Abstract

BackgroundVoltage gated sodium channels Nav1.7 are involved in nociceptor nerve action potentials and are known to affect pain sensitivity in clinical genetic disorders.Aims and ObjectivesTo study Nav1.7 levels in dental pulpitis pain, an inflammatory condition, and burning mouth syndrome (BMS), considered a neuropathic orofacial pain disorder.MethodsTwo groups of patients were recruited for this study. One group consisted of patients with dental pulpitis pain (n = 5) and controls (n = 12), and the other patients with BMS (n = 7) and controls (n = 10). BMS patients were diagnosed according to the International Association for the Study of Pain criteria; a pain history was collected, including the visual analogue scale (VAS). Immunohistochemistry with visual intensity and computer image analysis were used to evaluate levels of Nav1.7 in dental pulp tissue samples from the dental pulpitis group, and tongue biopsies from the BMS group.ResultsThere was a significantly increased visual intensity score for Nav1.7 in nerve fibres in the painful dental pulp specimens, compared to controls. Image analysis showed a trend for an increase of the Nav1.7 immunoreactive % area in the painful pulp group, but this was not statistically significant. When expressed as a ratio of the neurofilament % area, there was a strong trend for an increase of Nav1.7 in the painful pulp group. Nav1.7 immunoreactive fibres were seen in abundance in the sub-mucosal layer of tongue biopsies, with no significant difference between BMS and controls.ConclusionNav1.7 sodium channel may play a significant role in inflammatory dental pain. Clinical trials with selective Nav1.7 channel blockers should prioritise dental pulp pain rather than BMS.

Highlights

  • Voltage gated sodium channels Nav1.7 are involved in nociceptor nerve action potentials and are known to affect pain sensitivity in clinical genetic disorders

  • Patients scheduled for dental extraction, and those diagnosed with burning mouth syndrome (BMS), at Kings College London Dental Institute, London, were included in this study

  • A subset of nerve fibres was immunostained with the Nav1.7 antibody (Figure 1a, c) in both non-painful and painful pulp groups

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Summary

Introduction

Voltage gated sodium channels Nav1.7 are involved in nociceptor nerve action potentials and are known to affect pain sensitivity in clinical genetic disorders. Orofacial pain conditions are common and debilitating. Few studies have investigated the role of novel key pain ion channels, such as Nav1.7, in these conditions. Such studies may lead to the development of more effective treatments. Dental pain is the most common symptom of diseased tooth pulp, often as a result of coronal caries of the tooth [1]. Strong correlations have been reported between the afferent discharge frequency of human pulp nociceptors and pain levels [6]

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