期刊
SKELETAL BIOLOGY AND MEDICINE
卷 1192, 期 -, 页码 81-83出版社
BLACKWELL PUBLISHING
DOI: 10.1111/j.1749-6632.2009.05228.x
关键词
glucocorticoids; osteoporosis; bone fragility
资金
- NIAMS NIH HHS [P50 AR063043, K24 AR048841, R01 AR043052] Funding Source: Medline
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [P50AR063043, K24AR048841, R01AR043052] Funding Source: NIH RePORTER
Glucocorticoid (GC) use results in rapid bone loss and an elevated risk of fracture. The excess bone fragility from GC treatment is multifactorial. GCs increase bone remodeling through reductions in gonadal hormones, elevations in PTH from negative calcium balance, early stimulation of osteoclast maturation and activity, and delayed, sustained reduction in osteogenesis and osteoblast activity. GCs also alter the metabolism of osteocytes so that increased osteocyte lacunae size, with demineralization around the osteocyte and reduced elastic modulus, is observed in a mouse model of GC-induced bone loss. In summary, GC effects on bone fragility are multifactorial, and additional studies are now under way to clarify how GCs alter osteocyte metabolism and result in reduction in localized bone strength.
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