Bruxism

Last Modified: N/A
Date Created: September 2023

 

MPC 30680

ICD-11 DA0E.7

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DEFINITION

Bruxism is an umbrella term grouping together the repetitive masticatory muscle (jaw muscle) activities which include teeth clenching, teeth grinding and activity without tooth contact (bracing/thrusting of the mandible) either during sleep or when awake.

Bruxism is a repetitive masticatory muscle activity that may occur episodically but does not generally occur consistently.

Sleep bruxism and awake bruxism have different etiologies (causes) and comorbidities (other medical conditions that may occur at the same time).

  • Sleep bruxism (SB) is also referred to as nocturnal bruxism. It is a normal component of sleep behavior in healthy individuals. Sleep bruxism is rhythmic masticatory muscle activity (RMMA) side to side during sleep. It is not a movement disorder or a sleep disorder.
  • Awake bruxism (AB) is also referred to as diurnal bruxism. It is a normal involuntary behavior in healthy individuals. Most individuals are not aware of the activity. Awake bruxism is a masticatory muscle activity during wakefulness with repetitive or sustained tooth contact (clenching) and/or bracing or thrusting of the mandible. It is not a movement disorder.

For Veterans Affairs Canada entitlement purposes, Bruxism includes a diagnosis of sleep and/or awake Bruxism.

DIAGNOSTIC STANDARD

DIAGNOSIS: A diagnosis is required from a qualified dentist except for sleep bruxism which may also be confirmed by a Polysomnographic (PSG) test.

DIAGNOSTIC CONSIDERATIONS:

Supportive diagnostic evidence provided by the dentist should include the presence of relevant self-reported symptoms and clinical exam findings or investigations such as from Polysomnographic (PSG), Electromyography (EMG); and/or force sensing appliances.

Note: Attrition type tooth wear is not diagnostic for Bruxism. Attrition is a normal age-related process. The presence of attrition on exam, in the absence of any other symptoms or clinical findings, does not establish the diagnosis of current or ongoing Bruxism.

ANATOMY AND PHYSIOLOGY

The muscles responsible for movement of the mandible and chewing functions are called masticatory muscles. The primary masticatory muscles include:

  • the temporalis,
  • masseter,
  • medial pterygoid, and
  • lateral pterygoids.

The temporalis (lateral forehead) and masseter (cheek) muscles are responsible for jaw opening and closing while the pterygoid muscles move the jaw from side to side.

It is believed that the temporalis muscles are more prominently involved in tooth grinding activity which typically occurs during sleep; while the masseters are more involved in tooth clenching while awake. The primary masticatory muscle activity associated with awake bruxism is bracing/thrusting of the mandible without tooth contact and less commonly tooth clenching.

  • Sleep bruxism appears to be genetically determined. There is good evidence of an increase in sleep bruxism in individuals with familial history. Additionally, research has shown that several genes relating to dopamine biology appear to be associated with sleep bruxism in children. Since bruxism decreases with age this is consistent with the age-related reduction in dopamine receptors in the brain.

  • Sleep bruxism is considered to be part of the normal sleep cycle. Evidence supports it is a central nervous system phenomenon with activation of the autonomic nervous system which causes sleep-related micro-arousals.

    PSG studies have shown that sleep bruxism appears around micro-arousal episodes which are associated with an increase of brain activity, heart and respiratory rate elevation and increased jaw and oropharyngeal muscle tone. This is followed by an increase in masticatory muscle activity causing lateral tooth grinding.

    The episodes are typically short bursts of activity lasting 3-10 seconds, up to 8-15 times per hour, for a total of 2-6 min a night.

  • Awake bruxism is believed to play a positive role in coping with stress. While the physiology is unknown, it is believed that masticatory muscle activity including mastication, is a means of relieving tension and reducing stress. Current research has shown that individuals who perceive situations as threatening or stressful are more likely to have awake bruxism.

CLINICAL FEATURES

Bruxism is common and may cause transient tension or tenderness of the masticatory muscles and/or an acute inflammation of the joint lining with symptoms often described as tight, tired, tense, or painful facial muscles with jaw pain and difficulty opening. It should be noted that gum-chewing and nail biting may cause similar symptoms.

Treatment of Bruxism and/or reduction in gum chewing reduces any associated muscle pain.

Bruxism is considered to be a continuum of repetitive masticatory muscle activity which may be neutral, beneficial and/or be associated with a negative outcome as follows:

  • A harmless behavior considered a normal physiological process.
  • A protective factor when associated with a positive health outcome. For example, improving or restoring upper airway patency in relation to obstructive sleep apnea and/or as a relief factor for psychological stress.
  • In rare situations it may be a risk factor for development of other health outcomes.

