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Odontogenic gingival epithelial hamartoma (OGEH) is a rare odontogenic epitheliallesion. Distinguishing OGEH from peripheral ameloblastoma can pose a differential diagnostic challenge. We report a case of OGEH affecting the lower gingiva in a 78-year-old male patient. The lesion presented as a large, painless, pedunculated mass with a pleomorphic histological appearance. A diagnosis of OGEH was made after the exclusion of peripheral ameloblastoma and peripheral adenomatoid odontogenic tumour. Previous studies have reported differences in sex and age between patients with OGEH and peripheral ameloblastoma; this suggests that peripheral ameloblastoma is not derived from OGEH. Histological findings suggest that the lesions are independent entities.

Adenomatoid odontogenic tumor (AOT) is a rare odontogenic origin tumor that manifests as a slow-growing cystic neoplasm in the anterior maxilla, often in conjunction with an impacted tooth. AOTs are divided into three kinds based on their histology: follicular, extrafollicular, and peripheral. Because the source of the AOT is unknown, it's impossible to say whether the lining of an associated cyst reflects the cause i.e. a real dentigerous cyst, a cystic alteration within an AOT, or a separate entity. The diagnosis and treatment should be determined following a thorough clinical, radiographic, and histological investigation. The presented case is a rare occurrence of its sort due to the favorable patient's age and the AOT's site in the lower jaw. The current study reports on a case with follicular AOT in the anterior mandibular region (a rare location), with unusual histomorphology (snow flake and calcified areas) associated with impacted 43 and retained 83.

Adenoid ameloblastoma is a hybrid odontogenic tumour showing histopathological features of both ameloblastoma and adenomatoid odontogenic tumour (AOT), with approximately 40 cases reported in the literature. The aims of the report are to illustrate the diagnostic challenges of adenoid ameloblastoma using three new cases and to analyze evidence in literature to consider adenoid ameloblastoma as a new sub type of ameloblastoma. A literature review was performed with the key words—adenoid ameloblastoma, hybrid/composite odontogenic tumours, hybrid ameloblastoma and adenomatoid odontogenic tumour, ameloblastoma with inductive changes, dentinoid and dentinoma to select the cases compatible with the diagnosis of adenoid ameloblastoma. Out of the 40 cases reported in literature, 31 cases with sufficient information and 3 new cases were analyzed. Out of the 34 adenoid ameloblastomas majority of tumours (76.5%) occurred in adults with age ranging from 25 to 55 years. Slight female predilection with a male:female ratio of 0.9:1 was observed. Approximately, 64.7% occurred in the mandible. Radiologically, 82.4% of adenoid ameloblastomas presented as radiolucent lesions while 47.1% occurred with ill-defined margins and cortical perforation at diagnosis. Histopathologically, 70.8% of tumours presented as plexiform ameloblastomas, while duct like structures/glandular structures were the commonest feature supportive of adenomatoid odontogenic tumour observed in overwhelming majority of 95.9% of adenoid ameloblastomas. 91.6% of tumours showed inductive change in the form of dentinoid. Further, 45.4% of the tumours developed at least one recurrence following surgical excision. The report presents literature review based evidence to show the existence of adenoid ameloblastoma, which is demographically similar to conventional ameloblastoma but with histopathological differences and presenting with higher rate/multiple recurrences, indicating its biological aggressiveness. Thus, we would like to propose the inclusion of adenoid ameloblastoma as a sub type of ameloblastoma in the next revision of the WHO odontogenic tumour classification.

Adenomatoid odontogenic tumour, truly coined as one of the masters of disguise of orofacial pathologies, was first reported in the literature by Steen Lands.1 Philipson and Brin used the terminology adenomatoid odontogenic tumour for this pathology with its commonly accepted abbreviation AOT.2 Later on, adenomatoid odontogenic tumour (AOT) name was accepted by the World Health Organization (WHO) in 1971. In 2005, WHO revealed the histological variants of the adenomatoid odontogenic tumour and classified it as a tumour comprised of odontogenic epithelium showing various patterns in histopathologic view within a mature connective tissue stroma.3 It is seldom noticed neoplasm which comprises only 3 % of all the odontogenic tumours. It was commonly found in the maxilla with female predilection and mostly in association with impacted canines.4-6 Adenomatoid odontogenic tumour is an odontogenic epithelial tumour usually seen in females in their second decade of life. The tumour is slow growing in nature which eventually results in painless expansion of jaw. The maxilla is commonly affected than mandible. Being benign in nature, most of the AOT cases usually got treated with conservative surgical enucleation but the greater size of tumour can leave behind an oro-facial defect. To prevent such type of incident, it is important to diagnose them early and treat accordingly. Herewith, we are presenting a case report of adenomatoid odontogenic tumour of mandible in a male patient.

