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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.

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.

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.

Introduction: Dentascan is a CT imaging software that provides three dimensional display and high resolution panoramic views of the jaw. It has become an important aspect of evaluation of mandibular and maxillary pathologies due to its advantages over two dimensional techniques and conventional CT. Materials and Methods: 60 patients presenting with jaw lesions, were studied using Dentascan software. The aim of the study was to explore the spectrum of findings in various mandibular and maxillary pathologies as well as define their extent and involvement using DentaScan. Results: Impacted mandibular molars constituted 45% of cases followed by tumors and inflammatory lesions (36.6 %). Of the 22 tumors and inflammatory lesions, giant cell granulomas and radicular cysts, accounted for 22.7% each while osteomyelitis constituted 18%. Other lesions included osteosarcoma, buccal space infection, ameloblastoma, adenomatoid odontogenic tumor, dentigerous cysts and carcinoma alveolus. Trauma leading to facial fractures and TMJ pathologies constituted 8.3% and 10% of cases respectively. Conclusion: DentaScan is a valuable tool in evaluation of maxillary and mandibular pathologies including tumors/cysts, inflammatory /infectious lesions, TMJ ankylosis and facial fractures. By providing information superior to radiographs and conventional computed tomography, it plays a valuable role in pre-operative assessment of various pathologies.

An impacted tooth is the one which fails to erupt into its anatomic position due to various factors such as malposition, lack of space, or other impediments. The prevalence of impacted tooth varies with geographic locations and has been estimated to be between 8% and 38%. An impacted tooth can be a nidus for dental caries, infection, destruction of adjacent teeth, periodontal disease, and even oral and maxillofacial cysts or tumors. Therefore, careful evaluation of the history and the clinical and radiographic findings and knowledge about the various maxillofacial cysts and tumors help a clinician to arrive at early diagnosis and render proper treatment to a patient. The recent advancements made in the field of radiology, especially the cone-beam computed tomography (CBCT), is a boon to dentistry. The three-dimensional imaging has made CBCT the preferential imaging modality for the evaluation of unerupted/impacted or supernumerary teeth and also in the evaluation of odontogenic and nonodontogenic cysts/tumors of the jaws. The varied radiographic appearances of cysts/tumors in the maxillofacial region help in precise differentiation of the pathology and prompt the clinicians to arrive at an accurate early diagnosis. This article discusses three case reports of maxillofacial cysts/tumors associated with an impacted tooth where radiology plays an important role in the diagnosis of the lesions.

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.

Ameloblastic fibro-odontoma (AFO) is an uncommon benign tumor of the jaws and mostly found in patients aged less than 20 years. In this report, we describe two cases of AFO in a 5-year-old girl and a 3-year-old boy. In both cases, radiographic images showed a well-defined unilocular radiolucency with partial radiopacity in their jaws. Lesions were removed under general anesthesia and histopathologically examined, which revealed then to be AFOs. Although unerupted teeth that came in contact with the lesions were left as is, no recurrence was observed postoperatively. A common aspect of both cases was that a presurgical pathological diagnosis, which is usually made on the basis of findings of presurgical biopsy under local anesthesia, was not possible because of their immaturity. Differential diagnoses of AFO include calcifying epithelial odontogenic tumor (CEOT), calcifying cystic odontogenic tumor (CCOT), adenomatoid odontogenic tumor (AOT), and complex odontoma (CO). As this includes tumors with a high risk of recurrence such as CEOT, an accurate clinical diagnosis is quite important. However, it was difficult to distinguish AFO from other tumors on the basis of clinical features including radiographic findings. Our review of literature revealed that there have been no reports of cases of CEOT and CCOT in patients aged less than 6 years, whereas AFO was frequently detected. We concluded that radiographic findings in combination with the patient’s age were quite useful indicators for the differential diagnosis of AFO. Moreover, our case report supported the notion that impacted teeth adjacent to AFO can be preserved.

Adenamatoid odontogenic tumor (AOT) is an odontogenic tumor with a prevalence of 2.2–7.1%. AOT is a benign, noninvasive, and progressive lesion which is also known as “a two third tumor.” As the name suggests the tumor occurs in the maxilla in two third of cases. It occurs in young patients in two third of cases and associated with missing or unerupted teeth in two third of cases. Two third cases are associated with the maxillary canine. Characterized by slow growing, gradually enlarging, painless swelling associated with missing teeth. We report a case of a male patient of age 22 years, with characteristic findings. AOT resembles different odontogenic cysts and tumors which may include dentigerous cyst, globulomaxillary cyst, ameloblastoma, and other entities, hence must be well differentiated. Conservative surgical enucleation is the treatment of choice. Recurrence rate for AOT is 0.2%. Prognosis is excellent when completely removed in toto.