Subject based indicators of Bruxism include self-reported history from the patient based on interviews or questionnaires, and more recently the use of smartphone apps. For sleep bruxism, reports from a bed partner of the presence of regular or frequent tooth grinding sounds during sleep is considered witnessed reporting.

Note: Self-reported and witnessed reporting are insufficient alone to establish a diagnosis.

Clinical examination findings by a qualified dentist can identify a diagnosis of probable Bruxism.

Clinical signs and symptoms of Bruxism (sleep and/or awake) include:

  • Extraoral clinical findings:
    • Most commonly, masseter muscle hypertrophy with or without pain. Masticatory muscle tenderness is described as tight, tired, tense, or painful facial muscles with cheeks feeling tired or sore when chewing.
    • There can also be hypertrophy of temporalis muscles with the presence of muscle fatigue and temporal headaches.
    • Individuals with awake bruxism (jaw thrusting, clenching) typically have an increase in symptoms of jaw muscle pain or fatigue as the day progresses.
    • Individuals with sleep bruxism (grinding) describe masticatory muscle fatigue or tenderness/pain and/or headache on waking.
  • Intraoral clinical findings:
    • Tongue scalloping: wavy or rippled edges that appear along the sides of the tongue.
    • Linea alba: a white line on the inside of the cheek where upper and lower teeth meet. It is a build-up of keratin caused by friction (frictional keratosis).
    • Morsicatio buccarum a type of frictional keratosis due to chronic irritation or injury to the lining of the cheek mucosa; most commonly due to cheek biting but has been documented in individuals with Bruxism.
    • Generalized tooth sensitivity.

  • Supportive investigations used to measure masseter muscle activity can identify a definite diagnosis of sleep bruxism. Currently, there are no definitive supportive investigations to confirm a definite diagnosis of awake bruxism.

    These investigations include:

    • Polysomnographic (PSG) study: PSG study during sleep laboratory recordings is the gold standard.

      PSG criteria for diagnosis of sleep bruxism are:

      • more than four Bruxism episodes per hour,
      • more than six Bruxism bursts per episode and/or 25 Bruxism bursts per hour of sleep, and
      • at least two episodes with grinding sounds.
    • Electromyography (EMG): EMG measures contraction of muscles during sleep. EMG classifies sleep bruxism based on muscle activity and EMG signal as:
      • tonic contraction more than 2 seconds,
      • phasic contraction of at least three muscles for 0.25-2.0 seconds separated by intervals, and/or
      • a combination of phasic and tonic contraction.
    • Force sensing oral appliances with embedded pressure sensors: These are used to record frequency, duration, and intensity of tooth clenching and/or grinding episodes.

While there are few large-scale population studies, it has been estimated that the incidence of overall Bruxism is between 5-30% with no differences between males and females. Bruxism peaks in adolescence and young adults with a steady decline in incidence over 40 years of age to a rate of about 3% in patients over 60 years. While there have been studies based on self-report that suggest an average prevalence of awake bruxism of 5%; and an average prevalence of sleep bruxism of 17%; at the time of publication, diagnostically confirmed prevalence is unknown.

ENTITLEMENT CONSIDERATIONS

Each case should be decided on the evidence provided and its own merits. The following lists are not all inclusive.

The factors listed in Section A have been determined based on a review of medical evidence to cause or aggravate (permanently worsen) Bruxism.

A. CAUSES AND/OR AGGRAVATION

In healthy individuals, sleep bruxism is a normal part of sleep, and awake bruxism is a normal response to stress, anger, anxiety, depression and when concentrating or during focused work. For VAC purposes, certain medical conditions and/or medications may cause Bruxism to progress to a chronic condition, or may aggravate a pre-existing condition.

Aggravation is a permanent worsening of a disability from disease or injury between enrolment and discharge as outlined in the VAC Policy Disability Resulting From a Non Service Related Injury or Disease.

Factors, other than those listed in Section A, may be considered on a case-by-case basis. The timelines cited below are provided for guidance purposes.

Factors: Awake bruxism

  1. Neurological Movement Disorder: Having a significant neurological movement disorder before the clinical onset or aggravation of Bruxism. These neurological movement disorders include, but are not limited to:
    • Parkinsonian disorders,
    • Cerebral Palsy.
  2. Psychiatric Conditions: Having a clinically significant psychiatric condition at the time of clinical onset or aggravation.

