Adenomatoid Odontogenic Tumor Research Articles

Expression of anti - Apoptotic survivin in odontogenic keratocyst, adenomatoid odontogenic tumor and ameloblastoma.

The process of odontogenesis is complex involving epithelial-mesenchymal interactions, along with the molecular signalling pathways triggering the initiating process. The triggering factors and cells precisely involved in the pathogenesis of odontogenic cysts and tumors are unknown. There is a vast array of biomarkers used to stain different sites, thereby helpful in diagnosing and evaluating the prognosis of these cysts and tumors. In the following study, Anti Apoptotic survivin expression patterns were assessed quantitatively in 48 samples (12 each) of Reduced Enamel Epithelium, Adenomatoid Odontogenic Tumor, Odontogenic Keratocyst and Ameloblastoma. The Aim of this study is to assess the anti-apoptotic survivin expression in Reduced Enamel Epithelium, Adenomatoid odontogenic tumour, Odontogenic Keratocyst and Ameloblastoma. The present study is carried out with 12 samples in each group. Routine hematoxylin and eosin staining was performed for confirmatory diagnosis. Later Immunohistochemistry was performed using survivin antibody. Survivin protein expression was analyzed using the parameters like location, intensity, percentage of cells positivity with survivin protein and extent of staining. With the help of Olympus BX 43 microscope, with ProgRes microscope camera, the 48 slides obtained were examined. The region of interest was selected in each slide and number of cells positively stained was counted. Data was analyzed using SPSS software version 23. Descriptive for scale data, results were analysed by using ANOVA with Chi-square test for intergroup comparison. The results showed significant P value <0.05. Expression of survivin was highest in Ameloblastoma, followed by Odontogenic keratocyst, Adenomatoid odontogenic tumor, and Reduced Enamel Epithelium. Survivin was involved in the inhibition of apoptosis as well as the detailed understanding of the biological behaviour of odontogenic cysts and tumours, thereby increasing therapeutic approaches.

A RARE HYBRID AOT OF MAXILLARY ANTRUM: A CASE REPORT WITH 10 YEARS FOLLOW-UP

Introduction: Amongst all odontogenic tumors adenomatoid odontogenic tumor (AOT) accounts for only 3% of them. Being odontogenic in 1 origin, the tumor shows a plethora of histoarchitectural patterns. Sex predilection is towards females and likely occurs in second to third decades of life. Anterior maxilla is the commonest region for AOT; maxillary antrum being rare; in conjugation with dentigerous cyst (DC) then being the 2 rarest. Here we describe a case of gigantic AOT in 17-year-old male t Observation: hat occupied the left maxillary antrum with an impacted tooth which was clinically diagnosed as dentigerous cyst. In toto removal of the cystic tumor was accomplished with removal of retained impacted canine as well. Histopathological examination inferred the presence of an AOT with dentigerous like cystic lining. With uneventful healing no local recurrence was observed after 10 years of follow up. Implied take away lesson the Conclusion: prime importance of histopathological evaluation in all enucleated cysts, simultaneous more research into fourth type of a “hybrid variant” of AOT

The molecular basis of odontogenic cysts and tumours.

The advances in molecular technologies have allowed a better understanding of the molecular basis of odontogenic cysts and tumours. PTCH1 mutations have been reported in a high proportion of odontogenic keratocyst. BRAF p.V600E are recurrent in ameloblastoma and KRAS p.G12V/R in adenomatoid odontogenic tumour, dysregulating the MAPK/ERK pathway. Notably, BRAF p.V600E is also detected in ameloblastic carcinoma, but at a lower frequency than in its benign counterpart ameloblastoma. Recently, adenoid ameloblastoma has been shown to be BRAF wild-type and to harbour CTNNB1 (β-catenin gene) mutations, further suggesting that it is not an ameloblastoma subtype. CTNNB1 mutations also occur in other ghost-cell-containing tumours, including calcifying odontogenic cysts, dentinogenic ghost cell tumours and odontogenic carcinoma with dentinoid, but the link between CTNNB1 mutations and ghost cell formation in these lesions remains unclear. Regarding mixed tumours, BRAF p.V600E has been reported in a subset of ameloblastic fibromas, ameloblastic-fibrodentinomas and fibro-odontomas, in addition to ameloblastic fibrosarcoma. Such mutation-positivity in a subset of samples can be helpful in differentiating some of these lesions from odontoma, which is BRAF-wild-type. Recently, FOS rearrangements have been reported in cementoblastoma, supporting its relationship with osteoblastoma. Collectively, the identification of recurrent mutations in these aforementioned lesions has helped to clarify their molecular basis and to better understand the interrelationships between some tumours, but none of these genetic abnormalities is diagnostic. Since the functional effect of pathogenic mutations is context and tissue-dependent, a clear role for the reported mutations in odontogenic cysts and tumours in their pathogenesis remains to be elucidated.

