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Giving 'young blood' to old mice helps broken bones heal more quickly

Giving 'young blood' to old mice helps broken bones heal more quickly


Bone healing slows with age, but that process may one day be reversed

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Human bodies age. There’s really no way around it — at least for now. Sagging skin, weakened immune systems, and slow-healing bone fractures are pretty much inevitable above a certain age. But what if humans could reverse that process somehow? As it turns out, that might become possible — at least when dealing with bone fractures.

Researchers were able to "rejuvenate" bone-healing cells

By sharing the blood of young mice with older mice, researchers were able to "rejuvenate" bone-healing cells, and trigger healing speeds that rivaled those of younger mice. The research is still in its infancy, but it’s possible that it could one day lead to a drug that could help older individuals conserve the ability to quickly recover from a fracture.

About one out of five people who sustain a hip fracture dies within a year of their initial injury, according to the CDC. And the rate of hip fractures increases tremendously with age; people over the age of 85 are 10 to 15 times more likely to suffer hip fractures than those between the ages of 60 and 65. That’s why understanding the mechanisms that underly bone healing is so important; for some older people, the answer could be live-saving.

In the study, researchers injected the blood of young mice into older mice with broken legs. They found that the old mice that had received the "young blood" experienced faster fracture healing times than those that hadn’t — and those times matched those of younger mice.

One out of five people who sustain a hip fracture dies within a year

To narrow down the source of this change, the researchers performed bone marrow transplants in which they gave "young blood cells" to older mice. Once again, they found that the transplants helped the older mice heal more quickly than those who hadn't received the young blood cells.

The researchers then checked to see if a protein called beta-catenin, which had been linked to repairing fractures in previous studies, was responsible. Mice produce more of this protein as they age, which might explain the difference. To verify this link, the researchers used mice with lower levels of beta-catenin; they found that these mice were able to heal quickly, even when they were elderly. In contrast, mice that were genetically modified so that they couldn't lower their beta-catenin levels didn't get a boost from young blood. The two results taken together suggest that beta-catenin is directly involved in the old mice's response to young blood.

"Bone-healing cells don't lose their ability to heal fractures."

"Our most important finding is that as they age, bone-healing cells don't lose their ability to heal fractures the same as when they were younger," says Benjamin Alman, a stem cell biologist at the University of Toronto and a co-author of a new study published today in Nature Communications. Indeed, they can be stimulated to do just that. It might therefore be possible to "develop a drug treatment that can ‘rejuvenate’ fracture healing," he says — before adding that humans have already produced drugs that act on beta-catenin.

You probably shouldn’t get too excited about the potential for a "fast-acting bone-healing" drug, however. "It is likely that many factors" — instead of a single one — "are involved in the multi-faceted responses of aging animals," says Christopher Evans, a cell biologist at the Mayo Clinic who didn’t participate in this study. In addition, the results "suggest that the level and timing of beta-catenin signaling need to be very carefully modulated to enhance bone healing," Evans says. Doing that with drugs "could be tricky."

Doing that with drugs "could be tricky."

And any mouse study needs to be examined carefully; what works in mice doesn't always work in humans. That said, Alman thinks that this particular finding could eventually hold some benefits for our species. "Mice heal fractures the same as people, and previous data from fracture repair in mice has carried over quite well to patents, so I suspect the same is the case in our work," he says. Overall, we still have a lot to learn, Evans says — "but it is very exciting."

Alman and his team now hope to clearly identify the elements — the specific blood cell and the accompanying proteins — that are responsible for the bone-healing rejuvenation process in mice. "We already have some promising leads," he says. The researchers also want to test drugs that can alter beta-catenin levels in animals soon.

The study fits well with the emerging idea that the blood of younger animals can rejuvenate the tissues of old ones, Evans says. Indeed, the idea that the blood of younger individuals contains the ingredients for faster tissue repair isn’t new, but applying this technique to bone repair will certainly help extend this idea's reach. "This work shows the importance of blood cells in fracture repair," Alman says. "If we could reverse this, we would prevent complications of fractures in older patients."