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DECEMBER 2008

    From Dive Training Magazine December 2007

By Alex Brylske
Q:Craig Yamato sent in a question concerning his daughter. "You've addressed dental problems a few times in your past columns, and touched on a concern that seems to be having a great effect on my daughter. I'm an instructor and certified her as soon as she was old enough. The problem is that she suffers from temporomandibular joint (TMJ) syndrome, and holding a regulator in her mouth for any length of time is a problem. Her dentist has actually recommended that she stop scuba diving. However, he's not a diver, and before we consider anything that drastic, I want to find out as much as I can about whether there's anything we can do to relieve the problem. Both she and I would be deeply disappointed if she had to stop diving. Any advice?"


A:Your daughter is hardly alone in her problem, Craig. In fact, dental experts who are knowledgeable about diving believe that a good portion of headaches many complain about after diving are from undiagnosed cases of TMJ syndrome either brought on or exacerbated by the standard scuba regulator mouthpiece. There was even an article about the problem published in the March 2001 issue of the British Journal of Sports Medicine. Its author, Dr. Ross Hobson, is an orthodontist and professor at the United Kingdom's University of Newcastle. He's also an avid scuba diver.
The study involved six male subjects, each using three types of regulator mouthpieces - a standard rubber model, a semi-customized silicone model, and a fully customized molded mouthpiece that allowed the back teeth, as well as the front teeth, to grip. All subjects were between the ages of 25 and 35, and had no history of TMJ syndrome. Each bit on the mouthpieces for 45 minutes, about the length of an average dive. Tests of the different mouthpieces were separated by intervals of at least a week.
In the end, what the study found was hardly surprising. The standard rubber mouthpiece required twice as much effort to hold it in place as the fully customized silicone model, and caused twice as much pain. Lip numbness and jaw position - the latter determined by X-ray - were also worse with the standard mouthpiece. And with all three mouthpieces, muscle fatigue gradually got worse with time. Reiterating the result in an interview for the Internet site, WebMD, Hobson said, "The more diving they do, the worse the discomfort gets, [so] a customized mouthpiece increases comfort and decreases problems and should be worn whenever possible." He says that about half of all divers with TMJ syndrome experience pain while in the water, and the other half do sometime soon after leaving the water. Interestingly, no tooth pain was reported by any subject.
The study is anything but surprising because regulator mouthpiece design hasn't changed much since scuba diving began. The bite blocks are made of rubber or, more recently, silicone and are designed to be gripped only by the front (canine) and middle (premolar) teeth. This puts stress on the jaw joints and, according to some experts, causes inflammation in about two-thirds of divers. While this alone doesn't necessarily indicate full-blown TMJ syndrome, the condition can result if the stress continues. TMJ symptoms include headache, pain in the face or jaw, difficulty opening the mouth wide or chewing, and ringing in the ears.
According to Dr. Barbara Mousel, a Chicago-based dentist and scuba diver, the problem isn't just limited to those with TMJ syndrome. In any diver, she says, "Lip numbness and ear pain can be attributed to the commercial scuba mouthpiece." In the worst cases, standard mouthpieces can even make divers dizzy and disoriented by affecting the balance function of the ear. "I agree that the customized mouthpiece is the solution to many of these problems," Mousel said in the same WebMD interview. But she also said that the Hobson study left out one important factor - the effect of pulling on the high-pressure hose that's attached to the mouthpiece. The strain of constantly pulling sideways, she believes, may add significantly to TMJ strain. Experts agree that TMJ problems are like other joint injuries, and normally resolve with rest, hot or cold compresses, and aspirin or other anti-inflammatory drugs. But if this offers no relief, divers should see their dentist.
Fortunately, there have been a number of new products introduced recently to address the issue of jaw fatigue induced by regulator mouthpieces. I'd strongly advise that you consult with your local dive center to get an update on the new technology. A good dentist, who also has some background in diving medicine, might be helpful, too. Whatever the two of you do, don't give up without a fight.
 

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The next article is a research paper from a Canadian group who have been studying sleep bruxism and/or tooth clenching for several years. They have found some exciting information which may may lead to a medication approach to one of the most common causes and perpetuators of TMD problems.

