Rat Odontoblasts May Use Glutamate to Signal Dentin Injury

Objectives: Accumulating evidence indicates that odontoblasts act as sensor cells, capable of triggering action potentials in adjacent axons of nociceptive neurons, suggesting a paracrine signaling via a currently-unknown mediator. Since glutamate can mediate signaling by non-neuronal cells, and peripheral axons may express glutamate receptors (GluR), we hypothesized that the expression of high levels of glutamate and of thermo- and heat receptors in odontoblasts, combined with an expression of GluR in adjacent pulpal axons, is the basis for odontoblastic sensory signaling
Methods: To test this hypothesis, we investigated the expression of glutamate, the thermo- and mechano-sensitive ion channels TRPV1, TRPA1, and TREK-1, and the glutamate receptor mGluR5, in normal rat dental pulp, and following dentin injury, by light- and electron-microscopic immunocytochemistry and quantitative analysis. We also examined the glutamate release from odontoblast in cell culture
Results: Immunoreactivity for TRPV1, TRPA1, and TREK-1 was prominent in odontoblasts, and they were also enriched with glutamate, at the level as high as in adjacent pulpal axons. These pulpal axons expressed mGluR5. Both the levels of glutamate in odontoblasts, and the expression of mGluR5 in nearby axons, were upregulated following dentin injury. The extracellular glutamate concentration was increased significantly after treating of odontoblast cell line with calcium permeable ionophore, suggesting glutamate release from odontoblasts
Conclusions: These findings lend morphological support to the hypothesis that odontoblasts use glutamate as a neuroactive substance to activate adjacent pulpal axons, and may contribute to dental pain and hypersensitivity