Simulation output for your selection:
Mechanism: Denosumab is injected every 6 months. After every denosumab injection, the osteoclasts die because of the absence of RANKL. In the time between one injection and the next, osteoclasts are formed from precursors. As a result of accumulation of osteoclast precursors due to blocking of differentiation by denosumab, the osteoclast recovery increases over time.
Note it does not make sense to give this diabetic patient whose resorption and formation are already low denosumab which would lower resorption and formation even more. This would just stop the natural processes of bone repair and adaptation to loads.
This is not the best combination of treatment and exercise level for this osteoporotic patient. Try again!