The corpus luteum, which is the remnant of the antral cavity after ovulation, undergoes a series of changes. Initially, blood fills the cavity, resulting in a corpus hemorrhagicum. Over time, macrophages remove the red blood cells and debris, and fibroblasts fill in the cavity with a hyaline-like extracellular matrix. The granulosa cells, now called granulosa lutein cells, enlarge and accumulate cholesterol esters. These enlarged cells collapse into the old cavity. The theca, along with blood vessels, mast cells, macrophages, leukocytes, and other connective tissue cells, infiltrate the granulosa layer at various sites.

The lifespan of the human corpus luteum is around 14 days, with slight variations. However, if the LH-like hormone human chorionic gonadotropin (hCG) is produced by an implanting embryo, the corpus luteum of pregnancy can remain viable for approximately 9 months. The exact mechanism behind the regression of the corpus luteum during menstruation within 14 days is not completely understood. It is believed that the corpus luteum becomes less responsive to basal levels of LH, requiring hCG binding to the LH receptor for its continued function. Regression involves the release of prostaglandin PGF2α from both granulosa lutein cells and the uterus in response to declining levels of progesterone during the second week of the luteal phase. Paracrine factors from immune and vascular cells, such as endothelin and monocyte chemotactic protein-1, likely contribute to the demise and removal of granulosa lutein cells. Ultimately, the corpus luteum transforms into the corpus albicans, a scar-like structure that gradually gets absorbed into the ovary's medulla.

The LH surge triggers two parallel processes: ovulation and luteinization. If ovulation occurs normally, there is no gamete present in the corpus luteum. Before the LH surge, the granulosa cells have low capacity to convert cholesterol into steroid hormones. However, the LH surge induces the expression of CYP11A1, 3β-HSD, and StAR protein, enabling the granulosa lutein cells to convert cholesterol into progesterone. As CYP17 expression remains low, progesterone accumulates and exits the granulosa lutein cells, entering the vasculature. This production of progesterone by the corpus luteum is essential for its proper functioning.
•Fig. 44.22 Steroidogenicpathwaysinthecorpusluteum(ModifiedfromWhiteBA,PorterfieldSP.Endocrine Physiology. 4thed.Philadelphia:Mosby;2013.)LH LH receptor LDLR and HDLR-mediated uptake Acetate Cholesterol Stimulation of steroidogenesis LH LH receptor LDLR and HDLR-mediated uptake Cholesterol Pregnenolone Stimulation of steroidogenesis StAR protein CYP11A1 Androstenedione Androstenedione Progesterone Estradiol-17˜3˜-HSD
The Corpus Luteum
After ovulation the remnant of the antral cavity fills with blood from damaged blood vessels in the vicinity of the stigma. This gives rise to a corpus hemorrhagicum. Within a few days, red blood cells and debris are removed by macrophages, and fibroblasts fill in the antral cavity with a hyaline-like extracellular matrix. In the mature corpus luteum the granulosa cells, now called granulosa lutein cells, enlarge and become filled with lipid (cholesterol esters). The enlarged granulosa lutein cells collapse into and partially fill in the old antral cavity. The theca along with blood vessels, mast cells, macrophages, leukocytes, and other resident connective tissue cells infiltrate the granulosa layer at multiple sites.
The human corpus luteum is programmed to live for 14 days, plus or minus 2 days (corpus luteum of menstruation), unless “rescued” by the LH-like hormone human chorionic gonadotropin (hCG), which originates from an implanting embryo. If rescued, the corpus luteum of pregnancy will remain viable during the pregnancy (usually ≈ 9 months). The mechanism by which the corpus luteum of menstruation regresses in 14 days is not fully understood. The corpus luteum appears to become progressively less sensitive to basal levels of LH, so that hCG binding to the LH receptor is needed for continued health and function of the corpus luteum. Regression appears to involve release of the prostaglandin PGF2α from both granulosa lutein cells and the uterus in response to declining levels of progesterone during the second week of the luteal phase. Several paracrine factors (endothelin, monocyte chemotactic protein-1) from immune and vascular cells are likely to play a role in the demise and removal of granulosa lutein cells. The corpus luteum is ultimately turned into a scarlike body called the corpus albicans, which sinks into the medulla of the ovary and is slowly absorbed.
The Gamete
The LH surge induces two parallel events, ovulation and luteinization. If ovulation occurs normally, the corpus luteum is devoid of a gamete.
Before the LH surge, the granulosa cells have very low capacity to convert cholesterol into a steroid hormone. The LH surge induces the onset of expression of CYP11A1, 3β-HSD and StAR protein, allowing granulosa lutein cells to convert cholesterol into progesterone. Because CYP17 expression is extremely low, progesterone accumulates and moves out of the granulosa lutein cells and enters the vasculature. Progesterone production by the corpus luteum (see