Earl U, Bulmer J N, Briones A
Department of Pathology, University of Leeds, UK.
Placenta. 1987 May-Jun;8(3):273-82. doi: 10.1016/0143-4004(87)90051-8.
Trophoblast populations in four cases of placenta accreta were characterized using antibodies directed against cell membrane antigens, placental hormonal products and low-molecular-weight cytokeratins in standard immunoperoxidase techniques. The results obtained with antibody to syncytiotrophoblast membrane (rabbit anti-StMPM), antibody to an epithelial membrane antigen (HMFGI) and a cytokeratin marker (CAM 5.2) appeared identical to those reported for normal term placental tissues. Similarly the localization of human placental lactogen (hPL), human chorionic gonadotrophin (hCG) and pregnancy-specific beta 1-glycoprotein (SP1) within trophoblast populations in placenta accreta was identical to their reported distribution in term placenta. However, increased reactivity at the villous-maternal junction was demonstrated with NDOGI, an antibody raised against term syncytiotrophoblast membrane and directed against hyaluronic acid. NDOGI reactivity at this site is normally maximal during early placental development and is virtually absent in the third trimester. The results suggest that placenta accreta does not arise through excessive trophoblast invasiveness or proliferation and the absence of decidua is of more importance in the pathogenesis. Trophoblast may regulate its development at an unfavourable intramyometrial implantation site by the production of hyaluronic acid.
