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Open Access Highly Accessed Research article

Sodium channel Nav1.7 immunoreactivity in painful human dental pulp and burning mouth syndrome

Kiran Beneng1, Tara Renton1, Zehra Yilmaz1, Yiangos Yiangou2 and Praveen Anand2*

Author Affiliations

1 Dental Institute, King's College London, Guy's Hospital, Oral Surgery Department, Great Maze Pond, London, UK

2 Peripheral Neuropathy Unit, Hammersmith Hospital, Imperial College London, London, UK

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BMC Neuroscience 2010, 11:71  doi:10.1186/1471-2202-11-71

Published: 8 June 2010

Abstract

Background

Voltage 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 Objectives

To study Nav1.7 levels in dental pulpitis pain, an inflammatory condition, and burning mouth syndrome (BMS), considered a neuropathic orofacial pain disorder.

Methods

Two 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.

Results

There 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.

Conclusion

Nav1.7 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.