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The intensity of pain associated with deep infiltrating endometriosis relates to the depth of penetration and to the proximity or direct invasion of nerves.331 341
Whereas neural inflammation or invasion might explain the pain of women with deep infiltrating endometriosis, it cannot be the mechanism that produces pain in women wrho have superficial peritoneal/ovarian disease.3" The pain associated with mild disease more likely relates to inflammation resulting from cyclic focal bleeding in and around peritoneal implants or from the actions of inflammatory cytokines released by the larger numbers of macrophages and other immune cells in the peritoneal fluid of women with endometriosis.
eutopic cnde^meLr^uln^L,, JJ| ft is postulated that aberrant aclt- v.iiinn nf die Writ pathway negatively impact* endometrial development during the time of the implantation window, likely by adversely affecting the normal epithelial-stromal polarity,2'1: There is ajbo Increasing evidence that ectopic implants can lead, to tmpln nfation failure through ate riant endometrial gene expression in the truing it e icWmirtrium.
Whereas deep infiltrating endometriosis involving 'he ree tovagina!
(tm) '*1 Whereas ovarian endometriomas usually are accompanied by numerous other visible peritoneal lesions,383 deep infiltrating endometriosis is largely retroperitoneal, often not readily apparent, and frequently isolated; it may even represent a distinct entity, arising from mullerian rests within the rectovaginal septum.3*3-3*3
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