Sleep Bruxism



During sleep it is common for the lower jaw to move around. This is termed Rhythmic Masticatory Muscle Activity or RMMA. This consists of two forms of muscle activity: a series of repetitive contractions or an isolated sustained contraction of jaw clenching. These muscle contractions, when extreme, produce the tooth grinding sounds during sleep and are referred to as Sleep Bruxism (SB). It is often reported by a spouse that the sound of the teeth is disturbing and waking them. The patient is usually unaware that they are doing this as it occurs once they are asleep. It is often their bed partner that alerts them to this.

The World Health Organization (WHO) have created an international classification of diseases with a specific code being given to every disease known. They break the diseases down into categories or systems. The following flow chart summarizes this (click to enlarge):

This classification from WHO differentiates awake bruxism and sleep bruxism. Sleep bruxism is a disease of the nervous system, or neurogenic, whereas awake bruxism is classified under mental and behavioral disorders. They are diagnosed and treated very differently and cannot be considered related. It should be noted that both disorders can and do occur together in the same patient.

The Center for Disease Control (CDC) in the USA also use the WHO classification except that they add “clinical modifications” to it. This is designated as CM following the WHO coding (for example, sleep bruxism would be ICD-10 G47.63 CM under the CDC classification). The clinical modification for sleep bruxism is that it excludes awake bruxism and awake bruxism (ICD-10 F48.3 CM) excludes  sleep bruxism.

As sleep bruxism is a central mediated disorder (the brain triggers the event) there is a cascade of events that occurs:

  1. there is an increase in heart rate and blood pressure
  2. there is an increase in EEG (brain electrical) activity
  3. the muscles above the hyoid (Adam’s apple) bone activate
  4. the masseter and temporalis jaw muscles contract
  5. often finishes with a swallow reflex

This sequence of events occurs with every Sleep Bruxism event and can occur hundreds of times each night.

Rhythmic movements such as chewing and bruxing are controlled by central pattern generators (CPG) within the brain. Mastication (and sleep bruxism) are driven by the hypoglossal nucleus, which is controlled by the dorsal medullary reticular column (DMRC) and the nucleus of the tractus solitaries (NTS). It has been recently found that patients suffering from sleep bruxism have a genetic mutation of gene HTR2A rs2770304, which is involved in the release of serotonin (a neurotransmitter in the brain and gut) occurs in multiple copies (polymorphism) resulting in too much serotonin being released into the brain. This results in suppression of the neurons that prevent the jaw muscles from contracting too hard and inactivation of the masseter inhibitory reflex. The result is increased frequency and intensity of contraction of the masseter and temporalis muscles resulting in damage to the teeth, jaws, muscles and TMJ. Serotonin acts on the inhibitory neurons in another way. There is a connection from these neurons to the dorsal motor neuron of cranial nerve 10, the vagus nerve. This nerve controls heart rate (as well as a number of important functions) resulting in stimulation of the heart and an increase in heart rate with each bruxism event. This combination of serotonin suppressing the inhibitory neurons (allowing 100% muscle contraction) and stimulation of the dorsal motor neuron of the vagus nerve, explains the mechanism behind sleep bruxism. Because the cause is polymorphism of the HTR2A rs2770304 gene, sleep bruxism cannot be cured at this time, only controlled.

Recently, restless leg syndrome was linked to cardiovascular disease, due to the increase in heart rate and blood pressure associated with restless leg syndrome. To date, there have not been any studies of sleep bruxism, with its associated increase of heart rate and blood pressure but is likely only a matter of time before this relationship is also confirmed.

Those who suffer from sleep bruxism demonstrate an interesting finding: when they lightly touch their incisors together (as in biting a piece of thread), the lower jaw will begin to shake or tremor. This finding is a positive sign of active sleep bruxism.

