JAWBONE CAVITATIONS: Infarction, Infection & Systemic Disease

By Suzin Stockton MA

Reprinted by Permission to Y2K Health and Detox Center

  About seven years ago I made the eye-opening discovery that my chronic health problems, which had eluded resolution for many years, had their origin in – of all places – my jawbone. I would never have deduced this had it not been for a fortuitous chance finding:  the complete disappearance of bladder problems of one-year duration within days of having an abscessed tooth removed. When I reported the “coincidence” to my dentist, he was incredulous. He shouldn’t have been, for he considered himself to be a “holistic” practitioner.  That same dentist would later, despite his lack of understanding of focal illness, unknowingly help me to learn more about it by creating the conditions that triggered the full expression of a long silent jawbone disease – ischemic osteonecrosis. (a.k.a. cavitations and a dozen or so other names). This disease is actually quite common, though infrequently diagnosed, and is perhaps THE most common focal condition in the body. A “focus” is a walled-off area of concentrated toxins and necrotic (dead) and/or infected tissue.

            Ischemic osteonecrosis (bone death due to poor blood supply) is a disease of the entire skeleton – i.e., it can affect any bone in the body.  It is best known as a hip condition, and yet it is actually more common in the jawbone, though unacknowledged as such by mainstream medicine and dentistry. 

 A jawbone cavitation is simply a hollow space or pocket in the bone. It is not readily visible to the eye and often causes no local discomfort, though it can be the hidden cause of facial pain syndromes (hence one of its names, NICO – Neuralgia Inducing Cavitational Osteonecrosis).  The chief initiating factor is trauma to the jaw, often brought on by standard dental treatment.

I’d first encountered the word, “cavitation” many years ago in the writings of Dr. Hulda Clark. She’d described it in her books as “a bone infection resulting from an incompletely extracted tooth” – i.e., an extraction where tissue (bone and ligament) that should be completely extracted is not thoroughly removed. That description didn’t resonate in me then, despite the fact that it was exactly what had been silently going on in my jawbone for many years.  I guess I thought if I had an infection in my jaw, I’d know it: Surely there would be pain, inflammation, tenderness – and my dentist would find the problem in the course of my routine check-ups. WRONG!  Chronic osteomyelitis (cavitation) of the jawbone is not characterized by the usual signs of infection (inflammation, redness, fever, pus) – it most often is a silent condition. And it’s one that dentists are not trained in school to recognize. In fact, they’re not even taught that the condition exists. This is a somewhat perturbing state of affairs, for the jawbone cavitation is not a new disease. It was described as early as 1848 by Thomas Bond in the first oral pathology book. He wrote about a jawbone necrosis that existed independently of abscessed teeth and gums. In 1915, Dr. G.V. Black, the father of modern dentistry, described the condition as “chronic osteitis.”

 Jawbone cavitations are exquisitely described in an eye-opening book entitled Death and Dentistry written in 1940 by Martin H. Fischer, medical doctor and professor of physiology at the University of Cincinnati.  Citing the research of Drs. Frank Billings and E.C. Rosenow (early 1900s), Dr. Fischer speaks of “infarctions induced of microorganismal emboli” that have broken into the general circulation from a peripheral focal point in the jaw or tonsils. This “metastasis” of microorganisms is the cause of a surprising number of conditions according to Fischer (p.8, 9):

Embolic infection that has struck the heart valves will be endocarditis; the heart muscle, myocarditis;

the pericardium, pericarditis; if all are struck, it is pancarditis. Involving the skeletal muscles, the

same pathological background will give rise to myositis; when their tendinous junctions are struck,

fibrositis; and when the synovial bursae are affected, bursitis or tenosynovitis. The process in the

joints is arthritis; and in the nerves and nerve ganglia, neuritis. In the brain, this is cerebritis, and in

its coverings, meningitis.

