title: Molecular and cellular causes of abnormal uterine bleeding of endometrial origin.
abstract: Women today may reasonably anticipate in the order of some 400 menstrual cycles over their reproductive lifespan. The endometrium is thus subject to repeat cycles of shedding and repair and notably healing of the endometrium post menses is "scarless". The local molecular and cellular mechanisms involved in post menstrual resolution of the inflammatory events associated with menstruation and endometrial repair remain to be fully determined. Menstrual complaints are common. It is highly likely that unrestrained local inflammatory events and/ or deficient repair processes within the endometrium contribute to the women's experience of heavy menstrual bleeding (HMB). The management of women with HMB may need to utilize therapeutic approaches that optimize endometrial repair processes, post menses. These approaches may be necessary in addition to current therapies that hitherto have focused on limiting the local inflammation associated with menstruation. Research endeavors thus need to focus upon the molecular and cellular causes of problematic uterine bleeding. Herein the events associated with pre-menstrual progesterone withdrawal, limitation of blood loss, the expression of vasoactive mediators and factors that may modulate vascular morphology are described. Such lines of enquiry and knowledge will be essential if novel targets for treatment of menstrual bleeding complaints, such as HMB, are to be identified.
authors: MRC Centre for Reproductive Health, The University of Edinburgh, The Queen's Medical Research Institute, Edinburgh, Midlothian, United Kingdom. hilary.critchley@ed.ac.uk
authors: Hilary O D
authors: HO
authors: Critchley
authors: Jacqueline A
authors: JA
authors: Maybin
mesh_terms: D004717:Endometrium / Q000098:blood supply / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008598:Menstruation; D008599:Menstruation Disturbances / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D018570:Risk Assessment; D012307:Risk Factors; D014592:Uterine Hemorrhage / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy