Premature response to gonadotrophins by small follicles is the key answer of developing too many follicles in ovarian cortex!!
LH hyperfunction in PCOs : In a normal cycle, only the dominant follicle responds to LH action when it reaches 10 mm in diameter. In PCOS patients, the response to LH occurs inappropriately in smaller follicles; a large number of antral follicles reach a terminal differentiation before the appropriate time, producing a larger amount of steroids and inhibin B that have a negative feedback on the production of FSH: the result is the arrest of follicular growth. Over-response of even the small Follicles which are < 10 mm which normally should not respond to gonadotrophins but in case of PCO such small follicles do respond to both LH & FSH:
It has been shown that polycystic ovary presents a greater number of small antral follicles (2-9 mm in diameter) than the normal ovary. This morphological scenario could be the consequence of a potential dysregulation of the recruitment mechanism of primordial follicles that, on the contrary, are present in physiological number.
Finally, the increase in ovarian androgen level changes adrenal specific enzyme activities involved in the process of steroidogenesis.
On the other hand, the final pathway of follicular growth, which is gonadotropin dependent, is blocked in the majority of PCOS patients, and it is the basis of anovulation and oligo-/amenorrhea.
As underlined before, the etiology of this syndrome is still partly unknown, but it is likely to be multifactorial. The most significant theories are explained below:
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