The Toxic Tooth: CHAPTER TWELVE: BEYOND ROOT CANAL TREATMENT Hidden Gangrene: The Cavitation

 

 

 

 

 

CHAPTER TWELVE: BEYOND ROOT CANAL TREATMENT

Hidden Gangrene: The Cavitation

What is a Cavitation?

While the title of this chapter may seem a bit alarming and even a bit incredible, it is no exaggeration. A cavitation is a residual hole or defect in the jawbone at the site of an old, or “healed” tooth extraction. The contents of a cavitation typically consist of toxins, osteomyelitic and osteonecrotic (dead) bone, the presence of microbes, and various types of tissue fragments. Histologically, cavitation contents have distinct similarities to wet gangrene.

Cavitations are Common

It is a fact that cavitations are very commonly found in most people who have had tooth extractions; the vast majority of dental patients have one or more of them. The statistical incidence of cavitations was first presented in the winter 1996 issue of the Journal of Advancement in Medicine . In a review of 112 patients who were explored for possible cavitations, it was found that nearly 90% (313 out of 354) of wisdom tooth extraction sites had cavitated.1 Many of these cavitations were not at recent extraction sites. Typically, years and often decades had passed since the teeth had been extracted. All of the other extraction sites also demonstrated the ability to cavitate, although the incidence of cavitation lessened as the size of the teeth extracted became smaller or as the amount of infection present at the time of extraction was less. The bigger the hole and more pronounced the infection, the more likely that healing would be incomplete and remain incomplete. Once present, cavitations tend to remain; they will never heal spontaneously. Complete surgical debridement is required in order to get new, healthy bone to fill in the defect. Cavitations do not heal on their own without surgical intervention, no matter how much time is allowed.

Why Cavitations Develop

An important reason that cavitations develop is due to the nature of the standard extraction technique. The typical technique does not always remove the periodontal ligament and may not allow adequate blood flow through the cortical bone of the tooth socket to initiate new bone formation.

The tooth socket is a dense layer of cortical bone designed to withstand the forces of chewing. The tooth is held in place within the socket by the periodontal ligament. The periodontal ligament is a thin yet dense connective tissue layer that lines the socket, anchors the tooth to the cortical bone, and acts as a shock absorber to cushion the forces of chewing.

When the tooth is extracted but the periodontal ligament remains, the surrounding bone has no physiological awareness that the tooth is gone.

Oftentimes after extraction, the periodontal ligament remains attached to the cortical bone of the tooth socket. When the tooth is extracted but the periodontal ligament remains, the surrounding bone has no physiological awareness that the tooth is gone. The body may not initiate resorption of the periodontal ligament and cortical tooth socket bone, and new bone formation may not occur. Instead, only a small amount of new bone grows at the top of the extraction site, where the ligament ends, and the typical thin cap of bone over the extraction site results. Because new bone and the associated blood vessel plexus have failed to form, the bacteria introduced to the extraction site remain within the cavitation, creating a site of focal infection with the associated toxin release. Bone samples from the perimeter of the cavitation sent for microscopic analysis show both chronic osteomyelitis and osteonecrosis.

Because new bone and the associated blood vessel plexus have failed to form, the bacteria introduced to the extraction site remain within the cavitation, creating a site of focal infection.

Dentists should completely remove the periodontal ligament lining the tooth socket. If the extraction is due to periodontal disease or the tooth is a root canal-treated tooth, complete removal of the cortical bone socket is recommended in order to expose healthy, bleeding medullary bone. At the very least, the periodontal ligament should be removed, and a large number of closely spaced perforations through the cortical bone socket should be made with a burr to induce bleeding. This increased blood flow will increase the likelihood that the osteoclast cells will completely resorb the tooth socket and the osteoblast cells will initiate new bone formation. Failure of the cortical bone of the socket to resorb will produce the appearance on X-ray called laminar rain.

