Birth order has a significant impact on perinatal and long-term outcomes. Preterm birth rates, ranging from 5% to 18%, are regrettably still high in industrialized and developing countries, making them the main contributor to infant mortality and morbidity. Infection, cervical pathology, uterine overdistension, progesterone deficiency, stress on the mother and fetus, allograft reaction, allergic phenomena, and likely more unknown factors are just a few of the causes of preterm birth syndrome. These several causes may improperly stimulate the usual pathway between the decidua and the fetal membranes, resulting in cervical ripening, membrane rupture, and uterine contractility. Some of the mechanisms underpinning these actions include receptors, chemokines, and inflammatory cytokines. For early identification, treatment, and avoidance of negative consequences, it is essential to understand the cellular and metabolic mechanisms that cause preterm labor. Clinicians and researchers are crucial to improving our knowledge of the biochemistry of preterm delivery, identifying risk factors, and creating treatments for this challenging condition. Intrauterine growth restriction and pre-eclampsia or eclampsia are frequent causes of suspected preterm births. "Spontaneous preterm births" occur after preterm labor that develops without warning with an early membrane rupture. It is thought that the condition that may cause these births may have several causes, such as uterine overdistension, vascular disease, infection, or inflammation. Unplanned preterm births have several reasons, including the black race, periodontal disease, low mother body mass index (BMI), and previous preterm births. A short cervical length and a high cervical-vaginal fetal fibronectin concentration are the two best signs of premature birth.
Keywords: prematurity; preterm birth; progesterone; short cervical length; transvaginal ultrasound.
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