Academic literature on the topic 'Prognosis ameloblastomas'

Unicystic ameloblastoma is a distinguishable entity of ameloblastomas, characterized by slow growth and being relatively locally aggressive. Three histological types are recognized according to the degree of ameloblastomatous epithelial extension, namely, luminal, intraluminal, and mural types. This classification has a direct bearing on their biological behavior, treatment, and prognosis. However, there is difficulty in determining the most appropriate form of treatment for unicystic ameloblastoma. We present a case of unicystic ameloblastoma that occurred in the right posterior mandible of 19-year-old girl, which was enucleated and did not recur after 12-month follow-up.

Background: Ameloblastoma is a common benign aggressive odontogenic tumor with a tendency for high recurrence rate. Ameloblastic Carcinoma is the malignant counterpart of Ameloblastoma. However, they are usually difficult to be distinguished from one another. Therefore, using Immunohistochemical markers might be beneficial for diagnosing them accurately.Objective: Evaluation of SOX2 and GPC3 expressions as well as evaluating their roles in the tumorigenesis and the biological behavior of Ameloblastoma and Ameloblastic Carcinoma.Methods: Tissue samples are composed of 34 archived histopathologically confirmed cases of (19 Conventional Ameloblastomas, and 15 Ameloblatic Carcinomas). Sections were subjected to Immunohistochemical staining according to a standard protocol by applying antibodies to SOX2, and GPC3.Results: SOX2 and GPC3 expressions in recurrent Ameloblastoma were significantly higher than non- recurrent cases. Ameloblastic Carcinoma showed the highest immune-reactivity to SOX2 and GPC3 compared to the Conventional Ameloblastoma. Desmoplastic Ameloblastoma showed the highest scores of SOX2 and GPC3 compared to the other subtypes.Conclusions: SOX2 and GPC3 can be used as a panel for diagnosing the aggressive and the malignant odontogenic tumors accurately. Desmoplastic Ameloblastoma behaves more aggressively than other Conventional Ameloblastoma subtypes.

Ameloblastoma is an odontogenic neoplasm whose molecular pathogenesis has only recently been elucidated. The discovery of recurrent activating mutations in FGFR2, BRAF, and RAS in a large majority of ameloblastomas has implicated dysregulation of MAPK pathway signaling as a critical step in the pathogenesis of this tumor. Some degree of controversy exists regarding the role of mutations affecting the sonic hedgehog (SHH) pathway, specifically Smoothened (SMO), which have been postulated to serve as either an alternative pathogenetic mechanism or secondary mutations. Here, we review recent advances in our understanding of the molecular pathogenesis of ameloblastoma as well as the diagnostic, prognostic, and therapeutic implications of these discoveries.

BACKGROUND Ameloblastoma is a rare, benign odontogenic neoplasm which is locally aggressive and mostly present with a painless swelling. The enigma about the diagnosis of proliferative ameloblastoma and ameloblastic carcinoma is still a debate because the diagnostic criteria is not standardized or quantified which has a direct correlation on its biological behaviour and prognosis. Despite numerous studies, correlation between the histological patterns of ameloblastoma and tumour behaviour has not been consistently established. The present study was done to compare the expression levels of Ki-67 between conventional ameloblastoma, proliferative ameloblastoma and ameloblastic carcinoma and to assess the usefulness of these markers for diagnostic differentiation. METHODS A retrospective study of total of 18 cases of ameloblastoma were retrieved from the archives of Department of Oral and Maxillofacial Pathology, Saveetha Dental College from 2012 till 2019, which included conventional ameloblastoma, proliferative ameloblastoma and ameloblastic carcinoma. Immunohistochemical (IHC) analysis was done using the marker Ki-67 and labelling index were determined for the same. RESULTS The results of the current study showed that the cellular proliferative activity assessed using Ki-67 in follicular ameloblastoma was (55 %), 4 cases of plexiform ameloblastoma (22 %), 17 % of proliferative ameloblastoma and 6 % of ameloblastic carcinoma showed negative expression. CONCLUSIONS Immunophenotyping using the marker Ki-67 may be a useful tool for histological typing of ameloblastoma. KEY WORDS Ameloblastoma, Ki-67, IHC, Immunophenotyping

