Heat shock protein expression in oral lichen planus.
To assess the potential role of heat shock protein (HSP) in the pathogenesis of oral lichen planus (OLP), sections of OLP, normal oral mucosa, non-specific oral ulceration (NSOU) and dysplastic OLP were assessed for HSP expression using avidin-biotin complex immunohistochemistry with an anti-HSP 70 polyclonal antibody. There were statistically significant differences in both the vertical and horizontal staining distribution when other groups were compared with the OLP group (p < 0.01). Using microdensitometry, the mean staining intensity in OLP, dysplastic OLP and NSOU was elevated in comparison with normal oral mucosa (p < 0.001). In a standard tritiated thymidine uptake assay, lymphocytes extracted from nine OLP lesions demonstrated significant proliferation when stimulated with purified protein derivative (PPD), of which HSP is a major constituent, with stimulation indices ranging from 2 to 132. These results are consistent with the hypothesis that, in OLP patients, diverse exogenous agents may cause upregulated expression of HSP by oral mucosal keratinocytes. A reaction of cytotoxic T lymphocytes to these activated keratinocytes may then result in the tissue destruction which is characteristic of OLP lesions.
Sugerman
P B
PB
Department of Dentistry, University of Queensland, Brisbane, Australia.
Savage
N W
NW
Xu
L J
LJ
Walsh
L J
LJ
Seymour
G J
GJ
D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D016022:Case-Control Studies; D003720:Densitometry; D005260:Female; D018840:HSP70 Heat-Shock Proteins / Q000096:biosynthesis*; D006801:Humans; D007124:Immunoenzyme Techniques; D015603:Keratinocytes / Q000378:metabolism; D016018:Least-Squares Analysis; D017676:Lichen Planus, Oral / Q000209:etiology* / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009061:Mouth Mucosa / Q000276:immunology / Q000378:metabolism; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D015854:Up-Regulation
D018840:HSP70 Heat-Shock Proteins