Introduction: The adenomatoid odontogenic tumor is a relatively uncommon odontogenic neoplasm representing about 4.7% of all odontogenic tumors.
Objective: The aim of this study was to determine the demographic and clinical profile of the adenomatoid odontogenic tumors in a Sri Lankan population.
Methods: Data gathered from the cases received for a period of 38 years from the Department of Oral Pathology, Faculty of Dental Sciences, University of Peradeniya. Request forms, biopsy reports and electronic data base of the department were used to obtain relevant information. Demographic data including age, gender and location of the tumor were included in the analysis.
Results: Out of 116 cases of adenomatoid odontogenic tumor, the mean age was 21.02 ± 11.24. It occurs more fre quently in the second decade of life, more prevalent in females, most often associated with the maxilla, predominantly affecting anterior jaw bones and presenting mostly in the right side of the jaw bone. The results from the present study showed the statistically significant relationship with site of occurrence (maxilla/mandible) and age (p < 0.005). Further, depending on whether it occurs in anterior/mid/posterior site also showed a significant relationship with age (p ≤ 0.001). However, side of occurrence, left or right or site of occurrence, showed no statistically significance with age (p > 0.05).
Conclusion: Adenomatoid odontogenic tumor occurs more frequently in the second decade of life with a significant female predominance and the commonest site is anterior maxilla. This study revealed few differences on demographic and clinical presentations of adenomatoid odontogenic tumor from some regions of the world.
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http://dx.doi.org/10.1016/j.bjorl.2020.06.004 | 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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