New drug may reverse the effects of osteoporosis, but caution is warranted.
A new drug, recently featured in a top medical journal, could be that ‘magic bullet’ needed for the three million UK osteoporosis sufferers. Studies have highlighted a number of benefits, including increased bone formation and bone mineral density, whilst decreasing the bone decay rate.
Osteoporosis sees a general loss of bone particularly in postmenopausal women. This occurs everywhere, but the skull and jaw. Weakened and fracture-prone bones make falling a terrifying prospect. Persistent, unpleasant side effects to current drugs, mean effective therapies are still being sought after.
A research team, led by Dr Michael McClung, founding member of the Oregon Osteoporosis Center, spent one year evaluating the safety and efficacy of the drug.
”Most osteoporosis drugs work by stopping the progression of bone loss, but they don’t have the capability of rebuilding the skeleton,” McClung said. ”This really is a new day in the consideration of how we treat osteoporosis, with the capability of truly stimulating bone production and rebuilding the skeleton, not simply keeping it from getting worse”.
McClung’s team found bone mineral density to increase by 11.3% at the lower spine, large increases of bone mineral density at the hip, as well as decreased bone resorption. Importantly, no significant side effects were observed.
The drug, which is administered simply via injection, or orally, is designed to exploit a pre-existing bone forming process in the body. A protein, called Sclerostin, interrupts this process so bone is not formed.
The body naturally needs to control bone formation, very precisely as bone overgrowth could have all kinds of bad consequences.
The drug works by getting rid of Sclerostin, so that bone can be formed once again, in addition to the many other benefits mentioned.
The current standard treatment for osteoporosis is Teriparatide, a hormone based therapy. It has proved a safe and effective method since 2002. However, the need for daily injection and high cost mean it is not ideal.
Romosozumab, the sclerostin based therapy, lasts much longer in the body, potentially meaning it can be administered as scarcely as every three months.
Nevertheless, the novel drugs greatest feature may also be its worst. Sclerostin based therapy persists in the circulation, lasting for weeks or even months; once it has entered the body it cannot be taken out.
Currently in Phase Two human clinical trials, it may be a while before Romosozumab is readily available through the NHS. The initial promising findings must now be coupled with a cautious progression.
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