What is Sleep-Related Bruxism?
Sleep-related 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. In the latest classification of the World Health Organization, ICD-11, sleep-related bruxism is classified under Sleep-Wake Disorders, specifically under the classification of 7A83. New to this edition, they added three levels of severity not seen in ICD-10 for sleep-related bruxism. Awake bruxism (grinding when awake) is not the same and is classified under Dentofacial Anomalies, specifically under Dentofacial Parafunctional Disorders DA0E.7 Awake bruxism includes teeth clenching, teeth grinding, and bruxism and bruxomania while awake (bruxomania is a compulsive urge to clench and grind while awake).
Sleep-related bruxism occurs in 26% of children under 6 years of age, in 14% of teenage young adults and 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-related bruxism patients present with all symptoms and some may be symptom-free.
Sleep-related 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, blood pressure, gastric motility and disturbs sleep.
The following is a system by system summary of the current knowledge of sleep-related bruxism, and the effects it can have.
Central Pattern Generators (CPG)
Rhythmic controllers of repetitive movements…
Figure 1 Central pattern generators
Rhythmic movements such as chewing and bruxing are controlled by central pattern generators (CPG) within the brain (Figure 1). 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-related 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-related bruxism events, these central pattern generators are abnormally stimulated resulting in the “chewing” and “clenching” type events characteristic of sleep-related bruxism. The suppression of the masseter inhibitory reflex (a powerful protective reflex which is, discussed below), results in heavy clenching and grinding forces that are very damaging.
Genetics and Sleep-Related Bruxism:
Many disorders have a genetic basis to them and sleep-related bruxism is no exception. There is a growing body of evidence for a genetic basis for sleep-related 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.
Figure 2 Location of the HTR2A genetic mutation on chromosome 13
The HTR2A gene creates a protein that forms into the HTR (short for serotonin) 2A receptor (figure 2). This receptor, when activated, inhibits the nucleus it is connected to. The HTR1A gene, its counterpart, not affected by sleep-related bruxism, is excitatory, the opposite action of the 2A.
In sleep-related bruxism, there are multiple copies of the HTR2A gene, termed “polymorphism”. This creates too many serotonin receptors and a hyper-sensitivity of affected nerves and nerve centers.
In function, too many 2A receptors result in an increase of suppression of key centers of the brain.
Figure 3 Hyper-stimulation due to an excess of receptors for serotonin
With the polymorphism seen, there is an overstimulation of the affected nucleus (figure 3). The 2A receptor suppresses activity.
One of these key regions affected by this mutation is the control of the masseter inhibitory reflex, a protective reflex that prevents one from biting too hard. In sleep-related bruxism, the polymorphism of the HTR2A gene results in too many suppressor genes on the control center, and this protection is lost. The masseter, temporalis and posterior digastric muscles are all affected by this mutation and are allowed to contract with 100% force during sleep-related bruxism events. Women with sleep-related bruxism generate forces of 70-90 lbs and affected men generate forces of 100-120 lbs. Normally forces of 15-25 lbs are generated when chewing hard foods when awake.
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 but could account for the abnormal chewing movements seen in sleep-related bruxism. 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) but the research is scarce on this.
The inheritance pattern of the HTR2A mutation is an autosomal dominant meaning that if one parent has the HTR2A mutation (and sleep-related bruxism), 50% of the offspring will be affected (if both parents are affected, 75% of the offspring will be affected).
Figure 4 Autosomal dominant Mendelian inheritance pattern
Genes can be active or latent. A latent gene is an affected gene that is not active (silent) and is not causing disease. A latent gene for a condition can be activated by certain conditions. In sleep-related bruxism, trauma to the face or jaws (such as motor vehicle accident or injury) can activate the latent HTR2a gene resulting in sleep-related bruxism starting later in life. Certain medications can also active the mutated HTR2a gene. Modifier genes can activate other genes later in life as well. Not all patients with sleep-related bruxism are symptomatic for life, many are affected later in life. A good example of this is medication-induced sleep-related bruxism (below) that can activate the HTR2A gene and the sequella of sleep-related bruxism. Head trauma, such as a motor vehicle accident, may iniate sleep-related bruxism in suseptible people.
It is currently known that about 26% of children suffer from sleep-related bruxism, 14-15% of teenagers and 12% of adults. The numbers do not add up for a dominant genetic condition (figure 4) 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, modulated by other genes, or the genes become latent, reducing the number affected from 26% to 14%. This could explain the difference in reporting between the different age groups. This discrepancy could also be due to reporting errors between groups as well as the sudden onset of the condition in an otherwise asymptomatic adult. There are less than 500 articles written about sleep-related bruxism currently and many are meta-studies that simply report on other studies.