The forces generated by sleep bruxism are much greater than when awake:

  • Chewing meat = 25 psi (pounds per square inch)
  • Chewing a hard carrot = 28 psi
  • Biting as hard as you can when awake = ~30
  • Sleep Bruxism can exceed 100-150 psi in some individuals

This is due to a reflex of the jaw muscles, the masseter inhibition reflex (MIR) being suppressed by sleep bruxism. The MIR normally restricts how hard the masseter muscle contracts, limiting it to safe levels. During sleep bruxism, this reflex is effectively turned off and the masseter contracts with 100% of its force. The forward bite of the Luco Hybrid OSA Appliance re-establishes this reflex during sleep, preventing over-contraction of the masseter, allowing it, and the other associated muscles to relax and heal. This is the primary mechanism in which this advanced device reduces significantly or completely eliminates sleep bruxism events  and their duration during sleep.

The following screen shot of a sleep study of a sleep bruxism patient demonstrates the elimination of sleep bruxism events, stabilization of the patients respiration and stabilization of the heart rate (which was being affected by the sleep bruxism).


As you can see, the forces generated during sleep bruxism are substantial and can potentially cause very serious damage. Left untreated, this condition can cause progressive irreversible damage to the teeth, surrounding bone, jaw bones, musculature, and TMJ. Sleep bruxism is a significant cause of TMJ problems due to the considerable pressure placed on the TMJ during sleep bruxism events (it only takes about 15 psi to cause damage to the TMJ).

80% of the time, Sleep Bruxism occurs together with sleep apnea, as they are both sleep disorders. If is estimated that 8% of the population suffer from Sleep Bruxism and about 16% from sleep apnea. Sleep Bruxism occurs in over 30% of OSA cases! In 20%, Sleep Bruxism occurs independently of sleep apnea on its own.

Sleep Bruxism occurs in different forms:

  • Tonic or clenching type
  • Phasic or grinding type
  • Mixed or a combination of both types

Sleep related bruxism is usually diagnosed by either the patient (with changes to their teeth or jaws or pain symptoms), the dentist (with clinical signs such as premature failure of fillings, abfraction lesions etc.) or by a sleep specialist during a sleep study.

It has been proposed for a sub-classified into three subtypes:

  1. Possible: patient reported symptoms without clinical signs
  2. Probable: patient reported symptoms with clinical signs
  3. Definite: patient reported symptoms, clinical signs and an overnight sleep study with muscle recording (supported by a microphone or video recording).

Dental radiographs can identify the effects on the jaws from sleep bruxism. The following image shows a panorex (orthopantomograph) of a normal patient. The second shows the effects of sleep bruxism. The first demonstrates calcified stylomandibular ligaments (ligaments that restrict the range of motion of the lower jaw to normal movements) and antigonial notching or a bend in the lower jaw caused by tonic sleep bruxism (clenching type) involving the masseter and medial pterygoid muscles. The lower border of the mandible should be straight and not bent as seen. The ligaments are soft tissue and should not show on a radiograph. This is termed Eagle’s Syndrome. They should not be seen on a radiograph.

The second panorex demonstrates coronoid elongation or stretching of the coronoid process (attachment of the temporalis muscle) caused by tonic sleep bruxism involving the temporalis muscles. The orange dotted line marks the highest point of the coronoid process. In a normal individual, this line should pass through the yellow dots on the condyles (balls) of the TMJ.

SB does not require a sleep study for diagnosis and treatment, a dentist can diagnose this and treat it in their office from the signs and symptoms observed. If the dentist suspects a concurrent sleep disorder, they are obliged to refer the patient for a sleep study to ensure all the sleep problems are being addressed.  There are medical conditions that have bruxism as a symptom ( such as faciomandibular myoclonus, SRBD, RBD, abnormal swallowing, gastro-esophageal reflux, night terrors, confusional arousals, dyskinetic jaw movements persisting in sleep (dystonia, tremor, chorea, dyskinesia), and, rarely,  in sleep related epilepsy). If the dentist is unsure, a sleep study is the always the best course of action.

Sleep studies can accurately record sleep bruxism if equipped to record this. The following tracings are an actual patient’s recordings using a 12 channel Type 3 sleep monitor (Medibyte Event) with electromyographic (EMG) muscle recording module. The first is a tracing of normal sleep and the second demonstrates numerous sleep bruxism bursts (click to enlarge).