Historical Perspective on Cavitations

Although still not recognized by modern dentistry to be the common and toxic entity that it is, the cavitation was actually described as far back as 1915 by the dental pioneer, G. V. Black. While Dr. Black did not call what he found a “cavitation,” he nevertheless described very accurately the pathology and gross appearance as is described today. Dr. Black considered bone necrosis to be typical of the cavitation lesion and to be the ongoing factor that resulted in the hollowed-out area so often found at the site of an old extraction. The gradual death of bone produces a softening of the area until it eventually results in an actual hole.

Dr. Black labeled this process “chronic osteitis,” even though he did not completely understand how such extensive internal bone destruction could occur without obvious external signs of inflammation and swelling. He also noted that the patient was not typically acutely ill, and did not present with symptoms such as fever. Even though Dr. Black realized that the absence of such classical inflammation/infection-associated signs and symptoms flew in the face of standard medical and dental knowledge, he still recognized the existence of these lesions and advocated that they should be thoroughly debrided.

It is known that some disease-causing microorganisms such as mycoplasma do not present with the classic signs and symptoms of infection normally seen on blood tests or clinical evaluation. These “silent” infections often go initially undetected by our standard laboratory tests and

can later cause and/or promote the development of various chronic diseases. Even when such a disease becomes well-established, the possibility of occult, or hidden, infection is rarely entertained as a likely cause of the disease or even as a significant contributory factor in its development. Likewise, cavitations are chronically infected and toxic lesions that can also go undetected by standard tests and yet play a substantial role in the initiation and maintenance of chronic disease, especially when the bone necrosis continues to spread to previously healthy bone.

In his surgical approach to cavitation debridement, Dr. Black noted that it was usually easy to enter the thin cap of bone at the old extraction site and then proceed to remove all of the contents and softened, diseased bone until solid bone margins were reached.

Even though Dr. Black was a dental pioneer who is still held in high esteem by dentists today (he is known as the “father of operative dentistry”), his findings on cavitations never were incorporated into current dental thought or dental teaching. There is no way to know whether this omission was deliberate or inadvertent. Regardless of this oversight, the appreciation of the existence of cavitations by other dental authors once again emerged in the 1970s. Much of this writing associated cavitations with undiagnosed facial pain syndromes, and the literature began to talk about “NICO,” or neuralgia-inducing cavitational osteonecrosis. Neuralgia refers to pain extending along the pathway of one or more nerves. Patients who presented with trigeminal neuralgias and other atypical facial neuralgias were often found to have cavitations at old extraction sites. After the cavitations were properly debrided, many of these patients experienced resolution of their pain.

Much of this writing [from recent dental authors] associated cavitations with undiagnosed facial pain syndromes.

The scientific literature has also labeled cavitations with several other names. In addition to NICO, they have also been referred to as Ratner, Roberts, or trigger point bone cavities, as well as alveolar cavitational osteopathosis. But regardless of the name, the entity remains the same,

although the clinical consequences can vary widely among the afflicted patients.

Diagnosing Cavitations

While cavitations can occur in anybody, the work-up should always include an evaluation of the multiple initiating and predisposing risk factors for the development of a cavitation. A comprehensive oral examination should then be performed. Many (but not all) cavitations of the upper jaw can be detected by discomfort elicited by direct palpation (finger pressure on the bone). Upper jaw cavitations are easier to detect than lower jaw cavitations by palpation due to the differing bone densities of the upper and lower jaws. If the cavitation is near the surface of the bone, pain may be elicited when pressure is applied to the tissue directly overlying the area.

Sometimes cavitations or even root canal-treated teeth can cause referred pain to the head and other parts of the body such as the shoulder, hip, or knee. Root canal-treated teeth can share this ability with cavitations since the tissue specimen found in the socket of a freshly extracted root canal- treated tooth can have similar characteristics to the contents of a cavitation with regard to toxins, bacteria, and evidence of osteonecrosis and chronic osteomyelitis. In fact, almost any area of the body can experience referred pain from a cavitation or a root canal-treated tooth.