Thank Medications Affecting Sleep-Related Bruxism:
Secondary Sleep Bruxism
There are some medications known to initiate or worsen sleep-related bruxism. This includes the following classes of drugs:
|Class of Medication||Drug Name||Common Examples|
(selective serotonin reuptake inhibitors)
|paroxetine||Paxil, Pexeva, Brisdelle|
|citalopram HBr||CTP 30|
(selective serotonin-norepinephrine reuptake inhibitors)
|venlafaxine||Effexor, Effexor XR|
(non-SSRI, SSNRI medications)
|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-related bruxism. These drugs increase levels of serotonin or dopamine in the brain and have sleep bruxism as a side 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. There are likely to be more drugs shown with this effect over time as many affect the nervous system and the musculature. As well, if sleep-related bruxism has been initiated from one of these medications, it persists for life in more than 50%. Once activated, the genes can remain activated for life! Patients on these medications take longer to treat with the Luco Hybrid device as the medication is working against the treatment. They are also more prone to relapse. This is also very strong evidence that there are too many HTR2a receptors in the brains of those suffering from sleep-related bruxism.
The Effects of Sleep-Related Bruxism
It is important to note that signs and symptoms of sleep-related bruxism vary widely between individuals. Some show extensive tooth damage while others only suffer from fatigue and muscle pain. Men tend to demonstrate more tooth damage and bone changes while women tend to demonstrate more pain type symptoms. Over 90% of sleep-related bruxism patients demonstrate neurological signs discussed below.
As discussed, 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-related bruxism:
Cracked fillings: the pressure of sleep-related bruxism can easily fracture fillings and/or shorten their lifespan requiring frequent replacement (Figure 5).
Figure 5 Broken Fillings
Cracked teeth are also common. These teeth are very sensitive to biting only hard foods, as the crack opens and closes (Figure 5) and, as the crack deepens, the tooth may split, usually requiring removed. Many cracked teeth, if caught early enough, can be saved by the placement of a crown as this helps to prevent the spread of the crack under loading (biting). Once the crack reaches the nerve of the tooth, there is little chance of saving the tooth.
Figure 6 Painful Cracked Tooth
Abnormal Tooth Wear is very common. Acid reflux (GERD) occurs in many with sleep-related bruxism and, combined with the extreme forces of sleep-related bruxism, results in considerable wear in a short time. (Figure 6). The hydrochloric acid from the stomach is very powerful and softens the enamel. The abnormal excessive sleep-related bruxism movements remove the softened enamel flattening the teeth quickly.
Figure 7 Excessive Tooth Wear
The roots of the teeth can actually crack requiring removal of the tooth (Figure 7). Phasic or side-to-side, front-to-back sleep-related bruxism produces a considerable force on the teeth. In extreme cases, the root of a tooth may fracture. Figure 8 is the radiograph of a patient who woke with a loose lateral incisor. The radiograph shown demonstrated a complete root fracture occurring during sleep.
Figure 8 Fractured Root During Sleep
Localized bone loss can occur due to side-to-side forces concentrated on one tooth (Figure 9). If a tooth hits before the others in a side-to-side movement, the tooth will be rocked side-to-side. Over time, this abnormal movement can result in loss of the supporting bone.
Figure 9 Localised periodontal bone loss
Painful abfraction lesions (notches) can occur at the gumline on upper and lower teeth (Figure 10). Side-to-side motions seen in sleep-related bruxism may not fracture the root or damage the bone, but instead cause a notch, usually sensitive to brushing, sweets, and temperatures, can form. Figure 10 shows extensive abfraction lesions in the eyetooth and 1st bicuspid. Many dentists and hygienists refer to this as toothbrush abrasion, however, sleep-related bruxism has been shown to be the actual cause. Horizontal tooth brushing may result in sensitivity however it is not the cause of these lesions.
Figure 10 Abfraction lesions
Hypersensitivity of the teeth to hot and cold foods is a hallmark sign of sleep-related bruxism due to tooth wear, acid reflex, damage to the teeth as well as referred pain from the masseter and temporalis muscles (Figure 11). Stretching of the periodontal ligaments of the teeth can result in tooth pain as well as these ligaments contain over 100,000 mechano-receptors per tooth. Abstraction lesions are also intensively painful to temperatures in many.
Dental Implants and Sleep Bruxism
As one would expect, the forces of sleep-related bruxism can damage and shorten the lifespan of dental work Figures 12-13). Studies have shown that dental implants can be fractured due to the forces of sleep-related bruxism. Figure 8 demonstrates a broken implant and figures 13-14 demonstrate peri-implantitis, or bone loss similar to that seen in periodontal disease, in sleep-related bruxism patients.
