Mast Cells and Angiogenesis in Oral Malignant and Premalignant Lesions

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

PCB association with model phospholipid bilayers

We compare the association of an ortho-substituted and a planar PCB (polychlorinated biphenyls PCB-52 and PCB-77, respectively) with single-component phospholipid bilayers terminated with phosphocholine headgroups. First, fluorescence correlation spectroscopy (FCS) studies of diffusion on supported fluid-phase DLPC show that the ortho-substituted PCB diffuses more slowly, indicating either complex formation or obstructed diffusion. Differential scanning calorimetry (DSC) of vesicles formed from DMPC shows that the gel-to-fluid phase transition temperature is lower for vesicles containing this ortho-substituted PCB. Atomic force microscopy (AFM) shows that, whereas supported bilayers of DMPC containing this ortho-substituted PCB display two melting points, bilayers containing the coplanar PCB display just a single melting point. A model is proposed in which the ortho-substituted PCB resides within the lipid tails of these phospholipid bilayers but the coplanar PCB associates preferentially with the headgroups. This model is consistent with the known membrane disruptive ability of the ortho substituted isomer