How does raloxifene differ from estrogen therapy in osteoporosis?

• A. It causes more endometrial stimulation.
• B. It is a selective estrogen receptor modulator that preserves bone density with less endometrial stimulation; it carries a risk of DVT/PE.
• C. It increases osteoclast activity.
• D. It has no thromboembolic risk.

Answer: (B)

Raloxifene is a selective estrogen receptor modulator (SERM). It acts like estrogen on bone, helping preserve or improve bone density, but acts like an estrogen antagonist in the uterus (and breast), so it causes much less endometrial stimulation than estrogen therapy. This means you get bone protection without as much risk of endometrial hyperplasia or related problems. However, it still carries the risk of venous thromboembolism, such as DVT or PE. In contrast, estrogen therapy can stimulate the endometrium, increasing the risk of endometrial hyperplasia or cancer if not balanced, and it also has a thromboembolic risk. So the best summary is that raloxifene maintains bone density with less endometrial stimulation while preserving a risk of DVT/PE.