The Epidemiology of Sleep-Related Bruxism(SRB)
|14-17% of the pediatric population suffers from SRB. The primary or baby teeth only have 0.5mm of enamel and can wear very quickly.|
|12% of the teenage group suffers from SRB. Headaches are common in this group and is a common symptom of SRB.|
|12% of the 20- 29-year-old group suffers from SRB. This group tends to report the most severe symptoms. Headaches are very common in this group as well as hypersensitivity of the teeth to temperatures, especially cold and sweet.|
|8-10% of the 30-59-year-old group suffers from SRB. Often accompanied by neck and upper back pain. Headaches are common. SRB also affects the cervical or neck muscles and is closely related to tension headaches.|
|8% of the 60+-year-old group suffer from SRB. Longstanding symptoms are less severe than the other groups. Headaches are not as common in this group but often many teeth have been lost due to repeated breakage throughout life or supporting bone loss.|
The Genetic Link…
Most dentists have seen families of tooth grinders and have suspected an inherited origin. There is, in fact, a genetic component to SRB as well. researchers have found a genetic mutation on chromosome 13 on the gene HTR2A. In SRB patients there are multiple copies of the gene termed a polymorphism. This gene creates receptors in the central nervous system (CNS) for serotonin a neurotransmitter that suppresses activity in nuclei or nerve centers in the CNS (the HTR1A gene creates receptors that activate the CNS when stimulated). The multiple copies of the HTR2A gene result in a hypersensitivity to serotonin. It should be noted that medications that prevent the re-uptake (breaking down) of serotonin in the CNS have been shown to initiate or worsen existing SRB. This supports the HTR2A theory. Serotonin is also involved in the nuclei of the brain involved in chewing and in SRB these are activated during sleep and responsible for the side-to-side, front-to-back grinding, and clenching patterns seen in SRB. Other studies are linking SRB to another polymorphism of the DDR3 gene, which helps control in motivation and may affect the muscle contractions seen.
The inheritance pattern of the HTR2A mutation is dominant. If one parent suffers from this condition half of their children will similarly be affected…
If both parents are carriers of this mutation, then 3/4 of their offspring will be affected.
The epidemiology studies do not reflect genetic evidence. As there is limited research relating to SRB, the reporting in adults is likely low as it would be expected that all age groups would be affected similarly. Future research should confirm this.
It should also be noted that not all genes are activated at the same time, some remain dormant until another gene or stress on the body activates the latent gene. This is often the case with sleep-related bruxism and it only becomes clinically significant after a serious head or neck injury or by taking certain medications. Many patients are not symptomatic until later in life whereas many children are affected as soon as their teeth are in. As well, the degree of the mutation likely affects the severity, with some having hundreds or thousands of extra copies of the HTR2A gene while others may have much less. This could help explain why some people are much worse than others. Further research is definitely warranted in this field.
Sleep- related bruxism has also been shown in the research to hyper-sensitize the nervous system to serotonin. This means that an affected person with this condition will react to serotonin at lower concentrations than an unaffected person. Combined with more serotonin receptors, this is a recipe for disaster.