As shown in Table 1, the peripheral epithelial odontogenic cells

As shown in Table 1, the peripheral epithelial odontogenic cells of all studied tumours were positive for podoplanin while the central ones were negative. The exceptions were plexiform ameloblastoma, adenomatoid odontogenic tumour and ameloblastic fibroma. The plexiform ameloblastoma resembles the tooth germ in the dental lamina stage,17 when the differentiation process of the odontogenic epithelium has not initiated.

This lack of cellular differentiation may reflect the homogeneity of podoplanin expression found in those benign epithelial tumours, confirming previous results obtained by other authors.6 and 14 All nine adenomatoid odontogenic tumours showed membranous and cytoplasmic podoplanin expression in the central epithelial odontogenic cells, including the duct-like structures (Fig. 1C). These results are contradicting the previous12 and 13 reports, which described negative podoplanin immunostaining in superficial and luminal epithelia of duct-like structures of only two adenomatoid odontogenic tumours. The explanation for this apparent discrepancy may be associated with the proliferative activity of the epithelial cells with duct-like appearance within the benign odontogenic tumour. However, these results demand further confirmation by other series of representative adenomatoid odontogenic tumour with characteristic cellular duct-like pattern. In ameloblastic

fibromas, moderate podoplanin expression by reticulum stellate-like cells was observed, which might indicate cellular activity of these selected cells. The find protocol Glutathione peroxidase ectomesenchymal cells of mixed odontogenic tumour presented absent or weak immunoreaction for anti-podoplanin antibody, except for odontoblasts of ameloblastic fibro-odontoma. Although podoplanin distribution in benign odontogenic tumours has been recently identified,5, 6, 8, 12,

13 and 14 its precise biologic relevance and significance in tumoral or even in normal odontogenic tissues remains source of debate. The podoplanin expression accelerates cell motility in vitro and induces cell invasion and metastasis of the malignant epithelial tumour. 18 Furthermore, overexpression of podoplanin promotes the formation of elongated cell extensions and increases adhesion and migration of MDCK cells 3 and suggests a role for podoplanin in cytoskeletal reorganization. In ameloblastic fibro-odontoma, secreting ameloblasts expressed podoplanin while in non-secreting and reduced ameloblasts this immunoreaction was absent. Our findings are in line with González-Alva et al.’s 5 and we agree with them when they suggest that podoplanin, with its ability to remodel the actin cytoskeleton and form filopodia, is involved in the movement of ameloblasts away from odontoblasts and vice versa. Once enamel deposition has been completed and the ameloblasts no longer move, they lose their podoplanin expression.

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