Review Article
Bone Health in Patients with Multiple Sclerosis
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.
|
