Bruxism

The etiology of bruxism is a complex and controversial issue, especially the different manifestations relating to the circadian rhythm (i.e., sleep and awake). The condition should be viewed as a muscle behavior that reflects the presence of one or more underlying conditions or factors.[15]

Many etiologic theories for sleep bruxism (SB) have been proposed. The multifactorial model to explain its onset, postulating that a complex set of factors interact with central nervous system function and sleep regulation, seems to be the most plausible hypothesis.[16][17] Consensus suggests an ongoing paradigm shift from peripheral (i.e., occlusal) to central (i.e., stress, emotions, personality) regulation.[18] However, the belief that bruxism and dental (mal-)occlusion (the bite) are causally related has not been fully abandoned.

One review determined that neither occlusal interferences nor factors related to the anatomy of the orofacial skeleton are involved in the etiology of bruxism.[19] The lack of association of bruxism with occlusal morphology has important ethical implications for the dental profession.[20]

The etiologic focus in SB is mainly on central factors, such as psychosocial disorders (e.g., stress sensitivity, anxious personality traits), physiologic-biologic factors (e.g., neurochemicals), genetics, and exogenous factors (e.g., smoking).[21][22][23][24][25][26][27][28] In comparison, awake bruxism (AB) is associated with emotional tension or psychosocial disorders causing prolonged contraction of masticatory muscles. It may be the result of a transient anxious reaction to stressful daily events or related to a more chronic anxiety disorder.[21]

Trait anxiety is associated with both increased masseter muscle activity and intensity of wake-time tooth clenching episodes and, therefore, with an increased occurrence of AB episodes.[29][30]

Most literature on bruxism pathophysiology focuses on SB and comparatively little is known about the actual cascade of events leading to AB.

SB is part of a complex arousal response of the central nervous system, and features a combination of all bruxism activities, e.g., short- or long-lasting tonic clenching and phasic grinding of masticatory muscles, with or without teeth contact.[31]

AB is commonly characterized by teeth contacting habits or mandible bracing. This leads to the hypothesis that AB is mainly a consequence of stress sensitivity, such as stereotyped reaction to external stressors.[21]

The study of bruxism pathophysiology also involves its relationship with potential clinical implications. Prosthodontic complications, mechanical tooth wear and pain in the jaw muscles or the temporomandibular joints (TMJ), are examples of potential negative outcomes due to bruxism.[3][4][5][6]

The relationship between bruxism and pain is controversial, with contrasting literature findings.[6] Investigations based on self-reported or clinical bruxism diagnosis show a positive association with TMJ pain, but studies based on polysomnography (PSG) or electromyography (EMG) to diagnose bruxism show a much lower association with TMJ symptoms in general.[6]

Hypotheses to explain such contrasting findings suggest that bruxism, and consequently jaw muscle EMG activity, decreases with pain chronicity.[32] In addition, PSG/EMG devices can only offer a count of sleep bruxism episodes, without any information on the actual amount of muscle work or bruxism during wakefulness.

One study showed that patients with temporomandibular disorders (TMD)-related pain have elevated background levels of muscle activity during sleep, which may be indicative of tonic, prolonged, low intensity mandible bracing that provokes exhaustion of muscle fibers and joint load.[33] The amount of muscle work, in turn, is related to trait anxiety scores.[22]

Historically, classifications of bruxism have varied widely. An international consensus meeting in 2017 defined and classified bruxism as follows:[1]

Sleep bruxism (SB): a masticatory muscle activity during sleep that is characterized as rhythmic (phasic) or nonrhythmic (tonic) and is not a movement disorder or a sleep disorder in otherwise healthy individuals.
Awake bruxism (AB): a masticatory muscle activity during wakefulness that is characterized by repetitive or sustained tooth contact and/or by bracing or thrusting of the mandible and is not a movement disorder in otherwise healthy individuals.

The international consensus also proposed that bruxism may be classified according to clinical consequences:[1]

Not a risk factor or protective factor: bruxism is a behavior that does not cause harm.
A risk factor: bruxism is associated with one or more negative health outcomes. These include temporomandibular joint pain, masticatory muscle pain, excessive tooth wear and prosthodontic complications.[3][4][5][6]
A protective factor: bruxism is associated with one or more positive health outcomes. These may include preventing collapse of the upper airway while sleeping in patients with obstructive sleep apnea, releasing emotional tension, or promoting salivation to protect the teeth in patients with gastroesophageal reflux disease.[2]

Pathophysiology

Classification