The normal adult ovary measures approximately 3-5 cm in length, 1.5-3 cm in width, and 0.5-1.5 cm in thickness.A thin, fibrous layer called the tunica albuginea encapsulates the ovary. Within the capsule lies the ovarian stroma, a combination of fibroblasts, smooth muscle cells, arteries, veins, lymphatics, nerves, and follicles. The stroma is typically divided into a cortex and medulla. The medulla is a highly vascular region supplied by the ovarian artery and branches of the uterine artery, which enter the ovary via the broad ligament. From here, smaller arteries and arterioles penetrate the cortex. The peripheral zone, or cortex, is predominantly composed of follicles and spindle-shaped fibroblasts and smooth muscle cells.

      By the seventh month of gestation, primordial follicles have begun to develop in the fetal ovary. They consist of primary oocytes encapsulated by single layers of follicular cells. At birth, each ovary contains approximately 400,000 primordial follicles. After puberty and during each ovarian cycle, a number of follicles are hormonally stimulated to begin maturing. Usually, only a single follicle completes the process. Follicular cells proliferate and differentiate into the granulosa cell layer. The surrounding ovarian stroma differentiates into thecal cells (internal and external layers). Cell layers play a complex role in the development of the follicle; in hormonal variations during the menstrual cycle; and, ultimately, in ovulation.

      In the normal state, the hypothalamus secretes gonadotropin-releasing hormone (GnRH) in a pulsatile manner. The pituitary gland responds to GnRH by releasing luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in a similar cycle. In the follicular phase of the menstrual cycle, LH acts primarily on the theca cells of the ovary to increase the production of androgenic precursors. Concurrently, FSH acts on the granulosa cells to promote conversion of the androgens into estrogens, particularly estradiol, which assists in follicular development. During the follicular phase, increasing levels of estradiol lead to an LH surge. In a complex interaction, the LH surge, the elevated levels of estradiol, and an increase in the circulating progesterone level trigger the midcycle surge of FSH.

      In polycystic ovaries syndrome, the cycle is disturbed. Any of several possible precipitating factors may contribute to the imbalance. Evaluation of blood serum levels typically reveals elevated LH levels and normal or low FSH levels. Patients also have increased levels of free estrogen, primarily estrone and estradiol. Estrogens exert a complex feedback effect on the pituitary gland that results in the suppression of FSH secretion and the increased release of LH. Thus, the production and release of androgen precursors by ovarian theca cells is increased. The peripheral conversion of androgens to estrogens, primarily estrone, strengthens the feedback effect on the pituitary gland.

      The same androgens also inhibit the production of sex hormone-binding globulin in the liver, indirectly increasing levels of free estrogen in the bloodstream as well. Locally, elevated androgen levels in the ovary exert a direct inhibitory effect on follicular maturation. In conjunction with the diminished but steady presence of FSH, the follicles continue to develop without ever maturing. Thus, numerous follicles are present in the polycystic ovary and show varying phases of development and atresia.