Allen Anna, Jones Carolyn J P, Jauniaux Eric, Hussein Ahmed, Aplin John D
Maternal and Fetal Health Research Centre, Division of Developmental Biology & Medicine, School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Central Manchester University Hospital NHS Foundation Trust, Manchester Academic Health Sciences Centre, St Mary's Hospital, Oxford Road, Manchester, M13 9WL, UK.
Institute for Women's Health, Faculty of Population Health Sciences, University College London (UCL), London, UK.
Placenta. 2025 Aug;168:135-143. doi: 10.1016/j.placenta.2025.06.014. Epub 2025 Jun 24.
During normal placentation, extravillous trophoblast (EVT) colonises and, in synergy with maternal leukocytes, transforms the walls of uterine spiral arteries in the decidua and inner myometrium. In placenta accreta spectrum (PAS), migration of extravillous trophoblasts (EVT) is abnormally deep, reaching larger upstream arteries in myometrium. As little is known about their interactions in accreta areas, scar tissue and deeper arteries were examined for colonisation and remodelling by trophoblast and maternal inflammatory cells.
Samples (n = 79) were fresh hysterectomy specimens taken immediately after surgery in 11 patients presenting with placenta previa accreta at birth, at term or near term. They were obtained from accreta areas, non-accreta areas and, in cases of associated dehiscence of the lower uterine segment, from the adjacent shell (uterine boundary membrane). Samples were stained using antibodies to EVT (cytokeratin) or inflammatory cells (CD45). Arterial profiles positioned within 5 mm of villous placenta at scar sites were included in the analysis (54 lumina).
EVT colonisation of scar tissue was much more extensive than in adjacent myometrium (p < 0.001). Large arteries were remodelled (20.3 %), partially remodelled (22.2 %) or unremodelled (29.6 %). Unremodelled arteries were present in 10/11 specimens while 6/11 had one or more fully remodelled. Leucocytes/inflammatory cells were frequently associated with arteries undergoing remodelling. EVT also accumulated beneath the serosa but were not found to cross it.
Some remodelling of deep arteries occurs in most samples from accreta areas, but persistence of unremodelled arteries in distal segments with abnormally high velocity intraplacental blood flow is probably the main mechanism leading to lacuna formation.
在正常胎盘形成过程中，绒毛外滋养层细胞（EVT）定植，并与母体白细胞协同作用，改变蜕膜和子宫肌层内层子宫螺旋动脉的管壁。在胎盘植入谱系（PAS）中，绒毛外滋养层细胞（EVT）的迁移异常深入，到达子宫肌层中更大的上游动脉。由于对其在植入区域的相互作用了解甚少，因此研究了瘢痕组织和更深层动脉中滋养层细胞和母体炎症细胞的定植及重塑情况。
样本（n = 79）为11例出生时、足月或接近足月时患有前置胎盘植入的患者术后立即获取的新鲜子宫切除标本。它们取自植入区域、非植入区域，对于伴有子宫下段裂开的病例，取自相邻的蜕膜（子宫边界膜）。样本用针对EVT（细胞角蛋白）或炎症细胞（CD45）的抗体进行染色。分析瘢痕部位距绒毛胎盘5毫米内的动脉轮廓（54个管腔）。
瘢痕组织中的EVT定植比相邻子宫肌层广泛得多（p < 0.001）。大动脉发生重塑（20.3%）、部分重塑（22.2%）或未重塑（29.6%）。11个标本中有10个存在未重塑动脉，而11个标本中有6个有一条或多条完全重塑的动脉。白细胞/炎症细胞常与正在重塑的动脉相关。EVT也在浆膜下积聚，但未发现其穿过浆膜。
在大多数来自植入区域的样本中，深层动脉会发生一些重塑，但胎盘内血流速度异常高的远端节段中未重塑动脉的持续存在可能是导致腔隙形成的主要机制。