Adenomatoid odontogenic tumors: Rare cases in Enugu, Eastern Nigeria

Adenomatoid odontogenic tumors (AOTs) are very rare. We present a case series of eight AOTs seen and managed at University of Nigeria Teaching Hospital (UNTH), Ituku-Ozalla, Enugu State, Nigeria over a 10-year period, from 2012 to 2021. Their epidemiological data and clinic-pathological information were obtained from the biopsy forms, histopathology reports, and case files archived in the Records Department of the hospital. The AOTs were diagnosed in 8 patients out of the 225 odontogenic tumors seen during the period giving a prevalence of 3.6%. Five patients (62.5%) were males, whereas three (37.5%) were females giving a male-to-female ratio of 1.7:1. The mean (SD) age at onset of lesion was 12.4 (5.4) years with a range of 5–21 years. The location of the tumors was anterior in 62.5% of the jaw cases. A maxillary location was observed in 62.5% of the cases. Pain complaint was reported in 25% of the subjects. Tumor fluid was aspirated in 75.0% (n = 6) of the lesions: straw aspirate (83.3%),and dark-brown aspirate (16.7%). A tooth was associated with the tumor in 87.5% (n = 7) of the cases, with the canine impacted in 85.7% (n = 6) of these. Only one case (12.5%) was extrafollicular. The AOTs are uncommon and differed from other Nigerian studies by exhibiting a male gender prevalence, lower mean age, and frequent straw aspirates.

Correlation of amyloid and ameloblast-associated proteins to odontogenic cysts and tumors: A cross-sectional study.

Odontogenic cysts and tumors often form hard and soft structures that resemble odontogenesis. It is well known that amyloid is produced in Pindborgtumors; however, it is still debatable whether it is also formed in other odontogenic tumors and cysts. This study aimed to detect the presence of amyloid in different odontogenic cysts and tumors in correlation to matrix proteins secreted during enamel formation; namely amelogenin and odontogenic ameloblast-associated protein. This study included formalin fixed paraffin embedded tissue blocks of 106 different types of odontogenic cysts and tumors. Congo red and thioflavin T were performed to confirm the presence of amyloid; immunohistochemistry was used to detect amelogenin and odontogenic ameloblast-associated protein. Amyloid was detected in pindborg tumors (conventional), adenomatoid odontogenic tumors, odontogenic fibroma (Amyloid variant), follicular solid and unicystic ameloblastomas, radicular cysts, dentigerous cysts, dentinogenic ghost cell odontogenic tumor, ameloblastic fibroma, calcifying odontogenic cyst, and primordial Odontogenic tumor. Amelogenin was detected in 95.3% of the cases, while odontogenic ameloblast-associated protein was detected in 93.4% of the cases. The association between odontogenic ameloblast-associated protein and amyloid was highly significant at p < 0.01. However, there was no significant relationship between amelogenin and amyloid p > 0.05. Although pindborg tumor is the bonafide example of amyloid deposition in odontogenic tumors, this study concluded that amyloid may be deposited in traces to massive amounts in various odontogenic cysts and tumors, and it is significantly linked to odontogenic ameloblast-associated protein but not amelogenin matrix protein, since all amyloid cases were odontogenic ameloblast associated protein positive.

