The menstrual cycle is on average 28 days in length. It begins with menses (day 1–7) during the follicular phase (day 1–14) and followed by ovulation (day 14) and ending with the luteal phase (day 14–28). Unlike the follicular phase which can vary in length among individuals, the luteal phase is typically fixed at approximately 14 days (i.e. days 14–28) and is characterized by changes to hormone levels, such as an increase in progesterone and estrogen levels, decrease in gonadotropins such as follicle-stimulating hormone (FSH) and luteinizing hormone (LH), changes to the endometrial lining to promote implantation of the fertilized egg, and development of the corpus luteum. In the absence of fertilization by sperm, the corpus luteum atrophies leading to a decrease in progesterone and estrogen, an increase in FSH and LH, and shedding of the endometrial lining (menses) to begin the menstrual cycle again. Hormonal events
After ovulation and release of the oocyte, the anterior pituitary hormones–follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are released and cause the remaining parts of the dominant follicle to transform into the corpus luteum. It continues to grow during the luteal phase after ovulation and produces significant amounts of hormones, particularly progesterone, and, to a lesser extent, estrogen and inhibin. Progesterone plays a vital role in making the endometrium receptive to implantation of the embryo and supportive of early pregnancy. High levels of progesterone inhibit the follicular growth.
Overall, the purpose of the treatment improves self-identification of an individual, reduces the increased risk of cancer and reduces the possibility of infertility, if not already present. PMDS patients have a possibility of infertility in the future if not promptly operated on. When the affected males are adults, those who are not aware of the condition may find the presence of blood in their semen (hematospermia). The Müllerian structures and cryptorchidism can also  develop into cancer if ignored, or if there are pieces of Müllerian structures left from past surgery. If PMDS is found during adulthood, or if Müllerian structures had to be left behind due to risks in surgery, biopsies of the remaining Müllerian structures can be performed. Upon pathohistological observation, the endometrial tissues appear atrophied, and the fallopian tubes have begun to congest showing signs of fibrosis. Epidemiology
PMDS is a relatively rare congenital disease. From current data, approximately 45% of the known cases are caused by mutations in the AMH gene, being a mutation on chromosome 19 (Type I PMDS). Approximately, 40% are AMHR2 mutations, on the AMH receptor type 2 gene, which is on chromosome 12 (Type 2 PMDS). The remaining unknown 15% are referred to as idiopathic PMDS. Case studies
Especially before the 21st century, these conditions were hard to diagnose due to the lack of modern imaging capabilities. For this reason, the older population, or those in poorer countries found out later.