In this study, proliferating cell nuclear antigen (PCNA) and p53 protein expressions were analyzed in 16 cases of ameloblastoma and 8 cases of adenomatoid odontogenic tumor (AOT). The cases of ameloblastoma consisted of solid type tumors and histologic arrangements of different subtypes were observed. In some specimens, more than one histologic subtype was identified in the same lesion, and each tumor was categorized according to the predominant cell pattern. The odontogenic tumors were grouped as follows: follicular ameloblastoma (n=7), plexiform ameloblastoma (n=4), acanthomatous + follicular ameloblastoma (n=3), basal cell ameloblastoma (n=2), adenomatoid odontogenic tumor (n=8). PCNA immunohistochemical expression revealed stronger quantitative labeling index for the follicular ameloblastoma, while for p53 protein the strongest quantitative labeling index was detected in the plexiform type. Nevertheless, statistical analysis using ANOVA and Tukey's test did not detect significant differences (p>0.05) among the histologic subtypes of ameloblastoma. The findings of this study suggest that the different histologic patterns of ameloblastoma did not show a direct correlation with their clinical behavior and consequently with the prognosis of the cases. The results also indicated that the ameloblastoma has greater proliferative potential than the AOT, which can contribute to explain its more aggressive and invasive characteristics.

Ameloblastic carcinoma is a rare malignant odontogenic neoplasm with a poor prognosis. It can arise de novo or from a pre-existing ameloblastoma. Research into stemness marker expression in ameloblastic tumours is lacking. This study aimed to explore the immunohistochemical expression of stemness markers nestin, CD138, and alpha-smooth muscle actin (alpha-SMA) for the characterisation of ameloblastic tumours. Six cases of ameloblastoma and four cases of ameloblastic carcinoma were assessed, including one case of ameloblastic carcinoma arising from desmoplastic ameloblastoma. In all tumour samples, CD138 was positive, whilst alpha-SMA was negative. Nestin was negative in all but one tumour sample. Conversely, the presence or absence of these markers varied in stroma samples. Nestin was observed in one ameloblastic carcinoma stroma sample, whilst CD138 was positive in one ameloblastoma case, one desmoplastic ameloblastoma case, and in two ameloblastic carcinoma stroma samples. Finally, alpha-SMA was found positive only in the desmoplastic ameloblastoma stroma sample. Our results suggest nestin expression to be an indicator for ameloblastic carcinoma, and CD138 and alpha-SMA to be promising biomarkers for the malignant transformation of ameloblastoma. Our data showed that nestin, CD138, and alpha-SMA are novel biomarkers for a better understanding of the origins and behaviour of ameloblastic tumours.

ABSTRACT Ameloblastoma is a benign but locally aggressive odontogenic tumor. The knowledge about this tumor is gaining greater importance because of its emerging variants. It is very essential to know the clinical, radiological and histopathological features of all the subtypes of ameloblastoma along with their behavioral and prognostic characteristics. Worldwide, maxillary ameloblastoma is rare, but its late detection renders adequate treatment difficult. Majority occur in the mandible with about 5 to 20% occurring in the maxillary bone. Here, we report a case of follicular ameloblastoma of the anterior maxilla in a 60-year-old male. How to cite this article Vasan V, Balaji P, Latha S, Gupta A. Maxillary Ameloblastoma: A Rare Case Report. J Health Sci Res 2014;5(2):21-24.

