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Cysticercosis is a parasitic infestation caused by the larval stage of Taenia solium. It is common in regions where humans and animals live in close contact, with poor sanitation, and due to consumption of infected meat. The tissues affected are the subcutaneous layers, brain, muscle, heart, liver, lungs, and peritoneum. Oral manifestations are very rare. The most common intra-oral site is the tongue. Here, we present a case in a who sought treatment for an asymptomatic nodule in the upper lip. A gross specimen revealed a cystic cavity containing clear watery fluid and white membranous flecks. The histopathology showed features of cysticercosis.

Amaç: E-cadherin'in displazinin kansere dönüşmesinde rol oynayabileceğine dair bulgular vardır. Bu çalışmanın amacı E-cadherin'in ağız içi normal mukoza, yassı epitel hücreli karsinom ve displastik epitelde ekspresyonunu karşılaştırarak oral karsinogenez ile ilişkisini araştırmaktır. Gereç ve yöntem: Klinik olarak oral premalin lezyon ve yassı epitel karsinom şüphesi bulunan hastalar, histopatolojik tanıyı takiben çalışmaya alındı. Toplam olarak oral epitelyal displazili 20 hasta ve oral yassı epitel hücreli karsinomu bulunan 20 hasta çalışmaya alındı. Her hastada aşağıdaki değişkenler kaydedildi: Hastanın yaşı, cinsiyeti, tümör lokalizasyonu, TNM evresi ve klinik evre (I-IV). Hematoksilen-Eozin'le boyanmış kesitlerin ilk muayenesini takiben, her parçadan bir kısım alınarak 5 mikronluk kesitler halinde immunohistokimyasal çalışmaya alındı. Bulgular: E-cadherin ekspresyonu ile displazi arasında negatif bir bağlantıyı telkin eder tarzda, hafiften ağıra değişen derecedeki displazide E-cadherin ekspresyonu azalmış bulundu. Ayrıca E-cadherin ekspresyonu ile klinik tümör evresi ve prognoz skoru arasında anlamlı bir bağıntı saptanmadı. Sonuç: Oral yassı hücreli karsinomda displazi derecesi arttıkça E-cadherin ekspresyonu azalmaktadır. Azalmış E-cadherin ekspresyonu ağız içi yassı epitel hücreli karsinoma'da invazivlikte artışın güvenilir bir belirteci olabilir. Azalmış E-cadherin ekspresyonu displazini oral kansere dönüşmesini gösteren faydalı bir belirteç olarak düşünülebilir. Anahtar kelimeler: E-cadherin, oral epitelyal displazi, oral yassı epitel hücreli karsinoma ABSTRACT Objectives: There is evidence that E-cadherins may also play a role in progression of dysplasia to cancer. The aim of this study was to investigate the expression of E-cadherin during the process of oral carcinogenesis by comparing their expression in normal and oral dysplastic epithelium (OED) with oral squamous cell carcinoma (OSSC). Materials and methods: The patients who were clinical suspected of having premalignant lesion and oral squamous cell carcinoma were included in the study after the histopathological diagnosis. Totally 20 cases of OED and 20 Cases of OSSC were included in the study. From each case the following data were recorded: patient's age and sex, tumour location, TNM classification and clinical stage (I-IV). After preliminary examination of sections stained with haematoxylin/eosin, representative parts of each piece were selected and sectioned at 5 micron for immunohistochemical study. Results: There was reduced expression of E-cadherin from mild to severe degree of dysplasia suggesting the negative correlation with E-cadherin expression. However, there was no significant correlation between E-cadherin expression, clinical TNM stage and prognosis score. Conclusion: The E-cadherin expression is reduced with increase grade of dysplasia and in oral squamous cell carcinoma. The reduced expression of E-cadherin may be a reliable indicator of increase in invasiveness in oral squamous cell carcinoma. Reduced E-cadherin expression can...

