The clinical relevance of menstruation
Despite our increasing understanding of menstrual physiology, the mechanisms by which the denuded surface of the endometrium repairs without scarring or loss of function repeatedly throughout a woman's reproductive life remain unknown.
The unique physiological inflammatory response, hypoxic insult, and tissue repair and regeneration are only superficially understood. Investigation of the control, regulation, and coordination of menstruation will lead to improved understanding of endometrial physiology and ultimately improve the clinical management of women with menstrual disorders. Furthermore, knowledge of the processes involved in efficient repair may be applied to other tissue sites where persistent inflammation and scarring lead to severe pathology.
Figure 40.4 Impact of progesterone withdrawal on endometrial inflammation. Progesterone withdrawal in the late secretory phase drives local prostaglandin production. In addition, the withdrawal of progesterone inhibits breakdown of active prostaglandins resulting in a cascade of inflammation at menses. An increase in prostaglandins results in leucocyte influx, vasoconstriction of spiral arterioles, and resultant hypoxia. The process culminates in shedding of the functional layer of endometrium. COX-2, cyclooxygenase-2; IL-8, interleukin-8; MMP matrix metalloproteinase; PGE, prostaglandin E; PGEM, prostaglandin E metabolites; PGF2, prostaglandin F2 alpha; PGFM, prostaglandin F2 alpha metabolites; PGH2, prostaglandin H2; PLA2, phospholipase A2; VGEF, vascular endothelial growth factor.
Figure 40.5 Intrinsic and extrinsic coagulation pathways lead to production of fibrin clot and haemostasis. Activation of fibrinolysis is necessary to break down the fibrin clot. Perturbation of these pathways may lead to AUB-C.
Reproduced from JA Maybin and HO Critchley, Menstrual physiology: implications for endometrial pathology and beyond, Hum Reprod Update 2015;21:748-761 (https:// creativecommons.org/licenses/).