Polycystic ovary syndrome

In polycystic ovary syndrome, “poly” means many, and “cystic” refers to cysts.

So you might think that having many ovarian cysts is a crucial part of polycystic ovary syndrome.

But while some people with polycystic ovarian syndrome do have ovarian cysts, ovarian cysts are no longer a necessary characteristic of the condition.

Instead, polycystic ovary syndrome is a dysfunction in the hypothalamic-pituitary-ovarian axis, which are the hormones that regulate the menstrual cycle.

A normal menstrual cycle can be divided into two phases: the follicular phase, which takes place before ovulation, and the luteal phase, which takes place after ovulation.

During the follicular phase, the hypothalamus secretes gonadotropin-releasing hormone, or GnRH.

GnRH makes the anterior pituitary gland secrete two other hormones, called gonadotropins, in roughly equal amounts, which it releases in pulses.

One of these gonadotropins is the luteinizing hormone, or LH.

The other is the follicle-stimulating hormone, or FSH.

LH and FSH travel to the follicles in the ovaries.

The follicles are small clusters of theca and granulosa cells that protect the developing oocyte, or egg.

The theca cells develop LH receptors which allow them to bind LH, and in response they secrete a hormone called androstenedione.

Granulosa cells develop FSH receptors, which allow them to bind to FSH and produce an enzyme called aromatase, which converts the androstenedione into 17β-estradiol - a member of the estrogen family.

As follicles grow, the level of 17β-estradiol in the blood increases, and it acts as a negative feedback signal – that is, it tells the pituitary to secrete less FSH.

Less FSH in the blood means there’s only enough to stimulate one follicle.

The follicle that has the most FSH receptors grows the quickest, and becomes the dominant follicle.