Myomas and Adenomyosis: Impact on Reproductive Outcome

Table 2

Mechanisms proposed for fertility impairment on the presence of myomas and adenomyosis.

	Mechanism
Myomas	(i) Distortion of the uterine cavity rendering the endometrial contour anomalous may compromise implantation potential; (ii) An enlarged and deformed fibroid uterus may hamper sperm transport; (iii) Cervical displacement may hinder sperm passage into the cervical canal; (iv) Altered myometrial contractility may compromise sperm progression into the female reproductive system; (v) Alteration to the endometrial and myometrial blood supply may interfere with both uterine contractility and implantation; (vi) Retained menstrual efflux due to a deformity of the uterine cavity may interfere with both sperm transport and implantation; (vii) Deviation or obstruction of the tubal ostia may compromise tubal patency; (viii) Alteration of the tubo-ovarian anatomic relation may impede ovum collection from the fimbrial end following ovulation; (ix) Chronic endometrial inflammation due to myomas lying adjacent to the endometrium may alter endometrial milieu; (x) Histologic alterations attributed to myomas lying close or in contact to the endometrial surface may impair implantation; (xi) Among molecular markers of endometrial receptivity, a decrease in HOX gene expression throughout the endometrium and not simply over a submucosal myoma may suggest that impairment of fertility may be attributed to a global effect and not simply a focal change over the myoma
Adenomyosis	(i) Aberrant uterine contractility, originating from the junctional zone, which is broadened in case of adenomyosis, may impair rapid and sustained directed sperm transport; (ii) Abnormal myometrial activity during the peri-implantation period may hinder apposition, adhesion, and penetration of the embryonic pole of the blastocyst into the decidualized endometrium; (iii) Increased endometrial stroma vascularization in the secretory phase may derange the endometrial milieu, thus negatively affecting implantation; (iv) Alteration in the expression profile of cytokines and growth factors in the endometrium, such as increased expression of hypoxia-inducible factor 1α (HIF-1α) and interleukins (IL-6, IL-8, IL-10) as well as IL-8 receptors CXCR1 and CXCR2, matrix metalloproteinases (MMP2 and MMP9) and vascular endothelial growth factor (VEGF) and decreased expression of leukemia inhibiting factor (LIF), LIF receptor α, and IL-11 may be linked to adenomyosis-associated infertility; (v) Decreased expression of HOXA-10 gene during the midluteal phase, which is considered a necessary component of endometrial receptivity and peaks during the implantation window, may negatively affect implantation; (vi) Hyperestrogenic endometrial environment due to the increased expression of cytochrome P450 along with increased aromatase activity in the endometrium sustains the increased expression of the estrogen receptor α during the secretory phase. This in turn adversely affects cell-adhesion molecule expression, such as β3 integrins, which are deemed as key elements for the development of a receptive endometrium