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Nigerian Journal of Clinical Practice Sep 2022Ameloblastoma is a benign epithelial odontogenic tumor with a tendency for recurrence. The recurrent tumors behave unpredictably with atypical microscopic changes and...
BACKGROUND
Ameloblastoma is a benign epithelial odontogenic tumor with a tendency for recurrence. The recurrent tumors behave unpredictably with atypical microscopic changes and likelihood of malignant transformation.
AIMS
To study the clinicopathologic features and diagnostic outcome of recurrent tumors of ameloblastoma in Enugu. This is a six-year (2012-2017) retrospective study of 17 consecutive patients with recurrent tumors of ameloblastoma in a Teaching Hospital in Nigeria.
MATERIALS AND METHODS
The relevant clinicopathologic information, histology slides, and blocks were retrieved and reviewed. Descriptive analysis was used to determine the frequency, tables for categorical variables, and a Chi-square test was used to determine the statistical significance.
RESULT
Recurrent tumors constituted 33.3% (17/51) of all confirmed diagnoses of ameloblastoma. The diagnostic outcome of the recurrent tumors was conventional ameloblastoma 58.8% (10), unicystic ameloblastoma 5.9% (1), and ameloblastic carcinoma 35.3% (6). There was bilateral mandibular extension in 60.0% (9), pain 58.8% (10), ulceration 29.4% (5), and matted lymph nodes 5.9% (1). Tumors with positive fluid aspirates 82.4% (14) yielded dark-brown fluids in 90.0% (9) of recurrent ameloblastomas and in 66.7% (2) of ameloblastic carcinomas. Atypical peripheral hyperplasia, nuclear hyperchromatism, and increased vascularization were commonly observed in benign recurrences. The frequency of recurrence is significantly associated with the biological behavior of ameloblastoma P = 0.03.
CONCLUSION
Recurrent tumors of ameloblastoma presented atypical features and malignant transformation.
Topics: Ameloblastoma; Humans; Nigeria; Odontogenic Tumors; Retrospective Studies
PubMed: 36149215
DOI: 10.4103/njcp.njcp_82_22 -
Oral and Maxillofacial Surgery Sep 2023An increasing number of articles are published each year. The aim of this is to provide a list of the 100 most cited articles on the subject of ameloblastoma. (Review)
Review
OBJECTIVES
An increasing number of articles are published each year. The aim of this is to provide a list of the 100 most cited articles on the subject of ameloblastoma.
METHODS
A bibliographic search was performed on Google Scholar (GS), Microsoft Academic (MA), and Dimensions for ameloblastoma. A ranking was created in order of citation density. Graphical representations of keywords and authorship were created with VOSviewer. Statistical analysis was performed and only results with a 95% confidence interval were considered significant.
RESULTS
A helpful list of top 100 articles was developed to help professionals in a variety of ways. Some curiosities are discussed about this scientometric analysis in ameloblastoma articles.
CONCLUSIONS
A useful list of the top 100 most cited articles on ameloblastoma has been provided. Bibliometric and altmetric analysis using Google Scholar, Microsoft Academic, and Dimensions is a free and excellent tool, not only as a citation manager but also as a study reference.
Topics: Humans; Ameloblastoma; Bibliometrics; Publications; Authorship
PubMed: 35654987
DOI: 10.1007/s10006-022-01082-x -
Journal of Oral Biosciences Jun 2024Odontogenic tumors arise in the jawbone and originate from cells associated with tooth development. Therefore, understanding odontogenic tumors requires knowledge of all... (Review)
Review
BACKGROUND
Odontogenic tumors arise in the jawbone and originate from cells associated with tooth development. Therefore, understanding odontogenic tumors requires knowledge of all aspects of dental research, including tooth development and eruption. Ameloblastoma is the most common odontogenic tumor.
HIGHLIGHT
Although a benign tumor, ameloblastoma progresses with marked jawbone resorption. Because of its locally aggressive features, it can be treated surgically by resecting the surrounding bone. From a molecular pathology perspective, several genetic mutations and dysregulated signaling pathways involved in ameloblastoma tumorigenesis have been identified. Histopathologically, ameloblastomas consist of peripheral ameloblast-like cells and an inner stellate reticulum. The stromal region consists of fibrovascular connective tissue, showing a characteristic sparse myxoid histology. In general, the tumor microenvironment, including the surrounding non-tumor cells, contributes to tumorigenesis and progression. In this review, we focus on the tumor microenvironment of ameloblastomas. In addition, we present some of our recent studies on osteoclastogenesis, tubulin acetylation-induced cell migration, and hypoxia-induced epithelial-mesenchymal transition in ameloblastomas.
