Detection of human papillomavirus DNA in intraosseus ameloblastoma

Human Papillomavirus (HPV) infection has been shown as a risk factor in oral carcinogenesis. The association between HPV and benign and malignant neoplasm of oral mucosa, especially surface epithelium-derived tumors, is well established. The role of HPV in pathogenesis of odontogenic cysts and tumors has been published in few articles. The aim of this study was detection of HPV in Iranian patients with intrabony ameloblastoma and investigation of specific risk factors associated with ameloblastoma. One hundred intrabony ameloblastoma and 50 age-sex matched samples as controls were evaluated by polymerase chain reaction for the detection and typing of HPV. Fisher exact and chi square tests were used to assess the data. HPV DNA was detected in 32% of patients and 10% of controls. HPV-6 was the most prevalent genotype (31.6%) in infected cases. It was followed by HPV-11 (12.5%), HPV-16 (12.5%) and HPV-31 (3.1%). We found a significant association between presence of HPV and location of tumor (p = 0.02), traumatic history (p = 0.03) and ododontic therapy (p = 0.01). These findings indicated that HPV-6 probably is one of the most important etiologic agents in causing intraosseous ameloblastoma in Iranian population. © 2006 Academic Journals Inc., USA

Expression of RECK and matrix metalloproteinase-2 in ameloblastoma

<p>Abstract</p> <p>Background</p> <p>Ameloblastoma is a frequent odontogenic benign tumor characterized by local invasiveness, high risk of recurrence and occasional metastasis and malignant transformation. Matrix metalloproteinase-2 (MMP-2) promotes tumor invasion and progression by destroying the extracellular matrix (ECM) and basement membrane. For this proteolytic activity, the endogenous inhibitor is reversion-inducing cysteine rich protein with Kazal motifs (RECK). The aim of this study was to characterize the relationship between RECK and MMP-2 expression and the clinical manifestation of ameloblastoma.</p> <p>Methods</p> <p>Immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) were employed to detect the protein and mRNA expression of RECK and MMP-2 in keratocystic odontogenic tumor (KCOT), ameloblastoma and ameloblastic carcinoma.</p> <p>Results</p> <p>RECK protein expression was significantly reduced in KCOT (87.5%), ameloblastoma (56.5%) and ameloblastic carcinoma (0%) (P < 0.01), and was significantly lower in recurrent ameloblastoma compared with primary ameloblastoma (P < 0.01), but did not differ by histological type of ameloblastoma. MMP-2 protein expression was significantly higher in ameloblastoma and ameloblastic carcinoma compared with KCOT (P < 0.01). RECK mRNA expression was significantly lower in ameloblastoma than in KCOT (P < 0.01), lower in recurrent ameloblastoma than in primary ameloblastoma, and was negative in ameloblastic carcinoma. MMP-2 mRNA expression was significantly higher in ameloblastoma compared with KCOT (P < 0.01), but was no different in recurrent ameloblastoma versus primary ameloblastoma. RECK protein expression was negatively associated with MMP-2 protein expression in ameloblastoma (r = -0.431, P < 0.01).</p> <p>Conclusion</p> <p>Low or no RECK expression and increased MMP-2 expression may be associated with negative clinical findings in ameloblastoma. RECK may participate in the invasion, recurrence and malignant transformation of ameloblastoma by regulating MMP-2 at the post-transcriptional level.</p

CHARACTERISTIC OF AMELOBLASTOMA IN ORAL AND MAXILLOFACIAL SURGERY AT HASAN SADIKIN HOSPITAL : 2 YEARS RETROSPECTIVE STUDY

ABSTRACTBackground: Ameloblastoma is the most common odontogenic tumor. Ameloblastoma is a borderline tumor because it is a benign but locally aggressive tumor with a high recurrence rate if the excision is not complete. The principle of treatment for ameloblastoma is excision all the tumor. This article aimed to conduct a retrospective study to analyze the characteristics of ameloblastoma in patients at Oral and Maxillofacial Surgery Hasan Sadikin Hospital Oral Surgery between the period of January 2018-December 2019Method: This is a retrospective study with 37 patients diagnosed with ameloblastoma during 2018-2019. We took data from each patient such as gender, age, radiological features, histopathological diagnosis of the location of ameloblastoma, management, defects, reconstruction. Result: A total of 22 patients were diagnosed with plexiform ameloblastoma, 12 cases of follicular ameloblastoma, 3 cases of mixed plexiform and follicular ameloblastoma. 31 patients were treated radically, while 6 patients were treated conservatively. Radical treatment is more often used to reduce recurrence rates, whereas conservative measures are indicated in children and adolescents, as well as adult patients with unilocular ameloblastoma types. Conclusion: The most characteristic of ameloblastoma is plexiform ameloblastoma in the mandible. Ameloblastoma is usually performed radically and reconstructed with an AO plate

Treatment Modalities of Unicystic Ameloblastoma - A Case Series

Unicystic ameloblastoma is a unique variant of conventional ameloblastoma which has considerably less recurrence rate than its counterpart. Unlike conventional ameloblastoma which mostly requires aggressive management, unicystic ameloblastoma has different treatment modalities which can be conservative or aggressive depending upon the histological nature of the tumor. We report five cases of unicystic ameloblastoma with different treatment modalities with long term follow up and satisfactory results

