W I S D O M T E E T H or Teeth of Misfortune (Third Molars)

Facial Pain Linked To Infections
by Christopher J. Hussar, D.D.S., D.O.

For almost a century controversy has waged regarding the existence of a disease process with infectious origins within the dental alveolus. These localized infectious processes have been strongly implicated in generating facial pain including trigeminal neuralgia along with other cranial facial pain disorders including, remote pain disorders in distant regions of the body.
The Father of modem dentistry, G. V. Black, recognized and gave notice in one of his textbooks to the actuality of a hollow jaw bone, housing an infectious process within the dental alveolus. A review of the literature reveals numerous papers from the early 20th century written by both M.D. and D.D.S. alike, describing the surgical debridement of jaw infections including devital teeth, and localized osteomyelitis lesions that successfully treated, not only localized facial pain, but remote pain disorders such as arthritis as well.
Sir Wilfred Harris, a British neurosurgeon, proposed the reality of a chronic intra osseous infection within the alveolus causing neural degenerative changes and demyelination to trigeminal nerve branches. This was in 1926 and was widely accepted by dental surgeons in America nearly a century prior.
In the early part of this century the theory of "focal disease" arose in which a chronically infected area of the body was responsible for causing pathology elsewhere. Many tonsils as well as teeth were removed with miraculous, as well as not so miraculous, results. The clinician would script an article expounding the cure of arthritis after the patient had several diseased teeth removed. Anecdotal cases of blindness reversal was documented (your author has witnessed such an event)...

Much credit must be attributed to the brilliant research of Dr. Weston Price in the early part of our century. With incredibly reproducible results, this research dentist demonstrated the existence of multiple bacterial strains in dental teeth including root canals. In addition, he addressed the chronically infected periodontal membrane and periodicular bone resulting from infected teeth and the cavitation of such chronically infected bone if thorough socket curettabe was not performed properly.

With the ``disproving'' of the focal theory by our progressively autocratic medical/dental complex, the concept of chronic dental/alveolar infections has gone practically unrecognized for the past sixty years.
One of the reasons may be poor visuatlization of these chronically ``cavitated'' lesions on intra-oral radiographs. Usually housed within the cancellous bone, the cortical plates and their different x-ray absorption qualities obscure and alter the true picture lying deep within the jaw bone.

