ABSTRACT: In this study, the authors investigated the link between
jaw clenching/bruxism and temporal bone movement associated with
multiple sclerosis (MS). Twenty-one subjects participated in this study
(10 patients with MS and 11 controls). To quantity the change in
intracranial dimension between the endocranial surfaces of the temporal
bones during jaw clenching, an ultrasonic pulsed phase locked loop
(PPLL) device was used. A sustained jaw clenching force of 100 lbs was
used to measure the mean change in acoustic pathlength ([DELTA]L) as the
measure of intracranial distance. In the control subjects the mean
[DELTA]L was 0.27 mm[+ or -]0.24. In subjects with MS the mean [DELTA]L
was 1.71 mm[+ or -]1.18 (p<0.001). The increase in magnitude of
bi-temporal bone intracranial expansion was approximately six times
greater in subjects with MS compared to controls. Therefore, jaw
clenching/bruxism is associated with more marked displacement of the
temporal bones and expansion of the cranial cavity in patients with MS
than in control subjects.
Multiple sclerosis (MS) is the major cause of nontraumatic
neurological disability in young adults in North America. (1) Patients
with MS suffer from a progressive loss of normal brain function, leading
to disability, sometimes with severe pain, dementia and even death.
Current medical management offers palliative treatment and some slowing
of the disease process, but the etiology of MS remains elusive. One
early study suggested that there may be a link between MS and tooth
decay. (2) This study led researchers to investigateotherdental factors
associated with MS. Unpublished, three dimensional (3D) radiographic
imaging studies have demonstrated the presence of a malpositioned
superior border of the temporal bone in patients with MS, and evidence
is emerging of a shifting of the squamosal suture during sustained,
maximal jaw clenching in those patients. Studies of jaw clenching have
demonstrated pressures of 975 psi at the molars and as high as 175,000
psi at the incisors. (3) Although it is assumed that structures that
support the insertions of the masticatory muscles are stable and
stationary, and that the impact of clenching/bruxism is strictly a
dental issue, evidence is beginning to emerge that bruxism/TMD may be
associated with a compromised airway, (4) and TMJ health may be
important in overall cranial health. Moreover, modern radiographic
techniques have allowed critical evaluations of compliance in the
cranial sutures, suggesting that cranial mobility is detectable. With
external manipulation of the cranial vault, temporal bone movement (the
mean angle of change at the squamosal suture) is about 1.75[degrees].
For example, the mastoid process moves by 1.66[degrees], the malar line
moves by 1.25[degrees] and the sphenoid bone moves by 2.4[degrees].
Other measurements indicate that this amount of movement is common in
most sutures. (5)
It is thought that changes in intra-cranial pressure (ICP) lead to
corresponding changes in intra-cranial diameter. (6-7) These changes can
be measured using a pulsed phase locked loop (PPLL) device (8) (Figure
1). The PPLL device originally was used to measure pulsatile changes in
ICP. (9-10) The PPLL device transmits a 500 kHz ultrasonic tone burst
through the cranium via a transducer placed on the subject's head.
The tone burst passes through the cutaneous tissues, reflects off the
ipsilateral intracranial temporal bone (Echo 1), passes through the
intracranial contents; reflects off the endocranial surface of the
temporal bone on the opposite (contralateral) side of the skull, and is
received back (as Echo 2) by the originating transducer (Figure 2). Any
change in cranial diameter produces a phase shift in the ultrasound
signal. (9-10) The PPLL processing software is designed to track changes
in the phase of the ultrasonic signal as it strikes the intracranial
surfaces of the temporal bones and converts those changes into an
estimated target delay ([DELTA]L, change in acoustic pathlength). (8)
The resulting target delay estimates are then converted into a distance
measuring the intracranial distance using the equation:
[FIGURE 1 OMITTED]
[FIGURE 2 OMITTED]
where t is the target delay estimate and v is the speed of sound.