Hybrid odontogenic tumors are sporadic, where the distinctive areas of more than one odontogenic tumor tissue type have been reported. The occurrence of adenomatoid odontogenic tumor (AOT) with calcifying epithelial odontogenic tumor (CEOT) like areas histologically simulating salivary gland pathology is an unusual finding that has not been previously reported in the literature. We report the case of a 32-year-old female presenting with slow-growing firm swelling, radiographically as a pear-shaped radiolucent lesion in the interdental region of maxillary incisors. Histologically, the tissue showed nests and anastomosing strands of the bland cuboidal to squamoid epithelial cells showing nuclear pleomorphism, hyperchromatism, and abundant cytoplasm with prominent intercellular bridges focally. Multiple basophilic calcifications, amyloid-like material, duct-like formation, and mucinous spillage are seen. Tumor cells showed immunopositivity for CK 7, CK 19, CK 8/18 and low Ki67, p63, and immunonegativity for S100 suggesting of a hybrid lesion of CEOT with AOT.

Ki-67 is a marker of cell proliferation, used as an important diagnostic marker in the pathologic differentiation of various lesions. It is also relevant for developing targeted molecular therapies. We carried out a systematic review to assess the Ki-67 labeling index (LI) in odontogenic cysts and tumors. Databases were searched, including PubMed (MEDLINE), Scopus, CINHAL, PsycoInfo, the Cochrane Library, and Proquest. The meta-analysis was carried out based on the data of 608 lesions. When a 5% cut-off point was set, ki-67 LI of all benign odontogenic tumors dropped below this point. All the malignant tumors demonstrated an LI of over 15.3%; a significantly higher Ki-67 LI in malignant odontogenic lesions (17.59±2.80) was observed. Among benign tumors, the largest and the smallest Ki-67 LIs were seen in ameloblastoma (4.39±0.47) and adenomatoid odontogenic tumor (0.91±1.71). The mean values of Ki-67 LI in tumors and cysts were 4.23 (0.38) and 1.04 (0.07), respectively. Among odontogenic cysts, the highest Ki-67 LI was found in odontogenic keratocyst (OKC) (3.58±0.51), and the lowest in the radicular cyst (1.29±0.62%). Ki-67 LIs in all odontogenic cysts were

The calcifying odontogenic cyst is as a benign, rare developmental odontogenic cyst with a wide range of histologic characteristics. It may present along with other odontogenic pathologies such as odontoma, ameloblastoma, adenomatoid odontogenic tumor, ameloblastic fibroma, and ameloblastic fibro-odontoma. Clinically, it can be an either intra- or extraosseous painless swelling that can produce cortical expansion. It affects mostly the anterior area of the mandible. Radiographically, it appears as a well-circumscribed unilocular radiolucency containing flecks of indistinct radiopacities. In about one third of cases, an impacted tooth is associated. In this paper, we employ a patient with an enormous calcifying odontogenic cyst to review both the pathology and active decompression and distraction sugosteogenesis, a novel technique employed to treat odontogenic entities. This dual approach usually results in an accelerated bone healing (sugosteogenesis), partial removal of the cystic epithelium, thickening of the wall, and migration of chronic inflammatory cells which triggered epithelial modulation, ultimately causing a realignment in the biologic behavior of the lesion.

Occurence of combined odontogenic tumours is rare. These lesions are also named as hybrid lesions. Histologic features of these lesions are often identical to other odontogenic neoplasms such as ameloblastoma, adenomatoid odontogenic tumor, ameloblastic ?broma (AF), and ameloblastic ?bro-odontoma. With variable clinical presentation, ranging from cysts to neoplasms, these lesions show varying degrees of aggressive behaviour. Mostly these combined tumors contain features of one of the odontogenic tumors in combination with either a cyst or tumor. We present a case report of combined odontogenic tumor; an odontogenic keratocyst with an ameloblastic fibroma. Prediction of clinical outcome of such lesions becomes challenging owing to their paucity. It becomes important to understand their salient features so that differentiation from the more common conventional neoplasms distinctly helps to expand classi?cation and provide prognostic criteria. Keywords: Combined odontogenic tumors, Hybrid odontogenic tumors, Odontogenic keratocyst, Ameloblastic fibroma.

