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Does Dentistry Hold The Missing Link to Multiple Schlerosis, Alzheimers and Others?

March 1, 2018
by Dr. David Edmund Williams


The search for the cause of Multiple Sclerosis (MS) by mainstream medicine has followed a profound predilection for autoimmune conjecture, in spite of the absence of evidence for any “mechanism by which the immune system is tricked into seeing myelin as foreign in MS patients,” said Dr. Bruce Trapp of the Cleveland Clinic. He continues, “Is there a ‘missing link’ that is responsible for the disease, MS?” A. Chaudhuri comments that “Transplanting EAE (autoimmune theory) data to human MS is not science but an example of monumental incredulity that has only hindered proper MS research.” A new discovery from outside the neurological paradigm may hold the “missing link”. This article will describe this phenomenon and show how it may be a major component in the etiology of MS and other neurological illnesses like Alzheimer’s DementIa (AD) and Parkinson’s Disease (PD). A future article will delineate the specifics of dental and cranial physiology that lead to it. A third will discuss treatment implications.

We suggest that displacement of the cranial bones (discovered in anatomical studies of MS and Alzheimer’s crania) caused by jaw clenching, is responsible for short bursts of global and or regional cerebrospinal fluid pressure waves which a) directly damage the subpial brain tissues generally and specifically around periventricular veins and b) produce downstream turbulence through the ventricular fluid system and endothelial venous blockage, which further complicates the fluid dynamics and brain perfusion.This bone displacement begins slowly and occurs mostly at night or during clenching events called bruxing.

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The connection of MS to dentistry has been known for a long time but is rarely discussed in the literature. Craelius (1978) reported the global demographic “overlap” of deaths due to MS with the DMF (decayed, missing, filled) distribution. He said, “A review of the literature shows that the risk for dental caries is lower among… blacks compared with whites; and males compared with females. The dental caries risk is higher during pregnancy and lactation. All these trends have been described for MS as well.” The statistical significance of these findings were very high (P = <.001).

Could more women get MS (and Alzheimer’s) than men because of the presence of relaxin in their hormonal cycles? Nicozisis (2000) said, “Relaxin is responsible for the relaxing of the pubic symphysis; the birth canal is widened for parturition. Our results indicate the presence of relaxin within the cranial sutures. Histological observations revealed definite changes in the collagen fibril arrangement from being dense and highly organized with a perpendicular direction between the bones to randomly organized and loose, lacking any direction.” Do female hormone cycles cause loosening of joints and sutures? It is interesting that 2X more women suffer from TMJ symptoms than men.

The temporal-parietal suture is found to have the greatest variability of shape and complexity of bone-surface interlock. This variability is determined by dental loading patterns during formative years (Fig. 1). Zhang (2015) found that, “The morphology of the suture had large influences on the dynamics of the bone-suture complex… The suture elastic modulus and the arrangement of sutural fibers also had influence on the dynamics.” Interestingly, Poser 1995 discussed the possible connections of MS to the white race via viking heritage. Could inherited skull development and structure variation be a part of the demographic trends in MS? If the bone interface-configuration is not robust, the integrity of the suture would depend entirely on the collagenous ligaments. The ensuing tug-of-war between the clenching muscles and these ligaments is what this paper is about.

Fig. 1
Inner facing surface of squamous temporal bone.
Left: This suture morphology relies completely on collagen fiber strength for its integrity. Suture displacement limited by ligament integrity.
Right: Bony limits to muscle driven displacement. The structural complexity of this suture would resist sutural failure under loading.

The issue of collagen and sutural integrity is further illuminated by the connections between MS and Ehlers-Danlos (EDS) disease in which inherited flaws in the formation of collagen are present. Vilisaar reports a, “10-11 times increased prevalence of EDS in MS patients compared with the general population (P = 0.02). Suggested implications include a possible causal relationship on a connective tissue level with a higher susceptibility to MS in EDS.”