From Archives of Oral Biology vol52(4) April 2007

Genesis of sleep bruxism: Motor and autonomic-cardiac interactions
Gilles J. Lavigne, Nelly Huynh, Takafumi Kato, Kazuo Okura,
Kazunori Adachi, Dong Yao, Barry Sessle

a b s t r a c t
This is a short review paper presenting hypothesis to explain the mechanism that may be
involved in the genesis of sleep bruxism (SB). In humans, SB is a repetitive sleep movement
disorder mainly characterized by rhythmic masticatory muscle activity (RMMA) at a frequency
of 1 Hz and by occasional tooth grinding. Until recently, the mechanism by which
RMMA and SB episodes are triggered has been poorly understood. It is reported that during
light sleep, most SB episodes are observed in relation to brief cardiac and brain reactivations
(3–15 s) termed ‘‘micro-arousals’’. We showed that RMMA are secondary to a sequence of
events in relation to sleep micro-arousals: the heart (increase in autonomic sympathetic
activity) and brain are activated in the minutes and seconds, respectively, before the onset of
activity in suprahyoid muscles and finally by RMMA in jaw closing masseter or temporalis
muscles. In non-human primate study, we have shown that the excitability of cortico-bulbar
pathways is depressed during sleep; no rhythmic jaw movements (RJM) are observed
following intracortical microstimulation (ICMS) of cortical masticatory area (CMA) during
sleep compared to the quiet awake state.
The above results suggest that the onset ofRMMAand SB episodes during sleep are under
the influences of brief and transient activity of the brainstem arousal—reticular ascending
system contributing to the increase of activity in autonomic-cardiac and motor modulatory
networks.

1. Definition and recognition of sleep bruxism
    Sleep bruxism (SB) is defined as a stereotyped movement
disorder occurring during sleep and characterized by tooth
grinding (TG) and/or clenching. SB should be distinguished
from the daytime-awake bruxism that is mainly related to
‘‘stress/anxiety’’ reactivity and expressed as a jaw muscle
clenching habit/tic. In the presence of medical disorders,
medication or drug use, TG is described as secondary or
iatrogenic. In normal subjects, SB-TG is considered to be
primary and is reported by 8% of the adult population. Its
prevalence decreases with age from 14% in childhood to 3% in
the elderly; no gender difference is observed.
    The consequences of SB may be tooth destruction,
temporomandibular joint and muscle pain or jaw lock,
temporal headaches and cheek-biting (worse if xerostomia).
The odds ratio (OR) of reporting temporomandibular
disorders or chronic myofascial pain of masticatory muscles,
when clenching and/or grinding are concomitant, have been
estimated at between 4.2 and 8.4. Up to 65% of SB patients
of all ages report headaches. The noise made by the TG can
greatly disturb the sleep of bedroom partners. The following
major risk factors have been shown to exacerbate SB-TG: (1)
smoking, caffeine and heavy alcohol drinking; (2) type A
personality—anxiety; (3) sleep disorders such as snoring,
sleep apnea or periodic limb movements
(concomitant in 10%).
    Clinically, SB is diagnosed following report by the sleep
partner or parent of recent/frequent TG (this is the most
reliable criterion), the presence of tooth wear or jaw muscle
hypertrophy, and awareness of jaw clenching while awake.2
The sleep laboratory diagnosis of SB requires that it be
distinguished from other oromandibular activity during sleep
(e.g., oromandibular myoclonus, swallowing, coughing, grunting,
tooth tapping, vocalization, etc.) that may represent up to
30% of all oral activities during sleep. Episodes of jaw
muscle contractions are scored as moderate to severe SB if
more than four EMG events per hour of sleep are noted. The
final diagnosis is made if at least two SB episodes per night are
associated with TG noise.

