Gingival Hyperplasia Case Study

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Chronic Inflammatory Gingival Enlargement Associated with Orthodontic Therapy – A Case Report


Purpose: Gingival enlargement, also synonymous with the terms gingival hyperplasia or hypertrophy, is defined as an abnormal overgrowth of gingival tissues. A case of a 19–year–old male presenting with maxillary and mandibular chronic inflammatory gingival enlargement associated with prolonged orthodontic therapy is reported here. Surgical therapy was carried out to provide a good aesthetic outcome. No recurrence was reported at the end of 1 year. The importance of patient motivation and compliance during and after therapy as a critical factor in the success of treatment has also been highlighted through this case report.

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Gingival enlargement, a globally accepted terminology for an increase in the size of the gingiva, is a general feature of gingival diseases. It is a multifactorial condition that develops in response to various stimuli and interactions between the host and the environment. It may be plaque–induced or associated with systemic hormonal disturbances. It also occurs as a manifestation associated with several blood dyscrasias, such as leukemia, thrombocytopenia or thrombocytopathy. A rare variant, idiopathic gingival fibromatosis, with a familial inheritance, has also been reported.1 Based on the extent and severity, these enlargements may lead to functional disturbances like altered speech, difficulty in mastication and aesthetic and psychological problems.

Inflammatory gingival enlargement may be categorized as acute or chronic, wherein chronic changes are much more common.1 The ability to perform oral hygiene measures is compromised in some patients with gingival enlargements, which may be further complicated by the presence of prosthesis and fixed orthodontic appliances. This may lead to more inflammation and further plaque accumulation perpetuating this vicious cycle. Thus, there is a transformation of the gingival sulcus into a periodontal pocket creating an area where plaque removal becomes impossible.

One of the most important determinants of treatment outcomes is patient compliance. The willingness to perform adequate oral hygiene measures and receive timely periodic recalls and treatment are deemed essential for a successful outcome. The therapeutic approaches related to gingival enlargement are based on the underlying etiology and the subsequent changes it manifests on the tissues. The prime treatment modalities involve obtaining a detailed medical history and non–surgical periodontal therapy, followed by surgical excision to retain esthetical and functional demands.

This case report presents a case of chronic gingival enlargement associated with prolonged orthodontic therapy.

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Case Report

A 19–year–old male patient reported to the Department of Periodontology, Manipal College of Dental Sciences, Manipal, India. The patient complained of swelling of the upper and lower gums in the front tooth region. The patient had noticed the swelling 3 years prior and reported that it had not increased in size since then. He also complained of bleeding from the gums while brushing. The patient revealed that he had undergone incomplete orthodontic treatment which was initiated 6 years prior. There was no other relevant medical, dental or family history.

Consistent with the history of incomplete orthodontic treatment, intraoral inspection revealed orthodontic molar bands and brackets on all teeth except the maxillary left central incisor. On clinical examination, marginal and papillary gingiva appeared red and enlarged in the maxillary and mandibular arches, which was more prominent in the anterior sextants and also more pronounced on the right side as compared to the left (Figures 1, 2 and 3). Further soft tissue assessment revealed soft and edematous consistency and bleeding on probing on all teeth.

A treatment plan consisting of initial periodontal therapy followed by a gingivectomy procedure was planned to improve aesthetics and function. The initial periodontal therapy comprising supragingival and subgingival scaling was performed. Oral hygiene instructions were given and the use of chlorhexidine mouthwash (0.2% Clohex™, Dr. Reddy's Laboratories Ltd., India) twice a day for one week was advised. At the next visit, in spite of use of the prescribed medicated mouthwash, the gingival enlargement did not show considerable reduction in size, but the tissues appeared to be firm in consistency. At this stage, radiographs were taken and complete blood count investigations (RBC, WBC and platelet counts, ESR, bleeding time, clotting time, prothrombin time) were carried out (Figure 4).

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These investigations were non–contributory. An internal bevel gingivectomy was performed for the maxillary sextant. The excised tissue was sent for histopathological examination. Following this, the patient failed to report for subsequent recall appointments.