Adenomatoid odontogenic tumor (AOT) is benign tumor of the oral cavity characterized by its slow growth accounting to 3%–7% of the odontogenic tumors. AOTs mostly occur in the maxillary anterior region and most often than not associated with impacted anterior teeth. It affects the younger age group, especially below 20 years and is commonly seen in females. It occurs as two main variants – (a) central/intraosseous which is more common and (b) peripheral which is rare. The location of the lesion, its association with the impacted tooth, is the basis for the classification of AOT. The intraosseous type may be related to unerupted tooth (follicular variant) or may not be related to unerupted tooth (extra-follicular variant). Radiologically, AOT presents predominantly as a unilocular cystic lesion enclosing the unerupted tooth. The lesion presents rarely with a cystic component. Radiopacities on the intraoral periapical radiograph are seen as discrete foci having a flocculent pattern within radiolucency even with the presence of minimal calcified deposits. AOT being benign in nature is enucleated with least chances of recurrence. Here, we present a rare case of extra-follicular variant of adenomatoid odontogenic tumor in a 19-year-old female patient.

p16INK4a is a tumor suppressor protein that retards cell cycle progression from G1 to S phase. Prior studies have evaluated p16INK4a expression in odontogenic keratocyst and ameloblastoma, but data regarding other odontogenic cysts and tumors have been sparse.With IRB approval, cases from the following entities were identified from archives of the UF Oral Pathology Biopsy Service (2005-2015): benign incidental odontogenic rest, dentigerous cyst, lateral periodontal cyst, calcifying odontogenic cyst, glandular odontogenic cyst, odontogenic keratocyst, orthokeratinized odontogenic cyst, adenomatoid odontogenic tumor, calcifying epithelial odontogenic tumor, and ameloblastoma. All cases were submitted for p16INK4a immunohistochemical testing.Results were scored as follows: nuclear and cytoplasmic staining of5% cells (score 0), 5%-25% (score 1), 25%-50% (score 2),50% (score 3). No significant difference in p16INK4a staining was noted between odontogenic cysts and the listed odontogenic tumors (chi-square, P = .540). When comparing lesions with higher recurrence rates (over 25% as reported in the literature) versus lesions with low recurrence rates (under 25%), higher recurrence correlated to significantly higher p16INK4a positivity (chi-square, P = .001). Follow-up testing was performed on 18 cases with "2" or "3" p16INK4a expression scores for high-risk HPV strains through HPV in situ hybridization (ISH) messenger RNA testing with no cases exhibiting a positive result.This study exhibits an association between increased p16INK4a positivity and odontogenic lesions with higher recurrence rates and highlights the role of p16INK4a as a progression marker unrelated to HPV expression in this group of pathologic entities.

Objective Adenomatoid odontogenic tumor (AOT) was classified by WHO as a mixed odontogenic tumor in 1992 and reclassified as an epithelial-only tumor in 2005 without clear rationale. The purpose of this study was to investigate if there was any evidence to suggest AOT might be a mixed odontogenic tumor. Study Design Immunohistochemical studies with nestin, dentin sialophosphoprotein (DSPP), cytokeratin, and vimentin were performed using 21 cases of AOT and the staining results were analyzed according to the various morphologic patterns seen in AOT. Sirius red stain was used to detect presence of collagen types I and III in AOT products. Results Our results showed that 20/21 (95.23%), 0/21 (0%), 21/21 (100%), and 20/21 (95.23%) cases expressed nestin, DSPP, cytokeratin, and vimentin, respectively. Some cells in rosette/duct-like structures (RDS) expressed nestin, vimentin or both, without cytokeratin. Co-expression of vimentin and cytokeratin, or nestin, cytokeratin, and vimentin were noted in some cells. Sirius red was positive in eosinophilic products in RDS, double-layered spheres and dentinoid. Conclusion Although most AOT cells appear epithelial, there is a small population of cells expressing mesenchymal proteins and secreting collagen types I and III. These evidence suggests that AOT is a mixed odontogenic tumor.

Ameloblastoma and adenomatoid odontogenic tumors are the most common odontogenic neoplasms. However, hybrid variant of the two lesions, Adenoid Ameloblastoma with dentinoid is extremely rare. The lesion comprises of characteristic histopathological features of Ameloblastoma and Adenomatoid odontogenic tumor and also shares certain clinical characteristics with either of the entities. Adenoid Ameloblastoma with dentinoid may be considered at the more aggressive end of spectrum of benign odontogenic neoplasms. Owing to the frequent tendency of lesion to be underdiagnosed, careful histopathological screening of submitted biopsies is warranted. With the increase in number of reported cases in the recent years, it is likely to be included as a separate entity in the upcoming WHO classification. The present systematic review aims at collectively presenting the demographic, clinical, radiographic and histopathological features, treatment performed along with its outcome for all the cases of Adenoid Ameloblastoma with dentinoid reported in scientific literature till date. Keywords: Hybrid Odontogenic Tumor; Adenomatoid Odontogenic Tumor; Adenoameloblastoma; dentinoameloblastoma; Immunohistochemistry

