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CASE REPORT

Amlodipine-Induced Gingival Overgrowth in a Patient With UncontrolledType 2 Diabetes Mellitus With Hypercholesterolemia: A Case Report

K. Smitha*

Introduction: Gingival overgrowth, with its potential cosmetic implications and for providing new niches for the growthof microorganisms, is a serious concern for both patients and clinicians. Amlodipine is a comparatively new calcium channel

blocker and is being used with increasing frequency in the management of hypertension and angina. Although amlodipine is

considered a safe drug, it may induce gingival overgrowth in some individuals.

Case Presentation: A rare case of amlodipine-induced gingival overgrowth in a 60-year-old Indian woman who wason amlodipine for 3 years and subsequent periodontal management of the overgrowth is reported here. The patient did not

have any gingival overgrowth for 2 years despite the fact that she was taking amlodipine, but she developed the gingival over-

growth 9 months before her initial visit, coincident with uncontrolled diabetes mellitus and use of a cholesterol-lowering drug.Shewas treated with drug substitutionfor thesystemic conditionand surgical treatment forthe overgrowth. She wasfollowed

up for 1 year, regularly.

Conclusion: We speculate that overgrowth could have been triggered by uncontrolled type 2 diabetes mellitus and byaltered pharmacokinetics of amlodipine resulting from the drug interaction of amlodipine with a cholesterol-lowering drug.

Clin Adv Periodontics 2012;2:115-122.

Key Words: Amlodipine, adverse effects; calcium channel blockers; diabetes mellitus, type 2; gingival overgrowth;

periodontal pocket; risk factors.

Background

Gingival overgrowth (GO) has been associated with multi-ple factors, including inflammation, adverse drug reaction,neoplastic conditions, and systemic disorders. An increasingnumber of medications are associated with gingival enlarge-ment. Currently, >20 prescription medications are associ-ated with GO.1 Drugs associated with GO can be broadly

divided into three categories: 1) anticonvulsants; 2) calcium

channel blockers; and 3) immune suppressants.Calcium channel blockers (dihydropyridine, phenylal-kylamine, and benzothiazine derivatives) are used widelyin the management of hypertension and in the prophylaxisof angina. Many of these drugs have been implicated incausing GO. In a study by Ellis et al.2 in 1999 on 911 pa-tients on calcium channel blockers, a prevalence of GO of6% for nifedipine (NIF), 1.7% for amlodipine, and 2.2%for diltiazem was reported.

Amlodipine, an agent of dihydropyridine, a third-gen-eration calcium channel blocker that is used for treatment ofhypertension and angina, was first reported by Ellis et al.3 as

* Department of Periodontics, Bangalore Institute of Dental Sciences,

Karnataka, India.

Submitted March 16, 2011; accepted for publication July 6, 2011

doi: 10.1902/cap.2012.110026

Clinical Advances in Periodontics, Vol. 2, No. 2, May 2012 115

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causing GO as an adverse effect. Amlodipine is shown tohave longer action and weaker adverse effects comparedto first-generation blockers, such as NIF.2,3

The pathogenesis of GO is uncertain, and several factorsmay influence therelationshipbetweendrugs andgingivaltis-sues as discussed by Seymour et al.4 These factors include: 1)age; 2) genetic predisposition; 3) pharmacokinetic variables;4) alteration in gingival connective tissue homeostasis; 5) his-

topathology; 6) ultra-structural factors; 7) inflammatorychanges; and 8) drug action on growth factors. The combina-tion of periodontitis and GO presents a complicated condi-tion. GO creates an environment conducive to easy plaqueaccumulation, which affects conventional periodontal ther-apy, so that treatment may require resective techniques.

