The membranes surrounding the amniotic cavity are composed of the amnion and the chorion, which are closely adherent layers consisting of several cell types, including epithelial cells, mesenchymal cells, and trophoblast cells, embedded in a collagenous matrix. They retain amniotic fluid, secrete substances both into the amniotic fluid and toward the uterus, and guard the fetus against infection ascending the reproductive tract. The membranes normally rupture during labor. Premature rupture of the fetal membranes is defined as rupture of the membranes before the onset of labor.1 Premature rupture of the membranes occurring before 37 weeks' gestation is usually referred to as preterm premature rupture of the membranes. Despite advances in perinatal care, premature rupture of the membranes and preterm premature rupture of the membranes continue to be important obstetrical complications. At term, 8 to 10 percent of pregnant women present with premature rupture of the membranes; these women are at increased risk for intrauterine infection when the interval between the membrane rupture and delivery is prolonged.1 Preterm premature rupture of the membranes occurs in approximately 1 percent of all pregnancies and is associated with 30 to 40 percent of preterm deliveries. It is thus the leading identifiable cause of preterm delivery (after less than 37 completed weeks' gestation) and its complications, including respiratory distress syndrome, neonatal infection, and intraventricular hemorrhage.
Obstetricians have traditionally attributed rupture of the membranes to physical stress, particularly that associated with labor. However, more recent evidence suggests that membrane rupture is also related to biochemical processes, including disruption of collagen within the extracellular matrix of the amnion and the chorion and programmed death of cells in the fetal membranes. It has been proposed that the fetal membranes and the maternal uterine lining (decidua) respond to various stimuli, including membrane stretching and infection of the reproductive tract, by producing mediators, such as prostaglandins, cytokines, and protein hormones, that govern the activities of matrix-degrading enzymes. We review here the association between the degradation of the extracellular matrix within the fetal membranes and premature rupture of the membranes, in an effort to understand better the pathophysiology of such ruptures and identify potentially effective interventions