Abstract
The cervix functions as a barrier between the uterus and vagina and keeps the uterus closed until term so that the fetus can develop. For delivery the cervix must soften and dilate, and finally reconstitute to close the uterus. This complex process involves precisely timed activation of molecular and microstructural events. Spontaneous preterm birth (sPTB) can result from aberrant timing of these events in the cervix. Unfortunately, the pathophysiology of sPTB due to cervical causes remains unclear and thus our treatment options remain limited - even if all appropriate candidates were identified and correctly treated with currently available interventions, the rate of sPTB would only be reduced by 5%. Very recent molecular and microstructural investigation is challenging prevailing concepts about cervical remodeling in pregnancy. We believe that progress toward novel, targeted solutions for the diverse pathways to sPTB entails a paradigm shift in which the overlapping and complex interactions between the cervix, uterus, membranes, fetus, placenta, and surrounding (structural and molecular) environment are suitably honored.