Bruxism is a repetitive jaw-muscle activity characterized by clenching or grinding of the teeth, and it represents a significant clinical challenge in both dentistry and psychiatry. Selective serotonin reuptake inhibitors (SSRIs), the most widely prescribed class of antidepressants worldwide, have been increasingly implicated as a pharmacological trigger for the onset or exacerbation of bruxism. This narrative review synthesizes the available clinical evidence from case reports, case series, and observational studies examining the relationship between SSRI use and bruxism intensity. The putative neurobiological mechanisms linking serotonergic modulation to masticatory motor activity are explored, including the role of serotonin-dopamine interactions in the basal ganglia and the disruption of central pattern generators governing jaw movements during sleep. Current pharmacological management strategies, including the adjunctive use of buspirone, gabapentin, and dose modification, are critically evaluated. The review highlights the need for prospective controlled studies to establish causal relationships, quantify dose-response effects, and develop evidence-based treatment algorithms for SSRI-associated bruxism. In conclusion, although the current evidence is largely derived from case reports and small observational studies, the consistent temporal association between SSRI initiation and bruxism onset, the dose-dependent trend reported in prevalence studies, and the favorable response to adjunctive buspirone collectively support a likely causal role of SSRIs in inducing or intensifying bruxism, and justify routine clinical surveillance for this adverse effect in patients receiving serotonergic antidepressants.
Patricia Valério (Mon,) studied this question.