to stroma, suggesting a role for invadopodia in local invasiveness. At ameloblastoma invasion sites cortactin would recruit MT-MMP, inducing focal degradation in stroma. Correlating cortactin and MT1-MMP presence in ameloblastoma with our previous findings on MMPs and growth factors, 3,4 we suggest that cortactin, MT1-MMP, proteases and growth factors would combine forces to regulate ameloblastoma invasiveness.We demonstrated cortactin and MT1-MMP expression in ameloblastoma. These proteins were increased significantly compared to CCOT, a non-invasive odontogenic tumour. Our results indicate that invadopodia proteins cooperate to regulate ameloblastoma invasion. acknowledgements This investigation was supported by the State of São Paulo Research Foundation (FAPESP grants 2006 ⁄ 57079-4 and 2008 ⁄ 57103-8) and the Brazilian National Council for
Described for the first time in 1971, Schimke immuno-osseous dysplasia (SIOD) is an autosomal-recessive multisystem disorder that is caused by bi-allelic mutations of SMARCAL1, which encodes a DNA annealing helicase. To define better the dental anomalies of SIOD, we reviewed the records from SIOD patients with identified bi-allelic SMARCAL1 mutations, and we found that 66.0% had microdontia, hypodontia, or malformed deciduous and permanent molars. Immunohistochemical analyses showed expression of SMARCAL1 in all developing teeth, raising the possibility that the malformations are cell-autonomous consequences of SMARCAL1 deficiency. We also found that stimulation of cultured skin fibroblasts from SIOD patients with the tooth morphogens WNT3A, BMP4, and TGFβ1 identified altered transcriptional responses, raising the hypothesis that the dental malformations arise in part from altered responses to developmental morphogens. To the best of our knowledge, this is the first systematic study of the dental anomalies associated with SIOD.
Pseudocyst of the auricle is a benign condition predominantly affecting young Asian males. Histology characteristically reveals an intracartilaginous cyst devoid of epithelial lining, and there are no pathognomonic features. We postulate that an inflammatory response is crucial to the development of this condition on the basis of a consistent perivascular inflammatory response seen in all our specimens.
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