La tumeur adénomatoïde odontogène est une tumeur épithéliale bénigne, qui touche essentiellement la femme jeune, elle siège habituellement dans la partie antérieure du maxillaire supérieur. Son diagnostic peut être suspecté cliniquement devant une formation kystique, associée à une dent incluse, mais la confirmation repose sur l'examen histopathologie. Il s'agit de deux patients précédemment de 13 et de 37 ans, sans antécédents, qui consultaient suite à une tuméfaction siégeant respectivement au niveau du maxillaire et au niveau de la mandibule. L'examen anatomo-pathologique de ces lésions avait conclu à une tumeur adénomatoïde odontogène. A travers ces deux observations, nous rapportons les caractéristiques anatomo-cliniques, l'évolution et le traitement de ce type de tumeur.

Claudins are integral to the structure and function of tight junctions. Altered claudin expression has been shown to affect disease behavior and patient prognosis in various neoplasms. The objectives of this study were to analyze the claudin-1, -4 and -7 expression in odontogenic tumors and characterize their expression pattern in distinct tumor cell types in relation to the recurrence potential. Sixty-nine cases of odontogenic tumors, including 43 ameloblastomas (AM), 17 adenomatoid odontogenic tumors (AOT), 6 ameloblastic fibromas (AF) and 3 ameloblastic carcinomas (AC) were investigated for claudin-1, -4 and -7 expression immunohistochemically. The staining was analyzed semi-quantitatively and categorized into 4 levels, based on the percentage of positively stained neoplastic epithelial cells. Claudin-1 was expressed in all AOT and AF cases, whereas most AC (66.7%) showed no expression. The claudin-1 staining was moderate-to-intense in the odontogenic epithelium of AF. In contrast, its staining of ameloblast-like cells and stellate reticulum-like cells in AM was weak. Claudin-7 expression was noted in all tumor types studied, while the expression of claudin-4 was limited and mainly localized in the squamous differentiated cells of AM and AC. AM showed significantly higher claudin-4, but lower claudin-7 expression than AOT. In addition, AC showed diminished claudin-1 immunoreactivity, compared to AOT. Low claudin-1 expression in AM was significantly associated with the increased clinical recurrence. The loss of claudin-1 may underlie the locally invasive nature of AM.

To investigate the contribution of MMP-13 in tumor aggressiveness, by acting on the reorganization of the extracellular matrix, regulating the biological activity of cytokines in odontogenic epithelial lesions, as well as to evaluate the role of EMMPRIN as an inducer of MMP-13. Twenty solid ameloblastomas (SAs), 10 unicystic ameloblastomas (UAs), 20 odontogenic keratocysts (OKCs), and 20 adenomatoid odontogenic tumors (OATs) were selected. The expression of MMP-13 and EMMPRIN was evaluated in epithelial/connective tissue by determining the score of immunoreactive cells. Higher concentration of MMP-13 was observed in epithelium of SAs and OKCs (p = 0.316), while in connective, MMP-13 was more expressed in OKCs and UAs (p = 0.213). OKCs exhibited the highest immunoreactivity score for EMMPRIN in the epithelium (p = 0.091). In connective tissue, a larger number of immunoreactive cells were observed in OKCs and UACs (p = 0.357). There was a moderate correlation (r = 0.343/p = 0.004) between MMP-13/EMMPRIN in epithelium and strong correlation (r = 0.474/p

