Association between etiopathogenesis of morbidly adherent placenta and adenomyosis

Christopher A. Enakpene, Ozgul Muneyyirci‐Delale
In: Open Journal of Obstetrics and Gynecology · 2012 · vol. 02(03) , pp. 321–324 · doi:10.4236/ojog.2012.23067 · W2017303409
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This article proposes that pre-existing adenomyosis, caused by endometrial invasion into the myometrium, acts as a precursor to morbidly adherent placenta due to endometrial hyperplasia and bcl-2 oncogene overexpression.

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The paper discusses a proposed etiopathogenesis linking morbidly adherent placenta (placenta accreta/creta) to adenomyosis, arguing that rather than placenta accreta arising from trophoblast invasion into previously normal myometrium after uterine surgery, pre-existing adenomyosis may serve as a precursor. Drawing on the authors’ comparative framework of similar clinical/pathologic features and shared molecular components, they hypothesize that endometrial tissue invasion of the myometrium in the setting of disrupted decidua basalis leads to adenomyosis, and that endometrial over-expression of the bcl-2 oncogene inhibits apoptosis, removing a barrier that normally limits trophoblastic invasion to produce morbidly adherent placenta. They cite overlapping epidemiology (both increase with age and with prior uterine trauma such as surgery, childbirth, and endometritis) and the lack of identified genetic abnormalities (e.g., K-ras, p53, LOH) as additional support. The authors note that an ongoing study using uterine specimens from cesarean hysterectomies and pelvic MRI to evaluate retained placentas is near to conclusion, highlighting that the association remains largely hypothetical. This paper is centrally about adenomyosis—specifically proposing adenomyosis as a precursor mechanism for morbidly adherent placenta (placenta accreta).

