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Gingival
enlargement is a common manifestation of gingival and periodontal disease
having a multifactorial etiology. Anticonvulsants, immunosuppressants and
calcium channel blockers have been associated with gingival enlargement in
susceptible patients. Amlodipine is a new generation calcium channel blocker
used to manage hypertension and angina. Reports of amlodipine associated
gingival enlargement are uncommon.
The
current case reports gingival enlargement in a 45 years old female, associated
with the use of a small dosage (5 mg) of Amlodipine for hypertension. The
treatment protocol included non-surgical periodontal therapy, drug
substitution, surgical excision of minor fibrotic enlargement as well as extraction
and rehabilitation of the offending teeth to improve esthetics and function
resulting in an excellent clinical outcome.
Keywords: Amlodipine, Gingival enlargement,
Amlodipine-induced gingival overgrowth, Gingival inflammation
INTRODUCTION
Drug-induced
gingival enlargement could be an unwanted side-effect of certain group of drugs
given for non-dental conditions. Currently, more than 20 prescription
medications are associated with gingival enlargement [2]. Drugs associated with
gingival overgrowth are broadly categorized into three major groups according
to their therapeutic actions, namely, anticonvulsants, immunosuppressants and
calcium channel blockers [3,4]. Patients medicated with these drugs may be
implicated in this unwanted side effect, which may interfere with esthetics,
mastication or speech as well as decrease access for oral hygiene resulting in
an increased susceptibility to oral infection, caries and periodontal disease.
Amlodipine
is a newer dihydropyridine calcium channel blocker that used in the management
of both hypertension and angina. Ellis et al. [5] first reported gingival
sequestration of amlodipine and amlodipine-induced gingival overgrowth. Since
then, very few isolated cases of AIGO have appeared in the dental literature,
although there are numerous reports of nifedipine (another member of calcium
channel blocker-induced gingival overgrowth till date). There is less data on
reports of overgrowth with amlodipine at a dose of 5 mg, even after taking it
for more than 6 months.
But, in the
present case, the gingival overgrowth occurred at a dose of 5 mg within 6
months of use. AIGO was treated in the following phases: (1) thorough Phase-1
therapy, (2) substitution of the drug, (3) surgical excision of the residual
gingival overgrowth and (4) Restoration and replacement of teeth.
CASE REPORT
A 45 year
old female patient from a poor socio-economic background, reported to Dr.
Rishi’s Dental Clinic, Navi Mumbai with a chief complaint of swollen and
bleeding gums for 6-8 months along with bad breath. Patient was not aware of
such a type of gum growth previously until she saw diffused, nodular bright-red
gum growth in the lower front region and upper and lower right side of the
jaws. Her past medical history revealed that she was hypertensive since the
Her personal history revealed
that she used to brush her teeth once daily with brush and paste, but she
avoided brushing the teeth which had enlarged gums, as they bled on brushing.
Her general physical examination revealed a moderate built with vital signs
within the normal range.
Intraoral examination revealed
enlarged marginal and interdental gingiva starting from maxillary right canine
(13) up to 2nd molar (17) and from mandibular left lateral incisor
(32) up to right 2nd molar (47) (Figure
1).
The enlarged gingiva was nodular
in certain areas with bright red color. The contour was rolled-out with soft
and edematous consistency. There were visible bands of supra and sub-gingival
calculus. Pus exudation presented with mandibular right 2nd premolar
(45). Spacing was present between lower incisors along with labial version (Figure 2).
Patient was
subjected to complete hemogram and all the parameters were found to be within
normal range. Radiographic evaluation of the affected sites revealed extensive
bone loss with mandibular left (31) and right central incisor (41) along with
pathologic migration. The mandibular lateral incisors (32,42) had greater than
50% alveolar bone support remaining. Her
treatment started with non-surgical approach. Scaling and root planing were
performed in 2-3 sessions along with 5% Povidone-iodine irrigation for
periodontal pockets (Figure 3).
Simultaneously,
the patient's physician was consulted regarding drug substitution or withdrawal
of the drug. The physician changed the drug from the previous combination of
Telmisartan 40 mg + Amlodipine 5 mg to plain Telmisartan 40 mg, eliminating
Amlodipine. The patient was prescribed Folic acid supplements, once daily for
15 days. Patient was instructed to maintain good oral hygiene with the use of
chlorhexidine oral rinses. A dramatic response was noticed after four weeks of
drug substitution and maintenance of regular oral hygiene. There was regression
in the size of gingival enlargement with minimal fibrotic component left (Figure 4).
After about 2
weeks of healing, the lateral incisors and canines were prepared to receive
fixed partial denture prosthesis, replacing the extracted teeth as well as
restoring function and esthetics (Figure
6).
The patient has
been kept on a recall every 6 months.
DISCUSSION
Medication
associated gingival enlargement has been known for a long time. The widespread
use of calcium channel blockers began in 1980. The prevalence of Amlodipine
associated gingival enlargement has been reported to be 3.3%, which is
significantly lower as compared to Nifedipine [6]. Nifedipine is a second
generation dihydropyridine whereas amlodipine is a third generation
dihydropyridine. Amlodipine has a pharmacological action comparable to nifedipine,
but it is preferred over nifedipine due to its higher bio-availability, slow
hepatic degradation, near complete absorption and slow elimination making its
duration of action longer, thus it needs to be administered once daily,
improving patient compliance with minimal side effects as compared to
Nifedipine [6-8].
