Modified maxillary vestibular approach with subperiostal intranasal dissection for surgical extractions of mesiodentes impacted in the floor of the nasal cavity.

INTRODUCTION: Impacted mesiodentes in the inverted position may interfere with the base of the nasal cavity or the nasal septum. They can rarely erupt into the nose as well. Traditionally they are extracted via intraoral approaches (transpalatal or vestibular). Also, an endoscopically assisted transnasal approach can be used. In this paper, the authors are the first to present a group of patients suffering from impacted mesiodentes who have been surgically treated using a modified maxillary vestibular approach with subperiostal intranasal dissection. MATERIAL AND METHOD: The prospective study was completed in the time period 12/2013-6/2017. The inclusion criteria were: 1. Mesiodens impacted in the inverted position extending to the base of the nasal cavity or into the nasal septum without concomitant pathological lesion and without eruption into the nasal cavity. 2. Localization of the mesiodens at the level of or dorsally to the roots of the upper middle incisors in the sagittal plane or ventrally to the roots of these teeth, but with the crown extending significantly posteriorly to the base of the nasal cavity.3. Indication for extraction because of clinical or orthodontic reasons. RESULTS: In total, 9 patients were enrolled into the group. In these patients, surgical extractions of 9 mesiodentes were performed using the alternative approach described above. All extractions were done according to a uniform surgical protocol. The mean age of the patients was 11.7 ± 3.1 years (age range 7-17 years). The crown's most cranial point exceeded the bone of the nasal cavity on average by2.0 ± 1.4 mm (in the range 0-5 mm). 8 mesiodentes were conical, 1 was tuberculate. Surgical procedure and postoperative healing were always without any complications. CONCLUSION: For the removal of midline supernumerary teeth, the modified maxillary vestibular approach with subperiostal intranasal dissection in comparison to the intraoral palatal approach provides less postoperative morbidity and a lower risk of complications (smaller surgical wound, minimal exposure of maxilla, minimal bone loss, reduced risk of damage to the roots of the upper incisors, lower risk of damage to the nasopalatine neurovascular bundle, good visibility in the surgical field, easier surgery, and finally no need of postoperative palatal splint). For oral and maxillofacial surgeons the presented technique represents a more traditional way of surgical tooth extraction than the endoscopically assisted transnasal approach.

Langerhans cell histiocytosis in childhood - review, symptoms in the oral cavity, differential diagnosis and report of two cases.

BACKGROUND: Langerhans cell histiocytosis is a rare disease characterized by monoclonal proliferation and migration of special dendritic cells. This disease primarily affects bones, but occurs less frequently in other organ systems or may manifest as a multisystem disease. CASE REPORTS: Extraoral and intraoral symptoms of Langerhans cell histiocytosis are described in a 13-month-old female and a 5-month-old male infant. Dermatitis was found on the scalp, abdomen, flexures and in intertrigineous areas in both patients. The intraoral examination of the 13-month-old infant showed premature eruption of all maxillary deciduous molars, loosening and significant damage of periodontal tissues (gingivitis with bleeding, swelling of palatal mucosa, periodontal pockets) resembling severe periodontitis. In the oral cavity of the 5-month-old predentate infant bilateral swellings of maxillary alveolar mucosa with deep ulcerations were seen. The oral and skin symptoms in both infants were indications for biopsy. Langerhans cell histiocytosis was confirmed histologically and immunohistochemically. CONCLUSION: Oral findings in Langerhans cell histiocytosis may be the only clinical symptom of the disease; therefore the role of dentists in establishing diagnosis is very important.

Mammary analogue secretory carcinoma of salivary glands with high-grade transformation: report of 3 cases with the ETV6-NTRK3 gene fusion and analysis of TP53, ß-catenin, EGFR, and CCND1 genes.

Mammary analogue secretory carcinoma of salivary gland origin (MASC) is a recently described tumor resembling secretory carcinoma of the breast characterized by strong S-100 protein, mammaglobin, and vimentin immunoexpression and which harbors a t(12;15) (p13;q25) translocation resulting in ETV6-NTRK3 fusion product. Histologically, conventional MASC displays bland histomorphology and a lobulated growth pattern and is often composed of microcystic, tubular, and solid structures with abundant eosinophilic homogenous or bubbly secretions. Colloid-like secretory material stains positively for periodic acid-Schiff with and without diastase as well as for Alcian Blue. We present for the first time, 3 patients with MASC of the parotid gland in which high-grade (HG) transformation developed in each case characterized by an accelerated clinical course and poor outcome. The HG component revealed strong membrane staining for EGFR and ß-catenin, cytoplasmic/nuclear staining for S-100 protein, and nuclear staining for cyclin-D1, whereas HER-2/neu was absent. Analysis for the presence of the ETV6-NTRK3 fusion transcript revealed positivity in both HG and low-grade component of MASC in 2 of the 3 studied cases. The tumor in case 2 was negative in both its elements for the t(12;15) translocation, but ETV6 gene rearrangement was detected in both components in all 3 cases. Analysis of TP53 and CTNNB1 gene mutations in the HG component of MASCs as well as detection of copy number aberration of EGFR and CCND1 gene did not harbor any abnormalities. All 3 patients with HG-transformed MASC died of disseminated disease within 2 to 6 years after diagnosis. Recognizing HG-transformed MASC and testing for ETV6 rearrangement may be of potential value in patient treatment, because the presence of the ETV6-NTRK3 translocation may represent a therapeutic target in MASC.