Thus, the time of the phase shift is converted into millimeters of
movement (d) of the temporal bones (change in acoustic pathlength,
In addition, mechanical tensions placed on the teeth are
transmitted to the cranium. In one study, these tensile forces were
found to be positively correlated with osteogenic responses in the
interparietal sutures. (11) Thus, an abnormal bite relationship may
exert unequal pressure on the cranial bones, which may be a precursor of
cranial bone dysfunction. Therefore, the PPLL device offers a
non-invasive method for evaluating the physical stresses of bruxism on
the cranium and its components. In view of these technical developments
and clinical observations, it was hypothesized that periodic episodes of
bruxism/ clenching may, under certain circumstances, cause increased
cranial suture mobility. This mobility could result in pressure changes
inside the cranium, which might in turn alter CSF flow, venous flow, or
neurologic tissues directly. Therefore, the aim of this preliminary
study is to test the null hypothesis that clenching/bruxism is not
associated with hypermobility of the temporal bones in patients with MS.
Materials and Methods
The UCSD Human Research Protections Program approved this study.
After obtaining IRB approval, 11 control subjects and 10 patients with
MS diagnosed by a neurologist participated in this study. Inclusion
criteria for the control subjects were: 1. no relevant medical history;
and 2. aged 18-60 years old. Exclusion criteria for the control subjects
were: 1. history of chronic headaches; 2. history of cranial trauma; 3.
history of neurologic symptoms or diseases; 4. anodontia in one or both
dental arches; 5. advanced periodontitis with dental mobilities over
class 1; and 6. dental or muscular pain upon clenching. Similarly,
inclusion criteria for the MS patients were: 1. medical diagnosis of MS
by a neurologist; 2. aged 18-60 years old. Exclusion criteria for the MS
patients were: 1. anodontia in one or both dental arches; 2. advanced
periodontitis with dental mobilities over class 1; and 3. dental or
muscular pain upon clenching. The mean age of the control group was 44.9
years. The mean age of the MS group was 48.2 years. There were
approximately the same number of males and females in the control and MS
groups. All study subjects were of Caucasian ethnicity.
[FIGURE 3 OMITTED]
All subjects lay supine on a bed with their head resting in a
headrest to rigidly position the transducer, which sends and receives
ultrasound waves (Luna Innovations, Blacksburg, VA). The
transducer's position was adjusted manually, and the head was
rigidly fixed in a frame. After the transducer was placed over the right
temple of the subject, it was adjusted until strong ultrasonic echoes
were obtained from the endocranial surfaces of the temporal bones
(Figure 3). Once adjusted, a maximum strength test was conducted to
measure the maximum clenching strength of the subject, using a dental
bite I-scan sensor (Tekscan Inc., South Boston, MA). The subjects bit
down on the sensor that was a Mylar sheet with pressure sensitive ink
between metal tracings. The sensors have double layers of thin rubber
protectors to dissipate the forces and prevent perforation. The subjects
clenched as hard as they could for one second while data were acquired.
This procedure was used both to test the subject's maximum
clenching force, and to show them the desired clenching levels. Later
the subjects were able to judge their strength and maintain a 100 lb
clench-force for this test. The signal was determined with the muscles
at rest. The signal was checked again and data were acquired for 20
seconds, while the subject underwent the jaw clenching procedure, as
described in Table 1. The change in intracranial temporal bone diameter
was expressed as [DELTA]L (change in acoustic pathlength), which was
converted into intracranial distance in mm (using the aforementioned
[FIGURE 4 OMITTED]
To ensure that the subject was clenching at approximately 100 lbs,
the subject watched a video monitor, which showed clenching force. This
force was detected by a load cell developed by T-scan (Tekscan Inc.,
South Boston, MA). With care taken to ensure that the subject did not
move the head during this procedure, one member of the research team
monitored the clench strength, while a second member coached the subject
on proper jaw clenching. To ensure reproducibility, all study subjects
were tested several times under this protocol. For each test, the
ultrasonic data were saved to a file and processed in real time.