Fischer goes on to explain the role of metastatic infection in gastric and duodenal ulcers, cholecystitis, cystitis, pneumonia, bronchitis, rheumatism, asthma, pleuritis, nephritis, thyroid disease, herpes, iritis, poliomyelitis, multiple sclerosis, certain skin disorders, diabetes, migraines, hypertension and more. He gives case histories and much clinical and laboratory evidence, including impressive photographs of cross-sections of infected teeth and microscopy slides.

Although infection in the oral cavity may be a triggering event in the formation of a cavitation, biopsy of the site typically shows few, if any, bacteria.  It is the toxins produced by these anaerobic bacteria that are most damaging to the body.  However, until local defenses break down and these toxins gain systemic access, the problem remains localized and most likely silent. Symptoms develop when the body burden of toxins increases to the point that nutritional reserves are depleted, and the system is no longer able to confine the toxins to their point of origin. They then travel via blood and lymph channels and through nerve pathways to other areas of the body.

Toxins create an extremely acidic environment. As long as the body’s alkaline reserves (primarily calcium and sodium) remain intact, pH is kept within acceptable limits, homeostasis remains intact, and the body functions normally. Once alkaline reserves are depleted however, balance is disrupted. It is not only acid-forming foods (like grains and meat) so prevalent in the standard American diet, that deplete the alkaline reserves, but also the bacterial toxins generated at the site of jawbone cavitations. These toxins create an acid environment and destroy critical enzyme systems in the body, including enzymes essential for energy production. The inactivated enzymes are then unable to fulfill their function as mineral chaperones. The net result is that key minerals, even though present in the system, become bio-unavailable, for the enzymes needed to activate them have been destroyed by bacterial toxins. It is important to understand that such a mineral “deficiency” is unrelated to mineral intake. It can exist in the face of ample intake, though insufficient intake certainly compounds the problem. The toxins responsible for mineral deactivation and breakdown of homeostasis are carried throughout the system via blood and lymph vessels, tending to settle in areas of inherent or acquired weakness. This means that my jawbone cavitations may result in an entirely different symptom picture than yours, simply because my weaknesses are different than yours.

The over-acid conditions that result once alkaline reserves are depleted have many deleterious systemic effects. When the pH of the blood becomes too acid, its viscosity increases – that is to say it becomes thicker. Consequently, it does not flow as smoothly through the vessels as it once did. Clotting anomalies result. A tendency to excessive clotting is very common in chronic cavitation patients, affecting approximately 80% of them.  Hyper coagulation leads to infarctions in blood vessels. Jawbone infarctions were spoken of by Dr. Fischer more than half a century ago.

Although the word, “infarct” has come to be associated with heart attack, the condition is not confined to the large vessels associated with the heart. Webster defines an “infarct” as “an area of necrosis in a tissue or organ resulting from obstruction of the local circulation by a thrombus or embolus.”  Jawbone necrosis does indeed result from impeded circulation, commonly stemming from trauma to the jawbone. Such trauma is largely iatrogenic, the result of standard dental treatment. Any large fillings, crowns, bridges (including the once healthy teeth used as abutments for the bridge) veneers, endodontic treatment, periodontal scaling, tooth extractions, injections (particularly of vasoconstrictive anesthetics), placement of toxic and/or incompatible restorative materials – all of these insults to the jawbone seriously reduce the blood supply to it. Where blood supply is compromised, toxins can’t get out, nutrients and oxygen can’t get in. 

By the time toxins gain systemic access, alkaline reserves have become depleted.  The blood then becomes hyper viscous, and infarction can occur. Such infarction tends to occur initially in the small vessels associated with traumatized bone tissue in the jaw. These infarctions of the microcirculation, it would appear, are a major factor in the development and spreading of jawbone cavitations. Fischer understood this years ago when he wrote of “infarctions induced of microorganismal emboli.”