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.

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.

Introduction/Objective Adenomatoid odontogenic tumor (AOT) is an uncommon benign odontogenic tumor representing 3 to 7% of all odontogenic tumors. This tumor was first reported as adeno-ameloblastoma by Bernier and Tiecke in 1950 as it was initially assumed to be a type of ameloblastoma. In 1969, Philipsen and Bern proposed the term adenomatoid odontogenic tumor which was subsequently adopted by WHO and became the accepted terminology for this tumor. AOT is classified as a tumor of odontogenic epithelium but occasionally abnormal hard tissues consistent with dentinoid material may also be present as part of the tumor. AOT tends to occur in younger patients and 50% of the cases are diagnosed in teenagers. It occurs twice as commonly in females and frequently involves the anterior maxilla. Radiographically, AOT can appear as a radiolucent or mixed lucent-opaque lesion and may be associated with an impacted tooth. Methods/Case Report We report two unusually large expansile lesions of AOT that presented in the mandible. In the first case, the tumor presented as an expansile radiolucent lesion involving the right posterior mandible in a 32 year old female. In the second case, the tumor presented as an expansile mixed lucent-opaque lesion involving the left anterior mandible in a 21 year old female. The clinical presentation, radiographic and imaging findings, histopathologic features and treatment of these two cases will be discussed. The recommended treatment for AOT is surgical excision. The prognosis is good as this tumor seldom recurs after excision. Results (if a Case Study enter NA) NA Conclusion AOT is considered to be a non-aggressive, non-invasive and slow growing benign neoplasm. It is usually discovered on routine radiographic examination as the lesion is usually small and asymptomatic at the time of diagnosis but occasional cases that are larger in size have been reported in the literature.

Background. The diseases belonging to the group of benign epithelial odontogenic tumors have a high prevalence nowadays. Some tumors in this group are rare. One of such rare tumors is peripheral ameloblastoma. Description of the clinical case. Patient A., 40 years old, was first treated for adenomatoid odontogenic tumor in Stavropol in 2008, the treatment included cystectomy. In 2012, she referred to MSUMD with complaints on the changes in face configuration. The following treatment was carried out: removal of the tumor with segmental resection of the body and left branch of the lower jaw, followed by simultaneous reconstruction of the defect with an iliac crest bone autograft and replantation of the condylar process of the lower jaw on the left. In 2018–2019, the patient re-applied to the CMC MSUMD with complaints on the recurrent pain in soft tissues of the left mandible area. The following treatment was performed: removal of the tumor of the left buccal region. The pathological diagnosis: peripheral ameloblastoma. Conclusion. We have described the main clinical, radiological and histological characteristics of peripheral ameloblastoma and the main stages of treatment of patients with this pathology., Актуальность. Заболевания, входящие в группу доброкачественных эпителиальных одонтогенных опухолей на сегодняшний день, имеют большую распространенность в популяции. Некоторые нозоло- гические единицы из данной группы встречаются редко. Такой патологией является периферическая амелобластома. Описание клинического наблюдения. Пациентка А. 40 лет, впервые проходила лечение по поводу новообразования нижней челюсти (НЧ) слева в 2008 г. в городе Ставрополь, лечение выполнено в объеме цистэктомии. В 2012 г. обратилась в МГМСУ им. Евдокимова с жалобами на изменения конфигурации лица за счет новообразования НЧ слева. Гистологическое заключение: аденоматоидная одонтогенная опухоль. Проведено лечение в объеме: удаление новообразования с сегментарной резекцией тела и ветви НЧ и одномоментной реконструкцией дефекта костным аутотрансплантатом из гребня под- вздошной кости с реплантацией мыщелкового отростка НЧ слева. В 2018–2019 гг. пациентка повторно обратилась в КМЦ МГМСУ с жалобами на периодические боли в области мягких тканей окружающих НЧ слева. Проведено лечение: удаление новообразования щечной области слева. Гистологическое заключение: периферическая амелобластома. Заключение. Нами описаны основные клинико-рентгенологические и гистологические характеристики периферической амелобластомы, основные этапы лечения пациентов при данной патологии., Head and neck. Russian Journal, Выпуск 2 2021

Ameloblastoma is one of the most common types of oral odontogenic tumors. As per literature, ameloblastoma mostly occurs in the mandible butthe maxillary ameloblastoma has a more aggressive behavior due to anatomical features. Also, unicystic ameloblastoma may have lower recurrent rate. In this case report, we present a 60-year-old male patient with a history of unicystic ameloblastoma, which the intraluminal adenomatoid odontogenic tumor excisional biopsy surgery was performed but the patient didn’t follow the treatment completely, and after two years he came back with swelling of the right upper alveolar ridge. After the second surgery, the histopathologic report revealed a mixed plexiform-follicular ameloblastoma recurrence and it seemedthat previous surgery was not sufficient and more radical treatment is needed for the lesion. Keywords: Ameloblastoma; Maxilla; Adenomatoid odontogenic tumor.

