In one group of animals, plates screwed onto the bones to maintain limb stability prevented mechanical forces from being applied to the affected bone. In another group, plates allowed compressive loads along the bone axis to be transferred, but prevented twisting and bending of the limbs. The researchers used contrast-enhanced micro-computed tomography imaging and histology to quantify new bone and blood vessel formation.
The experiments showed that exerting mechanical forces on the injury site immediately after healing began significantly inhibited vascular growth into the bone defect region. The volume of blood vessels and their connectivity were reduced by 66 and 91 percent, respectively, compared to the group for which no force was applied. The lack of vascular growth into the defect produced a 75 percent reduction in bone formation and failure to heal the defect.
But the study found that the same mechanical force that hindered repair early in the healing process became helpful later on.
When the injury site experienced no mechanical force until four weeks after the injury, blood vessels grew into the defect and vascular remodeling began. With delayed loading, the researchers observed a reduction in quantity and connectivity of blood vessels, but the average vessel thickness increased. In addition, bone formation improved by 20 percent compared to when no force was applied, and strong tissue biomaterial integration was evident.
"We found that having a very stable environment initially is very important because mechanical stresses applied early on disrupted very small vessels that were forming," said Guldberg, who is also the director of the Petit Institute for Bioengineering and Bioscience at Georgia Tech. "If you wait until those vessels have grown in and they're a little more mature, applying a mechanical stimulus then induces remodeling so that
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Georgia Institute of Technology Research News