Peripheral mechanisms of odontogenic pain

By Henry M, Hargreaves K

Date: 01/2007
Journal: Dental Clinics

Purpose:

Discuss peripheral mechanisms of odontogenic pain

Results:

Function: allow peripheral terminals of nociceptors to detect & respond to noxious signals in their environment.

1.G-protein-coupled receptors (GPCRs)neuropeptide binds to GPCR, G protein (Gαi/o, Gαq, Gαs) activation.

a.Gαi/o = nerve activity inhibition. Neuropeptides: somatostatin, NPY, opioids.

b.Gαq = activation of phospholipase C & protein kinase C, sensitization of TRPV1 receptor, ↑ expression of bradykinin & CGRP , ↑ odontogenic pain. Neuropeptides: SP neuropeptide, bradykinin

c.Gαs = nerve activity activation = odontogenic pain. Neuropeptides: prostaglandins, CGRP.

2.Voltage gated ion channels essential in the formation & propagation of action potentials.

a.Na channels most focused. Activation à ↑ neuronal excitability in inflammatory & pain conditions.

b.K channels terminate nerve activity. Anticonvulsants have been shown to be effective in treating neuropathic and chronic pain. Thus, this could be a new drug target.

c.Ca channels play an important role in vesicle fusion and release of neurotransmitter during synaptic transmission. Mice lacking Cav2.2 channel show ↓ inflammatory & neuropathic pain behaviors. Pregabalin & gabapentin bind to α2-δ type 1 subunits on Ca channels as an analgesic.

d.Pulp of painful teeth show a “remodeling of Na channels within axons.” Expression of isoforms Nav 1.7 and Nav 1.8 is greater near areas of inflammation in painful teeth. They are also located at the nodes of Ranvier, which can lead to spontaneous activity of myelinated fibers (e.g., sharp, shooting pain).