The Discovery
Cranial suture displacement caused by dental loading in humans was discovered in 2006. This was published in CRANIO in 2011. In this study, we measured intertemporal bone displacement during jaw clenching in MS patients and age/sex matched controls. Using Pulsed Phase Locked Loop (PPLL) ultrasound,we measured lateral displacements of as much as 3.6 mm during a metered 100 pound jaw clench in 10 MS patients (Williams 2011). The non MS subjects showed displacement of .5 mm or less. It is assumed that this bone movement is capable of creating significant fluid and/or tissue displacement inside the cranium since outward movement of the squamous temporal would be accompanied by downward movement of the parietal bones (based on suture shape and orientation) under pressure from the temporalis muscles (jaw clenching forces) (Fig. 2).

Fig. 2
Illustration: Mechanism of Episodic Paroxismal Trauma caused by jaw clenching in MS.

In cadaver dissections leading up to this study we found 14 of 14 MS cadavers to have a visible displacement at the squamosal sutures. Eight of these were newly deceased and blood was easily expressed from this one suture by applying pressure with a thumb on the squamous temporal bones. This is highly suggestive of mobility under clenching loads (Fig. 3). Other sutures on these same cadavers had no such vascularization nor apparent deformation (structural or functional). By the sixth and seventh decade of life all healthy cranial sutures are thought to be physically fused with little or very slight displacement. This was found to be the case in over 300 normal skulls examined in medical school anatomy labs at U of A in Edmonton, UCSF San Diego and Dalhousie.
If jaw clenching causes chronic intracranial pressure waves in developing MS, are there any MS signs that this may be a contributing factor?

The earliest signs of pathology in MS occur around the small veins directly adjacent to the ventricles (Adams). As the disease progresses, these areas of inflammation and myelin loss extend along the veins into the surrounding white matter. These key facts are “elephants-in-the-room” – rarely mentioned – and their possible implications never discussed. A pressure wave passing through the brain and against the wall of the ventricle would certainly impact CSF fluid and the low pressure region around a vein differently than the surrounding tissue. Chronic pressure waves against these veins could lead to “arterialization” as is seen in the cardiac bypass veins (Obrien). Colin Adams’ Color Atlas of Multiple Sclerosis contains images of veins in early and late MS lesions. The early lesions show single cell thick venules with blood products surrounding the vein. The older lesions show veins that have taken on the appearance of arteries (Figs. 4 & 5). Little has been said in the literature about these common findings, but the accumulation of iron in MS brains is well documented (Stuber 2016). The source of iron seems to be clearly illustrated in these images of localized vein disruption. The exchange of antigenic myelin basic protein with blood born immune cells would be common place in this periventricular “brain storm” accounting for the immune cascade. What if simple trauma to these specific areas of the brain is the missing piece? This “trauma-engine” would be running in the background as long as chewing and bruxism are happening. Could attacks of MS be connected to increases in clenching? Negative stress is known to increase MS lesions.(Burns 2014) It also increases bruxism and TMJ pain.

Fig. 4 & 5
Recent haemorrhages around vein wall in plaques of multiple sclerosis. The presence of haemosiderin (brown) in the wall of the vein indicates that haemorrhage had occured on a previous occasion. Source: Adams C. W. M. 1989. Color Atlas of Multiple Sclerosis & Other Myelin Disorders.

Hyalinised vein wall (resembling an artery) with perivascular lymphocytes in multiple sclerosis. Source: Adams C. W. M. 1989. Color Atlas of Multiple Sclerosis & Other Myelin Disorders.
 

But does aberrant fluid pressure cause demyelination? According to the work of Bunge in 1957, the fluid pressure changes from cerebrospinal fluid pumping (called barbotage) as little as one cc exchanged 10 times in the fourth ventricle of cats caused demyelinated lesions and neurological deficits lasting several weeks. T-cell activation and inflammation were documented. Apparently, fluid pressure changes in the ventricles can cause demyelinating lesions in the adjacent white matter. Barz (2017) presented, “Experimental results which support the hypothesis that demyelinated lesions, as seen in multiple sclerosis, may be caused by increased tissue pressure.”