CRTC1-MAML2 and CRTC3-MAML2 fusions were not detected in metaplastic Warthin tumor and metaplastic pleomorphic adenoma of salivary glands.

The recurrent translocations t(11;19) and t(11;15) resulting in CRTC1-MAML2 or CRTC3-MAML2 fusion oncogenes, respectively, are identified in a large proportion of mucoepidermoid carcinomas (MECs) of the salivary gland and have impact on prognosis. However, there are conflicting data on the specificity of this translocation, in particular, on its putative occurrence in Warthin tumor (WT) of the parotid gland as reported in few previous cases. It was speculated that extensive squamous metaplasia could explain the presence of t(11;19) translocation in a subset of WTs. We evaluated 76 salivary gland tumors, including 16 cases of metaplastic WT and 8 cases of pleomorphic adenoma (PA) with squamous and/or mucinous metaplasia, extensive enough morphologically to mimic MEC. Detection of CRTC1-MAML2 and CRTC3-MAML2 fusion transcripts and MAML2 gene break was performed using nested reverse transcription-polymerase chain reaction and fluorescence in situ hybridization (FISH), respectively. None of 16 analyzed metaplastic WTs showed positivity for fusion transcripts CRTC1-MAML2 or CRTC3-MAML2, and none showed rearrangement of the MAML2 gene by FISH. Similarly, we did not detect these transcripts or break of MAML2 gene in any case of PA with extensive squamous/mucinous metaplasia. For comparison, 40 cases of low-grade MEC were also evaluated. CRTC1-MAML2 and CRTC3-MAML2 fusion transcripts were detected in 17 and 5 cases, respectively. The FISH method using break-apart probe demonstrated the MAML2 gene rearrangement in 25 cases of low-grade MEC. In contrast to low-grade MEC, neither metaplastic WTs nor metaplastic PAs harbored translocations t(11;19) and anticipated t(11;15) resulting in CRTC1-MAML2 and CRTC3-MAML2 fusion transcripts, respectively, and/or MAML2 gene rearrangement.

Human papillomaviruses are not involved in the etiopathogenesis of salivary gland tumors.

BACKGROUND: Tumor-related high risk human papillomaviruses (HPV) 16 and 18 have been repeatedly detected in head and neck cancers, particularly, they are well known risk factors in squamous cell carcinoma of the oropharyngeal and tonsillar region. Little is known, however, about the possible role of HPV in salivary gland tumors. METHODS: Fifty-five cases of benign and malignant salivary gland tumors were tested using p16 immunohistochemistry followed by HPV DNA polymerase chain reaction (PCR) using SPF, CPSGB, GP5+/GP6+ primers, and type specific primers for HPV 16, 18, 31, 33, 35, 45 in the cases with strong immunohistochemical expression for p16 protein (score 3+). RESULTS: Only 5 tumors of 55 (9 %) were completely devoid of any p16 staining, and in 10 cases (18 %), less than 25 % of tumor cells stained (score 1+). In the majority of cases (35 of 55; 64 %) there was a patchy nuclear and cytoplasmic strong staining in 26 to 50 % of tumor cells (score 2+). In five cases (9 %), strong nuclear and cytoplasmic staining in more than 51% of tumor cells was detected (score 3+). However, none of the p16-positive cases showed any evidence of high-risk HPV by PCR. CONCLUSIONS: The results of the study indicate that HPV, in particular oncogenic types 16 and 18, are not involved in the etiology of benign and malignant epithelial tumors of salivary glands. Therefore, it is likely that salivary gland tumors belong to the category of tissues in which the p16 positive immunohistochemistry is not biologically relevant to the oncogenic role of HPV infection.

Pleomorphic adenoma of the salivary glands with intravascular tumor deposits: a diagnostic pitfall.

The diagnosis of pleomorphic adenoma (PA) of salivary glands is usually straightforward posing few diagnostic problems for the general surgical histopathologist. The purpose of our investigation was to present a series of 22 cases of PA of major salivary glands, each of which contained small foci of tumor within vascular spaces. This feature has previously been described very rarely in PA and may represent a significant diagnostic pitfall. The patients included 12 women and 10 men, ranging in age at diagnosis from 17 to 82 years. Histopathologically, all 22 tumors displayed the features of PA with mixed epithelial and myoepithelial growth patterns and chondromyxoid areas. None of these neoplasms showed any cytologic evidence of malignancy. In all cases, there were multiple dilated thin-walled and/or muscular thick-walled blood vessels containing small intraluminal collections of neoplastic cells with or without myxoid stromal components. The intravascular tumor cells expressed cytokeratins, and in some cases they were also immunoreactive for S-100 protein, GFAP, D2-40, and p63 protein. The intravascular location of the neoplastic cells was confirmed by CD31, CD34, and factor VIII-related antigen immunostains. Reaction for D2-40 was negative in the endothelium of the involved vessel in all cases, confirming that they were vascular rather than lymphatic channels. Seven patients (36%) underwent fine-needle aspiration biopsy 25 days to several years before excision of the tumor. Follow-up of the patients in our series revealed no cases of recurrence or metastasis (range, 6 mo to 9.5 y; mean 3.8 y; median 3.5 y). The biological significance of intravascular tumor in PA is not clear, but there is growing evidence that it is an innocuous phenomenon that might be related to artifactual spillage caused by tumor injury presumably by either fine-needle aspiration or intraoperative trauma.