The dental trauma most often associated with cavitations is the standard tooth extraction, particularly if it involves the third molar (or wisdom tooth) sites. Although taught in dental school, it is not common practice today for the surgeon excavating these teeth to thoroughly remove the periodontal ligament that attaches tooth to bone. Once the tooth is removed, this ligament serves no purpose, and if any part of it is permitted to remain in the jaw, it serves as a barrier to healing, impeding blood flow and preventing re-growth of bone. While the extraction site will invariably “heal” shut, the healing is quite often incomplete, for below the healed-over surface, a pocket or hole has formed. This hollow space becomes a breeding ground for anaerobic microorganisms. It is very possibly these microorganisms that form the infarction-inducing embolus of which Fischer wrote so many years ago. When the metabolic waste products of these bacteria interact with chemical toxins (from restorative materials, anesthetics, etc.) in the oral cavity, the result is the production of super toxins.  The extreme toxicity thus created may well reduce bacterial population.

        Whether or not a cavitation forms following the standard extraction of a tooth will depend largely upon how much of the periodontal ligament happens to be removed with the tooth (some portion usually comes out, even when the surgeon is making no attempt at removal of it) AND the type of microorganisms which are present at the site. More damaging than the microorganisms themselves are the extremely potent toxins they produce. Once these bacterial toxins gain systemic access, they can do a great deal of harm through inhibition of enzymes and minerals as described above. The necrosis they produce is actually a gangrenous condition, which tends to spread to other areas of the jawbone. Detoxification is a significant challenge at this point and an absolute impossibility in the face of the continuance of the focal condition (infected tooth and/or jawbone).

        Treatment of choice for jawbone cavitations is surgical removal of the necrotic and infected bone, for in the presence of such bone, the conditions that created the infection remain, and blood supply continues to be impaired. This surgical procedure is a relatively simple one when done in conjunction with a new extraction. It is much more difficult where old extraction sites are concerned. Here the task is complicated by the fact that there has been, up until very recently, no way to clearly visualize the cavitation site and gain information about its dimensions and other distinguishing features short of opening up the site and ‘looking around.’ Even then, the site cannot be viewed from all angles. To the trained eye, the panoramic x-ray can reveal indications of the presence of a cavitation, but not always. Even when it does, details are often not clearly discernible, and the surgeon is still operating ‘in the blind’ to some degree. The 2-dimensional x-ray image cannot adequately reflect anomalies in the 3-dimensional jawbone. In some instances, cavitations can be depicted on x-ray; however, as much as 50% of the bone must be affected before their presence is apparent.

       The MRI, while the ‘gold standard’ for detecting osteonecrosis of the hip, does not work well with the flat bones of the face.  Tech 99 bone scans are about 70% effective when a special contrast medium is used.  Jawbone cavitations can also be imaged through CT scan, when a spiral scan is taken from about the middle of the sinus to the bottom of the mandible. These methods, however, are neither practical nor cost-effective for use by the dental profession. They expose the patient to the adverse effects of radiation and require the interpretive services of a radiologist who is unlikely to recognize jawbone cavitations because he has not been trained to do so. The aware dentist has long been in need of a reliable instrument for clearly and safely imaging jawbone cavitations; ideally an instrument that could be used “in house.” Such an instrument is now available, due to the unflagging efforts of Bob Jones. The story of his dental drama is interesting, more dramatic than my own (told in my book, Beyond Amalgam) and worth telling here.

         A decade ago, Bob was a specimen of perfect health – or so it seemed. He was employed full-time as a commercial airline pilot, worked part-time as a ski instructor. This avid outdoorsman was slim, trim and fit. That all changed in 1987 when he was stricken with chronic debilitating fatigue, muscle atrophy and a neurological condition that baffled specialists. By 1992, he had become completely disabled, was wheelchair bound, had lost use of his arms and gained an excessive amount of weight. While the MDs couldn’t come to agreement on the exact nature of the problem and finally settled upon a speculative diagnosis of ALS, they were in agreement on one thing:  Bob’s condition was terminal. They had given him no more than six months to live, when he stumbled upon an understanding of the source of his problem and a way to turn it around. His search for solutions led him to the realization that potent toxins, by-products of standard dental treatments were essentially poisoning his system. Bob’s symptoms subsided, and his condition dramatically improved once his diseased bone marrow and “silver” fillings were removed. Today he is completely mobile and moderately active. Much of his excess weight has been lost. Bob is quick to point out, however, that his recovery has not been 100%. At this point in time, chronic cavitation patients can expect improvement but often not complete cure, owing to the severity and duration of their condition.

