[Physiopathology of polycystic ovary syndrome]

The Polycystic Ovary Syndrome (PCOS) includes three phenotypic compartments, not always fully associated, consisting in hyperandrogenism, anovulation and metabolic syndrome, secondary to insulin resistance. The pathophysiological grounds lie upon two main components, i.e.: the theca-interstitial cell (TIC) and the granulosa cell (GC) dysregulations, the former accounting for hyperandrogenism and the latter for anovulation, and both of them being under the influence of hyperinsulinism. The former mainly results from an enzymatic overactivity, yielding an exaggerated output of androgens by the TIC, but the type(s) of enzymes as well as the genetic or adaptative nature of its (their) dysregulation are still controversial. The main consequence of the CG dysregulation is the follicular arrest just before the time of dominance. This might result from an intrinsic abnormality in CG, involving the IGFs and/or the Inhibin/Activin/Follistatin systems. Alternatively, the CTI might have deleterious effects on GC, mainly via the intra-ovarian hyperandrogenism. The latter should not be regarded any more as an atretogenic phenomenon. It is closely related to the two main morphological features of PCOS, i.e.: the stromal hyperplasia and the excessive follicular number.