Abstract
Morbid adherence remains a puzzling disease. This paper suggests that normal and morbidly adherent placentation may best be viewed in terms of trophoblastic stem cells, and the mutually exclusive branches of the trophoblastic differentiation pathway - villous trophoblast, interstitial and endovascular nonvillous trophoblast (NVT) at the implantation site, and a positional variation in the chorion. Based on hysterectomies for morbid adherence seen over 30 years at a community hospital; analyzed with routine keratin stains, with actin and trichrome stains as indicated, and attempts at sonographic-pathologic correlation; we present selected observations. In true accreta, the site of morbid adherence was to dilated basal plate vessels, infiltrated by endovascular NVT; with scant interstitial NVT, and normal myometrium. It appeared that excess blood flow into the placenta was due to excessively deep keratin-positive endovascular NVT that spread - independently of interstitial NVT - in an angiocentric fashion, in both accreta and increta. Retroplacental abnormalities were due to myometrial destruction by interstitial NVT in increta, sometimes requiring actin stains for detection; and to an admixture of markedly dilated endometrial glands and vessels in true accreta, best appreciated with keratin stains. Variations of depth and extent in increta may be due to variations in myometrial tone, and in the protease-antiprotease balance. Morbidly adherent fetal membranes are described. The role of C-section scars in incretas is addressed.