[Clinical and imaging features of 36 odontogenic keratocysts associated with an impacted tooth].

PURPOSE: To analyse the imaging features of odontogenic keratocysts (OKCs) associated with an impacted tooth. METHODS: Clinical and radiological data of 235 cases with OKCs were respectively investigated, with emphasis on imaging features of 36 OKCs, which were associated with an unerupted tooth. RESULTS: In 36 cases of OKCs associated with an impacted tooth, the ratio of male to female was 1.77:1, and molar-ramus was involved in 26 cases (72.22％). OKCs in association with an unerupted tooth occurred mostly in patients ranging from 20 to 30 years (19 cases, 52.8％). There were 27 cases (75％) of unilocular and 9 cases (25％) multilocualr radiolucency. Thirteen cases (36.11%) were related to the crown of the impacted teeth, and the unerupted teeth also were impacted as a result of malposition in which the entire teeth appeared to be enveloped by cysts (15 cases, 41.67%), or adjacent to cyst wall (8 cases, 22.22%). CONCLUSIONS: Radiographically, one of the most imaging features of OKCs in association with an unerupted tooth is that its entire tooth appears to be enveloped by cyst or adjacent to cyst, while pericoronal radiolucencies surrounding an impacted tooth are rarely seen.

Octreotide stimulates somatostatin receptor-induced apoptosis of SW480 colon cancer cells by activation of glycogen synthase kinase-3ß, A Wnt/ß-catenin pathway modulator.

BACKGROUND/AIMS: Peptide hormone somatostatin and its receptors (SSTRs) have a wide range of physiological functions and play a role in the treatment of numerous human diseases, including colorectal cancer. Octreotide, a somatostatin-analog peptide, inhibits growth of colonic cancer SW480 cells through Wnt/ß-catenin pathway modulation. However, the specific octreotide-stimulating SSTR subtypes and the signal-transduction mechanism responsible for the negative regulation of Wnt/ß-catenin pathway by octreotide have not been fully elucidated. METHODOLOGY: Octreotide-induced apoptosis in SW480 colon cancer cells mediated by SSTR2,SSTR5-dependent regulation of the Wnt/ß-catenin pathway components GSK-3ß and ß-catenin was investigated. Cell apoptosis of SW480 cells was measured by apoptosis-DNA ladder assay. SSTR1, SSTR2, SSTR3, SSTR4, and SSTR5 mRNA expression levels were confirmed by RT-PCR; ß-catenin, TCF-4, cyclin D1, c-Myc, and GSK-3ß protein levels were examined by Western blot. The distribution of ß-catenin in the cell was analyzed with immunocytochemistry. RESULTS: Octreotide treatment increased SSTR2,SSTR5-induced apoptosis of SW480 colon cancer cells, promoted the plasma membrane accumulation of ß-catenin, inactivated T-cell factor-dependent transcription, and downregulated Wnt target genes cyclin D1 and c-Myc. Further, octreotide treatment mediated the activation of GSK-3. CONCLUSIONS: These preliminary findings showed the negative regulation of the Wnt/ß-catenin pathway by peptide hormone G protein-coupled receptors SSTRs.