CONCLUSION
Further research on ameloblastomas can lead to the development of new treatments and improve patients' quality of life.
Topics: Ameloblastoma; Humans; Tumor Microenvironment; Cell Transformation, Neoplastic; Cell Movement; Jaw Neoplasms; Osteogenesis; Epithelial-Mesenchymal Transition; Osteoclasts
PubMed: 38734178
DOI: 10.1016/j.job.2024.05.002 -
Journal of Oral Biosciences Sep 2021Ameloblastoma is an odontogenic neoplasm of the mandible and maxilla with various histological types and subtypes. It has been reported that some ameloblastomas could...
OBJECTIVES
Ameloblastoma is an odontogenic neoplasm of the mandible and maxilla with various histological types and subtypes. It has been reported that some ameloblastomas could arise from dentigerous cyst walls; thus, the development of ameloblastoma from dentigerous cysts may be due to differential protein expression. Our aim was to identify a membrane protein that is differentially expressed in ameloblastomas with respect to dentigerous cysts.
METHODS
We analyzed the SDS-PAGE profiles of membrane proteins from ameloblastomas and dentigerous cysts. The protein in a band present in the ameloblastoma sample, but apparently absent in the dentigerous cyst sample was identified via mass spectrometry as the chaperonin Hsp60. We used western blotting and immunohistochemistry to analyze its overexpression and localization in ameloblastoma.
RESULTS
We found a differential band of 95 kDa in the membrane proteins of ameloblastoma. In this band, the chaperonin Hsp60 was identified, and its overexpression was corroborated using western blotting and immunohistochemistry. Hsp60 was localized in the plasma membrane of all ameloblastoma samples studied; in addition, it was found in the cell nucleus of the plexiform subtype of conventional ameloblastoma.
CONCLUSIONS
Our results suggest that Hsp60 may be involved in ameloblastoma development, and could therefore be a potential therapeutic target for ameloblastoma treatment.
Topics: Ameloblastoma; Chaperonin 60; Chaperonins; Dentigerous Cyst; Humans; Immunohistochemistry; Mitochondrial Proteins; Odontogenic Tumors
PubMed: 34010688
DOI: 10.1016/j.job.2021.05.001 -
Oral Diseases Oct 2022Ameloblastoma is an odontogenic epithelial tumour with a low expression of mismatch repair system components. We aimed to investigate the methylation status of the genes...
OBJECTIVES
Ameloblastoma is an odontogenic epithelial tumour with a low expression of mismatch repair system components. We aimed to investigate the methylation status of the genes MSH2, MSH3 and MSH6 (MutS group) in conventional ameloblastomas.
MATERIALS AND METHODS
The ameloblastoma and dental follicle samples (n = 10 each) were collected from 20 different patients. Each ameloblastoma sample was sectioned into two fragments: one was paraffin-embedded while the other one, likewise the dental follicle samples, was fixed in RNAlater and frozen at -196°C. All frozen samples were investigated for the MutS genes methylation levels, using the enzymatic restriction digestion and quantitative real-time PCR (qPCR) assay. The ameloblastoma paraffin-embedded samples were submitted to immunohistochemical reactions for MutS proteins detection and digitally quantification. Correlation analyses were performed between the immunohistochemical results and the respective gene methylation percentage.
RESULTS
There are no significant differences between the MutS genes methylation levels in the ameloblastoma and the dental follicle. However, a strong negative correlation was found between MSH2 and MSH6 gene methylation status and their respective proteins expressions evaluated by immunohistochemistry.
CONCLUSION
Our results show that the genes methylations is in part responsible for decreasing the expression of MSH2 and MSH6 genes in ameloblastoma.
Topics: Ameloblastoma; DNA Methylation; DNA-Binding Proteins; Humans; MutS Homolog 2 Protein; Odontogenic Tumors
PubMed: 33901323
DOI: 10.1111/odi.13887 -
International Journal of Oral Science Feb 2024Ameloblastoma is a benign tumor characterized by locally invasive phenotypes, leading to facial bone destruction and a high recurrence rate. However, the mechanisms...
