BACKGROUND: Reports on the proteomic studies of ameloblastoma and other common odontogenic lesions are limited. We thus explored the differential proteins among ameloblastoma, odontogenic keratocyst, dentigerous cyst, and normal gingival tissue using proteomics and identified hub proteins involved in the local aggressiveness and recurrence of ameloblastoma.
METHODS: Samples were obtained from 14 patients with ameloblastoma, 6 with odontogenic keratocyst, 9 with a dentigerous cyst, and 5 with normal gingival tissue. Proteins were then extracted, purified, quantified, and analysed using Easy-nLC chromatography and mass spectrometry. Further functional annotation and enrichment analyses were performed using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes on the target protein collection. Protein clustering and protein-protein interaction network analyses were used to screen the hub proteins. Proteins with significant interactions were screened according to their degree index. These results were verified by immunohistochemical staining. Proteins meeting the screening criteria of expression difference ploidy >1.2-fold (upregulation and downregulation) and p < 0.05 were considered differential proteins.
RESULTS: In ameloblastoma, 808 differential proteins were upregulated and 505 were downregulated compared with those in odontogenic keratocyst; 309 were upregulated and 453 were downregulated compared with those in dentigerous cyst; and 2210 were upregulated and 829 were downregulated compared with those in normal gingival tissue. The three groups of differential proteins were associated with cellular exosomes, antigen binding, complement activation, human papillomavirus infection, focal adhesion, cell adhesion molecules, and metabolic pathways.
CONCLUSIONS: CDH3 is associated with the local aggressiveness and recurrence of ameloblastoma and is a potential therapeutic target.

The solid variant of odontogenic keratocyst (SOKC) is an extremely rare odontogenic lesion, which remains poorly defined even in the 2017 World Health Organization odontogenic tumour classification. It is difficult to distinguish between SOKC and so called keratoameloblastoma (KAB), both rare lesions that have similarities in clinical, histological and biological characteristics. Here, we report clinicopathological data and results of molecular analysis of nine cases with a literature review. First, they were compared to previously reported cases of SOKC and/or KAB, and many overlaps were found in clinical and pathological characteristics. Second, we performed PCR analysis for BRAF V600E mutation. Although ameloblastoma-like epithelia were often encountered, none exhibited BRAF V600E mutation, which has been reported to occur frequently in ameloblastomas but not in odontogenic keratocysts (OKCs). One of two cases of SOKC in the present series from which fresh frozen tissue specimens were available was found to harbour PTCH1 mutations, indicating that these were more likely to be a subtype of OKC. Moreover, we also examined the differences between SOKC and primary intraosseous carcinoma (PIOC) with regard to the expression of cytokeratins (pan-CK, CK5/6, CK7, CK8/18, CK10, CK14 and CK19), p53 and Ki-67. The proportions of p53-and Ki-67-positive cells were significantly higher in PIOC than in SOKC. These findings suggest that immunostaining for p53 and Ki-67 would be useful to differentiate between SOKC and PIOC. We also conducted a review of SOKC and KAB cases reported in the English language literature.

OBJECTIVE: To illustrate the characteristic features of odontogenic myxoma (OM) on CBCT.
METHODS: From 52 subjects with histopathologically diagnosed OMs, 18 subjects who underwent a CBCT examination were retrieved between May 2009 and April 2016. Features on CBCT images and clinical records were carefully observed and analyzed.
RESULTS: Characteristic features include: (1) fine and straight septa that were recognized to separate the tumour into triangular, square or rectangular spaces, which appeared as \"tennis racket\" or \"honeycomb\" patterns; (2) septa that frequently scattered to the borders of lesions and appeared perpendicular to the margins; (3) tooth displacement and resorption that were seen in most of the OM lesions; (4) OMs that were noted to have a tendency to involve the alveolar process, scallop between the roots and affect the integrity of the alveolar ridge; (5) the cortex of OMs that appeared normally perforated and the edge of the cortex expanded into the soft tissue.
CONCLUSIONS: CBCT is highly effective in demonstrating the comprehensive internal structures of the lesions precisely and providing detailed information for the diagnosis of OM.

An otherwise healthy 14-year-old male was referred to our hospital for the evaluation of a mass that was noticed 2 months previously. The mass was located in the left submandibular area. Comprehensive imaging examinations including panoramic radiography, CT and positron emission tomography-CT were performed. Appropriate surgical management and histopathological examination were taken for the patient. Histopathological examination demonstrated an odontogenic myxoma.