Mending Broken Bones with Motion

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Athletes or not, people snap clavicles, phalanges, femurs, ribs – you name the bone – every day. According to the Centers for Disease Control and Prevention, 1 million fractures occur each year.

The vast majority of these injuries are easily treated with casts or internal screws, plates or rods. But for 1 in 20 people, these methods don’t work. Their bones won’t heal without an external fixator, a movable system of pins and bars fastened to the damaged bone from the outside (through skin and muscle).

Movable is really the key word here.

“Motion, in general, is detrimental to healing, which is why we get casts or bone plates. But for non-unions, bones that don’t heal, a small amount of motion can stimulate the body to stabilize the break with cartilage, which can be replaced by bone,” said Jennifer Currey, assistant professor of bioengineering. “The big question is how much motion and by what mechanisms does the body take this motion and mend itself.”

That’s what she’s trying to find out by studying broken bones in mice. She uses the rodents as models because they share over 80 percent of their genes with humans, and because they heal incredibly quickly (fractures in just 21-28 days).

In her lab, Currey attaches a fixator (miniature version of what’s used on humans) to a mouse’s injured tibia. She then moves the fixator, and hence the fractured bone it’s attached to, by connecting the fixator to a device that shifts forward and backward at a prescribed distance and rate. In people, the patient’s own body plays this role.

“In the clinical setting, the fixator is adjusted so that, under the weight of the patient, it can generate a certain amount of motion during walking,” Currey said, adding that the fixator is supportive enough to allow this kind of ambulation.

The controlled movement of fixators in her lab, though, combined with histology and microCT scans, makes it possible to determine how much healing (or lack thereof) correlates with how much motion.

Histology is the microscopic study of cell and tissue anatomy. In this case, Currey assesses the cellular mechanisms of healing. A microCT scanner is just a tiny version of the average CT scanner in hospitals. It takes x-ray images of fractures that are compiled to form a 3D image of the mice bones.

Preliminary findings indicate that if a fractured mouse tibia is moved forward and backward just 150 micrometers once every second for 60 seconds, once a day, there is a significant increase in fracture callus stiffness after 17 days of treatment, Currey said.

For perspective, the break in the bone itself is 500 micrometers across, and the average human hair is between 17 and 180 micrometers thick. And a facture callus is simply the site of the break, where healing occurs.

“I describe it like this. If you put two pencils eraser-to-eraser and wrap one piece of tape around them, they can still wiggle around,” Currey explained. “So you keep wrapping tape around it until the pencils are stable.”

“That is essentially what the body is doing when it creates a fracture callus,” she continued. “It is putting tissue in the break area that can withstand motion and stabilize the boney ends. Once stabilized, the body can start to remodel and replace the callus with bone.”

All of this, especially the part about motion helping calluses stiffen, is worth knowing.

“If we better understand how much motion is beneficial to healing we can better prescribe treatment for non-unions in humans,” Currey said. “We can provide physicians with data on how much motion patients need and when to start that motion.”

In short, maybe people’s bones will mend more efficiently too.

Former and current students involved in Currey’s efforts include Kaitlin Graham ’09, Alexandra Guernon ’10, Marc Nash ’11, Tom Albano ’12, William Barton Harris ’12, Sean Day ’14, Megan Mancuso ’15, Sylvie Kalikoff ’16 and Erin Miller (RPI).