Evangelinakis N, Polyzou E, Kassanos D

3rd Department of Obstetrics and Gynecology, University of Athens, Medical School, Attiko hospital, Athens, Greece

Correspondence: Evangelinakis Nikolaos, 3rd Department of Obstetrics and Gynecology, University of Athens, Attiko hospital, 1 Rimini St, GR-12464, Athens, Greece. E-mail: This email address is being protected from spambots. You need JavaScript enabled to view it.




Preterm birth, caused either by preterm onset of contractions (before 37 weeks’ gestation) or by preterm premature rupture of membranes (pPROM), accounts for ~80% of preterm deliveries. pPROM is associated with 30-40% of preterm deliveries and its incidence has increased during the past decade. A fundamental question that has to be addressed is why some women experience preterm pPROM and others experience preterm labor without rupture of membranes, although risk factors are common for both conditions. To date, studies have evaluated biological markers that are commonly elevated in preterm delivery regardless of rupture of membranes. A better understanding of the similarities and differences between the biomolecular pathways leading to each of these conditions may broaden our horizons in research and therapeutic intervention. In this review we emphasize on the possibly different roles of inflammatory mediators (cytokines and matrix metalloproteinases) in preterm labor with and without pPROM.

Key words: preterm premature rupture of membranes; inflammation; matrix metallinoproteinases; apoptosis; genetic variations