The histopathological examination revealed a hyperplastic parakeratinized epithelium overlying inflamed connective tissue. The underlying stromal tissue showed numerous proliferating young fibroblasts admixed with focal aggregates of chronic inflammatory cells. Few fibroblasts appeared stellate, with numerous nuclei distributed in a collagenized stroma. At places the stromal tissue exhibited myxoid degeneration. A histopathological diagnosis suggestive of inflammatory fibrous hyperplasia was given (Figure 5).

One year later, the patient reported back to the clinic. At this stage, the patient also expressed the unwillingness to continue the orthodontic therapy. Intraoral examination revealed that the maxillary surgical site had healed satisfactorily. There was no recurrence of the gingival enlargement in the maxillary anterior sextant (Figure 6). However, enlargements in the untreated areas persisted. Initial periodontal therapy was performed again and oral hygiene instructions were reinforced. To further improve plaque control measures, the orthodontic appliances were removed at this stage by the orthodontist. The patient was also counseled regarding the importance of follow up and maintenance with special emphasis on motivation.

Figure 1:

Intra–oral pre–operative right lateral view

Figure 2:

Intra–oral pre–operative frontal view

Figure 3:

Intra–oral pre–operative left lateral view

Figure 4:


Following this, gingivectomy was performed in the mandibular anterior sextant (Figure 7) and maxillary right posterior sextant at different scheduled appointments. Then the patient was reviewed and healing was found to be satisfactory.

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Gingival overgrowth varies from mild enlargement of isolated interdental papillae to segmental or uniform and marked enlargement affecting 1 or both of the jaws with a diverse etiopathogenesis.2

Here, we report a case of chronic inflammatory gingival enlargement. These enlargements are often associated with a long–standing bacterial plaque accumulation. Regular professional oral prophylaxis and good patient compliance are required in the management of such cases. In this case, patient compliance was lacking as evidenced by the history of incomplete orthodontic treatment and the failure to report for regular recall appointments. Also, the presence of the appliances may have further compromised the maintenance of adequate oral hygiene. This reflects the importance of patient education, motivation and compliance during and after dental treatment. Reinforcement of effective oral hygiene is essential, since patients have a tendency to revert to their original behavior. The patient must be placed into a maintenance schedule to preserve a healthy dentition.

Figure 5:

Histological section showing hyperplastic parakeratinized epithelium with fibro–collagenous connective tissue with chronic inflammatory cells (H&E 10X)

Consequently, it was noticed that once the appliances were removed and oral hygiene instructions were reinforced, the patient was able to maintain good oral hygiene. A study by Sallum et al showed significant impact of orthodontic appliance removal and professional prophylaxis on periodontal health.3

Figure 6:

Maxillary arch 12 months postoperative view after gingivectomy

The patient was recommended to undergo complete blood investigations to rule out underlying systemic disease and allergies. Some authors have reported a possible allergic reaction to orthodontic metal which may cause gingival enlargement. Allergic contact stomatitis by dental metals, particularly nickel, has shown to cause gingival hyperplasia. Özkaya et al reported 2 cases with nickel–induced oral mucosal hyperplasia.4 Although extremely rare, a hyperplastic form has also been reported in single cases from nickel in dental appliances5,6 and from gold and palladium in a dental clasp.7

Orthodontic treatment–induced gingival overgrowth shows a specific fibrous and thickened gingival appearance, different from fragile gingiva with marginal gingival redness, which is seen in allergic or inflammatory gingival lesions. Histologically, inflammatory gingival hyperplasia is mainly observed as an increase and thickening of mature collagen bundles in the connective tissue stroma. Microscopic appearance of fibroblasts in the connective tissue stroma and chronic inflammatory cell component is suggestive of non–specific gingival enlargement. Fibrous gingival enlargements associated with fixed orthodontic appliances seem to be transitory, and it is generally thought that enlargement resolves after orthodontic therapy.1 However, there are also studies reporting that this resolution is not complete.8,9

When chronic inflammatory gingival enlargements include a significant fibrotic component that does not resolve completely after initial periodontal therapy or does not meet the aesthetic and functional demands of the patient, surgical removal is the treatment of choice. The most widely employed surgical approaches for the treatment of gingival enlargements is gingivectomy or the flap technique.