Cavitations that produce facial neuralgias form the syndrome called NICO... Sometimes NICO sites can also cause referred pain to distant sites in the body.

Cavitations that produce facial neuralgias form the syndrome called NICO, already mentioned above. Sometimes NICO sites can also cause referred pain to distant sites in the body. Just as a heart attack can frequently cause referred pain to the jaw and left arm, cavitations can cause referred pain as well. However, it is very important to realize that most of the time there is no associated referred pain with cavitations and root canal-treated teeth. Furthermore, when referred pain at some remote site of the body is

present, the site of the cavitation itself is still frequently pain-free. This referred pain will only resolve after the cavitation has been surgically debrided or the root canal-treated tooth has been extracted and the extraction site properly debrided in a similar fashion.

A diagnostic test to determine any link between the area where pain is felt and the cavitation can be performed by injecting a non-vasoconstrictor anesthetic near the site of the cavitation. If the referred pain goes away or is significantly diminished after injection of the local anesthetic, it is probable that the cavitation is the cause of the referred pain.

Sometimes the referred pain does not go away when local anesthetic is placed near the cavitation. This does not necessarily mean that the cavitation is still not the source of the referred pain. Factors such as decreased blood supply to the bone and lack of adequate access of the anesthesia to the area most responsible for generation of the pain may prevent relief of symptoms. Surgical intervention may still produce positive results, although pain might sometimes persist. Diagnostic confirmation should always be attempted when referred pain is suspected.

Nevertheless, all suspected cavitation sites should be explored and properly debrided if possible, regardless of the presence or absence of associated symptomatology, as it is always desirable to clean out dead and infected tissue wherever it might be present in the body. An asymptomatic cavitation can always progress and evolve to a larger, symptomatic one.

As mentioned earlier, it needs to be emphasized that only a small percentage of cavitations produces either local or referred pain. This does NOT mean that these cavitations are toxin-free and incapable of potentially affecting other parts of the body. The toxicity test devised by Boyd Haley, PhD, has found all cavitation samples tested thus far to be toxic, with most of them proving to be very highly toxic. This same test found similar toxins in the 5,000+ consecutive extracted root canal-treated teeth that he tested (see Chapter Three).

All suspected cavitation sites should be explored and properly debrided if possible... as it is always

desirable to clean out dead and infected tissue wherever it might be present in the body.

How these toxins affect an individual will depend upon many factors including genetic susceptibility, immune system function, and the degree of access that the toxins have to the rest of the body. Root canal-treated teeth may disseminate their toxins throughout the body and impact health negatively, while a single small cavitation may have little to no substantive clinical impact. Conversely, multiple and/or large cavitations in a patient can contribute to a wide variety of advanced chronic degenerative diseases. The bottom line is that all cavitations should be completely debrided, unless some unique clinical circumstance or individual risk/benefit concern indicates otherwise.

X-Raying the Invisible?

The diagnostic tool that has been most used to diagnose cavitations is the panoramic dental X-ray. This large X-ray includes the upper jaw, lower jaw, teeth and sinuses. Sometimes a smaller periapical X-ray that focuses on the root of a tooth or a limited area of the jawbone is used to get a closer view of a particular area. Although many lesions can be seen on a panoramic X- ray, it does not reliably depict areas of bone in the beginning stages of osteonecrosis, or cavitation formation. Many times these lesions do not show up on X-ray until there is a 50% deterioration of the bone density relative to adjacent normal bone. This is due to the anatomical nature of bone, which is literally a substance comprised of multiple small holes superimposed upon each other and sandwiched between denser outer bone coverings. Remember that an X-ray is a two-dimensional picture of a three- dimensional object.

These lesions may take on a variety of X-ray appearances. One appearance is a dark space of variable size, indicating a relatively larger hole or space in the bone than is usually present within normal bone.

