Menstrual cyclicity: Pathogenicity, predictability, and reproducibility

The birth of every female child triggers the potential risk of endometriosis is yet to be ascertained. It has brought about the understanding of the untraceable pathophysiological relation between endometriosis and the onset of the menstrual period. It is an estrogen-dependent benign inflammatory disease characterized by the presence of ectopic endometrial implants such as endometrial glands and stroma outside the uterus. The occurrence of the earlier menarche before the onset of the adolescent stage is no longer restricted to the exposure of such metabolic disease. Rather, it is further extended to the normative and the late menarche according to the evidence-based studies. The widespread pathophysiological developments in different menarcheal age and its impact is implicated in disease onset has spurred researchers to investigate a causal relation between the range of menarcheal age and the concomitant increase of civilization chronic diseases due to having multiple factors which directly exacerbate a high degree of the metabolic investment in the widest area of the reproductive functioning, menarcheal age, nutritional status, and parity by virtue of the inextricably interwoven of complexity between the menstrual cycle and pathogen load of the retrograde menstruation. An evolutionary menstrual cyclical model predictably modulates hormonal milieu, inflammation, estrogen exposure, and pinpointing the migration of endometrial debris into the peritoneal cavity, which is up-regulated in the menstrual cycle and eventually increases the chances of the development of estrogen-dependent disease such as endometriosis. The present review evaluates the published evidence on the potential risk of endometriosis irrespective of any menarcheal age.