The placental factor in spontaneous preterm labor with and without premature rupture of membranes

The association between infection and inflammatory response in preterm labor (PTL) is well established. Our aim was to elucidate the roles of utero-placental perfusion and fetal component, in PTL.

Histopathologic findings in placentas from pregnancies complicated by preterm birth with or without premature rupture of membranes (ROM) (study group) were compared to placentas from pregnancies with delivery >34 weeks, with or without spontaneous ROM (control group). Placental lesions were classified as those consistent with maternal circulation abnormalities, maternal underperfusion, vascular or villous changes, and those consistent with fetal thrombo-occlusive disease, vascular or villous changes. Lesions were analyzed by maternal or fetal origin of inflammatory response.

The study group of 68 women, had a higher rate of vascular lesions than controls (136 women, 26.5% vs. 11%, P=0.005) and of inflammatory lesions of maternal and fetal origin (P<0.001). Within the study group, inflammatory lesions were more common in those with ruptured membrane than in those without (P<0.001).

Placentas from preterm birth demonstrate vascular lesions of maternal origin, in addition to the known inflammatory process. Preterm premature membrane rupture is associated with an increased rate of inflammatory lesions relative to spontaneous intact membranes-preterm birth, suggesting a different underlying mechanism.