Chemically-induced histopathological progression in the polycystic ovary syndrome (PCOS)- A review

Polycystic ovary syndrome (PCOS) is the most common endocrine-gynecological disorder, affecting 4-10% of women of reproductive age. Although a fragment of the involved mechanism behind the PCOS occurrence is discovered, the exact etiology and pathophysiology are not completely understood yet. The pathogenesis of the disease involves several genetic, epigenetic, and environmental factors, as well as poor lifestyle. Chemicals that interact adversely with the endocrine glands are ubiquitous in the ecosystem and are known as endocrine-disrupting chemicals. An exposed population, especially women at a growing age, undergoes many hormonal and physiological changes and is more susceptible to developing endocrinological disorders like PCOS. An effective diagnosis of the disease can be made by observing changes in cells that are associated with the progression of the disease. Histopathological changes provide abundant evidence that is directly or indirectly involved in its progression and help in the evaluation of the complexity of the disease. In case of environmental stress, the body responds via some visible changes in cells, including the position and size of small cysts, changes in atretic follicles and ovarian capsules, thickening of ovarian tunica, and increased intra-ovarian cysts are some of the examples that are involved in etiology of disease. Therefore, in this review, we will try to understand the progression of PCOS by observing morphological changes through the histopathology of associated tissues that can be a plausible predictor of malignant changes in the disease. Our primary aim is to summarize the existing literature of experiments and contribute to a better understanding of the disease and associated problems.