Rodent incisors are capable of growing continuously and the renewal of dental epithelium giving rise to enamel-forming ameloblasts and dental mesenchyme giving rise to dentin-forming odontoblasts and pulp cells is achieved by stem cells residing at their proximal ends. Although the dental epithelial stem cell niche (cervical loop) is well characterized, little is known about the dental mesenchymal stem cell niche. Ring1a/b are the core Polycomb repressive complex1 (PRC1) components that have recently also been found in a protein complex with BcoR (Bcl-6 interacting corepressor) and Fbxl10. During mouse incisor development, we found that genes encoding members of the PRC1 complex are strongly expressed in the incisor apical mesenchyme in an area that contains the cells with the highest proliferation rate in the tooth pulp, consistent with a location for transit amplifying cells. Analysis of Ring1a(-/-);Ring1b(cko/cko) mice showed that loss of Ring1a/b postnatally results in defective cervical loops and disturbances of enamel and dentin formation in continuously growing incisors. To further characterize the defect found in Ring1a(-/-);Ring1b(cko/cko) mice, we demonstrated that cell proliferation is dramatically reduced in the apical mesenchyme and cervical loop epithelium of Ring1a(-/-);Ring1b(cko/cko) incisors in comparison to Ring1a(-/-);Ring1b(fl/fl)cre- incisors. Fgf signaling and downstream targets that have been previously shown to be important in the maintenance of the dental epithelial stem cell compartment in the cervical loop are downregulated in Ring1a(-/-);Ring1b(cko/cko) incisors. In addition, expression of other genes of the PRC1 complex is also altered. We also identified an essential postnatal requirement for Ring1 proteins in molar root formation. These results show that the PRC1 complex regulates the transit amplifying cell compartment of the dental mesenchymal stem cell niche and cell differentiation in developing mouse incisors and is required for molar root formation.

Bio-MA, a calcium chloride accerelator-containing calcium-silicate cement, as a pulp capping material was evaluated on mechanically exposed rat molar pulp. Sixty maxillary first molars from Wistar rats were mechanically exposed and assigned to two capping materials: Bio-MA or white mineral trioxide aggregate (WMTA), and three periods: 1, 7, or 30 days. Nine molars were exposed and covered with polytetrafluoroethylene tape, as positive controls. From histological examination, inflammatory cell infiltration and reparative dentin formation were evaluated using grading scores. No significant difference in pulpal responses between the two materials was observed at any period (p>0.05). At 1 day, all experimental groups showed localized mild inflammation. At 7 days, dentin bridge was partially observed at exposure sites with few inflammatory cells. At 30 days, pulp appeared normal with complete tubular dentin bridges. Bio-MA with accerelator was biocompatible similar to WMTA and could be used as a pulp-capping material.

Objective  Tongue is regarded as one of the common sites of oral squamous cell carcinoma (OSCC). This study aimed to determine the prevalence and clinicopathological profile of OSCC and oral potentially malignant disorders (OPMDs) at the tongue. Materials and Methods  We retrospectively analyzed clinicopathological characteristics of 208 Thai patients diagnosed with SCC and OPMDs at the tongue in the period from 1996 to 2015. Chi-squared test was used to compare differences between patient’s clinical and histopathological features. Results  Seventy-eight tongue SCC and 130 tongue OPMD cases were present over the study period. Slight male predominance was found for tongue SCC, while a slight female predominance was present for tongue OPMDs. Both tongue SCC and tongue OPMDs were mostly diagnosed in the old age patients (>40 years old). The majority of tongue SCC and OPMDs occurred at the tip and lateral of the tongue. The most common histologic grading of tongue SCC was well differentiated and no poor differentiation was found in this study. More than a half of tongue OPMDs showed epithelial dysplasia. Both tongue SCC and OPMDs demonstrated no significant correlation between clinical feature and histopathologic diagnosis. Conclusions  Tongue SCC and OPMDs were particularly found in the elderly population and frequently developed at the tip and lateral of the tongue. Most of tongue OPMDs, particularly all of tongue erythroplakia, exhibited epithelial dysplasia. For dental practitioners, awareness in the early detection and diagnosis of these tongue lesions should be raised.