In reality, this is not the case as certain radiographic landmarks are quiate visible and will readily confirm the presence of these lesions. With continued x-ray evaluation along with curettage of a suspected lesion, they will become obvious.
The above mentioned as been well documented by Jerry Bouquot, D.D.S., M.S.D., in his numerous articles on NICO (Neuralgia Industing Cavitational Osteonecrosis) lesions describing ``laminar rain,'' the x-ray visible, boney changes resemblung the rungs of a ladder. This results when the bone of the extraction site refuses to heal properly, literally leaving the root outlined. Micro calcification within the confines of the original extraction site, further confirms the presence of an inflammatory bone lesion, often referred to as a cavitation.''.
In surgerizing mandibular lesions, involvement of the inferior alveolar nerve (IAN) by the obstructive process creates a characteristic appearance on the x-ray. The superior aspect of the mandibular canal, the ``roof,'' is usually eliminated and the fine, dense superior white line is seen to disappear as the IAN courses through the lesion site. Absolute certainty of course only occurs with biopsy confirmation of curettaged tissue from these lesions. With little practice and suspicion, near one hundred percent accuracy is possible when performing the surgical debridements.
Perhaps our subject matter has been ignored for decades because of a failure to biopsy on the part of dentistry as a whole. Do endodontists rely on the biopsy for verification of tissue? Hardly, for my dental training down-played the role. Do oral surgeons send their extracted teeth in for biopsy along with any abnormal bone that may be removed along with those teeth? It is my policy to biopsy every tissue fragment I remove from the mouth. My judgement in determining pathology has been incorrect less than .5% of the time. Once you begin to recognize the disease, the diagnosis becomes much easier.
When curetted, the contents of these intraosseous lesions may present varying types of diseased tissue. Commonly, when surgically opened, the lesion site is void of caancellous bone; thus the derivation of the term ``cavitation,'' a hollow cavity exists. Other presentations include hemorrhagic bone with easily curettaged spicules of both viable and non-viable bone. Multiple globules of adipose tissue representing degenerated bone can commonly be curettaged; in fact, **************opening up one of these lesions with a fissure burr causes an exudate not unlike bloody chicken soup with countless micelles of fat floating on the surface of the serium***************.
If an area of condensing osteomyelitis/osteitis is evident on an x-ray associated with a suspected cavitational area, surgically speaking the alveolar bone will usually possess a consistency of pearl-like hardness implying condensed bone that has been made devital by ischemia. This is extremely difficult bone to surgically eliminate especially in the presence of the inferior alveolar nerve. These patients will often develop facial pain syndrome and can be difficult to treat.
Microscopically most biopsy reports will demonstrate marrow fibrosis as the body attempts to regenerate itself, fibrotic material heals easier than bone. Multiple fragments of bone shard appear as the impaired blood supply cannot provide adequate flow to new bone attempting to replace diseased bone. When your patients come to you months after a difficult extraction, showing a small bone fragment that has worked its way through the gingiva, you didn't forget to irrigate it out; the body refused to nourish it and it sloughed. Lymphocytes may or may not be encountered depending on the chronicity of the infection, the immunity of the patient, nutritional status, and other factors. Neurophils, most commonly seen with acute inflammatory processes, are seen infrequently with cavitations. What is seen primarily is necrotic bone flake often intermingled with viable bone. Remarkably, very few osteoblasts or osteoclasts are observed in specimens.
Most articles covering facial pain are written dealing with trigeminal neuralgia, atypical facial pain (AFP) and TMJ, with the latter two being the most common. Most of these reading this article are well-versed in the treatment of TMJ disorders. However, what treatments do you prescribe to the patient who has had 5 or 6 bite splints from other practitioners and his facial pain persists without alleviation? You must always be suspicious of a ``NICO'' process smoldering in the patient's alveolus when consulted by such a patient.
********************Their orruccurrence is of epidemic proportions; if the patient has had any third molars removed, it's a safe bet to conclude that cavitations are present. Why do they cause pain in some and not others Multiple theories have been proposed as to what mechanisms exist allowing NICO's to generate pain
A general consensus agrees upon the initial development of an intra-alveolar infection from a devital tooth, root-canaled tooth, ir extraction site. This infection persists within the alveolus and can ``tunnel'' or remain localized. In the mandible, the bascula system is an end-organ type or terminal vessel allowing basically one-way flow of blood. Chronic infectious agents harboed in these cavities, namely bacteria and their endotoxins along with what appear to be viral agents causes a vasculitis in the arterial side eventually compromising the flow of blood.
With the onset of ischemia other changes occur. Antibiotics are not as effectivce for they rely on a blood supply to reach their target zone. Infectious agents often will die off or become rapidly attentuated and be rarely seen in biopsy. Bone necrosis develops, the affected alveolus cannot heal properly, and a pathologice entity arises called ``NICO.'' What caused the pain?

The physiology of the trigeminal nerval is extremely complex. Peripherally, the dentin contains 30,000 to 70,000 microtubules per square millimeter! Free sensory nerve endings and dentinoblasts course through these tubules and communicate with each other and pulped nerve fibers, The pulp itself contains at best 600 t 700 nerve fibers with a majority consisting of the myelinated type. This concentration of fibers is higher than the corney making human pulp an extremely pain sensitive structure. Sensory distribution of the trigeminal nerve is extensive as it supplies the ``central computer'' with information on pain, temperature and touch impulses from most of the head, skin, face, oral and nasal mucosa and dura mater.

*******************The axonal transport mechanism is capable of antegrade and retrograde flow, nourishing the periupheral branches with antegrade flow. Retrograde flow brings bacteria, viruses, endotoxins, and other degenerated compounds that are generated by devital teeth, N's, etc., to the central nervous system (CNS) and ultimately the main sensory trigeminal nucleus and spinal trigeminal nucleus. At some point, the CNS perceives a threat based on this feedback mechanism and goes on alert.

