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
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.