Objectives: Cancer is likely caused by alterations in gene structure or expression. Recently, next generation sequencing has documented mutations in 106 head and neck squamous cell cancer genomes, suggesting several new candidate genes. However, it remains difficult to determine which mutations directly contributed to cancer. Here, summarize the animal models which have already validated and may test cancer causing mutations identified by next generation sequencing approaches.

Material and Methods: We reviewed the existing literature on genetically engineered mouse models and next generation sequencing (NGS), as it relates to animal models of squamous cell cancers of the head and neck (HNSCC) in PubMed.

Results: NSG has identified an average of 19 to 130 distinct mutations per HNSCC specimen. While many mutations likely had biological significance, it remains unclear which mutations were essential to, or "drive," carcinogenesis. In contrast, "passenger" mutations also exist that provide no selection advantage. The genes identified by NGS included p53, RAS, Human Papillomavirus oncogenes, as well as novel genes such as Notch1, Dicer and SYNE1,2. Animal models of HNSCC have already validated some of these common gene mutations identified by NGS.

Conclusions: The advent of next generation sequencing will provide new leads to the genetic changes occurring in squamous cell cancers of the head and neck. Animal models will enable us to validate these new leads in order to better elucidate the biology of squamous cell cancers of the head and neck.

Objectives: Head and neck/oral cancer, predominantly head and neck squamous cell carcinoma (HNSCC), is the sixth most common cancer in the world. While substantial advances have been made to define the genomic alterations associated with head and neck/oral cancer, most studies are focused on protein coding genes. The aim of this article is to review the current literature on identified genomic aberrations of non-coding genes (e.g., microRNA) in head and neck/oral cancer (HNOC), and their contribution to the initiation and progression of HNOC.

Material and Methods: A comprehensive review of the available literature relevant to microRNA deregulation in HNSCC/HNOC, was undertaken using PubMed, Medline, Scholar Google and Scopus. Keywords for the search were: microRNA and oral cancer, microRNA and squamous cell carcinoma, microRNA deregulation and oral cancer, microRNA and carcinogenesis in the head and neck/oral cavity. Only full length articles in the English language were included.

Results: We recently identified a panel of microRNA deregulations that were consistently observed in HNSCC [Chen et al., Oral Oncol. 2012;48(8):686-91], including 7 consistently up-regulated microRNAs (miR-21, miR-7, miR-155, miR-130b, miR-223, miR-34b), and 4 consistently down-regulated microRNAs (miR-100, miR-99a, miR-125b, miR-375). In this review, we will first provide an overview on microRNA and HNSCC. We will then provide a comprehensive review on the roles of microRNA deregulations in HNSCC. The functional significance of the identified HNSCC-associated microRNAs and a number of other relevant microRNAs (e.g., miR-138, miR-98, miR-137, miR-193a and miR-218) will be discussed in detail.

Objectives: The aim of this study was to detect the presence of myofibroblasts and transforming growth factor-beta1 in fibrous and ossifying-fibrous epulis and their possible contribution to the collagenous connective tissue formation. The correlation between the myofibroblasts and the degree of inflammatory infiltration was also examined.

Material and Methods: The presence of myofibroblasts as well as transforming growth factor-beta1 was examined in twenty cases of fibrous epulis and 22 ossifying fibrous epulis, using immunohistochemistry.

Results: Myofibroblasts positive for alpha smooth muscle actin and vimentin but negative to desmin were found in 20% and 45% in fibrous epulis and ossifying fibrous epulis, respectively. Myofibroblasts were distributed in areas with and without inflammatory infiltration and their presence in inflammatory areas was not related with the degree of inflammatory infiltration. A percentage of 21 - 60% of fibroblasts and chronic inflammatory cells expressed transforming growth factor-beta1 in all cases.

Conclusions: These data suggest that transforming growth factor-beta1 and myofibroblasts contribute to the formation of collagenous connective tissue in fibrous epulis and ossifying fibrous epulis. Myofibroblasts are mainly presented in ossifying fibrous epulis than in fibrous epulis. It seems to be no relationship between the presence of myofibroblasts and the degree of inflammatory infiltration of the lesions.

Background: The aim of the present article is to report a case of ameloblastic carcinoma and use a marker alpha smooth muscle actin as a tool to differentiate cases of ameloblastic carcinoma from that of ameloblastoma.

Methods: Case study reporting a case of ameloblastic carcinoma (AC) with expression of alpha smooth muscle actin (alpha-SMA) as a marker for emergence of stromal myofibroblasts. The expression of myofibroblasts was also compared with that of ameloblastoma.

Results: Difference between the two lesions in the pattern of expression of alpha smooth muscle actin was also observed. There was increase in the number of myofibroblasts in the stroma of AC while in ameloblastoma, it was comparatively less. Secondly, few areas of the carcinomatous ameloblastic island also exhibited a mild positivity towards alpha smooth muscle actin.

Conclusions: Increase in number of stromal myofibroblast may be taken as a predictor for carcinomatous transformation. Further studies with greater sample size can validate the use of alpha-SMA as a marker to differentiate ameloblastic carcinoma from ameloblastoma.

Background: Giant cell fibroma is a type of fibrous tumour of the oral mucosa which rarely affects children under the age of 10. The purpose of this paper was to contribute two clinically and histologically documented cases of giant cell fibroma in the free gingiva of a 7 and 6 year old boys.

Methods: Both nodules were presented in the mandibular anterior region. In the differential diagnosis several fibrous hyperplastic lesions were considered such as traumatic fibroma, papilloma, peripheral ossifying fibroma, peripheral odontogenic fibroma, giant cell fibroma and odontogenic hamartoma.

Results: The lesions were removed and the histological examination revealed fibrocollagenous connective tissue with the presence of stellate giant cells which confirmed the diagnosis of giant cell fibroma.

Conclusions: Dentists should be aware of the existence of giant cell fibroma in children, which must be included in the differential diagnosis of nodular lesions of the gingiva and adequately diagnosed and treated by removal and histopathological examination.