This review examines evidence supporting the concept that menstruation occurs as a result of an inflammatory process. In the endometrium, leukocyte numbers rise in the late secretory phase following the fall in serum progesterone concentrations. It is postulated that products released following activation of these leukocytes are critically important for menstruation. Mast cells, eosinophils, neutrophils and macrophages in particular are involved. Endometrial granular lymphocytes may also play a role, although their increase in numbers is somewhat earlier during the menstrual cycle than that of the others, suggesting perhaps a primary role in embryo implantation. Leukocyte products include a range of proteases, chemokines and cytokines which in concert result in focal production and activation of matrix metalloproteinases by endometrial cells and the subsequent breakdown of tissue that characterizes menstruation. Regulation of leukocyte entry, proliferation, differentiation and activation within the endometrium is not yet well understood, although both chemokines and cytokines produced locally by endometrial cells are clearly implicated. The role of progesterone in regulating these events is still not understood although the lack of progesterone receptors on endometrial leukocytes suggests indirect actions.