INTRODUCTION: Odontogenic tumors are diverse groups of lesions derived from odontogenic tissues. Clinical behavior of these lesions varies widely, ranging from benign to malignant with differences in recurrence rate and growth pattern. A better understanding of the underlying molecular mechanisms will help to predict the course of odontogenic tumors and lead to the development of new therapeutic applications. Nucleolar organizer regions (NORs) are loops of DNA that codify the ribosomal RNA and are considered important for protein synthesis. The NORs stained histochemicaly by silver are named argyrophilic nucleolar organizer regions (AgNOR). Quantification of AgNOR represents a valuable parameter of cell kinetics and therefore cell proliferation. The number of AgNOR sites in malignant cells is significantly greater than those in their normal or benign counterparts. Proliferating cell nuclear antigen (PCNA) is a useful marker of cellular proliferation and DNA replication. Malignant tissue is characterized by an uncoordinated proliferating cell nuclear antigen (PCNA). OBJECTIVES: To evaluate the cell proliferation rate using the expression of Argyrophilic Organizing Region counts and Proliferating Cell Nuclear Antigen in epithelial odontogenic tumors and to assess the usefulness of AgNOR and PCNA as markers in malignant potential of epithelial odontogenic tumors. MATERIALS AND METHODS: This study was done on 45 surgical specimens of epithelial odontogenic tumors and one control specimen from normal tooth germ.The tissue biopsies were processed and paraffin sections were prepared. Hematoxylin and eosin-stained sections were examined for diagnosis. Other sections were subjected to AgNORhistochemical technique and immunohistochemical staining for PCNA. Immunohistochemical staining was performed using a Labeled Strept-Avidin Biotin complex method (LSAB). RESULTS: The mean AgNOR count of tooth germ was 1.21 and the benign odontogenic tumors was 1.862.The highest AgNOR count was recorded in Ameloblastic carcinoma and lowest was seen in adenomatoid odontogenic tumor. Statistically significant difference in AgNOR counts of ameloblastoma and adenomatoid odontogenic tumor, ameloblastoma and calcifying epithelial odontogenic tumor, benign odontogenic tumors and ameloblastic carcinoma were seen. AgNORs in ameloblastic carcinoma were more in number and more widely distributed.The highest mean value of PCNA-positive cell percentage was demonstrated in ameloblastic carcinoma followed by ameloblastoma. A significant difference was noted when the PCNA value of ameloblastoma was compared with that of ameloblastic carcinoma. CONCLUSIONS: AgNOR technique may be considered a good indicator of cell proliferation in epithelial odontogenic tumors.The PCNA expression, along with the clinical features, can predict the aggressiveness, chances of recurrence and malignant potential of these tumors.

Unilocular radiolucent lesions of the dental hard tissues can present regularly, however they are impossible to diagnose definitively without appropriate imaging and histopathology. A case is reported that involves a 14-year-old that presented with a history of an unerupted maxillary first premolar. An initial Dental Panoramic Tomograph (DPT) did not identify any localized opacities and was diagnosed as a dentigerous cyst. A Cone Bean Computed Tomogram (CBCT) identified calcified opacities resulting in a re-evaluated radiological interpretation. With the help of a multidisciplinary approach, the removal of the benign lesion allowed orthodontic traction to extrude the tooth and for it to be brought into alignment. CPD/Clinical Relevance: This report highlights the importance of three-dimensional imaging as an adjunct to aid diagnosis and highlights the importance of multidisciplinary teams in the management of clinical challenges.

Adenomatoid odontogenic tumor is a benign encapsulated epithelial odontogenic tumor that shows an indolent clinical behavior. We have reported in a few adenomatoid odontogenic tumors mutations in KRAS, which is a proto-oncogene frequently mutated in cancer such as lung, pancreas, and colorectal adenocarcinomas. We aimed to assess KRAS mutations in the hotspot codons 12, 13, and 61 in a large cohort of adenomatoid odontogenic tumors and to test the association of these mutations with clinical (age, site, tumor size, follicular/extrafollicular subtypes) and histopathological parameters. Thirty eight central cases were studied. KRAS codon 12 mutations were assessed by TaqMan allele-specific qPCR (p.G12V/R) and/or Sanger sequencing, and codon 13 and 61 mutations were screened by Sanger. Histological tumor capsule thickness was evaluated by morphometric analysis. Additionally, the phosphorylated form of the MAPK downstream effector ERK1/2 was investigated. Statistical analysis was carried out to test the association of KRAS mutations with clinicopathological parameters. KRAS c.35 G >T mutation, leading to p.G12V, was detected in 15 cases. A novel mutation in adenomatoid odontogenic tumor, c.34 G >C, leading to p.G12R, was detected in 12 cases and the other 11 were wild-type. Codon 12 mutations were not associated with the clinicopathological parameters tested. RAS mutations are known to activate the MAPK pathway, and we show that adenomatoid odontogenic tumors express phosphorylated ERK1/2. In conclusion, a high proportion of adenomatoid odontogenic tumors (27/38, 71%) have KRAS codon 12 mutations, which occur independently of the clinicopathological features evaluated. Collectively, these findings indicate that KRAS mutations and MAPK pathway activation are the common features of this tumor and some cancer types. Although it is unclear why different codon 12 alleles occur in different disease contexts and the complex interactions between tumor genotype and phenotype need clarification, on the basis of our results the presence of KRAS p.G12V/R favors the adenomatoid odontogenic tumor diagnosis in challenging oral neoplasm cases.

