Drug-induced gingival overgrowth is frequently associated with three particular drugs: phenytoin, cyclosporin, and nifedipine. As gingival enlargement develops, it affects the normal oral hygiene practice and may interfere with masticatory functions. The awareness in the medical community about this possible side effect of nifedipine is less when compared to the effects of phenytoin and cyclosporin. The frequency of gingival enlargement associated with chronic nifedipine therapy remains controversial. Within the group of patients that develop this unwanted effect, there appears to be variability in the extent and severity of the gingival changes. Although gingival inflammation is considered a primary requisite in their development, few cases with minimal or no plaque induced gingival inflammation have also been reported. A case report of gingival overgrowth induced by nifedipine in a patient with good oral hygiene and its nonsurgical management with drug substitution is discussed in this case report.
Gingival enlargement is a well-known consequence of the administration of some anticonvulsants, immunosuppressants, and calcium channel blockers and may create speech, mastication, tooth eruption, and aesthetic problems.
Not all the patients using these agents are affected by gingival overgrowth, and the extent and severity are variable in such patients. Phenytoin-induced overgrowth may be present in 50 to 100% of patients treated with such drug, whereas cyclosporin and calcium channel blocker-induced overgrowths seem to be less common, with a prevalence of 30% and 20%, respectively [
A 53-year-old male patient reported to the Department of Periodontology, with a complaint of swollen gums. On examination, generalized gingival enlargement was noticed in the lower arch, whereas an isolated nodular growth was observed in the right side of upper arch. The enlarged gingiva was firm, pale pink, and resilient with a minutely lobulated surface and displayed no tendency to bleed (Figure
(a) Preoperative view. (b) Preoperative view.
(a) Postoperative view (2 months after drug substitution). (b) Postoperative view (2 months after drug substitution).
The pathogenesis of drug-induced gingival overgrowths is still not completely understood. It has been demonstrated that gingival enlargement has a multifactorial nature and is affected by factors such as age, demographic variables, genetic predisposition, oral hygiene status, pharmacokinetic variables, and molecular and cellular changes in gingival tissues [
Despite their pharmacological diversity, the three major drugs causing gingival overgrowth, namely, anticonvulsants, calcium channel blockers, and immunosuppressants, have similar mechanism of action at the cellular level, where they inhibit intracellular calcium ion influx. The action of these drugs on calcium and sodium ion flux may prove to be the key in understanding why three dissimilar drugs have a common side effect upon a secondary target tissue, such as gingival connective tissue.
Calcium channel blockers are drugs developed for the treatment of cardiovascular conditions such as hypertension, angina pectoris, coronary artery spasms, and cardiac arrhythmias. Gingival enlargement associated with nifedipine was first reported in the early 1980s and was soon also described with diltiazem and verapamil and in cases with amlodipine and felodipine [
Some investigators believe that inflammation is a prerequisite for development of the enlargement, which therefore could be prevented by plaque removal and fastidious oral hygiene [
It has also been proposed that susceptibility or resistance to pharmacologically induced gingival overgrowth may be governed by the existence of specific genetically predetermined subpopulations of fibroblasts in each individual which exhibit a fibrogenic response to these medications [
Mast cells have been found to participate in many inflammatory oral diseases, particularly those associated with fibrosis. They possess very diverse roles ranging from proinflammatory to immunomodulatory. Upon their activation, they promote the local renin angiotensin system generation consequently able to stimulate endothelin and other profibrotic mediators [
The presence of the enlargement makes plaque control difficult, often resulting in a secondary inflammatory process that complicates the gingival overgrowth caused by the drug. The primary aim of nonsurgical approaches is to reduce the inflammatory component in the gingival tissues and thereby avoid the need for surgery. Patients at risk from or who have developed drug-induced gingival overgrowth will benefit from effective oral hygiene measures, professional tooth cleaning, scaling, and root surface instrumentation. For some patients these measures alone could reduce the gingival overgrowth to acceptable levels, and for others, it could make surgical correction easier [
The dose of the drug also has an impact on gingival oral growth. It is reported that nifedipine was found 15–316 times more in the gingival crevicular fluid compared to plasma [
The number of prescriptions for calcium channel blockers has been increasing in recent years. There is infinitesimal awareness about this effect of drugs on gingival tissues in medical community. There is a need for physicians and dentists to make a coordinated treatment plan for the patients indicated for these drug therapies. Our case showed that not every case of drug-induced gingival enlargement requires plaque induced gingival inflammation for their development. In such cases drug substitution should be considered a valid treatment option especially when the gingival enlargement is present in spite of good oral hygiene.
The authors declare that there is no conflict of interests regarding the publication of this paper.