Diabetes mellitus (DM) is a well-established risk factorfor periodontal disease and tissue destruction. It is reportedthat patients with type 2 DM were 2.8 to 4.2 times morelikely to have progressive periodontal disease comparedto individuals without DM.5 A previous report6 on fourcases demonstrated erythematous gingival enlargementassociated with hyperglycemic levels in patients with nohistory of taking the common drugs associated with GO.However, it remains unknown whether uncontrolled hyper-glycemic levels and their effectson gingival tissuewould playa synergistic role on drug-influenced gingival enlargement. Acase report7 documented a conservative clinical approach tothe management of felodipine-influenced gingival enlarge-ment and reported clinical and histologic aspects of a caseof felodipine-influenced GO in a patient with undiagnosedtype 2 DM.

A cross-sectional study8 showed that NIF intake may in-crease the risk of periodontal destruction in patients withtype 2 DM. These data imply that there might be a possible

synergistic effect of NIF intake on periodontal pathogene-sis in patients with DM. NIF and DM can induce hyper-responsive monotype/macrophage phenotype and therebyincrease the production of chemokines and proinflamma-tory cytokines.9,10

It is well recognized that calcium channel blockers, whichare strong inhibitors of cytochrome P450 3A4, coadminis-tered with statins that aremetabolized by the same isoenzymebefore biliary and renal excretion may lead to reduced clear-ance of both the drugs, with an increase in adverse effects.11

Indeed, in patients treated with verapamil and simvastatin,the serum levels of both drugs were increased,12 but as yetthere is little evidence for this with dihydropyridine calcium

antagonists. Nevertheless, when statins and calcium channelblockers are coprescribed, especially at high doses, there maypossibly be an increase in adverse effects, such as GO. How-ever, the exact mechanism remains an enigma. This case re-port presents the management of a case of a combination ofdrug-influenced gingival enlargement and uncontrolled DMwith hypercholesterolemia.

Clinical PresentationIn September 2007, a 60-year-old Indian woman who com-plained of swollen gums for the past 9 months was referredto the Department of Periodontics, Bangalore Institute of

Dental Sciences, affiliated with Rajiv Gandhi Universityof Health Sciences, Bangalore, India. She felt very uncom-fortable because the swelling interfered while chewing,was unsightly, and caused gingival bleeding while brushing

her teeth. She had hypertension for 3 years and was pre-scribed 10 mg amlodipine, daily. Table 1 shows her medi-cation history. She also had type 2 DM for 5 years, for whichshe was prescribed the combination of 500 mg metforminand 80 mg gliclazide. Medicalreports showed thather met-abolic status was not under control for >1 year (Table 2).She had hypercholesterolemia and had been taking statinsx

for 1 year. Dental history revealed that she had undergonescaling 6 months before her initial visit to this departmentfor the same complaint of swollen and bleeding gums. Al-though bleeding was reduced after scaling, gingival enlarge-ment remained. Generally, she looked well, was alert, andhad centralobesity. Periodontalparametersare shown in Ta-

bles 3 and 4. Intraorally, there was GO on the labial and lin-gual/palatal surface of the maxillary and mandibular teeth,which was more pronounced in the anterior region than theposterior region. The interdental papillae were enlarged,fibrous, and lobulated in appearance mainly around themandibular anterior teeth (Fig. 1). Gingival enlargementwas graded at six points around each tooth according tothe gingival overgrowth index (GOI) originally describedby Angelopoulous and Goaz13 and later modified by Millerand Damm,14 and the highest score of the three points oneach surface was recorded as the grade for that surface ofthe tooth. Her oral hygiene showed the presence of someamount of plaque and calculus, and plaque was abundant

around anterior teeth. Bleeding on probing (BOP) was de-tected on all affected areas. Range of probing depth (PD)of gingival sulcus was recorded from 3 to 8 mm. Grade 1tooth mobility was noticed in teeth #2, 23, 24, 25, and26.The examination of occlusion exhibited labioversionand diastema of anterior teeth. Panoramic radiographexamination revealed a generalized moderate horizon-tal bone loss (Fig. 2).

