Objectives: Ameloblastoma is a benign but highly infiltrative tumour, a behaviour that is lacking in adenomatoid odontogenic tumour but partly shared by the odontogenic keratocyst which possesses a unique intrinsic growth potential with marked ability for destroying bone and a high tendency recurrence. High frequency of stromal myofibroblasts (assessed with alpha smooth muscle actin (α-SMA) correlates with aggressive behaviour while p53-cell cycle regulation system is critical in odontogenic tumours with immunoreactivity signifying prognostic status. This study aims to determine and compare the immunoreactivity of these selected tumours to p53 and α-SMA in order to establish if a relationship exists between the frequency and pattern of distribution of myofibroblasts and the behaviour of these lesions.
Materials And Methods: 69 blocks of ameloblastoma, and 23 each of adenomatoid odontogenic tumor (AOT), and odontogenic keratocyst (OKC/KCOT) were retrieved. Immunohistochemistry technique was applied for evaluation of these two markers staining with primary antibodies to p53 and -SMA and the frequency and pattern of distribution of myofibroblasts and immunoreactivity to p53 analysed and compared using ANOVA. p was set at <0.05.
Results And Conclusion: Immunoreactivity to p53 and α-SMA was highest in ameloblastoma (solid compared to unicystic) with highest mean positive cells to α-SMA (29.7±20.1) and p53 (28.3±24.5) in plexiform ameloblastoma. This suggests that ameloblastoma was the most aggressive of tumours studied. Different pharmacological agents that can regulate stromal MF are useful aids to decrease the need for radical surgery in extensive and aggressive odontogenic tumours.
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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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