Hypervitaminosis A and Oral Pathology: Genomic Disruption, Enamel Defects, and Gingival Hazards
- 1Assistant lecturer at Oral Biology Department, Modern University for Technology and Information.
- 2Professor at Oral Biology Department, Al-Azhar University for Boys, Cairo, Egypt.
- 3oral biology department,faculty of dentistry,Ain Shams university, Cairo,Egypt
Abstract
Background: Vitamin A is essential for epithelial integrity, skeletal development, and immune function. However, when consumed in excess, it becomes a potent toxin. The oral cavity with its high rate of epithelial turnover, active bone metabolism, precisely regulated enamel formation, and complex immune interactions is particularly susceptible to vitamin A overload. Despite widespread supplement use, hypervitaminosis A remains an underrecognized cause of oral pathology. Methods: This narrative review synthesized evidence published between January 2016 and July 2026. We searched PubMed, Scopus, and Web of Science using keywords related to hypervitaminosis A and oral pathology. Studies were included if they examined vitamin A toxicity effects on oral tissues, enamel, gingiva, or alveolar bone. Key toxicity pathways analyzed included receptor-mediated genomic disruption and metabolite cytotoxicity. Results: Retinoid accumulation in alveolar bone disrupts osteoblast-osteoclast balance, shifting toward bone resorption. Multiple studies consistently report associations between vitamin A excess and enamel hypoplasia, opacities, and hypomineralization. In poly-supplement users, dysregulated collagen synthesis and inhibited clotting factors contribute to gingival hyperplasia and bleeding. Nutrient interactions with vitamins D, E, K, and iron exacerbate oral manifestations. High-risk groups include pregnant women, children, the elderly, and patients with hepatic dysfunction. Conclusion: Hypervitaminosis A is an underrecognized risk factor for oral pathology. Dentists should consider supplement overuse when evaluating unexplained enamel defects, gingival changes, or jawbone fragility. Early recognition and discontinuation of supplementation can reverse acute changes and prevent irreversible enamel and bone damage. Biomarker-based precision nutrition offers a promising approach for managing oral complications of vitamin A toxicity.
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BibTeX
@article{desouly2026hypervitaminosis,
title = {{Hypervitaminosis A and Oral Pathology: Genomic Disruption, Enamel Defects, and Gingival Hazards}},
author = {Nada Desouly and Hany Sherif and Iman Fathy},
journal = {The Egyptian Journal of Histology},
year = {2026},
month = oct,
doi = {10.21608/ejh.2026.508328.2492},
url = {https://doi.org/10.21608/ejh.2026.508328.2492},
note = {CC BY},
}
RIS
TY - JOUR
TI - Hypervitaminosis A and Oral Pathology: Genomic Disruption, Enamel Defects, and Gingival Hazards
AU - Nada Desouly
AU - Hany Sherif
AU - Iman Fathy
PY - 2026
DA - 2026/10/25
JO - The Egyptian Journal of Histology
DO - 10.21608/ejh.2026.508328.2492
UR - https://doi.org/10.21608/ejh.2026.508328.2492
AB - Background: Vitamin A is essential for epithelial integrity, skeletal development, and immune function. However, when consumed in excess, it becomes a potent toxin. The oral cavity with its high rate of epithelial turnover, active bone metabolism, precisely regulated enamel formation, and complex immune interactions is particularly susceptible to vitamin A overload. Despite widespread supplement use, hypervitaminosis A remains an underrecognized cause of oral pathology. Methods: This narrative review synthesized evidence published between January 2016 and July 2026. We searched PubMed, Scopus, and Web of Science using keywords related to hypervitaminosis A and oral pathology. Studies were included if they examined vitamin A toxicity effects on oral tissues, enamel, gingiva, or alveolar bone. Key toxicity pathways analyzed included receptor-mediated genomic disruption and metabolite cytotoxicity. Results: Retinoid accumulation in alveolar bone disrupts osteoblast-osteoclast balance, shifting toward bone resorption. Multiple studies consistently report associations between vitamin A excess and enamel hypoplasia, opacities, and hypomineralization. In poly-supplement users, dysregulated collagen synthesis and inhibited clotting factors contribute to gingival hyperplasia and bleeding. Nutrient interactions with vitamins D, E, K, and iron exacerbate oral manifestations. High-risk groups include pregnant women, children, the elderly, and patients with hepatic dysfunction. Conclusion: Hypervitaminosis A is an underrecognized risk factor for oral pathology. Dentists should consider supplement overuse when evaluating unexplained enamel defects, gingival changes, or jawbone fragility. Early recognition and discontinuation of supplementation can reverse acute changes and prevent irreversible enamel and bone damage. Biomarker-based precision nutrition offers a promising approach for managing oral complications of vitamin A toxicity.
SN - 2090-2417
SN - 1110-0559
ER -