Oral carcinoma: Clinical evaluation using diffusion kurtosis imaging and its correlation with histopathologic findings

PURPOSE: In this study, we aimed to determine the usefulness of diffusion kurtosis imaging (DKI) as a noninvasive method for evaluation of the histologic grade and lymph node metastasis in patients with oral carcinoma. MATERIALS AND METHODS: Twenty-seven patients with oral carcinoma were examined with a 3-T MR system and 16-channel coil. DKI data were obtained by a single-shot echo-planar imaging sequence with repetition time, 10,000ms; echo time, 94ms; field of view, 250x204.25ms; matrix, 120x98; section thickness, 4mm; four b values of 0, 500, 1000, and 2000s/mm(2); and motion-probing gradients in three orthogonal directions. Diffusivity (D) and kurtosis (K) were calculated using the equation: S=S0 exp(-b D+b(2) D(2) K/6). Conventional apparent diffusion coefficient (ADC) was also calculated. The MR images were compared with the histopathologic findings. RESULTS: Relative to the histologic grades (Grades 1, 2, and 3) of the 27 oral carcinomas, D values showed a significant inverse correlation (r=-0.885; P<0.001) and K values showed a significant positive correlation (r=0.869; P<0.001), whereas ADC values showed no significant correlation (r=-0.311; P=0.115). When comparing between metastatic and non-metastatic lymph nodes, significant differences in the D values (P<0.001) and K values (P<0.001), but not the ADC values (P=0.110) became apparent. CONCLUSIONS: In patients with oral carcinoma, DKI seems to be clinically useful for the evaluation of histologic grades and lymph node metastasis

The glomus tumor resorbed bone and teeth in the mandible: a case report

Abstract Background A glomus tumor is a rare neoplasm usually found in the dermis or subcutaneous tissue of the extremities. It is rare for the glomus tumor to occur on the head and face. Only 26 glomus tumors of the oral region and affected bone have been reported in the English-language literature (Table 1). We report a case of a glomus tumor at the mandible. As a new point, the glomus tumor resorbed a bone and teeth roots when the tumor progressed into the mandible. Case presentation The patient was a 44-year-old Japanese man who complained swelling of the right mandible. Radiographic examination showed a multilocular radiolucency area in the left mandible. Radiographic findings on our case resembled those of a common benign tumor. The lesion occupied to the premolar and molar area and revealed that the tumor resorbed the roots of the teeth. The lesion was removed surgically with the buccal cortical bone and buccal mucosa in contact with the mass of the tumor. The mass fully excised intraorally under general anesthesia, and the inferior alveolar nerve in contact with the mass was preserved. The specimen was pathologically diagnosed as a glomus tumor. Immunohistochemical staining was positive for vimentin, muscle-specific actin/HHF35, and calponin. A hairline-shaped area of positive staining for type IV collagen surrounding the tumor cells was also observed. In contrast, staining for alpha-SMA, cytokeratin (AE1/AE3), cytokeratin (CAM5.2), CK19, CD31, CD34, CD68, p63, S-100, Factor VIII, and desmin was all negative. The Ki-67 labeling index was almost 1%. A recurrent tumor was again detected in the site below the primary tumor at an 8-year follow-up, and it was surgically removed. The patient has had no symptoms of recurrence in 2 years after the second operation. Conclusion The glomus tumor resorbed a bone and teeth roots when the tumor progressed into the mandible. The immunohistochemical features of the tumor were consistent with those described in previous reports. It is important to completely remove the Glomus tumor

Genetic basis of calcifying cystic odontogenic tumors

<div><p>Calcifying cystic odontogenic tumors (CCOTs) are benign cystic tumors that form abnormally keratinized ghost cells. Mutations in <i>CTNNB1</i>, which encodes beta-catenin, have been implicated in the development of these tumors, but a causal relationship has not been definitively established. Thus, mutational hot spots in 50 cancer genes were examined by targeted next-generation sequencing in 11 samples of CCOT. Mutations in <i>CTNNB1</i>, but not in other genes, were observed in 10 of 11 cases. These mutations constitutively activate beta-catenin signaling by abolishing the phosphorylation sites Asp32, Ser33, or Ser37, and are similar to those reported in pilomatrixoma and adamantinomatous craniopharyngioma. In contrast, <i>BRAF</i> or <i>NRAS</i> mutations were observed in 12 and two control samples of ameloblastoma, respectively. In HEK293 cells, overexpression of mutated CTNNB1 also upregulated hair keratin, a marker of ghost cells. Furthermore, ghost cells were present in two cases of ameloblastoma with <i>BRAF</i> and <i>CTNNB1</i> mutations, indicating that ghost cells form due to mutations in <i>CTNNB1</i>. The data suggest that mutations in <i>CTNNB1</i> are the major driver mutations of CCOT, and that CCOT is the genetic analog of pilomatrixoma and adamantinomatous craniopharyngioma in odontogenic tissue.</p></div

Summarized landscape of gene mutations in CCOT and ameloblastoma.

<p>Filled boxes indicate relevant gene mutations detected by next-generation (cases #1–18) and/or Sanger sequencing (cases #19–25). Note that only <i>CTNNB1</i>, <i>BRAF</i>, and <i>MEK2K1</i> hot spots were examined in cases #19–25, while hot spots in 50 cancer genes were examined in cases #1–18.</p

PCR primers used.

<p>PCR primers used.</p

Photomicrographs of ghost cells in CCOT and ameloblastoma.

<p><b>A, and B</b>, Representative photomicrographs of ghost cells immunostained for hair cortex keratin (clone name AE13) in (<b>A</b>) CCOT (case #6) and (<b>B</b>) ameloblastoma (case #20). Scale bars; 20 μm.</p

Photomicrographs of CCOT and ameloblastoma.

<p><b>A, and D</b>, Representative photomicrographs of CCOT (case #6) and ameloblastoma (case #25) specimens stained with hematoxylin and eosin. <b>B, C, E, and F</b>, Immunostaining for (<b>B and E</b>) BRAF Val600Glu (clone name VE1) and (<b>C and F</b>) beta-catenin. Scale bars; 20 μm.</p

Electropherogram in CCOT and ameloblastoma.

<p><b>A</b>, Electropherogram of a TCT>TGT substitution at c.98 in CTNNB1, resulting in a Ser33Cys missense mutation in case #4. <b>B</b>, Electropherogram of a GTG>GAG substitution at position c.1799 in BRAF, resulting in Val600Glu missense mutation in case #25. Guanine is indicated by a black line, cytosine is indicated by a blue line, adenine is indicated by a green line, and thymine is indicated by a red line.</p

Case summaries.

<p>Case summaries.</p