ABSTRACT
Abstract Introduction Sclerosing odontogenic carcinoma was a new addition to the list of head and neck tumors by World Health Organization in 2017. This lesion has scarcely been reported and a lack of pathognomonic markers for diagnosis exists. Objective The aim of the study was to summarize findings from the available literature to provide up-to-date information on sclerosing odontogenic carcinoma and to analyse clinical, radiological, and histopathological features to obtain information for and against as an odontogenic malignancy. Methods We conducted a comprehensive review of literature by searching Pubmed, EBSCO and Web of Science databases, according to PRISMA guidelines. All the cases reported as sclerosing odontogenic carcinoma in English were included. Data retrieved from the articles were gender, age, clinical features, site, relevant medical history, radiographical findings, histopathological findings, immunohistochemical findings, treatments provided and prognosis. Results Mean age at diagnosis of sclerosing odontogenic carcinoma was 54.4 years with a very slight female predilection. Sclerosing odontogenic carcinoma was commonly reported in the mandible as an expansile swelling which can be asymptomatic or associated with pain or paraesthesia. They appeared radiolucent with cortical resorption in radiograph evaluation. Histologically, sclerosing odontogenic carcinoma was composed of epithelioid cells in dense, fibrous, or sclerotic stroma with equivocal perineural invasion. Mild cellular atypia and inconspicuous mitotic activity were observed. There is no specific immunohistochemical marker for sclerosing odontogenic carcinoma. AE1/AE3, CK 5/6, CK 14, CK19, p63 and E-cadherin were the widely expressed markers for sclerosing odontogenic carcinoma. Surgical resection was the main treatment provided with no recurrence in most cases. No cases of metastasis were reported. Conclusion From the literature available, sclerosing odontogenic carcinoma is justifiable as a malignant tumor with no or unknown metastatic potential which can be adequately treated with surgical resection. However, there is insufficient evidence for histological grading or degree of malignancy of this tumor.
Resumo Introdução O carcinoma odontogênico esclerosante é a nova adição à lista de tumores de cabeça e pescoço da Organização Mundial da Saúde em 2017. Essa lesão é pouco relatada e não há marcadores patognomônicos para o diagnóstico. Objetivo Resumir os achados da literatura disponível para fornecer informações atualizadas sobre o carcinoma odontogênico esclerosante e analisar as características clínicas, radiológicas e histopatológicas a favor e contra sua classificação como uma lesão odontogênica maligna. Método Uma revisão abrangente da literatura foi feita nos bancos de dados Pubmed, Ebsco e Web of Science, de acordo com as diretrizes do Prisma. Todos os casos relatados em inglês como carcinoma odontogênico esclerosante foram incluídos. Os dados recuperados dos artigos foram sexo, idade, características clínicas, sítio do tumor, histórico médico relevante, achados radiográficos, achados histopatológicos, achados imuno-histoquímico, tratamentos instituídos e prognóstico. Resultados A média de idade ao diagnóstico de carcinoma odontogênico esclerosante foi de 54,4 anos, com uma predileção muito leve pelo sexo feminino. Tumores do tipo carcinoma odontogênico esclerosante foram comumente relatados na mandíbula como um edema expansivo, que pode ser assintomático ou associado a dor ou parestesia. Eles têm aparência radiolucente com reabsorção cortical na radiografia. Histologicamente, o carcinoma odontogênico esclerosante é composto por células epitelioides em estroma denso, fibroso ou esclerótico com invasão perineural ambígua. Atipia celular leve e atividade mitótica imperceptível foram observadas. Não há um marcador imuno-histoquímico específico para SOC. AE1/AE3, CK 5/6, CK 14, CK19, p63 e E-caderina foram os marcadores amplamente expressos para carcinoma odontogênico esclerosante. A ressecção foi o principal tratamento feito sem recorrência na maioria dos casos. Nenhum caso de metástase foi relatado. Conclusão De acordo com a literatura disponível, é justificável classificar o carcinoma odontogênico esclerosante como um tumor maligno com nenhum ou desconhecido potencial metastático, que pode ser tratado adequadamente com ressecção cirúrgica. Entretanto, não há evidências suficientes para a graduação histológica ou de malignidade desse tumor.
ABSTRACT
@#Introduction: Ameloblastoma is a benign but locally invasive odontogenic epithelial neoplasm with a high recurrence rate after treatment. The two main subsets encountered clinically are unicystic (UA) and solid/multicystic ameloblastoma (SMA). Currently neoplastic progression of many tumour types are believed to be related to parenchyma-stromal cell-cell interactions mediated by cytokines notably interleukins (IL). However their roles in ameloblastoma remain ill-understood. Materials and Methods: Thirty-nine formalin-fixed paraffin-embedded ameloblastoma cases comprising unicystic ameloblastoma (n=19) and solid/multicystic ameloblastoma (n=20) were subjected to IHC staining for IL-1α, IL-1β, IL-6 and IL-8. A semi-quantitative method was used to evaluate the expression levels of these cytokines according to cell types in the tumoural parenchyma and stroma. Results: Major findings were upregulations of IL-1α and IL-6 in SMA compared to UA. Both cytokines were heterogeneously detected in the tumoural parenchyma and stroma. Within the neoplastic epithelial compartment, IL-1α expression was more frequently detected in PA-like cells in UA whereas it was more frequently encountered in SR-like cells in SMA. IL-6 demonstrated higher expression levels in the stromal compartment of SMA. IL-1β and IL-8 were markedly underexpressed in both tumour subsets. Conclusions: Overexpression of IL-1α in SMA suggests that this growth factor might play a role in promoting bone resorption and local invasiveness in this subtype. The expression levels of IL-1α and IL-6 in three cellular localizations indicate that parenchymal-stromal components of ameloblastoma interact reciprocally via IL-1α and IL-6 to create a microenvironment conducive for tumour progression.