Semin Reprod Med 2007; 25(1): 003-004
DOI: 10.1055/s-2006-956770

Copyright © 2007 by Thieme Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.

Parturition-Mechanisms and Clinical Aspects

R. Ann Word1  Guest Editor 
  • 1Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, Texas
Further Information

Publication History

Publication Date:
05 January 2007 (online)

R. Ann Word M.D.

In 2004, 12.5% of births in the United States occurred preterm (prior to 37 weeks gestation). This rate of preterm birth has increased in the last 10 years. The birth of a preterm infant is accompanied by a significant risk of death and a variety of health and developmental difficulties affecting virtually every organ system. Although infants born at the earliest gestational ages are at the greatest risk for mortality and morbidity, infants born from 32 to 36 weeks gestation are also at increased risk for neonatal complications compared with infants born at term. Despite the staggering economic, social, and emotional costs of preterm birth, strategies to prevent preterm birth have not been widely successful.

This issue provides an overview of the current concepts in parturition research. Our understanding of the physiologic processes that lead to normal parturition in women continues to evolve. Parturition at term is initiated by multiple, parallel, interactive pathways that bring about uterine contractions and cervical remodeling at a time when fetal maturity is sufficient for extrauterine life. The endocrine and paracrine signals from the mother and fetus are complex and the relative contribution of each signaling pathway in the onset of labor varies considerably among species. For example, in rodents, parturition is preceded by an acute decline in serum progesterone levels. In contrast to rodents and most other mammalian species, progesterone production continues to increase throughout gestation, and decreases in serum progesterone levels are not linked to the onset of labor in humans and a few other species, suggesting that continued progesterone production is crucial for maintaining prolonged pregnancy, thereby allowing full development of the fetus to the neonatal stage at birth. Several investigators have proposed that functional progesterone withdrawal occurs in human pregnancy through changes in progesterone receptor function or local metabolism of tissue progesterone. The role of functional progesterone withdrawal and myometrial responsiveness to progesterone during pregnancy and parturition is reviewed by Sam Mesiano in the first article of this issue.

Beginning with the pioneering work of Liggins indicating that fetal-derived cortisol initiates parturition in sheep, it was proposed that the onset of parturition involves signals from the developing fetus. The role of the fetal adrenal and corticotropin-releasing hormone signaling in the parturition cascade is discussed in the second article by Beshay et al, and the role of fetal inflammation in signaling preterm parturition is reviewed in the third article by Romero et al. Genetic influences on inflammatory processes in parturition and the potential role of environmental interactions with genetic predisposing factors in the initiation of preterm labor are presented in the fourth article by DeFrance et al.

The causes of preterm labor are multifactorial. Mechanisms that bring about preterm labor in some conditions may not be involved in the etiology of preterm labor in others or in physiologic labor at term. Despite the multifactorial etiology of preterm labor, the pathways of preterm and term labor converge on certain common biological events, namely uterine contractions and cervical dilation. Oxytocin receptor signaling and prostaglandin signaling through prostaglandin receptors are believed to be two processes that comprise certain aspects of these final common biological events (reviewed in the fifth [Blanks et al] and sixth [Makino et al] articles). Finally, the dynamics of cervical remodeling during pregnancy and parturition is reviewed in the last article by Word et al.

Although much progress has been made in our understanding of the initiation of parturition, the precise networks involved and the influence of infection and genetic or environmental factors leading to preterm birth remain elusive. Efforts to prevent preterm birth have focused primarily on the identification of risk factors because knowledge regarding the exact mechanisms leading to preterm birth is lacking. The next decade of research is predicted to bring new insights into the physiologic regulation of parturition at term and the pathologic interactions that result in preterm birth. Armed with this knowledge, focused strategies to prevent and treat preterm labor will be developed.