Odontogenic tumors are rare entities, often derived from the epithelial remnants in the gnathic bones following odontogenesis. This brief manuscript will seek to address recent developments pertaining to odontogenic tumors as well as particularly uncommon odontogenic tumors and the difficulties in their diagnosis.

Adenomatoid odontogenic tumor (AOT) is a relatively rare benign, epithelial tumor of odontogenic origin. There is varying class of thoughts contemplating this lesion to be a hamartoma or neoplastic growth of odontogenic epithelium. Controversy regarding the histogenesis of the lesion is plentiful in earlier literature. The recent advent of immunohistochemical and ultrastructural studies has aided in throwing light on the tissue of origin of this tumor. This review aims at understanding the evolving concepts of histogenesis of AOT to better understand the biological behavior of the lesion. The review of AOT was carried out using PubMed and Google Scholar databases and 39 articles from the year 2001 to 2016 which contributed to the histogenesis of AOT were included for review. Since the origin of the cystic lining is similar to a reduced enamel epithelium and not the dental lamina, we propose the former to be the progenitor of AOT. Furthermore, we consider extra-follicular, as well as peripheral AOTs, originate from the remnants of Hertwig’s epithelial root sheath (epithelial rests of Malassez), which complies with the common histology for all these variants.

Tumors and tumor-like growths arising from odontogenic tissues constitute a heterogeneous group of interesting lesions, as they display the various inductive interactions that normally occur among the embryologic components of the developing tooth germ. Adenomatoid odontogenic tumor is a benign tumor, most common in the maxilla, characterized by slow, progressive, painless growth of firm consistency, the size of which usually does not reach large proportions. They are of three types: extrafollicular, follicular, and peripheral. It usually develops around or overlaps adjacent teeth. How to cite this article Katiyar A, Gupta S, et al. Trauma to Tumor: A Hunt of Adenomatoid Odontogenic Tumor–A Rare Case Report. Int J Clin Pediatr Dent 2019;12(4):366–369.

Adenomatoid odontogenic tumor is an epithelial tumor thought to arise from the cells of enamel organ or reduced enamel epithelium. It shows predilection for young children and adolescence and occurs with greater propensity in the anterior maxilla. The tumor manifests characteristic histological features and has been well-described. The purpose of the present report is to document a developing or incipient AOT in the maxillae of a 5-year old girl.

Adenomatoid odontogenic tumor is a relatively rare tumor that typically occurs at the anterior part of the maxilla. Most cases arise as a central or intraosseous tumor accompanying an impacted tooth; thus, the radiological appearance resembles that of an odontogenic cyst. The tumor is divided into three subtypes depending on its location and relationship with the impacted tooth: the central variant associated with the crown of an unerupted tooth (follicular type); the central variant with no association with the crown of an unerupted tooth (extrafollicular type); and the peripheral (gingival) variant. Among them, the occurrence of peripheral variant is reportedly very rare, and they usually exhibit an epulis-like or fibroma-like appearance. This paper reports an unusual case of adenomatoid odontogenic tumor. Remarkably, the tumor extended into the buccal periodontal space, expanding the space possibly due to tumor growth without relevant absorption of labial alveolar bone. The adjacent gingiva looked normal except for the slight swelling. On histopathological analysis, the tumor showed no direct connection to the periodontal ligament, which may indicate the possible origin of this tumor as an epithelial remnant of the dental lamina in the peripheral gingiva.

Adenomatoid Odontogenic tumour is an uncommon benign lesion of odontogenic origin which affects young individuals mostly in second decade of life, with a female predominance. AOT is most commonly located in anterior maxilla usually associated with impacted canine. Through this paper we present a rare entity - Adenomatoid Odontogenic tumour with dentigerous cyst associated to impacted canine and lateral incisor in anterior maxilla in a 15 year old male patient.

This article reviews odontogenic and developmental oral lesions encountered in the gnathic region of pediatric patients. The process of odontogenesis is discussed as it is essential to understanding the pathogenesis of odontogenic tumors. The clinical presentation, microscopic features, and prognosis are addressed for odontogenic lesions in the neonate (dental lamina cysts/gingival cysts of the newborn, congenital (granular cell) epulis of the newborn, melanotic neuroectodermal tumor, choristoma/heterotopia, cysts of foregut origin), lesions associated with unerupted/erupting teeth (hyperplastic dental follicle, eruption cyst, dentigerous cyst, odontogenic keratocyst/keratocystic odonogenic tumor, buccal bifurcation cyst/inflammatory collateral cyst) and pediatric odontogenic hamartomas and tumors (odontoma, ameloblastic fibroma, ameloblastoma, adenomatoid odontogenic tumor, primordial odontogenic tumor). Pediatric odontogenic and developmental oral lesions range from common to rare, but familiarity with these entities is essential due to the varying management implications of these diagnoses.

