Follicle dynamics and anovulation in polycystic ovary syndrome.
BACKGROUND
Polycystic ovary syndrome (PCOS) is the commonest cause of anovulatory infertility and menstrual cycle abnormalities, but the factors responsible for failure to select a dominant follicle remain unclear.


METHODS
Source is authors' own studies and search of the relevant literature.


RESULTS
Arrest of antral follicle growth is associated with an abnormal endocrine environment involving hypersecretion of luteinizing hormone and insulin (and perhaps hyperandrogenism). The net effect is secondary suppression of FSH, which leads to inhibition of maturation of otherwise healthy follicles in the cohort. There is, however, emerging evidence for an intrinsic abnormality of folliculogenesis in PCOS that affects the very earliest, gonadotrophin independent, stages of follicle development. There is an increased density of small pre-antral follicles and an increased proportion of early growing follicles. These abnormalities in anovulatory PCOS are further defined by abnormal granulosa cell proliferation and disparate growth of oocyte and surrounding granulosa cells. This suggests that the normal 'dialogue' between oocyte and granulosa cells in these early growing follicles is altered. There is evidence that abnormal, local (follicle-to-follicle) signalling of anti-Müllerian hormone may play a part in disordered folliculogenesis, but it is plausible that other local regulators that have been implicated in normal and abnormal pre-antral follicle development-such as insulin-like growth factors and sex steroids-have a role in aberrant folliculogenesis in PCOS.


CONCLUSIONS
Significant abnormalities in the very earliest stages of folliculogenesis may be the root cause of anovulation in PCOS.
Franks
Stephen
S
Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Hospital, London W12 0NN, UK. s.franks@imperial.ac.uk
Stark
Jaroslav
J
Hardy
Kate
K
D000858:Anovulation / Q000209:etiology* / Q000378:metabolism; D054304:Anti-Mullerian Hormone / Q000378:metabolism / Q000502:physiology; D049109:Cell Proliferation; D005260:Female; D012739:Gonadal Steroid Hormones / Q000378:metabolism / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance; D008954:Models, Biological; D009865:Oocytes / Q000166:cytology / Q000502:physiology; D006080:Ovarian Follicle / Q000254:growth & development / Q000378:metabolism / Q000503:physiopathology*; D011085:Polycystic Ovary Syndrome / Q000150:complications* / Q000378:metabolism; D015398:Signal Transduction; D013002:Somatomedins / Q000378:metabolism / Q000502:physiology
D012739:Gonadal Steroid Hormones; D013002:Somatomedins; D054304:Anti-Mullerian Hormone