ArticleJournal of oral & maxillofacial research
Fibrosis in Oral Carcinoma and Leukoplakia: an Immunohistochemical Study.
Article in Journal of oral & maxillofacial research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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Authors and funding
6 authors.
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Abstract
Objectives: The objective of this retrospective study was to evaluate clinicopathologic profile and collagen type I expression in oral leukoplakia and oral squamous cell carcinoma to elucidate stromal alterations in malignant transformation. Material and Methods: The sample consisted of 40 cases, of which 20 oral leukoplakia (OL) were classified according to World Health Organization and binary systems for grading oral epithelial dysplasia (OED) as well as 20 oral squamous cell carcinoma (OSCC), moderately or poorly differentiated. Type I collagen was analysed by immunohistochemistry, Fisher's exact test and chi-square test evaluated the clinical data. One-way ANOVA and Tukey's test were applied to analyse type I collagen expression between groups. Associations between data were analysed by two-way ANOVA with Sidak's multiple comparison test. Results: Men were most affected with OSCC (90%) and 60% of OL were in women (P = 0.0022). Type I collagen expression was higher in mild (P = 0.04) and moderate (P = 0.03) OED than moderately differentiated OSCC. Severe OED had a lower expression when compared with moderate OED (P = 0.01) and well differentiated OSCC (P = 0.02). The binary system showed that low-risk had more collagen expression than high-risk (P = 0.03) and severe OED (P = 0.03). Conclusions: The binary system allows more effective correlations to be established between stromal changes and oral epithelial dysplasia. The higher expression of collagen in the benign lesions may represent changes in the microenvironment that will favour the process of epithelial transformation and the establishment of a more aggressive disease.
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