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Calcium Antagonist-Induced Gingival Overgrowth: A Case Report and Literature Review
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Background: Drug-induced gingival enlargement is a commonly documented adverse effect in patients administered with calcium antagonist medications. Nifedipine is the medicine most frequently linked to instances of gingival enlargement; nevertheless, amlodipine, likewise a calcium antagonist, can elicit this adverse effect. This case report aims to detail a case of amlodipine-induced gingival hyperplasia, emphasizing the significance of a multidisciplinary approach and outlining its therapy across various surgical phases. Methods: A 48-year-old hypertensive patient using amlodipine therapy presents with aberrant gingival tissue growth in the upper arch. Intraoral examination reveals localized inflammation and tissue enlargement in the papillae areas of the upper arch gingiva, leading to partial covering of the dental crowns. The patient experienced painful sensations and episodes of spontaneous bleeding in the enlarged gingival tissue. Following an initial professional dental hygiene treatment, which included root planning in the upper quadrants, and in consultation with the referring cardiologist, it was determined to discontinue amlodipine and initiate a replacement therapy with olmesartan medoxomil. Fifteen days following the cessation of amlodipine, surgical excision of the thickened interdental gingival tissues in the anterior region was conducted to obtain biopsies for histological confirmation of the observed pathological condition. Results: Histopathological examination validated the diagnosis of drug-induced gingival enlargement, characterized by chorion fibrosis and significant lymphoplasmacytic infiltration. Specifically, parakeratotic and acanthotic characteristics were seen in the gingival epithelium. Adjacent to the inflammatory regions, fibrosis was noted, along with the presence of cytoid bodies, which are typically linked to pathological diseases driven by inflammatory processes. These histological characteristics were consistent with the diagnosis of drug-induced gingival enlargement. Conclusions: A multidisciplinary approach involving the treating physician, dentist, and hygienist, incorporating drug replacement and targeted oral hygiene sessions, is crucial for the management and resolution of calcium channel blocker-induced gingival enlargement.
Title: Calcium Antagonist-Induced Gingival Overgrowth: A Case Report and Literature Review
Description:
Background: Drug-induced gingival enlargement is a commonly documented adverse effect in patients administered with calcium antagonist medications.
Nifedipine is the medicine most frequently linked to instances of gingival enlargement; nevertheless, amlodipine, likewise a calcium antagonist, can elicit this adverse effect.
This case report aims to detail a case of amlodipine-induced gingival hyperplasia, emphasizing the significance of a multidisciplinary approach and outlining its therapy across various surgical phases.
Methods: A 48-year-old hypertensive patient using amlodipine therapy presents with aberrant gingival tissue growth in the upper arch.
Intraoral examination reveals localized inflammation and tissue enlargement in the papillae areas of the upper arch gingiva, leading to partial covering of the dental crowns.
The patient experienced painful sensations and episodes of spontaneous bleeding in the enlarged gingival tissue.
Following an initial professional dental hygiene treatment, which included root planning in the upper quadrants, and in consultation with the referring cardiologist, it was determined to discontinue amlodipine and initiate a replacement therapy with olmesartan medoxomil.
Fifteen days following the cessation of amlodipine, surgical excision of the thickened interdental gingival tissues in the anterior region was conducted to obtain biopsies for histological confirmation of the observed pathological condition.
Results: Histopathological examination validated the diagnosis of drug-induced gingival enlargement, characterized by chorion fibrosis and significant lymphoplasmacytic infiltration.
Specifically, parakeratotic and acanthotic characteristics were seen in the gingival epithelium.
Adjacent to the inflammatory regions, fibrosis was noted, along with the presence of cytoid bodies, which are typically linked to pathological diseases driven by inflammatory processes.
These histological characteristics were consistent with the diagnosis of drug-induced gingival enlargement.
Conclusions: A multidisciplinary approach involving the treating physician, dentist, and hygienist, incorporating drug replacement and targeted oral hygiene sessions, is crucial for the management and resolution of calcium channel blocker-induced gingival enlargement.
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