ObjectiveTo determine whether gonadal steroids and insulin-like growth factor I influence the final cervical remodeling during parturition.MethodsCervical biopsies were obtained transvaginally before labor (n= 10) and after spontaneous cervical ripening and vaginal delivery (n= 20). Levels of estrogen and progesterone receptors, their messenger RNAs, insulin-like growth factor I messenger RNA, and serum estradiol and progesterone were measured. Collagen and proteoglycan concentrations and compositions were measured to estimate the degree of cervical ripeness.ResultsThe concentrations of estrogen and progesterone receptors decreased in comparison with the clinically unripe cervix before labor. The median estrogen receptor concentration (range) decreased from 10 (2–18) to 4.5 (2–14) fmol/mg protein (P< .01), and the progesterone receptor concentration from 105.5 (32–153) to 74 (30–115) fmol/mg protein (P< .05), whereas their messenger RNA levels were unchanged. The insulin-like growth factor I messenger RNA concentration declined from 16.1 (8.4–20.4) at term to 8.9 (1.5–18.5) amol/μg DNA after parturition (P< .01). The collagen solubility by pepsin increased, but not significantly, and the collagen concentration was unchanged. The concentration of small proteoglycans, mainly decorin, decreased from 1.59 (1.20–1.97) to 0.84 (0.24–1.41) μg/mg wet weight (P< .001), and the concentration of versican increased, but not significantly (P= .07).ConclusionConcentrations of estrogen and progesterone receptors and insulin-like growth factor I messenger RNA were decreased significantly after spontaneous cervical ripening in comparison to levels before labor. These changes coincided with a tendency toward increased collagen solubility and a decline in concentration of small proteoglycans, which probably alters collagen organization, thus allowing for cervical softening and dilation. These observations suggest that gonadal steroids influence the final cervical remodeling during parturition, an influence perhaps mediated by insulin-like growth factor I.