Roles of sex steroid receptors and cell cycle regulation in pathogenesis of pelvic organ prolapseChung, Da Jung; Bai, Sang WookCurrent Opinion in Obstetrics and Gynecology: October 2006 - Volume 18 - Issue 5 - p 551–554 doi: 10.1097/01.gco.0000242959.63362.1e Urogynecology Buy Abstract Author InformationAuthors Article MetricsMetrics Purpose of review The cause of pelvic organ prolapse is multifactorial and many inciting, promoting and decompensating factors play a role in developing pelvic organ prolapse. Various clinical parameters have been studied quite extensively, but estrogen and collagen metabolism and cell proliferation and apoptosis have not been widely evaluated. This review focuses on assessing the roles of estrogen and its receptor, relationship with collagen metabolism and cell proliferation and cell apoptosis in development and progression of pelvic organ prolapse. Recent findings Differential expressions of sex steroid receptors in various suspensory ligaments of prolapsed uteri have been studied. How different subtypes of estrogen receptor play a role in inducing and aggravating pelvic organ prolapse has yet to be defined. The role of estrogen in collagen metabolism and cell proliferation related to development of pelvic organ prolapse is still under study. Studies on the proliferation of fibroblasts in ligaments of pelvic organ prolapse have yielded conflicting results. Summary There is still a need for additional research on precise roles of sex steroids, their receptors and cell cycle regulatory proteins and cell proliferation in pathogenesis of pelvic organ prolapse. Some of them could be the cause of pelvic organ prolapse and some of them the direct result of tissue trauma in pelvic organ prolapse. Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea Correspondence to Sang Wook Bai, MD, Associate Professor, Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Shinchon-dong 134 Seodaemun-gu, Seoul 120-752, Korea Tel: +82 2 2228 2230; fax: +82 2 313 8357; e-mail: firstname.lastname@example.org © 2006 Lippincott Williams & Wilkins, Inc.