Figure 7:

Mandibular arch 3 months postoperative view after gingivectomy

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This report helps to highlight the importance of patient motivation and patient compliance in treatment planning. Oral hygiene education supplemented with positive motivation should be started at the initial stages of the treatment strategy in order to obtain predictable outcomes. At each recall visit, the patient should be notified about their ongoing dental condition and the effects of risk factors like poor oral hygiene, smoking and deleterious habits on the existing oral state. Even though revolutionary advances have taken place in dental specialties, these 2 factors still play a critical role in the success of a therapeutic program. An effective communication is, thus, vital in motivating and educating patients about their dental problems. As a consequence, successful treatment outcome is believed to relate to 2 sides of the same coin, necessitating the combined efforts of both the patient and the clinician.

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  • Tanya Jadhav, MDS, is involved in Private practice at Pune, Maharashtra-India. K Mahalinga Bhat, MDS, is a professor at the Department of Periodontics, Manipal College of Dental Sciences. G Subraya Bhat, MDS, is the Head of Department at the Department of Periodontics, Manipal College of Dental Sciences. Jothi M Varghese, MDS, is an associate professor at the Department of Periodontics, Manipal College of Dental Sciences.

  • This study supports the NDHRA priority area, Clinical Dental Hygiene Care: Assess the use of evidence–based treatment recommendations in dental hygiene practice.

  • Copyright © 2013 The American Dental Hygienists’ Association


1Department of Periodontology and Oral Medicine, Institute of Dentistry, Zdrave Korde 4, 78000 Banja Luka, Bosnia and Herzegovina
2Department of Endodontics, Institute of Dentistry, Zdrave Korde 4, 78000 Banja Luka, Bosnia and Herzegovina
3Department of Periodontology and Oral Medicine, Medical Faculty University of Banja Luka, Bulevar Petra Bojovica 1, 78000 Banja Luka, Bosnia and Herzegovina

Copyright © 2015 Verica Pavlic et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Amlodipine is a third generation dihydropyridine calcium channel blocker that is frequently used in therapy of hypertension. Among many side effects, amlodipine has been found associated with gingival overgrowth (GO) which usually occurs within the first three months of starting therapy at a dose of 10 mg/day. However, there are very few reports on amlodipine-induced gingival overgrowth (AIGO) at a lower dose (5 mg/day) and only after short term administration. A 64-year-old male patient with hypertension, who received amlodipine (5 mg/day) for four years, sought medical attention at the Department of Periodontology and Oral Medicine, Institute of Dentistry, Banja Luka, Bosnia and Herzegovina. The patient complained of masticatory problems due to extensive maxillary GO along with pain, bleeding, and foul odor. The clinical and the histological evidences were consistent with AIGO. The first line treatment consisted of the amlodipine substitution (amlodipine was replaced with enalapril, 5 mg/day) and the scaling and root planning/SRP. At one-month follow-up, drug replacement and SRP resulted in some reduction of the inflammation and significant reduction of symptoms. Further, gingivectomy/gingivoplasty helped overcome the effect of these drugs. The possibility of AIGO should be considered for a lower dose, as well as a late presentation.

1. Introduction

Gingival overgrowth (enlargement, hyperplasia) is benign painless condition, characterized by massive enlargement of the interdental papillae, which can range from mild to extremely severe [1–3]. It may be accompanied by swelling of the gingival margin and partial cover of the occlusal surface of teeth, causing aesthetic limitations and functional difficulties in swallowing, speaking, and mastication [1, 2]. Gingival overgrowth (GO) is usually more conspicuous at labial/buccal surface of both upper and lower anterior teeth [4]. GO can be caused by various factors, such as inflammatory changes, mouth breathing, vitamin C deficiency, heredity, malignancies, hormonal alterations (seen in puberty and pregnancy), and the adverse effects associated with the systemic administration of certain drugs/drug-induced gingival overgrowth (DIGO). The prevalence of the DIGO is 3–20% compared to other gingival enlargements [4]. DIGO was firstly observed in patients who were taking phenytoin for epilepsy, with approximately 50% having GO [1–6]. Currently, more than 20 drugs, mainly among anticonvulsants (e.g., phenytoin), immunosuppressants (e.g., cyclosporine A), and various calcium channel blockers (e.g., nifedipine, verapamil, and diltiazem), are associated with gingival enlargements [3–7]. The pharmacologic effect of each of these drugs is different but all of them seem to act similarly on secondary target tissue, such as gingival tissue, resulting in similar clinical and histopathological findings. Among calcium channel blockers, the dihydropyridines (e.g., nifedipine, felodipine, amlodipine, nitrendipine, nicardipine, and manidipine) tend to be more commonly associated with gingival enlargement [7]. Amlodipine is a third generation dihydropyridine calcium channel blocker that is frequently used in therapy of hypertension and angina pectoris [1]. The prevalence of GO associated with amlodipine is reported to be 3.3%, which is significantly lower than that associated with nifedipine, ranging from 14 to 83% [8].

