What is Sleep Bruxism?
Sleep bruxism is an inherited neurological sleep disorder classified by the American Academy of Sleep Medicine as a movement-type sleep disorder similar to restless leg syndrome. Sleep bruxism is not the same as awake bruxism which is classified as a reaction to severe stress.
Sleep Bruxism occurs in 26% of children under 6 years of age, in 14% of teenage young adults and in 12% of adults over 18 years of age. It affects men and women equally however the presentation of symptoms can be quite different. It should be noted that not all sleep bruxism patients present with all symptoms and some may be symptom free.
Sleep bruxism is very damaging to the teeth, jaws, muscles, and TMJ. It is a significant cause of tension/migraine type headaches and tooth sensitivity. It affects the heart and disturbs sleep. The following is a system by system summary of the current knowledge of sleep bruxism.
Central Pattern Generators
Rhythmic movements such as chewing and bruxing are controlled by central pattern generators (CPG) within the brain. These are neural loops that create cyclical signals independent of higher brain function for certain activities such as walking, swallowing and chewing. Chewing (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) (above).
During sleep bruxism events, these central pattern generators are abnormally stimulated resulting in the “chewing” and “clenching” type events characteristic of sleep bruxism.
Genetics and Sleep Bruxism:
Many disorders have a genetic basis to them and sleep bruxism is no different. There is a growing body of evidence for a genetic basis for sleep bruxism. It is common for family members to suffer from this condition, supporting this theory. One gene identified to date is the HTR2A gene on chromosome 13. HTR is short for serotonin, a neurotransmitter and the 2a refers to a receptor type.
The HTR2A Gene creates a protein that forms into the 2a receptor for serotonin.
In sleep bruxism, there are multiple copies of the gene termed “polymorphism”. This creates too many serotonin receptors.
In function, too many receptors result in an increase of stimulation/suppression of key centers of the brain.
In sleep bruxism, serotonin acts to turn off key control centers and activate others. as discussed, the central pattern generators controlling chewing are activated. Other key areas are shut down or suppressed.
One of these key regions is the masseter inhibitory reflex, a protective reflex that prevents one from biting too hard. In sleep bruxism, this protection is lost. The masseter, temporalis and posterior digastric muscles are all affected by this mutation and are allowed to contract with 100% bite force during sleep bruxism events. Women with sleep bruxism generate forces of 70-90 lbs and affected men generate forces of 100-120 lbs. Normally forces of 15-25 lbs are generated with chewing hard foods.
The HTR2A gene has been extensively studied in medicine relating to psychiatric disorders (a different mutation). A second gene identified is the DDR3 gene located on chromosome 5. This gene is involved with receptors for dopamine. This exact mechanism is not understood. The HTR1A gene, similar to the HTR2A, is also a serotonin receptor that usually has the opposite effect of the HTR2A gene and has also been implicated in sleep bruxism (the central pattern generators).
The inheritance pattern of the HTR2a mutation is dominant meaning that if one parent has the mutation and sleep bruxism, 1/2 of the offspring will be affected.
If both parents have the mutation, 3 out of 4 offspring are affected!
Both Parents Affected (Carriers):
Genes can be active or latent. A gene for a condition can be activated by certain events. In sleep bruxism, trauma to the face or jaws (if motor vehicle accident or injury) can activate the HTR2a gene system resulting in sleep bruxism starting later in life.
It is currently known that about 26% of children suffer from this disease, 14-15% of teenagers and 12% of adults. The numbers do not add up for a dominant genetic condition as one would expect 26% of all age groups to be affected. One possible explanation is that in puberty, the HTR2a gene expression is reduced or the genes are turned off, reducing the number affected from 26% to 14%. 12-14% between teens and adults could simply be errors in reporting with adults also being affected at 14%.
Medications Affecting Sleep Bruxism:
Medications can activate gene expression in some conditions and sleep bruxism is one. There are a number of medications that have been shown to initiate or worsen existing sleep bruxism. This includes the following classes of drugs:
|Class of Medication||Name||Example|
(selective serotonin reuptake inhibitors)
|paroxetine||Paxil, Pexeva, Brisdelle|
|citalopram HBr||CTP 30|
(serotonin-norepinephrine reuptake inhibitors)
|venlafaxine||Effexor, Effexor XR|
(non-SSRI, SSNRI reuptake inhibitors)
|Simulants||methylphenidate HCl||Ritalin, Concerta, Biphentin, Foquest,|
|Dopamine-Affecting||levodopa-carbidopa-entacapone||Stalevo, Bromocriptine, Prolopa, Comtan, Duodopa|
|Analgesics||buprenorphine||BuTrans, Suboxone, Belbuca|
All of the above medications have been shown to initiate or increase the severity of sleep bruxism. These drugs increase levels of serotonin or dopamine in the brain and have sleep bruxism as a side/adverse effect. It is interesting to note that when reviewing many patient’s jaw pain histories, their symptoms started soon after starting one of these medications.
The Effects of Sleep Bruxism
With inactivation or suppression of the masseter inhibitory reflex, the jaws muscles are allowed to contract with 100% of their bite force. In women, forces of 70-90 lbs of pressure are possible and in men, 100-120 lbs. These excessive forces, being applied to the teeth and jaws all night long, has very serious effects on the teeth, jaws, TMJ, and muscles.
The following are the structures of the face, head, and neck directly affected by sleep bruxism:
Cracked fillings: the pressure of sleep bruxism can easily fracture fillings and/or shorten their lifespan requiring frequent replacement (Figure 1).
Figure 1 Broken Filling
Cracked teeth are also common. These teeth are very sensitive to biting only hard foods as the crack opens and closes (Figure 2) and, as the crack deepens, often the affected tooth must be removed. Most cracked teeth must be crowned to prevent the spread of the crack.
Figure 2 Cracked Tooth
Abnormal Tooth Wear is very common. Acid reflux (GERD) occurs in many with sleep bruxism and, combined with the forces of sleep bruxism, results in considerable wear in a short time. (Figure 3).
Figure 3 Excessive Tooth Wear
The roots of the teeth can actually crack requiring removal of the tooth (Figure 4).
Figure 4 Fractured Root During Sleep
Localized bone loss can occur due to side-to-side forces concentrated on one tooth (Figure 5).
Figure 5 Localised Periodontal Bone Loss
Painful abfraction lesions (notches) can occur at the gumline on upper and lower teeth (Figure 6).
Figure 6 Abfraction Lesions
Hypersensitivity to hot and cold foods is a hallmark sign of sleep bruxism due to tooth wear, acid reflex, damage to the teeth as well as referred pain from the masseter and temporalis muscles (Figure 7).
Dental Implants and Sleep Bruxism
As one would expect, the forces of sleep bruxism can damage and shorten the lifespan of dental work. Studies have shown that dental implants can be fractured due to the forces of sleep bruxism. Figure 8 demonstrates a broken implant and figures 8-10 demonstrate peri-implantitis, or bone loss similar to that seen in periodontal disease, in sleep bruxism patients.
Bone loss can occur around implants just like teeth. The side to side forces seen in phasic sleep bruxism can cause this.
The Jaw Bones (Mandible and Maxilla):
In this view, the stylomandibular ligament has calcified. This is termed Eagle’s Syndrome. If it fuses completely there can be restrictions in opening the jaws and pain when turning the neck (Figure 11).
There is a bend in the mandible termed “antigonial notching” (Figure 11). This is due to excessive pressure of the masseter muscle during sleep bruxism events.
In this view (Figure 12), the coronoid process (the temporalis muscle attaches here) is elongated (higher, marked with the orange dotted line. The yellow dot shows the correct height) by excessive muscle pull during sleep bruxism events. If stretched too far, this restricts side to side mobility of the lower jaw as the coronoid process bumps into the zygomatic arch (cheekbone).
When excessive torquing pressure is placed on bone, the bone will adapt to prevent injury (breakage). In the case of the jaws, these are termed torus (singular) and tori (plural). Figure 13 demonstrates moderately sized tori and where they are most commonly seen in the lower jaw. This location is not by chance. This region is one of the higher risk areas for fracturing.
Figure 14 demonstrates a torus that developed on the palate. This is due to compressive forces on the upper jaw during sleep bruxism forcing the nasal septum through the palate at the mid-palatal suture. Often the sinuses will invade into these tori making removal very challenging. Tori (both upper and lower) are serious as they reduce the space for the tongue. This has ramifications with sleep apnea, where a crowded tongue can block the airway. Tori certainly do not help this!
