ECTS2014 Poster Presentations Bone development/growth and fracture repair (55 abstracts)
Aarhus University, Aarhus, Denmark.
Objective: In rodents, lactation is associated with a considerable and very rapid bone loss, which almost completely recovers after weaning. The aim of the present study was to investigate whether the bisphosphonate zoledronate (Zln) inhibits lactation induced bone loss during lactation. In addition, to study if Zln interferes with recovery of bone mass after lactation has ceased.
Materials and methods: 70 NMRI mice were divided into the following groups: baseline, pregnant, lactation, lactation+Zln, recovery, recovery+Zln, and recovery control (virgin). The lactation period was 12 days, then the pups were removed, and recovery took place for 28 days. Zln, 100 μg/kg s.c., was given at the day of delivery, and 4 and 8 days after delivery. The experiment was approved by the Danish Animal Experiments Inspectorate.
Results: In L4, lactation resulted in substantial loss of trabecular BV/TV (−40% vs pregnant, P<0.001), trabecular thickness (Tb.Th*) (−29% vs pregnant, P<0.001), bone material density (−4% vs pregnant, P<0.001) and bone strength (−55% vs pregnant, P<0.001). Zln completely prevented lactation induced changes in L4: BV/TV (+10% vs pregnant, NS), Tb.Th* (+0.03% vs pregnant, NS), bone material density (1.2% vs pregnant, NS), bone strength (+11% vs pregnant, NS). Similar results were found in the proximal tibia. Full recovery was found 4 weeks after weaning. Interestingly, L4 of the recovery group treated with Zln during the lactation period had higher BV/TV (+45%, P<0.05), Tb.Th* (+16%, P<0.05), and bone strength (+38%, P<0.05) compared with recovery controls. This indicates that Zln did not interfere with the substantial anabolic response, which takes place during recovery.
Conclusion: Zln fully prevented lactation induced loss of bone strength and architecture, and did not inhibit the anabolic response taking place after weaning.