Abstract
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.
Highlights
Glucocorticoids (GCs), such as prednisolone, are widely used to treat inflammatory diseases
The purpose of the study was to investigate whether the osteoanabolic effect of ABL was affected by short-term GC excess in mice
The main finding of the study was that GC mainly blunted the osteoanabolic effect of ABL in cortical bone
Summary
Glucocorticoids (GCs), such as prednisolone, are widely used to treat inflammatory diseases. 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. Continuous long-term treatment with glucocorticoids induces a series of adverse effects including severe influences on the musculoskeletal system like rapidly decreased muscle mass and bone density, which subsequently increases the risk of debilitating osteoporotic fragility fractures[9,10]. Patients with severe glucocorticoid-induced osteoporosis (T-score ≤ − 3.5 or T-score ≤ − 2.5 plus a fragility fracture) are usually candidates for treatment with teriparatide, since daily injections of 20 μg teriparatide results in a greater increase in bone mineral density (BMD) than treatment with alendronate[17].
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