Abstract
Preterm birth remains to be one of the most prevalent obstetric complications worldwide. Since there are multiple etiological factors associated with this disease process, an integrative literature search in PubMed and Scopus databases on possible mechanism of action and effect of bisphenols on exposure on human or animal placental samples in preterm birth was conducted. From 2332 articles on initial literature search, 63 studies were included for full data extraction. Altogether, several pathways were shown to be possibly affected by bisphenols, leading to dysregulations in structural and endocrine foundation in the placenta, potential induction of senescence and failure of decidualization in the decidua, and possible propagation of inflammation in the fetal membranes. Combined, these actions may eventually counteract bisphenol-induced relaxation of the myometrium and promote contractility alongside fetal membrane weakening. In totality, these individual impairments in gestation-critical processes may lead to failure of maintenance of pregnancy, and thus effecting preterm birth.
Highlights
15 million infants are born prior to 37 weeks of gestation, defined by theWorld Health Organization (WHO) as preterm birth (PTB)
This review explores the potential role of bisphenols in contributing towards a preterm birth phenotype
There have been studies published regarding the possible mechanisms of actions of bisphenols that may contribute to preterm birth, there is a relative lack of coherence due to the use of various in vitro, in vivo, and ex vivo models due to human experimentation barriers
Summary
15 million infants are born prior to 37 weeks of gestation, defined by theWorld Health Organization (WHO) as preterm birth (PTB). Short-term complications may arise and lead to hospital-acquired infections, intraventricular hemorrhage, and necrotizing enterocolitis [2]. About half of preterm births (PTB) are of spontaneous or idiopathic etiologies, in contrast with preterm rupture of membranes (about a third of PTB cases) or elective preterm deliveries (about a fifth of PTB cases). These pathways are not mutually exclusive of each other, since there are redundancies in downstream effectors for each factor listed; moderate changes brought upon by a single factor may not be adequate to bring about the definitive outcome of premature delivery [4,5]. Since spontaneous PTBs comprise the majority of these cases, determination of the exact pathophysiology becomes an important endeavor to allow possible interventions that can prevent PTB
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