Now let’s turn the argument around. If fluid trauma from skull bone displacement is the cause of local white matter lesions in MS, surely, in a closed system there would be damage to all areas of the brain. Improvements in MRI imaging have shown that even in the earliest stages of MS there are significant changes in normal appearing white matter (NAWM) and in the grey matter (GM). Enzinger (2015) states, “Grey matter atrophy in MS occurs both at global and regional level and can be quantitated using MRI. It also does not directly correlate with the number of white matter lesions and diffuse normal appearing white matter damage, suggesting partially independent pathological processes. Unfortunately, GM volume measures are inherently non-specific and reveal little about the exact cause of tissue injury.” (Unless both are the result of general pressure increases accompanied by regional flow dynamics dictated by anatomical restraints such as falx and pial membranes, tissue planes and variation in the specific sources of brain compression).

MS is still considered a demyelinating disease in spite of this “global” nature. Is it plausible that trauma from these pressure waves could be responsible for disruption of the blood brain barrier, demyelination, exposure of the blood to myelin antigens, T cell activation and inflammatory cascades? If it is, it would make sense that all of these elements could be a part of other kinds of brain trauma scenarios. In fact, traumatic brain injury (TBI) manifests all of them and adds a few other interesting correlations. These same elements are known to be an integral part of Alzheimer’s dementia, Parkinson’s disease and traumatic brain injury.

Is this hidden, continuous trauma a common factor in neurological illness? TBI studies provide a wealth of data connecting this new theory to possible etiologies for various other brain pathologies.

As we zero-in on a trauma based theory in MS it becomes important to look at other neurological conditions. Many share the same elements including: iron accumulation, history of head trauma, sleep disturbance, ventricular enlargement and headaches. We don’t have room to detail all of the overlap between these illnesses but a few deserve mentioning.

Dementia is a component of MS and Parkinson’s and traumatic brain injury (TBI) and is accompanied by increased cortical degeneration and amyloid accumulation. M. David reported, “In MS, amyloid precursor protein (APP) was associated with lesions and plaques. Furthermore, patients with primary progressive MS displayed increase of amyloid β and tau protein levels in their CSF.” Amyloid has been identified as an indicator of disease activity in MS. But wait, MS is all about demyelination!

Is Alzheimer’s caused by a similar mechanism?
Anatomy studies have shown that in MS this temporal bone displacement is bilateral which would create more symmetrical pressure directly on the fluid in the ventricles. In Alzheimer’s cadavers, an even greater degree of displacement was discovered but only on one side. The opposite side was completely normal. Interestingly, every case of Alzheimer’s and Parkinson’s demonstrate a consistent left (or right) dominance of degeneration. In AD the areas that see the greatest loss are the hippocampus (directly above the petrous temporal bone) and the temporoparietal regions (beneath the squamousal suture). Patients with AD and PD demonstrate extreme imbalances between right and left chewing forces which, with age, may precipitate the described unilateral bone shifting.

CCSVI
CCSVI has been shown to be highly correlated with MS but clearly not the cause. It is now known to be present in most Parkinson’s sufferers. The importance of the extracranial venous stenosis and downstream fluid dynamics makes more sense in light of these intracranial pressure waves. Consider the following images from MS, Parkinson’s and Normals (Fig. 6). Should we not take such findings into full account, given the lack of progress in recent decades?

Fig. 6
MRI jugular venograms.

Summary

  • Human bite forces can reach 275 lbs per square inch. Nighttime bruxing can be even higher than day time. (Nishigawa)
  • Genetics, gender, trauma, Vitamin D, pregnancy and ageing etc. can lead to muscle hypertrophy and temporal bone mobility during jaw clenching.
  • Temporal bone mobility could cause pressure waves and direct impingement on the brain.
  • This unseen chronic trauma worsens with time and stress as the bones move more and more.
  • The impact on brain health may be a factor worth considering in all neurodegenerative illness.
  • This often goes on at night when no one is aware.

Other healthcare professionals who specialize in cranial bone health and cervical spine physiology should work closely with dentists to develop a better understanding of these components of brain health.

Questions

  • What if correction of dental and cranial elements opens up better long term treatment outcomes for MS and other degenerative diseases?
  • How can we measure the specifics of these structural and functional elements?
  • What if enigmatic neurological illness of all descriptions be prevented and eventually eliminated?

