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Gennaro Scutiero [1] and Piergiorgio Iannone [1] and Giulia Bernardi [1] and Gloria Bonaccorsi [1] and Savino Spadaro [2] and Carlo Alberto Volta [2] and Pantaleo Greco [1] and Luigi Nappi [3]
Academic Editor: Victor M. Victor
1, Department of Morphology, Surgery and Experimental Medicine, Section of Obstetrics and Gynecology, Azienda Ospedaliero-Universitaria S. Anna, University of Ferrara, Via Aldo Moro, 8, 44121 Cona, Ferrara, Italy, unife.it
2, Department of Morphology, Surgery and Experimental Medicine, Section of Anaesthesia and Intensive Care University of Ferrara, Azienda Ospedaliero-Universitaria S. Anna, Via Aldo Moro, 8, 44121 Cona, Ferrara, Italy, ospfe.it
3, Department of Medical and Surgical Sciences, Institute of Obstetrics and Gynecology, University of Foggia, Viale L. Pinto, 71100 Foggia, Italy, unifg.it
Received May 23, 2017; Revised Jun 22, 2017; Accepted Aug 24, 2017
This 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.
1. Introduction
Endometriosis is an estrogen-dependent pelvic inflammatory disease characterized by implantation and growth of endometrial tissue (glands and stroma) outside the uterine cavity [1]. It affects about 10–15% of women of reproductive age [2, 3]. The most common symptoms of the disease are pelvic pain and infertility [1]. In fact, the prevalence of endometriosis in women with pelvic pain ranges from 30 to 45% of infertile population [4]. However, endometriosis can be also asymptomatic or accompanied by symptoms such as dysmenorrhea and dyspareunia [3, 5, 6]. The etiology of endometriosis is still unclear: the implantation theory of Sampson, the coelomic metaplasia theory of Mayer, and the theory of induction are the three classic theories that have tried to designate the definitive pathogenetic mechanism of endometriosis but they have failed to establish it [7, 8]. Recent studies have addressed the role of other factors in the development of endometriotic lesions such as familiar tendency and genetic predisposition [9]. It is now widely accepted that oxidative stress, defined as an imbalance between reactive oxygen species (ROS) and antioxidants, may be implicated in the pathophysiology of endometriosis causing a general inflammatory response in the peritoneal cavity [10–12]. Reactive oxygen species are intermediaries produced by normal oxygen metabolism and are inflammatory mediators known to modulate cell proliferation...