Osteoporosis International

, Volume 26, Issue 9, pp 2223–2241 | Cite as

Presentation and management of osteoporosis presenting in association with pregnancy or lactation

  • C. S. KovacsEmail author
  • S. H. Ralston


In this review, we summarize our current understanding of the pathophysiology of fragility fractures that occur for the first time during pregnancy and lactation, and provide guidance on appropriate investigations and treatment strategies. Most affected women will have had no prior bone density reading, and so the extent of bone loss that may have occurred during pregnancy or lactation is uncertain. During pregnancy, intestinal calcium absorption doubles in order to meet the fetal demand for calcium, but if maternal intake of calcium is insufficient to meet the combined needs of the mother and baby, the maternal skeleton will undergo resorption during the third trimester. During lactation, several hormonal changes, independent of maternal calcium intake, program a 5–10 % loss of trabecular mineral content in order to provide calcium to milk. After weaning the baby, the maternal skeleton is normally restored to its prior mineral content and strength. This physiological bone resorption during reproduction does not normally cause fractures; instead, women who do fracture are more likely to have additional secondary causes of bone loss and fragility. Transient osteoporosis of the hip may affect one or both femoral heads during pregnancy but it involves localized edema and not skeletal resorption. Case reports have described the use of calcitonin, bisphosphonates, strontium ranelate, teriparatide, vertebroplasty, and kyphoplasty to treat post-partum vertebral fractures. However, the need for such treatments is uncertain given that a progressive increase in bone mass subsequently occurs in most women who present with a fracture during pregnancy or lactation.


Lactation Osteoporosis Parathyroid hormone-related protein Pregnancy Transient osteoporosis of the hip 



The study received research grant support to CSK from Canadian Institutes of Health Research (grant no. 133413 and no. 84253).

Conflicts of interest

SHR reports having received consultancy fees on behalf of his institution from Novartis and Merck and research grants to his institution from Amgen and Eli Lilly. CSK has received honoraria from Amgen for work unrelated to the topic of this review.


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Copyright information

© International Osteoporosis Foundation and National Osteoporosis Foundation 2015

Authors and Affiliations

  1. 1.Faculty of Medicine—EndocrinologyMemorial University of NewfoundlandSt. John’sCanada
  2. 2.Rheumatology and Bone Disease Research Group, Institute of Genetics and Molecular MedicineEdinburgh University, Western General HospitalEdinburghUK
  3. 3.Health Sciences CentreSt. John’sCanada

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