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Table of Contents
Year : 2021  |  Volume : 5  |  Issue : 2  |  Page : 91-96

Periodontal management of amlodipine-induced gingival hyperplasia in a hypertensive patient: A surgical approach

Department of Periodontology, Rabat Dental Consultation and Treatment Center, Faculty of Dental Medicine, Mohammed V University in Rabat, Rabat. Morocco

Date of Submission13-Nov-2020
Date of Decision07-Feb-2021
Date of Acceptance16-Apr-2021
Date of Web Publication23-Jun-2021

Correspondence Address:
Houda El Ayachi
Department of Periodontology, Rabat Dental Consultation and Treatment Center, Faculty of Dental Medicine, Mohammed V University in Rabat, Rabat. Morocco

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/SDJ.SDJ_59_20

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Background: Amlodipine is a third-generation dihydropyridine calcium channel blocker used to treat hypertension and angina. Gingival hyperplasia (GH) is an unwanted side effect associated with this therapy. It causes unsatisfactory esthetics, difficulty in maintaining good oral hygiene, abnormal tooth movement, and difficulty in mastication. GH can be managed by nonsurgical therapy alone or using a combination of nonsurgical and surgical therapy. Case Report: A 55-year-old female patient came to the clinical department of periodontology, University Hospital of Rabat, with a chief complaint of gingival enlargement. It was diagnosed and initially managed by nonsurgical periodontal treatment. Drug substitution and surgical intervention were executed. Regular supportive periodontal therapy showed a good and stable outcome over 2 years of follow-up. Conclusion: Amlodipine-induced GH can be managed using periodontal procedures combined with good oral hygiene and regular supportive periodontal therapy.

Keywords: Amlodipine, gingival hyperplasia, surgical approach

How to cite this article:
El Ayachi H, Ennibi OK. Periodontal management of amlodipine-induced gingival hyperplasia in a hypertensive patient: A surgical approach. Sci Dent J 2021;5:91-6

How to cite this URL:
El Ayachi H, Ennibi OK. Periodontal management of amlodipine-induced gingival hyperplasia in a hypertensive patient: A surgical approach. Sci Dent J [serial online] 2021 [cited 2023 Jun 4];5:91-6. Available from: https://www.scidentj.com/text.asp?2021/5/2/91/319051

  Background Top

Gingival hyperplasia (GH) is a periodontal disease characterized by an increase in gingival size.[1] This condition is also referred to as gingival overgrowth, gum overgrowth, and gum enlargement. Many factors have been implicated in the etiology of GH, such as inflammatory changes, hormonal alterations, Vitamin C deficiency, heredity, neoplasms, and systemic medications.[1],[2] However, the most commonly hypothesized cause is a reaction to prescribed drugs. More than 20 drugs are associated with GH most of which are classified as anticonvulsants, immunosuppressants, or antihypertensive agents.[2],[3]

Amlodipine, a third-generation dihydropyridine calcium channel blocker, is used to manage high blood pressure and angina.[4] The side effects associated with this medication include headache, dizziness, edema, flushing, palpitations, and GH.[5],[6] Signs and symptoms related to gingival enlargement may occur within 1–3 months of starting drug therapy.[7],[8] The first manifestation of the condition is an overgrowth of the interdental papilla that may extend coronally and is usually limited to the attached gum. This increased gingival volume frequently affects the anterior gingiva and the labial surfaces.[7],[9] GH can be managed using either a nonsurgical approach or by surgery, in the event that the fibrotic growth of the gingival tissue persists.[7],[10] In both approaches, it is recommended to reduce the dosage of the drug the patient is already taking or to switch to a different drug under the supervision of the attending physician.

In this report, we describe and discuss the relevant data available in the literature and the case study of a hypertensive patient with amlodipine-associated gingival over growth who underwent a successful surgical periodontal treatment and supportive periodontal therapy for over 24 months of follow-up.

  Case Report Top

A 55-year-old female patient was referred to the clinical department of periodontology, University Hospital of Rabat. She was complaining about anesthetic gingival enlargement on the buccal side of lower incisors. The GH had begun 4 months previously. The patient had difficulties to clean her teeth and suffered from bleeding when cleaning.