The typical treatment of ameloblastoma is by surgery. The result of the procedure nevertheless does not always lead to complete healing of the sickness but to a recurrence during the post-operative period. It has been reported by a number of authors that the recurrence of the condition is influenced by a number of factors such as the kind of surgical intervention, the histological variant of the ameloblastoma and the incomplete removal of the tumor. The purpose of this research is to study the incidence of recurrence of ameloblastoma after surgery, taking into consideration type of surgery and size of the tumor. A study of 76 cases of ameloblastoma with different histological structures was undertaken in the laboratory of pathological anatomy of Central Research Institute of Dental and Maxillofacial Surgery. Data such as the recurrence of the disease and tumors size was collected, registered and analysed. The size of the tumors was expressed in conventional units. The analysis showed that basal cell and plexiform variants of ameloblastoma are often relate to cases with aggressive clinical courses. The tendency to the recurrence of the disease was also observed in the follicular and acanthomatous variants. According to the results of this study, cases of peripheral variants of ameloblastoma have the best prognosis.

Objective: To report a case of extragnathic sinonasal ameloblastoma and discuss its clinical features, approach to diagnosis, pathology, and management.
 
 Methods:
 Study Design: Case report
 Setting: Tertiary government university hospital
 Subject: One
 
 Results: A 40-year-old female consulted for a rapidly enlarging right intranasal mass of 4 months duration associated with recurrent profuse epistaxis and nasal obstruction. Previous specimens of the mass were histopathologically interpreted as ameloblastoma versus craniopharyngioma. Examination revealed a pink, fleshy, smooth right intranasal mass with associated nasomaxillary bulge and supero-lateral displacement of the right eye. Computed tomography (CT) scan and magnetic resonance imaging (MRI) of the nasal cavity and paranasal sinuses demonstrated a soft-tissue density occupying the entire nasal cavity with erosion but no invasion of the maxillary sinus and no intracranial extension despite erosion of the skull base. The mass was completely excised via lateral rhinotomy and the final histopathologic diagnosis was ameloblastoma.
 
 Conclusion: Extragnathic sinonasal ameloblastoma is a benign but locally aggressive variant of ameloblastoma involving the nasal cavity and/or paranasal sinuses often mimicking malignant tumors. Diagnosis is primarily based on histopathology but radiologic and intraoperative findings help distinguish it from differentials. Complete surgical excision remains the treatment of choice, and coupled with good follow up, may improve the prognosis of patients.
 
