Nifedipine is a very potent and effective anti-hypertensive drug. However, long term use of these anti-hypertensive drugs causes gingival enlargement. In a community-based study, it was noticed that more than 6% of subjects taking Nifedipine had significant overgrowth and it was directly proportional to amount of gingival inflammation [
3]. As suggested by Seymour eat al [
8] drug induced gingival hyperplasia is a multifactorial disease. Gingival enlargement in our case persisted even in edentulous state. It might be due to persistence of gingival overgrowth which did not resolve completely after extraction or might be due to incorporation of specific population of gingival fibroblast in alveolar ridge mucosa [
9]. The other reason for gingival enlargement in edentulous state can be due to defective collagen activity or due to decreased uptake of folic acid, blockage of aldosterone synthesis from adrenal cortex and an increase in adreno corticotropic hormone (ACTH) level and up regulation of keratinocyte growth factor [
10]. Drugs like Nifedipine, block influx of calcium ions thereby affecting homeostasis of collagen. Synthesis and degradation of collagen being altered leads to the abnormal growth [
11].Also a link to androgen metabolism has been suggested. Evidence from animal studies confirms that, nifedipine when added to gingival fibroblast in culture, increase the conversion of testosterone to 5α dihydrotestosterone and this active metabolite would target subpopulations of fibroblasts [
12,
13]. Idiopathic/Hereditary gingival enlargement from our case was ruled out as these enlargements are commonly detected at an early age and in few cases even at birth. Histological findings of present case suggested drug induced gingival enlargement. Genetic factors like Polymorphism of enzymes that are involved in transport (P-glycoprotein MDR1, CYP2C) and metabolism (cytochrome P450) of pharmacological active substances have been investigated in various studies. A relationship has been described between gingival enlargement and the expression of human leukocyte antigen (HLA; HLA-DR2-positive patients) [
14]. Other factors like heparin sulfate glycosaminoglycan (HSPG), basic fibroblast growth factor (bFGF), and transforming growth factor – beta (TGF-β) were found to be high in drug induced gingival enlargement [
10]. Dose of drug in present case was not altered as the dose was very low. Several studies in literature have suggested that a dose range of 30-60 mg/day is more associated with gingival enlargement [
3]. Dose of Nifedipine taken by patient was below the threshold limit of gingival overgrowth. Relation between gingival hyperplasia and pharmacokinetics of the drug has been investigated and are much debatable. This threshold might differ from patient to patient which might not be a suitable prognostic factors for gingival enlargement [
8]. Normal ridges were noticed after surgical excision in our patient. There was no recurrence of growth on a year follow up and on regular use of denture by our patient.
In conclusion, Nifedipine induced gingival enlargement is rare to occur in edentulous patients as there are no such reported cases from the past. The possible etiology for its occurrence is obsolete. Further studies are required to explain the association and existence of Nifedipine induced gingival enlargement in edentulous patients. Hence, there is a need for physicians and dentist to make a coordinated treatment plan and practice care while prescribing these drugs which are associated with gingival overgrowth.