1Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, NC, USA.
Reprod Sci. 2013 Oct;20(10):1246-54. doi: 10.1177/1933719113483009. Epub 2013 Mar 27.
Preterm premature rupture of the membranes (PPROM) is an important etiology of preterm birth and source of significant neonatal morbidity. We propose that PPROM occurs in the setting of long-standing altered tissue remodeling, which creates a vulnerable environment for the fetal membranes and pregnancy. We tested the hypothesis that PPROM is the result of tissue remodeling in the fetal membranes, specifically the chorion, and this weakening of the chorion compromises the protection provided to the amnion. The purpose of this study was to quantify thickness and apoptosis in the choriodecidua of fetal membranes in patients with PPROM, preterm labor (PTL), preterm no labor (PTNL), and women with term labor (TERM). We conducted a retrospective evaluation of fetal membrane samples from 86 placentas. Immunohistochemistry was performed using a cytokeratin antibody, and mean chorion cellular thickness was compared between each clinical group. To evaluate chorion apoptosis, fetal membranes from patients with PPROM, PTL, and TERM were stained with the M30 antibody, and the degree of cellular apoptosis was determined. Statistical analysis was performed using analysis of variance with corrections for multiple comparisons. The chorion cellular layer was thinner in patients with PPROM compared to patients with PTNL and TERM (62, 140, and 169 µm, respectively, P < .0001), though not significantly different from PTL (95 µm, P > .05). The percentage of apoptotic cells within the chorion among the patients with PPROM was greater compared to PTL and TERM (24.2%, 13.1%, and 8.4%, respectively, P < .001). The chorion cellular layer is thinner and demonstrates increased apoptosis in PPROM compared to patients with PTL, PTNL, and TERM, suggesting differential remodeling between clinical phenotypes.
胎膜早破（PPROM）是早产的重要病因，也是新生儿发病率显著增加的原因。我们提出，PPROM 发生在长期组织重塑改变的情况下，这为胎膜和妊娠创造了一个脆弱的环境。我们检验了以下假设，即 PPROM 是胎膜组织重塑的结果，特别是绒毛膜，这种绒毛膜的弱化损害了对羊膜的保护。本研究的目的是定量分析 PPROM、早产临产（PTL）、未临产早产（PTNL）和足月临产（TERM）患者胎膜的绒-蜕膜厚度和细胞凋亡。我们对 86 例胎盘的胎膜样本进行了回顾性评估。采用细胞角蛋白抗体进行免疫组织化学染色，并比较了每个临床组的绒毛膜细胞平均厚度。为了评估绒毛膜细胞凋亡，用 M30 抗体对来自 PPROM、PTL 和 TERM 患者的胎膜进行染色，并确定细胞凋亡的程度。采用方差分析进行统计分析，并对多重比较进行校正。与 PTNL 和 TERM 患者相比，PPROM 患者的绒毛膜细胞层较薄（分别为 62、140 和 169 µm，P <.0001），但与 PTL 患者相比无显著差异（95 µm，P >.05）。与 PTL 和 TERM 患者相比，PPROM 患者绒毛膜中的凋亡细胞百分比更高（分别为 24.2%、13.1%和 8.4%，P <.001）。与 PTL、PTNL 和 TERM 患者相比，PPROM 患者的绒毛膜细胞层较薄，且凋亡增加，提示临床表型之间存在差异重塑。
