Currently, there is no animal model in which
to evaluate the underlying physiological processes leading to the heterotopic
ossification (HO) which forms in most combat-related and blast wounds.
We sought to reproduce the ossification that forms under these circumstances
in a rat by emulating patterns of injury seen in patients with severe
injuries resulting from blasts. We investigated whether exposure
to blast overpressure increased the prevalence of HO after transfemoral
amputation performed within the zone of injury. We exposed rats
to a blast overpressure alone (BOP-CTL), crush injury and femoral
fracture followed by amputation through the zone of injury (AMP-CTL)
or a combination of these (BOP-AMP). The presence of HO was evaluated
using radiographs, micro-CT and histology. HO developed in none
of nine BOP-CTL, six of nine AMP-CTL, and in all 20 BOP-AMP rats.
Exposure to blast overpressure increased the prevalence of HO. This model may thus be used to elucidate cellular and molecular
pathways of HO, the effect of varying intensities of blast overpressure,
and to evaluate new means of prophylaxis and treatment of heterotopic
ossification. Cite this article:
Heterotopic ossification (HO) is perhaps the
single most significant obstacle to independence, functional mobility, and
return to duty for combat-injured veterans of Operation Enduring
Freedom and Operation Iraqi Freedom. Recent research into the cause(s)
of HO has been driven by a markedly higher prevalence seen in these
wounded warriors than encountered in previous wars or following
civilian trauma. To that end, research in both civilian and military
laboratories continues to shed light onto the complex mechanisms
behind HO formation, including systemic and wound specific factors,
cell lineage, and neurogenic inflammation. Of particular interest,
non-invasive
