**1. Introduction**

Endometriosis is a chronic inflammatory disease, estrogen-dependent and progesterone-resistant, with a multifactorial etiology, which can appear from intrauterine life [1, 2] and can progress and aggravate as a hidden disease in adolescence [3], being more common during reproductive years, when it is more studied. It is an invasive and metastatic disease, being different from malignancies by missing nuclear atypia [4]. Endometriosis is characterized and diagnosed by

the presence and growth of endometrial-like glands and stroma outside the uterine cavity and musculature, which undergoes cyclic proliferation and breakdown similar to the eutopic endometrium, with peculiar symptoms in most cases, and non-specific also in others. The genetic predisposition, and the epigenetic changes, the systemic, and local environmental factors, and the dysfunctions in endocrine and immune systems, which make possible the new cellular connections induced by exosomes between original tissues and ectopically attached adult stem cells, with bone marrow or endometrial source, are believed to a play significant role in the establishment, maintenance, and progression of endometriosis [5, 6] and its consequences on women's fertility and quality of life. The human endometrium is an angiogenic tissue, with enormous waves of regenerative capacities through cell proliferation, differentiation, and recruitment of inflammatory cells, with episodes of apoptosis and events of breakdown and regeneration without scar, but in ectopic endometrium progression to deeply infiltrative lesions, the scar is present in the form of important fibrosis. The ovarian hormones, estrogens, and progesterone through their receptors—genetic and epigenetic regulated—play an important role in physiology and pathophysiology of eutopic and ectopic endometrium. Excess estradiol and progesterone resistance are documented in eutopic and ectopic endometrium of ill women.