Another bone adaptation seen in sleep bruxism are exostoses or bone outgrowths on the jaw bones. Figures 15 and 16 demonstrate this on the lower and upper jaws. If a sufferer of sleep bruxism requires dentures, these bone outgrowths must all be removed before dentures can be made.
The TMJ (Jaw Joints):
Sleep bruxism causes considerable pressure on the TMJ. This causes pain in the TMJ, clicking and closed locking in the morning. Over time, if left untreated, the TMJ can break down irreversibly. Figure 17 below demonstrates normal TMJ movement. The disk (yellow in animation) remains between the bones the entire opening and closing cycle.
In the early stages, the disk starts to slip out of alignment when biting, but “clicks” into place when the jaw starts to open and remains there for most of the opening and closing cycle (Figure 18).
When biting, the disk is dislocated forward. With sleep bruxism, the teeth are together most of the night resulting in the progression of damage to the TMJ over time.
If this continues, the disk can tear free and never resets into position. This is termed a closed lock. This is where the dislocated disk completely blocks full opening and usually restricts opening to a finger or two. The American Academy of Sleep Medicine list closed locks on waking, resolving as the day goes on, as a common sign of sleep bruxism (Figure 19). Over time, this can permanently lock, requiring surgical intervention to stabilize the joint(s).
TMJ problems (TMD) are very common in those suffering from sleep bruxism. Conventional TMJ therapies do not take into account (or in most cases) even mention sleep bruxism. Conventional upper or lower TMJ splints do not treat sleep bruxism and the associated TCR activation. Over time, the TMJ splints can break and the treatment fails. Upper bruxism appliances have been shown to not only be ineffective in treating sleep bruxism but can also affect the airway resulting in sleep-disordered breathing. The American Academy of Sleep Medicine list non-reducing closed locks as a common finding in sleep bruxism.
The two main muscles involved in sleep bruxism are the temporalis (Figure 20), located on the side of the head and temple region, and the masseter, which is the main chewing muscle in your cheek. These muscles are seriously overworked in sleep bruxism and can become damaged or diseased over time, causing pain.
Sleep bruxism can cause these muscles to fatigue very easily making chewing harder or chewy foods very difficult. Over time, areas of these muscles can become damaged and form myofascial trigger points. These are areas where the muscle tightens and remains tightened. The trigger points are painful to palpate and have the characteristic of referring pain to adjacent regions, very predictably.
As can be seen in Figure 18, the temporalis pain referral pattern for the front fibers is into the temple, upper molars, upper bicuspids, and upper incisor region. Headaches in the temples on waking, or later in the day, are a hallmark symptom of sleep bruxism and this is one of the causes.
In Figure 21, the masseter muscle pain referral patterns include both upper and lower molars, over the eye and temples as a tension headache. The masseter muscle is also a common cause of morning headaches. These headaches are reported by patients as moderate to severe in nature and can occur in waking, or later in the day. Waking to a severe headache is not a pleasant way to start the day and depression can also occur in susceptible people. There is also referral into the maxillary sinus area that mimics chronic sinusitis in some.
Tooth pain from the masseter and temporalis muscles is very common and may be mistaken for a real toothache. Root canal therapy may be inadvertently performed on a healthy tooth due to the similarity in the symptoms.
The muscles under the jaw also are involved in sleep bruxism. They are activated just as the masseter and temporalis and contract with considerable opposing force, attempting to open the jaw. As they are much smaller, they cannot and often develop trigger points. Figure 20 shows the trigger point referral pattern for the digastric muscles (anterior and posterior):
The posterior digastric muscle (Figure 23) shows how this causes pain under the jawline as well as into the mastoid region. Many patients awake with what they believe is a sore throat due to this pain referral pattern.
Figure 23 Posterior Digastric Referral
Muscles are responsible for most headaches. With the damaged muscles due to sleep bruxism, headaches (and sensitive teeth) are the most commonly reported symptoms. Development of myofascial trigger point in these muscles can result in tooth pain, ear pain, and a numbner of other symptoms. The American Academy of Sleep Medicine list headaches in the temple region and sensitive teeth as the two most commonly reported symptoms of sleep bruxism.
Sleep bruxism affects the masseter inhibitory reflex (MIR) by blocking the control centers.
The Masseter Inhibitory Reflex
The masseter inhibitory reflex (or MIR) is a cranial reflex located in the brainstem region called the pons. This is located just under the skull in the spinal cord. If you have ever been chewing a soft food, and unexpectedly bite into something hard, you immediately stop chewing, remove the hard object and slowing start chewing again. This is the MIR in action normally.
