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Na(v)1.7 sodium channel expression in human lingual nerve neuromas
E V Bird1, P P Robinson, F M Boissonade
1Department of Oral and Maxillofacial Medicine and Surgery, School of Clinical Dentistry, University of Sheffield, Claremont Crescent, Sheffield S10 2TA, United Kingdom. e.v.bird@sheffield.ac.uk
Archives of Oral Biology
|January 11, 2007
Summary
Sodium channel Na(v)1.7 is present in damaged human lingual nerves after dental surgery. Its expression alone does not appear to cause neuropathic pain, suggesting complex factors are involved.
Area of Science:
- Neuroscience
- Oral Surgery
- Pain Research
Background:
- Peripheral trigeminal nerve damage during lower third molar extraction can lead to persistent chronic pain.
- The underlying mechanisms of this neuropathic pain are unclear, and effective treatments are lacking.
Purpose of the Study:
- To investigate the expression of the sodium channel subtype Na(v)1.7 in damaged human lingual nerves.
- To determine if Na(v)1.7 expression correlates with symptoms of dysesthesia.
Main Methods:
- Analyzed 11 neuromas-in-continuity (NICs) and 11 nerve-end neuromas (NENs) from patients undergoing lingual nerve repair.
- Utilized indirect immunofluorescence and image analysis to quantify Na(v)1.7 expression.
- Categorized specimens based on patient-reported symptoms of pain, tingling, or discomfort.
Main Results:
- Confirmed Na(v)1.7 expression in human lingual nerve neuromas.
- Found no direct correlation between Na(v)1.7 levels and dysesthesia symptoms.
- Observed an inverse correlation between Na(v)1.7 and macrophage expression in NICs, and a direct correlation with axonal apposition in symptomatic NICs.
Conclusions:
- Na(v)1.7 expression alone does not appear to be the primary driver of painful dysesthesia.
- Neuropathic pain development likely involves intricate interactions, including alterations in nerve ultrastructure and ion channel density.
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