Prevalence of Odontogenic Tumours: A Study of 122 Cases among Karnataka Population

Introduction: Tumours arising from odontogenic tissues are rare and constitute a heterogeneous group of interesting lesions. Studies on incidence of Odontogenic Tumours (OT) published from many countries show a distinct geographic variation. Aim: The aim of present study was to compare and correlate the frequency of individual OT in India as well as the other parts of the world based on 2005 World Health Organization (WHO) classification. Materials and Methods: This institution-based retrospective study conducted in Department of Oral Pathology and Microbiology at Government Dental College and Research Institute, Bengaluru, Karnataka, India, from April 2015 to September 2016. Total of 122 cases of odontogenic tumours documented in duration of 10 years (2005 to 2014) were categorised based on World Health Organization 2005 classification. The histological type, age, gender, anatomical site and symptoms were systematically tabulated. Results: Odontogenic tumours constituted 9.5% (122 cases) of the total oral biopsies (1284 cases) received in a 10 year period. Among these, 95.9% of the tumours were benign and 4.1% were malignant. The most frequent tumour being ameloblastomas 39.3% followed by keratocystic odontogenic tumour 35.2%, odontome 4.9%, calcifying cystic odontogenic tumour 4.9% and adenomatoid odontogenic tumour 4%. While odontome, generally regarded as the most frequent OT in American and European countries, only accounted for 4.9%, the third most common tumour in the present study. The mean age of patients was 32.37 years (range: 9-70 years). Their exist a slight male predominance, more predilection to posterior region of mandible and majority of tumours presented with pain and swelling. Conclusion: The relative frequency of Odontogenic tumours reported in our institution was similar to the studies reported in India, Asian and African population but differs from that of European and American countries. There is a definite geographic variation in the prevalence of OT published worldwide.

An unusual presentation of aneurysmal bone cyst of the maxillary sinus in a child: A rare case report

ABSTRACT Aneurysmal bone cyst(ABC) is a rare vascular tumor arising usually from long bone and vertebrae,very rarely involves the skull and facial bone. Here, we present a case of a 9-year-old child presented with progressive proptosis and strabismus of the left eye associated with nasal obstruction and epistaxis. Computed tomography was done which gave us an insight into the possibilities of ABC, giant cell tumor, adenomatoid odontogenic tumor, etc., Biopsy was taken for histopathological confirmation. Usually, ABC of the maxillary sinus presents with pain, cheek swelling, and nasal obstruction. Our patient presented with ocular findings which are rare among maxillary bone ABCs.

Extra-follicular Variant of Adenomatoid Odontogenic Tumor: A Diagnostic Enigma

Adenomatoid odontogenic tumor (AOT) is an uncommon, slow-growing, noninvasive odontogenic tumor mostly in the anterior maxilla with three well-recognized clinico-pathological variants: follicular, extra-follicular, and peripheral. Extra-follicular variant presents as a well-defined, unilocular, radiolucency in between, above, or superimposed on the roots of an erupted tooth. A 19 years female reported with the chief complaint of a loose tooth in the right front region of the upper jaw for 6 months, associated with firm swelling without pain or discharge. On orthopantomogram and cone-beam computed tomography, the lesion appeared as a single, localized, well-defined, roughly oval unilocular radiolucency with flecks of radiopacity integrating radicular and cervical third of 13. Complete surgical enucleation followed by histopathological examination revealed the lesion as AOT. The extra-follicular AOT can cause diagnostic dilemmas and is often misdiagnosed as an odontogenic cyst.

Expression of Fascin and SALL4 in odontogenic cysts and tumors: an immunohistochemical appraisal.

Background: Various stemness markers (SOX2, OCT4, and NANOG) have been studied in odontogenic cysts and tumors. However, studies on SALL4 having similar properties of stemness has not been documented. Additionally, insight into fascin as a migratory molecule is less explored. In this study, the expression of SALL4 and fascin were evaluated in ameloblastoma, adenomatoid odontogenic tumor (AOT), odontogenic keratocyst (OKC), dentigerous cyst (DC), radicular cyst (RC), and calcifying odontogenic cyst (COC). Methods: Semi-quantitative analysis of fascin and SALL4 immuno-positive cells was done in a total of 40 cases of ameloblastoma (11 plexiform, 12 follicular, 12 unicystic, and 5 desmoplastic) variants, 6 cases of AOT, 15 each of OKC, DC, RC and 5 of COC. Chi-square test was applied to evaluate the association between SALL4 and fascin expression in odontogenic cysts and tumors. Results: Fascin immunopositivity was observed in peripheral ameloblast-like cells, and weak or absent in stellate reticulum-like cells. A moderate to weak immune-reactivity to SALL4 was observed in the cytoplasm of ameloblastoma, epithelial cells of dentigerous and radicular cysts, having a marked inflammatory infiltrate, which is an interesting observation. COC and AOT had negative to weak expressions. No recurrence has been reported. Conclusions: Expression of fascin in ameloblastomas elucidate their role in motility and localized invasion. Its expression in less aggressive lesions like DC, COC, AOT will incite to explore the other functional properties of fascin. SALL4 expression in the cytoplasm of odontogenic cysts and tumors may represent inactive or mutant forms which requires further validation.