         Even before his recovery, Bob set out to develop an instrument designed to detect jawbone cavitations. Since these lesions routinely elude detection through standard diagnostic procedures, the need for an improved imaging device was apparent. As a design engineer with a background in sonar technology, Bob was convinced from the onset that such an imaging device could be developed using sonography. Six months after commencing the arduous task of ‘cleaning out’ his jawbone, Bob had developed the first working prototype of the CAVITAT™. There would be many design revisions and obstacles put in his path in the years to follow, but he worked diligently to make his vision of a perfected CAVITAT™ the reality that it has now become.

         The CAVITAT’s proprietary analog to digital circuitry has been awarded 19 patents. There are 22 additional patents pending on the flexible circuit receiver and its advanced cross-channel noise suppression technique. The device is unique in the sonography market in that it is engineered to show only bone, no soft tissue. All other ultrasound devices do just the opposite – show tissue but no bone. And, the image they display is 2-dimensional, while the CAVITAT™ displays a 3-dimensional color-coded image. These colors (green, yellow, red) reflect the degree of bone loss and necrosis. The 3-D computer images may be rotated so that they can be viewed from all angles. One image is generated for each of the 32 tooth sites, and all can be displayed on the screen simultaneously. This allows the operator to see the overall picture and how one affected site can influence adjacent ones. Each of the 32 images consists of 64 elements or pixels. These detailed images are identified as to orientation – “B” for buccal and “D” for distal.

        The new Generation 4 CAVITAT™ differs from its prototype precursor in many important respects.  The resolution has been increased 800%, making for a much clearer image and enabling detection of smaller cavitations. The Generation 4 is capable of detecting jawbone defects down to 1/64 of an inch in diameter.

         Bob Jones had introduced a limited number of Generation 3 CAVITATs to a select number of dentists at the end of 1999. These were prototype models used for field evaluation. The feedback from the dentists using them provided the data necessary to make desired improvements. The software was totally rewritten, and the net result was a user-friendly state-of-the-art precision instrument. It is this version of the CAVITAT™ that is now being made available to doctors and dentists to assist in diagnosis of jawbone cavitations and other bony defects of the jaw.

        The significance of this technological break through cannot be overemphasized. The success of cavitation surgery is dependent upon many variables. A major one is the extent to which necrotic tissue is removed. Before the advent of the CAVITAT™, dentists were operating very much in the blind, unable to see the full extent of the necrosis and therefore unable to remove all necrotic bone.  The result for many patients was poor bone healing, unchecked spreading of necrotic lesions and consequent need for repeat surgeries. While excision of all diseased bone will not necessarily assure full recovery, it certainly does improve the odds. Most patients have had jawbone cavitations for a number of years before they are discovered. Consequently, by the time treatment is initiated, a great deal of serious damage has been done. Dr. Fischer had stated in Death and Dentistry, “It is only in the earliest stages of oral disease that arrest of progressive infection seems possible.” With the development of the CAVITAT™, early detection is finally possible. It may be our only hope of putting the reigns on this silent, insidious condition that appears to have reached epidemic proportions.

        While thorough excision of osteonecrotic lesions is necessary in the treatment of cavitations, for the chronic cavitation patient, it is often not sufficient. Aggressive detoxification measures are also in order. These must be tailored to the needs of the individual patient with regard to his/her specific detoxification capabilities and overall condition. Nutritional support is also essential – for rebuilding bone, improving circulation, combating infection, chelating heavy metals.

        While surgical treatment of cavitations falls within the domain of the dental profession, the metastatic infection seeded by these lesions has systemic consequences that should be of interest to all physicians. It is therefore imperative that every patient history taken by all physicians and health care providers include questions about dental treatment. Remember:  Any trauma to the jaw can be the beginning of cavitations.

