Journal of cutaneous pathology · 2008
Desmocollin expression in oral atrophic lichen planus correlates with clinical behavior and DNA content.
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Mattila Riikka, Alanen Kalle, Syrjänen Stina
Аннотация
BACKGROUND: Oral lichen planus (OLP) is a chronic mucocutaneous inflammatory disease, with some tendency toward malignant transformation. Markers are needed to identify the lesions at risk.
METHODS: A series of 82 biopsies from 70 patients with atrophic OLP was analyzed for desmocollin-1, E-cadherin, cyclin-dependent kinase 1 (cdk-1) and Rad-51 expression using immunohistochemistry and static DNA cytometry, with particular reference to clinical outcome.
RESULTS: Desmocollin-1 and E-cadherin expression were each detected in 24.4% (20/82) of the samples. Of the positive samples, only eight specimens expressed both desmocollin-1 and E-cadherin. Strong desmocollin-1 and E-cadherin expression was found in 8.5% and 3.7% of OLP biopsies, respectively. Desmocollin-1 expression increased the risk of dysplasia 31.8-fold (95% confidence intervals (CI) 3.6-280.9; p = 0.0001), while E-cadherin was significantly related to cancer (odds ratio (OR) = 5.13; 95% CI 3.3-8.1; p = 0.001). In univariate survival analysis, desmocollin-1 was a significant predictor of both cancer (log-rank test; p = 0.033) and dysplasia (p = 0.0001), while E-cadherin predicted the development of cancer (p = 0.0001). Neither cdk-1 nor Rad-51 had any predictive value. Importantly, desmocollin-1 retained its value as the only independent predictor of dysplasia in the multivariate (Cox) model (adjusted Hazard Ratio (HR) = 44.13; 95% CI 3.7-525.6).
CONCLUSIONS: In atrophic OLP, desmocollin-1 is a powerful predictor of an important intermediate endpoint marker (dysplasia) in the causal pathway toward oral cancer.
METHODS: A series of 82 biopsies from 70 patients with atrophic OLP was analyzed for desmocollin-1, E-cadherin, cyclin-dependent kinase 1 (cdk-1) and Rad-51 expression using immunohistochemistry and static DNA cytometry, with particular reference to clinical outcome.
RESULTS: Desmocollin-1 and E-cadherin expression were each detected in 24.4% (20/82) of the samples. Of the positive samples, only eight specimens expressed both desmocollin-1 and E-cadherin. Strong desmocollin-1 and E-cadherin expression was found in 8.5% and 3.7% of OLP biopsies, respectively. Desmocollin-1 expression increased the risk of dysplasia 31.8-fold (95% confidence intervals (CI) 3.6-280.9; p = 0.0001), while E-cadherin was significantly related to cancer (odds ratio (OR) = 5.13; 95% CI 3.3-8.1; p = 0.001). In univariate survival analysis, desmocollin-1 was a significant predictor of both cancer (log-rank test; p = 0.033) and dysplasia (p = 0.0001), while E-cadherin predicted the development of cancer (p = 0.0001). Neither cdk-1 nor Rad-51 had any predictive value. Importantly, desmocollin-1 retained its value as the only independent predictor of dysplasia in the multivariate (Cox) model (adjusted Hazard Ratio (HR) = 44.13; 95% CI 3.7-525.6).
CONCLUSIONS: In atrophic OLP, desmocollin-1 is a powerful predictor of an important intermediate endpoint marker (dysplasia) in the causal pathway toward oral cancer.