 Keywords: sinonasal ameloblastoma, extragnathic, craniopharyngioma

O ameloblastoma é um tumor odontogênico agressivo, localmente invasivo e altamente recorrente. Estudos demonstram que é a neoplasia odontogênica benigna mais comum e eventualmente pode apresentar comportamento de lesões malignas. A detecção da mutação BRAF V600E tem sido demonstrada como uma das principais vias de proliferação tumoral dos ameloblastomas. Portanto, a identificação desses marcadores poderão ser úteis para elaborar estratégias mais eficientes de tratamento dessa patologia, bem como melhorar a qualidade de vida dos pacientes. Este estudo pesquisou a mutação BRAF V600E, por meio da técnica de imunohistoquimica, em ameloblastomas mandibulares bem como correlacionou com dados clínicos e imaginológicos relevantes. A amostra consistiu de 84 casos diagnosticados como ameloblastoma e localizados na mandíbula dos acervos do Serviço de Patologia Cirúrgica do Departamento de Estomatologia da FOUSP e do Serviço de Cirurgia Bucomaxilofacial do Hospital Erasto Gaertner, Curitiba, PR. Os blocos obtidos foram submetidos a reação imunohistoquímica para detectar a mutação da proteína BRAF e foram coletados todos os dados clínicos e imaginológicos dos pacientes como sexo, idade, tamanho do tumor, localização mandibular, aspecto radiográfico, tipo e subtipo histológico e status do tumor. Análise estatística foi realizada buscando estabelecer correlação entre o marcador BRAF e dados clínicos e imaginológicos. Como resultados, dos 84 pacientes, 44 eram pacientes do sexo masculino (52,38%) e 40 feminino (47,62%). A mediana da idade encontrada foi de 25,5 anos sendo que em 42 casos foi observada idade inferior a mediana (50%) e 42 superior (50%). Com relação a presença ou ausência da mutação BRAF V600E, 66 casos apresentaram positividade para o marcador estudado (78,57%) e 18 foram negativos (21,43%). Ao relacionar a expressão de BRAF com as variáveis, foi observado significância estatística para a variável localização (P= 0,0353) e tamanho do tumor (P=0,008). Não foi observado resultados com significância estatística com relação às variáveis sexo (P=0,969), idade (P=1,0), aspecto radiográfico (P=0,977), padrão histológico (P=0,910), subtipo histológico (P=0,5141) e status do tumor (P=0,336). Os autores concluíram que a mutação BRAF V600E é comum em ameloblastomas mandibulares e é mais frequente tumores maiores de 4 cm e na região posterior de mandíbula. Além disso, independe do tipo histológico do tumor, idade e sexo do paciente, aspecto radiográfico e status do tumor (primário x recorrente).<br>Ameloblastoma is an aggressive odontogenic tumour, being locally invasive and highly recurrent. Studies have demonstrated that it is the most common benign odontogenic neoplasia, sometimes exhibiting behaviour of malignant lesions. Detection of BRAF V600E mutation has been shown to be one of the main proliferation pathways of ameloblastomas. Therefore, the identification of these markers can be useful to elaborate more efficient treatment strategies for this pathology as well as to improve the patient\'s quality of life. This study investigated the BRAF V600E mutation in mandible ameloblastomas by using the immunohistochemical technique and by correlating clinical and imaging data of the patients. The sample consisted of 84 cases diagnosed as mandibular ameloblastoma, with all blocks being obtained from the Surgery Pathology Service of the FOUSP Department of Stomatology and the Maxillofacial Surgery Unit of the Erasto Gaertner Hospital, Curitiba, PR. The blocks were submitted to immunohistochemical reaction for detection of BRAF protein mutation, with clinical and imaging data such as age, gender, tumour size, mandibular location, radiographic aspect, histological type and subtype, and tumour status were collected. Statistical analysis was performed in order to establish a correlation between BRAF marker and clinical and imaging data. The results showed that, of the 84 patients, 44 were male (52.38%) and 40 female (47.62%). The median age was 25.5 years old, with 42 cases having age below the median (50%) and 42 above it (50%). With regard to the presence or absence of BRAF V600E mutation, 66 cases were found to be positive for the marker (78.57%) and 18 were negative (21.43%). The correlation between BRAF expression and variables showed statistical significances for mandibular location (P = 0.0353) and tumour size (P = 0.008), whereas no statistical significance was observed for gender (P = 0.969), age (P = 1.0), radiographic aspect (P = 0.977), histological pattern (P = 0.910), histological subtype (P = 0.5141) and tumour status (P = 0.336). The authors concluded that BRAF V600E mutation is common in mandibular ameloblastomas, with tumours larger than four cm being more frequent in the posterior region of the mandible. In addition, this pathology occurs regardless of histological type of the tumour, age, gender, radiographic aspect and tumour status.