Adenomatoid odontogenic tumour- revisted

Adenomatoid odontogenic tumor, fourth most common odontogenic tumor in the Indian population. It is the most common odontogenic tumor associated with impacted teeth. The diagnosis stands important as it is most commonly associated with an impacted maxillary canine. An adenomatoid odontogenic tumor (AOT) is a tumor of epithelial origin that shows duct-like structures and the epithelium forms whorled masses of cells in a scant fibrous stroma. AOT is not a common odontogenic neoplasm and it was first described by Steensland in the year 1905. Initially, AOT was described as pseudoadenoameloblastoma by Dreibladt in the year 1907 and it was considered a distinct entity and some of them believed it to be a variant of ameloblastoma by Stafne in the year 1948.

An Unusual Presentation of “Two-Thirds Tumor” in the Mandible – A Diagnostic Quandary with a Review of the Literature

An adenomatoid odontogenic tumor (AOT) is an uncommon benign tumor of the oral cavity commonly found in the maxillary anterior region and is associated with impacted canines in young females. It rarely occurs in the mandibular region with no impacted or missing teeth. A 21-year-old female reported to the clinic with swelling on the right side of the face for the past six months with no history of pain. Radiographic features such as unilocular radiolucency with thinning of the cortical borders and considerable buccal cortical expansion, as well as some evidence of radiopaque specks were noted. Histopathological examination revealed cells with hyperchromatic nuclei, rosette-like structures with focal areas of calcified mass, and concentric rings resembling Liesegang rings, suggestive of AOT. The tumor was treated surgically by enucleation and cauterization. Although follicular type is a common variant, the tumor presented in this case was of extrafollicular type noted in the mandibular canine and premolar regions of a young female patient with no related impacted tooth.

Immunohistochemical expression of Ki-67 and Glypican-3 to distinguish aggressive from nonaggressive benign odontogenic tumors.

The benign neoplasms are normally slow growing, indolent with no invasive potential. However, there exist a few locally aggressive benign odontogenic tumors that have a tendency to invade and deform the surrounding structures. The exact reason for the aggressiveness of these benign neoplasms remained an enigma. Their biology and clinical expression can often be destructive and ominous. An appropriate treatment protocol needs to be followed to combat the high recurrence rate and aggressiveness of these entities. Aggressive and noniaggressive epithelial odontogenic tumors were analyzed immunohistochemically with Ki-67 and glypican 3 (GPC3). Fifty-nine cases of tumors were divided into aggressive odontogenic tumors (20 solid ameloblastomas, four unicystic ameloblastoma, and 28 keratocystic odontogenic tumors) and nonaggressive odontogenic tumors (five adenomatoid odontogenic tumors and two calcifying cystic odontogenic itumors). Statistical analysis using Pearson correlation showed Ki-67 to be a better marker for differentiating aggressive from nonaggressive odontogenic tumor as compared to GPC3 (P < 0.001, highly significant), whereas among aggressive tumors, GPC3 turned out to be more useful as compared to Ki-67 (P < 0.001, highly significant). The present study provides an insight into the different biological behavior of odontogenic tumors, which can thus be helpful in determining the therapy strategies for more aggressive odontogenic tumors.

CDC7 Expression in Selected Odontogenic Tumors.

