摘要
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.
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.
