Background: The AOT is an atypical tumor of odontogenic origin that comprises about 0.1% of jaw tumors and cysts as well as up to 3% of odontogenic tumors (OTs).
Aim And Objective: This review describes the clinical, radiographical, histopathological, and immunohistochemical properties of adenomatoid odontogenic tumor (AOT) and reports an occurrence of an AOT in a boy, 13 years of age.
Case Description: A male, 13 years of age, presented with a swelling with respect to the left maxilla, painless, and with obvious facial asymmetry. The orthopantomogram and computed tomography scan revealed a large unilocular radiolucency in the left maxilla with permanent lateral incisor embedded within the lesion and permanent canine pushed away from its normal position. After complete enucleation of the cyst under local anesthesia and extraction of associated impacted permanent teeth and retained deciduous teeth related to the lesion, the defect was filled with a bone graft and closed. Postoperative follow-up was uneventful.
Conclusion: An accurate diagnosis should be established through clinical, radiographical, and pathological correlations in order to be able to differentiate AOT from other conditions for early diagnosis.
Clinical Significance: This report highlights the salient features of the AOT to be able to correctly diagnose and manage the lesion.
How To Cite This Article: Kamble A, Shimpi MR, Dash JK, Adenomatoid Odontogenic Tumor of the Maxilla in a 13-year-old Patient: A Rare Case Report with a Review of Literature. Int J Clin Pediatr Dent 2021;14(4):596-600.
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http://dx.doi.org/10.5005/jp-journals-10005-1771 | DOI Listing |
Eur J Dent
November 2024
Department of Oral Surgery and Oral Medicine, Faculty of Dentistry, Srinakharinwirot University, Bangkok, Thailand.
Objectives: Histone modification in odontogenic lesions is mostly unexplored. Trimethylation of histone H3 at lysine residue 9 (H3K9Me3) has been studied in various pathologic conditions and showed biological significance promising for future therapeutic application. This study aimed to investigate the level and clinical relevance of the H3K9Me3 histone modification in odontogenic cysts and tumors.
View Article and Find Full Text PDFCureus
September 2024
Department of Oral and Maxillofacial Clinical Sciences, Faculty of Dentistry, Universiti Malaya, Kuala Lumpur, MYS.
Objectives: This study endeavors to bridge the long-term diagnostic and management gap through a comprehensive audit of odontogenic cysts and tumors in Kenya, offering crucial insights for both clinicians and policymakers.
Methods: Patient records (2001-2020) with odontogenic cysts and tumors were retrospectively abstracted from two major referral hospitals in Nairobi, Kenya, covering demographics, lesion location, and histological diagnosis. IBM SPSS Statistics for Windows, Version 29.
Oral Dis
October 2024
Cell Culture Laboratory, School of Dentistry, Federal University of Pará, Belém, Brazil.
The acetylation of histones H2A on lysine 5 (H2AacK5) and H3 on lysine 27 (H3AcK27) modulate several cellular mechanisms through the p300 enzyme in pathological lesions; however, their role in odontogenic lesions has not been addressed. This study aims to evaluate the immunoexpression of p300, H2AacK5, and H3AcK27 in samples of ameloblastoma (AMB) (n = 30), odontogenic keratocyst (OK) (n = 15), adenomatoid odontogenic tumor (AOT) (n = 10), odontogenic fibroma (OF) (n = 8), calcifying odontogenic cyst (COC) (n = 8), odontogenic myxoma (MIX) (n = 10), and ameloblastic fibroma (AF) (n = 06). The percentage of p300-positive cells was higher in AOT and decreased in COC, OK, AMB, AF, OF, and MIX.
View Article and Find Full Text PDFSemin Diagn Pathol
October 2024
Department of Oral Pathology & Microbiology, King George's Medical University, Lucknow 226003, UP, India. Electronic address:
J Oral Maxillofac Pathol
July 2024
Department of Oral Pathology and Microbiology, SDM College of Dental Sciences and Hospital, Dharwad, Karnataka, India.
Background: It is a well-recognized fact that abnormal cell proliferation plays a crucial role in the development of odontogenic lesions. p53 is a tumour-suppressor gene which assists in cell cycle regulation and p63 is a homolog of p53 responsible for ectodermal differentiation and maintenance of stratified epithelial progenitor-cell. Analysing the tissue expression of p53 and p63 in odontogenic lesions may provide us with an insight into their potential role in the development of these lesions.
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