Bone loss can occur around implants just like teeth. The side to side forces seen in phasic sleep-related bruxism can cause this. This is termed peri-implantitis and can lead to loosening and failure of the implant.
The Jaw Bones (Mandible and Maxilla):
In Figure 16, 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.
There is a bend in the mandible termed “antigonial notching” (Figure 16). This is due to the excessive pressure of the masseter muscle during sleep-related bruxism events.
In Figure 17, the coronoid process (the temporalis muscle attaches here) is elongated (higher, marked with the orange dotted line. The yellow dot (and green dotted line) shows the correct height) by excessive muscle pull during sleep-related 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 a bone, the bone will adapt to prevent injury (breakage). In the case of the jaws, these are termed torus (singular) and tori (plural). Figure 18 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. These forces are produced in phasic or side-to-side sleep-related bruxism.
Figure 19 Palatal Torus
Figure 19 demonstrates a torus that developed on the palate. This is due to compressive forces on the upper jaw during sleep-related 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-related bruxism are exostoses or bone outgrowths on the jawbones. Figures 20 and 21 demonstrate this on the lower and upper jaws. If a sufferer of sleep-related bruxism requires dentures, these bone outgrowths must all be removed before dentures can be made.
The two main muscles involved in sleep-related bruxism are the temporalis (Figure 22), 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-related bruxism and can become damaged or diseased over time, causing pain.
Sleep-related 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 may 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 23, 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-related bruxism and this is one of the causes.
In Figure 24, 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-related bruxism. They are activated just as the masseter and temporalis and contract with a considerable opposing force, attempting to open the jaw. As they are much smaller, they cannot and often develop trigger points. Figure 21 demonstrates the trigger point referral pattern for the digastric muscles (anterior and posterior):
Figure 25 Posterior digastric pain referral pattern
The posterior digastric muscle (Figure 25) demonstrates 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.
Muscles are responsible for most headaches (Figure 26). With the chronic injury to these muscles during sleep-related 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 number 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-related bruxism.
Figure 26 Headaches associated with sleep-related bruxism
The Masseter Inhibitory Reflex
Everyone is familiar with the knee-jerk reflex (Figure 27). The doctor taps your knee and your leg jumps up.
This reflex is located in the spinal cord and is termed a “spinal reflex”.
We have many reflexes that are located inside the brain and brainstem. These are termed “cranial reflexes”. The masseter inhibitory reflex (or MIR) is one such 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 and is 10 milliseconds (ms) in length. 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 that suppresses or stops muscle contraction. Ligaments in the bicuspid and molar teeth contain stretch receptors that activate this reflex the mental nerve (V3 of the trigeminal nerve) also activates the reflex. Of significance, this phase of the MIR only affects the side stimulated, or is unilateral. Figure 24 is an animation of the normal ESI phase of the masseter inhibitory reflex.
The ES1 phase (Figure 28) lasts 10-12 ms and only affects the side that has been stimulated.
The second stage termed exteroceptive suppression two, or ES2 last for 40-60 seconds and occurs 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 ES2 phase occurs after the ES1 phase but lasts longer, about 40-60 ms (figure 29). It also affects both sides independently of which side has been stimulated.
The ES2 phase actives the 2nd inhibitory nucleus of the reflex labeled as 2IN in the animation.
On an electromyographic (EMG) tracing, the reflex looks like this:
Of note, in mild sleep-related bruxism, the ES2 stage is shortened, the ES1 fairly normal. In severe sleep-related bruxism, however, the ES2 stage is completely absent and the ES1 state is shortened and advanced (figure 30). This is due to the effect of the HTR2a polymorphism and over-stimulation by serotonin in the brainstem.
TENSION HEADACHES AND THE MIR
Tension headaches also affect the MIR, very similarly to sleep-related bruxism. The following image shows both a severe sleep-related bruxism patient and a patient suffering from a tension-type headache:
Note in the EMG tracing (figure 31) how similar severe sleep-related bruxism and tension-type headaches affect the MIR; they are almost identical. In both the ES2 stage is absent. This is likely the reason tension-type headaches are one of the most commonly reported symptoms of sleep-related bruxism. Those affected by tension headaches also share the HTR2a polymorphism mutation as 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 32). This also increases the strength of the muscle resulting in even greater damage to the teeth during sleep-related bruxism events.
