Gingival enlargement can be associated with a number of entities: hereditary, infectious, localized inflammatory, systemic inflammatory/autoimmune, neoplasia (localized or hematologic), medications. Microscopically, the enlargement is generally notable for either increased extracellular matrix/interstitial fluid or cells (resident or infiltrating). Current evidence suggests that medication-associated gingival enlargement results from collagen accumulation in the extracellular matrix. Increased plaque/poor oral hygiene positively correlates with this enlargement. “The big three” medications that the dental team are coached to look out for are phenytoin (anti-epileptic), nifedipine (calcium channel blocker), and cyclosporine (immunosuppressant), with gingival hyperplasia being reported in approximately 25% to 50% of users.
A number of additional medications have been reported to cause gingival enlargement, and the below cross-sectional study evaluated gingival enlargement and plaque index in 162 patients taking one or more anti-epileptic medications for at least 1 year. Individuals on calcium channel blockers or cyclosporine were rightfully excluded from the study; however, no control group was included.
Abstract
Objective: The aim was to estimate the prevalence of gingival overgrowth (hyperplasia) and to determine whether active molecules affect the severity of overgrowth in a group of patients with epilepsy.
Background: The effects of phenytoin on oral health have been explored in different studies, yet little information is available on other antiepileptic drugs.
Methods: Data were collected from 213 participants of both sexes, from 5 to 80 years. Patients taking the same antiepileptic therapy for at least 1 year and meeting the inclusion criteria of the study (n = 162) were subjected to measurement of gingival overgrowth according to the modified Harris and Ewalt classification and O’Leary’s plaque control record (OLR). Descriptive statistics were calculated. Data were analyzed using Pearson’s r correlation coefficient and chi‐square test. Significance level was set at 5%.
Results: The active drugs lamotrigine, oxcarbazepine, and phenobarbital were significantly associated with gingival overgrowth in 61%, 71%, and 53% of cases, respectively, and phenytoin, valproic acid, and carbamazepine in 50%, 44%, and 32% of cases, respectively.
Conclusion: Different antiepileptic molecules may be related to gingival overgrowth. In addition to phenytoin, also lamotrigine, oxcarbazepine, and phenobarbital were associated with increased prevalence of gingival overgrowth. In the management of patients with epilepsy, oral health professionals should take into account different drugs as possible causes for gingival overgrowth and warn for possible alternatives.
