Abstract
Adenomyosis and endometriosis are common gynecological disorders, but their pathophysiology
is still under debate. The aim of this review is to discuss whether adenomyosis and
endometriosis represent two different entities or different phenotypes of a single
disease. We searched PubMed electronic databases published between January 2000 and
April 2020. Endometriosis is classified into three phenotypes; superficial peritoneal
disease (SUP), ovarian endometrioma (OMA) and deep infiltrating endometriosis (DIE)
lesions. Adenomyosis presents several different subtypes, including intrinsic adenomyosis,
extrinsic adenomyosis, adenomyosis externa and focal adenomyosis located in the outer
myometrium (FAOM). Human uterus is embryologically composed of archimetra, originating
from the Müllerian duct, and neometra, arising from the non-Müllerian duct, and adenomyosis
and endometriosis are diseases of archimetra. The outer myometrial layer of the uterus
is composed of highly differentiated smooth muscle cells (SMCs), while the inner myometrial
cells are immature. Inappropriate uterine contractions can cause retrograde menstruation
and chronic inflammation in the pelvic cavity, then influencing the development of
pelvic endometriosis. Furthermore, hyperperistalsis results in physiological and pathological
changes to the endometrial-myometrial junctional barrier, allowing invagination of
the normal endometrial tissue into the inner myometrial layer. This can trigger the
development of intrinsic adenomyosis. There are insufficient data available to draw
conclusions, but extrinsic adenomyosis may result from pelvic endometriosis and FAOM
from rectal and bladder DIE/adenomyosis externa. In conclusions, this paper contributes
to the debate in the possibility that adenomyosis and endometriosis represent different
phenotypes of a single disease.
Keywords
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Article info
Publication history
Published online: August 23, 2020
Accepted:
August 21,
2020
Received in revised form:
August 10,
2020
Received:
July 13,
2020
Identification
Copyright
© 2020 Elsevier B.V. All rights reserved.
