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As people age, bone healing becomes slower and poorer. But a new drug may provide hope of restoring to seniors the rapid bone healing of youth, according to a recent study.
The research, which is presented in the Journal of Bone and Mineral Research, offers hope to the roughly 560,000 Americans a year who suffer bone fractures that heal slowly or incompletely, leaving many in wheelchairs, unable to walk or live on their own. Even though the study is just on mice, it’s relevant to humans because of the similarity between a key human and mouse bone-building gene, and because the study mice, specially engineered by the National Institute on Aging, led to several important insights into aging that have been confirmed in humans.
The key bone-building gene is called the COX-2 gene, shorthand for cyclooxygenase-2, an enzyme that plays a vital role in cartilage and bone repair. COX-2 declines dramatically with age.
“The skeleton loses the ability to repair itself as we age,” said Regis J. O’Keefe, chairman of the Department of Orthopaedics at the University of Rochester Medical Center and corresponding author of the article. “Our results position the COX-2 pathway as one of several under exploration with the common goal of accelerating healing in aging humans, and with the potential to come together in future combination therapies.”
In the O’Keefe study, the bone-healing rates of two groups of mice – one young (seven-nine weeks of age) and one old (52-56 weeks of age) – were compared using imaging and gene-expression techniques. The expression of the COX-2 gene was far less in older mice than in young, and corresponded exactly with the onset of the key healing period.
Most important, the researchers were able to reverse the loss of bone-healing ability in aging mice by using an experimental Pfizer drug that boosts the effect of COX-2. The drug fills a missing link that develops in the COX-2 cell-stimulation pathway in aged mice. As COX-2 levels diminish with age, the chain reaction that’s required to stimulate bone marrow stem cells, cartilage cells and bone-producing cells (osteoblasts) weakens to a trickle.
The experimental drug, CP-734432, apparently mimicked one element in the COX-2 pathway, boosting fracture repair in the older mice with more efficient formation of mature bone. The drug was also recently used to prevent osteoporosis in early animal studies.
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