|Year : 2014 | Volume
| Issue : 2 | Page : 226-228
Incidence of amlodipine-induced gingival overgrowth in the rural population of Loni
Avneesh Tejnani1, Ameet Mani2, Neha Kaur Sodhi3, Alok Mehta4, Sonal Gourkhede5, Vinayak Thorat6, Pramod Marawar2
1 GSBS Medical Trust, Loni, Maharashtra, India
2 Department of Periodontology, Rural Dental College, Loni, India
3 Private Practitioner, Loni, Maharashtra, India
4 Hiranandani Hospital, Thane, Maharashtra, India
5 Late Shri Yashwantrao Chavan Memorial Medical and Rural Development Foundation's Dental College, Maharashtra, India
6 BVP Dental College, Navi Mumbai, Maharashtra, India
|Date of Submission||19-Dec-2012|
|Date of Acceptance||17-Oct-2013|
|Date of Web Publication||23-Apr-2014|
Gods Gift, 103, Prof. Almeida Park, TPS IV, 9th Road, Bandra (W), Mumbai - 400 050, Maharashtra
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Aims: Since the incidence of gingival overgrowth induced by amlodipine remains poorly defined, this study was carried out with an aim to determine the incidence. Materials and Methods: Dental patients who received amlodipine (N = 115), for more than 3 months were studied to determine the drug-induced gingival overgrowth. Clinical diagnosis of drug-induced overgrowth was verified by disappearance or decreased severity of gingival overgrowth after withdrawal of the causative drug. Results: The prevalence rate of amlodipine-induced gingival hyperplasia among experimental patients was 3.4%, while it was not observed among the control subjects. Oral examination revealed gingival overgrowth as a lobular or nodular enlargement on interdental papilla located in the anterior interproximal regions. Conclusions: In this study, there was a significant relationship between gingival inflammation resulting from dental plaque and drug dosage, and hyperplasia.
Keywords: Gingival hyperplasia, gingival overgrowth induced by amlodipine, hyperplasia
|How to cite this article:|
Tejnani A, Mani A, Sodhi NK, Mehta A, Gourkhede S, Thorat V, Marawar P. Incidence of amlodipine-induced gingival overgrowth in the rural population of Loni. J Indian Soc Periodontol 2014;18:226-8
|How to cite this URL:|
Tejnani A, Mani A, Sodhi NK, Mehta A, Gourkhede S, Thorat V, Marawar P. Incidence of amlodipine-induced gingival overgrowth in the rural population of Loni. J Indian Soc Periodontol [serial online] 2014 [cited 2021 Jul 28];18:226-8. Available from: https://www.jisponline.com/text.asp?2014/18/2/226/131332
| Introduction|| |
Calcium channel blockers are used widely in the management of hypertension and in the prophylaxis of angina. Drug-induced gingival enlargement is a well-documented unwanted side effect reported in the literature, and many of these drugs have been implicated in causing gingival overgrowth. Amlodipine, a long-acting calcium channel blocker, is used as an anti-hypertensive and for the treatment of angina. For a substantial period of time, this drug was considered a "safe drug" having relatively less adverse drug reactions (ADR). In conjunction with an increase in the usage of amlodipine, however, an adverse effect of gingival overgrowth has been reported. Evidence regarding gingival overgrowth has come from several case reports, although there have been only two studies on the incidence to evaluate the magnitude of this effect. , Because the incidence of amlodipine-associated gingival overgrowth remains poorly defined, we determined the incidence rate of amlodipine-associated gingival overgrowth.
| Materials and Methods|| |
Dental patients (N = 115) who received amlodipine for more than 3 months were surveyed to determine the rate of drug-induced gingival overgrowth. Medical histories were taken, and the patients' medical charts were examined.
Patients were included in the study if they:
- Had been taking no other medications that could cause gingival hyperplasia
- Had not been switched from one calcium antagonist to another while they were included in this study and
- Had received no periodontal therapy within 6 months before inclusion in this study.
Clinical diagnosis of amlodipine-induced gingival overgrowth was verified by the disappearance or decreased severity of gingival overgrowth after the withdrawal of amlodipine.
