Biochemistry and physiology of preterm labour and delivery

Human parturition is associated with profound changes in uterine connective tissue affecting mainly the cervix, but the endocrine control of cervical ripening remains obscure. Connective tissue changes are also implicated in premature rupture of the membranes, a problem often associated with preterm delivery, and it is believed that local inflammatory infiltration may play a role in both this condition and cervical ripening, but it is difficult to define which changes precede parturition and which are a consequence of the trauma of labour. Chorioamnionitis can cause preterm labour by provoking the release of inflammatory mediators in the decidua/fetal membranes area and it is likely that activation of prostaglandin release by decidual macrophages is involved in triggering labour. However, the role of macrophages and other bone marrow derived cells in normal labour and in labour associated with chorioamnionitis needs to be defined. It is likely that treatment with a combination of antibiotics and prostaglandin synthase inhibitors and/or other anti-inflammatory drugs is the most appropriate therapeutic approach. Idiopathic preterm labour and spontaneous labour at term are probably due to changes in the sensitivity of the myometrium to endogenous agonists. Recent progress in cell signalling pathways, such as the characterization of regulatory G proteins and the cloning of hormone receptors, should clarify the mechanism of action of relaxing and contracting agents on myometrial cells and should provide the means for the development of new therapeutic agents of high effectiveness and selectivity. This approach should result in better management of both term and preterm labour.