Short-term glucocorticoid excess blunts abaloparatide-induced increase in femoral bone mass and strength in mice

Glucocorticoids (GCs), such as prednisolone, are widely used to treat inflammatory diseases. Continuously long-term or high dose treatment with GCs is one of the most common causes of secondary osteoporosis and is associated with sarcopenia and increased risk of debilitating osteoporotic fragility f...

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Bibliographic Details
Published in:Scientific reports 2021-06, Vol.11 (1), p.12258-12258, Article 12258
Main Authors: Brent, Mikkel Bo, Thomsen, Jesper Skovhus, Brüel, Annemarie
Format: Article
Language:English
Subjects:
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Animals
Apposition
Bone density
Bone growth
Bone mass
Bone mineral content
Bone mineral density
Bone strength
Cancellous bone
Cortical bone
Fractures
General anesthesia
Glucocorticoids
Humanities and Social Sciences
Hypercalcemia
Inflammatory diseases
multidisciplinary
Osteogenesis
Osteoporosis
Parathyroid
Parathyroid hormone
Parathyroid hormone-related protein
Prednisolone
Sarcopenia
Science
Science (multidisciplinary)
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Summary:Glucocorticoids (GCs), such as prednisolone, are widely used to treat inflammatory diseases. Continuously long-term or high dose treatment with GCs is one of the most common causes of secondary osteoporosis and is associated with sarcopenia and increased risk of debilitating osteoporotic fragility fractures. Abaloparatide (ABL) is a potent parathyroid hormone-related peptide analog, which can increase bone mineral density (aBMD), improve trabecular microarchitecture, and increase bone strength. The present study aimed to investigate whether GC excess blunts the osteoanabolic effect of ABL. Sixty 12–13-week-old female RjOrl:SWISS mice were allocated to the following groups: Baseline, Control, ABL, GC, and GC + ABL. ABL was administered as subcutaneous injections (100 μg/kg), while GC was delivered by subcutaneous implantation of a 60-days slow-release prednisolone-pellet (10 mg). The study lasted four weeks. GC induced a substantial reduction in muscle mass, trabecular mineral apposition rate (MAR) and bone formation rate (BFR/BS), and endocortical MAR compared with Control, but did not alter the trabecular microarchitecture or bone strength. In mice not receiving GC, ABL increased aBMD, bone mineral content (BMC), cortical and trabecular microarchitecture, mineralizing surface (MS/BS), MAR, BFR/BS, and bone strength compared with Control. However, when administered concomitantly with GC, the osteoanabolic effect of ABL on BMC, cortical morphology, and cortical bone strength was blunted. In conclusion, at cortical bone sites, the osteoanabolic effect of ABL is generally blunted by short-term GC excess.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-021-91729-8