ABSTRACT
Burning mouth syndrome (BMS) is characterized by oral dysesthesia, xerostomia and dysgeusia without visible alterations of oral mucosa. While secondary BMS results from an underlying general condition such as diabetes or iron deficiency, no causal disorder can be identified in primary BMS. The estimated prevalence is 1 - 2%, postmenopausal women are substantially more frequently affected than men. Current etiologic concepts assume a focal peripheral and central neuropathy. Only few controlled drug trials have yet been conducted. Thioctic acid appears the medical treatment of choice due to its comparatively good evidence for efficacy and low incidence of adverse reaction. Gabapentin and pregabalin are modern GABA-analogue anticonvulsants, which are also efficient in the treatment of peripheral neuropathies. Also conceptually appropriate for BMS treatment, current evidence for efficacy in BMS is insufficient. In two trials, local oral treatment with clonazepam has been beneficial in BMS. The efficacy of antidepressants is equivocal.
Subject(s)
Burning Mouth Syndrome/etiology , Glossitis/etiology , Stomatitis/etiology , Age Factors , Anticonvulsants/therapeutic use , Burning Mouth Syndrome/drug therapy , Burning Mouth Syndrome/epidemiology , Clonazepam/therapeutic use , Cranial Nerve Diseases/diagnosis , Cranial Nerve Diseases/drug therapy , Cross-Sectional Studies , Female , Glossitis/drug therapy , Glossitis/epidemiology , Humans , Incidence , Male , Middle Aged , Mouth/innervation , Mouth Mucosa/innervation , Sex Factors , Stomatitis/drug therapy , Stomatitis/epidemiology , Tongue/innervationABSTRACT
OBJECTIVE: An increased mucosal expression of transforming growth factor-beta (TGF-beta) and hepatocyte growth factor (HGF) has been reported in patients with active inflammatory bowel diseases (IBD) and in proximity to injured gastric and intestinal mucosal surfaces. The aim of this study was to measure systemic concentrations of TGF-beta and HGF and to assess their potential value to predict disease activity or severity of inflammation in patients with inflammatory bowel diseases. DESIGN AND METHODS: Plasma HGF and TGF-beta1 peptide levels were determined in 29 patients with ulcerative colitis, 45 patients with Crohn's disease and 28 healthy controls using commercial ELISA assays. Peptide levels were correlated with disease activity indices and various laboratory parameters. RESULTS: HGF and TGF-beta1 plasma levels were detected in all control and IBD subjects. Although a tendency towards increased HGF and TGF-beta1 peptide levels in IBD patients was observed, differences between groups were not significant In ulcerative colitis patients HGF plasma levels positively correlated with white blood cell counts and negatively correlated with serum albumin concentrations and haematocrit. In Crohn's disease patients, a positive correlation between TGF-beta and platelet count was observed. CONCLUSIONS: HGF and TGF-beta1 plasma concentrations are not significantly different in IBD and healthy control subjects. Stratification of IBD patients according to disease activity did not reveal any substantial differences, suggesting that HGF and TGF-beta plasma levels have no value in the assessment of disease activity or severity of inflammation in patients with IBD.
