altered gene expression and local environment. They can adhere to pelvic organs, forming nodules, cysts (e.g. ovarian endometriomas) and fibrotic strands. Cyclical bleeding within a closed space triggers irritation of the peritoneum and surrounding nerves.

Several mechanisms are proposed:

• Retrograde menstruation: menstrual blood containing endometrial cells flows through the fallopian tubes into the peritoneal cavity.
• Coelomic metaplasia: peritoneal cells transform into endometrial-like tissue.
• Stem/progenitor cell involvement and immune dysfunction, позволяющие имплантам выживать и расти.

Hormonal Dependence and Immune Microenvironment

Lesions are highly responsive to estrogens and often exhibit increased local estrogen production via aromatase. Progesterone signalling may be altered ("progesterone resistance"), reducing anti-inflammatory effects.
The surrounding microenvironment shows elevated pro-inflammatory cytokines (IL‑1β, IL‑6, TNF‑α), growth factors and angiogenic signals (VEGF), supporting lesion survival and innervation.

Immune cells (macrophages, NK-cells, T-cells) demonstrate functional changes: сниженная способность очищать эктопические клетки и усиленное поддержание хронического воспаления.

Pain Mechanisms

Pain in endometriosis is multifactorial:

• Nociceptive pain from inflamed and fibrotic tissue, stretched adhesions, organ tethering.
• Neuropathic components due to nerve fiber ingrowth into lesions and repeated irritation of pelvic nerves.
• Central sensitization, when repeated nociceptive input lowers pain thresholds in the spinal cord and brain, making even mild stimuli feel intense.

This helps explain why pain severity does not always correlate with visible lesion extent.

Fertility and Organ Function

Endometriosis can impair fertility by:

• Distorting pelvic anatomy (adhesions, tubal fixation).
• Altering peritoneal fluid composition (inflammatory mediators affecting gametes and embryos).
• Impacting ovarian reserve through endometriomas and their treatment.

Symptoms such as dyschezia, dysuria and deep dyspareunia arise from lesions on bowel, bladder or uterosacral ligaments, affecting quality of life beyond menstruation.

Treatment Approaches

• Medical management: hormonal therapies (combined oral contraceptives, progestins, GnRH analogues) aim to reduce estrogen exposure and induce decidualization/atrophy of lesions.
• Surgical treatment: laparoscopic excision or ablation of lesions and adhesiolysis, particularly in cases of severe pain or infertility.
• Multidisciplinary care: pain management, pelvic floor physiotherapy, psychological support.

Endometriosis thus represents a network-level disorder involving ectopic endometrial tissue, hormonal signalling, immune responses and pain processing systems. Understanding these interconnected mechanisms позволяет строить более точные и индивидуализированные стратегии терапии.