Note: The observation of abnormalities in the bite and related joint position of three late stage MS patients lead to the investigation and discoveries contained in this paper. The details of these observations represent a new way of looking at and treating human dental occlusion and invite collaborative work between all dental and cranial related health professionals. The dental components of this connection will be discussed in the next instalment of Oral Health. OH

Oral Health welcomes this original article.

References

  1. Barz H, Schreiber A, Barz U. 2017. “Demyelinating diseases as a result of cerebral edema?” In Medical Hypotheses. 104: 10-14.
  2. Bunge RP, Settlage PH. 1957. “Neurological lesions in cats following cerebrospinal fluid manipulation” In Journal of Neuropathology and Experimental Neurology. 16: 471-490.
  3. Burns MN, Nawacki E, Kwasny MJ, Pelletier D, Mohr DC. 2014.
  4. “Do positive or negative stressful events predict the development of new brain lesions in people with MS?” In Psychological Medicine. 2: 349-59
  5. Chaudhuri A, Behan P. 2004. “Multiple Sclerosis Is Not an Autoimmune Disease” In Archives of Neurology. 61: 1610-1612.
  6. Craelius W. 1978. “Comparative epidemiology of multiple sclerosis and dental caries” In Journal of Epidemiology and Community Health. 32: 155-165.
  7. David M A, Tayebi M. 2014. “Detection of protein aggregates in brain and cerebrospinal fluid derived from multiple sclerosis patients” In Frontiers in Neurology. December: 02.
  8. Enzinger C, Fazekas F. 2015. “Measuring Gray Matter and White Matter Damage in MS: Why This is Not Enough” In Frontiers in Neurology. 6: 56.
  9. Nicozisis JL, Nah-Cederquist HD, Tuncay OC. 2000. “Relaxin affects the dentofacial sutural tissues” In Clinical Orthodontics and Research. 3: 192-201.
  10. Nishigawa K. 2001. “Quantitative study of bite force during sleep associated bruxism” Journal of Oral Rehabilitation. 5: 485-91
  11. Poser CM. 1995. “Viking voyages: the origin of multiple sclerosis? An essay in medical history” Acta Neurologica Scandinavica. 161: 11-22
  12. Poser CM. 2006. “The multiple sclerosis trait and the development of multiple sclerosis: Genetic vulnerability and environmental effect” In Clinical Neurology and Neurosurgery. 108: 227-233.
  13. Stuber C, Pitt D, Wang Y. 2016. International Journal of Molecular Sciences. 17: 100.
  14. Trapp BD, Nave K. 2008. “Multiple Sclerosis: An Immune or Neurodegenerative Disorder?” In Annual Review of Neuroscience. 31: 247-269.
  15. Vilisaar J, Harikrishnan S. 2008. “Ehlers—Danlos syndrome and multiple sclerosis: a possible association” In Multiple Sclerosis. 14: 567-570.
  16. Williams D. 2011. “Bruxism and Temporal Bone Hypermobility in Patients with Multiple Sclerosis” In Journal of Craniomandibular Practice. 29: 178-186.
  17. Zamboni P. 2009. “Chronic cerebrospinal venous insufficiency in patients with multiple sclerosis” In Journal of Neurology, Neurosurgery and Psychiatry. 80: 392-399.
  18. Zhang ZQ, Yang JL. 2015. “Biomechanical Dynamics of Cranial Sutures during Simulated Impulsive Loading” In Applied Bionics and Biomechanics. Article ID 596843.

About the Author
David E. Williams obtained a Bachelor of Science in Vertebrate Zoology from the University of Lethbridge in 1976 and DDS from the University of Edmonton in 1980. He is a practicing general dentist.


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1 Comment » for Does Dentistry Hold The Missing Link to Multiple Schlerosis, Alzheimers and Others?
  1. Norman Thomas says:

    Yes David .You will remember that collagen crosslinkage is significant in tooth eruption Thomas PhD 1966. It is also significant in top block physiology lectures I gave at LVIADS .Congratulations on this update . Norman Thomas Professor Emeritus U.of A and Chancellor of ICCMO and Director of Neuromuscular Dentistry Research BDS Hons;BSC Hons;PhD;Cert Oral Maxillo Facial Pathology;FRCD;FADI.

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