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Placenta accreta and placenta increta: an approach to pathogenesis based on the trophoblastic differentiation pathway
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Placenta accreta and placenta increta: an approach to pathogenesis based on the trophoblastic differentiation pathway

Stewart F. Cramer and Debra Heller
Pediatric and Developmental Pathology, Vol.19(4), pp.320-333
2016
DOI:
https://doi.org/10.7282/T3HQ41ZG

Abstract

Decidua Trophoblast Placenta accreta Placenta--Abnormalities
Objectives: Although classical teaching is that morbidly adherent placentas are due to absence of decidua, recent thinking suggests there may be a major role for abnormalities of trophoblast. Methods: This report presents representative cases of placenta accreta and increta collected over 30 years; analyzed with sonographic-pathologic correlation; with adjunctive trichrome , actin and keratin stains. Results: The sonographic finding of an abnormal retroplacental zone differed between accreta and increta. The site of morbid adherence was also different. Accreta was adherent to smooth muscle of large dilated vessels in the basal plate; with irregular destruction of vascular smooth muscle; endovascular trophoblast on keratin stain, and foci of intravascular villi. Increta was adherent to myometrium, while the fetal membranes could also be morbidly adherent. In increta, keratin stains showed nonvillous trophoblast (NVT) as the invading front, with villous trophoblast following behind. In accreta, there was a retroplacental spongy zone composed of dilated vessels and dilated glands. In increta there was a retroplacental zone of shriveled, inflamed, edematous myometrium, with foci of intravascular villi. In both accreta and increta, the sonographic finding of intraplacental blood lakes appeared to be due to supply from larger deeper vessels than seen in normal implantation, transformed by endovascular NVT. Conclusions: True accreta primarily reflects excessive action of endovascular NVT while increta also reflects excessive action of interstitial NVT. We speculate that there may be a role for protease inhibitor deficiency abnormalities.
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http://dx.doi.org/10.2350/15-05-1641-OA.1View
Pediatric and Developmental Pathology
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