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.

Background: The incidence and frequency of odontogenic cysts and tumors depends on the different geographic location. Odontogenic cysts and tumors are lesions that arise from the tooth apparatus or its remnants. The purpose of this study was to determine the prevalence of odontogenic cysts and tumors over a period of 5 years 9 months and to compare our results with other published studies. Aim and Objective: The purpose of this study was to evaluate the prevalence of odontogenic cysts and tumors diagnosed at the Department of Oral Pathology, M.M. College of Dental Sciences & Research, Mullana (Ambala) and to compare the results with findings in the literature. Materials and Method: Data of odontogenic cysts and tumors diagnosed during 2014 to 2019 (till September) w4ere collected from the files of the Oral Pathology Department, M.M. College of Dental Sciences & Research, Mullana (Ambala). Results: Out of the total 71 cases of odontogenic cysts, most prevalent odontogenic cysts were found to be radicular cysts (n=42, %= 59.1%), followed by dentigerous cysts (n=17, %=23.9%) and odontogenic keratocyst (n=12, %=16.9%). Among the odontogenic tumors out of 49 cases reported, the most prevalent was ameloblastoma (n=28, %=57.1%) followed by, ameloblastic fibroma (n=06, %=12.2%), odontoma (n=05,%=10.2%), adenomatoid odontogenic tumor (n=03, %=6.1%), peripheral odontogenic fibroma (n=02, %=4.08%), ameloblastic carcinoma (n=02, %=4.08%), odontogenic fibroma (n=02, %=4.08%) and odontogenic myxofibroma (n=01, %=2.04%). The anterior and posterior portion of the body of mandible was the most common site for both odontogenic cysts and tumors. The age group for odontogenic cysts ranged from 07 to 72 years of age, whereas for the odontogenic cysts the range was 10 to 75 years of age. The male to female ratio for the odontogenic cysts was 1:1.2, whereas for the odontogenic tumors it was found to be having more female predilection with the ratio of 1:1.3. Conclusion: The prevalence of odontogenic cysts was similar to that reported in the literature, with incidence of radicular cysts seen most frequently. In case of odontogenic tumors the findings vary to the reported literature with ameloblastoma being more commonly reported.

Submitted by Jean Medeiros (jeanletras@uepb.edu.br) on 2022-02-18T13:47:58Z No. of bitstreams: 1 PDF - Walter Gleybson Antas de Morais.pdf: 2583981 bytes, checksum: 725ecb443489ac3ea6c8ec51009b3138 (MD5) Approved for entry into archive by Secta BC (secta.csu.bc@uepb.edu.br) on 2022-02-22T13:52:41Z (GMT) No. of bitstreams: 1 PDF - Walter Gleybson Antas de Morais.pdf: 2583981 bytes, checksum: 725ecb443489ac3ea6c8ec51009b3138 (MD5) Made available in DSpace on 2022-02-22T13:53:08Z (GMT). No. of bitstreams: 1 PDF - Walter Gleybson Antas de Morais.pdf: 2583981 bytes, checksum: 725ecb443489ac3ea6c8ec51009b3138 (MD5) Previous issue date: 2020-07-10 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES Background: Ameloblastoma (AM) and adenomatoid odontogenic tumor (AOT) are benign odontogenic tumors with ephitelial origin, but exhibiting distinct clinical behavior. This fact leads to development of research that try to better understand the possible differences in the pathogenesis and biological behavior of these lesions. Galectins are proteins involved in various pathological mechanisms of the oral cavity, however, until the presente moment, its role in odontogenic tumors is still poorly elucidated. Objective: To evaluate the immunoexpression of galectins -1, -3 and -7 in a series of cases of AM and AOT, comparing it with clinicomorphological parameters. Material and Methods: A total of 31 cases of AM and 20 cases of AOT were analyzed in a retrospective and cross-sectional study. Clinical data (sex, age, anatomical location, radiographic aspects and primary or recurrent lesion) were collected from biopsy request forms. In the morphological study, classification proposed by the WHO (2017) was considered. For the immunohistochemical study, it were established percentages of imunopositives cells to galectins -1, -3 and -7, considering differents cell compartments, in 10 microscopy fields in the parenchyma of AM and AOT. In the stroma, absence/presence of galectin immunoexpression was considered. Data obtained were submitted to statistical analysis using the Mann-Whitney and Fisher’s exact tests (p

