Introduction: Pathogenesis of Endometriosis Endometriosis is a benign gynecological disease that is characterized by the presence and proliferation of endometrial tissue outside the uterus . The pathophysiology of endometriosis remains an enigma. Although several theories exist to explain why this disease can occur, no single theory can explain the pathophysiology of endometriosis. In the 1920s, Sampson proposed the retrograde menstruation theory in which endometriotic cells moved retrogradely through the reproductive system to emerge in the peritoneal cavity . By contrast, Meyer interprets endometriosis as a metaplastic process of the epithelium to produce endometriotic cells. Meyer’s theory implies that celomic metaplasia, or endometriosis, can occur in women without a uterus and the incidence is higher as aging progresses . However, the incidence of endometriosis is much lower after the onset of menopause . Neither of these two hypotheses can explain thoracic endometriosis . For this reason, the theory of benign metastasis proposed by Halban explains the presence of endometriotic cells outside the uterus because of lymphatic and vascular spread . Halban’s theory is supported by the finding that endometrial stromal cells were significantly increased in lymph nodes of baboons with induced endometriosis compared with controls . Another theory that presents the complete story of endometriosis is implantation theory. The development of endometriosis in the peritoneal cavity needs a complete process from attachment, invasion, proliferation, and maintenance . Currently, stem cell theory broadens the understanding of endometriosis pathophysiology. The existence of human endometrial stem cells and their possible involvement in the pathogenesis of endometriosis has been proven . However, none of the theories described above can provide a clear explanation of how endometriosis occurs. A complex interplay of genetic, immunologic, inflammatory, and environmental factors comes together in endometriosis. Endometriosis as an Estrogen-Dependent and Inflammatory Disease Endometriosis is known to be an estrogen-dependent disease that plays a role in the development and maintenance of endometriotic cells. This is evident because endometriosis starts to develop after puberty and regresses after menopause . Several proteins such as 17β-hydroxysteroid dehydrogenase (HSD17B) type I, HSD3B, P450 aromatase, StAR protein, and P450 side-chain cleavage enzyme (P450scc) required for synthesizing estrogen occur in endometriotic stromal cells . Estrogen also regulates the expression of anti-apoptotic genes that dysregulate the capability of endometriotic cells to enter “cell death” cycles.
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