         The high-speed drill routinely used by dentists cracks enamel, thus allowing bacterial toxins to penetrate the dentine. There is evidence that such drills cause actual pulp damage. Drilling done then in preparation of a tooth for routine fillings, crowns and bridges can be damaging to the jawbone. Root canals will unquestionably cause cavitations sooner or later, as will routine extractions (where the socket is not properly cleaned out, with all necrotic/infected bone removed). The eclectic physician will not only want to question his patients about these procedures, s/he will also want to be in a position to diagnose jawbone cavitations, or to refer patients to a dentist who is able to make such a diagnosis. Once the diagnosis is made, it is desirable that the dentist and primary physician work together in instigating a treatment plan and following up with patient.

         In working with the chronic cavitation patient, it is imperative that the entire jawbone be considered and examined – not just the site(s) of extractions.  A mistake that is frequently made is to clean out new extraction sites, while ignoring old ones. If all necrosis is not removed, it will spread – and will ultimately re-infect a new extraction site, even one that was properly cleaned out. Taking things a step further, it is important to be aware that the spreading of jawbone cavitations is not confined to edentulous areas. When the bone beneath an apparently “vital” tooth becomes affected/infected, blood supply to that tooth is greatly reduced, and it begins to die. Neither oral exam, nor x-ray evaluation will likely reveal a problem with such a tooth. ElectroDermal Screening and muscle testing may also miss the problem.  The patient, however, frequently has a sense of something being “not quite right” with the tooth.  (The chronically sensitive tooth often is an indication of the presence of jawbone necrosis beneath it) If he or she insists upon its extraction (usually against the advice of the dentist) and manages to talk his/her dentist into removing it, that dentist is counseled to carefully examine the extracted tooth. Chances are very good that upon drilling into the pulp chamber, s/he will find that the tooth is dead or dying.  This avitality is reflected by lack of moisture in the pulp chamber, a result of severely restricted blood flow.  I say all of this from personal experience, for three of my mandibular extractions done in ’99 and ’00 were performed at my insistence against the initial protestations of my dentist, who fortunately was open-minded and curious enough to drill open the pulp chambers of the extracted teeth. 

        Dentists are taught to save the tooth at all costs. Frequently, however, the price paid is the systemic health of the patient.  Dead and dying teeth should not remain in the jaw, even if they are causing no acute distress to the patient. If CAVITAT™ scan of the jawbone shows pronounced necrosis under a “vital” tooth, please entertain the possibility that the tooth only appears to be vital, and is, in fact, dying. Healthy teeth don’t grow out of necrotic bone.

        For the chronic cavitation patient, extraction may be both the beginning and end of his or her health problems. The improperly done extraction (usually of a wisdom tooth) is frequently the beginning of a problem which may go undetected for decades, and then only be resolved by the proper extraction of some, or possibly all, of the remaining teeth, along with removal of necrotic bone from edentulous areas and aggressive systemic detoxification.  Prevention and early detection are the keys to avoiding this outcome. Improved imaging capabilities give us the tool for such early intervention.. The first step in solving the problem, however, is awareness of it. You have taken that step and are urged to take the next one.  Doctors:  Learn to recognize jawbone cavitations and to either treat them surgically, or refer your patient to a qualified cavitation surgeon for treatment.  Patients: Seek out a dentist familiar with jawbone pathology:  It may be the unsuspected cause of your systemic problems.

Fischer, Martin H. Death and Dentistry. Charles C. Thomas, LTD: Springfield, IL, 1940.

Stockton, Susan. Beyond Amalgam: The Health Hazard Posed by Jawbone Cavitations.  Power of One Publishing:  Aurora, CO, 2000.

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Suzin Stockton, MA, is a recognized writer and researcher in the field of natural health and medicine. She is author of a number of books and articles, including Beyond Amalgam and The Terrain is Everything (available through Power of One Publishing, 1-727-539-1700). Susan lives and works in Clearwater, FL, where she is a writer with Renew Life Formulas. More of her articles and information on her books and videos may be accessed on her web site www.healthcarealternatives.net.