Gingival Overgrowth Induced by Anticonvulsant Drugs

 

TAKE-HOME MESSAGE

  • This cross-sectional study aimed to evaluate the prevalence of gingival overgrowth and the differences among causative drugs in epileptic patients. A total of 162 patients were included, with the incidence of overgrowth among those taking a single drug (37%) being comparable with that among those taking multiple drugs (45%). Drugs in decreasing order of associated incidence of overgrowth were oxcarbazepine (71%), lamotrigine (61%), phenobarbital (53%), phenytoin (50%), valproic acid (44%), and carbamazepine (32%).

  • Phenytoin and valproic acid have historically been known to cause gingival overgrowth in epileptic patients. The findings of this study remind us that multiple other drugs used in the management of epileptic patients have varying potential to cause gingival overgrowth, some with even higher potential than phenytoin and valproic acid.
– Tapan N. Koticha, BDS, MDS

 Clinical Dentistry

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 present cross-sectional study evaluated gingival enlargement and plaque index in 162 patients taking 1 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. Additionally, the gingival enlargement index used is subjective compared with other available indices and it appears that localized gingival changes were scored equivalently to generalized changes. Considering the many possible etiologies for localized gingival enlargement, with inadequate oral hygiene being most common, longitudinal data and/or addition of a control group would have significantly enhanced the quality of evidence.

The authors do report hyperplasia in a high percentage of patients taking a number of anti-epileptic phenytoin alternatives: valproic acid (44%), carbamazepine (32%), levetiracetam (29%), lamotrigine (61%), phenobarbital (53%), and oxcarbazepine (71%). Some of these percentages are orders of magnitude larger than those reported in other studies. This may be related to the scoring limitations discussed above. Overall, only 13.58% of patients on anti-epileptics in this study were reported as having greater than what I would consider as mild gingival enlargement and 45.06% of patients had no gingival changes reported at all. Thus, I think it wise to coach your dental team to defend against gingival enlargement/overgrowth with more than just “the big three,” including any anti-epileptics or calcium channel blockers. Routine prophylaxis and oral hygiene instruction will be your most reliable defense 

OBJECTIVE

Our 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 epileptic patients.

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 subjects 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 epileptic patients, dentists should take into account different drugs as possible causes for gingival overgrowth and warn for possible alternatives. 

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