Sleep bruxism is characterized by the involuntary clenching or grinding of the teeth during sleep and can cause severe health problems, including the destruction of tooth structure, temporo-mandibular joint dysfunction, myofascial pain, and severe sleep disturbances. Iatrogenic sleep bruxism may be common during treatment with psychotropic medications, such as anti-psychotics and antidepressants, especially selective serotonin reuptake inhibitors (SSRIs). Bruxism is a common movement disorder that affects 8–21% of the population. The majority of bruxism symptoms are mild or moderate, although rare but severe cases may lead to serious periodontal damage, temporo-mandibular dysfunction, sleep disturbances, jaw pain, and stiffness. As a result, such cases must be treated with medication. It has been hypothesized that the mechanism of SSRI-induced bruxism may involve excessive serotonergic action on the meso-cortical neurons arising from the ventral tegmental area. It has been argued that,the addition of buspirone, was necessitated by the high level of residual anxiety. As a result, these symptoms may have been prevented through the use of buspirone alone. Buspirone, is an agonist of the 5-HT1A receptor that increases dopaminergic neuron, firing in the ventral tegmental area and increases the synaptic release of dopamine in the prefrontal cortex. These effects ameliorate drug-induced bruxism. Buspirone can also ameliorate extrapyramidal side effects, such as akathisia and tardive dyskinesia, and this property may be an additional explanation for the bruxism-related effects of the drug. Furthermore, buspirone may be an effective treatment for the bruxism associated with the use of these medications.