Parturition at term in normal pregnancy follows a predictable sequence of events. There is some evidence that a state of inflammation prevails in the reproductive tissues during labor at term, but it is uncertain whether this phenomenon is the initiating signal for parturition. The absence of a clear temporal sequence of inflammatory events prior to labor casts doubt on the concept that normal human labor at term is primarily the result of an inflammatory cascade. This review examines evidence linking parturition and inflammation in order to address whether inflammation is a cause of labor, a consequence of labor, or a separate but related phenomenon. Finally, we identify and suggest ways to reconcile inconsistencies regarding definitions of labor onset in published research, which may contribute to the variability in conclusions regarding the genesis and maintenance of parturition. A more thorough understanding of the processes underlying normal parturition at term may lead to novel insights regarding abnormal labor, including spontaneous preterm labor, preterm premature rupture of the fetal membranes, and dysfunctional labor, and the role of inflammation in each.
Human labor has features suggestive of inflammatory processes. However, data indicate that inflammation may not be necessary for labor initiation at term. Further research is needed to understand the events leading to normal human parturition.