Abstract
ObjectiveTo determine the relationship between maternal bone resorption and bone development in fetuses.MethodsFemale SD rats were injected with either fluorescent calcium indicator calcein alone or together with tetracycline 1 week before pregnancy, followed by fluorescence detection in fetal tibias 21 days post-treatment. Alendronate was subsequently administered to pregnant rats to inhibit maternal bone resorption, while maternal bone turnover and fetal bone development were both examined.ResultsThe maternal fluorescent labeled calcium before pregnancy was found in the fetal tibia. This indicated that the calcium of maternal bones may be released into the maternal circulation through high bone resorption during pregnancy, thereby participating in the fetal bone development. Bone histomorphometry and serum biomarker results showed that Alendronate significantly inhibited maternal bone resorption in pregnant rats when compared to normal pregnant rats. Moreover, the body weight, bone mass, and bone length of the fetuses in the Alendronate group were significantly decreased; while no apparent abnormality in placental morphology was observed. The above results implied that when maternal bone resorption is suppressed, the development of the fetal bone shall also be suppressed.ConclusionCalcium in the maternal bone is released into the maternal circulation through bone resorption during pregnancy which represents an important material source in fetal bone development. Therefore, high bone turnover during pregnancy is essential for mammalian embryonic bone development.
Highlights
Pregnancy is an exhaustive period of persistent calcium demand, especially toward late gestation; the placenta actively transports vast amounts of calcium to allow rapid fetal skeletal mineralization (Hacker et al, 2012)
Maternal bone resorption and bone formation are both increased during pregnancy, which are elevated in clinical studies and animal studies, mainly by measurements of plasma bio-markers (Cross et al, 1995; Naylor et al, 2000, 2003)
These fluorescent signals mainly localized at the fetal cortical bone (Figure 1). This indicated that the fluorescent-labeled calcium deposited in the mothers’ bones is released during pregnancy and is directly recruited to assist fetal bone development
Summary
Pregnancy is an exhaustive period of persistent calcium demand, especially toward late gestation; the placenta actively transports vast amounts of calcium to allow rapid fetal skeletal mineralization (Hacker et al, 2012). Accumulating clinical evidence indicates that women having high calcium intake during pregnancy do not increase the development of fetal bones compared to those who have normal calcium intake (Kovacs, 2000; Vargas Zapata et al, 2004). It is implied that no additional calcium intake is required during pregnancy, and the maternal physiological adaptation process is sufficient to maintain the calcium requirement for fetal growth (Prentice, 2000). Those findings did not topple the mainstream concept for the importance in calcium supplementation during pregnancy. The missing link appears to be any direct evidence to demonstrate how liberation of calcium from maternal skeleton shall provide the calcium necessary for fetal bone development, perhaps surprisingly, even in animal studies
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