ORIGINAL ARTICLE
Year : 2021  |  Volume : 13  |  Issue : 2  |  Page : 148-154

Assessment of Inflammatory Domain on the Proliferative Activity of Odontogenic Keratocyst in Comparison with Dentigerous Cyst and Perapical Cyst


1 Department of Oral and Maxillofacial Pathology and Oral Microbiology, Nitte (Deemed to be University), AB Shetty Memorial Institute of Dental Sciences, Deralakatte, Mangalore, Karnataka, India
2 Department of Public Health Dentistry, Manipal College of Dental Sciences, Mangalore, Manipal Academy of Higher Education, Manipal, Karnataka, India

Correspondence Address:
Dr. Reshma Amin
Department of Oral and Maxillofacial Pathology and Oral Microbiology, Nitte (Deemed to be University), AB Shetty Memorial Institute of Dental Sciences, Deralakatte 575018, Mangalore, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jofs.jofs_257_21

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Introduction: Ki67 is a proven marker in assessing the aggressiveness of various neoplasms expressed in proliferating cells. The recognized role of p53 in a stress-induced cell represents gene mutation or disturbance of growth regulation. Therefore, a comparative analysis of p53 can give a better picture of proliferation in odontogenic keratocyst (OKC). In recent years, minichromosome maintenance (MCM) proteins are frequently in use for the application and evaluating cell proliferation. Our study plan was to compare the inter-relationship of p53, Ki67, minimicrosome (MCM2) markers in OKC, and other odontogenic cysts in inflammation, further checking the markers as a valuable tool in the prognosis and treatment of OKC. Materials and methods: Selected cases of 40 OKCs, 10 cases each of dentigerous cyst (DC) and periapical (PA) cyst showing mild to moderate inflammation were chosen from the department archives. Immunohistochemical procedure was carried out on all cases; interexaminer reliability was checked with Cronbach Alfa; and Chi-square was applied to check the association between the data. Results: Immunoexpression was significantly higher in OKC among p53, Ki67, and MCM2. The positivity of cells observed in OKC in the three markers did not show much difference (P = 0.666), though the intensity was statistically significant (P = 0.010). Comparative analysis among OKC, DC, and PA in all the three markers indicated statistical significance in the percentage of the positive cells and intensity. Conclusion: Considering the proportion of cycling cells relative to the expression of three markers, OKC imparts valuable information on proliferation. We speculate that the biological potential of OKC’s histopathogenesis lies within the lining epithelium, inflammatory cytokines contributing to the changes.


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