Background: Phosphatase and tensin homolog (PTEN) acts as a tumor suppressor gene. Inactivation of PTEN has been reported in various types of cancers. PTEN promoter methylation possibly underlies PTEN inactivation, which results in tumorigenesis. The aim of this study was to investigate whether PTEN promoter methylation contributes to PTEN inactivation in ameloblastoma and its associated protein expression. Material and Methods: In total, 20 fresh-frozen ameloblastoma samples were evaluated for PTEN promoter methylation using methylation-specific polymerase chain reaction (MS-PCR). A subset of 10 paraffin-embedded ameloblastoma samples was examined for PTEN expression through immunohistochemistry. Four primary cultured ameloblastoma cells were investigated for PTEN promoter methylation and PTEN transcriptional expression via reverse transcription PCR. Results: PTEN promoter methylation was detected in 65% (13/20) of the ameloblastoma samples. Of 10 ameloblastoma samples, 4 exhibited reduced PTEN expression. Of 5 samples with methylated PTEN, 3 (60%) were associated with loss of PTEN expression. However, PTEN expression was detected in 4 (80%) of 5 samples with unmethylated PTEN. In addition, 3 (75%) of 4 primary ameloblastoma cell cultures exhibited an inverse correlation between PTEN promoter methylation and PTEN transcription level. Conclusions: PTEN promoter methylation is found in a number of ameloblastomas but not significantly correlated with loss of PTEN expression. Genetic or epigenetic mechanisms other than PTEN promoter methylation may contribute to PTEN inactivation in ameloblastoma tumor cells.

Granular cell ameloblastoma is a rare, benign neoplasm of the odontogenic epithelium. A case of massive granular cell ameloblastoma in a 44-year-old Thai female is reported. Histopathological features displayed a follicular type of ameloblastoma with an accumulation of granular cells residing within the tumor follicles. After treatment by partial mandibulectomy, the patient showed a good prognosis without recurrence in a 2-year follow-up. To characterize the granular cells in ameloblastoma, we examined the expression of basement membrane (BM) proteins, including collagen type IV, laminins 1 and 5 and fibronectin using immunohistochemistry. Except for the granular cells, the tumor cells demonstrated a similar expression of BM proteins compared to follicular and plexiform ameloblastomas in our previous study, whereas the granular cells showed strong positivity to laminins 1 and 5 and fibronectin. The increased fibronectin expression in granular cells suggests a possibility of age-related transformation of granular cells in ameloblastoma.

ObjectivesDirect pulp capping is a treatment for mechanically exposed pulp in which a biocompatible capping material is used to preserve pulpal vitality. Biocompatibility tests in animal studies have used a variety of experimental protocols, particularly with regard to the exposure site. In this study, pulp exposure on the occlusal and mesial surfaces of molar teeth was investigated in a rat model.Materials and MethodsA total of 58 maxillary first molars of Wistar rats were used. Forty molars were mechanically exposed and randomly assigned according to 3 factors: 1) the exposure site (occlusal or mesial), 2) the pulp-capping material (ProRoot White MTA or Bio-MA), and 3) 2 follow-up periods (1 day or 7 days) (n = 5 each). The pulp of 6 intact molars served as negative controls. The pulp of 12 molars was exposed without a capping material (n = 3 per exposure site for each period) and served as positive controls. Inflammatory cell infiltration and reparative dentin formation were histologically evaluated at 1 and 7 days using grading scores.ResultsAt 1 day, localized mild inflammation was detected in most teeth in all experimental groups. At 7 days, continuous/discontinuous calcified bridges were formed at exposure sites with no or few inflammatory cells. No significant differences in pulpal response according to the exposure site or calcium-silicate cement were observed.ConclusionsThe location of the exposure site had no effect on rat pulpal healing. However, mesial exposures could be performed easily, with more consistent results. The pulpal responses were not significantly different between the 2 capping materials.

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