  The recent discovery of bone flexoelectricity (electrical polarization
induced by strain gradient) suggests that flexoelectricity could have
physiological effects in bones, and specifically near bone fractures, where
flexoelectricity is theoretically highest. Here, we report a cytological study
of the interaction between crack stress and bone cells. We have cultured
MC3T3-E1 mouse osteoblastic cells in biomimetic microcracked hydroxyapatite
substrates, differentiated into osteocytes and applied a strain gradient to the
samples. The results show a strong apoptotic cellular response, whereby
mechanical stimulation causes those cells near the crack to die, as indicated
by live-dead and caspase staining. In addition, analysis two weeks after
stimulation shows increased cell attachment and mineralization around
microcracks and a higher expression of osteocalcin, an osteogenic protein known
to be promoted by physical exercise. The results are consistent with
flexoelectricity playing at least two different roles in bone remodelling:
apoptotic trigger of the repair protocol, and electrostimulant of the
bone-building activity of osteoblasts.
