ArticleCureus2025
Immunohistochemical Evaluation of Ki-67 Proliferation Marker in Various Biological Variants of Ameloblastoma.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Introduction Ameloblastoma remains one of the most enigmatic and locally destructive benign odontogenic tumors, posing significant therapeutic challenges owing to its variable biological behavior across histopathological subtypes. The present study aimed to evaluate and compare the proliferative activity using Ki-67 labelling index (LI) among solid/multicystic ameloblastoma (SMA), unicystic ameloblastoma (UA), and desmoplastic ameloblastoma (DA), and to correlate the findings with their known clinical aggressiveness and recurrence potential. Materials and methods Thirty archival formalin-fixed, paraffin-embedded blocks of ameloblastoma were retrieved. The ameloblastoma cases comprised 12 SMA (predominant plexiform pattern), 10 UA, and 08 DA cases. Four or five micrometer sections were subjected to immunohistochemical staining using a ready-to-use mouse monoclonal anti-Ki-67 antibody. Three blinded oral pathologists independently counted Ki-67-positive tumor nuclei in three hot spot high-power fields (×100), and the labelling index was calculated as the percentage of positive nuclei per 1,000 tumor cells. Data were analyzed using one-way analysis of variance (ANOVA) and Tukey's post-hoc test; p <0.05 was considered significant. Results Ki-67 LI was significantly higher in SMA (mean 75.44 ± 18.58%, range 20.56-93.89%), followed by UA (22.81 ± 4.81%), and lowest in the DA (11.7 ± 15.44%; p=0.001). Post-hoc analysis confirmed significantly higher expression in SMA than in UA (p=0.001) and DA (p=0.001), with no significant difference between UA and DA (p=0.353). Excellent interobserver agreement was achieved (ICC=0.99). Conclusion SMA exhibited markedly higher proliferative activity than UA and DA, explaining their greater local aggressiveness and recurrence risk. The Ki-67 LI is a reliable and reproducible immunohistochemical marker that can aid risk stratification, treatment planning, and prognostic prediction in ameloblastoma.
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