Case Presentation: A 31-year-old male with a past medical history of hypertension, ischemic lacunar stroke and alcohol use disorder presents to the outpatient clinic with a 6-month history of gingival enlargement. He denied any elements of fever, chills, weight loss, nor night sweats. His previous antihypertensive regimen consisted of amlodipine 10 mg daily, losartan 100 mg daily, and hydrochlorothiazide 25 mg daily. However, his hypertension was uncontrolled, and his amlodipine was switched to nifedipine 60 mg daily 2 years ago. In order to optimize blood pressure control, his nifedipine dose was escalated to 90 mg daily 6 months ago. On physical exam, there was a nodular non-tender enlargement of the gingival planes, most prominently at the maxillary alveolar ridges with no evidence of bleeding. The patient underwent a thorough evaluation for secondary causes of hypertension. His renin levels were elevated at 27.621 ng/mL/hr. However, aldosterone levels, aldosterone-renin ratio, thyroid function studies were unremarkable. A follow up renal artery doppler ultrasound demonstrates no significant stenosis in proximal, middle, and distal renal arteries bilaterally. The patient’s nifedipine was discontinued and was instructed to record a blood pressure diary at home. On his 1-month and 4 -month follow ups, there was a notable decrease in size of gingival hyperplasia that was previously demonstrated on the maxillary ridges. His blood pressure remained controlled.
Discussion: Gingival hyperplasia is a clinical entity characterized by excessive enlargement of gingival tissues along the maxillary and mandibular ridges. It can be associated with a multitude of etiologies including genetic, autoimmune, neoplastic, and drug-induced causes. Nifedipine, a well-established antihypertensive agent, has been previously reported to be associated with gingival hyperplasia. In a community-based study, such an adverse effect was implicated in 6.3% of the study population. Although the risk increases with prolonged use, clinically apparent gingival overgrowth can be seen in as early as 3 months after initiating treatment with nifedipine. The pathogenesis behind such an association has not been clearly defined. However, a proposed mechanism may involve blockage of calcium influx leading to alteration in collagen homeostasis resulting in gingival tissue overgrowth. Despite prior reported cases requiring periodontal interventions, a unique recovery was seen in our patient by exhibiting signs of gingival hyperplasia reversal after 4 months of nifedipine suspension.
Conclusions: Nifedipine induced gingival hyperplasia represents a unique adverse effect occurring with prolonged drug administration. Healthcare professionals should be vigilant regarding prescribing calcium channel blockers, especially in patient with poor oral hygiene. In addition, regular surveillance for periodontal adverse effect is essential, as early detection can be associated with improved clinical outcomes.