The Ticklish Gene
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iosteum.* At the same time, the bone generated its own current
piezoelectrically due to residual stress in the mangled apatite-collagen
matrix. These signals combined to stimulate the cells that formed new
bone.
Except for the identity of the target cells, bone repair seemed to be
basically the same in all vertebrates, proceeding through the stages of
blood clot, blastema, callus, and ossification. In fish, amphibians, rep-
tiles, and birds, the red cells in the clot dedifferentiated in response to
the electric field, especially the positive potentials at the broken ends of
the bone. They then redifferentiated as cartilage cells and continued on
In some animals the periosteal cells responded to the current of injury
by migrating into the gap and specializing a bit further into bone cells.
This process seemed to be available to amphibians only at high tem-
peratures, but it was the dominant method in mammals, whose thick
periosteum made up for the lack of nuclei in their red corpuscles. By
this time we'd become pretty sure that the marrow component of bone
healing in humans involved the dedifferentiation of at least the immature
*The lack of the periosteal (nerve-derived) current may explain the uncontrolled, de-
formed growth that often follows fractures in the limbs of paraplegics and lepers. Their
bones still generate a positive potential in the gap, but because of nerve damage it isn't
balanced by the negative periosteal potential that normally surrounds the break.