Study of Mechanical Forces Could Lead to New Wound-Care Technologies

Bob Michaels

November 8, 2011

2 Min Read
Study of Mechanical Forces Could Lead to New Wound-Care Technologies

A new study from researchers at the Georgia Institute of Technology (Georgia Tech; Atlanta) demonstrating that mechanical forces affect the growth and remodeling of blood vessels during tissue regeneration and wound healing could lead to future-generation wound-care and implant technologies. The study shows that the forces diminish or enhance the vascularization process and tissue regeneration depending on when they are applied during the healing process.

Microcomputed tomography reconstructions show bone formation when the injury site experienced no mechanical force for seven weeks (left) and when mechanical forces were exerted on the injury site beginning after four weeks for a duration of three weeks (left). (Images by Joel Boerckel)

Conducted by Robert Guldberg, a professor in the George W. Woodruff School of Mechanical Engineering at Georgia Tech, and graduate student Joel Boerckel, the study was based on healing bone defects in rats and on the understanding that blood vessel growth is required for the regeneration of many different tissues, including bone. Following removal of eight millimeters of femur bone, they treated the gap with a polymer scaffold seeded with a growth factor called recombinant human bone morphogenetic protein-2 (rhBMP-2), a potent inducer of bone regeneration.

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 the limbs from twisting and bending. The researchers used contrast-enhanced microcomputed 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%, respectively, compared with the group for which no force was applied. The lack of vascular growth into the defect produced a 75% reduction in bone formation and failure to heal the defect.

However, the same mechanical force that hindered repair early in the healing process was beneficial later on. When mechanical force was applied to the injury site 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% compared with when no force was applied.

The study may help researchers optimize the mechanical properties of tissue-regeneration scaffolds in the future. "Our study shows that one might want to implant a material that is stiff at the very beginning to stabilize the injury site but becomes more compliant with time, to improve vascularization and tissue regeneration," Guldberg says.

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