CDC7 is a serine-threonine kinase that plays a key role in initiating DNA replication. It has been implicated in the growth and invasion of many pathologic lesions and suggested as a diagnostic marker. The aim of this study was to evaluate CDC7 in some odontogenic tumors. In this cross-sectional study, 45 cases, including 19 ameloblastomas, 15 dentigerous cysts, 7 ameloblastic fibromas, and 4 adenomatoid odontogenic tumors (AOT), were studied immunohistochemically. ANOVA and post hoc methods were used for statistical analysis. CDC7 expression was observed in 93% of tumors and all dentigerous cysts. The expression rate was low. The results showed a higher expression rate of CDC7 in ameloblastoma and ameloblastic fibroma compared to AOT (p=0.009 and p=0.048, respectively). Ameloblastoma and ameloblastic fibroma were not significantly different in CDC7 expression (p=0.6). According to the results, the expression of the CDC7 protein in odontogenic tumors is low. The higher expression of CDC7 in ameloblastoma and ameloblastic fibroma in comparison with AOT confirms the hamartomatous growth of the latter, so it can be considered as a potential diagnostic marker. Future studies with a larger sample size are suggested to obtain a cut-off point for diagnostic purposes.

Molecular diagnostics in odontogenic tumors.

Odontogenic tumors (OTs) are rare, with an estimated incidence rate of less than 0.5cases per 100,000 per year. The causes of OTs remain unclear. Nonetheless, the majority of OTs seem to arise de novo, without an apparent causative factor. Although the etiopathogenesis of most OTs remains unclear, there have been some recent advances in understanding the genetic basis relating to specific histologies and clinical features. Molecular analyses performed by different techniques, including Sanger sequencing, next-generation sequencing, and allele-specific PCR, have uncovered mutations in genes related to the oncogenic MAPK/ERK signaling pathway. Genetic mutations in these pathway genes have been reported in epithelial and mixed OTs, in addition to odontogenic carcinomas and sarcomas. Notably, B‑RAF proto-oncogene serine/threonine kinase (BRAF) and KRAS proto-oncogene GTPase (KRAS) pathogenic mutations have been reported in ahigh proportion of ameloblastoma and ameloblastoma-related tumors and adenomatoid odontogenic tumors, respectively. To discuss how molecular profiling aids in diagnostic classification of odontogenic tumors. Molecular profiling of odontogenic tumors helps to identify patients for neoadjuvant therapies and reduces postoperative morbidity.

Homeobox Genes in Odontogenic Lesions: A Scoping Review.

Homeobox genes play crucial roles in tooth morphogenesis and development and thus mutations in homeobox genes cause developmental disorders such as odontogenic lesions. The aim of this scoping review is to identify and compile available data from the literatures on the topic of homeobox gene expression in odontogenic lesions. An electronic search to collate all the information on studies on homeobox gene expression in odontogenic lesions was carried out in four databases (PubMed, EBSCO host, Web of Science and Cochrane Library) with selected keywords. All papers which reported expression of homeobox genes in odontogenic lesions were considered. A total of eleven (11) papers describing expression of homeobox genes in odontogenic lesions were identified. Methods of studies included next generation sequencing, microarray analysis, RT-PCR, Western blotting, in situ hybridization, and immunohistochemistry. The homeobox reported in odontogenic lesions includes LHX8 and DLX3 in odontoma; PITX2, MSX1, MSX2, DLX, DLX2, DLX3, DLX4, DLX5, DLX6, ISL1, OCT4 and HOX C in ameloblastoma; OCT4 in adenomatoid odontogenic tumour; PITX2 and MSX2 in primordial odontogenic tumour; PAX9 and BARX1 in odontogenic keratocyst; PITX2, ZEB1 and MEIS2 in ameloblastic carcinoma while there is absence of DLX2, DLX3 and MSX2 in clear cell odontogenic carcinoma. This paper summarized and reviews the possible link between homeobox gene expression in odontogenic lesions. Based on the current available data, there are insufficient evidence to support any definite role of homeobox gene in odontogenic lesions.

Synchronous odontogenic tumors: A systematic review.