Since the exact pathogenesis of amlodipine-induced gingival hyperplasia (AIGO) is not well-understood, it has become a serious challenge for both the patients and dentists/periodontists to diagnose and manage the cases effectively. The first line management of AIGO is withdrawal or substitution of amlodipine with the patient’s physician consent [1–4]. Unfortunately, in most of the cases, withdrawal is not possible and drug substitution alone is not enough to overcome the AIGO effects. Usually GO are traps for debris and plaque, causing difficulties in maintenance of oral hygiene, further enhancing secondary inflammation and susceptibility of periodontal disease and caries [1–3]. Therefore, stringent maintenance of oral hygiene measures, ensuring that the accumulated plaque is removed from around the necks of the teeth and gums (professional tooth cleaning, scaling, and root planning/SRP), is, however, necessary [1–4, 9]. Situations when GO persists after careful consideration of the previously mentioned approaches and/or in which the chronic inflammatory gingival enlargement includes significant fibrotic components are treated with surgical removal of the excess tissue, either gingivectomy/gingivoplasty or flap surgery [9, 10].

To date reports related to AIGO are very rare. Majority of available literature are case studies/presentations which demonstrated that the AIGO occurs within 2-3 months of onset at a dose of 10 mg/day and rarely within first 6 months of onset at a lower dose of 5 mg/day [3]. The present case is interesting as AIGO occurred with a low dose of amlodipine (5 mg/day) and appeared on after several years of administration.

2. Case Report

A 64-year-old male patient with hypertension, who received amlodipine (Amlopin, Lek, Ljubljana, Slovenia) 5 mg/day, one dose orally for four years, sought medical attention at the Department of Periodontology and Oral Medicine, Institute of Dentistry, Banja Luka, Bosnia and Herzegovina, with the chief complaint of the swollen gums. Until 3 months back, patient firstly noted bead like nodular growth over the upper arch gums which progressively enlarged causing masticatory problems due to extensive gingival overgrowth along with pain, bleeding, and foul odor. The medical history of the patient revealed that the patient was hypertensive and that he was under amlodipine for a period of 4 years. The physical examination revealed noncyanosed moderately built and nourished man with no signs of anaemia. His vital signs were within the normal range. An intraoral examination revealed generalized diffused GO in the maxilla. The enlarged gingiva was firm, pink, and resilient with tendency to bleed (Figure 1). Poor oral hygiene status of patient was assessed by the presence of local irritating factors which surrounded the teeth. Due to the outward (rather than vertical) enlargement of gingiva, the deep periodontal pockets were not detected. Orthopantomogram revealed generalized moderate horizontal bone loss. Based on drug history and clinical examination of the patient, provisional diagnosis of combined GO (amlodipine-induced GO complicated by inflammatory effects) was made. After this, incisional gingival biopsy was done. Histopathological report revealed the increase in the gingival connective tissue volume (a mixture of dense and loose fibrous components) with the chronic inflammatory cell infiltrate and acanthosis of overlying epithelium. According to medical history, clinical examination, and investigations, final diagnosis of AIGO was made. Firstly, a patient’s physician was consulted in order to substitute amlodipine, whom replaced amlodipine with angiotensin-converting-enzyme (ACE) inhibitor enalapril (Enap, Krka, Novo Mesto, Slovenia) 5 mg/day, one dose orally. Along with drug substitution, complete SRP was performed for supragingival and subgingival calculus removal. At subsequent follow-up after one month, first line therapy resulted in some reduction of the inflammatory component, reduction of the size of the GO, and significant reduction of symptoms (Figure 2). Later, remaining aesthetic and functional limitations were overcome by the surgical reduction of the enlarged tissue (gingivectomy and gingivoplasty).

