The article discusses the concept of preterm parturition as a syndrome, distinct from term labor, and highlights the role of multiple etiologies in its pathogenesis. It proposes that preterm labor arises from pathological signaling in the common pathway of parturition, which includes uterine contractility, cervical dilatation, and activation of membranes/decidua. The term "great obstetrical syndromes" is introduced to describe conditions like preterm labor, which are characterized by multiple etiologies, long preclinical stages, frequent fetal involvement, adaptive clinical manifestations, and gene-environment interactions. The article reviews evidence linking preterm labor to intrauterine infection, uterine ischemia, over-distension, abnormal allograft reaction, allergy, cervical insufficiency, and hormonal disorders. It emphasizes the importance of understanding these mechanisms for prevention, diagnosis, and treatment. The article also discusses the role of inflammation in preterm labor, highlighting the involvement of cytokines like IL-1 and TNF-α, and the importance of the fetal inflammatory response syndrome (FIRS) in fetal injury. It further explores gene-environment interactions, such as the association between bacterial vaginosis and the TNF-α allele 2, in predisposing to preterm labor. The article concludes by emphasizing the complexity of preterm labor and the need for a multifaceted approach to its management.The article discusses the concept of preterm parturition as a syndrome, distinct from term labor, and highlights the role of multiple etiologies in its pathogenesis. It proposes that preterm labor arises from pathological signaling in the common pathway of parturition, which includes uterine contractility, cervical dilatation, and activation of membranes/decidua. The term "great obstetrical syndromes" is introduced to describe conditions like preterm labor, which are characterized by multiple etiologies, long preclinical stages, frequent fetal involvement, adaptive clinical manifestations, and gene-environment interactions. The article reviews evidence linking preterm labor to intrauterine infection, uterine ischemia, over-distension, abnormal allograft reaction, allergy, cervical insufficiency, and hormonal disorders. It emphasizes the importance of understanding these mechanisms for prevention, diagnosis, and treatment. The article also discusses the role of inflammation in preterm labor, highlighting the involvement of cytokines like IL-1 and TNF-α, and the importance of the fetal inflammatory response syndrome (FIRS) in fetal injury. It further explores gene-environment interactions, such as the association between bacterial vaginosis and the TNF-α allele 2, in predisposing to preterm labor. The article concludes by emphasizing the complexity of preterm labor and the need for a multifaceted approach to its management.