This systematic review aimed to incorporate published information about synchronous odontogenic tumors (SOTs) with an analysis of the demographic and clinical characteristics from the cases published in the literature. Case reports and case series of SOT were searched in PubMed, Web of Science, Scopus, and EMBASE. A descriptive statistical analysis was performed. Twenty-eight studies comprising 30 cases of SOTs were included. Considering all cases published, SOTs mostly occurred simultaneously in the maxilla and mandible (n=19/63.3%). Lesions were bifocal in 13 (43.3% of all the 30 cases) and multifocal in 17 cases (56.7% of all the 30 cases). All SOTs available in the literature presented the same type of lesion, and two of them also involved another different SOT (n=2/6.7% of all the 30 cases). Out of all published cases, the most frequent SOTs in the literature were odontomas (n=10/33.3% of all the 30 cases), squamous odontogenic tumors (OTs) (n=8/26.7% of all the 30 cases), calcifying epithelial OTs (n=8/26.7% of all the 30 cases), and adenomatoid OTs (n=2/6.7% of all the 30 cases). Considering all SOTs cases included, the overall recurrence was 13.3%. Inside a subgroup of the lesion, synchronous calcifying epithelial OT presented the highest (25%). Five cases (16.7% of all the 30 cases) had a previously associated syndrome, with two cases of Schimmelpenning syndrome being reported. Among published SOTs, odontomas were the most common. All SOTs available in the scientific literature showed the same type of OT and mainly affected both jaws simultaneously. Only a few of these cases were associated with a syndrome.

Immunohistochemical analysis of SHH, SMO and GLI-1 proteins in epithelial odontogenic lesions.

The present study analyzed the expression of proteins involved in the sonic hedgehog signaling pathway (SHH, SMO, and GLI-1) in benign epithelial odontogenic lesions (odontogenic keratocyst - OKC, ameloblastoma - AB, and adenomatoid odontogenic tumor - AOT) in order to identify the role of these proteins in the pathogenesis of these lesions. The sample consisted of 20 OKCs, 20 ABs, and 10 AOTs. The Kruskal-Wallis, Mann-Whitney U, and Spearman's (r) tests were used for statistical analysis, with the level of significance set at 5% (p < 0.05). The membrane/cytoplasmic expression of SHH was significantly higher in AB compared to AOT (p = 0.022) and OKC (p = 0.02). No differences were found in the membrane/cytoplasmic expression of SMO between the lesions studied. Regarding GLI-1, significant differences were observed at the nuclear level for AB and OKC compared to AOT (p < 0.0001). In addition, significant positive correlations were found between cytoplasmic and nuclear GLI-1 in AB (r = 0.482; p = 0.031) and OKC (r = 0.865; p < 0.0001), and between membrane/cytoplasmic SMO and cytoplasmic GLI-1 in AOT (r = 0.667; p = 0.035) and OKC (r = 0.535; p = 0.015). The results of this study confirm the participation of the sonic hedgehog signaling pathway in the pathogenesis of the lesions studied. Overexpression of SHH in ABs and nuclear expression of GLI-1 in ABs and OKCs indicate that these proteins contribute to the more aggressive behavior of these two lesions when compared to AOT.

IMMUNOEXPRESSION OF GALECTINS-1, -3, AND -7 IN AMELOBLASTOMAS AND ADENOMATOID ODONTOGENIC TUMORS

<h3>Objectives</h3> To investigate immunoexpression of galectins -1, -3, and -7 in ameloblastoma (AM) and adenomatoid odontogenic tumor (AOT), comparing them with clinicomorphologic parameters. <h3>Study Design</h3> A total of 31 cases of AM and 20 cases of AOT were analyzed. Immunoexpression of galectin-1, -3, and -7 was analyzed in parenchyma (quantitatively) and stroma (presence/absence). In the parenchyma, immunopositivity of cell compartments (nucleus and/or cytoplasm) was also considered. Mann-Whitney and Fisher's exact tests were used (<i>P</i> < .05). <h3>Results</h3> In parenchyma, AM showed the highest nuclear expression of galectin-1 (<i>P</i> < .001), galectin-3 (<i>P</i> < .001), and galectin-7 (<i>P</i> < .001). Significant differences were observed in the immunoexpression of nuclear galectin-1 with recurrent AM (<i>P</i> < .001) and nuclear galectin-7 with conventional AM (<i>P</i> = .040). In tumor stroma, AM showed higher expression of galectin-1 than AOT (<i>P</i> = .007). AOT exhibited the highest levels of expression of cytoplasmic galectin-3 (<i>P</i> = .003) and galectin-7 (<i>P</i> = .015). Significant differences were observed in the immunoexpression of nuclear galectin-1 with mandibular AOT (<i>P</i> = .009). <h3>Conclusions</h3> Galectin-1, -3, and -7 play a role in the pathogenesis of AM and AOT. Nuclear expression of galectin-1 and -7 in recurrent and conventional AM suggests a possible proliferative and/or antiapoptotic function of these galectins related to the distinct pattern of aggressiveness of AM.