Development of a 3D Model of Ameloblastoma

Introduction: Ameloblastoma is a benign yet aggressive tumour of the jawbones causing bone resorption and has a high rate of recurrence after surgery. The precise molecular mechanisms driving ameloblastoma remain unclear and it is critical to study the association between ameloblastoma and its native bone microenvironment if we are to develop new therapeutic interventions. Current 3D ameloblastoma in vitro models lack an active bone component and there is no 3D bone model which canß biomimetically recapitulate active bone formation. Methods: First, an in vitro 3D ameloblastoma model was established and characterised the ameloblastoma cell lines within. Then a novel active bone-forming stroma model (3D bone stroma model) was created, and fully characterised bone nodules produced therein. The ameloblastoma tumour mass was placed on top of active 3D bone stroma compartments and conducted gene work to understand the genetic alterations in bone cells as well as ameloblastoma cells. Results: 3D tumouroid model successfully mimicked the ameloblastoma tumour microenvironment and native subtype cell morphology and caused ameloblastoma cells to produce more bone resorption proteins in earlier days. Then, a novel active bone-forming model was developed by forming bone nodules in 3D stiff matrix with high collagen density. This model allowed detection of early and late bone formation markers. The compositional and structural characterisation of the bone nodules was completed. The 3D bone stroma was used as a compartment of 3D ameloblastoma tumouroid model. This compartmentalised model showed that ameloblastoma directly inhibits bone nodule formation by targeting osteoblast differentiation genes and bone matrix development genes. Conclusion: The development of the first 3D ameloblastoma tumouroid model with of active bone stroma provided novel information about ameloblastoma microenvironment and some of the mechanisms associated with bone damage. The genes involved in ameloblastoma-induced inhibition of bone formation were identified. Further work is ongoing in order to include osteoclast-like cells in the 3D model, with a view to increase its biomimetic complexity, study the interaction between ameloblastoma cells, active bone formation cells, and osteoclasts, and explore potential drug targets

Desmoplastic ameloblastoma of maxilla: a case report

Ameloblastoma is the most common neoplasm affecting the jaws, arising from the odontogenic epithelium. Despite its locally aggressive nature, it is considered to be benign. The chief histopathological variants of ameloblastoma are the follicular and plexiform types, followed by the acanthomatous and granular cell types. Uncommon variants include desmoplastic, basal cell, clear cell ameloblastoma, keratoameloblastoma and papilliferous keratoameloblastoma. When the desmoplastic type co-exists with other types, it is called as “hybrid” ameloblastoma. There are significant anatomic, histopathological and radiological differences between desmoplastic ameloblastoma and the classical type. The purpose of this article is to report a case and to review the relevant literature, emphasizing peculiar aspects of this unusual lesion

Screening of Ameloblastoma Cases in Ibadan for HPV and EBV Genes.

Context: This study investigated the presence or absence of β-catenin and Patched1 (PTCH1) genes involved in the developmental pathway in ameloblastoma, in order to clarify the genetic etiology of this tumor. Aim: The aim of this study was to investigate whether PTCH1 and β-catenin genes are involved in the development of ameloblastoma. Subjects and Methods: Archived formalin-fixed paraffinembedded specimens of 89 ameloblastoma cases from the year 2000 to 2010 were genotyped by polymerase chain reaction (PCR). Results: A total of 21 (23.6%) of the 89 ameloblastoma cases were positive for β-catenin gene, where 14/21 (66.7%) cases were mandibular ameloblastoma. Plexiform 5/21 (23.8%) and cystic 5/21 (23.8%) ameloblastoma were the most regular histological type positive for β-catenin. However, β-catenin positive was more in the feminine gender (11/19, 57.9%) than the masculine (8/19, 42.1%). Only one case was positive for PTCH1 gene and this was histologically a mandibular site and plexiform-type ameloblastoma. Conclusions: This study suggested that β-catenin and PTCH1 genes may play an important role in the pathogenesis of ameloblastoma

Role of Apoptotic Biomarkers in Ameloblastoma and Dental Follicle

Objectives Ameloblastoma is an odontogenic neoplasm with locally aggressive behavior. Fas and FasL play important roles in apoptotic pathways. The aim of this study was to determine the possible role of expression of apoptotic pathways (Fas and FasL) in human ameloblastoma and the relationship of apoptosis with the clinical biological characteristics of ameloblastoma. Methods In this descriptive retrospective study, we investigated the anti-Fas and anti-FasL antibody expression in 11 dental follicles and 56 ameloblastoma specimens (35 conventional, 15 unicystic and 6 ameloblastic carcinoma samples) by immunohistochemical (IHC) staining and polymerase chain reaction (PCR). The percentage of positive cells was calculated by using the Mann-Whitney U test and Kruskal-Wallis test. Results The rate of expression of markers was significantly lower in dental follicles than all subtypes of ameloblastoma (P=0.01 for Fas, and P=0.0001 for FasL). The FasL proportional score was significantly higher in conventional ameloblastoma than in unicystic ameloblastoma and ameloblastic carcinoma (P=0.003). There was no significant relationship between the type of ameloblastoma and expression of Fas. Conclusion This study shows that the process of apoptosis in ameloblastomais a sign of behavioral change in odontogenic epithelial cells especially in conventional ameloblastoma and that the apoptotic factors may not play an effective role in the malignancy of ameloblastoma

Intraosseous ameloblastoma masquerading as exophytic growth: a case report

Intraosseous ameloblastoma is the most common and simple type of ameloblastoma prevalent among odontogenic tumors. Clinico-radiographically intraosseous ameloblastoma presents as slow, painless swelling or expansion of the jaws and described as multilocular expansile radiolucency that occurs most frequently in mandibular molar/ramus area. This article describes a case of follicular ameloblastoma involving 45 year old male which is different from the usual presentation, which includes-exophytic growth, different location and without expansion of the cortex

High frequency of BRAF V600E mutations in ameloblastoma

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