TABLE 1 Medication History

Medication Administered Period of Administration

10 mg amlodipine May 2004 to September 2007

80 mg gliclazide plus

500 mg metformin

Since 2002

25 mg atenolol Since September 2007

10 mg simvastatin Since October 2006

0.3 mg voglibose Since September 2007

Amlogard, Pfizer, Mumbai, India. Diabend-M, Bal Pharma, Bangalore, India.x Zocor, Merck, Mumbai, India.

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Case ManagementBefore local management, the patient was referred to a phy-sician who thoroughly assessed her, substituted atenololk foramlodipine, prescribed voglibose{ (0.3 mg) along with met-formin and gliclazide,# and also advised diet control andphysical exercise. The treatment plan was explained, and in-formed written consent was obtained from the patient forthe treatment, as well as for reporting of the case. She under-went thorough scaling. She was prescribed chlorhexidinemouthwash and was given oral hygiene instructions. She re-ported after 1 month, requesting correction of the unsightlygingival enlargement.

Under local anesthesia, the enlargement was resected seg-ment-wise by a modified flap surgical procedure. The tissue

that was resected was sent for histpathologic examination.The routine hematoxylin and eosinstained sections re-vealed hyperplastic parakeratinized stratified squamousepithelium overlying the connective tissue. The underlyingconnective tissue was dense with numerous collagen bun-dles arranged in haphazard manner interspersed withfibroblasts. The inflammatory component was observedmore toward the epithelium, with lymphocytes being thepredominant cells (Fig. 3). The case was diagnosed as am-lodipine-induced gingival enlargement based on clinicaland histopathologic features.

Clinical OutcomesThere were no postoperative complications, and the healingwas uneventful (Fig. 4). The patient was followed up regu-larly for 1 year. A marginal inflammatory recurrence, how-ever, was noticed that could easily be managed by routinetherapeutic procedures. Clinical parameters 1 year post-sur-gery are shown in Tables 3 and 4.

DiscussionGO, with its potential cosmetic implications and for pro-vidingnew niches forthe growthof microorganisms, is a se-rious concern for both patients and clinicians. Clinical

manifestation of gingival enlargement frequently appearswithin 1 to 3 months after initiation of treatment with

the associated medication.15

In the present case,although the patient wastaking 10 mgamlodipine for 3 years, GO was noted only 9 months beforeher initial visit. Coincident with this, her medical history re-vealed uncontrolled DM forthepastyear. A previous report6

has shown cases of gingival enlargement in patients withDM. It remains unknown whether hyperglycemic statusand its effects on gingival tissue would have played a syner-gistic role on drug-influenced gingival enlargement in thiscase.

Furthermore, the patient was taking statins for the pastyear, which was coprescribed with amlodipine. This couldhave aggravated the adverse effects, resulting in clinicallyevident GO.

In this case, GO was more pronounced in the anteriorregion and was less severe around the posterior teeth. Thiscould be attributable to accumulationof more plaquein theanterior region especially around mandibular anteriors,due to the wasting disease noted in these teeth leading toless effective plaque removal. Gingival inflammation and

TABLE 2 Metabolic Status

Time (date of investigation)

FBS

(mg/dL)

PPBS

(mg/dL)

Total Cholesterol

(mg/dL)

HDL

(mg/dL)

LDL

(mg/dL)

Triglycerides

(mg/dL)

VLDL

(mg/dL)

Reference value 70 to 110 110 to 140

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presence of dental plaque have been reported as significantrisk factors for development of GO.16

Calcium antagonists are almost exclusively prescribedin older patients, and these patients might have preexistingperiodontitis. The combination of periodontitis and GOpresents a complicated condition. The present case hadperiodontal pockets with the PD ranging from 3 to 8 mm.These deeper pockets serve as an ecological niches for peri-odonto-pathogenic bacteria leading to an increased bacte-rial load and concomitantly to an increased inflammationand may exacerbate the drug induced gingival enlarge-ment.17,18 Morisaki et al.19 observed that germ-free rats in-fected with a strain of Streptococcus mutans had greater