In the second tracing above, the amplitude or amount of force being generated is in the range of 10-14 x the normal maximum bite when awake. These bruxism events or bursts can occur hundreds of times per night, disturbing the patient’s sleep. The Epworth Sleepiness Scale is used to screen patients for excessive sleepiness. With OSA it is >10. With only Sleep Bruxism patients score in the 6-9 range for sleepiness.

SB can be destructive to the teeth, the supporting bone and gum tissues, the TMJ complex including the neck, and the musculature. The effects often result in hypersensitivity of the teeth to temperatures, headaches (particularly in the temple region upon waking), repeated damage to the teeth and sleep disruption. SB can jam cranial sutures affecting normal CSF flow (from the ventricles of the brain through the spinal cord). These excessive forces cause shifting of the teeth and can relapse orthodontic treatment.

This condition is usually diagnosed when a patient brings the symptoms up to the attention of their dentist or doctor. In younger healthy patients with SB, there is less sleep disruption.  Often jaw muscle pain affecting the massater (main cheek muscle) and temporalis (the muscle on the side of the head) muscles are reported with associated morning headaches. Fatigue in the muscles and limitation is opening upon waking are common with SB.

SB can shorten the life of an OSA appliance. Acrylic appliances can break under the increased force of SB. This is a concern as small pieces of broken appliance may be swallowed or aspirated into the lungs during sleep. The Luco Hybrid OSA Appliance is designed to withstand this and breakage is extremely rare (less than 3 cases in 3000). Because of this, this appliance can last in excess of 4 years with some lasting much longer.

There are a number of signs and symptoms related to SB. It should be noted however, that some people with SB have very few symptoms and only experience disturbances in sleep. The following table outlines the signs and symptoms of SRB commonly seen:

Unpleasant tooth and muscle sensations Flattening or excessive wear of the teeth
Limitations of jaw movement, TMJ pain Fractured teeth and fillings, vertical cracks in teeth
Orofacial Pain (pain around the face region) Waking with the jaw locked, unable to open wide for a few minutes.
Temporal/tension headaches on waking or later in the day Abfraction lesions (painful notching of the roots at the gum line

SB varies considerably between individuals regarding intensity and duration. In most cases it occurs hundreds of times a night. There is no direct link, however, between the severity of SB and the symptoms a patient will present to their dentist or doctor with. SB is indexed by the number of SB events per hour. Interestingly, patients with RMMAs of 2-4 per hour are much more likely to report muscle pain than more severe cases of > 4 RMMA/hour. The normal range of sleep bruxism events is <5 per hour or a bruxism index of <5.

Psychological factors may also be linked to SB. Currently there is a weak correlation between SB and psychological stress in both adults and children. Healthy patients with SB tend to have higher scores regarding stress, anxiety and psychiatric scales compared to patients without SB.

There are two subtypes of SB: Primary SB which occurs without any clear cause and Secondary SB which often occurs in children with medical diseases such as Cerebral Palsy, and other forms of mental retardation.  Myoclonus is a muscular disorder (either oro-mandibular or facio-mandibular) that is associated with SB in adults.  Sleep related breathing disorders (OSA and UARS) commonly occur with secondary SB.

The research has shown that SB is highest in children at about 14-17%. In teenagers and young adults, it has been reported to drop to about 12%. It drops to 8% in young to middle age patients and down to around 3% in elderly patients. In elderly, the significant drop may actually be due to decreased reporting and may actually be higher. Because of the overlap of symptoms of other conditions such as migraine syndrome (headaches in the same regions) and the variability in symptoms (some patients have no symptoms and would therefore not be included in these stats). Clinically however, most dentists see the results of SB much more often and more research is needed regarding epidemiology of this disease.

As well, severe SB in childhood may persist as severe throughout the lifetime of the patient. In these patients, the symptoms do not follow the normal progression of decreasing with age. There is also a relationship between SB in children and Attention Deficit Disorder Syndrome (ADHD), parasomnias  (such as confusion arousals, sleep-walking, sleep talking, head banging and sleep relating eating disorder), sleep related breathing disorders, snoring, and many psychological and medical conditions. Variability is high resulting in many patients not being diagnosed. SB occurring in childhood persists into adulthood in more than 65% of the cases!