Adenomatoid odontogenic tumour (AOT) is a rare tumour of odontogenic origin with distinct clinicopathological appearance but is often clinically misdiagnosed as a cyst. The most common site is the anterior maxilla in the canine region. We present here two cases, one at its commonest location in the maxillary canine while the other is at the uncommon location of the anterior mandible. Its clinical features of painless slow growing swelling, association with impacted tooth and radiographic appearance of well defined predominantly radiolucent lesion are overlapping with other oral pathologies like dentigerous cyst, radicular cyst, calcifying odontogenic cyst, calcifying epithelial odontogenic tumour, unicystic ameloblastoma etc. One must be aware and updated with the variation in appearance of AOT. Encapsulation of tumour causes less cumbersome enucleation of the tumour, a successful treatment as it reduces the chances of recurrence.

Background/purpose There are few studies comparing the expression of enamel proteins, such as amelogenin, and cytokeratins in cyst and odontogenic tumors like in ameloblastoma and odontogenic keratocyst, indicating that amelogenin could be a potential biomarker for the aggressiveness in the odontogenic tumors. The aim of this study was to evaluate if the expression of amelogenin, cytokeratin AE1/AE3 (CKAE1/AE3) and cytokeratin 14 (CK14) in cysts and odontogenic tumors with calcified matrices such as calcifying odontogenic cyst (COC), compound (CdO) and complex (CxO) odontomas, adenomatoid odontogenic tumor (AOT) and calcifying epithelial odontogenic tumor (CEOT) as an aggressiveness indicator. Materials and methods Three COC, eight CxO, three CdO, twelve AOT, two CEOT and three dental germs were submitted to an immunohistochemistry panel of antibodies composed of amelogenin, CKAE1/AE3 and CK14. Results CKAE1/AE3 and CK14 was present in all odontogenic epithelia. The amelogenin protein was detected in prismatic and amorphous calcified matrices of epithelial origin belonging to CxO, CdO, AOT, COC and the tooth germs used as controls. On the other hand, the CEOT was the only tumor or cyst studied that did not present immunostaining for amelogenin in calcified matrices. Conclusion Amelogenin was detected in pathologies with a low or absent recurrence rate and excellent prognosis. CEOT was the lesion of greater clinical aggressiveness which did not express amelogenin. The presence of amelogenin in calcified matrices of odontogenic arise could be an indicator of low aggressiveness.

The objective of this chapter was to present specific histologic criteria for the diagnosis of the main tumors and pseudotumors of the jaws. Illustration of the histologic findings of these entities was provided in correlation with their clinical and radiographic manifestations, including histologic differential diagnoses. The histologic, clinical, and radiographic presentation of benign epithelial odontogenic tumors (ameloblastoma, calcifying epithelial odontogenic tumor, adenomatoid odontogenic tumor, and squamous odontogenic tumor), mixed odontogenic tumors (ameloblastic fibroma, ameloblastic fibro-odontoma, odontoameloblastoma, primordial odontogenic tumor, odontoma, and dentinogenic ghost cell tumor), and mesenchymal odontogenic tumors (odontogenic fibroma, odontogenic myxoma, and cementoblastoma) was offered. Two malignant odontogenic tumors (ameloblastic carcinoma and ameloblastic fibrosarcoma) were also considered. Additional tumors and pseudotumors affecting the gnathic bones included melanotic neuroectodermal tumor of infancy, juvenile solitary myofibroma of the jaws, extranodal T/NK lymphoma nasal type, rhinoscleroma (respiratory scleroma), and necrotizing sialometaplasia.

