|Year : 2022 | Volume
| Issue : 5 | Page : 55-57
Amlodipine-induced gingival hyperplasia: A report of two cases
G Sri Lakshmi1, G Tejaswini1, B Alekhya2, Maria Bethasaida Manuel2, R Ram2, V Siva Kumar2
1 Sri Venkateswara Institute of Medical Sciences Sri Padmavathi Medical College for Women, Tirupati, Andhra Pradesh, India
2 Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India
|Date of Submission||25-Mar-2020|
|Date of Acceptance||04-Sep-2020|
|Date of Web Publication||19-Nov-2021|
Professor and Head, Sri Venkateswara Institute of Medical Sciences, Tirupati 517 507, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
Drugs associated with gingival overgrowth fall into three broad categories – anticonvulsants, immune suppressants and calcium channel blockers. Amlodipine is a third-generation dihydropyridine. The prevalence of amlodipine-induced gingival hyperplasia is 4.2%. We report two patients with the amlodipine-induced gingival hyperplasia.
Keywords: Amlodipine, anticonvulsants, calcium channel blockers, drug-induced gingival overgrowth, gingival hyperplasia, immune suppressants
|How to cite this article:|
Lakshmi G S, Tejaswini G, Alekhya B, Manuel MB, Ram R, Kumar V S. Amlodipine-induced gingival hyperplasia: A report of two cases. J Clin Sci Res 2022;11, Suppl S1:55-7
|How to cite this URL:|
Lakshmi G S, Tejaswini G, Alekhya B, Manuel MB, Ram R, Kumar V S. Amlodipine-induced gingival hyperplasia: A report of two cases. J Clin Sci Res [serial online] 2022 [cited 2022 Oct 6];11, Suppl S1:55-7. Available from: https://www.jcsr.co.in/text.asp?2022/11/5/55/355073
| Introduction|| |
Kimball reported gingival hyperplasia for the first time in 1939 in a patient following phenytoin use. Drugs associated with gingival overgrowth fall into three broad categories – anticonvulsants, immune suppressants and calcium channel blockers (CCBs)., Among CCBs, the dihydropyridines (e.g., nifedipine, felodipine, amlodipine, nitrendipine, nicardipine and manidipine) have a propensity to be more associated with gingival hyperplasia. Amlodipine is a third-generation dihydropyridine. It was patented in 1982 and approved for medical use in 1990. We report two patients with amlodipine-induced gingival hyperplasia.
| Case Reports|| |
A 50-year-old man, with hypertension, chronic kidney disease Stage 3 was receiving oral telmisartan 40 mg/day. When blood pressure was not controlled, amlodipine was added. After 3 months, the patient reported the overgrowth of the gums [Figure 1]a. There were no other complaints except for the cosmetic disquiet. Intraoral examination revealed a generalised enlargement of the gingiva extending up to marginal and interdental gingiva. The surface of the gingiva appears lobulated with loss of scalloping. Oral hygiene was poor. We substituted amlodipine with prazosin. After 12 weeks, the gingival hyperplasia had regressed [Figure 1]b. We referred the patient to a dental surgeon for improvement in oral hygiene.
|Figure 1: Clinical photograph showing gingival hyperplasia 3 months after the use of amlodipine (a). Clinical photograph of the same patient showing regression of gingical hyperplasia after amlodipine withdrawal (b)|
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A 55-year-old man, known to have type 2 diabetes mellitus, hypertension on maintenance haemodialysis for end-stage renal disease presented with complaints of bleeding from gums. The patient had been receiving amlodipine for the past decade. An intraoral examination revealed generalised diffused gingival hyperplasia. The gingival enlargement was painless, lobulated, firm, pink and resilient and had a tendency to bleed. Extensive plaque formation and periodontal disease were also present [Figure 2]. We replaced the amlodipine by an angiotensin-converting enzyme inhibitor and sought a dental surgeon consultation.
|Figure 2: Clinical photograph showing gingival hyperplasia after 3-months use of amlodipine|
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| Discussion|| |
The clinical manifestations of gingival hyperplasia are of a wide spectrum. The appearance ranges from non-inflamed, firm and fibrous gingiva to one that is dominated by oedema, erythema and bleeding. The latter form is especially seen in patients with poor oral hygiene. Although most of the drugs that cause gingival hyperplasia do not directly affect the underlying alveolar bone, the gingival enlargement may increase the accumulation of bacterial biofilm and prevent adequate oral hygiene measures, thus inducing inflammation, periodontitis, bone and tooth loss and halitosis.
In the CCBs-induced gingival enlargement, the increase in the gingival tissue volume is primarily due to a connective tissue response rather than an epithelial cell proliferation. It is characterised by an excessive accumulation of extracellular matrix proteins, such as collagen, amorphous ground substance and of non-collagenous proteins, such as glycosaminoglycans.
Both inflammatory and non-inflammatory pathways are proposed to explain the gingival hyperplasia after the use of drugs. The proposed non-inflammatory mechanisms are initiated by the decreased uptake of folic acid, blockage of aldosterone synthesis in the adrenal cortex and consequent feedback increase in adrenocorticotropic hormone level and upregulation of keratinocyte growth factor. The direct toxic effects of concentrated drug in crevicular gingival fluid may initiate the inflammatory process. The risk factors include poor oral hygiene and bacterial dental plaque formation. Age has not been identified as a risk factor for CCBs-induced gingival hyperplasia, as these drugs are usually prescribed to middle-aged and older patients, preventing any attempt to stratify them. Nifedipine increased the conversion of testosterone to 5-dihydrotestosterone. The active androgen metabolite appears to target subpopulations of fibroblasts and induces collagen synthesis or decreases its degradation. Therefore, the drug-induced gingival hyperplasia is reported more in males than in females. There is a lack of a clear correlation between dosage of nifedipine and occurrence of gingival hyperplasia. Some reports on amlodipine suggest that a daily dose of 5 mg or higher could be a risk factor for gingival overgrowth in some patients. Lederman et al. were the first to report its negative oral effects of nifedipine in 1984; subsequent studies showed that its prevalence varied from 14% to 83%., As for verapamil and amlodipine, the prevalence was significantly lower (4.2% and 3.3%, respectively) than that of nifedipine., The most effective treatment of gingival hyperplasia is cessation of the offending medication and a substitution with another class, or substitution with another CCB that has a lower risk of inducing gingival enlargement, such as verapamil and isradipine. In addition, surgical and non-surgical management may be required. As many as 40% of the patients are at risk of recurrence as early as 3–6 months. It appears that the risk of recurrence is higher in patients with poor oral hygiene or lack of dental care.
Financial support and sponsorship
Conflicts of interest
The authors are faculty members/Undergraduate/postgraduate students/residents of Sri Venkateswara Institute of Medical Sciences, Tirupati, of which Journal of Clinical and Scientific Research is the official Publication. The article was subject to the journal's standard procedures, with peer review handled independently of these faculty and their research groups.
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[Figure 1], [Figure 2]