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Abstract

been described in medical literature. Contrary to the believe that MAP is due to direct invasion of trophoblastic tissues into the adjacent normal myometrium due to prior uterine surgeries, this article describes how pre-existence of adenomyosis acts as a precursor for the development of placenta cretas. It elucidates how prior uterine traumas such as surgeries, repeated childbirths and endometritis cause endometrial tissues to invade the myometrium as a result of disruption of decidua basalis. The invaded endometrial tissues cause hyperplasia and hypertrophy of surrounding myometrium to form the clinical entity called adenomyosis. The over-expression of bcl-2 oncogene in the endometrium causes inhibition of apoptosis of endometrial cells removing the barrier of trophoblastic tissues to invade the myometrium to form MAP. This hypothesis is based on the similarity of their clinical perspectives, similar pathological description of the two disease entities and their common molecular components. Both diseases increase with age; more in women older than 35 years and also in those with history of previous endometrial traumas such as surgeries, childbirth and endometritis. Both diseases also share common pathological factors and molecular components due to absence of deciduas basalis and over-expression of bcl-2 oncoprotein gene, inhibition of cell apoptosis and failure to find genetic abnormalities such as mutations of K-ras, P53 or LOH. An on-going study looking at uterine specimens from cesarean hysterectomies and pelvic MRI evaluation of patients with retained placentas to prove that preexisting adenomyosis may be a precursor to the development of morbidly adherent placenta is near to conclusion.
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Association between etiopathogenesis of morbidly adherent placenta and adenomyosis () Christopher A. Enakpene, Ozgul Muneyyirci-Delale Department of Obstetrics and Gynecology, SUNY Downstate Medical Center, New York, USA. DOI: 10.4236/ojog.2012.23067 PDF HTML 4,812 Downloads 7,483 Views Citations Department of Obstetrics and Gynecology, SUNY Downstate Medical Center, New York, USA. DOI: 10.4236/ojog.2012.23067 PDF HTML 4,812 Downloads 7,483 Views Citations The association between etio-pathogenesis of morbidly adherent placenta (MAP) or placenta cretas and adenomyosis has never been described in medical literature. Contrary to the believe that MAP is due to direct invasion of trophoblastic tissues into the adjacent normal myometrium due to prior uterine surgeries, this article describes how pre-existence of adenomyosis acts as a precursor for the development of placenta cretas. It elucidates how prior uterine traumas such as surgeries, repeated childbirths and endometritis cause endometrial tissues to invade the myometrium as a result of disruption of decidua basalis. The invaded endometrial tissues cause hyper-plasia and hypertrophy of surrounding myometrium to form the clinical entity called adenomyosis. The over-expression of bcl-2 oncogene in the endometrium causes inhibition of apoptosis of endometrial cells removing the barrier of trophoblastic tissues to invade the myometrium to form MAP. This hypothesis is based on the similarity of their clinical perspectives, similar pathological description of the two disease entities and their common molecular components. Both diseases increase with age; more in women older than 35 years and also in those with history of previous endometrial traumas such as surgeries, childbirth and endometritis. Both diseases also share common pathological factors and molecular components due to absence of deciduas basalis and over-expression of bcl-2 oncoprotein gene, inhibition of cell apoptosis and failure to find genetic abnormalities such as mutations of K-ras, P53 or LOH. An ongoing study looking at uterine specimens from cesarean hysterectomies and pelvic MRI evaluation of patients with retained placentas to prove that pre-existing adenomyosis may be a precursor to the development of morbidly adherent placenta is near to conclusion. Keywords Morbidly Adherent Placenta (Placenta Accretes); Adenomyosis, Association; Epidemiology; Etio-Pathogenesis and Clinical Perspective Share and Cite: Enakpene, C. and Muneyyirci-Delale, O. (2012) Association between etiopathogenesis of morbidly adherent placenta and adenomyosis. Open Journal of Obstetrics and Gynecology, 2, 321-324. doi: 10.4236/ojog.2012.23067. Conflicts of Interest The authors declare no conflicts of interest. | [1] | Rokitansky, K. 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Placenta, 23, 210-214. doi,10.1053/plac.2001.0764 | | [14] | ACOG committee on obstetric practice (2002) ACOG committee opinion number 266 January 2002, placenta accrete. Obstetrics & Gynecology, 99, 169-170. | | [15] | Morken, N.H. and Henriksen, H. (2001) Placenta percreta two cases and review of the literature. European Journal of Obstetrics & Gynecology and Reproductive Biology, 100, 112-115. doi,10.1016/S0301-2115(01)00422-5 | | [16] | Benirschke, K. and Kaufmann, P. (2000) Pathology of the human placenta. 4th Edition, Springer, New York. | | [17] | Thompson, J.R. and Davion, R.J. (1986) Adenomyosis of the uterus, an enigma. Journal of the American Medical Association, 78, 305-307. | | [18] | Panganamamula, U.R., Harmanli, O.H., Isik-Akbay, E.F., et al. (2004) Is prior uterine surgery a risk factor for adenomyosis? Obstetrics & Gynecology, 104, 1034-1038. doi,10.1097/01.AOG.0000143264.59822.73 | | [19] | Matsumoto, Y., Iwasaka, T., Yamasaki, F. and Sugimori, H. (1999) Apoptosis and ki-67 expression in adenomyotic lesions and the corresponding eutopic endometriosis. Obstetrics & Gynecology, 94, 71-77. doi,10.1016/S0029-7844(99)00279-3 | | [20] | Miller, D.A., Chollet, J.A. and Goodwin, T.M. (1997) Clinical risk factors for placenta previa-placenta accreta. American Journal of Obstetrics & Gynecology, 177, 210-214. doi,10.1016/S0002-9378(97)70463-0 | | [21] | Tantbirojn, P., Crum, C.P. and Parast, M.M. (2008) Pathophysiology of placenta creta, the role of decidua and extravilloustrophoblast. Placenta, 29, 639-645. doi,10.1016/j.placenta.2008.04.008 | | [22] | Kong, T.Y. and Abdul Rahman, H. (1997) Bcl-2 expression delays postpartum involution of pregnancy-induced vascular changes in the human placenta bed. International Journal of Gynecological Pathology, 16, 138-142. doi,10.1097/00004347-199704000-00009 | | [23] | Ueki, K., Kumagai, K., et al. (2004) Expression of apoptosis related protein in adenomyotic uteri treated with danazol and GnRh agonists. International Journal of Gynecological Pathology, 23, 248-258. doi,10.1097/01.pgp.0000130109.80359.57 | | [24] | Rabinovici, J. and Stewart, E.A. (2006) New interventional techniques for adenomyosis. Best Practice and Research Clinical Obstetrics and Gynecology, 20, 617-636. doi,10.1016/j.bpobgyn.2006.02.002 | | [25] | Muneyyirci-Delale, O., Chandrareddy, A., Battala, N., et al. (2008) Norethindrone acetate in the medical management of adenomyosis. Obstetrics and Gynecology, 111, 29S. | Copyright © 2026 by authors and Scientific Research Publishing Inc. This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.

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