Abstract
Drug-induced gingival overgrowth (DIGO) is a major problem for general dentists and periodontists. Patients curated with explicit medications perhaps are drawn into this unsolicited after-effect (DIGO), which may perhaps impede comeliness, chewing, or articulation. Overgrowth of gingival tissues influenced from causative drugs are not only hampering patient’s aesthetics but prejudicing sustenance and permission to perform ongoing oral cleanliness practice, bringing about an enhanced feebleness to oral septicity, dental caries, and periodontal pathoses. 1
For many of these drug-related gingival pathology, previously known as “gingival hyperplasia”/“gingival enlargement”/“"gingival hypertrophy,” presently the preferred term is “gingival overgrowth.” The above terms do not accurately reflect our current understanding of gingival overgrowth and its histopathology. Generally, DIGO can be divided into 3 basic categories based on their causative drug involved in the etiopathology, namely the drugs from anticonvulsants, immunosuppressants, and calcium channel blockers. 2
The extensive usage of calcium channel blockers was launched in the early 1980s. Dihydropyridine (such as nifedipine) is often concomitant with enlarged gingiva, paralleled to other subsets of calcium channel antagonists such as amlodipine. Recommendation of calcium channel blockers is comparatively communal, making it challenging to conclude the exact commonness of DIGO.
Amlodipine is a third-generation dihydropyridine calcium antagonist, and its pharmacodynamics is equivalent to nifidipine. 1 However, amlodipine has unique physical and chemical properties, which are characterized by almost complete absorption in the liver, high plasma concentration, high bioavailability, and slow biodegradation. Due to the slow and long-lasting elimination of amlodipine, only one dose per day is required. This in turn leads to having better pharmacological efficacy in comparison with nifedipine, alongside higher patient compliance and less severe side effects.1, 2
Compared with patients taking amlodipine, patients taking nifedipine have a higher risk of significant overgrowth. The difference between nifedipine and amlodipine is important because both drugs are dihydropyridine and are therefore similar in structure. In addition, they are all secreted in the gingival crevicular fluid, but their physical and chemical profiles are different. Amlodipine is extra polar than other dihydropyridine with pKa (acid dissociation constant) value of 8.7. In contrast, nifedipine is highly lipophilic, soluble in cell membranes, and penetrates the cytoplasm.
Although it is believed that the mechanism of DIGO is multifactorial, drug–cell interactions play an important role in the pathogenesis of this effect.3, 4 Clinicians should determine plaque control measures as the main stage of DIGO treatment. While the relationship between DIGO and plaque are still challenging to extricate, there is evidence that eliminating local factors and maintaining good oral hygiene regularly reduces the severity of DIGO via reducing inflammatory components. Typically, a 3-month intermission for periodontal maintenance therapy has been acclaimed in management of DIGO. 3
The choice of treatment for DIGO should be based on the drugs used and the clinical manifestations of the case. First, consider stopping or altering the medicine/drug. Moreover, these conditions ought to be scrutinized in consultation with the patient’s physician. Modest termination of the aberrant causative agent is generally not a real-world elucidation. Conversely, its auxiliary with alternative medication might be the practical elucidation. The average time taken for the resolution of DIGO is 1 to 8 weeks. 3
Contemplation may be set to the usage of alternative course of antihypertensive drugs, which are recognized to be not concomitant with the DIGO. 4 Currently the ancillary medicine, that is, Tablet Normadate 100 mg, alongside thorough Phase-1 therapy occasioned in momentous clinical improvement in 6 weeks of time.
The necessity and timing of surgery must be carefully considered. Surgery is usually performed for cosmetic/aesthetic reasons before any functional consequences occur. The classic surgical method is gingivectomy with an external bevel. However, Mavrogiannis et al 5 concluded in his study that open flap debridement and conventional gingivectomy delivered similar effects with reverence to the degree of reappearance of DIGO. In the present case, as the overgrowth of the gingiva was clinically associated with the true periodontal pockets, open flap debridement was performed. The postoperative results were very satisfactory in terms of aesthetics and functions.
Even low-dose amlodipine (5 mg/day) can induce DIGO. Physicians and dentists/periodontists should pay attention to the patients consuming amlodipine group of drugs that can induce DIGO to detect oral changes to successfully prevent, diagnose and control their adverse side effects. However, in order to obtain the best results, we need to adopt the multi- and interdisciplinary team approach involving cardiologist.
