Abstract

Available therapeutic interventions for managing preterm labour have not been consistently successful due to controversies related to its aetiology. However, multiple mechanisms including inflammation play a significant role in the pathogenesis of preterm labour. The extracellular matrix of the amniochorion contains collagen fibres that maintain the tensile strength of the amniochorion, resisting mechanical stress and preventing rejection of the foetal allograft. Expression of pro-inflammatory mediators in the amniochorion triggers production of prostaglandins in the uterus and enzymatic degradation of the resilient extracellular matrix of the foetal membranes by matrix metalloproteinases leading to uterine contractions, cervical remodelling resulting in preterm labour.