The primary oocytes within the primordial follicles begin the first meiotic division in the embryo, but the process is arrested at the diplotene stage of meiotic prophase (see the section on meiosis in Chapter 3). The first meiotic prophase is not completed until just before ovulation. Therefore, primary oocytes remain arrested in the first meiotic prophase for 12 to 50 years. This long period of meiotic arrest exposes the primary oocyte to adverse environmental inﬂuences and may contribute to errors in meiotic division such as nondisjunction. Such errors result in anomalies such as trisomy of chromosome 21 (Down syndrome).
As the first meiotic division (reduction division) is completed in the mature follicle (Fig. 23.9), each daughter cell of the primary oocyte receives an equal share of chromatin, but one daughter cell receives most of the cytoplasm and becomes the secondary oocyte. It measures 150 m in diameter. The other daughter cell receives a minimal amount of cytoplasm and becomes the frst polar body.
The secondary oocyte is arrested at metaphase in the second meiotic division just before ovulation.
As soon as the first meiotic division is completed, the secondary oocyte begins the second meiotic division. As the secondary oocyte surrounded by the cells of the corona radiata leaves the follicle at ovulation, the second meiotic division (equatorial division) is in progress. This division is arrested at metaphase and completed only if the secondary oocyte is penetrated by a spermatozoon. If fertilization occurs, the secondary oocyte completes the second meiotic division and forms a mature ovum with the maternal pronucleus containing a set of 23 chromosomes. The other cell produced at this division is a second polar body. In humans, the first polar body persists for more than 20 hours after ovulation and does not divide; therefore, the fertilized egg can be recognized by the presence of two polar bodies (diploid first polar body and haploid second polar body). In some mammals, the first polar body can divide, so the final outcome of meiosis consists of one oocyte and three haploid polar bodies (see Fig. 23.9). The polar bodies, which are not capable of further development, undergo apoptosis.
Polycystic ovarian disease is characterized by bilaterally enlarged ovaries with numerous follicular cysts. When asso-ciated with oligomenorrhea, scanty menstruation, the clinical term Stein-Leventhal syndrome is used. The individual is infertile because of lack of ovulation. Morphologically, the ovaries resemble a small, white balloon filled with tightly packed marbles. Affected ovaries, often called oyster ovaries, have a smooth, pearl-white surface but do not show surface scarring because no ovulations have occurred. The condition is attributable to the large number of fluid-filled fol-licular cysts and atrophic secondary follicles that lie beneath an unusually thick tunica albuginea. The pathogenesis is not clear but seems to be related to a defect in the regulation of androgen biosynthesis that causes production of excessive amounts of androgens that are converted to estrogens. The selection process of the follicles that undergo maturation also seems to be disturbed. The individual has an anovula-tory cycle characterized by only estrogenic stimulation of the endometrium because of the inhibition of progesterone pro-duction. Progesterone inhibition is caused by failure of the Graafian follicle to transform into a progesterone-producing corpus luteum. The treatment of choice is hormonal to stabi-lize and reconstruct the estrogen-to-progesterone ratio, but in some cases, surgical intervention is necessary. A wedge-shaped incision is made into the ovary to expose the cortex, thus allowing the ova, after hormonal treatment, to leave the ovary without physical restrictions created by the preexisting thickened tunica albuginea (Fig. F23.1.1).