After completing this article, readers should be able to: 1. Describe the components of the common terminal pathway of human parturition. 2. Define the preterm parturition syndrome. 3. Describe the pathways of intrauterine infection. 4. Explain the relationship between intrauterine infection and preterm birth. 5. List the organisms most frequently involved in intra-amniotic infections. 6. Describe the role of inflammation and proinflammatory cytokines in the mechanisms of parturition. 7. Describe the fetal inflammatory response syndrome and its consequences. The implicit paradigm that has governed the clinical management and investigation of preterm parturition is that term and preterm labor are fundamentally the same processes except for the gestational age at which they occur. Indeed, term and preterm labor share a common terminal pathway composed of myometrial contractility, cervical ripening, and decidual/membrane activation (Fig. 1)⇓. Clinical tests to identify the patient at risk for preterm birth have focused on detection of premature activation of each of these components (Fig. 2)⇓. For example, uterine activity monitoring, ultrasonographic examination of the cervix, and measurement of fetal fibronectin can be used to detect myometrial activation, cervical ripening, and membrane/decidual activation, respectively. Interventions to prevent preterm birth also are also aimed at the common terminal pathway. Pharmacologic inhibition of uterine contractility (ie, tocolysis) and cervical cerclage have been proposed as methods to prevent preterm birth (Fig. 2)⇓. Antibiotic administration to patients who have positive fetal fibronectin (an indirect marker of membrane/decidual activation) has been attempted as a means of decreasing preterm birth based on the belief that a positive fibronectin finding is due to subclinical intrauterine infection. None of these interventions has proven successful. Figure 1. Term and preterm labor share a common terminal pathway composed of myometrial contractility, cervical ripening, and decidual/membrane activation. MLCK=myosin light chain kinase. Modified from an original drawing of Professor Gabor Haszor, Yale University. …