title: Cell proliferation activity and the expression of cell cycle regulatory proteins in oral lichen planus.
abstract: BACKGROUND
  In oral lichen planus (OLP), destruction of the basal cell layer, which is one of the characteristic histological features, is seen and many changes in cell proliferation, cell repair and cell death occur in the injured mucosal epithelium.
  
  
  METHODS
  We studied mucosal tissues from 19 patients of OLP and 10 controls, with immunohistochemistry for Ki-67, p53, cyclin dependent kinase inhibitors (CDKI) and cyclins. Mitotic count was calculated. TUNEL assay was also performed for evaluation of apoptotic cell death.
  
  
  RESULTS
  Mitotic count, Ki-67 and cyclin D1 labeling indices in the basal and parabasal layers of OLP mucosa were elevated in comparison with those of controls. p53, p21Cip1 and TUNEL indices of OLP mucosa were also increased.
  
  
  CONCLUSIONS
  These complex changes, which concomitantly occur in the injured mucosal epithelium, could contribute to the development and maintenance of characteristic mucosal epithelial architectures seen in OLP.
authors.affiliation: Department of Oral and Maxillofacial Surgery, Yokohama City University School of Medicine, Yokohama, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Hirota
authors.forename: Takaaki
authors.initials: T
authors.lastname: Ito
authors.forename: Koji
authors.initials: K
authors.lastname: Okudela
authors.forename: Ryoichi
authors.initials: R
authors.lastname: Kawabe
authors.forename: Takuya
authors.initials: T
authors.lastname: Yazawa
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Hayashi
authors.forename: Yukio
authors.initials: Y
authors.lastname: Nakatani
authors.forename: Kiyohide
authors.initials: K
authors.lastname: Fujita
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Kitamura
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000502:physiology; D015153:Blotting, Western; D018797:Cell Cycle Proteins / Q000032:analysis* / Q000235:genetics; D016923:Cell Death / Q000502:physiology; D002455:Cell Division / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D019938:Cyclin D1 / Q000032:analysis; D019927:Cyclin E / Q000032:analysis; D050759:Cyclin-Dependent Kinase Inhibitor p21; D050760:Cyclin-Dependent Kinase Inhibitor p27; D018844:Cyclin-Dependent Kinases / Q000037:antagonists & inhibitors; D016213:Cyclins / Q000032:analysis; D004791:Enzyme Inhibitors / Q000032:analysis; D004848:Epithelium / Q000378:metabolism / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D019394:Ki-67 Antigen / Q000032:analysis; D017676:Lichen Planus, Oral / Q000235:genetics / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D008938:Mitosis; D009061:Mouth Mucosa / Q000378:metabolism / Q000473:pathology; D018709:Statistics, Nonparametric; D016159:Tumor Suppressor Protein p53 / Q000032:analysis; D025521:Tumor Suppressor Proteins / Q000032:analysis
chemical_list: C493956:CDKN1A protein, human; D018797:Cell Cycle Proteins; D019927:Cyclin E; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D004791:Enzyme Inhibitors; D019394:Ki-67 Antigen; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; D019938:Cyclin D1; D050760:Cyclin-Dependent Kinase Inhibitor p27; D018844:Cyclin-Dependent Kinases