ADENOID AMELOBLASTOMA WITH DENTINOID: A CASE REPORT

A 58-year-old afrodescendant man presented a chief complaint of pain in tooth 48. Clinical examination revealed mobility, a deep periodontal pocket, and purulent secretion in teeth 48, 47, and 46. Cone beam computed tomography revealed a multilocular osteolytic lesion involving teeth 46, 47, and 48, promoting root resorption, with involvement of the ascending branch of the mandible. The diagnostic hypotheses were infected ameloblastoma or odontogenic keratocyst. Incisional biopsy revealed areas of typical ameloblastoma, in addition to epithelial spirals, duct-like microcysts, and the deposition of extracellular material consistent with dentinoid. The histopathologic diagnosis was adenoid ameloblastoma with dentinoid (AAD). The patient is in preoperative preparation for further definitive surgical procedure. AAD is an extremely rare odontogenic tumor with histologic features of ameloblastoma and adenomatoid odontogenic tumor and formation of hard tissue. Oral pathologists should have a thorough understanding of this histologic spectrum of ameloblastoma to avoid misdiagnosis. A 58-year-old afrodescendant man presented a chief complaint of pain in tooth 48. Clinical examination revealed mobility, a deep periodontal pocket, and purulent secretion in teeth 48, 47, and 46. Cone beam computed tomography revealed a multilocular osteolytic lesion involving teeth 46, 47, and 48, promoting root resorption, with involvement of the ascending branch of the mandible. The diagnostic hypotheses were infected ameloblastoma or odontogenic keratocyst. Incisional biopsy revealed areas of typical ameloblastoma, in addition to epithelial spirals, duct-like microcysts, and the deposition of extracellular material consistent with dentinoid. The histopathologic diagnosis was adenoid ameloblastoma with dentinoid (AAD). The patient is in preoperative preparation for further definitive surgical procedure. AAD is an extremely rare odontogenic tumor with histologic features of ameloblastoma and adenomatoid odontogenic tumor and formation of hard tissue. Oral pathologists should have a thorough understanding of this histologic spectrum of ameloblastoma to avoid misdiagnosis.

AMELOBLASTOMA WITH ADENOID STRUCTURES: A SURVEY OF 6 NEW CASES

<h3>Objectives</h3> The aim of the present study was to analyze the clinicopathologic profile of ameloblastomas with adenoid structures. <h3>Study Design</h3> This retrospective observational study consisted of cases diagnosed as ameloblastoma between 2014 and 2021 that were microscopically reviewed. The included cases were only those exhibiting focal (<50% of the tumor) or predominant (>50% of the tumor) duct-like spaces of variable size, lined by cuboidal to columnar cells containing mucoid material. Clinical data were collected from biopsy request forms and tabulated for descriptive analyses. <h3>Results</h3> There were 125 ameloblastomas (1.2%; ∼15 cases per year). Adenoid structures were observed in 6 samples (4.8%) from 5 males and 1 female, with a mean age of 41 years (range, 25 to 61). The posterior region of the mandible was most frequently affected (<i>n</i> = 5). The cases presented as asymptomatic unilocular (<i>n</i> = 1) or multilocular (<i>n</i> = 4) radiolucency. Three cases exhibited predominant adenoid structures, 1 of which exhibited exuberant dentinoid material. The other 3 cases of conventional ameloblastoma showed focal areas of adenoid features. <h3>Conclusions</h3> Adenoid structures in ameloblastoma appear to be an uncommon event of unknown clinical significance and may be associated with dentinoid material and should not be misinterpreted as an adenomatoid odontogenic tumor.