The technique provided high-resolution measurements of the change
in the position of the echo from the initial estimate. For these tests,
the position of three echoes was tracked with the PPLL: an echo from the
transducer's surface at the skin; an echo from the endocranial
surface of the right temporal bone just as the signal entered the
cranium (Echo 1); and an echo from the endocranial surface of the left
temporal bone after the signal had passed through the cranial cavity
(Echo 2). After tracking changes in the position of these echoes with
time, the data were saved to a file. By subtracting the difference in
the position between Echo 2 and Echo 1, it was possible to measure
changes in the width of the intracranial distance between the two
temporal bones, eliminating dimensional changes due to the motion of the
temporal muscle during clenching. This value is the intracranial length
or distance between the inner tables of the temporal bones (derived from
the change in acoustic pathlength, [DELTA]L). In essence, the PPLL
tracks changes in the distance between the transducer, the proximal
(right) and the distal (left) intracranial wall. To subtract out soft
tissue movement between the transducer and the proximal wall, the saved
data were reprocessed, this time locked on the echo from the proximal
wall (Echo 1). By subtracting the second result (Echo 2) from the first,
the authors were able to monitor changes in the distance between the
proximal and distal temporal bones during clenching.
For tests of reproducibility, one subject was chosen at random.
Thirteen tests and data points were obtained. The data are displayed in
Table 2 with statistical analysis in Table 3.
The results of the reproducibility test showed there was no
statistical difference in the measurement procedure. Therefore, analysis
of variance (ANOVA) was used on the data obtained from the control
subjects and MS patients who participated in this study.
Figures 4 and 5 show the PPLL locked at the back surface and front
surface of a patient with MS, and the changes in target delay can be
seen at these points. With the PPLL locked on the back surface, the PPLL
tracks changes in the distance between the transducer and the distal
skull wall. To subtract out soft tissue movement between the transducer
and the proximal skull wall, the saved data was reprocessed, this time
locked on the echo from the proximal skull wall, as shown in Figure 5.
By subtracting the second result from the first, the authors are able to
monitor changes in the distance between the ipsilateral and
contralateral temporal bones during clenching.
As can be seen in Figure 4, as the subject clenched, the distance
between skull plates increased. Figure 5 shows that, as the subject was
clenching, the soft tissue distance was actually decreasing, so the
resulting change in skull was actually greater than that shown in Figure
After subtracting soft tissue movement for all subjects, Figure 4
shows the results that were recorded for the cranial movements in the
temporal region. The results of ANOVA of the data obtained from the
subjects who participated in this study are summarized in Table 4.
Figure 6 shows the results recorded for cranial movements in the
temporal region: Distance is the change in intracranial distance
(derived from the change in the acoustic pathlength, [DELTA]L) in mm
with jaw clenching, i.e., widening of the diameter at the intracranial
surfaces of the temporal bones.
The results in Table 4 demonstrate a statistically significant
difference in temporal bone movement, as measured by the PPLL, between
the two groups (p<0.001). In other words, as the subject clenched,
the distance between the endocranial surfaces of the temporal bones
increased. As the subject was clenching, the soft tissue distance was
decreasing, so the resulting change in intracranial diameter (Echo 2
minus Echo 1) was greater, especially in the group with MS. The increase
in magnitude of bi-temporal bone intracranial expansion was nearly six
times greater in subjects with MS compared to controls.
[FIGURE 5 OMITTED]
The pathogenesis of MS involves autoimmune driven breakdown of the
myelin sheath surrounding the nerve fibers in the white matter. (12)
There are several ideas on the patho-etiology of MS. A significant
relationship between decreased vitamin D levels in patients with MS is
documented. (13-14) Vitamin D deficiency could lead to reduced bone
density in patients with MS, which, in turn, could lead to greater
cranial compliance along the layered bone (15) and sutures. (16) Indeed,
some investigators believe that trauma may be an instigating factor (17)
in its development. Thus, briefly, externally derived forces might cause
paroxysmal pressure spikes in the fluids surrounding the brain and
spinal cord that could act as a traumatic factor. In addition, it is
well documented that changes in intracranial pressure (ICP) lead to
corresponding changes in cranial diameter. (6-7) Furthermore, ICP
changes in many neurodegenerative diseases manifest idiosyncratic
phenomena and are often accompanied by cellular disruptions that
resemble elevated ICP conditions. For example, studies have shown that
hydrocephalus may produce significant periventricular demyelination,
probably as the result of mechanical stretching. (18)
The cranium was once thought to be a rigid configuration of bone
and ossified sutures. However, modern techniques have allowed critical
evaluation of the compliance in the sutures. For example, Kokich (19)
showed that the temporo-parietal (squamosal) suture does not begin to
synostose until the 3rd--4th decade in humans. Indeed, temporal bone
movement (mean angle of change at the suture) is about 1.75[degrees].