Background Keratin has shown promising outcomes as a biomaterial due to its inherent bioactivity, biocompatibility and regenerative effects. The effect of keratin on repair and regeneration of dental tissues has never been studied before. Current therapies to treat pulp tissues involve its replacement with inert, synthetic materials that do not have a proper biological function, leading to failure and tooth loss. This study aimed to develop a biocompatible keratin hydrogel (KH) suitable for pulp therapies. Methods Keratins extracted from sheep wool were isolated, quantified and reconstituted to form KH. Different concentrations of keratin gel suitable for dental application were characterized by rheological analysis. The optimized gel based on flow characteristics was studied further for microstructure including porosity, percentage swelling ratio and contact angle measurements, using analytical tools such as scanning electron microscopy (SEM), micro-computed tomography and goniometer. To assess both biocompatibility and pulpal response, KH was implanted into rat upper molar teeth following partial pulpotomy. After 28 days, the tissue sections were analyzed by histological and immunohistochemical methods to identify dentin matrix protein 1 (DMP-1) formation and compared with control (Ca(OH) 2 -treated) teeth. Results The results of the study demonstrated a viscous and injectable, porous, dimensionally stable, hydrophilic and biocompatible gel that allowed pulp healing to occur by a reparative response, with widespread DMP-1 expression. Conclusions The findings of this study indicate that keratins can be developed as a biomaterial source for alternate biological treatment options for pulp therapies.

Although the tumour cells themselves did not express IL-17, a range of cell types did, suggesting multiple cellular sources for IL-17 in OSCC. The spatial distribution of IL-17 cells suggests specific interactions with cells within the tumour microenvironment, implying that IL-17 cells are likely to play a role in the pathogenesis of OSCC.

Background: Interleukin 17 (IL17) is a proinflammatory cytokine with increased expression in some cancers. It has been demonstrated to exhibit both pro- and anti-tumor effects. Our group has previously demonstrated expression of IL17 from multiple cells in oral squamous cell carcinoma (OSCC) such that the aim of the current study was to examine the role of IL17 in OSCC progression. Methods: The cytoplasmic SEFIR sequence of the transmembrane IL17 receptor (IL17R) was detected in formalin Fixed Paraffin Embedded (FFPE) OSCC tissues (n = 14) using immunohistochemistry. Soluble IL17R was detected in the cell culture supernatants of three OSCC cell lines (SCC4, SCC15 and SCC25) using a sandwich ELISA. Human recombinant IL17 over a range of concentrations (0, 10, 50, 100 ng/mL) was used to stimulate the three OSCC cell lines.Proliferation at 0, 24, 48, 72 hours was then assayed by cell titer blue and invasion at 48 hours using a QCM ECMatrix cell invasion assay. The data were analyzed using unpaired Student's t test and ANOVA as appropriate using GraphPad Prism 6 software. Results:Cytoplasmic expression of transmembrane IL17R was detected in all FFPE OSCC tissues. Soluble IL17R was detected in the cell culture supernatants of all three OSCC cell lines and its concentration increased in a time dependent manner. SCC25 had significantly higher concentration of soluble IL17R at 72 hours than SCC4 and SCC15. The rate of proliferation of all three OSCC cell lines was not affected with the addition of recombinant IL17. However, IL17 promoted the in vitro invasion of SCC25 and SCC15 in a dose dependent manner. At the highest concentration of IL17 (100ng/mL), the SCC25 cells showed significant invasion compared to control cells (p<0.05), while the SCC15 cells exhibited significant invasion at both 50ng/mL and 100 ng/mL of IL17 (p<0.05). In contrast, IL17 failed to stimulate invasion in the SCC4 cell line. Conclusions: This study is the first to demonstrate in vitro association between IL17 and possible invasion of OSCC. The exact mechanism by which IL17 enhances invasion and thereby tumor progression in vivo remains to be elucidated and could involve a number of different mechanisms including cell adhesion and extracellular matrix proteins. Citation Format: Avadhoot Avadhani, Trudy Milne, Gregory Seymour, Alison Rich. Interleukin 17 promotes tumor progression in oral squamous cell carcinoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4151. doi:10.1158/1538-7445.AM2015-4151

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