Abstract
Gingival overgrowth (GO) is a side effect associated with some distinct classes of drugs, such as anticonvulsants, immunosuppressant, and calcium channel blockers. GO is characterized by the accumulation of extracellular matrix in gingival connective tissues, particularly collagenous components, with varying degrees of inflammation. One of the main drugs associated with GO is the antiepileptic phenytoin, which affects gingival tissues by altering extracellular matrix metabolism. Nevertheless, the pathogenesis of such drug-induced GO remains fulfilled by some contradictory findings. This paper aims to present the most relevant studies regarding the molecular, immune, and inflammatory aspects of phenytoin-induced gingival overgrowth.
Highlights
Gingival overgrowth (GO) comprises any clinical condition in which an increase in the size of the gingiva is observed
The aim of this work was to review the most relevant studies published about phenytoin-induced GO (PGO) and outline the possible mechanisms associated with this condition
Kato et al [34] showed a reduction in mRNA expression of collagen type I and III associated with a higher density of these fibers in the PGO. These results suggest that the imbalance that leads to PGO might be related to decreased collagen degradation, not to an increase on its synthesis (Figure 1)
Summary
Gingival overgrowth (GO) comprises any clinical condition in which an increase in the size of the gingiva is observed. The first report of GO associated with the chronic use of phenytoin was made in 1939 [6]. This agent remains as one of the most commonly prescribed medications to treat epilepsy and it may be used in cases of neuralgias and cardiac arrhythmias [7]. The aim of this work was to review the most relevant studies published about phenytoin-induced GO (PGO) and outline the possible mechanisms associated with this condition. The level of inflammatory cell infiltrate varies significantly [20]
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