Expression of Nav1.9 Channels in Human Dental Pulp and Trigeminal Ganglion

The iontophoresis of lignocaine with epinephrine into carious dentine for pain control during cavity preparation in human molars

“…The most likely explanation for the greater resistance to anaesthesia of carious dentine compared with normal dentine is that, as a result of inflammatory changes in the pulp associated with the caries, Na+ channels of a type that are not sensitive to lignocaine were expressed in the nerve terminals and that these continued to support the propagation of action potentials despite the presence of the anaesthetic. [7][8][9][10][11] There are several other possible explanations: for example, the dentine under the caries is likely to have been less permeable to the lignocaine than the normal dentine due to the presence of secondary and tertiary dentine. The hydraulic conductance of dentine under a carious lesion has been shown to be much lower than that of normal dentine.…”

Quantitative Ultrastructural Analysis of the Neurofilament 200–Positive Axons in the Rat Dental Pulp

“…It is difficult to inhibit impulse transmission by using anesthesia on the inflamed pulp (30). Recent studies have reported that expression of tetrodotoxin-resistant voltage-gated Na channels NaV1.8 and NaV1.9 increase and voltage-gated K channel Kv1.4 decreases in the inflamed pulp, contributing to increase in neuronal excitability and sometimes to failure of local anesthetics (31)(32)(33). Application of blockers for these Na and K channels can also block inflammatory pain through blocking the propagation of nociceptormediated action potential.…”

Expression of Metabotropic Glutamate Receptor mGluR5 in Human Dental Pulp

“…The expression of TRPV1 in a large number of the mGluR5+ pulp afferents supports this notion and suggests that the increase in the TRPV1 response may be downstream from the activation of mGluR5 within the same axons. With the activation of mGluR5 at the site of inflammation, changes in the expression of various ion channels on pulpal afferents may lead to hyperexcitability of pulpal neurons and hyperalgesia during pulpal inflammation (21)(22)(23). mGluR5+ was expressed strongly by axons that branched extensively in the peripheral pulp, but the immunostaining was weaker and the immunopositive axons branched less in the central portion of coronal pulp and in the radicular pulp.…”