Table 2.
The mechanisms of bone loss during long-term GCs treatment.
| Inhibition | Stimulation | |
|---|---|---|
| Bone cells direct effects | ||
| Bone marrow/stromal cells | differentiation into | differentiation into |
| osteoblasts | adipocytes | |
| Osteoblasts | differentiation, activity | — |
| synthesis of type I collagen | apoptosis | |
| Osteocytes | metabolism and function | apoptosis |
| Osteoclasts | apoptosis | stimulation |
|
| ||
| Indirect effects | ||
| Gut | Ca2+ absorption | — |
| Renal tubule | Ca2+ reabsorption | — |
| Parathyroid-PTH | Tonic secretory rate* | Pulse secretory |
| rate* | ||
| Fractional pulsatile | ||
| secretion* | ||
| Pituitary | Growth hormone/IGF-1 | — |
| FSH, LH | — | |
| Testes, ovaries | Testosterone, estradiol | — |
*Data from Bonadonna et al. [46]; abbreviations: FSH: follicle stimulating hormone; LH: luteinizing hormone; IGF-1: insulin like growth factor 1.