NIF-influenced gingival enlargement than germ-free con-trols. In contrast, different reports have suggested that druginduced GO may aggravate inflammatory periodontal dis-ease with conflicting results. Recently, an epidemiologicstudy found greater periodontal attachment loss/bone lossin patients using NIF.8 A cross sectional study involving4,290 individuals investigated the association between theintake of calcium antagonists and periodontitis, and con-cluded that calcium antagonists leads to gingival enlarge-ment without aggravation of periodontitis.20 A consensusreport of the editors of the American Journal of Cardiologyand Journal of Periodontology21 stated that there are no

specific reports of the effect of calcium channel blockerson the severity of periodontitis.

The most effective treatment of drug-related gingivalenlargement is withdrawal or substitution of medica-tion. When this treatment approach is taken as sug-gested by another case report,22 it may take from 1 to8 weeks for resolution of gingival lesions. Unfortu-nately, notall patients respond to this mode of treatmentespecially those with long standing gingival lesions.23

Surgical reduction of the overgrowntissues is frequentlynecessary to accomplish an esthetic and functional out-come. In the present case report, the antihypertensivedrug was changed to atenolol by the physician. The pa-

tient was conscious of the unesthetic GO and she hadmoderate chronic periodontitis. Hence, surgical reduc-tion of the enlargement was done after 1 month ofnon-surgical treatment. The case was followed for 1year. Although, studies5-8,10 have shown the potentialaf-fect of uncontrolled type 2 DM on gingival tissues, it re-mains speculative whether the pathologic process causedby uncontrolled DM and use of cholesterol-lowering drugsmay have contributed to the onset, severity, and clinicaloutcomes of this case. Further controlled investigationsshould be carried out to unravel this possible complexinteraction. n

TABLE 4 Periodontal Parameters

Tooth #

Parameter 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16

Maxillary (labial)

BL PD (mm) 4,5,6 7,5,8 8,6,6 3,5,5 6,4,6 5,3,6 6,4,6 6,3,5 5,3,5 5,3,4 5,6,7 6,5,6 6,5,6 6,5,7 7,5,6 7,4,5

BL GOI 1 1 1 0 1 1 1 1 1 1 1 1 1 1 1 1

NS PD (mm) 4,5,5 6,5,6 6,6,6 3,4,5 6,3,5 4,2,5 5,4,6 5,2,5 5,2,5 5,3,4 5,5,6 5,5,6 5,4,5 6,4,6 6,4,5 5,4,5

NS GOI 0 0 0 0 1 1 1 1 1 1 1 0 0 0 0 0

PS PD (mm) 3,3,3 5,3,5 4,3,3 2,2,3 4,2,3 3,2,3 2,1,2 2,1,2 2,1,2 3,2,2 3,3,3 3,3,4 4,3,4 4,4,5 5,3,5 4,3,3

PS GOI 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

Maxillary (palatal)

BL PD (mm) 5,5,7 7,6,5 6,5,5 5,4,5 4,4,5 5,5,6 6,6,6 6,4,6 6,5,6 5,4,6 5,4,6 6,5,5 6,6,6 6,5,6 7,6,5 7,5,5

BL GOI 1 1 1 0 0 1 1 1 1 1 1 0 0 0 1 0

NS PD (mm) 5,5,6 6,6,5 5,5,5 4,4,4 4,3,5 5,5,5 5,5,5 5,4,5 5,4,5 5,4,5 4,4,5 5,5,5 5,5,5 5,5,5 6,5,5 5,4,4

NS GOI 1 1 1 0 0 1 1 1 1 1 1 0 0 0 0 0

PS PD (mm) 3,3,3 3,3,4 3,3,3 3,2,3 3,2,3 3,3,3 2,2,2 2,1,2 2,1,1 2,2,2 2,2,3 3,3,3 3,3,3 3,3,3 4,3,3 3,3,3

PS GOI 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

BL baseline; NS 1 month after non-surgical treatment; PS 1 year after surgery; X extracted tooth.

