Selective Serotonin Reuptake Inhibitor-Associated Bruxism: Neuropharmacologic Mechanisms and Clinical Implications

Selective serotonin reuptake inhibitor (SSRI)-associated bruxism is an increasingly recognized medication-associated phenomenon, although its incidence, neuropharmacologic mechanisms, and optimal management remain incompletely understood. This focused narrative review examines the clinical evidence, proposed mechanisms, and therapeutic implications of SSRI-associated bruxism. Available literature demonstrates recurring temporal associations between SSRI initiation or dose escalation and the emergence of jaw clenching, tooth grinding, pain, and related orofacial symptoms across multiple agents. Proposed mechanisms are multifactorial and may involve altered monoaminergic regulation within central motor networks, including serotonergic-dopaminergic interactions, 5-hydroxytryptamine (serotonin) receptor 1A (5-HT1A) signaling, and possible noradrenergic contributions; however, these mechanisms remain unconfirmed in affected patients. Adjunctive buspirone is the most consistently described pharmacologic strategy and may permit the continuation of an otherwise effective SSRI, although evidence for benefit remains primarily case-based. The literature is limited by heterogeneous bruxism definitions, inconsistent differentiation between awake and sleep manifestations, variable antidepressant exposures, and sparse objective physiologic assessment. Prospective studies using standardized assessment methods and controlled treatment designs are needed to clarify incidence, susceptibility, pathophysiology, and treatment response.