Endometriosis is defined by the presence of endometrial glands and stroma in a location outside the uterus. It occurs in as many as 10% of women in their reproductive years and in nearly half of women with infertility. It frequently is multifocal and often involves pelvic structures (ovaries, pouch of Douglas, uterine ligaments, tubes, and rectovaginal septum). Less frequently, distant areas of the peritoneal cavity or periumbilical tissues are involved. Uncommonly, distant sites such as lymph nodes, lungs, and even heart, skeletal muscle, or bone are affected.
Four hypotheses have been put forth to explain the origin of dispersed endometriotic lesions, all of which are viable:
The regurgitation theory, which is currently favored, proposes that menstrual backflow through the fallopian tubes leads to implantation.
The benign metastases theory holds that endometrial tissue from the uterus can “spread” to distant sites via blood vessels and lymphatics.
The metaplastic theory, on the other hand, posits endometrial differentiation of coelomic epithelium (mesothelium of pelvis and abdomen from which endometrium originates) as the source.
The extrauterine stem/progenitor cell theory, proposes that circulating stem/progenitor cells from the bone marrow differentiate into endometrial tissue.
Studies suggest that endometriotic tissue is not just misplaced but is also abnormal (
Fig. 19.9 ). As compared to normal endometrium, endometriotic tissue exhibits increased levels of inflammatory mediators, particularly prostaglandin E2. It is proposed that the inflammation results from the recruitment and activation of macrophages by factors made by endometrial stromal cells. Stromal cells also make aromatase, leading to local production of estrogen. These factors enhance the survival and persistence of the endometriotic tissue within a foreign location (a key feature in the pathogenesis of endometriosis) and help to explain the beneficial effects of COX-2 inhibitors and aromatase inhibitors in the treatment of endometriosis.
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Fig.19.9Proposedoriginsofendometriosis.Ovary Uterus Fallopian tube Endometriotic cysts Endometriotic implants Retrograde menstruation Activated macrophages Stromal proinflammatory factors PGE2 and other inflammatory mediators COX2 COX2 PGE2
MORPHOLOGYEndometriosistypicallyconsistsoffunctioningendometrium,whichundergoescyclicbleeding.Becausebloodcollectsintheseaberrantfoci,theyappeargrosslyasred-brownnodulesorimplants.Theyrangeinsizefrommicroscopicto1to2cmindiameterandlieonorjustundertheaffectedserosalsurface.Often,individuallesionscoalescetoformlargermasses.Whentheovariesareinvolved,thelesionsmayformlarge,blood-filledcyststhatturnbrown(chocolatecysts)asthebloodages(
Fig.
19.10 ).Withseepageandorganizationoftheblood,widespreadfibrosisoccurs,leadingtoadhesionsamongpelvicstructures,sealingofthetubalfimbriatedends,anddistortionofthefallopiantubesandovaries.Thediagnosisdependsonfindingbothendometrialglandsandstromaatsitesexternaltotheendometrium.
Fig.19.10Ovarianendometriosis.Sectioningofovaryshowsalargeendo-metrioticcystwithdegeneratedblood(“chocolatecyst”).