A post on bruxism (part 2)

From Contemporary oral medicine 2019

The etiology of SB is largely unknow but current theories hypothesise that SB is centrally mediated probably in the brainstem and has a multifactorial etiology.

• Sleep arousal is a brief awakening from sleep (3-15s) characterised by increased EEG, autonomic, cardiac and muscular activities without a complete return to consciousness. These normally occur <15 times an hour in response to external or internal stimuli. The association between sleep arousals and RMMA is well estabilished but they shouldn't be considered as the only cause or trigger of SB as they may be the window that allows RMMA during sleep. Additionally, arousals represent the end result of a multitude of physiological events involving the SNS, movement and respiration that may be more to blame.
• Genetics and familial predisposition: The level of evidence supporting a genetic predisposition to SB is low however there is a high proportion of SB subjects who have a family member who exhibits SB.
• Breathing and breathing disorders: A recent hypothesis is that SB may be triggered by respiratory changes during sleep e.g desaturations, RERAs, apnoeas, hypopneas and the associated RMMA may allow the restoration of upper airway patency. This aligns with the observation of snoring and OSA as a common comorbidity to SB. A reduction in SB can be seen following treatments for OSA such as MAS, T+A surgery and CPAP. This can be supported in PSG studies where RMMA events correlated with the severity of AHI and had a temporal relationship after desaturations. Conversely, a proportion of RMMA can be seen before OSA events or even temporally unrelated.
• Personality traits, stress and anxiety: The level of evidence is low but anxious and stress prone personality types have been linked to increased SB. SB subjects appear to have maladaptive coping strategies, be more anxious, stressed and task oriented. Confounding factors need to be considered such as alcohol caffiene and cigarette consumption as well as medication and drug use.

Pathophysiology of SB:

RMMA doesn't appear to have cortical involvement which diferentiates it from conscious awake chewing but it does appear to have strong autonomic nervous system involvement. RMMA is more frequently observed in NREM sleep, during sleep stage shifts especially in the transition from NREM to REM sleep. The majority of RMMA episodes in the young and healthy population occur in association with sleep arousals and has a characteristic sequence of events: 1. a rise in sympathetic cardiac activity 4-8 minutes before RMMA. 2. EEG activity frequency increases 4 seconds before RMMA. 3. Tachycardia occurs 1 second before RMMA. 4. Suprahyoid muscle activity increases 0.8 seconds before RMMA. In some individuals a big breath is noted. 5. RMMA activity occurs in the masseter muscles resulting in tooth grinding

Comorbidities:
SB has been associated with other sleep disorders (e.g PLMS, OSA, insomnia), pain complaints (e.g headache, orofacial pain, TMD), neurologic disorders (e.g epilepsy, REM behaviour disorder, traumatic brain industry, Parkinson's disease) and behavioural disorders especially in children (e.g inattention and hyperactivity).