Abstract

Endometriosis, defined as the presence of endometrial glands and stroma outside the uterine cavity, is a common gynecological disease. It is an estrogen-dependent and chronic inflammatory disease, affecting 10% of women during their reproductive years. It is frequently associated with chronic pelvic pain, dyspareunia, and subfertility, negatively impacting on the afflicted women's quality of life. Although the etiology and pathogenesis of endometriosis are still unclear, Sampson's theory of implantation of endometrial cells and fragments refluxed during menstruation is generally accepted. It holds that endometriosis is caused by retrograde menstruation with intraperitoneal spilling of endometrial cells, from the mucosa lining of the uterine cavity, and then implanted into the endoabdominal structures, in particular the peritoneal wall and ovaries. However, nearly all healthy women with patent fallopian tubes undergo retrograde menstruation, yet only 1%–10% of women are diagnosed with endometriosis. Given such a huge gap, it is likely that the genesis of endometriosis is affected by many factors, such as the immune state, inflammation and the changes of hormones levels. It is generally regarded that the pathogenesis of endometriosis is complex, characterized by inflammation of peritoneum, macrophage chemotaxis and polarization, nerve infiltration and increased local estrogen biosynthesis.

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