Ameloblastoma is a benign tumor characterized by locally invasive phenotypes, leading to facial bone destruction and a high recurrence rate. However, the mechanisms governing tumor initiation and recurrence are poorly understood. Here, we uncovered cellular landscapes and mechanisms that underlie tumor recurrence in ameloblastoma at single-cell resolution. Our results revealed that ameloblastoma exhibits five tumor subpopulations varying with respect to immune response (IR), bone remodeling (BR), tooth development (TD), epithelial development (ED), and cell cycle (CC) signatures. Of note, we found that CC ameloblastoma cells were endowed with stemness and contributed to tumor recurrence, which was dominated by the EZH2-mediated program. Targeting EZH2 effectively eliminated CC ameloblastoma cells and inhibited tumor growth in ameloblastoma patient-derived organoids. These data described the tumor subpopulation and clarified the identity, function, and regulatory mechanism of CC ameloblastoma cells, providing a potential therapeutic target for ameloblastoma.
Topics: Humans; Ameloblastoma; Neoplasm Recurrence, Local; Phenotype; Cell Transformation, Neoplastic; Gene Expression Profiling
PubMed: 38424060
DOI: 10.1038/s41368-024-00281-4 -
Oral Diseases Nov 2022Ameloblastoma is a locally aggressive odontogenic tumor. Etiopathogenesis and locally aggressive growth properties of ameloblastoma can be attributed to a hypoxic...
Ameloblastoma is a locally aggressive odontogenic tumor. Etiopathogenesis and locally aggressive growth properties of ameloblastoma can be attributed to a hypoxic microenvironment conducive to tumor cell survival. Epithelial-derived follicular ameloblastoma cells (EP-AMCs) display enhanced basal autophagy, but the interplay of hypoxia and autophagy in EP-AMCs survival and ameloblastoma recurrence is unclear. We evaluated differential expression of autophagic markers in primary and recurrent ameloblastomas and hypothesized that hypoxia-induced autophagy supports EP-AMC survival. Primary and recurrent ameloblastomas were comparatively assessed for expression levels of pan-cytokeratin, Vimentin, and autophagic markers SQSTM1/p62, LC3, and pS6. EP-AMCs compared with human odontoma-derived cells (HODCs) were subjected to severe hypoxia to determine the interplay of hypoxia and autophagic process in posthypoxia survival. Pan-cytokeratin and SQSTM1/p62 were expressed by both primary and recurrent ameloblastoma epithelial cells while the ameloblastoma connective tissues displayed weak reactivity to vimentin. Under hypoxia, EP-AMC expression levels of hypoxia-inducible factor (HIF)-1α, p62, and LC3 were increased while pS6 was decreased posthypoxia. The combined decrease in pS6 and enhanced LC3 in EP-AMCs under hypoxia indicate that EP-AMCs re-establish basal autophagy under hypoxia. Taken together, these suggest a possible role of LC3-associated phagocytosis (LAP) in ameloblastoma cell survival.
Topics: Ameloblastoma; Autophagy; Cell Hypoxia; Cell Line, Tumor; Epithelial Cells; Humans; Hypoxia; Hypoxia-Inducible Factor 1, alpha Subunit; Keratins; Sequestosome-1 Protein; Tumor Microenvironment; Vimentin
PubMed: 33721362
DOI: 10.1111/odi.13848 -
Archives of Oral Biology Oct 2022Primary cilium is a cellular organelle with growing significance confirmed in tumour biology. Primary cilia have been associated with fine tuning of numerous cell...
OBJECTIVES
Primary cilium is a cellular organelle with growing significance confirmed in tumour biology. Primary cilia have been associated with fine tuning of numerous cell signalling pathways and the role of this structure in cancer initiation and progression is recently at the forefront of attention. Here, we investigated possible alterations in the occurrence of primary cilia and changes of associated signalling in ameloblastoma, which represents the most common odontogenic tumour.
METHODS
We performed immunohistochemistry to assess the number and morphology of primary cilia in ameloblastoma tissues. The gene expression of key SHH pathway members was analysed by qPCR. As a functional experiment, we treated a primary ameloblastoma cell line by a SHH pathway inhibitor Sonidegib (LDE225).
