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Author Spotlight: Developing a Rat Model for Weight-Bearing Intervention to Investigate Osteonecrosis of the Femoral Head
Published on: September 27, 2024
[Glucocorticoid-induced Osteoporosis; Epidemiology, Pathogenesis and Treatment]
Anna Madrid1, Catherine Lamm1, Daniel Aeberli1,2
1Medizinische Klinik, Spital Emmental, Burgdorf.
Introduction:
Glucocorticoid (GC) therapy has been shown to be associated with a dose-dependent significantly elevated risk of osteoporosis and fractures. It is estimated that about 3 % of the population are prescribed systemic GC on a daily basis, and approximately 30-50 % of patients treated with GC experience an osteoporotic fracture. Evidence has been mounting that inhaled, topical, and locally infiltrated GC also adversely affect bone mineral density. At the cellular level, GC have been shown to activate osteoclasts and inhibit the activity of osteoblasts and osteocytes, resulting in a loss of bone mass and a deterioration in bone quality, thereby increasing fracture risk. Patients prescribed a daily dosage of ≥ 5 mg of prednisone equivalents for a period of at least three months should undergo a bone density assessment and a fracture risk evaluation. Lifestyle modifications, including physical activity as well as calcium and vitamin D supplementation are recommended for all patients with GC therapy. In cases of a very high risk for fracture, the administration of osteoanabolic therapy followed by antiresorptive therapy is imperative. In patients with high fracture risk, antiresorptive therapy is recommended, whereas for those at moderate/low risk for fracture selective estrogen receptor modulators or oral bisphosphonates can be considered.
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