School of Nutrition and Translational Research in Metabolism (NUTRIM), Department of Pharmacology and Toxicology, Maastricht University Medical Center+, Maastricht, the Netherlands.
Department of Reproductive Medicine, University Hospital Ghent, Ghent, Belgium.
Histol Histopathol. 2020 Aug;35(8):849-862. doi: 10.14670/HH-18-205. Epub 2020 Jan 27.
Chorioamnionitis and preeclampsia account for the majority of preterm births worldwide. Thus far, adequate methods for early detection or prevention of these diseases are lacking. In preeclampsia, accelerated villous maturation is believed to compensate placental insufficiency. However, little is known about the effects of placental inflammation in chorioamnionitis on villous maturation. Therefore, we established a set of morphological parameters to evaluate histological villous maturity in pregnancies complicated by chorioamnionitis and preeclampsia. Preterm placentas complicated by chorioamnionitis or preeclampsia were compared to idiopathic preterm placentas and term controls. Histological villous maturation was analyzed by means of 17 histological markers. Fourteen of these markers provided information on absolute and relative numbers of the terminal villi (TV), the extent of their vascularization (using CD31-stained sections) and their exchange capacities. In addition, the numbers of syncytial bridges, syncytial apoptotic knots and shed syncytiotrophoblasts were counted. Accelerated villous maturation in preeclampsia was demonstrated by means of histological villous remodeling and confirmed by 11 relevant markers. Chorioamnionitis, however, only showed increased area of fetal capillaries. In preeclampsia, placentas may transition from growth to maturation earlier than placentas in normal pregnancies, whereas in chorioamnionitis placental changes are more acute and therefore less elaborated at a structural level. Regression analysis suggests the number of all villi and the number of terminal villi as a percentage of all villi as parameters to evaluate histological villous maturity in preeclamptic placentas and to assist diagnosis. However, we would recommend to analyze all 11 relevant parameters to judge placental maturity in detail.
绒毛膜羊膜炎和子痫前期是导致全球大多数早产的主要原因。到目前为止,还缺乏这些疾病的早期检测或预防的充分方法。在子痫前期中,加速的绒毛成熟被认为是补偿胎盘功能不全的一种方式。然而,对于绒毛膜羊膜炎中的胎盘炎症对绒毛成熟的影响知之甚少。因此,我们建立了一套形态学参数来评估合并绒毛膜羊膜炎和子痫前期的妊娠的组织学绒毛成熟度。将合并绒毛膜羊膜炎或子痫前期的早产胎盘与特发性早产胎盘和足月对照组进行比较。通过 17 种组织学标志物分析组织学绒毛成熟度。其中 14 种标志物提供了关于终末绒毛(TV)的绝对和相对数量、其血管化程度(使用 CD31 染色切片)及其交换能力的信息。此外,还计数了合体细胞桥、合体细胞凋亡结和脱落的合体滋养层细胞的数量。通过组织学绒毛重塑证明子痫前期存在绒毛成熟加速,并通过 11 个相关标志物得到证实。然而,绒毛膜羊膜炎仅显示胎儿毛细血管面积增加。在子痫前期中,胎盘可能比正常妊娠中的胎盘更早地从生长过渡到成熟,而在绒毛膜羊膜炎中,胎盘变化更为急性,因此在结构水平上的发育程度较低。回归分析表明,所有绒毛和终末绒毛的数量以及终末绒毛占所有绒毛的百分比,是评估子痫前期胎盘组织学绒毛成熟度并协助诊断的参数。然而,我们建议分析所有 11 个相关参数以详细判断胎盘成熟度。