When a cavitation is surgically explored, it is common to “fall into” a hole in the bone after very little drilling through the thin cap of bone typically covering the cavitation. The bone surrounding these holes tends to be ischemic, contributing to the failure of the bone to fully heal. With

marginal blood supply, the hole itself may have little, and sometimes no bone covering it, just the layer of gingiva (gum tissue) covering the hole.

Even though the X-ray remains the tool most commonly used to visualize a cavitation, it is very important to know that an X-ray is generally sub- optimal for this application. Many times a cavitation will not be seen on an X-ray, except by a highly experienced surgeon with an extensive background in working with and diagnosing cavitations.

Because they are difficult to consistently image on X-ray, cavitations have been labeled the “invisible osteomyelitis.” Practically speaking, what this also means is that an X-ray in which no cavitation is clearly visualized can NEVER be used as the sole reason for concluding that a cavitation is not present. In other words, a positive X-ray picture can rule IN the presence of a cavitation, but a negative, normal-appearing X-ray picture can never rule OUT the presence of a cavitation. Even some dentists who are very aware of the presence of cavitations persist in concluding that they cannot be present in a patient who has a normal-appearing panoramic dental X-ray. This approach will always miss more cavitations than it finds. The increased utilization of 3D X-ray imaging is improving cavitation diagnosis.

Physical Appearance and Characteristics of Cavitations

The physical appearance of the contents of cavitations can vary widely. Sometimes cavitations are composed of very mushy bone that can contain scattered globules of fat, with an overall likeness to chicken soup without the fat being skimmed. Cavitation contents may also have a sawdust-like appearance. The contents can even resemble melted chocolate ice cream. Colors described include green, yellow-green, or tarry black. Sometimes the contents are even clear. Consistencies of the contents range from clumps resembling cottage cheese to a loose, runny liquid. Distinctive unpleasant odors are sometimes present. Sometimes a sulfurous, “rotten egg” smell is present. Any odor that is associated with tissue breakdown and death secondary to chronic anaerobic bacterial growth and toxicity can occur. Interestingly, the dentist will sometimes miss the smell, but the patient will not.

The degree of development of a cavitation inside the jawbone can vary

significantly from one patient to the next. Depending on a number of local and systemic factors, the progressive cellular death of bone tissue as described long ago by Dr. Black can proceed largely unchecked, or it can “stall out” after only a relatively small cavitation has formed. Because of this, the actual configurations of cavitations inside the jawbone vary widely. They can be very focal and virtually impossible to delineate from the adjacent “normal” holes found in non-diseased, cancellous bone. They can also be quite large, in the range of one centimeter in length or even more. Fingerlike projections can evolve, and the overall cavitation can develop an “amoeba-like,” amorphous appearance. Sometimes they are rounded and sometimes they are very ragged and irregular along their boundaries. On occasion, the boundaries will calcify to a degree, and the ability for such a cavitation to show up on X-ray will be greatly enhanced.

When a patient has had consecutive teeth extracted, or is completely edentulous (without teeth), it is very common for cavitations to extend to a degree such that interconnections among them are formed. These progress to the point that some patients who have had all of their teeth extracted will actually have a tubular defect throughout much of their jawbone containing exceptionally large amounts of the toxic cavitation contents. This is referred to as a “channel cavitation.” This is also why many patients who have few or no teeth can have as much or more dental toxicity as patients with many remaining teeth. Many edentulous patients are dealing with an enormous amount of toxicity on a daily basis from their extensive cavitation disease.

Risk Factors for Cavitation Development

Bisphosphonates. Bisphosphonate drugs are used in the treatment of osteopenia and osteoporosis. These drugs inhibit the bone-resorbing osteoclast cells. Normally, bone is continually resorbed by osteoclasts and new bone formed by osteoblasts. When the balance of bone resorption to bone formation is negatively altered, more bone will be resorbed than is formed, and the bone will become less dense. The end result of this process is osteoporosis. Bisphosphonates alter osteoclast function, significantly slowing down bone resorption. Unfortunately, we need bone resorption to remove the residual tooth socket bone to allow the tooth socket to properly

heal and fill in with new medullary bone. Bisphosphonates significantly increase the likelihood of cavitation formation.