Figure 1: Clinical presentation of generalized diffused gingival overgrowth of upper arch (at patient’s first visit).

Figure 2: Gingival overgrowth one month after therapy (visible regression after amlodipine substitution and SRP).

3. Discussion

AIGO has a multifactorial nature and its appearance and severity are strongly influenced by dosage, duration, and blood level of amlodipine, as well as sex, genetic predisposition (fibroblasts with an abnormal susceptibility to the drug and/or the functional fibroblast heterogeneity), oral hygiene status/preexisting gingival inflammation, and activation of growth factors [3, 4, 9]. The underlying mechanism behind AIGO is still not completely understood [3, 4]. It is basically described as multifactorial model, involving noninflammatory and inflammatory mechanisms [3, 4]. The proposed noninflammatory mechanisms include defective collagenase activity due to decreased levels of matrix metalloproteinases-1 and -3 secretions and uptake of folic acid, blockage of aldosterone synthesis in zona glomerulosa of the adrenal cortex, and upregulation of keratinocyte growth factor [1]. However, majority of the available literature suggested that the gingival inflammation is essential for the interaction between drugs and fibroblasts [11]. An inflammation may develop as a result of direct toxic effects of concentrated drug in crevicular gingival fluid, since the crevicular fluid concentrations of the drugs were found to be up to 292 times of those found in plasma [9]. This inflammation could lead to the upregulation of several cytokine factors such as fibroblast growth factor-2 (FGF-2), transforming growth factor-β1 (TGF-β1), interleukin-6 and interleukin-1β (IL-6, IL-1β), and platelet derived growth factor-β (PDGF-β) predisposing the tissue to a localized toxic effect and the development of fibrotic gingival hyperplasia [5]. Released proinflammatory cytokines are also involved in the mast cells migration, influencing fibroblast proliferation, extracellular matrix synthesis, and degradation. Further, amlodipine may stimulate the production of IL-2 by T-cells causing fibrosis [9]. The strong relation between the inflammation and AIGO is demonstrated with the fact that AIGO can be successfully controlled even under the continuous amlodipine administration by meticulous professional and individual oral hygiene [8–10]. Also, the fact that DIGO, in general, does not affect edentulous areas further supported the statement that the presence of GO is most probably related to inflammatory factors from dentition, such as dental plaque [8]. However, the evidence based clinical trials regarding the correlation between periodontal inflammation and AIGO are lacking.

Clinical manifestation of GO commonly appears within 2-3 months after initiation of treatment with the amlodipine, usually at a dose of 10 mg/day. There are very few reports on AIGO at a lower dose (5 mg/day) and only after short term administration. However, according to some authors, amlodipine dose of 5 mg/day cannot induce gingival hyperplasia even if taken more than 6 months [12]. In the present case, GO occurred with a low dose of amlodipine (5 mg/day) and appeared after several years of administration. It is still unknown why AIGO in this case exacerbates after 4 years of continuous use. Apart from previously mentioned well-known possible risk factors, our patient did not have a habit of regular/daily tooth brushing. Further, possible explanation is the fact that our patient was a man, and AIGO occurs three times more often in men than in women [13]. Another potential explanation could be a patient’s sensitivity to a specific drug’s metabolic pathway [13] or patient’s sensitivity to a specific amlodipine concentration in the crevicular gingival fluid [7].

Medical doctors and dentists/periodontists should be aware of the use of medications with the potential to cause/contribute to the development of the GO, to prevent, diagnose, and successfully manage unwanted side effects of drugs by cooperative teamwork. Since it is expected that number of these drugs is likely to increase in the years to come, the thorough understanding and clear establishment of the DIGO molecular pathogenesis and novel preventive and treatment modalities are however necessary.

4. Conclusion

The gingival overgrowth could occur with amlodipine even at a small dose (5 mg/day) and after a long term application. Medical doctors and dental clinicians/periodontists need to be aware of the etiologic medications, such as amlodipine, that can induce GO in order to identify changes in the oral cavity in such patients and to prevent, diagnose, and successfully manage its unwanted side effects. The cooperative teamwork between the patient, his physician, and the periodontist is however necessary in order to obtain the best AIGO treatment outcome.

Conflict of Interests

The authors declare that there is no conflict of interests regarding the publication of this paper.


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