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Adenoid ameloblastoma revisited: A discursive exploration of its histological dualism, molecular aberrations, and clinical recurrence. | LitMetric

Adenoid ameloblastoma revisited: A discursive exploration of its histological dualism, molecular aberrations, and clinical recurrence.

Semin Diagn Pathol

Department of Oral Pathology & Microbiology, King George's Medical University, Lucknow 226003, UP, India. Electronic address:

Published: October 2024

AI Article Synopsis

  • Adenoid ameloblastoma (AA) is a rare but locally aggressive benign tumor derived from dental tissue remnants, and it was recently classified as a new type of odontogenic lesion by the WHO in 2022.
  • This tumor behaves more aggressively than similar types, presenting as a painless jaw swelling with a high recurrence rate and local invasiveness, and exhibits unique histopathological features such as a cribriform pattern and differential marker expression.
  • Due to its complex nature and unclear origins, AA requires thorough clinical evaluation and customized treatment approaches to manage recurrence and improve patient outcomes, with the latest research contributing to its understanding post-classification.

Article Abstract

Adenoid ameloblastoma (AA) is a rare benign but locally aggressive odontogenic tumor originating from the remnants of the dental lamina or enamel organ. It was newly incorporated into the 2022 WHO classification of odontogenic lesions, standing as the sole novel entity in this update. AA is also regarded as a hybrid tumor because of the combination of histological characteristics observed in both adenomatoid odontogenic tumors and ameloblastoma. Clinically, it presents similarly to other ameloblastoma variants, with patients typically exhibiting a painless, slow-growing jaw swelling. However, this subtype is noted for its more aggressive behavior, including a higher recurrence rate and greater local invasiveness. Histopathologically, AA is distinguished by an intricate arrangement of epithelial islands, cords, and strands, generating a cribriform architectural pattern, with peripheral palisading and central stellate reticulum-like formations. Immunohistochemical profiling reveals the expression of epithelial differentiation markers, including cytokeratins, and proliferative markers such as Ki-67, further corroborating its aggressive phenotype. While its precise etiopathogenesis remains obscure, the unique histological characteristics imply a potentially distinct underlying molecular pathway. Due to its aggressive nature, AA necessitates meticulous clinical and histopathological evaluation and tailored therapeutic strategies to mitigate recurrence risks and optimize patient prognoses. Furthermore, this review integrates histological and molecular insights from recent studies conducted after its inclusion in the updated WHO classification.

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Source
http://dx.doi.org/10.1053/j.semdp.2024.10.001DOI Listing

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