Genetic patterns in SB are possible as this tends to be seen in families with approximately 20-25% of affected patients having a close family member with a history of sleep related bruxism. To date, no gene mutations have been linked to primary SB in genetic testing, but in the future genetic testing may identify genes and could be used to screen patients for this disorder.

Interestingly, SB can start at any age. It is very difficult to study as the symptoms are so variable they are not reported by the patients to their doctors until the symptoms are affecting them significantly. The condition could have been present for years before being reported. Often the symptoms are not related to sleeping and treated (sometimes inappropriately) as other conditions, leaving the condition untreated and allowing it to persist.

It should be noted as well that RMMA occurs in everyone. In normal sleep RMMA is observed at about 1 episode per hour of sleep. However, with SRB the contractions are not only more often, but with much greater intensity (in the range of 10-14X normal chewing pressure). SRB also can vary considerably night to night. Sleep studies can miss this at a rate of up to 25% of the time due this nightly variability in some cases.

E.E.G. Findings:

Electroencephalogram (EEG) tracings have found differences between men who suffer from sleep bruxism. Women affected by sleep bruxism show a significantly lower Theta and Alpha EEG activity during sleep compared with normal subjects. This was found to be true regardless of level of associated pain reported. When muscle recording is included in the EEG tracing, a significant increase in activity of the masseter and temporalis muscles is seen. This is associated with an increase in heart rate and blood pressure.

Clinical Findings:

Abnormal wear of the teeth and dental damage are the most common signs of SB. It is important though to differential SB and tooth wear from an abrasive diet which can look similar. Disorders of the TMJ are common (pain and clicking in the TMJ, closed locking).

Muscular Hypertrophy:

Hypertrophy or enlargement of the jaw muscles can occur in some people, primarily in the massater and temporalis muscles. The following sections will outline the types of dental problems that are commonly seen with SB. The following image demonstrates hypertrophy or bulking up of the masseter muscle as is seen with severe sleep bruxism.

Fractured Roots: Although rare, root fractures are very painful and require urgent dental care (removal). Root fractures are caused by excessive lateral or side-to-side pressure on the teeth such as occurs in sleep-related bruxism.

Cracked Teeth: These are common and also are very painful requiring urgent dental care (removal). Cracked teeth are caused by excessive vertical pressure or downward pressure on a tooth causing it to split through the roots. This can be caused by the pressure of sleep-related bruxism over time. Initially, the tooth will be hypersensitive to hot and cold as well as biting on hard foods. As it progresses, the symptoms worsen until the tooth cracks in two.

Cracked Fillings: Fillings are not as strong as teeth and the effects of sleep-related bruxism accelerates wearing of the filling.  The life span of fillings in the presence of sleep bruxism is dramatically reduced.

Abfraction Lesions: Painful notches at the neck of the tooth used to be blamed on aggressive tooth brushing. It is now known that this is a direct result of excessive lateral side-to-side pressure on teeth as is seen in sleep bruxism. The enamel at the gum line  chips off and the exposed dentin, which is softer, wears away very quickly leading to the characteristic notches seen in abfraction lesions. These are challenging to manage as fillings do not hold well in these areas unless the source of the problem, the sleep bruxism, is treated. Gum recession in the area of the abfraction lesion is common and can lead to bone loss between the teeth and loosening of the teeth.

Excessive Tooth Wear

Tooth wear is a normal part of aging. It becomes a concern when it occurs at an accelerated rate. With sleep bruxism, this occurs often disfiguring of the teeth or shortening them so far that root canals become necessary due to exposure of the nerves. Sometimes the teeth are so badly worn they can only be removed. If this occurs in primary teeth in children, this can affect the position of the erupting permanent teeth as the permanent teeth only erupt to the height established by the primary teeth.

