Immunolocalization of tumor necrosis factor-α expressing cells in recurrent aphthous ulcer lesions (RAU)

: Tumor necrosis factor (TNF)‐α is a pro‐inflammatory cytokine and crucial mediator in many aspects of immunity. Although several studies have shown that recurrent aphthous ulcers (RAU) can be prevented by treatment that prevents the synthesis of endogenous TNF‐α, little is known about the location...

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Veröffentlicht in:Journal of oral pathology & medicine 2000-01, Vol.29 (1), p.19-25
Hauptverfasser: Natah, Sirajedin S., Häyrinen-Immonen, Ritva, Hietanen, Jarkko, Malmström, Maria, Konttinen, Yrjö T.
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Sprache:eng
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Zusammenfassung:: Tumor necrosis factor (TNF)‐α is a pro‐inflammatory cytokine and crucial mediator in many aspects of immunity. Although several studies have shown that recurrent aphthous ulcers (RAU) can be prevented by treatment that prevents the synthesis of endogenous TNF‐α, little is known about the location and distribution of TNF‐α‐expressing cells at disease sites. The aim of the present work is, therefore, to investigate TNF‐α and its cellular distribution in RAU lesions compared with those in induced oral traumatic ulcers (TUs). Twelve biopsies of RAU lesions of oral mucosa were obtained from 12 patients with RAU. They were compared to a control group consisting of ten samples of induced TUs. All samples were analyzed for TNF‐α expression by using monoclonal mouse anti‐human TNF‐α antibody in avidin‐biotin‐peroxidase complex (ABC) staining. Results were quantified by a semi‐automatic VIDAS image analysis system. TNF‐α immunoreactivity was contained mainly in monocyte/macrophages and lymphocytes within the mononuclear inflammatory infiltrates. TNF‐α was often seen in mast cells and vascular endothelial cells in connective tissue lateral to the inflammatory infiltrates. Interestingly, 32%–60% of the mononuclear cells were found to be TNF‐α immunoreactive in RAU lesions. TNF‐α‐containing cells were more numerous in aphthae (188±46 cells/0.2 mm2) compared with controls (52±14 cells/0.2 mm2, P
ISSN:0904-2512
1600-0714
DOI:10.1034/j.1600-0714.2000.290104.x