Follicular dynamics in the polycystic ovary syndrome

Anovulation in women with polycystic ovary syndrome (PCOS) is characterised by arrested growth of antral follicles. A relative lack of FSH may contribute to the persistence of anovulation but is unlikely, by itself, to be a major cause of it. Granulosa cells from anovulatory women with polycystic ovaries hypersecrete oestradiol, compared with size-matched follicles from normal ovaries or polycystic ovaries from ovulatory women. This phenomenon appears to reflect a condition of advanced maturation of medium-sized antral follicles. The underlying basis for the abnormalities in anovulatory PCOS remains uncertain, but it is possible that there are intrinsic differences in folliculogenesis between polycystic and normal ovaries which affect preantral as well as antral follicles. An alternative - but not mutually exclusive - explanation of this disorder is the abnormal endocrine environment. Hypersecretion of both LH and insulin are typical of anovulatory women with PCOS. Studies in isolated granulosa cells, have shown, that insulin greatly augments the action of LH on steroidogenesis but this interaction may compromise further growth of medium-sized antral follicles by generation of 'preovulatory' concentrations of cAMP within the granulosa cell and thereby leading, prematurely, to terminal differentiation of granulosa cells.