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Updated: May 30, 2026

Taste Exam: A Brief and Validated Test
Published on: August 17, 2018
Morphological evaluation of tongue mucosa in burning mouth syndrome
Andrea Sardella1, Alice Gualerzi, Giovanni Lodi
1Università di Milano, Dipartimento di Medicina, Chirurgia e Odontoiatria, Unità di Medicina Orale, Patologia Orale e Odontoiatria Geriatrica, Italy. andrea.sardella@unimi.it
Objective:
The aim of the present study was to perform a morphological evaluation by immunofluorescence of biomarkers of keratinocyte intercellular adhesion, and of differentiation in the tongue mucosa of burning mouth syndrome patients (BMS), compared with a control group.
Design:
A prospective blinded evaluation of tongue mucosal specimens processed for light microscopy was performed. Intercellular adhesion was evaluated by investigating the expression of desmoglein 1, desmoglein 3, and of occludin. Keratin 10 and keratin 14 (markers of epithelial differentiation) were also evaluated, as keratin 16 (marker for activated keratinocytes after epithelial injury). Apoptotic cascade was investigated by p53 and activated caspase-3 expression. The basal membrane integrity was analysed through laminin immunoreactivity.
Results:
In both groups, a preserved three-dimensional architecture of the tongue was observed. Desmoglein 1 and desmoglein 3 epithelial distributions were similar in the desmosomes of patients and control subjects. Again, keratin 10 immunoreactivity and distribution pattern of keratin 14 in the epithelial compartment was similar in both groups. In control samples, keratin 16 immunoreactivity was scant throughout the epithelium with a punctuate and scattered cytoplasmic labelling. In contrast, in all BMS patients keratinocyte cytoplasm was homogeneously labelled for keratin 16, with a more intense staining than controls. Furthermore, keratin 16 staining progressively decreased proceeding towards the most superficial epithelial layers.
Conclusions:
The results of this study are consistent with and support the clinically normal features of oral mucosa in BMS, and suggest that keratin 16 may be involved in the cell mechanisms underlying the syndrome occurrence.
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