Vitamin C prevents hypogonadal bone loss.

Epidemiologic studies correlate low vitamin C intake with bone loss. The genetic deletion of enzymes involved in de novo vitamin C synthesis in mice, likewise, causes severe osteoporosis. However, very few studies have evaluated a protective role of this dietary supplement on the skeleton. Here, we show that the ingestion of vitamin C prevents the low-turnover bone loss following ovariectomy in mice. We show that this prevention in areal bone mineral density and micro-CT parameters results from the stimulation of bone formation, demonstrable in vivo by histomorphometry, bone marker measurements, and quantitative PCR. Notably, the reductions in the bone formation rate, plasma osteocalcin levels, and ex vivo osteoblast gene expression 8 weeks post-ovariectomy are all returned to levels of sham-operated controls. The study establishes vitamin C as a skeletal anabolic agent.

The crossover of bisphosphonates to cancer therapy.

Bisphosphonates form a class of drugs commonly used to treat disorders of osteoclastic bone resorption, including osteoporosis, Paget's disease of the bone, rheumatoid arthritis, and bone metastases. Although long established as the therapy of choice to treat such disorders, bisphosphonates' potential in treating cancer is garnering interest. Bisphosphonates have been demonstrated to inhibit tumor growth and metastasis, induce apoptosis in tumor cells, and encourage immune reactions against tumor cells. Current applications of bisphosphonates in cancer treatment include their use to treat skeletal metastases and as an adjuvant to endocrine therapy. This review explores bisphosphonates' current clinical utility and potential as a crossover cancer therapy.