In case you haven’t noticed, the number of courses now available on sleep apnea has dwarfed even the number of implant-related courses. Economic motivation seems to be the driving force for the entrepreneurs who are offering these courses, but hopefully the quest for knowledge dissemination is driving the interest in them.
Let’s start with the connection between sleep bruxism and sleep apnea.
Sleep bruxism has two forms: static clenching and lateral/protrusion jaw shifts with the teeth in contact. The theory at the moment suggests that bruxism is the result of micro-arousals occurring in the brain, which then prompt an increase in sympathetic tone (heart rate elevation), a brief change in respiratory dynamics, and an ultimate increase in muscle EMG activity in the jaw.
So, initiation appears to be driven by central nervous system activity and not peripheral factors.
There are infinite possibilities that can theoretically arouse the brain and upset the quality and quantity of sleep, the most common being:
- Daily emotional upset.
- Challenging life circumstances that put the brain under siege.
- The needs and crying of a newborn baby.
- Stimulants consumed late in the day such as caffeine.
- Sympathetic upregulation driven by medications taken for attention deficit (such as Strattera, Concerta, and Adderall).
- A snoring bed partner.
- Pain-producing medical conditions such as IBS and back problems.
- Airway problems inclusive of UARS, RERAs, hypopneas and obstructive sleep apnea.
I find it fascinating that the result of sleep bruxism activity is rather variable. The static clencher may only build and condition the masseter and or temporalis muscles without active symptoms ever emerging. But others wake up with stiff sore muscles, headaches and limited jaw motion often persisting well into the morning.
The same scenario is played out in the lateral bruxer where the end result may be non-painful worn teeth (or sore worn teeth) combined with associated jaw muscle and joint problems.
It may be that the source of arousal along with chronicity, gender and other medical-co-morbidities, may be influencing this outcome.
Traditionally, treatments for sleep bruxism have included formal meditation training, dietary supplements and medications that induce and support sleep, and oral appliances. The oral appliance world is a bit murky. We have the traditional flat plane/stabilization option; the anterior contact option (for you NTI fans) and the now much promoted sleep appliance option to bring the jaw and tongue forward and facilitate airway patency (the assumed deficit driving arousals and the bruxism).
I clearly understand the last option but I try to never forget that a huge number of patients with moderate and/or severe sleep apnea do not exhibit uncommon levels of bruxism activity during overnight studies.
From my own experience I have theorized this airway compromise as a prompter of bruxism in countless patients, only to be disappointed by a normal sleep study absent even of respiratory related arousals (RERAs). I continue to respect this etiologic possibility but now I feel strongly that airway problems are not trumping the other potential sources of brain arousal.
Now, onto Neurotoxins (Botox/Disport) as a therapeutic option. Certainly, there is rationale for using this injectable option particularly in the patient who can’t, won’t, or has failed oral appliance therapy. Once the neurotoxin is on board, the patient is taken out of the equation in terms of compliance. The source of arousal is unchanged but the muscles will simply not be able to contract as vigorously for three to four months.
Outcomes have been encouraging but not perfect and repeated administrations may be necessary. This becomes costly for the patient, as the typical dosage necessary to cover the masseter and temporalis muscles is 100 units.
This brings me to the last piece. From what I hear there is conjecture out there that postulates that if the bruxism can be stopped with neurotoxin, then the indices of OSA, etc. will drop as well. Essentially then, those making these claims believe that bruxism (a sleep-related movement disorder) is responsible for airway insufficiency.
This thinking is confusing especially in light of the fact that some of the supporters of these claims once postulated (in the not too distant past) that lateral and protrusive bruxism was, in fact, the body’s way of opening the airway. If this were correct, using Botox to stop bruxism would be a big mistake.
I am hopeful that well-controlled studies are being pursued to sort this all out. I would love to hear your comments.