The MIR has two distinct stages. The first stage termed exteroceptive suppression one or ES1 for short, occurs in 10 milliseconds (ms). It only affects the side that is stimulated. The following animation shows this. Sensory nerves in the ligaments of the teeth as well as branch three of the trigeminal nerve, the mental nerve activate this stage. The reflex control center indicated as 1IN in the animation controls the trigeminal motor nucleus (the control center for the masseter and temporalis muscles). It is an inhibitory nucleus.
Of note, the ES1 state only activates the reflex center on the side stimulation (is unilateral).
The second stage termed exteroceptive suppression two, or ES2, occurs 40-60 seconds after the ES1 stage. It, however, affects both sides, unlike the ES1 stage. Stretch receptors in the masseter and temporalis muscles activate this stage of the reflex. The following animation demonstrates this:
The ES2 phase actives the 2nd inhibitory nucleus of the reflex labeled as 2IN in the animation. The ES2 reflex activates both sides, unlike the ES1 which affects only one side.
On an electromyographic (EMG) tracing, the reflex looks like this:
Of note, in mild sleep bruxism, the ES2 stage is shortened, the ES1 fairly normal. In severe sleep bruxism, however, the ES2 stage is completely absent and the ES1 state is shortened and advanced. This is the effect of the HTR2a polymorphism and over-stimulation by serotonin.
Note that is mild sleep bruxism the ES1 stage is relatively normal however the ES2 stage is shortened. In severe sleep bruxism, the ES1 stage is advanced and the ERS2 is completely absent.
Tension headaches also affect the MIR, very similarly to sleep bruxism. The following image shows both a severe sleep bruxism patient and a patient suffering from a tension-type headache:
Note in the EMG tracing above how similar severe sleep bruxism and tension-type headaches affect the MIR, they are almost identical. Both show the ES2 stage to be absent. This is likely the reason tension-type headaches are one of the most commonly reported symptoms of sleep bruxism.
If sleep bruxism is present in the severe form for an extended time, the jaw muscles can enlarge, like a bodybuilder’s. This is termed “hypertrophy”.
This alters the appearance of the person (Figure 24). This also increases the strength of the muscle resulting in even greater damage to the teeth during sleep bruxism events.
Figure 24 Masseter Hypertrophy
The only effective treatment for reducing this muscle hypertrophy is with the use of Botox injections, which has been shown to reduce excessive muscle mass over a few treatments. Botox, however, has not been shown to treat sleep bruxism or reduce the associated increase in heart rate and is not FDA cleared for this use.
The Digestive System: GERD
Sleep bruxism has been shown in the research to be associated with gastroesophageal reflux disorder (GERD) or acid reflux (heartburn) while sleeping as well as increased gastric motility or activity in the gut.
This acid reflux into the mouth, combined with the sleep bruxism results in accelerated tooth erosion/wear due to softening of the enamel of the stomach acid, coupled with the extreme forces of sleep bruxism on the teeth.
The Nervous System: Trigeminal Cardiac Reflex
Sleep bruxism has been shown in the research to activate a powerful cranial reflex known as the Trigeminal Cardiac Reflex (TCR). This reflex is well researched in medicine as certain forms of it can result in rapid and dangerous drops in blood pressure and heart rate during surgical procedures.
Recently, a new classification for the TCR was proposed, helping to explain the effect we see in sleep bruxism. Stimulation of the TCR on the outside of the head (skin and eyeballs) results in a drop in heart rate (bradycardia), blood pressure (hypotension), decreased respiration (apnea), intracranial pressure and an increase in gastric motility.
Stimulation at the level of the Gasserion results in the opposite effect of increased heart rate (tachycardia), increased blood pressure (hypertension), increased rate of breathing (hyperpnea), increased 0cranial pressure and as well as increased gastric motility. This is where sleep bruxism affects the TCR.
This stimulation of the TCR reflex is of great importance in medical research as this places stress on the heart.
In the sleep tracing above, the heart rate increases from 49 to 94 beats per minute (bpm) with is a 91.8% increase. It is medically accepted that an increase (0r decrease) of 20% or greater is an indication that the TCR has been activated. With sleep bruxism, the activation is very significant.
