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Survival signalling in keratinocytes of erythematous oral lichen planus
Author(s) -
Karatsaidis Andreas,
Hayashi Katsuhiko,
Schreurs Olav,
Helgeland Kristen,
Schenck Karl
Publication year - 2007
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.2007.00519.x
Subject(s) - keratinocyte , oral lichen planus , apoptosis , programmed cell death , fadd , epithelium , caspase , caspase 8 , pathology , necrosis , oral mucosa , biology , tumor necrosis factor alpha , immunology , cancer research , medicine , cell culture , biochemistry , genetics
Background: Keratinocytes in oral lichen (OL) planus have been shown to be exposed to potentially cell death‐inducing factors such as tumour necrosis factor‐ α (TNF‐ α ) and FasL, produced by the cells of the inflammatory infiltrate and by the keratinocytes themselves. Mostly, however, the lesions do not show ulceration, the clinical manifestation of substantial keratinocyte death. The aim of this study was to find support for the contention that there is activation of protecting anti‐apoptotic mechanisms in keratinocytes in a form of chronic OL (erythematous OL; ERY OL), simultaneously with the pathological cell death signals. Methods: Biopsies from patients with normal oral mucosa (NOM) or with ERY OL were compared by immunohistological staining. Results: In ERY OL keratinocytes, both the pro‐apoptotic FADD and the anti‐apoptotic molecules p‐IKK, NF‐ κ B/p50, FLIP L , cIAP‐1 and cIAP‐2 were strongly upregulated when compared with NOM. There were no significant differences in the staining patterns for active caspase‐3 and caspase‐8 with only few positive cells for both enzymes. Conclusions: The presently observed marked increase in expression of anti‐apoptotic molecules in ERY OL epithelium may counteract the pro‐apoptotic assault and rescue the epithelium from rampant cell death and thereby clinical ulceration.