Senior author Yongwon Choi, PhD, professor of Pathology and Laboratory Medicine at the University of Pennsylvania and colleagues report their findings in Nature Medicine. “The main challenge is how to prevent bone decay while also encouraging bone growth,” states Choi.
The basic principles behind bone metabolism are largely understood, hence a handful of drugs treating osteoporosis are available. Most drugs inhibit osteoclasts, which cause bone decay. But there is also at least one that stimulates osteoblasts, enhancing bone formation. A combined treatment will not only prevent the occurrence of osteoporosis, but also make the quality of bone even better. “Our discovery proves that inhibiting osteoclasts while simultaneously stimulating new bone formation can be done.”
Bone health is maintained by the balanced activities of osteoblasts and osteoclasts. The study shows that the inactivation of gene Atp6v0d2 in mice results in dramatically increased bone mass due to defective osteoclasts as well as enhanced bone formation. These findings may provide some clarity into the regulation of bone metabolism and show that targeting the function of a single gene could possibly inhibit bone decay while stimulating bone formation.
“We have finally proven the theory that targeting one gene can do both,” said Choi. “Now that we have demonstrated a new approach that is theoretically attainable, one that combines the best of both worlds, we can go to work on the genes up and down stream from our target gene. If we can find a way to get to our target gene with a drug we may be able to help the millions of seniors with osteoporosis.”
MEDICA.de; Source: University of Pennsylvania