The chorion layer of fetal membranes is prematurely destroyed in women with preterm premature rupture of the membranes.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Canzoneri, BJ; Feng, L; Grotegut, CA; Bentley, RC; Heine, RP; Murtha, AP

Published Date

  • October 2013

Published In

Volume / Issue

  • 20 / 10

Start / End Page

  • 1246 - 1254

PubMed ID

  • 23536574

Pubmed Central ID

  • 23536574

Electronic International Standard Serial Number (EISSN)

  • 1933-7205

Digital Object Identifier (DOI)

  • 10.1177/1933719113483009


  • eng

Conference Location

  • United States