Fundación para la Investigación Sanitaria y Biomédica (FISABIO)Juan de Garay 21, 46017 Valencia, SpainDepartment of GeneticsUniversity of Valencia and Research Foundation, INCLIVA, Avenida Blasco Ibáñez 15, 46010 Valencia, SpainDepartment of Functional Biology and Physical AnthropologySchool of Biological Sciences, University of Valencia, Burjasot Campus, Valencia, SpainDepartment of PediatricsObstetrics and Gynecology, Facultad de Medicina, University Hospital Dr Peset, University of Valencia, Avenida Blasco Ibáñez 15, 46010 Valencia, Spain.
Fundación para la Investigación Sanitaria y Biomédica (FISABIO)Juan de Garay 21, 46017 Valencia, SpainDepartment of GeneticsUniversity of Valencia and Research Foundation, INCLIVA, Avenida Blasco Ibáñez 15, 46010 Valencia, SpainDepartment of Functional Biology and Physical AnthropologySchool of Biological Sciences, University of Valencia, Burjasot Campus, Valencia, SpainDepartment of PediatricsObstetrics and Gynecology, Facultad de Medicina, University Hospital Dr Peset, University of Valencia, Avenida Blasco Ibáñez 15, 46010 Valencia, Spain
Eur J Endocrinol. 2015 Feb;172(2):R53-65. doi: 10.1530/EJE-14-0424. Epub 2014 Sep 10.
Changes in bone density and bone markers suggest that pregnancy is associated with deterioration of bone mass in the mother. The metabolism of calcium resets to allow for the needs imposed by the building of the fetal skeleton. The fetus contributes to the process through the output of regulators from the placenta. Understanding of the whole process is limited, but some changes are unambiguous. There is an increase in the circulating levels of vitamin D, but its functional impact is unclear. Fetal parathyroid hormone (PTH) and PTH-related peptide (PTHrp) play an indirect role through support of a calcium gradient that creates hypercalcemia in the fetus. Placental GH, which increases up to the end of pregnancy, may exert some anabolic effects, either directly or through the regulation of the IGF1 production. Other key regulators of bone metabolism, such as estrogens or prolactin, are elevated during pregnancy, but their role is uncertain. An increase in the ratio of receptor activator of nuclear factor kappa B ligand (RANKL) to osteoprotegerin (OPG) acts as an additional pro-resorbing factor in bone. The increase in bone resorption may lead to osteoporosis and fragility fracture, which have been diagnosed, although rarely. However, the condition is transitory as long-term studies do not link the number of pregnancies with osteoporosis. Prevention is limited by the lack of identifiable risk factors. When fractures are diagnosed, rest, analgesics, or, when indicated, orthopedic intervention have demonstrated efficacy. Systemic treatment with anti-osteoporotic drugs is effective, but the potential harm to the fetus imposes caution in their use.
骨密度和骨标志物的变化表明，妊娠会导致母体骨量恶化。钙的代谢会重置以满足胎儿骨骼生长的需要。胎儿通过胎盘输出调节剂来促进这个过程。尽管对整个过程的了解有限，但有些变化是明确的。循环中维生素 D 的水平增加，但它的功能影响尚不清楚。胎儿甲状旁腺激素（PTH）和甲状旁腺激素相关肽（PTHrp）通过支持钙梯度间接发挥作用，从而导致胎儿高钙血症。胎盘生长激素（GH）在妊娠末期增加，可能通过调节 IGF1 的产生发挥一些合成代谢作用，无论是直接还是间接的。其他关键的骨代谢调节剂，如雌激素或催乳素，在怀孕期间升高，但它们的作用尚不确定。核因子κB 受体激活剂配体（RANKL）与骨保护素（OPG）的比值增加是骨吸收的另一个促分解因素。骨吸收的增加可能导致骨质疏松症和脆性骨折，尽管很少有诊断病例，但这种情况是短暂的，因为长期研究并未将妊娠次数与骨质疏松症联系起来。预防措施受到缺乏可识别的危险因素的限制。当发生骨折时，休息、止痛剂或在必要时进行矫形干预已被证明是有效的。全身性抗骨质疏松药物治疗有效，但对胎儿的潜在危害要求在使用时谨慎。
