Abstract:
In vivo studies suggest that cyclic and low-magnitude loading can be useful over
pharmaceutical drugs in normalizing bone loss as it encourages osteogenesis (i.e. new bone
formation) at the sites of elevated strain magnitude. In silico models assumed normal strain or
strain energy density (SED) as the stimulus to predict loading-induced osteogenesis,
however, these models may have limited success in fitting the in vivo new bone formation at
several instances. For example, rest-inserted cyclic loading amplifies the new bone formation
as compared to continuous-cyclic loading even though similar strain magnitude were induced
in both the cases. It is also believed that loading-induced interstitial fluid flow can also be a
potential stimulus of osteogenesis. The present study hypothesizes that fluid motion as
osteogenic stimulus may explain the afore-mentioned anomalies. Accordingly, this work
studies osteogenesis as functions of SED and canalicular fluid motion using an in silico
model. Therefore, the new bone formation is considered roughly proportional to stimuli
above their osteogenic thresholds. This model attempts to simulate in vivo new bone
formation noticed in rest-inserted cantilever loading studies. The model‘s prediction of sitespecific
new bone formation improves when fluid flow is considered as the stimulus. It is also
noticed that fluid motion as the stimulus closely fits the new bone formation for another in
vivo study where the effects of aging on osteogenesis were examined. These attempts to
establish fluid flow as a potential osteogenic stimulus can be useful in the prediction of sitespecific
new bone formation. The findings will ultimately be useful in designing
biomechanical interventions such as prophylactic exercises to cure bone loss.