Other measurements indicate that this magnitude of movement is common in
most sutures in most crania. (5) Indeed our current, unpublished 3D
radiographic imaging studies demonstrate the presence of a malpositioned
superior border of the temporal bone in patients with MS. This
observation led the authors to hypothesize that periodic episodes of
bruxism may be associated with increased intracranial pressure, which in
turn, might be associated with demyelination in patients with MS. In
this study, using a jaw clenching protocol and the PPLL, the aim was to
establish a link between hypermobility of the temporal bones and jaw
clenching/bruxism, reflecting increased intracranial pressure in the
development of MS. In fact, it was found that an increase in magnitude
of bi-temporal bone intracranial expansion was nearly six times greater
in subjects with MS compared to controls. Therefore, jaw
clenching/bruxism is associated with more marked displacement of the
temporal bones and expansion of the cranial cavity in patients with MS
compared to control subjects. Nevertheless, it must still be determined
whether clenching/bruxism leads to temporal bone hypermobility in
patients with MS or whether it is a latent sign of the disease.
[FIGURE 6 OMITTED]
It has been postulated that patients with MS exhibit the
parafunctional abnormality of night-time clenching/bruxism, which may
cause increased ICP waves. These waves could lead to significant
periventricular demyelination. (12,20-21) Our original hypothesis was
that bruxism caused an increased ICP, but we now suspect that marked
expansion and contraction of the intracranial cavity by the hypermobile
temporal bones might induce pressure waves. As the intracranial distance
between the temporal bones expands and contracts during bruxism, the
compression may decrease cranial cavity volume with a corresponding
increase in ICP pressure, at least in principle, and may precipitate MS
in subjects with a genetic predisposition for the disease. There are
several reports of elevated CSF pressure in patients with MS. (17,22-25)
However, there are several limitations with this present preliminary
study. First, the sample is small and not matched as thoroughly as is
optimal. Second, for this investigation, a constant speed of sound of
1540 [ms.sup.-1] in tissue was estimated, due to the nonhomogeneity of
tissues in the intracranial space. However, based on previous studies,
(10) the conversion error could be as large as 5-6%, as variations in
intracranial distance are more significant than temperature- or
pressure-dependent variations in the speed of sound that may also affect
the target delay. Despite these constraints, much greater temporal bone
displacement was found with jaw clenching in patients with MS compared
to control subjects. Such changes in intracranial diameter could
generate high-pressure intracranial waves, which could cause
periventricular alterations in the blood-brain barrier (BBB) and promote
demyelination, in subjects with a genetic susceptibility to the
condition. Such alterations in the BBB could lead to lymphocytes
entering the periventricular tissues to form ectopic lymph nodes. (26)
Therefore, there is considerable interest in regulation of ICP, venous
outflow, and the venous systems. (27)
If bruxism compromises normal outflow of blood from the brain in
at-risk individuals, chronic cerebraspinal venous insufficiency might be
exacerbated, leading to intracerebral iron deposition and inflammatory
lesions. (28-29) However, an alternative process might be a sudden
reduction in the ICP when the jaw clenching ceases, followed by a sudden
wave of increased pressure as the cranial bones deflect back to their
original position. Moreover, the marked expansion of the cranial cavity
could cause a drop in ICP until blood enters the cranial cavity acutely.