Although the
exact role of dental plaque in the pathogenesis of drug associated gingival
enlargement is unclear, there is evidence that elimination of local factors and
maintenance of good oral hygiene, decreases the severity of gingival
enlargement and improves gingival health. In the present case, there were
abundant deposits of calculus and plaque retentive factors, at the sites with
gingival enlargement. Scaling and root planing removed the local factors along
with substitution of Amlodipine by the Physician was done.
Various possible
mechanisms have been proposed to explain drug associated gingival enlargement
in the past. CCBs affect calcium metabolism by reducing the Ca2+ cell
influx, leading to a reduction in the uptake of folic acid, thus limiting the
production of active collagenase [9]. As a result of the reduction in collagen
degradation, increased collagen accumulation occurs.
Proinflammatory cytokines, such as
interleukin-1b and interleukin-6 seem to have a synergistic effect in the
enhancement of collagen synthesis by human gingival fibroblasts [10].
Interleukin-6 has been shown to target connective tissue cells, such as fibroblasts,
both by enhancing their proliferation and by increasing collagen production and
glycosaminoglycan synthesis [11]. This mechanism explains the role of the
bacterial biofilm in inducing gingival inflammation, production of cytokines
and gingival enlargement.
In the present case, immediately after drug substitution, folic acid
supplements were prescribed to the patient to replenish the folic acid
depletion.
The treatment
options for drug-induced gingival enlargement should be based on the medication
being used and the clinical presentation of the individual case. The presence
of local factors adds to the inflammatory component of the drug induced
gingival enlargement. Timely removal of local factors by non-surgical
periodontal therapy partially resolves the gingival enlargement. The need for,
and timing of, any surgical intervention must be carefully assessed. Surgery is
normally performed for cosmetic/aesthetic needs, most commonly being external
bevel gingivectomy. In the present case, the persistent fibrotic enlargement
was excised by electrocautery as it was minor and nodular in nature.
Prosthetic
rehabilitation was carried out to replace the extracted mandibular central
incisors, obtaining support from and using the adjacent incisors and canines as
abutments. The prosthesis completely changed the smile as well as entailed
immense confidence into the patient.
In this case,
drug substitution had an additional advantage for the patient. Amlodipine
frequently resulted in pedal as well as facial edema. This side effect of
Amlodipine was also resolved post drug substitution. The post-treatment results
were found to be extremely satisfactory, esthetically as well as functionally.
The patient was also extremely delighted with the results and has been
maintaining her oral hygiene satisfactorily.
CONCLUSION
In this case, a
combination of drug substitution and periodontal therapy, resolved the gingival
overgrowth.
1. Bhatia V, Mittal A, Parida AK,
Talwar R, Kaul U (2007) Amlodipine induced gingival hyperplasia: A rare entity.
Int J Cardiol 122: 23-24.
2. Rees TD, Levine RA (1995) Systemic
drugs as a risk factor periodontal disease initiation and progression.
Compendium of Continuing Education in Dentistry, pp: 20-42.
3. (2004) Drug associated gingival
enlargement. J Periodontol, pp: 1424-1431.
4. Garzino-Demo P, Carbone M,
Carrozzo M, Broccoletti R, Gandolfo S (1998) An increase in gingival volume
induced by drugs (phenytoin, cyclosporine and calcium antagonists). A review of
the literature. Minerva Stomatologica, pp: 387-398.
5. Ellis JS, Seymour RA, Steele JG, Robertson
P, Butler TJ, et al. (1999) Prevalence of gingival overgrowth induced by
calcium channel blockers: A community-based study. J Periodontol, pp: 63-67.
6. Jorgensen MG (1997) Prevalence of
amlodipine-related gingival hyperplasia. J Periodontol, pp: 676-678.
7. Triveni MG, Rudrakshi C, Mehta DS
(2009) Amlodipine-induced gingival overgrowth. J Indian Soc Periodontol, pp:
160-163.
8. Seymour RA, Ellis JS, Thomason JM,
Monkman S, Idle JR (1994) Amlodipine-induced gingival overgrowth. J Clin
Periodontol 21: 281-283.
9. Barclay S, Thomason JM, Idle JR,
Seymour RA (1992) The incidence and severity of nifedipine-induced gingival
overgrowth. J Clin Periodontol 19: 311-314.
10. Johnson RB, Zebrowski EJ, Dai X
(2000) Synergistic enhancement of collagenous protein synthesis by human
gingival fibroblasts exposed to nifedipine and interleukin-1-beta in vitro. J Oral Pathol Med 29: 8-12.
11.
Duncan
MR, Berman B (1991) Stimulation of collagen and glycosaminoglycan production in
cultured human adult dermal fibroblasts by recombinant human interleukin-6. J
Invest Dermatol 97: 686-689.
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