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.