Introduction:primary maxillofacial tumors are uncommon in pediatric patients. When they do occur, the tissue damage caused directly alters facial growth, development as well as psycho-social evolution. This study was carried out to determine the pattern, sociodemographic characteristics and histologic peculiarities of paediatric jaw tumors in our environment. Methods:a retrospective hospital-based study where the case notes of children below the age of 14 years who presented with jaw tumors and tumor-like lesions from January 2014 to December 2018 were studied. Results:eighty-two patients were studied; patients aged 10-14 years had the highest representation. Mean time of presentation was 8 months with jaw swelling being the commonest presentation (84.1%). Majority of the fathers were in their 4thdecade of life while most of the mothers were in their third decade of life and both parents possessed primary school certificate as their highest level of educational attainment. Fathers were mostly traders, while mothers were mostly full-time housewives. The maxilla and mandible were most commonly affected with the left side showing higher preponderance. Burkitt lymphoma (19 (23.2%)) and adenomatoid odontogenic tumor (14 (17.1%)) were the commonest lesions. When the tumor involved both the maxilla and the mandible, the tumor was most likely malignant. Conclusion:in our center, paediatric jaw tumors are commonest in male children with the 10-14 years´ age group most commonly affected. Burkitt lymphoma and adenomatoid odontogenic tumors were the commonest tumors. Early presentation must be encouraged since these tumors if presented early can be successfully treated.

A 70-year-old man consulted for a mass of unspecified duration in the anterior area of the mandible. Radiologic information was not provided. An incision biopsy was performed by the dentistry service. The specimen received at the laboratory was labeled “cystic lining” and consisted of two light-gray to dark brown, irregularly shaped tissue fragments measuring 0.3 cm and 0.4 cm in diameters. Histological sections show biloculated cyst wall segments composed of fibrocollagenous tissue lined by an epithelial lining of varying thickness. (Figure 1) The latter consists of a thin layer of non-keratinizing epithelium with plaque-like thickenings that are composed of cells with a whorled pattern and variably clear cytoplasm. (Figures 2 & 3) Based on these microscopic features we signed the case out as a botryoid odontogenic cyst. Botryoid odontogenic cyst (BOC) is a developmental, non-inflammatory odontogenic cyst derived from residual odontogenic epithelium such as the dental lamina.1,2 It occurs between the roots of erupted teeth and is typically multilocular. It represents less than 1% of odontogenic cysts. Most cases occur in the sixth and seventh decades of life and a slight preponderance of males has been observed.1 Other studies report an equal distribution between sexes.2 It most often occurs in the mandible anterior to the molars, particularly the incisive/canine and premolar regions.1,2 Most BOCs are asymptomatic and discovered incidentally on radiographs although occasionally bone expansion is observed.1 Radiologically, BOCs often present with a multilocular radiological appearance.2 This multilocular feature has been likened to a “bunch of grapes” (botryoid: from the Greek botrys – bunch of grapes, and oeides – in the shape of).3 Microscopically, the cyst locules are lined by a one-to-two cell thick non-keratinizing epithelium with plaque-like thickenings of cells in a whorled arrangement and connective tissue septa.1,3 Cytoplasmic clearing may be observed because of glycogen.1 The differential diagnosis includes a lateral periodontal cyst (LPC) and a gingival cyst (GC). Although their histological features are largely identical, a LPC is unilocular while a GC occurs in the alveolar ridge of infants.1-3 A BOC is often considered a multilocular variant of lateral periodontal cyst.2,3 Making this distinction however is more than just of morphologic interest but is important as BOCs are reported to give rise to recurrences unlike LPCs and GCs.2,3 An ameloblastoma may be considered because of the multilocular appearance although the microscopic features are sufficiently distinct to rule out this entity. An adenomatoid odontogenic tumor (AOT) may be considered because of the nodular thickenings with a whorled pattern. However, AOT is a solid tumor characterized in addition by the presence of rosette- or duct-like spaces with dentinoid matrix. The recommended treatment is by enucleation.1 Successful conservative management with Carnoy’s solution has also been described.4 Peripheral ostectomy has also been recommended – a more aggressive approach being proposed as appropriate to extirpate any residual lesion.3 Recurrence has been stated to be between 15 to 30% which is largely ascribed to the multilocular characteristic of BOCs and consequent difficulty of complete removal, or of larger lesions.1-3 Thus, appropriate follow-up of cases or adjunctive therapy after enucleation might be warranted.2,3 To the author’s awareness, this is the first locally reported case of BOC after a search of local health research databases.

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.