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). During sleep bruxism events, these CPG’s are abnormally stimulated resulting in the “chewing” and “clenching” type events characteristic of sleep bruxism.
Genetics and Sleep Bruxism:
There is a growing body of evidence that there is a genetic basis for sleep bruxism. It is common for family members to suffer from this condition, supporting this theory. One gene identified is the HTR2A gene on chromosome 13. In sleep bruxism, there are multiple copies of the gene (termed polymorphism), which creates a protein in the nervous system for receptors for serotonin, a neurotransmitter that suppresses nerve activity in the brain. The excessive number of the gene is termed “polymorphism”.
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 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.
Medications Affecting Sleep Bruxism:
There are a number of medications that have been shown to initiate or worsen existing sleep bruxism. This includes the following classes of drugs:
SSRI (selective serotonin reuptake inhibitors) including:
- sertraline (Zoloft)
- fluoxetine (Prozac, Sarafem)
- citalopram (Celexa)
- escitalopram (Lexapro)
- paroxetine (Paxil, Pexeva, Brisdelle)
- fluvoxamine (Luvox)
- citalopram HBr (CTP 30)
SNRI (serotonin-norepinephrine inhibitors) including
- desvenlafaxine (Pristiq)
- duloxetine (Cymbalta)
- venlafaxine (Effexor, Effexor XR)
- levomilnacipran (Fetzima)
- milnacipran (Savella)
Non-SSRI, SNRI Antidepressants:
- Bupropion (Wellbutrin)
- Amytal Sodium
- Butisol Sodium
- Nembutal Sodium
- Sinemet CR
- Adderall XR
Dopamine-Affecting Medications including:
- Buprenorphine (Belbuca)
- aripiprazole (Abilify)
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.
The Effects of Sleep Bruxism
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
Figure 2 Cracked Tooth
Abnormal Tooth Wear is very common. Acid reflux 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).
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 8).
There is a bend in the mandible termed “antigonial notching” (Figure 8). This is due to excessive pressure of the masseter muscle during sleep bruxism events.
In this view (Figure 9), 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 10 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 11 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 10 and 11 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 14 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 15).
When biting, the disk is dislocated forward. With sleep bruxism, the teeth are together most of the night resulting in 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 16). 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 apnea symptoms.
The two main muscles involved in sleep bruxism are the temporalis (Figure 17), 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.
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 19, 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 anterior digastric muscle (Figure 20) shows how the lower incisors are affected.
Figure 20 Anterior Diagstric Referral
The posterior digastric muscle (Figure 21) 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 21 Posterior Diagstric Referral
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 22). This also increases the strength of the muscle resulting in even greater damage to the teeth during sleep bruxism events.
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.
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 activy 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 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 however inside the head, specifically at the level of the Gasserion or trigeminal ganglion of the brainstem results in the opposite effect of increased heart rate (tachycardia), increased blood pressure (hypertension), increased rate of breathing (hyperpnea), increased cranial pressure and decreased 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 of 20% or greater is an indication that the TCR has been activated. With sleep bruxism, the activation is significant.
The Sleep Bruxism “Cascade of Events”
Every sleep bruxism event results in a cascade of events including an increase in blood pressure and heart rate.
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, increase in rate of respiration, and increase in gastric motility.
Activation of the central pattern generators that control the massester 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
Activation of the shallowing 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. This is due to the activation of the trigeminal cardiac reflex (TCR) at the level of the Gasserion (trigeminal) ganglion of the brain. This stimulates the vagus dorsal motor nucleus which results in an increase in heart rate, blood pressure and rate of respiration. It is medically accepted that an increase or decrease of 20% in heart rate is required before a diagnosis of TCR activation may be made.
The tracing below (Figure 24) 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 24 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 26) 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 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).
Headaches on waking (or later in the day) and tooth sensitivity to temperatures are the two most common symptoms of sleep bruxism. Overloading of the masseter and temporalis muscles results in severe, chronic headaches due to referred pain from trigger points within them. As discussed, the masseter (and temporalis) inhibitory reflexes are inactivated with sleep bruxism resulting in excessive contractile forces being generated. Over time, the muscles may be damaged resulting in referred pain, and headaches (Figure 27).
Quality of Sleep:
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.
With sleep bruxism, 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!
Dental Work 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 28 demonstrates a broken implant and figures 29-30 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.
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.
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 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…