Abstract
Endometriosis is defined as aberrant islands of endometrium found in extrauterine locations that exhibit the histology and hormone responsiveness of the functional layer of the native endometrium (1–3). In the 1890s, the pathology of endometriosis was described by von Recklinghausen (4) and Russell (5). However, definitive investigation of this interesting disease began with Sampson’ s classic papers (3,6–21). Early studies focused on histopathology, natural history, and speculation as to etiology(3–23). Although the etiology of endometriosis remains unknown, the main theories of histogenesis can be summarized:
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1.
Transtubal regurgitation and implantation. This was initially proposed by Sampson (13,15), with experimental and clinical support by TeLinde and Scott (24,25), and others (26–33).
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2.
Celomic metaplasia. Ivanoff (34) and Meyer (35) theorized that repeated inflammation could induce metaplasia of celomic epithelium to endometrial epithelium. Novak suggested that hormonal stimuli might be the activating factor (2,36,37). Endometrium may contain an inducer of celomic metaplasia that does not require implantation for activity (38).
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3.
Lymphatic (23,29,40) and/or hematogenous (16,41,42) spread may be necessary to explain extraperitoneal endometriosis (23, 39–50), although thoracic lesions may be caused by peritoneal seeding through known diaphragmatic fenestrations (48,49). Sampson concurred that regurgitation/implantation could not explain all tissue involvement (2,16).
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Malinak, L.R., Wheeler, J.M. (1984). Endometriosis. In: Aiman, J. (eds) Infertility. Clinical Perspectives in Obstetrics and Gynecology. Springer, New York, NY. https://doi.org/10.1007/978-1-4613-8265-2_16
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