Intrauterine growth restriction (IUGR) has been associated with low bone mass in infancy and increased risk for osteoporosis development in adult life. We aimed to investigate the effect of IUGR on bone metabolism in mother/infant pairs, by determining circulating biochemical markers of bone turnover in IUGR and appropriate for gestational age (AGA) pregnancies. Circulating markers of bone formation [bone specific alkaline phosphatase (BALP), total alkaline phosphatase (ALP), osteocalcin (OC)] and bone resorption [cross-linked N-telopeptide of type I collagen (NTx)], as well as intact parathormone (PTH), calcium and phosphorus levels were measured in 40 mothers and their 20 IUGR and 20 AGA singleton full-term fetuses and neonates on postnatal days 1 (N1) and 4 (N4). No significant differences in BALP, ALP, OC, NTx, PTH, calcium or phosphorus levels were observed between the AGA and the IUGR groups. In both groups, maternal BALP levels were lower compared to fetal, N1 and N4 levels (p< or =0.005 in all cases). In the AGA group, maternal NTx and OC levels were lower compared to fetal, N1 and N4 levels (p<0.001 in all cases), and fetal NTx levels were lower compared to N1 and N4 ones (p<0.001 and p=0.002, respectively). In the IUGR group, maternal OC levels were lower compared to fetal, N1 and N4 ones (p<0.001 in each case) and fetal OC levels were elevated compared to N1 and N4 ones (p<0.001 and p=0.003, respectively). N4 NTx levels were elevated compared to maternal, fetal and N1 levels (p=0.009, p<0.001 and p=0.002, respectively) and fetal NTx levels were lower compared to N1 and N4 ones (p=0.001 and p<0.001, respectively). Finally, positive correlations were found between maternal NTx and BALP (r=0.332, p=0.037), as well as ALP (r=0.329, p=0.038) levels, and between maternal, fetal, N1, N4 BALP and respective ALP levels (r=0.432, p=0.005, r=0.534, p=0.001, r=0.778, p<0.001, r=0.694, p<0.001, respectively). In conclusion, maternal, fetal and neonatal bone turnover in IUGR cases may not differ from respective bone metabolism in AGA controls. In addition, fetal and neonatal bone remodeling is markedly enhanced and independent of maternal bone turnover in late pregnancy.