Engineer says new study forces researchers to rethink how elderly break their bones

Reaching the breaking point
University of Utah mechanical engineering assistant professor Claire Acevedo. Credit: Dan Hixson/University of Utah College of Engineering.

To better understand why many elderly people are prone to break a bone in a fall (known as bone fragility fractures), perhaps doctors and researchers should look at the human skeleton in much the same way civil engineers analyze buildings and bridges, according to a new study from a University of Utah mechanical engineering professor.

A team of researchers led by U assistant professor Claire Acevedo believes the bones of an older person, say above the age of 50, become more susceptible to a break due to repeated stress from everyday activities such as walking, creating microdamage that affects the quality of the . That is in contrast to the common-held belief that bone breaks in the elderly are largely due to one massive impact or force on the bone, such as a fall.

"It really starts with a small microcrack that grows over time under repeated loading," says Claire Acevedo, who has just joined the University of Utah College of Engineering faculty. "You need to be doing something like just walking or moving, and the crack is slowly propagating. At some point, the remaining cross-section of the bone that is still connected is too small and will break suddenly."

In that case, such in the elderly would be the cause of a fall rather than the result of a fall.

The study, "Fatigue as the missing link between bone fragility and fracture," was published online this week in the latest issue of Nature Biomedical Engineering.

Acevedo says this theory that "cyclic loading" (repeated and fluctuating loads) might be a bigger contributor to bone breaks is similar to the study of structures and engineered materials. This type of stress in structures and materials resulted in a rise of catastrophic accidents near the turn of the 20th Century and has led to the development of "fracture mechanics."

"In engineered materials and structures, cyclic fatigue is the most ubiquitous mode of failure," wrote Acevedo, who studies fractures and stress on skeletal tissue. "Cyclic fatigue accounts for more than 80 percent of all failures, leading to catastrophic and sudden accidents such as the failure of railway axles, the collapse of metallic bridges, the failure of ships and the cracking of aircraft airframes and engines."

The research is based on examining not just the bone's mineral density () but its quality, specifically how well the collagen that provides the ductility of the bone deforms to resist fractures. And as one gets older, the more microdamage that person accumulates over time and the weaker the bones get.

"Bone quality is much more important than what we have been thinking," she says. "Old bones gradually lose their mechanical properties, their ability to self-repair and to recover bone quality to prevent the formation of a fracture."

"Fatigue is really important, and bone is really important. We need to change our mind about that," she says. "We need to change our approach on how to study it and not just look at the effect of a single load if we want to prevent such fractures and the high risk of mortality associated with them."

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More information: Claire Acevedo et al. Fatigue as the missing link between bone fragility and fracture, Nature Biomedical Engineering (2018). DOI: 10.1038/s41551-017-0183-9
Journal information: Nature Biomedical Engineering

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Jan 23, 2018
Assuming that we have drugs to encourage bone cell growth and encourage bone reabsorption, I would be surprised if this research didn't lead to a treatment. Perhaps a short intensive session on a combination of the two drugs to turnover as much bone mass as possible, coupled with a program of exercise and a special diet would allow the microcracks to be healed. Doing something like that every 10 years or so could not only add years to lives, but reduce the amount of infirmary suffered during those years.

Just speculating of course.

Jan 23, 2018
I always assumed that it was inactivity and lack of exercise that led to fractures. Now it is usage that is the problem. We shall see which is proven to be true.

Jan 23, 2018
But steel doesn't heal while living tissue does or can. Bone heals after a complete break in younger people. Why would microcracks not heal, at least later in life?

Jan 24, 2018
Assuming that we have drugs to encourage bone cell growth and encourage bone reabsorption,

Well, we sorta do.

Bone remodeling is done by two types of cells (osteoclasts and osteoblasts). Both are at work all the time. You can imagine it this way: Clasts eat away at places where there is little bone stress. Blasts build bone mass at places where there is much bone stress.

Some drugs (e.g. for treatment of osteoporosis) simply inhibit the osteoclasts. This seems fine at first glance because you get more bone mass because the blasts keep buidling (technically you get more bone mineral density - BMD).

But a high BMD alone doesn't tell you whether the bone is prone to breaking or not, because most of the resilience and stability of bone is not in its density but in its trabecular structure.

Think of it like half timbred and full timber houses. A half timbred house can be as sturdy (or even sturdier) than a full timbred one because of its intricate force balancing.

Jan 24, 2018
Unfortunately the US intelligencia spends more time trying to figure out how to score the next grant monies than they they do trying to improve useful knowledge.

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