Why clotting does not occur during Menstruation
The endometrium changes throughout the menstrual cycle in response to hormones. During the first part of the cycle, the hormone estrogen is made by the ovaries. Estrogen causes the lining to grow and thicken to prepare the uterus for pregnancy. In the middle of the cycle, an egg is released from one of the ovaries (ovulation). Following ovulation, levels of another hormone called progesterone begin to increase. Progesterone prepares the endometrium to receive and nourish a fertilized egg. If pregnancy does not occur, estrogen and progesterone levels decrease. The decrease in progesterone triggers menstruation (the shedding of the uterine lining). Once the lining is completely shed, a new menstrual cycle begins. (ACOG)

The uterine lining secretes an anti-clotting factor during periods to assist the blood flow. If the substance is not sufficient to overcome the natural clotting factor menstrual blood clots can form, a process known as hemostasis. Flow may slow down toward the end of a period, and blood can clump. When women are reclining for a time, such as while sleeping, the discharge will pool, and blood clots will be dislodged when upon standing. The blood darkens as it sits and sometimes looks brown or black.
During menstruation, the endometrial cells that line the uterus strip away and leave the body. As this happens, the body releases proteins that cause the blood in the uterus to coagulate. This coagulation prevents the blood vessels in the uterine lining from continuing to bleed. The blood that the body has already shed also contains these coagulation proteins. When the flow is most substantial, the coagulation proteins within the blood may start to clump together, resulting in menstrual clots. This generally occurs when menstrual blood pools in the uterus or vagina before leaving the body.
Menstrual blood clots can be caused by an imbalance in the clotting and anti-coagulating factors in blood or by hormonal changes. Fibroids and endometriosis contribute to excess buildup of the uterine lining, which breaks free as clots.

Under normal physiological circumstances menstruation is a highly regulated, complex process that is under strict hormonal control. During normal menstruation, progesterone withdrawal initiates menstruation. The cessation of menstrual bleeding is achieved by endometrial haemostasis via platelet aggregation, fibrin deposition and thrombus formation. Local endocrine, immunological and haemostatic factors interact at a molecular level to control endometrial haemostasis. Tissue factor and thrombin play a key role locally in the cessation of menstrual bleeding through instigation of the coagulation factors. On the other hand, fibrinolysis prevents clot organisation within the uterine cavity while plasminogen activator inhibitors (PAI) and thrombin-activatable fibrinolysis inhibitors control plasminogen activators and plasmin activity. Abnormalities of uterine bleeding can result from imbalance of the haemostatic factors.
Endometrial haemostasis is a vital process for the control and cessation of menstruation. It is influenced by systemic clotting systems that react to the hormone induced shedding of the endometrium, forming the haemostatic platelet plug and fibrin deposition. Local factors within the endometrium are paramount to ensure the process is highly regulated, with adequate blood vessel occlusion, breakdown of thrombus, and tissue regeneration.
Davies, J., &amp; Kadir, R. A. (2012). Endometrial haemostasis and menstruation. Reviews in Endocrine and Metabolic Disorders, 13(4), 289-299. doi:10.1007/s11154-012-9226-4


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