The objective of the study is to present the clinico-pathological features of cystic and classic adenomatoid odontogenic tumors (AOTs) in order to identify the differences between the two variants of AOT. Materials and method: The study sample comprised of 41 AOTs, which were categorized into cystic and classic AOTs. Cystic AOTs are diagnosed as such when macroscopic and microscopic evidence of a cyst is present together with histopathological criteria of AOT (WHO&ndash, 2017). Results: The study sample comprised of eleven cystic and thirty classic AOTs. Eight cystic AOTs were regarded as arising from dentigerous cysts as these lesions were attached to the cemento-enamel junction of the impacted teeth. Though not statistically significant, in contrast to classic AOTs which showed female predilection, cystic AOTs were more prevalent in males. Cystic AOTs tend to present as significantly larger lesions compared to classic AOTs (p &lt, 0.02). In both cystic and classic AOTs, duct-like structures and epithelial whorls were the two most prominent histopathological features present in the majority of tumors. Two AOTs with massive amounts of dentinoid occurred in the mandible and presented as large lesions that eroded cortical bone. None of the 12 patients with follow-up information presented with recurrences. Conclusion: Except for the size of the lesion, no significant clinico-pathological differences were observed between cystic and classic AOTs. Therefore the cystic AOTs can be considered as a variant of AOT with enucleation, simple excision, or radical excision as the treatment of choice depending on the extent of the lesion, similar to classic AOTs.

Adenomatoid odontogenic tumor is a benign (hamartomatous), noninvasive lesion with slow but progressive growth. It develops from the dental lamina or its remnants. There are two variants of this tumor: Central and Peripheral. Central variant further get classified as follicular and extrafollicular on the basis of its association with the unerrupted tooth. Clinically this tumor has resemblance with other odontogenic lesions like dentigerous cysts, ameloblastoma etc. Thus histopathological examination is an important aid to confirm its diagnosis. Here we report a rare case of follicular type of Adenomatoid odontogenic tumor associated with impacted mandibular premolar.

Adenomatoid odontogenic tumor (AOT) is a relatively rare and distinct odontogenic tumor that is exclusively odontogenic epithelium in origin. Although considerable numbers of reports are available with regard to the clinical and histological spectrum of AOT, very few have highlighted its rare aggressive nature. This article focuses on an AOT causing jaw swelling in the mandibular anterior region with cortical plate expansion and perforation, root resorption and paresthesia. The present case had remarkably unusual clinical and radiographic features that distinguished it from most conventional AOTs and supported its neoplastic nature.

Adenomatoid odontogenic tumor (AOT) is a rare noninvasive odontogenic tumor that occurs mostly in the second decade of life. Based on its tooth association, AOT can be classified into three categories of follicular, extrafollicular, and peripheral types; the follicular classification is considered as the most common type of AOT. This study reported a large extrafollicular case of AOT in a 40-year-old female. She was asymptomatic and tumor was detected accidentally by her dental practitioner. Since the panoramic radiograph showed a well-defined unilocular radiolucent lesion, we observed radiopaque spots within the lesion by using cone beam computed tomography. The extrafollicular type can mimic a periapical radiolucent lesion.

Ameloblastic fibro-odontoma is a rare benign mixed odontogenic tumor exhibiting the histologic characteristics of ameloblastic fibroma and complex odontoma. Clinically, it represents a well-defined asymptomatic swelling with deformity of face, and radiographically a well-defined radiolucent area, which contains radiopaque foci of various sizes and shapes. These features overlap with other lesions such as calcifying odontogenic cyst, calcifying epithelial odontogenic tumor, and adenomatoid odontogenic tumor which makes a diagnostic dilemma for oral clinicians. Hereby we report such a rare case in a 7-year-old boy.

Background The calcifying odontogenic cyst is an uncommon lesion with an incidence of 1% of all odontogenic cysts and tumors. It is characterized microscopically by ameloblastoma-like odontogenic epithelial proliferation, presence of ghost cells, and dentinoid-like material. It was previously described by Gorlin et al. in 1962 and because of its diverse histologic picture, several terms have been used over time by different authors to describe this lesion. Case Report This is a case report on a variant of the calcifying odontogenic cyst. A 47-year-old male patient attended the Oral and Maxillofacial Surgery Department with an overgrowth of inflamed tissue and exophytic appearance on the gingivae in the lower right molar region. Initial imaging revealed a uniloculated and well-circumscribed osteolytic lesion in the edentulous area of the lower first molar. The histopathologic examination of the incisional biopsy sample did not establish a definitive diagnosis. Differential diagnosis included calcifying odontogenic tumor and adenomatoid odontogenic tumor. The patient underwent complete resection of the tumor along with the adjacent molar under general anesthesia. No postoperative complications were encountered. A lesion comprising keratin with ghost cells and calcification was sampled. It appears to be continuous with the surface epithelium and not present in the bone. The presence of ameloblastic cells at the periphery of the calcified foci led to the diagnosis of the controversial lesion known as Gorlin cyst and more recently as dentinogenic ghost cell tumor. One year after the resection, no clinical or radiological recurrence was observed. Yearly follow-ups are planned.