Figure 32 Masseter hypertrophy’s effect on facial form in the jaw region
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-relatedbruxism or reduce the hyperstimulation of the trigeminal cardiac reflex and is not FDA cleared for this use.
The Digestive System: GERD
sleep-related 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 Figure 33). This is due to sympathetic activation of the trigeminal cardiac reflex.
This acid reflux into the mouth (Figure 34), combined with the sleep-related bruxism results in accelerated tooth erosion/wear due. This is due to softening of the enamel due to stomach acid entering the mouth during sleep (GERD), coupled with the extreme forces of sleep-related bruxism on the teeth (figure 34).
The Nervous System: Trigeminal Cardiac Reflex
Sleep-related 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, sometimes life-threatening.
Figure 35 The trigeminal cardiac reflex stimulation at the level of the Gasserion ganglion
Figure 35 The trigeminal cardiac reflex stimulation at the level of the Gasserion ganglion
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 body (skin and eyeballs) results in a drop in heart rate (bradycardia), blood pressure (hypotension), decreased respiration (apnea), decreased intracranial pressure and changes in gastric motility.
Stimulation at the level of the Gasserion (figure 35) 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.
Sleep-related bruxism affects the TCR at the level of the Gasserion Ganglion and this effect is seen in most SRB patients.
The Sleep Bruxism “Cascade of Events”
Figure 36 The sleep-related bruxism cascade
What is unusual about sleep-related bruxism is that each event is not simply a grinding event, it is a cascade of events that occur with each sleep-related bruxism 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)
- Increased cranial activity, seen as sleep arousal from deeper to shallower sleep (reduction in REM sleep)
- 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-related bruxism event, often hundreds of times each night.
The tracing below (Figure 37) demonstrates a typical sleep-related bruxism event and below the effect on heart rate (increasing from 70 bpm to 96 bpm. It is medically accepted that there must be a change (increase or decrease in heart rate greater than 20% to state that the TCR has been activated. sleep-related bruxism far exceeds this level. This is a 37.1% increase in heart rate strongly suggesting sleep-related bruxism has a profound effect on the TCR and is far in excess of the 20% recognized standard (hyper-stimulation).
Research has shown that during sleep-related bruxism events, there is also an increase in pressure on the brain (figure 38) due to increased blood flow resulting from activation of the trigemino-cardiac reflex. This may have ramifications for those who are at risk of aneurysms of the brain. The trigeminal nerve innervates the cranial blood vessels controlling blood flow in the front half of the brain. This vascular control has been shown to be associated with migraine headaches.
Figure 38 Increased cranial pressure
Sleep-Related 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 39 is an animation demonstrating this.
During REM sleep, glial (star) 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-related bruxism, REM sleep is reduced due to sleep arousals occurring during the bruxism events, and the Glymphatic System is less effective at removing these damaging proteins. Reduced REM sleep is associated with depression. Antidepressants, which are very often prescribed for the depression, activate and intensify sleep bruxism. Intensified sleep-related bruxism further causes depression. A vicious cycle is established and the symptoms can intensify very rapidly in many people.
Sleep-related bruxism results in hundreds of sleep arousals each night (figure 40), prevented deep restorative sleep. The increase in brain activity seen during the sleep-related bruxism cascade disturbs 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.
In sleep-related bruxism, ESS scores of 4-9 are common. In sleep apnea, ESS scores of 10 and much higher are diagnostic of the condition. Sleep-related bruxism can cause daytime tiredness almost as severe as mild sleep apnea and can result in decreased productivity, poor memory consolidation, poor quality sleep and increased risk of accidents.
Research tends to focus on the disease and rarely on the family members. With sleep-related 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 and is universally described as noxious.
As discussed above, sleep-related bruxism is strongly associated with depression. Sleep deprivation is also associated. SSRI and SSNRI antidepressants are often prescribed which only worsen the sleep-related bruxism and, in turn, the depression. Stronger or more antidepressants are needed and a vicious circle is established.
Considering the effects of sleep-related bruxism discussed here, it is obvious that it can have a significant effect on the quality of life. Damage to the teeth and jaws are a significant concern and should always be considered when dentists are providing treatment. Most significantly, however, is the stimulation of the TCR reflex as this places a tremendous strain on the heart, numerous times each night. This increase in heart rate results in an increase in blood pressure. The increase in blood pressure places a strain on not only the heart but the kidneys. It is not just another dental condition. It is also, and more importantly, a serious medical-dental condition significantly affecting the cardiovascular system.
Treatment of sleep-related 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. The device effectively reduces the sleep-related bruxism to normal levels. It also reduces the hyperstimulation of the TCR reflex and the significant risks this 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…