Abstract
Preterm birth accounts for the majority of fetal morbidity and mortality in both the developed and developing world. The multifactorial etiology and inherent of molecular mechanisms resulting in preterm labor continue to be elucidated. Inflammatory mechanisms are increasingly recognized as playing a major role not only in cervical ripening and induction of myometrial contractions but also in the interaction between the fetus and mother in signaling labor at term. This review aims to describe recent developments in the understanding of the pathophysiology of preterm labor and how these molecular triggers and effector systems can interact, facilitating early delivery despite interruption of single pathways.
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