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MOLECULAR BASIS OF AMELOBLASTOMA PATHOGENESIS: A REVIEW

Original title: BASES MOLECULARES DE LA PATOGÉNESIS DEL AMELOBLASTOMA: UNA REVISIÓN
*Corresponding author for this work
  • Universidad Nacional Mayor de San Marcos
    ,
  • Universidad Científica del Sur
    ,
  • Universidad Federico Villareal
    ,
  • Niigata University Graduate School of Medical and Dental Sciences
Research Output:
Contribution to journal
Article
Peer-review

Publication Information

Output type

Research Output:
Contribution to journal
Article
Peer-review

Original language

Spanish

Article number

e212

Journal (Volume, Issue Number)

Revista Cientifica Odontologica (Volume 12, Issue 3)

Publication milestones

  • Published - 17/09/2024

Publication status

Published - 17/09/2024

ISSN

2310-2594

Publication IDs

  • Scopus: 105002452289

Abstract

Ameloblastoma is the most common and highly invasive benign odontogenic tumor. Its pathogenesis is not yet fully understood. Objective: To describe the most important molecular findings that promote the proliferative activity of ameloblastoma and the factors involved that encourage invasion into surrounding bone tissues. Methodology: A search for scientific evidence was conducted through the following databases: Science Direct, Medline, Wiley, Web of Science, and Google Scholar. A total of 32 articles were reviewed, with inclusion criteria being articles published in English and Spanish; descriptive and analytical studies, narrative and systematic reviews published from January 2015 to June 2021. Letters to the editor were excluded. Results: The biological molecular findings that allow ameloblastoma to invade surrounding tissues involve alterations in the RANK/RANKL/OPG pathways, transforming growth factor beta (TGF-β), Wnt/β-catenin pathway, and matrix metalloproteinases, as well as alterations in MAPK and SHH pathways that facilitate the proliferation and tumor development of ameloblastoma. Conclusions: These findings are fundamental for a better understanding of the pathways involved in the pathogenesis of ameloblastoma.