The biological basis and prevention of preterm birth

Abstract

The time of birth is a critical determinant of perinatal and long-term outcomes. Preterm birth is still the first cause of infant mortality and morbidity; unfortunately, rates of preterm birth remain high in both high- and low-resource countries, ranging from 5% to 18%. Preterm parturition is a syndrome, which can be induced by various factors such as infection, cervical pathology, uterine overdistension, progesterone deficiency, vascular alterations (utero-placental ischemia, decidual hemorrhage), maternal and fetal stress, allograft reaction, allergic phenomena, and probably other several unknown factors. These various etiologies can lead to the pathological activation of a common pathway of decidua/fetal membranes, which causes uterine contractility, cervical ripening, and rupture of membranes. Moreover, the mechanisms responsible for these processes have been identified, which involve receptors, chemokines, and inflammatory cytokines. It is very important to understand the cellular and biochemical pathways responsible for preterm labor to identify, treat, and prevent negative outcome in a timely manner. Clinicians and researchers play a key role in improving biochemical knowledge on preterm delivery, identifying risk factors, and shaping interventions that can address this complex syndrome.

Keywords: Cell-free fetal DNA; Decidual activation; Genetic predisposition; Inflammation; Microbiome; Preterm labor.