PDs are shown for the mesio, mid, and buccal aspects of each tooth.

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Tooth #

Parameter 32 31 30 29 28 27 26 25 24 23 22 21 20 19 18 17

Mandibular (labial)

BL PD (mm) 5,5,7 6,5,6 6,5,6 X 5,4,5 5,5,5 6,5,6 6,5,6 5,5,4 5,5,5 7,6,7 6,5,6 6,5,6 5,5,6 8,6,7 7,6,4

BL GOI 0 1 1 X 1 2 2 2 2 2 2 1 1 1 0 1

NS PD (mm) 4,4,5 5,3,5 5,5,5 X 4,4,4 4,4,4 5,5,5 5,5,5 5,4,4 4,4,4 5,4,6 5,5,5 6,5,5 5,5,5 6,4,5 6,5,3

NS GO 0 0 0 X 0 2 2 1 1 1 2 1 0 0 0 0

PS PD (mm) 3,3,3 3,2,3 3,3,3 X 3,2,3 2,2,2 2,1,2 2,1,2 3,2,2 3,2,3 3,2,3 2,1,2 2,1,2 2,2,2 5,3,4 4,3,3

PS GOI 0 0 0 X 0 0 0 0 0 0 0 0 0 0 0 0

Mandibular (lingual)

BL PD (mm) 5,5,6 6,6,5 5,5,5 X 4,4,4 5,5,5 6,6,6 6,5,6 6,5,5 5,5,5 6,6,6 6,5,5 5,5,5 5,5,6 6,5,5 7,5,4

BL GOI 0 1 0 X 1 1 1 1 1 1 1 1 1 1 0 0

NS PD (mm) 4,4,5 5,5,5 5,4,4 X 4,3,3 4,3,4 4,4,5 5,4,5 4,4,4 5,4,4 5,5,4 5,3,4 5,4,5 5,4,5 6,4,5 6,3,3

NS GOI 0 0 0 X 1 1 1 1 1 1 1 1 0 0 0 0

PS PD (mm) 3,3,3 3,4,4 4,3,3 X 3,2,3 3,3,3 3,3,2 2,2,2 2,1,2 3,2,3 3,2,2 3,2,3 3,3,3 3,2,3 3,2,3 3,2,3

PS GOI 0 0 0 X 0 0 0 0 0 0 0 0 0 0 0 0

BL baseline; NS 1 month after non-surgical treatment; PS 1 year after surgery; X extracted tooth.

PDs are shown for the mesio, mid, and buccal aspects of each tooth.

TABLE 4 (Continued) Periodontal Parameters

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FIGURE 1 Photograph at baseline visit showing GO.

FIGURE 2 Panoramic radiograph at baseline visit demonstrating gener-alized moderate periodontal involvement.

FIGURE 3 Histopathology of anterior maxillary gingival tissue. 3a he-matoxylin and eosin; 4. 3b hematoxylin and eosin; 10.

FIGURE 4 Postoperative photograph, 1 year post-surgical treatment anddrug replacement.

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Summary

Why is this case report new

information?

Clinical manifestation of this case appeared to be triggered by:j poorly controlled metabolic statusj interaction of drugs leading to increased adverse effects

What are the keys to successful

management of this case?

j consultation with a physicianj

alteration of the drugj control of the metabolic statusj surgical treatment

What are the primary limitations to

success in this case?

j patient compliancej lack of controlled investigation to unravel the complex interactionj interaction is speculative

AcknowledgmentThe author reports no conflicts of interest related to thiscase report.

CORRESPONDENCE:

Dr. K. Smitha, Department of Periodontics, Government Dental Col-lege and Research Institute, Bangalore 560002, Karnataka, India. E-mail:periosmitha@gmail.com.

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Smitha Clinical Advances in Periodontics, Vol. 2, No. 2, May 2012 121

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