Lactation in mice is associated with a substantial bone loss, which almost completely recovers within four weeks after weaning. The post-lactational recovery mechanism is considered one of the most potent physiological bone anabolic responses in adult life. The aim of the study was to investigate whether the post-lactational bone anabolic response could attenuate or prevent a disuse bone loss induced by botulinum toxin (BTX) in mice. Eighty-one 10-week-old female NMRI mice were divided into the following groups: Pregnant, Lactation, Recovery + Vehicle, Recovery + BTX, No Lactation, No Lactation + Vehicle, No Lactation + BTX, and Virgin Control. The mice lactated for 12 days before weaning followed by 21 days of recovery. On the last day of lactation, disuse was induced by injecting 2 IU of BTX per 100 g body weight into the right hind limb. Mechanical testing, μCT, and dynamic bone histomorphometry were performed on the right femur. Lactation induced a loss of aBMD and of vBMD, Tb.Th, and MS/BS at the distal femoral metaphysis, Ct.Th and bone strength at the femoral mid-diaphysis, and femoral neck bone strength compared to pregnant mice. This bone loss was partly or fully reversed after 21 days of recovery from lactation. In non-lactating mice, BTX resulted in a loss of aBMD and of vBMD, BV/TV, Tb.Th, MS/BS, and BFR/BS at the distal femoral metaphysis, Ct.Th at the femoral mid-diaphysis, and femoral neck bone strength compared to ambulating non-lactating mice. The post-lactational response attenuated the BTX-induced loss of aBMD, Tb.Th, Ct.Th, trabecular MS/BS and BFR/BS, and femoral neck bone strength indicating that the recovery after lactation had reduced the negative effects of BTX on these parameters. In contrast, it was unable to counteract the loss of BV/TV and vBMD at the distal femoral metaphysis. In conclusion, the post-lactational response attenuated disuse-induced decrease of femoral aBMD, femoral neck bone strength, trabecular and cortical thickness, and trabecular MS/BS, BFR/BS, while it could not counteract the disuse-induced loss of BV/TV and vBMD.
This article was published in the following journal.
Name: Bone
ISSN: 1873-2763
Pages: 115183
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Bone Density
The amount of mineral per square centimeter of BONE. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by X-RAY ABSORPTIOMETRY or TOMOGRAPHY, X RAY COMPUTED. Bone density is an important predictor for OSTEOPOROSIS.
Bone Demineralization Technique
Removal of mineral constituents or salts from bone or bone tissue. Demineralization is used as a method of studying bone strength and bone chemistry.
Bone Demineralization, Pathologic
Decrease, loss, or removal of the mineral constituents of bones. Temporary loss of bone mineral content is especially associated with space flight, weightlessness, and extended immobilization. OSTEOPOROSIS is permanent, includes reduction of total bone mass, and is associated with increased rate of fractures. CALCIFICATION, PHYSIOLOGIC is the process of bone remineralizing. (From Dorland, 27th ed; Stedman, 25th ed; Nicogossian, Space Physiology and Medicine, 2d ed, pp327-33)
Bone Density Conservation Agents
Agents that inhibit BONE RESORPTION and/or favor BONE MINERALIZATION and BONE REGENERATION. They are used to heal BONE FRACTURES and to treat METABOLIC BONE DISEASES.
Bone Remodeling
The continuous turnover of bone matrix and mineral that involves first, an increase in resorption (osteoclastic activity) and later, reactive bone formation (osteoblastic activity). The process of bone remodeling takes place in the adult skeleton at discrete foci. The process ensures the mechanical integrity of the skeleton throughout life and plays an important role in calcium homeostasis. An imbalance in the regulation of bone remodeling's two contrasting events, bone resorption and bone formation, results in many of the metabolic bone diseases, such as OSTEOPOROSIS.
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