Abstract Squamous cell carcinoma (SCC) of the mobile tongue is the most common type of cancer of the oral cavity, accounting for 30-40% of oral cancers. It behaves aggressively and almost half of the affected patients still die of the disease despite great advances in its medical and surgical care. Ameloblastomas are the most common clinically significant type of odontogenic tumors, constituting approximately 1% of all cysts and tumors of the jaw. They are benign but locally invasive tumors with a strong tendency to recur after surgery. Ameloblastic carcinoma combines the histological features of ameloblastoma with cytologic atypia irrespective of the presence or absence of metastasis. The effectiveness of tight junction proteins (claudins 1, 4, 5, 7 and occludin) and cancer-associated fibroblasts (CAFs) as prognostic markers in OTSCC and as markers of malignancy in ameloblastomas was studied. Abundance of CAFs and Claudin 7 derangement was found to be associated with poor disease-specific survival in oral (mobile) tongue cancer. Appearance of CAFs within the epithelial islands of ameloblastoma was found to be a marker of malignancy in the tumor. The prognostic predictability of CAF density, Ki-67 (cell proliferation marker), maspin (tumor suppressor marker) and tumor DNA content (tumor ploidy using image cytometry) in tongue cancers was also tested. CAF density was the only marker strongly predictive of prognosis. In ameloblastomas, α-SMA (for CAFs), Ki-67, epithelial membrane antigen (EMA) and DNA content (using image and flow cytometry) were assessed as markers of ameloblastic carcinoma. Only α-SMA was able to predict ameloblastic carcinoma when found in the epithelial islands. In conclusion, staining for α-SMA and claudin 7 seems to be beneficial for prognostication in tongue cancer, while α-SMA staining may be beneficial in differentiating ameloblastoma from ameloblastic carcinoma.

Introduktion: Ameloblastom (AB), adenomatoid odontogen tumör (AOT), ameloblastiskt fibrom (AF) och odontogent fibrom (OF) är odontogena tumörer som innehåller epiteliala komponenter. Frekvensen av recidiv hos dessa varierar från låg förekomst till relativt hög förekomst. Syftet med denna studie är att undersöka om Ki-67, p53 och BRAF kan användas som prognostiska markörer i recidivmönstret hos dessa tumörer.Material och metod: Studien genomfördes genom immunohistokemi med monoklonala antikroppar av Ki-67, p53 och BRAF på respektive tumör. Tumörerna hämtades från avdelningen för Oral patologi på Malmö högskola. En statistisk analys utfördes med hjälp av Kruskal-Wallis envägs-ANOVA.Resultat: I de tio AB-fallen kunde en hög proliferation och en hög prevalens av muterade p53 ses. I de sju fallen av AOT kunde en måttligt hög proliferation och en generellt hög prevalens av muterade p53, jämförbara med värden för AB, ses. De sju fallen med AF och de fem fallen med OF visade båda en låg proliferation och en låg förekomst av muterade p53. Skillnaden mellan gruppen AB och AOT och gruppen AF och OF visade en signifikant högre infärgningsintensitet för både Ki-67 (p<0.001) och p53(p=0.001) för gruppen med AB och AOT.Konklusion: Proliferations index med Ki-67 och förekomst av p53-mutationer kan användas som en prognostisk markör för recidiv hos AB och AOT. Det är å andra sidan inte tillämpbart för AF och OF.<br>Introduction: Ameloblastoma (AB), adenomatoid odontogenic tumour (AOT), ameloblastic fibroma (AF) and odontogenic fibroma (OF) are all odontogenic tumours with an epithelial component. The recurrence rate for these odontogenic tumours varies from low frequencies to quite high frequencies. The aim of this study is to evaluate the expression of Ki-67, p53 and BRAF and the possibility of these antibodies acting as prognostic markers in the recurrence pattern of odontogenic tumours.Material and method: An immunohistochemical study using Ki67, p53 and BRAF monoclonal antibodies was performed on 29 paraffin blocks from the respective tumours obtained at the department of Oral Pathology in the Faculty of Odontology at Malmö University. Statistical analysis was performed with Kruskal-Wallis one-way ANOVA.Results: In the series of ten AB cases high proliferation activity and a high prevalence of p53 mutations was observated. In the seven AOT cases a moderately high proliferative activity as well as a generally high prevalence of p53 mutation, comparable to AB, was observed. The seven cases of AF and the five cases of OF demonstrated a low proliferative activity and a low prevalence of p53 mutation. The difference between AB and AOT versus AF and OF as two separate groups, showed a significantly higher staining intensity for both Ki-67 (p < 0.001) and p53 (p = 0.001) in AB and AOT as a group.Conclusion: Ki-67 proliferation index and p53-mutation status can be considered to be a prognostic marker for AB and AOT recurrence. This is, however, not applicable to AF and OF.