Selective serotonin reuptake inhibitors (SSRI) and bruxism.

Nocturnal bruxism (involuntary repetitive grinding or clenching of the teeth during sleep) affects approximately 8-21% of adults. The force on the teeth from the repetitive contractions can be up to three times greater than that which occurs during chewing and can result in broken, worn, or loosened teeth. Therefore, the main focus of bruxism treatment is to protect the teeth from becoming damaged. To that end, the most commonly prescribed therapy for bruxism is a custom-fitted rigid acrylic mold usually placed over the lower teeth. This creates a barrier between the upper and lower teeth and dampens the force of grinding and clenching. Approximately 1.6 million dental splints are prescribed for bruxism each year in America. Scientists are perplexed why bruxism occurs but a certain class of antidepressants--the selective serotonin reuptake inhibitors (SSRIs)--may give a clue: SSRI use can induce bruxism suggesting a serotonergic influence in the pathogenesis of bruxism.

Chewing is a two-step process beginning with serotonergic neurons located within the midbrain raphe. (The raphe is the median seam formed where the two halves of the brainstem unite; it extends the length of the brainstem.) In the first step, signals from the raphe neurons travel to the ventral tegmental area (VTA) located within the cerebral peduncles. There in the VTA, the axons of the raphe serotonergic neurons nearly touch the cell bodies of dopaminergic neurons. The serotonergic neurons release the neurotransmitter serotonin into the synapse between the serotonergic and dopaminergic cells. The neurotransmitter then travels across the synapse and attaches to the dopaminergic neurons. Once attached, the second step of the process begins. The dopaminergic neurons relay signals along the mesocortical tract which extends from the VTA to the prefrontal cortex of the brain. The prefrontal cortex plays a role in voluntary movement. This part of the brain needs sufficient levels of dopamine to prevent involuntary movement such as bruxism.

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The function of the mesocortical tract may be most responsible for SSRI-induced bruxism since this tract is extremely sensitive to changes in serotonin production. Although the mesocortical cells are dopaminergic (i.e., they release dopamine), they contain receptors on the surface which respond to serotonin rather than dopamine. Increased levels of serotonin induces the mesocortical dopaminergic neurons to release less dopamine while decreased levels of serotonin induces the neurons to release more dopamine.

SSRIs cause increased amounts of serotonin to remain in a synapse. When SSRIs exert this effect in the VTA, the mesocortical dopaminergic cells correspondingly release reduced amounts of dopamine. This ultimately means less dopamine reaches the prefrontal cortex since there is less dopamine traveling through the mesocortical tract. With less dopamine in the prefrontal cortex, there is less control over voluntary movements and bruxism can manifest.

Also pointing to serotonergic influence in bruxism is that various studies show that the antidepressant drug buspirone can decrease SSRI-induced bruxism. For example, Bostwick and Jaffee prescribed buspirone to four patients after the SSRI sertraline had induced bruxism. Although sertraline had successfully ameliorated depression in all four, the patients began to complain of daytime as well as nocturnal bruxism 1-4 weeks after starting the drug. The patients also reported chronic headaches; awakening with sore or tight jaws; or broken teeth as a result of their bruxism. After adding buspirone to the regimen, the symptoms of bruxism disappeared within one to four weeks in all four patients.

Bostwick and Jaffee hypothesize that buspirone counteracts bruxism through its effect on the serotonin 1A (S1A) receptor. In the VTA, S1A receptors are found on the serotonergic neurons as well as the dopaminergic neurons. When buspirone attaches to the presynaptic S1A receptors, serotonergic neurons release less serotonin into the synapse. When buspirone attaches to the post-synaptic S1A receptors, dopaminergic neurons release increased amounts of dopamine which travels throughout the mesocortical tract ultimately reaching the prefrontal cortex. This restores dopamine levels in the prefrontal cortex preventing bruxism.

Interestingly, Dan J. Stein reported two cases in which SSRI antidepressants reduced bruxism. The first case was a young woman who had been prescribed paroxetine for obsessive-compulsive disorder. Before treatment, her nocturnal bruxism was so severe that her husband was kept awake by the noise. After starting the medication, her husband noted that she had fewer episodes. The second case involved an elderly woman who had been prescribed citalopram for depression. Before treatment, she frequently awoke with jaw soreness as a result of nocturnal bruxism. After starting citalopram, she reported she no longer had nocturnal bruxism as evidenced by lack of jaw soreness.

Some researchers have found that bruxism is associated with rapid eye movement (REM) sleep so it may be that SSRI antidepressants reduce bruxism by reducing the amount of REM sleep. Bruxism is also known to increase during times of high emotion (e.g., anxiety, stress, etc.) so it may be that the SSRI antidepressants reduce bruxism by alleviating the psychological factors associated with it. M. E. Jan Wise suggests a third possibility. Wise believes that decreased bruxing with SSRI use may be dose-dependent. This conclusion was based on the experience of two patients taking citalopram. The first took citalopram at a dose of 20 mg/day. At six weeks, the dose was increased to 40 mg/day. Ten days later at this new dose, the subject developed bruxism severe enough that a tooth had to be removed. The second patient took citalopram at 40 mg/day in combination with 10 mg of buspirone each day. After four months, buspirone was discontinued but the subject remained on citalopram. Bruxism began three weeks later with citolopram alone. When the dosage of citalopram was reduced to 20 mg/day, the bruxism stopped.

Scientists continue to investigate the influence of the serotonergic system in bruxism with the hope that the disorder can be treated by manipulating serotonin transmission. Currently, buspirone is the most successful drug in accomplishing this goal. However, another drug which has recently shown promise is the anti-convulsant drug gabapentin.

In 1999, E. Sherman Brown and Sunhee Hong inadvertently found that gabapentin could reduce bruxism. They prescribed it to reduce anxiety in a patient being treated for obsessive-compulsive disorder. The patient also had been prescribed venlafaxine. As a result, he had venlafaxine-induced bruxism which stopped after two days of using gabapentin.

Scientists, including Brown and Hong, do not know how gabapentin counteracts bruxism. It is similar to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). Yet research suggests that gabapentin does not attach to GABA receptors, serotonin (S1, S2) receptors, or dopamine (D1, D2) receptors.

Bruxism can result in worn or loose teeth; pain in the face, neck, ear, or temporal mandibular joint (TMJ); jaw tenderness or pain; migraine headache; difficulty chewing; clicking of the jaw during eating or talking; and difficulty opening one's mouth wide. Lesser known consequences of bruxism can be hearing loss; inflammation and obstruction of the parotid and salivary glands; and a swollen, painful mouth. People with SSRI-induced bruxism may be spared these consequences by changing to a different type of antidepressant medication or by changing the dosage of a medication. Since SSRI-induced bruxism can be reversed, it is important for sleep technologists to be aware that bruxism in a sleep study patient may also be a sign that the patient is using an SSRI (sertraline, fluoxetine, paroxetine, fluvoxamine, citalopram, venlafaxine).

by Regina Patrick RPSGT