In view of these preliminary findings, it is suggested that dental
professionals evaluate the need to prevent, diagnose and treat
bruxism/clenching as a preventive measure in the putative development of
MS. Future studies should endeavor to investigate the existence of a
temporal relationship between the onset of MS and bruxism, and seek to
identify a causal relation between the presence of MS and bruxism. In
addition, as patients with MS frequently suffer marked fatigability,
studies with polysomnography to investigate nocturnal bruxism and
evaluate compromised airway space in patients with MS are warranted.
This research was supported by a research grant from Stryker Corp.,
Kalamazoo, MI. The authors would like to thank G.W. Ellison, UCSD
Department of Neurosciences, San Diego, CA, and B.R. Macias, Department
of Health and Kinesiology, Texas A&M University, for technical
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David E. Williams, D.D.S.; John E. Lynch, Ph.D.; Vidhi Doshi, B.S.;
G. Dave Singh, D.D.Sc., Ph.D., B.D.S.; Alan R. Hargens, Ph.D.
Manuscript received June 29, 2010; revised manuscript received
October 11, 2010; accepted January 12, 2011
Address for correspondence:
Dr. Dave Singh
BioModeling Solutions, LLC
Cornell Oaks Corporate Center
15455 NW Greenbrier Pkwy.
The Commons Building, Suite 250
Beaverton, OR 97006 E-mail: firstname.lastname@example.org
Dr. David Williams received his B.Sc. degree in Zoology from the
University of Lethbridge in 1976. He obtained a D.D.S. degree from the
University of Alberta in 1980 and has a private dental practice in
Okotoks, Alberta, Canada. He has an interest in craniomandibular
physiology and anatomy and participated in the ISNVD conference in
Glasgow, Scotland in October 2010 and has been invited to attend the
inaugural meeting in Bologna, Italy in March 2011. Dr. Williams is a
board member of the National CCSVI Society.
Dr. John E. (Ted) Lynch is the Scientific Director for Luna's
Medical Products group. Prior to that, he was the Principal Investigator
on five Phase I SBIR programs and three Phase II programs. He is a
graduate of the NDE Group in the Applied Science Department at the
College of William & Mary. For his PhD research, he developed
technology for the ultrasonic diagnosis of ear(v-stage periodontal
Ms. Vidhi Doshi received her B.S. degree at the University of
California, San Diego in Bioengineering/Biotechnology. She is a
currently second year medical student at the Michigan State University,
College of Human Medicine and hopes to pursue a career in pediatrics.
Dr. G. Dave Singh was born, educated and trained in England. He
holds three doctorates, including a Degree in Dental Surgery, a Ph.D. in
Craniofacial Development, and a D.D.Sc. in orthodontics. At the Center
for Craniofacial Disorders (UPR), he led a NIH-funded program of
craniofacial research and was awarded First Prize at the International
Association for Orthodontics (2005). Dr Singh holds three U.S. patents,
has published numerous articles, and has lectured in Australia, Asia,
Europe and North America.
Dr. Alan R. Hargens is a professor and Director of the Orthopaedic
Clinical Physiology Lab at the University of California. San Diego. He
previously served as Chief of Space Physiology and Space Station Project
Scientist at NASA and Consulting Professor of Human Biology at Stanford
University. He is the recipient of a NIH Research Career Development
Award, Elizabeth Winston Lanier Award from the American Academy of
Orthopaedic Surgeons and Orthopaedic Research Society, Recognition Award
from the American Physiology' Society, and two NASA Honor Awards.
Jaw Clenching Procedure Performed
by Each Subiect
Time (sec) Action
5-10 Clenching begins, gradually increasing
the force until reaching 100 lbs
10-15 Maintain clench at 100 lbs
15-20 Clench is released
Reproducibility Tests on Subjects
Chosen at Random *
Test number [DELTA]L (mm)
* These data show a 0.0332 standard error and a small
sample variation compared to the standard deviation.
Statistics on Reproducibility of Measurements
of Study Subjects
Standard error 0.0332
Standard deviation 0.1197
Sample variance 0.0143
Confidence level (95%) 0.0723
ANOVA of Data from Figure 6
Groups Number Mean SD p value
Control 11 0.27 0.24 0.0008
MS 10 1.71 1.18