This study was conducted to determine the frequency and clinical significance of intra amniotic inflammation in patients with preterm premature rupture of the membranes. Amniotic fluid was retrieved from 219 patients with preterm premature rupture of the membranes; the fluid was cultured for aerobic and anaerobic bacteria and mycoplasmas and assayed for neutrophil collagenase, which is also known as matrix metalloprotein ase- 8. Matrix metalloproteinase- 8 was used because previous studies indicated that this was a sensitive and specific index of inflammation and that is correlated with the amniotic fluid white blood cell count. Intra amniotic inflammation was defined as an elevated amniotic fluid matrix metalloproteinase- 8 concentration (>23 ng/mL). Nonparametric and survival techniques were used for statistical analysis. The overall rate of intra amniotic inflammation was 42% (93/219 samples); proven intra amniotic infection was detected only in 23% (50/219 samples). Intraamniotic inflammation with a negative amniotic fluid culture for micro organisms was found in 23% (51/219 samples) and was as common as proven intra amniotic infection. Pregnancy outcome was worse in patients with intra amniotic inflammation and a negative culture than in those patients with a negative culture and without inflammation. There were no differences in the interval to delivery or rate of complications between patients with intra amniotic inflammation and a negative culture and patients with proven amniotic fluid infection. We conclude that intra amniotic inflammation, regardless of culture result, is present in 42% of patients with preterm premature rupture of the membranes and that it is a risk factor for impending preterm delivery and adverse outcome. We propose that intra amniotic inflammation, rather than infection, be used to classify and treat patients with preterm premature rupture of the membranes. This study was conducted to determine the frequency and clinical significance of intra amniotic inflammation in patients with preterm premature rupture of the membranes. The fluid was cultured for aerobic and anaerobic bacteria and mycoplasmas and assayed for neutrophil collagenase, which is also known as matrix metalloprotein ase- 8. Matrix metalloproteinase-8 was used because previous was indicated that this was a sensitive and specific index of inflammation and that is correlated with the amniotic fluid white blood cell count Intra amniotic inflammation was defined as an elevated amniotic fluid matrix metalloproteinase- 8 concentration (> 23 ng / mL). Nonparametric and survival techniques were used for statistical analysis. The overall rate of intra amniotic inflammation was 42% (93/219 samples) ; proven intra amniotic infection was detected only in 23% (50/219 samples). Int raamniotic inflammation with a negative amniotic fluid culture for micro organisms was found in 23% (51/219 samples) and was as common as proven intra amniotic infection. Pregnancy outcome was worse in patients with intra amniotic inflammation and a negative culture than in patients with a negative culture and without inflammation. There were no differences in the interval to delivery or rate of complications between patients with intra amniotic inflammation and a negative culture and patients with proven amniotic fluid infection. We conclude that intra amniotic inflammation, regardless of culture result , is present in 42% of patients with preterm premature rupture of the membranes and that it is a risk factor for impending preterm delivery and adverse outcome. We propose that intra amniotic inflammation, rather than infection, be used to classify and treat patients with preterm premature rupture of the membranes.