title: Vanilloid receptor 1 (TRPV1) expression in lingual nerve neuromas from patients with or without symptoms of burning pain.
abstract: The lingual nerve, a peripheral branch of the trigeminal nerve, can be damaged during the surgical removal of lower third molar teeth. This damage can lead to the development of dysaesthesia, with some patients complaining of burning pain. We investigated the hypothesis that vanilloid receptor 1 (TRPV1), a transducer of noxious heat stimuli, was involved in the development of this burning pain. Neuroma specimens were obtained from patients undergoing microsurgical repair of a damaged lingual nerve. Repair was undertaken where there was little evidence of spontaneous recovery, 7-41 months after the initial injury. Preoperatively the incidence of dysaesthesia was determined by reported symptoms and using visual analogue scales (VAS) for pain, tingling and discomfort. Nine neuromas were studied from patients with burning dysaesthesia and six from patients with a sensory deficit but no dysaesthesia. Indirect immunofluorescence for protein gene product (PGP) 9.5 and TRPV1 was used to quantify the percentage area of PGP 9.5 positive neuronal tissue that also expressed TRPV1. The results showed no significant difference between the mean percentage area of TRPV1 expression in neuromas from patients with or without burning dysaesthesia. Furthermore, there was no correlation between TRPV1 expression and the VAS scores for pain, tingling or discomfort. However, if data from all patients was pooled, there was a negative correlation between the level of TRPV1 expression and the time after initial injury. These data do not rule out involvement of TRPV1 in the aetiology of burning dysaesthesia following lingual nerve injury but suggest that TRPV1 at the injury site does not play a primary role.
authors.affiliation: Department of Oral and Maxillofacial Surgery, School of Clinical Dentistry, University of Sheffield, Claremont Crescent, Sheffield, S10 2TA, UK. j.biggs@sheffield.ac.uk
authors.forename: James E
authors.initials: JE
authors.lastname: Biggs
authors.forename: Julian M
authors.initials: JM
authors.lastname: Yates
authors.forename: Alison R
authors.initials: AR
authors.lastname: Loescher
authors.forename: Nick M
authors.initials: NM
authors.lastname: Clayton
authors.forename: Fiona M
authors.initials: FM
authors.lastname: Boissonade
authors.forename: Peter P
authors.initials: PP
authors.lastname: Robinson
mesh_terms: D000328:Adult; D002908:Chronic Disease; D005260:Female; D006801:Humans; D008036:Lingual Nerve / Q000378:metabolism* / Q000503:physiopathology; D061222:Lingual Nerve Injuries; D008297:Male; D008875:Middle Aged; D008964:Molar, Third / Q000033:anatomy & histology; D009437:Neuralgia / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D009463:Neuroma / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D009619:Nociceptors / Q000378:metabolism; D019647:Oral Surgical Procedures / Q000009:adverse effects; D010148:Intractable Pain / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D010292:Paresthesia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D011183:Postoperative Complications / Q000209:etiology / Q000503:physiopathology; D050916:TRPV Cation Channels / Q000378:metabolism*; D020433:Trigeminal Nerve Diseases / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D050916:TRPV Cation Channels; C494482:TRPV1 protein, human