title: Activation of nuclear factor-kappa B correlates with tumor necrosis factor-alpha in oral lichen planus: a clinicopathologic study in atrophic-erosive and reticular form.
abstract: BACKGROUND
  Nuclear factor-kappa B (NF-kappaB) is believed to be involved in the pathogenesis of various inflammatory diseases, including oral lichen planus (OLP). The objective of the present study was to investigate the possible relationship between NF-kappaB activation and expression of tumor necrosis factor-alpha (TNF-alpha) in OLP and their expression pattern in relation to several clinical features.
  
  
  METHODS
  Thirty OLP cases were divided into atrophic-erosive form (14 cases) and reticular form (16 cases) according to their clinical manifestations. The expression of NF-kappaB p65 and TNF-alpha of both two groups were investigated by immunohistochemical staining, and the percentage of positive cells was calculated in each case. Biopsies of 10 normal oral mucosa (NOM) also underwent the same procedure as controls.
  
  
  RESULTS
  Nuclear factor-kappa B p65 nuclear staining was found in nuclei of basal and suprabasal epithelial keratinocytes in OLP, however, no positive staining was found in NOM. Positive TNF-alpha staining was detected in cytoplasm of basal epithelial keratinocytes in OLP, and only scattered staining was detected in NOM. Expression of NF-kappaB p65 and TNF-alpha were significantly different with respect to clinical forms and lesion sites (P < 0.05), except for genders (P > 0.05) in 30 OLP cases. NF-kappaB nuclear staining positively correlated (r = 0.676, P < 0.01) with TNF-alpha overexpression in OLP.
  
  
  CONCLUSIONS
  Nuclear factor-kappa B activation and its correlation with overexpression of TNF-alpha may play an important role in pathogenesis of OLP. There might be a positive regulatory loop between NF-kappaB and TNF-alpha, which may contribute to inflammation in OLP; NF-kappaB may also protect epithelial keratinocytes from excessive apoptosis.
authors.affiliation: Department of Oral Medicine, School and Hospital of Stomatology, Wuhan University, Wuhan 430079, China. gordonzhou@tom.com
authors.forename: Gang
authors.initials: G
authors.lastname: Zhou
authors.forename: Kun
authors.initials: K
authors.lastname: Xia
authors.forename: Ge-fei
authors.initials: GF
authors.lastname: Du
authors.forename: Xin-ming
authors.initials: XM
authors.lastname: Chen
authors.forename: Xue-yi
authors.initials: XY
authors.lastname: Xu
authors.forename: Rui
authors.initials: R
authors.lastname: Lu
authors.forename: Hong-mei
authors.initials: HM
authors.lastname: Zhou
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D004847:Epithelial Cells / Q000166:cytology / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology / Q000502:physiology; D006801:Humans; D015603:Keratinocytes / Q000276:immunology / Q000378:metabolism*; D017676:Lichen Planus, Oral / Q000145:classification / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D051996:Transcription Factor RelA / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D055815:Young Adult
chemical_list: D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha