Abstract
Endometriosis is a poorly understood disease of unknown aetiology and histogenesis. It affects women as well as menstruating female primates of other species. The disease is characterized by ectopic growth and function of endometrial cells. Current data indicate that endometriosis begins with retrograde transport through the fallopian tubes into the peritoneal cavity of endometrial cells or fragments desquamated during the menstrual period. These cells (or tissue fragments) then implant, proliferate and develop into characteristic endometriotic lesions. Under cyclic stimulation of the ovarian hormones, ectopic endometrial cells undergo similar cyclic changes to those of the uterine endometrium. From the peritoneal cavity, endometriosis may spread through lymphatic and vascular channels into distant locations. Alternatively, endometrial cells from the uterus may disseminate systemically into the pelvic cavity and distant locations. It is unclear why, in some women, endometrial cells are transported through lymphatic and vascular channels to various parts of the body, and why they are allowed to implant and function in the ectopic sites. In many respects, this process resembles metastases of neoplastic cells and is the reason why endometriosis in the past has been referred to as ‘a benign cancer’.
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Dmowski, W.P., Braun, D., Gebel, H. (1991). The immune system in endometriosis. In: Thomas, E.J., Rock, J.A. (eds) Modern Approaches to Endometriosis. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-3864-2_6
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DOI: https://doi.org/10.1007/978-94-011-3864-2_6
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