Apoptosis and cell cycle arrest in oral lichen planus hypothesis on their possible influence on its malignant transformation

被引:51
作者
Bascones, C
Gonzalez-Moles, MA
Esparza, G
Bravo, M
Acevedo, A
Gil-Montoya, JA
Bascones, A [1 ]
机构
[1] Univ Complutense Madrid, Fac Odontol, Dept Estamatol, E-28040 Madrid, Spain
[2] Univ Granada, Dept Oral Med, E-18071 Granada, Spain
[3] Univ Complutense Madrid, Dept Oral Med Dent, E-28040 Madrid, Spain
[4] Univ Granada, Dept Prevent & Community Dent, E-18071 Granada, Spain
[5] Dept Princesa Hosp, Dept Anatomopathol, Madrid, Spain
[6] Univ Granada, Dept Dent, E-18071 Granada, Spain
[7] Univ Complutense Madrid, Dept Periodont, E-28040 Madrid, Spain
关键词
oral lichen planus; apoptosis; TUNEL assay; Caspase-3; p21;
D O I
10.1016/j.archoralbio.2005.02.005
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
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. (c) 2005 Elsevier Ltd. ALL rights reserved.
引用
收藏
页码:873 / 881
页数:9
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