BIOS 4500 Lecture Notes - Lecture 10: Denosumab, Bone Remodeling, Medical Device

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Document Summary

Effects of glucocorticoids on bone cells: effect of glucocorticoid therapeutic use. 1950 bone loss due to glucocorticoid excess was rare. Today, glucocorticoid-induced osteoporosis is almost entirely due to use of glucocorticoid treatment. 30-50% of patients receiving long-term glucocorticoid therapy present with one bone fracture. Thyroid hormone: skeleton considered a t3 target tissue, stimulate osteoblast activity. Insulin increases proliferation and differentiation of osteoblasts and increases collagen synthesis, bone formation and mineralization. Longitudinal growth- gh (& igf-1) stimulate prechondrocyte proliferation: gh directs mesenchymal stem cells toward condrocytic and osteoblastic lineages, gh stimulate opg and activation of osteoblasts and bone formation. Osteocalcin: originally thought to act primarily in bone as the glue that binds the mineral to collagen, recently recognized that osteocalcin has endocrine actions. Promotes testosterone synthesis in the leydig cell. Rankl inhibitor: human monoclonal antibody that prevents rankl-rank interaction, denosumab(prolia, stimulators of bone formation (anabolic)