Introduction And Importance: An adenomatoid odontogenic tumor is a rare medical condition. Large tumor (or several) often appears in the maxillae. In a minority of cases, the tumor(s) appear in the mandible.
Case Presentation: We report on a case of a 24-year-old female diagnosed with a mandibular adenomatoid odontogenic tumor, a giant tumor measuring approximately 22 × 25 × 17 cm. The tumor was located on the side of the mandible, causing facial deformity, malnutrition, and hemorrhaging. We assessed the patient's overall condition, carried out a resection of the tumor and mandible from the right condyle to the left mandibular angle, and reconstructed the mandibular defect with a fibula free flap. After the treatment, the patient was followed up for 1 year, with no recurrence detected over this period.
Clinical Discussion: Because adenomatoid odontogenic tumors are benign odontogenic lesions, which are painless and slow-growing, most are surgically removed or treated conservatively. However, the above treatment measures cannot be applied in the case of a giant tumor that causes facial deformity, destroys the entire jawbone, and has complications such as hemorrhaging and malnutrition. After the tumor resection, the defect is still significant. Accordingly, reconstruction using a microsurgical bone flap is an effective method instead.
Conclusion: Large adenomatoid odontogenic tumors in the mandible are rare, and treatment cannot follow conventional methods. Accordingly, defect reconstruction after tumor resection is essential.
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http://dx.doi.org/10.1016/j.ijscr.2022.107295 | 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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