Other Dental Problems that Can Occur:

  • loosening of teeth due to excessive pressure during grinding, bone loss around the tooth, and/or stretching of the ligaments that attach the teeth to the jaw bone
  • acceleration of periodontal bone loss due to excessive loading of the teeth during sleep
  • fractured cusps of teeth (corners of the teeth breaking off)
  • hypersensitivity to hot, cold and sweet
  • healthy teeth requiring root canal therapy for unknown reason (due to the teeth being compressed into their sockets restricting blood flow into the tooth and tooth nerve death).

Chronic Myofascial Pain (CMP)

Myofascial pain refers to pain originating in the muscles and fascia covering of the muscles that refers pain to adjacent regions or structures. The hallmark of myofascial pain is the development of trigger points, which are painful spasms inside a larger muscle group that feel like a knot or lump in the muscle. These muscle spasms can persist for months and even years and cause a myriad of symptoms. A primary trigger point can spread into other muscle groups and form secondary trigger points. in this way, the condition can spread and cause widespread pain symptoms. There is some evidence that CMP has a genetic basis and is activated by a trauma. In the case of sleep-related bruxism, the trauma is obvious: the overloading of the muscles.

When a trigger point develops in the muscles of the head and neck regions, the  referred pain is interpreted as a headache. Depending upon which muscle is affected will determine where the headache occurs. It should be noted that hypoxia or low oxygen levels while sleeping also causes headaches (sleep apnea, UARS) from the low oxygen levels. There are a series of muscles of the jaws that are involved in opening, closing, retracting, advancing and moving the jaw laterally side-to-side. The closing muscles are the chewing muscles however there are a series of neck muscles also involved that support the mandible, support the skull and support the neck when chewing. Sleep-related bruxism and UARS are both associated with chronic myofascial pain and the development of trigger points in these muscle groups. The following images show the most common areas in these muscles where trigger points commonly develop (x) and the expected referral patterns (headaches) from the trigger points (in red).

The Masseter Muscle

The Medial Pterygoid Muscle

 The Temporalis Muscle

 The Digastric Muscles

 The Sternocleidomastoid Muscle

 Trapezius Muscle

Jaw Problems: TMD (Temporomandibular Dysfunction)

Temporomandibular Dysfunction refers to disorders involving the TMJ or jaw joints. Excessive pressure exerted by the chewing muscles may cause a compression of the TMJ. This can trigger capsulitis of the back joint compartment of the TMJ resulting in severe pain when biting. This pain is caused by inflammation of the TMJ and, as it is encapsulated or in a capsule, the posterior or back joint compartment swells painfully forcing the entire mandible forward. This alters the bite resulting in difficulty closing the back teeth together and the front teeth hitting harder than normal. This is usually self-limiting and heals in a few weeks. It should be noted that patients with deep overbites can have this last much longer as their lower jaws naturally sit too far back. The back area of the TMJ is where all of the nerves and blood vessels reside. The American Academy of Sleep Medicine recognizes that patients with severe Sleep Related Bruxism can experience TMD problems and locking of the jaw upon waking is a common symptom in severe SRB.

 Normal TMJ Function: The disk (yellow in animation) stays between the bones at all times preventing bone wear and arthritis. The loading or pressure of the bite is directed through the disk at all times protecting the bones from damaging wear. There is never any pressure on the back portion of the joint and the nerves and blood vessels. (click to see animation)

Clicking TMJ: When the upper jaw does not develop to a normal size (as seen in many SB and OSA patients), the lower jaw can become too long for the upper. When biting, this excessive length of the lower jaw is expressed back towards the ear canals. The disk in the joint slips forward and, when the patient is biting, the TMJ becomes dislocated. On opening, the disk must re-seat into normal position with the characteristic click or popping sound. With this type of misalignment, the lower jaw is positioned too far back in the joint compressing the nerves and blood vessels of this region. Patients with clicking jaw are at much higher risk of capsulitis (pain and swelling of the TMJ) due to this positioning. Many chronic ear conditions can be attributed to capsulitis of the TMJ. This can also result in abnormal function of the Eustachian tubes resulting in difficulty in equalizing pressure in the inner ear.