2. Hypotheses on genesis of SB
    Various hypotheses have been proposed to explain SB:
changes in dental occlusion but no strong evidence-based
data support this hypothesis; stress and anxiety has also
been suggested; involvement of the dopaminergic
system that remains to be confirmed since in most randomised
experimental trials with dopaminergic medications
(e.g., L-dopa, bromocriptine), the onset of SB episodes is only
marginally reduced. During wakefulness, dopamine has a
role in the execution of movement and in maintaining
vigilance; during sleep the dopaminergic system is probably
minimally active at the exception of brief period of arousal
related movements such as periodic limb movements.
    2.1. Descending influences from cortex during sleep
Another hypothesis on genesis of RMMA during sleep is that,
conversely to wake state, cortico-bulbar influences are not
dominant during sleep. The top-down circuits seem to be
partially de-activated during sleep to preserve the so-called
sleep continuity. The following evidences support this
hypothesis in the physiopathology of SB: (1) a specific increase
in the cortical activity, over the motor cortex, precedes most
limbmovements. This brief and large deflection of brain wave
activity is termed pre-motor potential. We have found that
RMMA are not preceded by such pre-motor cortical potential
during sleep (Kato et al., unpublished observation). This
suggests that SB is not generated by a clear pattern of cortical
activation. (2) We also found, during sleep of SB patients, that
SB episodes are not associated with the so-called cortical K
complexes that are electroencephalographic (EEG) marker of
sudden changes in brain endogenous activity or secondary to
sounds influences. (3) In order to better understand the
‘‘basis’’ of the genesis of RJM, we directly tested if corticobulbar
pathways remain active during sleep of primates
(macaca fascicularis). We observed that the intracortical
microstimulation (ICMS) threshold did not evoke RMMA (or
a rhythmic jaw movements = RJM) responses from the cortical
masticatory area (CMA) during light non-REM sleep (stages 1
and 2 in humans) in comparison to the quiet awake state.
However, as soon as the animal wakes up, there is a rapid
return of RJM at ICMS threshold levels comparable to presleep.
These preliminary data suggest that the geneses of RJM
or RMMA during sleep are probably not directly under the
influence of the cortical network as seen during wake state.
    2.2. Sleep micro-arousal: brain and autonomic
reactivation toward arousal
It is possible that the sudden onset of RMMA during sleep is
occurring in brief time windows at which the brain is
switching from sleep to an aroused state. These periods are
termed micro-arousal which is defined as 3–15 s abrupt shifts
in EEG activity accompanied by a rise in heart rate and muscle
tone.31 Micro-arousals (MA) tends to recur 8–15 times per hour
of sleep in young healthy subjects.
    To better understand the role of MA in sleep it is important
to revise how sleep in initiated and maintained. To initiate
non-REM (rapid eye movement) sleep, a massive inhibition of
GABA on brain arousal ascending system is needed to reverse
the influences of arousal related orexin/hypocretin, from the
hypothalamus, and on acetylcholine, noradrenalin, histamine
and serotonin brain networks. Moreover, from the onset of
sleep, a reduction in muscle tone to a clear hypotonia or a near
limb paralysis in the REM sleep stages is observed. It is further
suggested that the reduction of muscle tone during REM sleep
is under the influences of noradrenergic neurons of the
peduculopontine tegmentum (PPT) neurons and of GABA and
glycine inhibition on both brainstem and spinal cord motoneurons.
    SB tends to occur in relation to recurrent MA within the socalled
cyclic alternating pattern or CAP. As described above
MA are characterized by a repetitive rise in heart and brain
activity within sleep and are thought to reflect a natural
process that acts as a sensor for maintaining body homeostasis
and as a protective sentinel during sleep. We
explored the role of MA, as a physiological state that may
increase the probability of initiating an episode of SB, with the
use of a sensory vibrator during sleep. Experimentally induced
RMMA related MA were followed by TG in over 70% of trials in
SB patients only and not in control subjects. Our laboratory
has further demonstrated that the onset of SB is related to a
sequence of physiological activations in relation to the MA:

(1) A rise in
sympathetic cardiac activity around 4min before         
RMMA.
(2) A rise in the frequency of EEG activity 4 s before RMMA.
(3) A tachycardia starting one heart beat before RMMA.
(4) An increase in jaw-opener ‘‘suprahyoid’’ muscle activity
(probably responsible for mandible and airway opening)
0.8 s before RMMA.
(5) Finally, RMMA EMG episodes scored as SB on masseter
muscles, with or without TG.
Interestingly, we have recently shown that we can
prevent the cardiac-sympathetic over-activation associated
to SB episodes (step #1 of SB sequence, Fig. 1) by the use of
the alpha-adrenergic agonist clonidine. The administration
of clonidine at bedtime reduces cardiac-sympathetic activity
and, secondarily, the number of SB episodes by 60%.44
We further showed in a preliminary study that we could
reduce the number of SB episodes by opening the airway
(step #4 of SB sequence) since a mandibular advancement
device (MAD) used in SB patients reduced (by 60%) the
probability of SB episodes. However, these preliminary data
require cautious interpretation since the MADs tend to
trigger jaw discomfort that may have influenced the
outcomes.

Then, our data suggest that the episodic and transient reactivation
of arousal ascending system may be associated to
the sudden apparition of RMMA in relation to ‘‘permissive’’
excitation or disinhibition (inhibition of inhibition) on some
motor trigeminal neuron or interneuron of the central pattern
generator (CPG) network responsible of RMMA. The rhythm of
jaw movements generated during bruxism is at 1 Hz frequency.
Also, in contrast to mastication, sleep-related RMMA
are characterized by co-contraction of opening and closing jaw
muscles and these purposeless movements rarely last more
than 8 s.

3. Conclusion
The above results suggest that the onset of RMMA and SB
episodes during sleep are under the influence of the brainstem
arousal—reticular ascending system contributing to the
increase of activity in motor and autonomic-cardiac neuronal
networks.