Crohn's disease (CD) is a chronic inflammatory bowel disease characterised by localised areas of nonspecific, noncaseating granulomas. Approximately 1/3 of CD patients develop extraintestinal manifestations in the course of their disease. This review focuses on oral manifestations of CD to understand if oral lesions could help clinicians in the diagnosis of systemic CD. MATERIALS AND METHODS: Literature for the review was retrieved using PubMed Medline, Ebsco Library and Web of Science. RESULTS: After a careful preliminary evaluation, only 43 articles were eligible for inclusion in the qualitative evaluation, whereas only 7 mentioned oral CD as the first sign of a systemic disease and were included in the quantitative evaluation. CONCLUSIONS: Oral manifestations of CD can be classified as specific and non-specific. The aetiology of oral CD seems to be linked to particular bacterial infections. Although the evidence from the literature is weak, it seems that in some cases the inspection of the mouth could assist in the diagnosis of a systemic Crohn's disease.

Reprogramming of metabolism is a well-established property of cancer cells that is receiving growing attention as potential therapeutic target. Oral squamous cell carcinomas (OSCC) are aggressive and drugs-resistant human tumours displaying wide metabolic heterogeneity depending on their malignant genotype and stage of development. Dichloroacetate (DCA) is a specific inhibitor of the PDH-regulator PDK proved to foster mitochondrial oxidation of pyruvate. In this study we tested comparatively the effects of DCA on three different OSCC-derived cell lines, HSC-2, HSC-3, PE15. Characterization of the three cell lines unveiled for HSC-2 and HSC-3 a glycolysis-reliant metabolism whereas PE15 accomplished an efficient mitochondrial oxidative phosphorylation. DCA treatment of the three OSCC cell lines, at pharmacological concentrations, resulted in stimulation of the respiratory activity and caused a remarkably distinctive pro-apoptotic/cytostatic effect on HSC-2 and HSC-3. This was accompanied with a large remodeling of the mitochondrial network, never documented before, leading to organelle fragmentation and with enhanced production of reactive oxygen species. The data here presented indicate that the therapeutic efficacy of DCA may depend on the specific metabolic profile adopted by the cancer cells with those exhibiting a deficient mitochondrial oxidative phosphorylation resulting more sensitive to the drug treatment.

TheraCal LC (TLC, Bisco Inc., Schaumburg, IL, USA) is a light-cured, resin-modified, calcium silicate-filled base/liner material designed for direct and indirect pulp-capping. In this study the result of the evaluation in vitro of the biocompatibility and chemical-physical properties of TLC are reported. TLC specimens were prepared under aseptic conditions in strict compliance with the manufacturer’s instructions and sterilized. Osteoblast-like cells (MG63) were used. For different time points, solubility, water uptake, alkalinizing activity and cytotoxicity were evaluated. In ddH20 and in DMEM+FBS, TLC showed a loss of material increasing simultaneously with the absorption capacity. The increase of water uptake of the material promoting the solubilization of mineral ions in medium is a requisite for a bioactive material. The alkalinizing activity is correlated to antimicrobial/bacteriostatic activity and to the ability to favor the formation of apatite deposits. The pH values for water absorption after immersion of the disks ranged between 8 and 9 at each times of evaluation. Cytotoxicity was not observed in MG63 cells treated with TLC and after 5 days, the cells were organized to form a confluent monolayer as demonstrated by fluorescence microscopy observation. TLC showed biocompatibility on MG63 cells allowing a physiologic cell growth and differentiation. The chemical-physical properties and biocompatibility of TLC observed in vitro in the present study, allows considering this cement as an innovative pulp-capping material for the vital pulp therapy.

Tongue squamous cell carcinoma (TSCC) is increasing in incidence, especially among young patients and preferably females. Infection with human papilloma virus (HPV) has been suggested as a cause of SCC in the head and neck, and the proportion of oropharyngeal cancers caused by HPV has steadily increased.

More than 30% of patients with squamous cell carcinoma (SCC) of the mobile tongue have clinically unde-tectable lymph node metastasis. Tumour cells can spread as single cells or collectively. A protein known toplay a role in both processes is podoplanin, which is expressed in endothelial cells not only in lymph vesselsbut also in some aggressive tumours with high invasive and metastatic potential. Here we studied samplesfrom 129 patients with primary SCC of the tongue for expression of podoplanin using immunohistochemistry.mRNA levels were analysed in another 27 cases of tongue SCC with adjacent clinically tumour-free tonguetissue and 14 tongue samples from healthy donors. Higher levels of podoplanin were seen in tumours com-pared to both normal tongue and clinically normal tongue in the tumour vicinity. No association was foundbetween levels of podoplanin, presence of lymph node metastases or other clinical factors. Patients aged 40or less were more likely to express high levels of podoplanin protein compared to older patients (p5 0.027).We conclude that levels of podoplanin in primary tongue SCCs are not associated with lymph node metasta-ses. However, tongue SCCs arising in young patients (40 years of age) are more likely to express high levelsof podoplanin than tongue SCCs that arise in the more elderly. The data suggest that podoplanin has a dis-tinctive role in young patients, who are known to have a poor prognosis: these patients may, therefore, bene-fit from podoplanin inhibitory therapies.

Head and neck squamous cell carcinoma (HNSCC) ranks sixth worldwide for tumor-related mortality. A subpopulation of tumor cells, termed cancer stem cells (CSCs), has the ability to support cancer growth. Therefore, profiling CSC-enriched populations could be a reliable tool to study cancer biology.

Oral squamous cell carcinoma (OSCC) represents about 90% of all oral neoplasms with a poor clinical prognosis. To improve survival of OSCC patients, it is fundamental to understand the basic molecular mechanisms characterizing oral carcinogenesis. Dysregulation of oncogenes and tumor suppressor genes seems to play a central role in tumorigenesis, including malignant transformation of the oral cavity.