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Changes in the minor salivary glands and ductal carcinoma resulting from induction of oral carcinogenesis

Caio Rodrigues Maia; Raissa Cláudia Eufrázio de Oliveira; Viviane Tainá Carvalho da Silva; Cecília Cerqueira Souza; Vivian Gracielly Nascimento de Oliveira; Alana Beatriz Brito Costa; Pedro Paulo de Andrade Santos
Journal of Molecular Histology · Vol. 57, Issue 5 · 2026

Abstract

Given the scarcity of experimental studies on the effects of induced oral carcinogenesis on the minor salivary glands, the aim of this study was to analyze the histopathological changes present in the lingual and palatal minor salivary glands (MiSGs) resulting from 4NQO exposure in rats from the 8th to the 30th week of the experiment. Eleven rats were used in the control group and 45 rats in the experimental groups that received 4NQO/propylene glycol diluted in drinking water. Histopathological analysis revealed evidence of hyperplasia, metaplasia, and ductal dysplasia, saliva buildup in the ducts, inflammatory infiltrate, lobular atrophy, degeneration of the secretory portion, fibrosis/replacement, and invasion of the minor salivary glands. The most evident change in both tongue and palate MiSGs was degeneration of the secretory portion, which reduced salivation and promoted the oncogenic action of 4NQO. However, changes such as hyperplasia, metaplasia, and dysplasia, which may promote the development of neoplastic changes, were more prevalent in tongue MiSGs. In the present study, we also identified an incidental case of salivary ductal carcinoma in palatal MiSGs. Given this, it is important to be vigilant regarding potential changes in MiSGs, as they may be related to the development of malignancies.

Bibliographic Information

JournalJournal of Molecular Histology
PublisherSpringer
Publication Date2026-10-01
Publication Year2026
Volume57
Issue5
Document TypeJournal Article
Print ISSN1567-2379
eISSN1567-2387
DOI10.1007/s10735-026-10938-5

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NARA Access Coverage1968-01-01~Current
Journal Homepagehttps://www.springer.com/journal/10735
Publisher PageOpen Publisher Page
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