Clotting disorders. People with underlying blood clotting disorders are more prone to cavitations simply because blood flow to the extraction site can be compromised (see Appendix C).

Vasoconstrictors in local anesthetics. Dentists often use local anesthetics with vasoconstrictors. Vasoconstrictors such as epinephrine constrict blood vessels. They are used to both keep the local anesthetic in the area for a longer period of time and to reduce bleeding. If blood supply to the bone is already compromised by factors such as a clotting disorder, infection, previous trauma, etc., the use of a local anesthetic containing a vasoconstrictor might induce enough ischemia to the bone to cause some cell death, resulting in osteonecrosis.

Further, direct injection of local anesthetic into the bone under pressure as is used in a periodontal ligament tooth injection or an intra-osseous injection should never be used. The high pressure induced within the bone can constrict the capillary bed causing ischemia, and a local anesthetic that contains a vasoconstrictor only compounds the problem.

Treatment of Cavitations

Currently, the most effective method of treating cavitations is complete surgical removal of the dead, diseased, and toxin-containing bone. Appendix D details the surgical protocol for cavitation debridement. A complete protocol will also include measures to help optimize the patient’s ability to grow new, healthy bone, which will eventually fill in the cavitation as fully as possible.

Too many dental practitioners advocate injecting different substances into the cavitation lesion with the hope of resolving the lesion non- surgically. One substance that has been injected into cavitations and elsewhere in the body is what is known as a Sanum remedy. The Sanum remedies used by dentists are homeopathic in nature, with the hope that so-called “interference fields” and other “blockages” of normal energy flow will be removed or minimized. However, Sanum remedies also contain and employ “apathogenic” microorganisms normally found in the body. As we have discussed earlier, both cavitations and root canal-treated teeth develop their

incredible toxicities because of what happens when the normal, largely apathogenic, microbial flora of the mouth becomes trapped in the oxygen- deprived environments found in these diseased areas of the jawbone. The last thing any clinician should want to do would be to inject any amount of any kind of microorganism into a cavitation, in or around a root canal- treated tooth, or into any other area with little or no oxygen and blood supply. This is like throwing gasoline onto the fire. This method of just injecting something into a cavitation and expecting healing will always prove to be ineffective at best and harmful at worst. Once a tissue is dead, it is dead.

Even if a Sanum remedy were able to improve the “energy dynamics” of the mouth and body, the body will not be able to clean out a relatively large area of osteonecrosis and osteomyelitis without a good blood supply. Placing new microorganisms into a cavitation may well result in a “reactivation” and expansion of what had been an area that had been relatively fixed in size.

Also, even when the cavitation is not actually worsened by the Sanum remedy, the patient will lose precious time and money. Ironically, Sanum remedies are quite expensive and using them to treat a sick patient with cavitations will only result in that patient remaining sicker for a longer period. This can result in that patient also losing hope that this condition can be satisfactorily treated.

The surgical protocol for treating the cavitation should utilize proven surgical principles. Every aspect of the surgical procedure should be based on sound scientific research and established principles documented to promote good healing. To this end, a great deal of time and energy was spent researching every aspect of this surgical procedure beginning with the methods for diagnosing these cavitation lesions right down to the type of sutures used for closing the surgery site. This is not to say that the protocol that is presented in this book cannot be improved upon. In fact, as new technology and new research becomes available, these treatment procedures will undoubtedly evolve and change to keep up with new findings. However, this current protocol is quite effective, and it has proven to be successful in the resolution of cavitations. For information on the pathology of cavitations, go to www.maxillofacialcenter.com . See Appendix B for cavitation images and X-rays and see Appendix C for cavitation causes.

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