RESULTS
We uncovered differences in primary cilia distribution and appearance in histological subtypes of ameloblastoma with the highest number of ciliated cells in plexiform and follicular subtypes. SHH protein was located close to primary cilia in ameloblastoma epithelial cells and the expression of molecules downstream of SHH signalling was upregulated. Moreover, the inhibition of SHH pathway by Sonidegib caused downregulation of SHH effector gene GLI1 and cell cycle regulator CCND1 in ameloblastoma primary cell line. The inhibition of SHH signalling also altered the expression of molecules involved in intraflagellar transport.
CONCLUSIONS
In conclusion, our study uncovered alterations in number of ciliated cells and associated signalling in ameloblastoma, which indicate SHH inhibitors as potential therapeutic target to treat this disease.
Topics: Ameloblastoma; Cilia; Hedgehog Proteins; Humans; Odontogenic Tumors; Signal Transduction
PubMed: 35863182
DOI: 10.1016/j.archoralbio.2022.105499 -
Journal of Cancer Research and... 2019Metastasizing ameloblastoma (MA) is a very rare odontogenic tumor with 2% of incidence rate. It exhibits benign histopathological features and malignant intrinsic... (Review)
Review
Metastasizing ameloblastoma (MA) is a very rare odontogenic tumor with 2% of incidence rate. It exhibits benign histopathological features and malignant intrinsic quality in the form of metastasis which makes it a little more than a pathological curiosity. Various molecular aspects related with malignant behavior have been discussed. Because of this, it provides a diagnostic challenge for clinicians and surgeons. It is an elusive lesion which should be more researched and studied so that definitive diagnostic features can be put forward. The objective of this paper is to review the molecular aspect involved in the pathogenesis of MA which will aid in differentiating non-MA from MA and thus helping in providing proper treatment at an early stage.
Topics: Ameloblastoma; Biomarkers, Tumor; Disease Management; Disease Susceptibility; Epithelial-Mesenchymal Transition; Humans; Neoplasm Metastasis; Neoplasm Staging; Tumor Microenvironment
PubMed: 31169204
DOI: 10.4103/jcrt.JCRT_268_17 -
Journal of Oral Pathology & Medicine :... Nov 2023CTNNB1 gene encodes beta catenin, a transcriptional activator of Wnt pathway involved in the pathogenesis of odontogenic lesions. Though located intramembranously, its... (Review)
Review
BACKGROUND
CTNNB1 gene encodes beta catenin, a transcriptional activator of Wnt pathway involved in the pathogenesis of odontogenic lesions. Though located intramembranously, its translocation into cytoplasm and nucleus could trigger cell proliferation, inhibition of apoptosis, invasion and migration of the tumour cell.
MATERIALS AND METHODS
Five electronic databases including MEDLINE by PubMed, Google scholar, Scopus, Trip, Cochrane library and EMBASE until 1 January 2023 without period restriction were thoroughly searched. Those articles that identified CTNNB1 mutation and beta catenin in odontogenic lesions were included for review. Risk of bias was analysed for each study using QUADAS 2 tool and Review Manager 5.3 was used to output its result.
RESULTS
Thirty four published articles were included for data synthesis. A total of 1092 cases of odontogenic lesions were assessed for both CTNNB1 mutation and beta catenin expression. CTNNB1 mutation was observed in ameloblastoma, calcifying odontogenic cyst, calcifying cystic odontogenic tumour and all malignant odontogenic tumours. The beta catenin expression (nuclear and cytoplasmic) was maximum in odontogenic keratocyst and calcifying odontogenic cyst. The expression was variable in ameloblastomas, membranous in odontomas, calcifying cystic odontogenic tumour and nuclear in all malignant tumours.
DISCUSSION AND CONCLUSION
High recurrence of odontogenic keratocyst and aggressiveness of solid ameloblastoma and malignant odontogenic tumours could be associated with the nuclear translocation of beta catenin. Disparity between CTNNB1 mutation and beta catenin expression within odontogenic lesions suggests alternate routes of beta catenin activation. The review results support the unique localisation of beta catenin as a helpful diagnostic factor in the pathogenesis of odontogenic lesions.
Topics: Humans; Ameloblastoma; beta Catenin; Odontogenic Cyst, Calcifying; Odontogenic Cysts; Odontogenic Tumors
PubMed: 37840228
DOI: 10.1111/jop.13487