The patient’s medical history revealed that she had high blood pressure and she had been prescribed amlodipine (10 mg, once daily) 4 months previously. An intraoral examination revealed weak oral plaque control: The Loe and Silness plaque index (PI) was 1.65 and her Loe and Silness gingival index (GI) was 2.75. She also had localized nodular growth over the lower teeth, with the attached gingiva extending up to the marginal and interdental gingiva [Figure 1].[11],[12] The depth and clinical attachment loss of the periodontal pockets were found to be between 3–6 mm and 2–3 mm, respectively. Periapical X-rays revealed generalized moderate horizontal bone loss [Figure 2]. Based on the 2017 classification of periodontal diseases and conditions, the diagnosis was “gingival overgrowth associated with amlodipine with underlying localized moderate periodontitis Stage II, Grade B.”[13]
Figure 1: Preoperative clinical photo (J0)

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Figure 2: Initial periapical radiographs

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We explained the etiology of the disease and the possible treatment protocols to the patient. She signed an informed consent stating that she had been informed about the disease and the treatment and accepted to have her clinical data and pictures shared through a scientific publication.

Before starting the periodontal treatment, the patient’s physician was contacted to request that the amlodipine she was prescribed be replaced with another anti-hypertensive drug. The patient was then switched to ramipril (5 mg, once per day). The initial periodontal management consisted of nonsurgical periodontal therapy based on dental education and oral hygiene instruction, combined with a full-mouth debridement. A 0.12% chlorhexidine mouthwash was prescribed twice a day for 10 days. Three months after the etiologic phase of periodontal treatment, a clinical evaluation revealed a decrease in the depth of pockets and improvement of plaque and GI scores (PI: 0.3 and GI: 1.5). Surgical intervention was then scheduled to correct the fibroblastic gingival mass [Figure 3]. Surgical management of the enlargement consisted of a gingivectomy and gingivoplasty (internal bevel incision) under local anesthesia. Sutures were applied for the patient’s comfort and to promote good healing [Figure 4]. Re-evaluation and a periodontal examination showed that the periodontium was stable, so supportive periodontal maintenance was scheduled, including the reinforcement of oral hygiene instruction and full-mouth scaling after 3 months and then every 6 months.
Figure 3: View after periodontal revaluation (3 months)

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Figure 4: Gingivectomy, gingivoplasty (internal bevel incision), and sutures

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Two years of regular follow-up, clinical examination, and X-ray evaluations showed a healthy reduced periodontium with a stable outcome [Figure 5].
Figure 5: Periapical radiographs, 2 years posttreatment, showing stable outcomes

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  Discussion Top

Gum enlargement is a side effect associated with the administration of calcium channel blocker drugs, including amlodipine. The present case report showed GH months after starting amlodipine at a daily dose of 10 mg.

Some studies have found that amlodipine-induced gingival enlargement affects <4% of patients prescribed the drug, for example, Jorgensen (3.3%), Ellis et al. (1.7%), and Tejnani et al. (3.4%), while other studies have reported a higher prevalence.[14],[15],[16],[17],[18],[19] A recent systematic review revealed that 26.7% of patients on amlodipine developed GH.[20] This broad variation in the prevalence can be explained by differences in the studied populations, drug dosages, and the duration and efficacy of oral hygiene practices.[21] The patient reviewed in this case study received 10 mg/day of amlodipine, a dosage that many studies have found to be associated with severe GH.[22],[23],[24],[25]

Jorgensen suggested that 5 mg/day of amlodipine could not result in GH, but this has been refuted by many later studies, which found that GH occurred with 5 mg/day or less of amlodipine (see, for example, Jayanthi et al.’s 2017 report).[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23] More recently, amlodipine has been reported to cause GH in dosages ranging from 2.5 to 10 mg.[20] This variance may be explained by the fact that the majority of such studies evaluated GH within the first 6 months of therapy, even though amlodipine-induced gingival enlargement can occur after this period.[14],[16],[21],[22],[23],[24],[25],[26],[27]

