• Biomarker-based cervicovaginal profiling, centering on fetal fibronectin and vaginal infection markers, emerged as a core approach to predict spontaneous preterm birth across diverse cohorts, enabling risk stratification beyond clinical history [1], [9], [8], [17].

• Clinical risk assessment systems and prevention programs consolidated risk stratification by integrating demographic, obstetric, and twin gestation risk factors, with multicenter trials and program implementations shaping targeted prevention for high-risk pregnancies [15], [3], [2], [12], [14].

• Recurrence risk analyses and gestational-age–specific outcome studies highlighted the persistence and evolution of preterm risk across pregnancies, including maternal stress effects, emphasizing etiologic heterogeneity of preterm birth [4], [7], [19].

• Expanded biomarker panels beyond fetal fibronectin, including maternal plasma corticotropin-releasing hormone (CRH) and α-fetoprotein (AFP), cytokines such as interleukin-6 (IL-6), and immune-modulating factors like granulocyte colony-stimulating factor (G-CSF), represent a trend toward mechanistic risk models integrating endocrine and inflammatory signals [16], [17], [5].

• Public health-oriented prevention studies and program evaluations demonstrate how coordinated care for high-risk women and community-based interventions impact preterm birth rates, informing scalable policy options [12], [2], [10], [14].