Infection and the role of inflammation in preterm premature rupture of the membranes

Best Pract Res Clin Obstet Gynaecol. 2007 Jun;21(3):467-78. doi: 10.1016/j.bpobgyn.2007.01.008. Epub 2007 Apr 19.


Spontaneous preterm birth, caused by preterm labor (contractions before 37 weeks' gestation) or preterm premature rupture of the membranes (pPROM) (membrane rupture before the onset of labor) or both account for approximately 80% of preterm deliveries. pPROM is associated with 30-40% of preterm deliveries and the incidence of pPROM has increased in the past decade. The question we address here is why some women experience pPROM and some experience preterm labor with no rupture of membranes (ROM) when the etiologic factors associated with both these pathologic complications are the same. To date, studies had evaluated the markers that are commonly elevated in both preterm labor and pPROM. A better understanding of the similarities and differences between the biomolecular pathways leading to each of these conditions may open new avenues for research and intervention. In this chapter we review the role of inflammatory mediators (cytokines and matrix metalloproteinases), and programmed cell death (apoptosis) in preterm labor with no ROM and preterm labor with pPROM to delineate the differences in pathways between the two conditions.

Publication types

  • Review

MeSH terms

  • Apoptosis / physiology
  • Female
  • Fetal Membranes, Premature Rupture / etiology*
  • Humans
  • Inflammation Mediators / physiology*
  • Matrix Metalloproteinases / physiology*
  • Obstetric Labor, Premature / etiology*
  • Pregnancy
  • Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / physiology*
  • Tumor Suppressor Protein p53 / physiology*


  • Inflammation Mediators
  • Tumor Necrosis Factor Receptor-Associated Peptides and Proteins
  • Tumor Suppressor Protein p53
  • Matrix Metalloproteinases