The pathogenesis of drug-induced GH is multifactorial, including genetic predisposition, age, gender, drug variables, and poor oral hygiene.[28],[29] Genetic susceptibility plays a central role in its etiopathogenesis: In fact, the inflammatory response to amlodipine seems to be altered by the multidrug-resistant gene MDR1.[20],[30],[31] Biofilm accumulation is also considered an important risk factor for the occurrence of amlodipine-induced GH. Several studies have confirmed the role of inflammation induced by dental plaque in the pathogenesis of gingival enlargement.[20],[32],[33],[34] The precise mechanism by which amlodipine-induced enlargement occurs remains unclear, although a number of hypotheses have been suggested. It seems that amlodipine and its metabolites disturb protein synthesis and collagen production in gingival fibroblasts.[35],[36] Thus, patients who develop drug-induced gingival enlargement should be well educated on how to keep clean their teeth, and close collaboration between these patients’ physicians and dentists is essential for their general wellbeing.

If gingival enlargement occurs, the patient’s physician may decide to substitute amlodipine with another drug and periodontal treatment should be implemented.[7],[37] Periodontal therapy is based on nonsurgical interventions that can be followed by surgical interventions. Nonsurgical approaches, including an oral hygiene education program, removal of local irritants, and scaling and root planing, can reduce the size of the clinical lesions, due primarily to the elimination of bacteria. Montebugnoli et al. showed that, after 3 months, nonsurgical periodontal treatment was effective in decreasing plaque and gingival indices, but changes in gingival overgrowth took longer to show significant improvement.[38] Aimetti et al. also reported that oral hygiene and periodontal debridement significantly reduced GH within 3 months.[39] The prescription of antibiotics is not a standard intervention and at present remains controversial; however, the adjunctive use of chlorhexidine showed beneficial effects in reducing the severity of gingival overgrowths.[40],[41] When nonsurgical treatments fail to reduce the hyperplastic tissue, surgical excision is recommended.[36],[42] Indeed, surgical treatment produces satisfactory steadyresults, as it removes the fibrotic tissue: This allows for the improvement of plaque control and restores the esthetic appearance of the gingiva.[20]

Surgical management of amlodipine-induced GH, although effective, does not necessarily prevent recurrence of the lesions. The recurrence rate of amlodipine-induced GH after surgical periodontal therapy was found to be approximately 40% within 18 months among patients whose drug therapy could not be altered.[43] Any recurrence of lesions after surgical excision requires repeated surgical interventions.[3] In this case study, it was decided that a surgical excision was necessary 3 months after the substitution of amlodipine and etiologic therapy. The patient complied with plaque control practices and experienced reduced inflammation, but she was not satisfied with the persistence of the fibrous component of the GH. If the GH persists despite drug substitution, good oral hygiene, and nonsurgical treatment, overgrown gingiva should be surgically removed. Classic gingivectomy remains the therapy of choice for several practitioners.[10] However, this technique, which involves an external bevel, causes loss of attached tissue, postoperative pain and bleeding, and delayed healing; it could also be contraindicated in cases of severe drug-induced GH.[44] Flap surgery, electrosurgery, and laser excision are useful alternative therapeutic options to external bevel gingivectomy for surgical correction in cases of amlodipine-induced GH.[10] Compared to conventional techniques, laser surgery has numerous advantages: It allows a clear operating field, better visibility, and reduced intervention time, as well as hemostatic and bactericidal advantages. It also causes generally fewer and less severe postoperative consequences and less pain. The rate of recurrence following laser excision is lower than that of scalpel gingivectomy in the first few months postsurgery.[45] The recurrence rate (34%) of drug-induced gingival overgrowth remains a challenge for dentists.[43] For this reason, a regular supportive periodontal therapy must be systematically established to avoid the need for repeated surgical interventions and to reduce the risk of recurrence, especially when the etiological factors particularly the involved drugs cannot be altered.[46]

  Conclusion Top

GH may occur in patients being treated with amlodipine. A patient’s medical history and a periodontal examination help clinicians to produce a diagnosis. Bacterial biofilm is an important risk factor for the occurrence of amlodipine-induced GH. Treatment can be based on a nonsurgical approach alone or in combination with surgery. When possible, amlodipine should be substituted with another drug to eliminate this side effect. Finally, a steady supportive periodontal therapy should be implemented to maintain the health of the periodontium and reduce the recurrence of GH.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

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