Journal
ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTOLOGY
Volume 110, Issue 3, Pages 351-356Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.tripleo.2009.08.013
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Funding
- BONFOR research foundation of the Medical Faculty of the University of Bonn
- Deutsche Forschungsgemeinschaft [KFO 208]
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Objective. The aim of this study was to investigate the expression pattern of oncogenes, antimicrobial peptides, and genes involved in inflammation in leukoplakia of the oral cavity compared with healthy gingiva. Study design. Biopsies of healthy gingiva (n = 20) and leukoplakia (n = 20), were obtained during routine surgical procedures. RNA was extracted according to standard protocols. Transcript levels of alpha-defensin (DEFA) 1/3, DEFA-4, S100-A7, deleted-in-oral-cancer (Doc) 1, interleukin (IL) 1 beta, IL-6, IL-8, IL-10, tumor necrosis factor (TNF) alpha, cyclooxygenase (Cox) 2, epidermal growth factor (EGF), keratinocyte growth factor (KGF), transforming growth factor (TGF) beta 1, TGF-alpha, collagen-IA1 (Col-1), and tenascin-c were analyzed by real-time reverse-transcription polymerase chain reaction. The proteins encoded by the different genes were visualized by immunostaining. Results. Compared with healthy gingiva (set as 1), there was an increased gene expression of DEFA-4 (179.2-fold), S100-A7 (25.4-fold), EGF (24.8-fold), TGF-beta 1 (25.2-fold), and tenascin-c (34.3-fold) in oral leukoplakia. The expression of IL-1 beta and Doc-1 was decreased (0.01-fold and 0.2-fold, respectively). Conclusions. The combination of an increased expression of the antimicrobial peptide DEFA-4, the oncogene S100-A7, EGF, and tenascin-c, and a decreased Doc-1 expression in oral leukoplakia might characterize its potency of malignant transformation. Chronic inflammation seems not to be involved in the development of this lesion. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2010;110:351-356)
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