Current treatments for osteoporosis focus on preventing cells called osteoclasts from removing minerals from the bone. A new treatment that may be more effective tries to stop the osteoclasts from being formed in the first place.

This effect was strongest at the hip, where denosumab increased bone density over thirty-three percent more than alendronate did.

Bones may seem like such solid, unchanging objects. In reality, they're very dynamic. New bone tissue is constantly being laid down while old bone is being removed. This works something like the deposits and withdrawals in a bank account. The system usually works well. This changes as people get older. Withdrawals exceed deposits; bones become less dense and more fragile. They fracture more easily and when they do, fractures heal much more slowly and poorly. This weakening of the bones is known as osteoporosis. The problem is most severe in post-menopausal women. The lack of estrogen tilts the balance in favor of withdrawals from the bone account.

The most common drug used for treatment and prevention of osteoporosis is alendronate (Fosamax®), a phosphate containing substance known as a bisphosphonate. While it has been effective, it sometimes causes side effects. These include upper GI problems, particularly to the esophagus. There is also an alleged link between oral bisphosphonate usage and osteonecrosis of the jaw.

Maybe there's a better way.

Clinical trials of a substance called denosumab indicate that it may be a more effective treatment for osteoporosis. Much of the bone loss in osteoporosis is caused by cells known as osteoclasts. Denosumab is an antibody to a protein the body produces called RANKL. RANKL is involved in the process which creates new osteoclasts. When people are given denosumab, fewer osteoclasts are produced and bone loss decreases, leading to denser and stronger bones.

A recent clinical trial compared the effect of denosumab to alendronate. Denosumab was better at increasing bone density. This effect was strongest at the hip, where denosumab increased bone density over thirty-three percent more than alendronate did.

The trial involved nearly 1,200 post-menopausal women, who were followed for over a year. Participants received either an injection of denosumab every six months plus a weekly oral placebo or they received a weekly oral dose of alendronate and an injection of placebo every six months. Both groups also took calcium and Vitamin D. The results were presented at the American College of Rheumatology annual meeting in San Francisco, October 29, 2008. A comparison of the effects of denosumab to alendronate in a clinical trial can be found in the September 3, 2008 online edition of the Journal of Bone and Mineral Research.

While RANKL and osteoclasts are best known for their role in removing bone tissue, it's entirely possible that they're involved in other processes which are in important in the day to day functioning of the body. Having fewer of them around could cause unexpected problems. So far, none have shown up, but these findings are preliminary and require further study.

Denosumab has completed its phase III clinical trials. Your rheumatologist is likely to know more about its potential availability as a treatment.