The aetiologies of secondary osteoporosis are multiple and often intricated, we studied in humans and in animals some of them: iatrogenic osteoporosis induced by glucocorticoids (GCs) and aromatase inhibitors, disuse osteoporosis and osteoporosis associated with systemic mastocytosis. We developed a murine model of glucocorticoid-induced osteoporosis to study the effects of GCs on the long bones and the mandible. We confirmed that GCs exposure leads to a reduction of trabecular bone at the tibia and showed for the first time in the mouse that GCs decrease the alveolar bone. We studied apoptosis of osteoblasts and osteocytes under GCs by cytodynamic method and we didn't find any increase in apoptosis but morphological modifications of osteocytes under Dexamethasone. In another study, we studied by microCT the effects of disuse induced by botulinum toxin on the muscle and bone at the tibia in growing rats. We showed that disuse leads to a rapid muscle and bone loss, a decrease of the growth in thickness but has no effect on the growth in length and doesn't modify the shape of tibia. In a clinical study we described the bone effects of systemic mastocytosis by analyzing the microarchitectural parameters after transiliac bone biopsy in 60 patients. Lastly, we showed in a 3 year prospective study the bone effects of aromatase inhibitors in a series of 497 women. We showed that 20% of the women have already at least one osteoporotic vertebral fracture at the beginning of aromatase inhibitor. After 3 years of treatment, the patients without osteoporosis have a low risk of bone loss and of osteoporotic fracture. Treatment with bisphosphonates blocks bone loss but does not prevent new vertebral fractures occurrence.
