C. A. Enakpene, O. Muneyyirci-Delale / Open Journal of Obstetrics and Gynecology 2 (2012) 321-324 323
vaginal sonogram and MRI features of widening of the
junctional zone of 12 mm or greater increase the risk of
future de velopment of placenta accretas in pregnancy. The
presence of irregular endometrium, endometrial defects,
hypervascularization, strawberry pattern or cystic hem-
orrhagic lesions which are hysteroscopic characteristics of
possible adenomyosis are also proposed in this hypothesis
as risk factors for the development of placenta cretas.
Adenomyosis and placenta cretas share common other
risk factors such as multiparity, endometritis and previous
uterine surgeries such as dilatation and curettage, myo-
mectomy and cesarean section. Any condition that leads
to disruption of the endometrium can alter decidualization
and placentation during pregnancy which can lead to
invagination of placenta tissues.
4.2. Pathological and Molecular Perspectives
The apparent similarity between the etio-pathogenesis of
morbidly adherent placenta and adenomyosis is based on
the common pathological factors such as absence of de-
ciduas basalis and over expression of bcl -2 in both disease
entities. There is a possibility that the invading endo-
metrial tissues leaves the decidua basalis devoid of nor-
mal endometrium covering leading to invasion of corre-
sponding myometrium by immortal endometrial tissues
due to over-expression of the bcl-2 oncoprotein gene, an
inhibitor of cell apoptosis. The pathogenesis of placenta
cretas is multi-dimensional involving increased but in-
complete trophoblast invasion in a background of absent
decidua. Placenta cretas result from prim ary deficie ncy of
decidua, abnormal maternal vascular remodeling and
excessive trophoblastic invasion of the myometrium [21].
4.3. The Role of Bcl-2 Oncoprotein Gene in the
Etiology of Morbidly Adherent Placenta
and Adenomyosis
Morbidly adherent placenta is associated wit h retention of
a piece or the whole placenta tissue resulting in uterine
sub-involution and delayed secondary postpartum hem-
orrhage. Increase bcl-2 oncoprotein is associated with
inhibition of apoptosis and prolonged cell survival. It is
seen mostly in sub-involuted placenta bed as compared
with involuted bed. The expression of bcl-2 gene is asso-
ciated with sub-involution of the utero-placental arteries
which inhibit complete resolution of pregnancy induced
changes [22]. There is also a decrease cellular apoptosis
in adenomyosis and ectopic endometrium due to high
bcl-2 gene e xpression in ectopi c endometrium tissues. In a
study by Ueki et al, occurrence of adenomyosis was cor-
related to bcl-2 expression regulated by estrogen and
estrogen receptor rather than genetic mutation [23]. Con-
stant expression of bcl-2 with estrogen receptor (ER) and
hyper-estrogenic metabolic states promote invagination
and spreading of a denomyosis into the myomet rium. This
hypothesis is also an chored on the failure to find genetic
abnormalities such as mutations of K-ras, P53 or LOH
[23].
5. CONCLUSION
Any patient with retained placental tissues following
delivery should be evaluated for prior history of sym-
ptoms, ra di ol o gi c or hyster oscopic feat ures of adenomy o-
sis. Till date, transvaginal sonogram and magnetic reso-
nance im aging are the m ainstay of pre-operative diagnosis
of adenomyosis with sensitivity of 68% and 70% and
specificity of 65% and 86% respectively [24]. When
available, they should be utilized without hesitation.
Other diagnostic approaches are pre-operative biopsy,
hysterosalpingography and hysteroscopy. The definitive
treatment and diagnosis of adenomyosis is hysterectomy
and pathological examination of extirpated uterus. How-
ever, conservative management such as norethindrone
acetate, levonorgestrol impregnated IUD (mirena), est-
rogen, danazol, GnRH agonists, resection of lesions, hys-
teroscopic endometrial ablation, uterine artery emboli-
zation (UAE) and magnetic resonance guided focused
ultrasound surgery (MRgFUS) can be employed [24,25].
Our hypothesis suggesting an association between etiopa-
thogenesis of placenta cretas and pre-existing adeno-
myosis may be factual rather than a mere proposition.
Fertility preserving management of adenomyosis may
play a great role in reducing the incidence of placenta
cretas. More research study to explore temporal associa-
tion between the etiology of MAP and adenomyosis is
under way. The result of our on-going study on this topic
will finalize whether this association is true or not.
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