title: Apoptosis and cell cycle arrest in oral lichen planus Hypothesis on their possible influence on its malignant transformation.
abstract: The quantitative importance of cell cycle arrest and apoptosis mechanisms in oral lichen planus (OLP) was analysed in order to assess the cell response to T lymphocyte aggression and establish a hypothesis on the influence of these phenomena in the malignant transformation process. The TUNEL assay and immunohistochemical methods were used to detect caspase-3, bax, and p21 in 32 tissue samples of oral mucosa with OLP and in 20 samples of normal oral mucosa. Positivity for TUNEL, caspase-3 and p21 was significantly more frequent in cases than in controls (p<0.001). Both TUNEL and caspase-3 positivity was significantly greater in the basal versus suprabasal layer (p=0.004 and 0.052, respectively). The basal and suprabasal expression of p21 was significantly higher in cases with a more intense liquefaction degeneration (p<0.01). There was no significant difference in basal expression of bax between cases and controls. The quantitative importance of apoptosis was small in OLP. Epithelial cells attacked in OLP have a very low response to apoptosis and cell cycle arrest mechanisms, which may produce an epithelial substrate that favours malignant transformation.
authors.affiliation: Departamento de Estomatología, Facultad de Odontología, Universidad de Madrid, Complutense University, Madrid, Spain. cristinabascones_i@hotmail.com
authors.forename: C
authors.initials: C
authors.lastname: Bascones
authors.forename: M A
authors.initials: MA
authors.lastname: Gonzalez-Moles
authors.forename: G
authors.initials: G
authors.lastname: Esparza
authors.forename: M
authors.initials: M
authors.lastname: Bravo
authors.forename: A
authors.initials: A
authors.lastname: Acevedo
authors.forename: J A
authors.initials: JA
authors.lastname: Gil-Montoya
authors.forename: A
authors.initials: A
authors.lastname: Bascones
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis / Q000502:physiology*; D053148:Caspase 3; D020169:Caspases / Q000032:analysis; D002453:Cell Cycle / Q000502:physiology*; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000032:analysis; D004847:Epithelial Cells / Q000473:pathology / Q000502:physiology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D020287:In Situ Nick-End Labeling / Q000379:methods; D017676:Lichen Planus, Oral / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009061:Mouth Mucosa / Q000473:pathology / Q000503:physiopathology; D009062:Mouth Neoplasms / Q000473:pathology / Q000503:physiopathology*; D013601:T-Lymphocytes / Q000502:physiology; D051028:bcl-2-Associated X Protein / Q000032:analysis
chemical_list: C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D051028:bcl-2-Associated X Protein; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases