Ameloblastoma Research Articles

Assessment of Tumor Angiogenesis by Expression of CD 105 in Ameloblastoma, Odontogenic Keratocyst and Central Giant Cell Lesion.

Angiogenesis is critical for tumor growth and reflects the aggressive behavior of invasive odontogenic lesions [like Ameloblastoma (AM), Odontogenic Keratocyst (OKC) and Central giant cell lesion (CGCL)]. Mean vascular density (MVD) shows the angiogenic potential and CD105 is an ideal endothelial biomarker due to its specificity to new blood vessels for MVD detection. The aim of the study was to compare the MVD (angiogenic potential) among AM, OKC and CGCL in comparison to Pyogenic Granuloma (PG) using CD105 biomarker. Sixty-four primary cases of odontogenic invasive tumors (AM, OKC and CGCL) and PG, diagnosed clinically and histologically were included in the study, with 16 samples in each group. Tissue samples of peripheral AM, Peripheral GCL of jaws, malignant AM, and specimen with insufficient tissue were excluded. Tissue sections were embedded, processed and stained using Hematoxylin and Eosin (H and E). Immunohistochemistry was performed using antibodies against CD105, with positive brown cytoplasmic staining in the endothelial cells of neo-vasculature. Distinct countable, positively stained endothelial cell or clusters were evaluated under light microscope for identification of MVD. ANOVA and t-test were applied for statistical analysis of data. Highest MVD was displayed in CGCL (32.99±0.77) and the minimum was observed in OKC (7.21± 0.75) respectively. CGCL showed significantly higher MVD to AM, OKC and PG lesions (p <0.05). AM (8.07± 0.36) and Odontogenic Keratocyst (7.21± 0.75) showed comparable MVD, which was lower than PG (14.7± 0.96) and CGCL vascular density (p < 0.01) respectively. CGCL was most aggressive, with highest MVD among the investigated odontogenic lesions (OKC, AM and PG). The proliferative aggressive behavior of Odontogenic Keratocyst is comparable to AM due to comparable mean vascular density.<br />.

Expression of caveolin-1 in tooth germ, ameloblastoma and ameloblastic carcinoma.

Background The caveolin-1 protein (structural component of membrane caveolae) plays important roles in several biological functions, such as endocytosis, cell adhesion, and cell signaling. However, this protein has been associated with mechanisms of tumorigenesis in several neoplasms. The expression patterns and roles of caveolin-1 in the oral epithelium and in embryonic and odontogenic tumor tissues are still unclear. Material and Methods The expression of caveolin-1 was evaluated in samples of the normal gingival epithelium (n=7), human tooth germ (TG) (n=12), ameloblastoma (AM) (n=83), and ameloblastic carcinoma (AC) (n=9) by immunohistochemistry. Additionally, AM samples were analyzed by qRT-PCR and Western blot. Results Most TG (91.7%), AM (73.5%) and AC (100%) samples showed diverse patterns of immunohistochemical positivity for caveolin-1, while only one gingival sample was positive. The transcript levels of cav-1 were significantly upregulated by 14.9-fold in AM tissue (P = 0.0014) compared to those in normal gingival epithelial tissue, as shown by qRT-PCR. Presence of caveolin-1 protein was confirmed by Western blot analysis. The caveolin-1 immunoexpression patterns throughout the stages of TG show its importance during odontogenesis. Conclusions The overexpression of caveolin-1 in AM and AC compared to its expression in normal gingival epithelium (adult tissue) suggests a possible role of caveolin-1 in protumoral events, but due to the similar immunoexpression observed in AM and AC, caveolin-1 may not necessarily participate in the malignant transformation process. However, future studies are needed to clarify and confirm these hypotheses. Key words:Ameloblastoma, ameloblastic carcinoma, caveolin-1, immunohistochemistry, real-time polymerase chain reaction.

A firm mass of the maxillary gingiva

A firm mass of the maxillary gingiva

AMELOBLASTOMA WITH ADENOID CHARACTERISTICS: A CASE REPORT

The ameloblastoma (AM) with adenoid characteristics is a rare variant with presence of ductile structures similar to adenomatoid odontogenic tumor (TOA), but with aggressive biologic behavior. A 24-year-old patient, male, white, presented with an increased volume in the anteroposterior region of the mandible, with no pain and slow growth. The clinical and tomographic diagnoses were dentigerous cyst and odontogenic keratocyst. Subsequently, after complementary biochemical examinations, surgical resection was performed, in which the final histopathologic diagnosis confirmed the AM, but was associated with ductal structures with cell proliferation in a solid and storiform pattern, similar to TOA. Due to the aggressive form of ameloblastoma, the patient is under periodic follow-up. Thus, the need for a careful assessment of the odontogenic tumors is emphasized, because in this case, the prognosis of TOA and AM is different, affecting the surgical therapy used.

IMMUNOEXPRESSION OF OSTEOCLASTOGENIC FACTORS IN ODONTOGENIC CYSTS AND TUMORS

The osteolytic activity of odontogenic cysts and tumors is directly associated with their growth and aggressiveness. Objective: The objective of this study was to evaluate and compare the immunohistochemical expression of factors that stimulate receptor activator of nuclear factor kappa-Β ligand (RANKL), cathepsin K (CatK), matrix metalloproteinase 8 (MMP8) and inhibit osteoclastogenesis (osteoprotegerin [OPG]) in dentigerous cyst (DC), glandular odontogenic cyst (GOC), odontogenic keratocysts (OKCs), and ameloblastomas (ABs). Study design: Paraffin-embedded sections of 9 DCs, 9 GOCs, 20 OKCs, 21 ABs, and 4 dental follicles (DFs) were obtained and submitted to immunohistochemistry by the immunoperoxidase technique. Results: Immunoexpression of the proteins was observed in the epithelial and mesenchymal cells of all lesions studied. Higher expression of OPG and MMP8 was found in DC and DF compared to the other markers (P

IMMUNOEXPRESSION OF DNA BER AND NER PROTEINS IN BENIGN EPITHELIAL ODONTOGENIC LESIONS

Objective: To evaluate DNA base excision repair (BER) in APE-1 and XRCC1; and nucleotide excision repair (NER) in XPF proteins in benign epithelial odontogenic lesions with different biological behaviors. Study design: Thirty solid ameloblastomas (AMEs), 30 isolated odontogenic keratocysts (NSOKCs), 29 syndromic odontogenic keratocysts (SKOCs), 30 dentigerous cysts (DCs; n = 30), and 20 dental follicles (DFs) were evaluated quantitatively for APE-1, XRCC1 and XPF through immunohistochemistry. Results: All the odontogenic lesions studied revealed a statistically significant expression of APE-1 (nuclear), XRCC1 (nuclear), and XPF (nuclear and cytoplasmic) compared with DFs (P

Maspin, Syndecan-1, and Ki-67 in the Odontogenic Keratocyst: An Immunohistochemical Analysis.

The odontogenic keratocyst (OKC) is a controversial lesion that was reclassified as a tumor with the name “keratocystic odontogenic tumor” in 2005. The reclassification was revoked recently in 2017, with a conclusion on the need for further studies on the subject. In this study, the expressions of an important regulatory protein (maspin), an important integral membrane proteoglycan (syndecan-1), and a universal proliferation marker (Ki-67) in the epithelium of the OKC were investigated in comparison with the dentigerous cyst (DC) and ameloblastoma (AB). Twenty-six OKCs, eleven DCs, and ten conventional ABs were immunohistochemically stained for maspin, syndecan-1, and Ki-67. ImageJ was used to analyze the positivity of maspin and syndecan-1. The Ki-67 score was calculated as the percentage of positive nuclei in 5 high power fields. Analysis of variance (ANOVA) test and Student t-test were used as appropriate. Lower expressions of maspin were noted in OKC and DC compared to those in AB, and lower expressions of syndecan-1 were noted in OKC and AB compared to those in DC. The differences, however, did not reach statistical significance (ANOVA and t-test: P > 0.05). The Ki-67 score was significantly higher in OKC than in DC (t-test: P < 0.05), and not significantly different from AB (t-test: P > 0.05). In conclusion, expressions of maspin and syndecan-1 are not strongly representative of differences in behavior between OKC, AB, and DC. However, the expression of Ki-67 indicates comparable proliferative activities of OKC and AB, which are higher than that of DC. Further investigation on the biologic behavior of OKC is still recommended to arrive at more specific conclusions regarding its classification.

Automatic diagnosis for cysts and tumors of both jaws on panoramic radiographs using a deep convolution neural network.

The purpose of this study was to automatically diagnose odontogenic cysts and tumors of both jaws on panoramic radiographs using deep learning. We proposed a novel framework of deep convolution neural network (CNN) with data augmentation for detection and classification of the multiple diseases. We developed a deep CNN modified from YOLOv3 for detecting and classifying odontogenic cysts and tumors of both jaws. Our data set of 1282 panoramic radiographs comprised 350 dentigerous cysts (DCs), 302 periapical cysts (PCs), 300 odontogenic keratocysts (OKCs), 230 ameloblastomas (ABs), and 100 normal jaws with no disease. In addition, the number of radiographs was augmented 12-fold by flip, rotation, and intensity changes. We evaluated the classification performance of the developed CNN by calculating sensitivity, specificity, accuracy, and area under the curve (AUC) for diseases of both jaws. The overall classification performance for the diseases improved from 78.2% sensitivity, 93.9% specificity,91.3% accuracy, and 0.86 AUC using the CNN with unaugmented data set to 88.9% sensitivity, 97.2% specificity, 95.6% accuracy, and 0.94 AUC using the CNN with augmented data set. CNN using augmented data set had the following sensitivities, specificities, accuracies, and AUCs: 91.4%, 99.2%, 97.8%, and 0.96 for DCs, 82.8%, 99.2%, 96.2%, and 0.92 for PCs, 98.4%,92.3%,94.0%, and 0.97 for OKCs, 71.7%, 100%, 94.3%, and 0.86 for ABs, and 100.0%, 95.1%, 96.0%, and 0.97 for normal jaws, respectively. The CNN method we developed for automatically diagnosing odontogenic cysts and tumors of both jaws on panoramic radiographs using data augmentation showed high sensitivity, specificity, accuracy, and AUC despite the limited number of panoramic images involved.

Review of Ameloblastoma Case

Ameloblastoma is a benign epithelial neoplasm and ranges from 10% of the entire odontogenic tumor. Ameloblastoma is characterized by a slow growth pattern and can grow to a very large size and cause severe facial deformities. These tumors are most common at the age of the third and fourth decades, and most often occur in the posterior mandibular, especially in the third molar tooth, as well as associated with the impacted follicular or dental cyst. Classification of Ameloblastoma According to WHO distinguishable into benign ameloblastoma which include: (1) solid/multicystic ameloblastoma, (2) unicystic Ameloblastoma, (3) the peripheral (or extraosseous) ameloblastoma, (4) the desmoplastic ameloblastoma and malignant ameloblastoma based on the frequency sequence which includes: (a) metastasizing ameloblastoma, (b) Primary ameloblastic carcinoma, (c) Secondary intraosseous ameloblastic carcinoma, (d) secondary peripheral ameloblastic carcinoma. A radiological examination that can be conducted to diagnose ameloblastoma is plain photo, CT Scan and MRI. The image of Meloblastoma radiography may vary. Some of the depictions of lusent lesions are firmly, unilocular, well-orticated, which often relate to Corona tooth impacted or no eruption, so that it cannot be distinguished by odontogenic keratosis and dentigerous cysts on radiography. Some of the other, multilocular, internal septa and honey comb or soap appearance bubbles are often similar to the large odontogenic keratosis. However, only histopatological findings can help to determine the malignant tumors and the alteration of carcinomatose.

A New Look at the History of Peripheral Ameloblastoma.

Peripheral ameloblastoma (PA) is a prototype form of extraosseous odontogenic tumor. As knowledge of PA has accumulated on the basis of more than 200 cases reported worldwide over a 60-year timeframe, it is important to comprehend the historical evolution of this entity. In 2018, we summarized the American history of PA, stressing the important early strides made by Bloodgood in 1904 with his many original observations of the "epulis form of ameloblastoma". During the preparation of our previous report, we were able to find several earlier and interesting descriptions in the literature. This review covers the early history of PA since the nineteenth century, chronologically focusing on meritorious articles published in the United States and Europe.

Fluorescently Labeled Cetuximab-IRDye800 for Guided Surgical Excision of Ameloblastoma: A Proof of Principle Study

Fluorescently labeled epidermal growth factor receptor (EGFR) antibodies have successfully identified microscopic tumors in multiple invivo models of human cancers with limited toxicity. The present study sought to demonstrate the ability of fluorescently labeled anti-EGFR, cetuximab-IRDye800, to localize to ameloblastoma (AB) tumor cells invitro and invivo. EGFR expression in AB cells was confirmed by quantitative real-time polymerase chain reaction and immunohistochemistry. Primary AB cells were labeled invitro with cetuximab-IRDye800 or nonspecific IgG-IRDye800. An invivo patient-derived xenograft (PDX) model of AB was developed. The tumor tissue from 3 patients was implanted subcutaneously into immunocompromised mice. The mice received an intravenous injection of cetuximab-IRDye800 or IgG-IRDye800 and underwent imaging to detect infrared fluorescence using a Pearl imaging system (LI-COR Biosciences, Lincoln, NE). After resection of the overlying skin, the tumor/background ratios (TBRs) were calculated and statistically analyzed using a paired t test. EGFR expression was seen in all AB samples. Tumor-specific labeling was achieved, as evidenced by a positive fluorescence signal from cetuximab-IRDye800 binding to AB cells, with little staining seen in the negative controls treated with IgG-IRDye800. In the animal PDX model, imaging revealed that the TBRs produced by cetuximab were significantly greater than those produced by IgG on days 7 to 14 for AB-20 tumors. After skin flap removal to simulate a preresection state, the TBRs increased with cetuximab and were significantly greater than the TBRs with the IgG control for PDX tumors derived from the 3 patients with AB. The excised tissues were embedded in paraffin and examined to confirm the presence of tumor. Fluorescently labeled anti-EGFR demonstrated specificity for AB cells and PDX tumors. The present study is the first report of tumor-specific, antibody-based imaging of odontogenic tumors, of which AB is one of the most clinically aggressive. We expect this technology will ultimately assist surgeons treating AB by helping to accurately assess the tumor margins during surgery, leading to improved long-term local tumor control and less surgical morbidity.

LGR5+ epithelial tumor stem-like cells generate a 3D-organoid model for ameloblastoma

Ameloblastoma (AM) is a benign but locally aggressive tumor with high recurrences. Currently, underlying pathophysiology remains elusive, and radical surgery remains the most definitive treatment with severe morbidities. We have recently reported that AM harbors a subpopulation of tumor epithelial stem-like cells (AM-EpiSCs). Herein, we explored whether LGR5+ epithelial cells in AM possess stem-like cell properties and their potential contribution to pathogenesis and recurrence of AM. We found that LGR5 and stem cell-related genes were co-expressed in a subpopulation of AM epithelial cells both in vivo and in vitro, which were enriched under 3D-spheroid culture. As compared to LGR5− counterparts, LGR5+ AM epithelial cells showed increased expression of various EMT- and stemness-related genes, and functionally, exhibited increased capacity to form 3D-spheroids and generate human tumor 3D organoids, which recapitulated the histopathologic features of distinct subtypes of solid AM, thus, contributing a useful human tumor platform for targeted therapeutic screening. Treatment with a selective BRAFV600E inhibitor, vemurafenib, unexpectedly enriched the subpopulation of LGR5+ AM-EpiSCs in tumor 3D organoids, which may have explained therapeutic resistances and recurrences. These findings suggest that LGR5+ AM-EpiSCs play a pivotal role in pathogenesis and progression of AM and targeted inhibition of both BRAF and LGR5 potentially serves a novel nonsurgical adjuvant therapeutic approach for this aggressively benign jaw tumor.

Mandibular ameloblastoma with papillary hyperplasia in the gingiva: A case report

Although ameloblastomas are relatively common tumors, they rarely occur in the gingiva or oral mucosa. Most gingival or oral ameloblastomas are peripheral (that is, soft-tissue) ameloblastomas; therefore, an exophytic peripheral lesion from an intraosseous ameloblastoma is unusual. Here, we report a 63-year-old man who had an ameloblastoma with papillomatous proliferation in the lingual gingiva. Magnetic resonance imaging showed a well-defined mass in the mandible. These tumors were enucleated intraorally under general anesthesia. Histopathological and immunohistochemical examinations revealed that the respective tumors were a papilloma and an ameloblastoma, with different origins. The histopathological diagnosis was an intraosseous ameloblastoma with papillary hyperplasia. The patient’s postoperative course was uneventful during his 20-month post-enucleation follow-up period.

Upregulation of Neural Cell Adhesion Molecule 1 (NCAM1) by hsa-miR-141-3p Suppresses Ameloblastoma Cell Migration.

BackgroundNeural cell adhesion molecule 1 (NCAM1; CD56) and E-cadherin are both involved in cell-cell adhesion and cell development processes, and their dysregulation is associated with various tumors. We hypothesized that dysregulated NCAM1 could suppress the invasive behavior of ameloblastoma (AB), and its expression was regulated by miR-141-3p.Material/MethodsReal-time qPCR was performed to examine differences in miR-141-3p expression between AB tissues and normal oral tissues (NOMs). The potential target NCAM1 of miR-141-3p was predicted by bioinformatics analysis, which was validated through dual-luciferase assay. The mRNA and protein levels of NCAM1 were detected by real-time qPCR and Western blot, respectively. Furthermore, the expression and distribution of NCAM1 in AB were investigated through immunohistochemical staining, and immunohistochemical staining of E-cadherin was also performed. After overexpression of NCAM1, the migration of AM-1 cells was examined using wound-healing assay.ResultsReal-time qPCR results confirmed that miR-141-3p was significantly downregulated in AB tissues. According to bioinformatics analysis, NCAM1 was a target of miR-141-3p, which was confirmed by dual luciferase assay. We found that NCAM1 was significantly upregulated in AB tissues at the mRNA and protein levels. Furthermore, NCAM1 and E-cadherin were mainly expressed on the cell membrane of AB. Downregulation of E-cadherin was found in AB tissues. As shown in wound-healing assay results, NCAM1 overexpression significantly inhibited the invasiveness of AM-1 cells.ConclusionsIn this study, highly expressed NCAM1 was found in AB, and it suppressed the migration of AB cells and was regulated by miR-141-3p, suggesting its potential value as a therapeutic target for AB.

Differential expression of nicotinamide N-methyltransferase in primary and recurrent ameloblastomas and odontogenic keratocysts.

Odontogenic tumours are a group of rare heterogeneous diseases that range from hamartomatous tissue proliferations to benign and malignant neoplasms. Recurrences can occur after 10years, so long-term clinical and radiological follow-up is required. The study of the molecular mechanisms involved in the development of these lesions is necessary to identify new prognostic markers. In this study, we evaluate the possible role of nicotinamide N-methyltransferase (NNMT) in ameloblastomas (AM) and odontogenic keratocysts (OKC). A total of 105 surgical specimens of primary and recurrent lesions were obtained from 55 patients (25 AM, 30 OKC). In particular, 50 AMs (25 primary, 25 recurrences) and 55 OKCs (30 primary, 25 recurrences) were retrieved. We carried out immunohistochemical analyses to evaluate the cytoplasmic expression of NNMT, measuring the percentage of positive cells and the value of NNMT expression intensity. NNMT expression was significantly higher in recurrent than primary AMs (P=.0430). This result was confirmed by staining intensity, showing more cases with moderate/intense staining in recurrent AMs (P=.0470). NNMT expression was significantly lower in recurrent than primary OKC (P=.0014). Staining intensity showed more cases with moderate/intense staining in primary OKCs (P=.0276). This report is the first to evaluate NNMT expression in odontogenic lesions and to demonstrate a differential expression in recurrent AMs and OKCs, suggesting that there is potential for use of NNMT as prognostic marker.

A Novel lncRNA ENST00000512916 Facilitates Cell Proliferation, Migration and Cell Cycle Progression in Ameloblastoma.

ObjectiveOur purpose was to identify up-regulated long noncoding RNA ENST00000512916 in ameloblastoma (AB) and explore its role in the progression of AB.MethodsWe analyzed lncRNA microarray expression profile between six paired AB and normal oral mucosa (NOM) tissues. An up-regulated lncRNA, ENST00000512916 was identified and validated by real-time qPCR. Cell proliferation, migration and cell cycle were detected by CCK-8 assay, transwell chamber and flow cytometry, respectively. Western blotting analysis was used to measure the expression of cell-cycle-related proteins including CyclinD1 and Cyclin-dependent kinase (CDK) 2/4/6. In addition, Xenograft tumor model was constructed to investigate tumor growth.ResultsReal-time qPCR confirmed that lncRNA ENST00000512916 was up-regulated in AB tissues. ENST00000512916 knockdown significantly inhibited cell proliferation, migration and the expression of CDK2/4/6 in AM-1 cells. Moreover, ENST00000512916 knockdown suppressed tumor growth in vivo. We also found that ENST00000512916 overexpression significantly promoted the expression of HOXC13 in AM-1 cells. Overexpression of ENST00000512916 promoted cell cycle progression in AM-1 cells, which was reversed by HOXC13 knockdown.ConclusionOur findings reveal that lncRNA ENST00000512916 promotes cell proliferation, migration and cell cycle progression of AB.

Current concepts in ameloblastoma-targeted therapies in B-raf proto-oncogene serine/threonine kinase V600E mutation: Systematic review.

BACKGROUNDAmeloblastomas are common benign epithelial odontogenic neoplasms that present an aggressive and unpredictable behavior that may modify treatment strategies. Different signaling pathways that participate in the progression of these tumors have been identified. B-raf proto-oncogene serine/threonine kinase (BRAF) is a protein involved in the behavior of ameloblastomas, and it is related to many cell mechanisms. BRAF gene mutations have been identified in ameloblastomas, of which the BRAF V600E (valine substituted by glutamic acid at amino acid 600) mutation has been the most common and can be present concomitantly with other mutations that may be involved in its behavior. Targeted therapies have been used as an alternative in the case of resistance or contraindications to conventional treatments.AIMTo document the presence of BRAF V600E and additional mutations, their behavior, and targeted therapies in these tumors.METHODSAn electronic literature search was conducted according to PRISMA guidelines in PubMed/MEDLINE, Cochrane, EMBASE, and SpringerLink using the terms “ameloblastomas”, “BRAF V600E”, “additional mutations”, and “targeted therapies”. Ameloblastomas were classified according to WHO guidelines. Inclusion criteria were articles in English, published not more than 10 years ago, and studies with laboratory works related to BRAF V600E. Articles were evaluated by two independent reviewers and retrieved for full-text evaluation. The EBLIP Critical Appraisal Checklist was used to evaluate the quality of the eligible studies. Descriptive statistical analysis was performed.RESULTSTwo independent reviewers, with a substantial concordance indicated by a kappa coefficient of k = 0.76, evaluated a total of 19 articles that were included in this study. The analysis registered 521 conventional ameloblastomas (AM), 81 unicystic ameloblastomas (UA), 13 ameloblastic carcinomas (AC), three metastatic ameloblastomas (MA), and six peripheral ameloblastomas (PA), of which the histopathological type, anatomic location, laboratory tests, expression of BRAF mutation, and additional mutations were registered. The BRAF V600E mutation was found in 297 AM (57%), 63 UA (77.7%), 3 AC (23%), 1 MA (50%), and 5 PA (83.3%). Follicular type predominated with a total of 116 cases (40%), followed by plexiform type with 63 cases (22.1%). Furthermore, both types presented additional mutations, in which alterations in JAK3 P132T, SMARCB1, PIK3CA, CTNNB1, SMO, and BRAF G606E genes were found. Four case reports were found with targeted therapy to BRAF V600E.CONCLUSIONThe identification of BRAF V600E and additional mutations as an aid in targeted therapies has been a breakthrough in alternative treatments of ameloblastomas where surgical treatments are contraindicated.

Downregulated miR-524-5p Participates in the Tumor Microenvironment of Ameloblastoma by Targeting the Interleukin-33 (IL-33)/Suppression of Tumorigenicity 2 (ST2) Axis.

BackgroundAmeloblastoma (AB) is a common odontogenic epithelial tumor, with locally invasive behavior and high recurrence. In this study, we hypothesized that miR-524-5p could be involved in the tumor microenvironment by targeting interleukin-33 (IL-33)/suppression of tumorigenicity 2 (ST2) in AB.Material/MethodsThe microRNA (miRNA) expression profile of AB tissues and normal oral mucosa tissues (NOM; 6 paired samples) was analyzed. The miRNAs with fold change ≥2 and P<0.05 were considered to be differentially expressed. Among them, downregulated miR-524-5p was verified by real-time qPCR. Potential targets of miR-524-5p were predicted by bioinformatics analysis. The expression levels of target genes were detected using real-time qPCR and Western blot, respectively. Immunohistochemistry analysis of target genes was performed, and we also assessed the correlation between miR-524-5p and its target.ResultsMicroarray analysis results first indicated miR-524-5p is a downregulated miRNA in AB tissues. Real-time qPCR results confirmed the expression pattern of miR-524-5p in AB tissues. Moreover, IL-33 and its receptor ST2 were significantly overexpressed. As shown in immunohistochemistry results, IL-33 was positively expressed in lymphocytes and plasma cells, suggesting that IL-33/ST2 participates in tumor immune responses in the tumor microenvironment. Correlation analysis suggested that miR-524-5p expression was negatively correlated with IL-33/ST2.ConclusionsOur findings reveal that downregulated miR-524-5p can participate in the tumor microenvironment of AB by targeting the IL-33/ST2 axis.

Peripheral ameloblastoma- A rare case report

Peripheral ameloblastoma- A rare case report - JOOO- Print ISSN No: - 2395-6186 Online ISSN No:- 2395-6194 Article DOI No:- 10.18231/j.jooo.2019.031, Journal of Oral Medicine, Oral Surgery, Oral Pathology and Oral Radiology-J Oral Med Oral Surg Oral Pathol Oral Radiol

Peripheral ameloblastoma: A case report

An ameloblastoma is benign and locally aggressive odontogenic tumor of epithelial origin. This tumor comprises about 1% of tumors and cysts arising in the jaws. Because of its slow-growing nature, there is often a delay in the diagnosis. There may be a high local recurrence rate when the tumor is not properly removed, due to remaining tumor cells. Treatment decisions for ameloblastoma are based on the individual patient situation and the best judgment of the surgeon. This is a case report of a peripheral ameloblastoma that was treated with surgical excision, but resulted in recurrence after eight months. Keywords: Ameloblastoma, Peripheral ameloblastomas (PA).