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Updated: Aug 17, 2026

Assessment of Maternal Vascular Remodeling During Pregnancy in the Mouse Uterus
Published on: December 5, 2015
Feto-maternal bone remodeling in normal pregnancy and preeclampsia
Mohamed Shaarawy1, Sameh Zaki, Abdel-Megid Ramzi
1Department of Obstetrics and Gynecology, Kasr Al-Aini School of Medicine, Cairo University, Cairo, Egypt. Shaarawy@mednet3.camed.eun.eg
Objectives:
To investigate feto-maternal bone turnover in normal pregnancy and preeclampsia and to test the hypothesis whether the reported low bone mass at birth in small-for-gestational age infants is associated with decreased bone formation or increased bone resorption.
Methods:
Thirty-two patients with preeclampsia (17 mild and 15 severe) and 20 normotensive women (controls) with singleton gestations in the third trimester participated in this study. Furthermore, 25 nonpregnant healthy women were chosen as nonpregnant controls. Maternal 24-hour urine specimens and venous blood samples were collected. In addition, fetal cord blood and the first voided neonatal urine were also collected. The freshly separated sera were assayed for osteocalcin (OC) and carboxy-terminal propeptide of type 1 collagen (PICP) by radioimmunoassay. Urine samples were assayed for N-telopeptide of type 1 collagen (NTx) by enzyme-linked immunosorbent assay.
Results:
Maternal and cord serum OC and PICP levels were significantly decreased in severe preeclampsia, whereas maternal and first-voided neonatal urinary NTx level were significantly increased compared to the corresponding levels of controls. In both mother and fetus, the coupling index of markers of bone turnover in normal pregnancy or mild preeclampsia was in favor of bone formation, whereas in severe preeclampsia the markers suggested marked bone resorption.
Conclusion:
Increased bone resorption and decreased bone formation occur in preeclampsia in both mother and fetus, being more pronounced in the latter. The increased osteoclastic activity in preeclampsia may be attributed to increased RANKL induced by increased interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor beta2 (TGF-beta2) production.
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