Abstract

BackgroundTo explore the hypothesis that burning mouth syndrome (BMS) probably is a neuropathic pain condition, thermal and mechanical sensory and pain thresholds were tested and compared with age- and gender-matched control participants using a standardized battery of psychophysical techniques.MethodsTwenty-five BMS patients (men: 8, women: 17, age: 49.5 ± 11.4 years) and 19 age- and gender-matched healthy control participants were included. The cold detection threshold (CDT), warm detection threshold (WDT), cold pain threshold (CPT), heat pain threshold (HPT), mechanical detection threshold (MDT) and mechanical pain threshold (MPT), in accordance with the German Network of Neuropathic Pain guidelines, were measured at the following four sites: the dorsum of the left hand (hand), the skin at the mental foramen (chin), on the tip of the tongue (tongue), and the mucosa of the lower lip (lip). Statistical analysis was performed using ANOVA with repeated measures to compare the means within and between groups. Furthermore, Z-score profiles were generated, and exploratory correlation analyses between QST and clinical variables were performed. Two-tailed tests with a significance level of 5 % were used throughout.ResultsCDTs (P < 0.02) were significantly lower (less sensitivity) and HPTs (P < 0.001) were significantly higher (less sensitivity) at the tongue and lip in BMS patients compared to control participants. WDT (P = 0.007) was also significantly higher at the tongue in BMS patients compared to control subjects . There were no significant differences in MDT and MPT between the BMS patients and healthy subjects at any of the four test sites. Z-scores showed that significant loss of function can be identified for CDT (Z-scores = −0.9±1.1) and HPT (Z-scores = 1.5±0.4). There were no significant correlations between QST and clinical variables (pain intensity, duration, depressions scores).ConclusionBMS patients had a significant loss of thermal function but not mechanical function, supporting the hypothesis that BMS may be a probable neuropathic pain condition. Further studies including e.g. electrophysiological or imaging techniques are needed to clarify the underlying mechanisms of BMS.

Highlights

  • To explore the hypothesis that burning mouth syndrome (BMS) probably is a neuropathic pain condition, thermal and mechanical sensory and pain thresholds were tested and compared with age- and gender-matched control participants using a standardized battery of psychophysical techniques

  • In this study performed in Chinese patients fulfilling the ICHD-3 criteria for BMS, thermal and mechanical quantitative sensory testing (QST) were measured based on previous experience, i.e., we focused on 4 thermal and 2 mechanical psychophysical tests instead of the complete DFNS protocol which includes a total of 13 different tests

  • We found that BMS patients had lower cold detection and pain thresholds and higher warm detection and pain thresholds at the tongue and lip than healthy participants

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Summary

Introduction

To explore the hypothesis that burning mouth syndrome (BMS) probably is a neuropathic pain condition, thermal and mechanical sensory and pain thresholds were tested and compared with age- and gender-matched control participants using a standardized battery of psychophysical techniques. Burning mouth syndrome (BMS) is characterized by the presence of a persistent burning sensation of the oral mucosa in the absence of clinical or laboratory data to explain these symptoms [1, 2]. It is a chronic orofacial pain condition, unaccompanied by obvious mucosal lesions or other evident clinical signs upon examination [1–3]. Several studies have been performed to examine the possible underlying mechanisms of BMS [7–9]. Neurophysiological studies have elucidated that several neuropathic mechanisms, mostly subclinical, act at different levels of the neuraxis and may contribute to the pathophysiology of primary BMS [3, 6]. All these research methods have been applied in the study of BMS patients, which, together with more rigorous clinical diagnostic definitions, has resulted in progress in the understanding of the pathophysiological mechanisms underlying BMS [3]

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