Molecular, cellular and behavioral changes associated with pathological pain signaling occur after dental pulp injury

作者：Lee Caroline S; Ramsey Austin A; De Brito Gariepy Helaine; Michot Benoit; Podborits Eugene; Melnyk Janet; Gibbs Jennifer L^*

来源：Molecular Pain, 2017, 13: 1744806917715173.

DOI：10.1177/1744806917715173

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 (DPI) in mice causes changes to the sensory nervous system associated with pathological pain. In some experiments we compared findings after DPI to a model of orofacial neuropathic pain, in which the mental nerve is injured (MNI). After unilateral DPI we observed increased expression of ATF3 and NPY mRNA and decreased TAC-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 immunoreactive cells, and no change in the number of cells labeled with IB4. Mice with DPI transiently exhibit hindpaw mechanical allodynia, out to 12 days, while mice with MNI have persistent hindpaw allodynia. Mice with DPI increased spontaneous consumption of a sucrose solution for 17 days while MNI mice did not. Finally, after DPI, an increase in expression of the glial markers Iba1 and GFAP occurs in the transition zone between nucleus caudalis and interpolaris, ipsilateral to the injury. Collectively these studies suggest that DPI is associated with significant neuroplasticity that could contribute to persistent pain after of dental pulp injury.

• 出版日期2017-6-5