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Bruxism and temporal bone hypermobility in patients with multiple sclerosis.
Article Type:
Report
Subject:
Bruxism (Development and progression)
Bruxism (Diagnosis)
Bruxism (Care and treatment)
Bruxism (Research)
Multiple sclerosis (Risk factors)
Multiple sclerosis (Diagnosis)
Multiple sclerosis (Care and treatment)
Multiple sclerosis (Research)
Radiography (Usage)
Authors:
Williams, David E.
Lynch, John E.
Doshi, Vidhi
Singh, G. Dave
Hargens, Alan R.
Pub Date:
07/01/2011
Publication:
Name: CRANIO: The Journal of Craniomandibular Practice Publisher: Chroma, Inc. Audience: Academic Format: Magazine/Journal Subject: Science and technology Copyright: COPYRIGHT 2011 Chroma, Inc. ISSN: 0886-9634
Issue:
Date: July, 2011 Source Volume: 29 Source Issue: 3
Topic:
Event Code: 310 Science & research
Geographic:
Geographic Scope: United States Geographic Code: 1USA United States

Accession Number:
262884652
Full Text:
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.

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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:

d=1/2v*t

[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, [DELTA]L).

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

Sample

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]

Measurement Procedures

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 equation).

[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.

Results

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 4.

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]

Discussion

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.

Acknowledgement

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 assistance.

References

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(3.) Attansio R: Nocturnal bruxism and its clinical management. Dental Clinics of NAm 1991; 35:245-252.

(4.) Singh GD, Olmos S: Use of a sibilant phoneme registration protocol to prevent upper airway collapse in patients with TMD. Sleep Breath 2007; 11: 209-216.

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(8.) Ueno T, Macias BR, Yost WT, Hargens AR: Noninvasive assessment of intracranial pressure waveforms by using pulsed phase lock loop technology. J Neurosurg 2005; 103:361-367.

(9.) Ueno T, Ballard RE, Shuer LM, Cantrell JH, Yost WT, Hargens AR: Noninvasive measurement of pulsatile intracranial pressure using ultrasound. Acta Neurochir Suppl 1998; 71:66-69.

(10.) Ueno T, Shuer LM, Yost WT, Hargens AR: Development of a noninvasive technique for the measurement of intracranial pressure. Biol Sci Space 1998; 12:270-271.

(11.) Miywaki S, Forbes DP: The morphologic and biochemical effects of tensile force application to the interparietal suture of the Sprague-Dawley rat. Am J Orthod Dentofacial Orthop 1987; 92:123-133.

(12.) Bunge RP, Settlage PH: Neurological lesions in cats following cerebrospinal fluid manipulation. J Neuropath Exp Neural 1957; 16:471-490.

(13.) Munger KL, Zhang SM, O'Reilly E, Hernan MA, Olek MJ, Willett WC, Ascherio A: Vitamin D intake and incidence of multiple sclerosis. Neural 2004; 62:60-65.

(14.) Ascherio A, Munger KL, Simon KC: Vitamin D intake and multiple sclerosis. Lancet Neural 2010; 9:599-612.

(15.) Hubbard RP: Flexure of layered cranial bone. J Biomech 1971; 4;251-263.

(16.) Hubbard RP, Melvin JW, Barodawala IT: Flexure of cranial sutures. J Biomech 1971; 4;491-496.

(17.) Chebel S, Rekik O, Boughammoura-Bouatay A, Frih-Ayed M: Pseudotumoral presentation of multiple sclerosis. Neurochirurgie 2007; 53:379-382. [Article in French]

(18.) Silverberg GD: Normal pressure hydrocephalus (NPH): ischaemia, CSF stagnation or both. Brain 2004; 127: 947-948.

(19.) Kokich VC: The biology of sutures. In: Cohen Jr MM, ed. Craniosynostosis. Diagnosis, evaluation and management. New York: Raven Press 1986; 94.

(20.) Schulz M, Engelhardt B: The circumventricular organs participate in the immunopathogenesis of experimental autoimmune encephalomyelitis. Cerebrospinal Fluid Res 2005; 2:8.

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(22.) Newman NJ, Selzer KA, Bell RA: Association of multiple sclerosis and intracranial hypertension. J Neuroophthalmol 1994; 14:189-192.

(23.) O'Brien T, Paine M, Matotek K, Byrne E: Apparent hydrocephalus and chronic multiple sclerosis: a report of two cases. Clin Exp Neural 1993; 30:137-143.

(24.) Talbert DG: Raised venous pressure as a factor in multiple sclerosis. Med Hypotheses 2008; 70:1112-1117.

(25.) Williams B J, Skinner H J, Mafia BL: Increased intracranial pressure in a case of pediatric multiple sclerosis. J Child Neural 2008; 23:699-702.

(26.) Serafini B, Rosicarelli B, Franciotta D, Magliozzi R, Reynolds R, et al.: Dysregulated Epstein-Barr virus infection in the multiple sclerosis brain. J Exp Med 2007; 204:2899-2912.

(27.) Gard G: An investigation into the regulation of intra-cranial pressure and its influence upon the surrounding cranial bones. J Body Mov Ther 2009; 13:246-254.

(28.) Zamboni P, Galeotti R, Menegatti E, Malagoni AM, Gianesini S, et al.: Chronic cerebrospinal venous insufficiency in patients with multiple sclerosis. J Neural Neurosurg Psychiatry 2009; 80:392-399.

(29.) Singh AV, Zamboni P: Anomalous venous blood flow and iron deposition in multiple sclerosis. J Cereb Blood Flow Metab 2009; 29:1867-1878.

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: drsingh@drdavesingh.com

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 disease.

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.
Table 1
Jaw Clenching Procedure Performed
by Each Subiect

Time (sec)                 Action

   0-5       Relaxed
   5-10      Clenching begins, gradually increasing
             the force until reaching 100 lbs
  10-15      Maintain clench at 100 lbs
  15-20      Clench is released

Table 2
Reproducibility Tests on Subjects
Chosen at Random *

Test number   [DELTA]L (mm)

    1         0.385
    2         0.077
    3         0
    4         0.385
    5         0.154
    6         0.1386
    7         0.077
    8         0.1078
    9         0.0924
    10        0.1694
    11        0.231
    12        0.0462
    13        0.077

* These data show a 0.0332 standard error and a small
sample variation compared to the standard deviation.

Table 3
Statistics on Reproducibility of Measurements
of Study Subjects

                         Value

Mean                     0.1493
Standard error           0.0332
Standard deviation       0.1197
Sample variance          0.0143
Confidence level (95%)   0.0723

Table 4
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
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