This lecture addresses our current understanding of the pathophysiology of bone loss and fragility fractures that occur during pregnancy and lactation, and provides guidance on appropriate investigations and treatment strategies. Most affected women present with no prior bone density reading, and so the extent of bone loss that may have occurred during pregnancy or lactation is uncertain. Several characteristic changes in bone metabolism do occur during normal reproductive cycles. 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 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 through an interval of rapid bone formation and mineralization that may not require the known calciotropic and phosphotropic hormones. The physiological bone loss that occurs during pregnancy and lactation does not normally cause fractures; instead, women who do fracture seem more likely to have additional secondary causes of bone loss and fragility. In women who fracture, calcitonin, bisphosphonates, strontium ranelate, teriparatide, vertebroplasty, and kyphoplasty have occasionally been used. However, the need for such treatments is uncertain given that a progressive 10-25% increase in bone mass subsequently occurs in most women who present with a fracture during pregnancy or lactation. In the long term, dozens of epidemiological studies have reported that parity and lactation are neutral or protective against long-term risk of low bone mass, osteoporosis, and fragility fractures.