Context: Experimental and clinical studies in a variety of non-primate species demonstrate that progesterone withdrawal leads to changes in gene expression that initiate parturition at term. Mice deficient in 5-reductase type I fail to undergo cervical ripening at term despite the timely onset of luteolysis and progesterone withdrawal in blood.

Objective: To test the hypothesis that estrogen and progesterone metabolism is regulated in cervical tissues during pregnancy even in species in which parturition is not characterized by progesterone withdrawal in blood.

Design: Estradiol and progesterone metabolism was quantified in intact cervical tissues from nonpregnant and pregnant women at term before or after labor.

Setting: The study was conducted at a university hospital.

Patients: Tissues were obtained from 5 nonpregnant and 21 pregnant women (9 before labor and 12 in labor).

Main Outcome Measures: Enzyme activity measurements, Northern blot analysis, quantitative real-time RT-PCR, and immunohistochemistry were utilized to quantify steroid hormone metabolizing enzymes in cervical and myometrial tissues.

Results: During pregnancy, 17-hydroxysteroid dehydrogenase (17HSD) type 2 was induced in glandular epithelial cells to catalyze the conversion of estradiol to estrone and stroma-derived 20-hydroxyprogesterone to progesterone. During parturition, 17HSD type 2 was downregulated in endocervical cells thereby creating a microenvironment favorable for cervical ripening.

Conclusions: Taken together, the data indicate that cervical ripening during parturition involves localized regulation of estrogen and progesterone metabolism through a complex relationship between cervical epithelium and stroma, and that steroid hormone metabolism in cervical tissues from pregnant women is unique from that in mice.