**1. Introduction**

Gingival overgrowth may have multiple causes, however drugs assumption is the most common [1,2]. In addiction, drug-induced gingival overgrowth may be associated with a patient's genetic predisposition [3,4].

The three main classes of drugs inducing gingival overgrowth are anticonvulsants, immunosuppressive, and antihypertensive agents [3,5–7]. The first report regarding gingival overgrowth by the administration of amlodipine was published in 1994 [8]. Subsequently, other authors reported the onset of gingival overgrowth as a side e ffect in patients who received 10 mg per day of amlodipine within two months [9]. Gingival overgrowth manifests as a side e ffect within one to three months after amlodipine administration [7,10]. Amlodipine shows a pharmacological profile, as follows: long-acting dihydropyridine; coronary and peripheral arterial vasodilatation; headaches, facial flushing, dizziness, and oedema. The main oral side e ffect that is induced by amlodipine is gingival overgrowth [11,12].

Gingival overgrowth that is induced by amlodipine (GOIA) must be stimulated by a threshold concentration of amlodipine [13]. However the severity of GOIA is supposed to be related to the concentration of amlodipine in oral fluids [13]. The mean dose of amlodipine reported to cause GOIA in most of the subjects is 5 mg/day. Therefore, it may be suggested that the dosage and duration of amlodipine may have an impact on GOIA [13]. Usually, the gingival manifestations of GOIA appear within the first three months of the drug administration [14]. A longer duration of therapy may increase the exposure of cells to amlodipine, and this may modify the apoptosis of cells, resulting in hyperplasia [14]. Genetic susceptibility is one the factors influencing the severity of GOIA; in fact multidrug resistant (*MDR1*) gene polymorphisms is supposed to alter the inflammatory response to the amlodipine [15].

Poor plaque control is another risk factor in developing of GOIA. In fact, GOIA hampered routine oral hygiene measures. Additionally, GOIA can favour the accumulation of bacterial plaque, which in turn determines gingival inflammation, causing gingival overgrowth [14]. Amlodipoine, in presence of proinflammatory cytokines (for example TNFα), may favour the inhibition of apoptosis of human gingival fibroblasts, thus promoting hyperplasia [16].