One hundred and fifteen patients under amlodipine treatment were classified as the study group and 100 patients were taken as the control subjects treated with other hypertension drugs in this study. In order to investigate the plaque score and gingival inflammation in the study and control groups, Loe and Silness plaque index (PI) and gingival index (GI) methods were used, respectively. A questionnaire including personal information, dosage and type of consumed drugs, plaque and gingival indices coding, and methods for oral hygiene preservation was prepared and completed by all patients. Hyperplasia was measured from the cemento-enamel junction to the free gingival margin. The hyperplasia was graded according to the gingival overgrowth index described by McGaw et al. (1987) as follows: 
0 = no overgrowth, feather-edged gingival margin
1 = blunting of gingival margin
2 = moderate gingival overgrowth (<1/3 of crown length) and
3 = marked gingival overgrowth (>1/3 of crown length).
Multiple logistic regression analysis was carried out to identify whether PI and GI were significant risk factors in the development of gingival hyperplasia. In the present study, P < 0.05 was considered as significant at 5% level of significance. P <0.001 was considered as significant at 1% level of significance.
| Results|| |
The severity of gingivitis and the GI level were greater in the amlodipine (study) group as compared to the control group, but the difference was not statistically significant (P > 0.05) [Table 1]. In this study, the amlodipine group had statistically significant higher PI values, as compared to the control group (P < 0.05) [Table 2]. In the study group, 4 (3.4%) patients were affected with gingival hyperplasia. Gingival hyperplasia was not observed in any of the control patients. The highest prevalence of gingival enlargement was in the fourth decade of life, with the incidence of overgrowth being higher in males compared to females [Table 3].
The clinical findings of amlodipine-induced gingival overgrowth were similar to those seen with use of other calcium channel blockers such as nifedipine and diltiazem. Clinical observation in patients with gingival overgrowth showed a lobular or nodular enlargement of interdental papilla in the anterior region [Figure 1]. Generally, gingival overgrowth was more obvious in the anterior region. Despite long-term amlodipine consumption, in patients with a good oral hygiene, no gingival changes were seen, whereas patients with hyperplasia had poor oral hygiene with plaque accumulation.
|Figure 1: Clinical appearance of amlodipine-associated gingival overgrowth. Gingival lobulations at the interdental papillae in the anterior segment of the labial surfaces of both lower and upper gingiva|
Click here to view
| Discussion|| |
Amlodipine is a dihydropyridine calcium antagonist that inhibits the transmembrane influx of calcium ions into vascular smooth muscle and cardiac muscle. It is frequently used as an anti-hypertensive and for the treatment of angina. 
The mechanisms by which calcium antagonists induce gingival hyperplasia have yet to be fully explained.  Among the several proposed mechanisms, the best hypothesis so far is that calcium antagonists inhibit the influx of calcium ions which is needed for the degradation and synthesis of collagen.  The accumulated collagen and extracellular matrix not degraded owing to inhibition of calcium influx by calcium antagonists is suggested to cause gingival hyperplasia. In addition to this mechanism, the importance of good oral hygiene for prevention of gingival hyperplasia is emphasized. 
The first case of amlodipine-associated gingival overgrowth was reported by Ellis in 1993.  Like other calcium channel blockers, clinical manifestation of gingival overgrowth frequently appears within 2-3 months after starting treatment with amlodipine. ,
There are two previous reports concerning the prevalence of amlodipine-associated gingival overgrowth. , The prevalence rates of the two previous reports (1.7% and 3.3%) showed a small difference. The prevalence rate in the present study (3.4%) was higher than the previous ones, but the difference was slight.
In this study, gingival hyperplasia was related to drug dosage and gingival inflammation caused by dental plaque. It is suggested that bacterial inflammation, resulting from dental plaque, is essential for gingival hyperplasia induced by amlodipine. Therefore, as expected, higher the PI, more severe will be the hyperplasia. Considering the predominance of lymphocytes, plasma cells, and mast cells in the connective tissue, the significant role of inflammation in the incidence and severity of gingival hyperplasia will be more obvious.
Finally, it should be noted that one question still remains ambiguous, i.e., why is it that despite there being similar conditions concerning plaque and amlodipine dosage, some of the drug receivers become affected with hyperplasia and others do not? Probably, this can be attributed to the biological differences among human beings, such as the existence of different subgroups of gingival fibroblasts. Therefore, investigating the interactions between factors such as the metabolism of gingival fibroblast subgroups, hormonal effects, and growth agents can be a guide to discover such differences.
We can conclude from this study that the overall incidence of gingival overgrowth related to chronic medication with amlodipine is low. Males seem to be more susceptible to the development of gingival overgrowth; the presence of gingival inflammation is an important cofactor in the expression of this effect.
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[Table 1], [Table 2], [Table 3]