The Sleep Bruxism “Cascade of Events”
What is unusual about sleep bruxism is that each event is not simply a grinding event. There is a predictable sequence of events that occurs with each event.
Each event includes:
- Activation of the TCR seen as an increase in heart rate of 50-120%, increase in blood pressure, increase in intracranial pressure, an increase in the rate of respiration, and an increase in gastric motility (GERD)
- Activation of the central pattern generators that control the masseter and temporalis muscles, seen as clenching (tonic events), grinding (phasic events) or a combination of both types (mixed events)
- Activation of the posterior digastric muscles
- Activation of the brain seen as a sleep arousal
- Activation of the sucking reflex (cheek biting)
- Activation of the swallowing reflex
This cascade of events occurs with each sleep bruxism event, often hundreds of times each night.
A normal sleeping heart rate is generally much less than 90 beats per minute (bpm). With sleep bruxism, the heart rate can climb as high as 140-150 bpm, placing significant stress on the heart.
The tracing below (Figure 28) demonstrates a typical sleep bruxism event and below the effect on heart rate (increasing from 70 bpm to 96 bpm. The horizontal dotted lines in the tracing indicate the normal range of jaw movement during sleep. Sleep bruxism far exceeds this level. This is a 37% increase in heart rate strongly suggesting sleep bruxism has a profound effect on the TCR and well in excess of the 20% recognized standard.
Figure 28 Sleep Study Demonstrating Activation of the TCR by Sleep Bruxism
Research has shown that during sleep bruxism events, there is also an increase in pressure on the brain (figure 29) due to increased blood flow due to the activation of the trigemino-cardiac reflex. This may have ramifications for those who are at risk of aneurysms of the brain.
There is also an increase in intracranial pressure seen with sleep bruxism. The long-term effects of this are not currently known.
Sleep bruxism and Sleep:
There is also reduced REM sleep with sleep bruxism. This means that the Glymphatic System is not functioning optimally and there may be an increase in Amyloid Beta and Tau protein accumulation within the brain (which is strongly associated with dementia). Figure 30 is an animation demonstrating this.
During REM sleep, glial cells in the brain release massive amounts of cerebral spinal fluid (CSF) into the brain. The CSF effectively washes the brain from the arterial side to the venous side removing the free amyloid beta and tao proteins, flushing them into the lymphatic system, outside of the brain, where they are carried off to the liver to be broken down.
In sleep bruxism, REM sleep is reduced and the glymphatic system is less effective at removing these damaging proteins.
Sleep bruxism results in hundreds of sleep arousals each night, prevented deep restorative sleep. The Epworth Sleepiness Scale (ESS) is used internationally to screen for tiredness during the daytime. Less than ideal sleep has been associated with many different diseases as well as in increasing the risk of a motor vehicle or industrial accident. It impairs memory formation and learning and can cause depression in some.
ESS scores of 4-9 are common. Sleep apnea starts at 10+. Sleep bruxism can cause daytime tiredness almost as bad as mild sleep apnea and can result in decreased productivity, poor memory consolidation, poor quality sleep and increases the risk of accidents.
Research tends to focus on the disease and rarely on the family members. With sleep bruxism, the sound of grinding teeth has been shown to be very disturbing to most people. This can disturb the sleep of the bed partner or even family members in adjacent rooms! Tooth grinding is not a pleasant sound!
Sleep bruxism causes depression in a significant number of affected individuals.
As discussed above, SSRI and SSNRI antidepressants are often prescribed which only worsen the sleep bruxism and, in turn, the depression. Stronger antidepressants are needed and a vicious circle is established.
Considering the effects of sleep Bruxism discussed here, it is obvious that it can have a significant effect on quality of life. The most significant effect, however, is the stimulation of the TCR reflex as this places a tremendous strain on the heart, numerous times each night. There is a growing body of evidence that sleep bruxism is a risk factor for the development of heart disease. It is not just another dental condition. It is also, and more importantly, a serious medical condition.
Treatment of sleep bruxism with the only FDA cleared treatment, the Luco Hybrid OSA Appliance, can dramatically improve the quality of life for those suffering from this disease, as well as their family members. It can also reduce the effects of the TCR reflex as well as the significant risks this condition imposes.
The Luco Hybrid OSA Appliance is currently available in Canada and the USA. Contact your dentist today if you feel you suffer from this common and serious disorder and begin…