Nikos F. Vlahos, Theodoros D.Theodoridis and George A. Partsinevelos

1. 2nd Department of Obstetrics and Gynecology, Aretaieion Hospital, National and Kapodistrian University of Athens, School of Medicine, 76 Vasilissis Sofas Av., 11528 Athens, Greece
2. 1st Department of Obstetrics and Gynecology, Papageorgiou General Hospital, Aristotle University of Tessaloniki, Faculty of Health Sciences, School of Medicine, Ring Road, Municipality of Pavlos Melas, Area of N. Efarpia, 56403 Tessaloniki, Greece
3. Assisted Reproduction-IVF Unit, MITERA Hospital, 6 Erithrou Stavrou Str., Marousi, 15123 Athens, Greece
   

Correspondence should be addressed to George A. Partsinevelos; partsiobgyn@yahoo.com

Received 24 February 2017; Revised 19 August 2017; Accepted 30 August 2017; Published 6 November 2017
Academic Editor: Vasilis Tanos
Copyright © 2017 Nikos F. Vlahos et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Among uterine structural abnormalities, myomas and adenomyosis represent two distinct, though frequently coexistent entities, with a remarkable prevalence in women of reproductive age. Various mechanisms have been proposed to explain the impact of each of them on reproductive outcome. In respect to myomas, current evidence implies that submucosal ones have an adverse effect on conception and early pregnancy. A similar effect yet is not quite clear and has been suggested for intramural myomas. Still, it seems reasonable that intramural myomas greater than 4 cm in diameter may negatively impair reproductive outcome. On the contrary, subserosal myomas do not seem to have a signifcant impact, if any, on reproduction. Te presence of submucosal and/or large intramural myomas has also been linked to adverse pregnancy outcomes. In particular increased risk for miscarriage, fetal malpresentation, placenta previa, preterm birth, placenta abruption, postpartum hemorrhage, and cesarean section has been reported. With regard to adenomyosis, besides the tentative coexistence of adenomyosis and infertility, to date a causal relationship among these conditions has not been fully confrmed. Preterm birth and preterm premature rupture of membranes, uterine rupture, postpartum hemorrhage due to uterine atony, and ectopic pregnancy have all been reported in association with adenomyosis. Further research on the impact of adenomyosis on reproductive outcome is welcome.

1. Introduction
Embryo implantation into the endometrial cavity has been long believed to be mainly driven by endometrial receptivity and to a lower extent by the embryo itself. In this context, impaired endometrial receptivity accounts for two-thirds, whereas embryo quality, in terms of both morphology under the microscope and genetic composition, accounts for onethird of implantation failures [1, 2]. Terefore the role of the endometrium in adverse reproductive outcome should not be disregarded. In this respect, endocrine disorders, inherited and acquired thrombophilias, immunologic abnormalities, and chronic inflammation may be responsible for reduced endometrial receptivity. Structural abnormalities, either congenital such as Mullerian anomalies or acquired ones, such as endometrial polyps, intrauterine adhesions, myomas, and
adenomyosis, may compromise embryo implantation following both natural conception and assisted reproduction technologies. Besides an adverse impact on implantation, both myomas and adenomyosis may interfere by various means throughout the duration of pregnancy and affect the obstetrical outcome [3–11].

2. Uterine MyomasUterine myomas, also called leiomyomata, fbroids, fbromyomas, leiomyofbromas, and fbroleiomyomas, are the most common benign uterine tumors. Evaluation by ultrasound reveals the incidence of fbroids as high as 60% by age of 35 years in African-American women and 40% in Caucasian women. Te incidence increases to 80% and 70% by age  50 of years, respectively [12]. Tereby, race along with age represents risk factors for myoma development. Interestingly, race is associated with myoma growth rate, given that women of African descent hold a relatively constant rate throughout reproductive life, whereas in Caucasian women myomas keep up a faster growth rate until 35 and a slower one afer the

age of 45 [13]. Early menarche, nulliparity, caffeine, and alcohol consumption, obesity, and high blood pressure have all been found to increase the risk, whereas smoking, possibly implicated in relative alteration in estrogen metabolism, has been shown to decrease the risk of developing fbroids [14– 21].

The pathogenesis of myomas is considered multifactorial. A somatic mutation in a single smooth muscle cell of the uterus is the triggering event, which explains the monoclonal origin of these tumors [14]. However, genetic and epigenetic factors, including steroid hormones, growth factors, cytokines, and chemokines, are also implicated in the development and growth of myomas [20, 22]. Although initially signifcant attention had been paid to estrogens, nowadays, progesterone and its receptors (PR-A and PR-B) are believed to play a key role in myoma growth, modulating the expression of growth factor signaling proteins and, among others, regulating genes associated with proliferation, apoptosis, and differentiation [14, 20].

Anatomically, myomas are monoclonal tumors expanding, as they grow, between normal myometrial cells creating apseudocapsule, which consists a fbro-neurovascular bundle, which surrounds the fbroid and separates it from healthy myometrium [23]. Basically, thickened collagen fbers and blood vessels form a vascular ring, which has been described as the “ring of fre” by color Doppler, whereas by conventional grey scale ultrasonography forms a hyperechogenic ring around the myoma [23, 24]. Accumulating evidence
supports the importance of this pseudocapsule in secreting, neurotransmitters, and neuropeptides, such as substance P (SP) and vasoactive intestinal peptide (VIP) as well as other molecules all of which are implicated in wound healing [25–27].

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