Persistent pain can occur after routine dental treatments in which the dental pulp is
injured. To better understand pain chronicity after pulp injury, we assessed whether
dental pulp injury in mice causes changes to the sensory nervous system associated with
pathological pain. In some experiments, we compared findings after dental pulp injury to a
model of orofacial neuropathic pain, in which the mental nerve is injured. After
unilateral dental pulp injury, we observed increased expression of activating
transcription factor 3 (ATF3) and neuropeptide Y (NPY) mRNA and decreased tachykinin
precursor 1 gene expression, in the ipsilateral trigeminal ganglion. We also observed an
ipsilateral increase in the number of trigeminal neurons expressing immunoreactivity for
ATF3, a decrease in substance P (SP) immunoreactive cells, and no change in the number of
cells labeled with IB4. Mice with dental pulp injury transiently exhibit hindpaw
mechanical allodynia, out to 12 days, while mice with mental nerve injury have persistent
hindpaw allodynia. Mice with dental pulp injury increased spontaneous consumption of a
sucrose solution for 17 days while mental nerve injury mice did not. Finally, after dental
pulp injury, an increase in expression of the glial markers Iba1 and glial fibrillary
acidic protein occurs in the transition zone between nucleus caudalis and interpolaris,
ipsilateral to the injury. Collectively these studies suggest that dental pulp injury is
associated with significant neuroplasticity that could contribute to persistent pain after
of dental pulp injury.