A Grinding Issue: Drug-Induced Bruxism

Bruxism is defined as an unproductive grinding or gnashing of the teeth and clenching of the jaws that can occur while awake or during sleep. ¹ This condition is, for the most part, an unconscious behaviour affecting both genders of all ages. ² The overall prevalence of bruxism is difficult to pinpoint. It may be self-reported or identified only when family members or bedroom partners report sounds of clicking or grinding. The incidence of sleep bruxism in children has been estimated at 15%, becoming more prevalent in the 7- to 10-year age group, and often resolving with the eruption of permanent teeth. In adults, the reported incidence varies widely (5%–96%).^1,2

Mild bruxism often goes undetected and does not always require treatment. In more severe cases, patients may complain of tooth hypersensitivity, painful masseter and temporal muscles, as well as headache. Tooth damage or fractured dental restorations can occur.^1,2 Damage is understandable, given that patients can have 8 episodes of teeth grinding per night with an average maximum biting force of 162 lb per square inch. Forces as high as 975 lb per square inch are recorded. ² Dental professionals may observe the signs and symptoms of bruxism during a regular dental visit and subsequently investigate a potential cause. Box 1 lists the symptoms associated with bruxism.

Primary bruxism may not have an identifiable cause, but current and ongoing research suggests a link to genetic and environmental factors, as well as life or psychological stresses. Secondary bruxism may be related to diseases, irregular sleep cycles or drug-induced oral movement disorders such as dystonia and dyskinesia. Box 2 contains a list of medications and illegal drugs reported to cause bruxism. ⁴ Occurrence has been linked to both drug consumption and withdrawal. ⁵

Drug-induced movement disorders are often referred to as extrapyramidal adverse reactions. The mechanism for these disorders is complex, variable and not fully understood. An imbalance of central nervous system neurotransmitters appears to be involved to varying degrees.^1–3 Hypersensitivity to or deficiencies/excesses of dopamine, serotonin and, in some cases, gamma-aminobutyric acid (GABA) and norepinephrine, may contribute to the problem. ⁶ Antipsychotic drugs can cause tardive dystonias, dystonic reactions or oral dyskinesias that can then manifest as bruxism. Amphetamine analogues can cause hyperactivity that leads to tooth grinding and jaw clenching during periods of acute use. ⁷

The time to onset of drug-induced bruxism is variable. In a review article of movement disorders associated with selective serotonin-reuptake inhibitors (SSRI), this adverse drug reaction (ADR) was detected as early as 1 day to as late as 11 months following initiation of therapy. ⁵ Another case series indicated that the onset of bruxism with SSRIs ranged from 6 hours to 8 weeks. ⁸ One case report described bruxism in a 77-year-old female suffering from Parkinson's disease when her total daily dose of levodopa/carbidopa was increased from 550 to 700 mg. The ADR was detected during the first 2 weeks of her dose increase, appearing 1 to 2 hours after administration of the daytime immediate-release doses and during the night. Symptoms subsided following a dose reduction to 550 mg daily. ⁹

Bruxism has also been associated with drug interactions. Two cases of bruxism were reported in children within hours (1.5 and 4) of taking concomitant valproic acid for seizure prophylaxis and methylphenidate for attention-deficit hyperactivity disorder. It was postulated that the serum levels of methylphenidate were elevated due to competitive metabolism of the 2 medications via the cytochrome 2D6 pathway. The symptoms in both cases resolved spontaneously on methylphenidate discontinuation. ⁸

Several options for managing drug-induced bruxism are proposed and used with varying success.^3,5,8 A dose reduction or discontinuation of the offending drug can be attempted to alleviate symptoms. In Canada, no drugs are officially indicated for the treatment of bruxism. The off-label use of several agents (Box 3) was found to be effective, but according to case reports, results are not always consistent. Paradoxically, some drugs used to treat bruxism may also induce it (e.g., levodopa/carbidopa, buspirone).

Two published cases report the success of buspirone for SSRI-induced bruxism. A bedtime dose of 5 mg over 4 days significantly improved paroxetine-induced bruxism in a 20-year-old woman. ¹⁰ In a second report, 4 adults with sertraline-associated bruxism were successfully treated with buspirone. Responses were observed within 1 to 8 weeks of initiating doses ranging from 20 to 50 mg daily. ¹¹ A bedtime dose of gabapentin 300 mg was effective for bruxism occurring in a man taking venlafaxine 75 mg twice daily for depression. Injections of botulinum toxin A to the masseter muscles of 2 patients successfully treated flecainide- and SSRI-induced dystonia of the jaw and bruxism that persisted despite discontinuation of the offending agent. Two adult patients responded to propranolol (60–240 mg/day) when they experienced night-time bruxism associated with the use of haloperidol for psychosis. ⁸