[Morphological basis for endometrial bleeding].

Endometrial morphology is discussed. The endometrium consists of a basal and a functional part. The functional part comprises compact and spongy tissues. The celis of the uteral stroma differentiate in the secretion phase of the menstrual cycle into predecidual cells and granules. Spiral arteries extend rapidly from the basal part of the endometrium and reach the upper surface of the endometrium by the end of the proliferation phase. Enzymes proteolytic enzymes and fibrinolytic activators play important roles in the development of the endometrium. Estrogens induce the growth and proliferation of endometrial cells. Progesterone causes the growth of spiral arteries and cell differentiation. Relacsin triggers the dissolution of the reticular network in preparation for menstruation. After no fertilized ovum is implanted in the uterus the blood supply from the spiral arteries is greater than is actually needed and there is a change in the hormonal balance of the endometrium causing menstruation. The compact and spongy tissues dissolve due to the loss of fluid in the endometrium. Some doctors believe that some of these tissues are retained as a basis for the building up of the next endometrium. 4-48 hours before menstruation a decrease in the progesterone level in the endometrium causes vasodilation of the spiral arteries. Menstrual bleeding stops as the ends of the arteries regenerate the surface of the endometrium reepithelializes and new capillaries grow. Anovulatory cycles are characterized by incompletely developed spiral arteries. Breakthrough bleeding is caused by either too high or too low estrogen levels depending on the condition of the endometrium. Juvenile bleeding is caused by increased estrogen concentration in the bloodstream. Preclimacteric bleeding can be caused by cystic glandular hyperplasia or secretory hypertrophy.