The timing of the click in the opening cycle determines the prognosis for the TMJ. An early click, meaning the disk pops back into alignment quickly, indicates a relatively healthy disk. If the click is later, nearer to wide opening, the prognosis is not as good as the disk is dislocated for more of the opening cycle. If the ligaments that attach the disk to the jaw bone (condyle) stretch so much that they tear, a closed lock occurs. The symptoms of a closed lock are very restricted opening and side to side movement, severe muscle pain in the jaw and neck muscles, and disturbed sleep patterns (due to the pain).


Non-Reducing Closed Lock: This occurs when the disk tears free of the jaw bone sliding forward (and usually inward) blocking the normal movement of the jaw. This is often a very sudden and painful occurrence requiring urgent dental attention. If acute,  the jaw will be restricted to about 28mm and accompanied by severe muscle spasms on the affected side. If left untreated, it will stretch out to 32-34 mm but the muscles usually develop painful trigger points. A normal opening is 45-52 mm or three fingers wide, and about 10 mm left, right and forward. With a closed lock, the jaw movement is blocked on the locked side so the jaw cannot move forward or to the side.  Typically, the jaw would deviate to the affected side as the healthy joint would move and the locked joint would not. If both joints are involved, there would be no movement to either side, and no movement forward possible.

Patients with chronic closed locks eventually stretch their ligaments and can open up to 38-40mm with 4-5 mm side to side and 5-6 mm forward. This restriction is functional but almost always accompanied by painful headaches due to numerous trigger points.


Before a diagnosis of sleep bruxism can be made, there are other medical conditions with similar symptoms that must be ruled out. TMD or Temporomandibular Dysfunction is fairly common disorder of the jaw joints and chewing muscles that can have similar symptomology. It is not uncommon for TMD sufferers to have disturbed sleep patterns due to chronic pain. Limitation in opening is common due to myopathy, as are waking with headaches and headaches lasting into the day. Clenching is more common than grinding (tonic awake bruxism) in this group and damage to teeth such as excessive wear and abfraction lesions are also common (phasic awake bruxism). There is usually cervical (neck) involvement of the pain in TMD and often a precipitating event (such as a whiplash injury, jaw injury, blow to the face etc.). It should be noted however, that SB and TMD can and do often occur in the same patients, as TMD patients may also have OSA or UARS predating the TMD. These are, by far, the most difficult patients to treat but also the most rewarding when treatment succeeds in treating both conditions. The Luco Hybrid OSA Appliance was designed specifically for these patients. It effectively treats TMD, Chronic Myofascial Pain, Sleep Bruxism  and Sleep Apnea simultaneously. With thousands of patients treated, this appliance is clinically proven and very effective.

As discussed earlier, there are some medical conditions that overlap symptoms with SB as well. Some of these include oro-mandibular myoclonus, facio-mandibular myoclonus, SRBD, RBD, abnormal swallowing, GERD, night terrors, confusional disorders, dyskinetic jaw movements persisting into sleep (dystonia, tremor, chorea and dyskinesia) and rarely, sleep related epilepsy. SRB is much more common than any of these disorders but they still must be considered before initiating treatment for SRB as they may require other medical treatments to manage.

Oro-mandibular or Facio-mandibular Monoclonus occurs in a fairly high number of SRB patients (10%). It is also seen in patients with excessive RMMA events during sleep. Facio-mandibular Monoclonus is much different than SRB. It consists of very short bursts of muscle activity of very short duration as opposed to longer sessions of grinding and clenching associated with SRB. This can only be diagnosed with a sleep study recording the muscle activity.

With partial complex or generalized seizure disorder, rhythmic jaw movements are also seen. Because of this, these disorders should always be considered in the differential diagnosis of SRB and a medical consultation is always prudent before treatment.

Until recently there were no recognized treatments of Sleep Bruxism. The Luco Hybrid OSA Appliance is now the first and only recognized treatment of sleep bruxism making this device truly unique and separates it from all other OSA appliances.

The Luco Hybrid OSA Appliance is the only sleep apnea appliance that is FDA cleared for the treatment of patients suffering from sleep apnea and sleep bruxism. These two diseases occur in over 30% of sleep apnea cases!