Definition and Classification
Bruxism is defined as a repetitive masticatory muscle activity characterized by clenching, grinding, or bracing of the teeth. The condition manifests in two distinct phenotypes with different etiological and clinical profiles:
Sleep Bruxism (SB)
Classified as a sleep-related movement disorder, sleep bruxism occurs unconsciously during sleep, typically during transitions between sleep stages or periods of cortical arousal. Patients remain unaware of the condition until a bed partner reports grinding sounds or a clinician identifies characteristic dental wear patterns.
Awake Bruxism (AB)
This phenotype involves semi-conscious or unconscious tooth clenching during waking hours, frequently associated with periods of concentration, cognitive load, or emotional stress. Unlike sleep bruxism, awake bruxism predominantly features static clenching rather than dynamic grinding movements.
Neurophysiology of Bruxism
Central Nervous System Mechanisms
Sleep bruxism demonstrates strong associations with sleep micro-arousals—brief cortical activations lasting 2-12 seconds that fragment sleep architecture without full awakening. Polysomnographic studies reveal that bruxism episodes occur predominantly during transitions from deeper (N3) to lighter (N2) sleep stages, preceded by autonomic nervous system activation including increased heart rate and sympathetic tone.
The trigeminal motor system plays a central role in bruxism pathophysiology. This involuntary motor activity generates occlusal forces substantially exceeding physiological mastication—ranging from 450-870 N in the molar region compared to typical chewing forces of 100-200 N.
Relationship With TMD and Craniofacial Pain
The relationship between bruxism and temporomandibular disorders (TMD) remains clinically significant yet mechanistically complex. Contrary to common belief that bruxism causes TMD, an in-depth analysis of the 4 muscle of mastication and the temporomandibular joint suggests that bruxism is in fact caused by a Temporomandibular disorder, largely defined by a change (deformation or displacement of the articular disc). TMD-induced bruxism represents a more accurate pathophysiological model in many cases.
The Articular Disc Displacement
The temporomandibular joint contains an articular disc that serves to absorb shock, stabilize the joint, and distribute occlusal forces uniformly. Following any trauma to the head (typically experienced by approximately 75% of the population), whether it is through a fall at the playground, sports injuries, or accidents—this disc may become displaced or deformed.
The masseter, temporalis, and pterygoid muscles repeatedly contract in unconscious attempts to reposition the compromised disc, manifesting as bruxism. This parafunctional activity represents failed repair attempts, as the structurally altered disc cannot return to normal anatomical configuration.
Clinical Sequelae
Painful TMD demonstrates strong comorbidity with both sleep bruxism and chronic pain conditions including headaches and migraines. The shared trigeminal nerve pathways create neuroanatomical substrates for pain referral patterns extending from masticatory structures to temporal, frontal, and cervical regions.
Systemic and Sleep Associations
Tinnitus and Otological Symptoms
The anatomical and neurological proximity of the TMJ to auditory structures creates substrate for somatic tinnitus. Research demonstrates significant associations between TMD, sleep bruxism, and tinnitus—perceived ringing or buzzing in the ears. In somatic tinnitus phenotypes, jaw movements or clenching modulate tinnitus intensity.[1]
Sleep Quality Disruption
Sleep bruxism episodes fragment sleep continuity through repeated micro-arousals, preventing progression into restorative deep sleep stages. This sleep architecture disruption manifests clinically as non-restorative sleep, excessive daytime somnolence, irritability, and impaired cognitive performance.[2]
Diagnosis
Clinical Assessment
Definitive sleep bruxism diagnosis requires polysomnographic recording combined with audio-video monitoring. However, this approach remains impractical for routine clinical use.
Probable bruxism diagnosis relies on:
- Patient or bed partner report of grinding sounds
- Clinical signs of tooth wear (flattened occlusal surfaces, enamel fractures)
- Masseter or temporalis muscle hypertrophy and tenderness
- Temporal relationship between bruxism events and symptoms
Differential Considerations
Clinicians must distinguish bruxism from other conditions producing similar symptoms, including primary headache disorders, sleep apnea, medication side effects, and neurological movement disorders.
Evidence-Based Treatment Overview
Behavioral and Lifestyle Interventions
Stress management represents a cornerstone of awake bruxism management. Mindfulness-based stress reduction, cognitive-behavioral therapy, and relaxation techniques demonstrate efficacy in reducing daytime clenching frequency. Sleep hygiene optimization addresses sleep quality factors that may exacerbate sleep bruxism.
Appliance Therapy
Custom-fabricated occlusal splints represent first-line management for sleep bruxism and TMD-induced bruxism. These hard acrylic or plastic devices worn over lower or upper dentition provide:
- Physical barrier protection preventing destructive tooth contact
- Occlusal force redistribution reducing peak loading
- Altered proprioceptive feedback potentially modulating trigeminal motor activity
- Possible vertical dimension changes improving muscle length-to-tension relationships
While evidence conclusively supports dental protection, debate persists regarding whether all appliances reduce bruxism frequency or merely protect teeth from bruxism consequences. Appliances with specific design intents to address the signs of TMD will be required to truly help with the frequency and severity of Sleep-Bruxism. Custom-fitted appliances demonstrate superior outcomes compared to over-the-counter devices.
Pharmacological Approaches
Limited evidence supports pharmacological management. Muscle relaxants may reduce muscle pain but show inconsistent effects on bruxism frequency. Botulinum toxin injections into masseter and temporalis muscles demonstrate efficacy reducing muscle force and bruxism intensity in refractory cases, though concerns exist regarding muscle atrophy and mandibular bone density changes with prolonged use.[3]
Comprehensive Management
Current management of sleep bruxism primarily involves oral appliance therapy, particularly stabilization splints, to reduce excessive mechanical loading on teeth and the masticatory system. Additional approaches such as biofeedback therapy and selected pharmacological interventions have been investigated; however, overall evidence for efficacy remains limited and further high-quality trials are needed.[4]
Conclusion
The association between TMD-induced bruxism and displaced articular discs provides important mechanistic insights, suggesting that addressing underlying joint dysfunction alongside protective appliance therapy offers optimal clinical outcomes.
Bruxism represents a complex orofacial behavior involving intricate interactions between central motor control, autonomic regulation, psychological factors, and biomechanical influences. Current understanding recognizes bruxism's multifactorial nature, requiring individualized assessment. The primary strategy should be focused on an oral, partially occlusal appliance while using the other multimodal management strategies as a backup.
