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.