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Mitoses become prominent and pseudostratification is observed.
All tissue components (glands, stromal and endothelial cells) show proliferation, with DNA nuclear and RNA cytoplasmic syntheses, which peak on days 8-10 of the cycle, reflecting maximum concentration of estrogen receptors in the endometrium.
The first was the meeting of the National Institutes of Health (1990), which defined as PCOS diagnostic criteria the presence of clinical or laboratory hyperandrogenism and spaniomenorrheic cycles or amenorrhea (fewer than six menstrual cycles per year), provided that other alterations such as Cushing's syndrome, hyperprolactinemia, adrenal enzyme deficiency and thyroid disorders had been ruled out The second was the consensus of Rotterdam (2003), carried out by the European Society for Human Reproduction and Embryology (ESHRE) and the American Society for Reproductive Medicine (ASRM), which established as diagnostic criteria: spaniomenorrheic cycles or amenorrhea (chronic anovulation), clinical or biochemical signs of hyperandrogenism and the presence of polycystic ovaries (identified by ultrasonography), with at least two of three criteria being necessary to define the diagnosis of PCOSThe third consensus was proposed by the Androgen Excess and PCOS Society (AE-PCOS) in 2006, which established as diagnostic requirements: hyperandrogenism (hirsutism and/or hyperandrogenemia), ovarian dysfunction (oligo-/anovulation and/or polycystic ovaries), while ruling out other causes of androgen excess The pathophysiology of PCOS has puzzled gynecologists and endocrinologists for many years and is very difficult to be defined.
The clinical features of PCOS demonstrate a disorder of follicular development resulting in chronic anovulation, where the endocrine environment is characterized by a state of equilibrium in which the concentrations of gonadotropins and sex steroids have little variation in comparison with the cyclic pattern of hormone concentrations that occurs during the normal cycles PCOS usually displays increased serum concentrations of luteinizing hormone (LH) in 60% of cases, low levels of follicle stimulating hormone (FSH) and increased LH/FSH ratio.
This classic study is still much used for the chronological analysis of endometrial alterations; however, deficiencies have been identified.
The dating is more specific in the early and late luteal phases, but not during the period of the "window of implantation", demonstrating few histological parameters and great inter-observer variability, especially in infertile women in this cycle phase Recent gene expression studies in endometrial tissue have shown that some genes present in the proliferative phase of the menstrual cycle are essentially related to DNA replication, leading to cell proliferation and remodeling.
Progesterone can inhibit specific genes that undergo cyclical changes during the menstrual cycle and also antagonize the stimulatory action of many oncogenes that are likely to mediate estrogen-induced growth.
The end result is the stability of the endometrial lining and, consequently, the prevention of hyperplastic states The luteal phase is the most widely studied and the histological changes are of clinical importance, serving as a guideline for the diagnosis of imperfect ovulation, unsuitable for the process of implantation.
In the middle secretory phase, the vacuoles are located near the lumen of the glands and the nuclei are located in the basal position and there is secretion in the glandular lumen as well as stromal edema. In the late luteal phase, alterations occur in the stroma with prominent and dilated arterioles, reaching up to the surface layer and the endometrium is called pre-deciduous.
This fact is perhaps best illustrated with in vitro fertilization (IVF), where success rates also remain low in spite of the excellent quality of transferred embryos.
This suggests that anovulation is not the only cause of infertility We conducted a search at electronic database using the following keywords: (I) "implantation", (II) "implantation AND PCOS", (III) "implantation markers", (IV) "endometrium", (V) "polycystic ovarian syndrome AND endometrium", (VI) "implantation window".
The proliferation ceases three days after ovulation, with a decline in mitosis and DNA synthesis due to progesterone interference with the estrogen receptor expression The secretory phase shows signs of the combined reaction of estrogen and progesterone activity on the endometrium.
Progesterone stimulates the 17-^-hydroxysteroid dehydrogenase and sulfotransferase, which converts estradiol to estrone sulfate, and this is rapidly excreted from the cell.
This article aims at reviewing the endometrial aspects of the "window of implantation" in women with polycystic ovary syndrome, focusing mainly on adhesion molecules.