VEGF expression from human dysplastic or malignant oral epithelium may be related to mast cell density and the subsequent angiogenetic phenomena.

Vascular endothelial growth factor (VEGF) is an angiogenic cytokine and mast cells play a role in neoangiogenesis in various malignancies. The aim of the present study was to elucidate the role of VEGF and mast cells in the early stages of tumorigenesis in oral squamous cell carcinoma (OSCC). Immunohistochemistry was conducted to study VEGF expression and microvessel density (MVD) in 49 tissue samples, 31 OSCCs, 13 leukoplakias (8 with and 5 without dysplasia) and 5 samples from normal oral tissue. Counterstaining with tolouidine blue was conducted to reveal mast cells. The number of microvessels and mast cells were counted at the same optical field. A gradually increased VEGF expression was observed from normal oral epithelium to leukoplakia and OSCC. MVD was found to increase significantly between normal oral tissue and OSCC (p=0.000). The number of mast cells was found to increase significantly between normal oral tissue, dysplasia (p=0.012) and OSCC (p=0.000). In the early stages of tumorigenesis in OSCC, VEGF, which is secreted by the epithelium, is gradually increased immediately affecting the population of mast cells, which are then related to the increase of microvessels.

Mast cells and angiogenesis in oral malignant and premalignant lesions.

UNLABELLED: Mast cell contribution to neoangiogenesis during tumorigenesis in oral squamous cell carcinoma is not determined yet. OBJECTIVES: To associate numerical mast cell density (MCD) to numerical microvessel density (MVD) during the progression of oral leukoplakia without dysplasia and leukoplakia with dysplasia to squamous cell carcinoma (OSCC). MATERIALS AND METHODS: MVD was analysed immunohistochemically (mouse monoclonal anti-human CD34) in 49 paraffin-embedded specimens, 35 OSCCs, 9 leukoplakias and 5 normal oral tissues. Toluidine blue counterstaining revealed mast cells. MCD and MVD were assessed at the same optical field. RESULTS: MVD increased between: normal oral mucosa, dysplasia (p=0.004), OSCC (p=0.001), leukoplakia and OSCC (p=0.041). MCD increased between: normal oral mucosa, dysplasia (p=0.003), OSCC (p=0.000), leukoplakia and OSCC (p=0.007). MVD was found to depend on MCD (p=0.000) in a percent 28.3% (power curve fit model). CONCLUSIONS: Mast cells are attracted at the lesion site and may turn on an angiogenic switch during tumorigenesis in OSCC.