  3. Medication Use: Treatment with certain medications at the time of clinical onset or aggravation. Awake bruxism may be caused or aggravated by certain selective serotonin reuptake inhibitors (SSRIs) and/or certain serotonin and norepinephrine reuptake inhibitors (SNRIs). Symptoms typically present within 2-4 weeks of medication introduction or dose titration. Symptom resolution has been shown with the addition of buspirone, dose reduction or medication cessation.

    Medications that may cause or aggravate Bruxism include, but are not limited to:

    • Duloxetine / Cymbalta
    • Fluoxetine / Prozac
    • Paroxetine / Paxil
    • Sertraline / Zoloft
    • Venlafaxine / Effexor (XR).

    Note: If it is claimed a medication caused or aggravated Bruxism, the following must be established:

    1. The individual was receiving the medication at the time of clinical onset or aggravation of the Bruxism.
    2. The medication was used for the treatment of an entitled condition.
    3. The medication is unlikely to be discontinued, substituted, or the medication is known to have enduring effects after discontinuation (with stopping of the above medications, Bruxism typically resolves).
    4. The current medical literature supports the medication can result in the clinical onset or aggravation of Bruxism.

Note: Individual medications may belong to a class, or grouping, of medications. The effects of a specific medication may vary from the grouping. The effects of the specific medication should be considered and not the effects of the group.

Factors: Sleep bruxism

  1. Neurological Movement Disorder: Having a significant neurological movement disorder before the clinical onset or aggravation of Bruxism. These neurological movement disorders include, but are not limited to:
    • Parkinsonian disorders,
    • Cerebral Palsy.

  2. Medication Use: Treatment with certain medications at the time of clinical onset or aggravation. Sleep bruxism may be caused or aggravated by certain selective serotonin reuptake inhibitors (SSRIs) and/or certain serotonin and norepinephrine reuptake inhibitors (SNRIs). Symptoms typically present within 2-4 weeks of medication introduction or dose titration. Symptom resolution has been shown with the addition of buspirone, dose reduction or medication cessation.

    Medications that may cause or aggravate Bruxism include, but are not limited to:

    • Duloxetine / Cymbalta
    • Fluoxetine / Prozac
    • Paroxetine / Paxil
    • Sertraline / Zoloft
    • Venlafaxine / Effexor (XR).

    Note: If it is claimed a medication caused or aggravated Bruxism, the following must be established:

    1. The individual was receiving the medication at the time of clinical onset or aggravation of the Bruxism.
    2. The medication was used for the treatment of an entitled condition.
    3. The medication is unlikely to be discontinued or the medication is known to have enduring effects after discontinuation (with stopping of the above medications, Bruxism typically resolves).
    4. The individual’s medical information and the current medical literature support the medication can result in the clinical onset or aggravation of Bruxism.

    Note: Individual medications may belong to a class, or grouping, of medications. The effects of a specific medication may vary from the grouping. The effects of the specific medication should be considered and not the effects of the group.

  3. Intake of Alcohol, Tobacco, and Caffeine: Clinical onset or aggravation of sleep bruxism is positively associated with alcohol, tobacco, and caffeine use.
  4. Obstructive Sleep Apnea (OSA): OSA at the time of clinical onset or aggravation of sleep bruxism. There is good evidence of an increase in sleep bruxism in individuals with Obstructive Sleep Apnea (OSA) as a protective factor to prevent the collapse or restore the patency of the upper airway.
  5. Neurological disorder: Having a neurological disorder before the clinical onset or aggravation of Bruxism. These neurological disorders include, but are not limited to:
    • epilepsy
    • stimulation of brain activity in individuals with cognitive decline.

Note: There is insufficient evidence at the time of publication to establish for entitlement purposes a consequential relationship between Gastroesophageal Reflux Disease (GERD) and the clinical onset or aggravation of Bruxism.

B. MEDICAL CONDITIONS WHICH ARE TO BE INCLUDED IN ENTITLEMENT/ ASSESSMENT

Section B provides a list of diagnosed medical conditions which are considered for VAC purposes to be included in the entitlement and assessment of Bruxism.

  • None

C. COMMON MEDICAL CONDITIONS WHICH MAY RESULT IN WHOLE OR IN PART FROM BRUXISM AND/OR ITS TREATMENT

Where the merits of the case and dental evidence indicate that a possible consequential relationship may exist related to Bruxism, consultation with a Disability Consultant and/or Dental Advisor may be required.

Note: At the time of publication, the medical evidence indicates Bruxism does not cause or aggravate Dental Erosion or Dental Abrasion.

TAGS: Veterans Affairs Canada, Disability Benefits, Pain and Suffering Compensation, Entitlement, EEG, Guideline, Bruxism, Sleep Bruxism, Awake Bruxism.

REFERENCES

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