As dentists, we are faced daily with challenges that are related to sleep-related bruxism (SRB). You spent 45 minutes perfecting a restoration. You check the occlusion meticulously. Two days later, the patient returns with the side fractured off the restoration, disgruntled. Another patient experiences pain halfway through a restorative appointment so severe in their jaw muscles you must stop for a few minutes until it passes. Another patient is having difficulty opening wide enough for you to work due to jaw pain.
The two most commonly reported symptoms of sleep-related bruxism are tooth sensitivity and headaches in the temple region. How many of your patients report these symptoms frequently? How often do you recommend a desensitizing tooth paste or rinse? There are many other signs and symptoms relating to sleep-related bruxism. Please read on.
Sleep-related bruxism is common, affecting 10-12% of the adult population. From over 30 years in clinical dentistry, I am convinced it is higher than this. Other clinicians have confirmed this to me. There are medications that can initiate the condition or worsen it in some. Some patients are symptomatic yet others have a serious reduction in quality of life. This can be very challenging to manage clinically. It can be primary and secondary to other conditions. Unfortunately, sleep-related bruxism is not taught in dental or medical schools currently and very few clinicians are even aware of it’s existence.
What do we know from the research?
There is a genetic component as it is inherited in a dominant inheritance pattern. Studies have shown that a significant number of SRB patients demonstrate a polymorphism of the HTR2a gene on chromosome 13. This gene creates proteins that fold into receptors for serotonin (HTR) specifically the 2a receptor. This receptor is a suppressor receptor, reducing activity in the tissues or regions supplied. Its counterpart, the 1a receptor is excitatory in the CNS and gut.
Evidence for the HTR2A polymorphism affecting SRB is that medications that are serotonin suppressing such as the SSRI (selective serotonin re-uptake inhibitor) and SSNRI (selective serotonin-norepinephrine re-uptake inhibitor) type medications have been shown to either initiate SRB or worsen SRB symptoms that are already present. These are commonly prescribed for depression and anxiety disorders. This makes perfect sense as more serotonin in a system already hypersensitive to serotonin (due to an increase in receptors) would be expected to increase the effects seen and this is exactly what happens in SRB. This provides clear evidence of the HTR2a polymorphism being a driving force behind SRB.
There is evidence that the 1a receptor is also mutation as polymorphism is SRB which could explain why SRB is associated with GERD (Gastroesophageal Reflux Disease).
Another gene, in the dopaminergic system, has been also shown to be prevalent in sleep-related bruxism patients, at least in children as a polymorphism. A polymorphism mutation of the DRD2 gene on chromosome 11 has been associated with sleep-related bruxism. It is not fully understood how this mutation relates to this condition at this time.
The genetic theory has merits in that we know that genetic expression is highly variable between individuals and many diseases occur at different levels of severity as a result. This may be due to the degree of mutation, where a greater number of duplicate genes are present to demonstrate more severe symptoms. Many genes have modifier gens that can suppress or enhance their activity. This likely occurs in SRB as some patients are very symptomatic while others are less so. Trauma may also play a role as sleep-related bruxism sometimes only appears following a trauma to the head or neck regions.
Supporting the HTR2a theory is that serotonin sparing drugs have been shown in initiate or worsen preexisting sleep-related bruxism, strongly supporting a hypersensitivity to serotonin in the central nervous system.
Sleep-related bruxism directly affects a number of cranial reflexes and, as discussed, may be primary or secondary.
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