The multiplicy and overlapping peripheral innervation (dentinoblasts, pulpal fibers, periodevital ligament fibers) further complicates the picutre by converging as it approaches the CNS. An inflamed pulp from a hot tooth could be causing impulses that are below the threshold of pain perception of the patient. Add to this, a root canal and two NICO leasions from old third molar sites and the CNS, via cranbial nerve #5, is aroused it lets the patient know there is something wrong causing pain. The pain can be intermittend and excruciating like that of trigeminal neuralgia or vague and heavy, disguised as a headache, ear pain, sinus pain or non-specific jaw pain, troublesome enough to cause suicide.**********************

Localization of these pathological ``foci'' of pain-causing disease is best accomplished by anesthetic confirmation of ``neural therapy''. This technique utilizes local anesthetic, both vasoconstrictor and preservative free, that is injected into and about the periapical mucosal area of suspect N leasions or teeth in order to ascertain their effect on the patient's perception of pain. Approximately 1/2 cc of anesthetic solution is delivered to the suspected site via 30 gauge needle. If the pain is abolished, it is with high certainty that you have found the primary lesion. If only some of the pain has been attenuated, then continued testing in other regions both ipsilaterally and contralaterally in the arches is necessary. Be suspicious of any edentulous regions.

******************* You will discover every third molar area is usually associated with a NICO lesion prior to extraction. W I S D O M T E E T H are misnamed; they are teeth of misfortune.**********************

References in my files /I think I typed enough for now/gg

quote:

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Originally posted by GiGi:
If you have not been able to get better and/or totally well, please read this very, very carefully and/or take it to your dentist. Whatever you do, do not ignore this. Taking this seriously, saved me and got me totally well after a long struggle.

By the way, I had no idea what an ``alveolus'' was ----- it refers to the bony socket of a tooth.......

W I S D O M T E E T H or Teeth of Misfortune (Third Molars)

Facial Pain Linked To Infections
by Christopher J. Hussar, D.D.S., D.O.

For almost a century controversy has waged regarding the existence of a disease process with infectious origins within the dental alveolus. These localized infectious processes have been strongly implicated in generating facial pain including trigeminal neuralgia along with other cranial facial pain disorders including, remote pain disorders in distant regions of the body.
The Father of modem dentistry, G. V. Black, recognized and gave notice in one of his textbooks to the actuality of a hollow jaw bone, housing an infectious process within the dental alveolus. A review of the literature reveals numerous papers from the early 20th century written by both M.D. and D.D.S. alike, describing the surgical debridement of jaw infections including devital teeth, and localized osteomyelitis lesions that successfully treated, not only localized facial pain, but remote pain disorders such as arthritis as well.
Sir Wilfred Harris, a British neurosurgeon, proposed the reality of a chronic intra osseous infection within the alveolus causing neural degenerative changes and demyelination to trigeminal nerve branches. This was in 1926 and was widely accepted by dental surgeons in America nearly a century prior.
In the early part of this century the theory of "focal disease" arose in which a chronically infected area of the body was responsible for causing pathology elsewhere. Many tonsils as well as teeth were removed with miraculous, as well as not so miraculous, results. The clinician would script an article expounding the cure of arthritis after the patient had several diseased teeth removed. Anecdotal cases of blindness reversal was documented (your author has witnessed such an event)...

Much credit must be attributed to the brilliant research of Dr. Weston Price in the early part of our century. With incredibly reproducible results, this research dentist demonstrated the existence of multiple bacterial strains in dental teeth including root canals. In addition, he addressed the chronically infected periodontal membrane and periodicular bone resulting from infected teeth and the cavitation of such chronically infected bone if thorough socket curettabe was not performed properly.

With the ``disproving'' of the focal theory by our progressively autocratic medical/dental complex, the concept of chronic dental/alveolar infections has gone practically unrecognized for the past sixty years.
One of the reasons may be poor visuatlization of these chronically ``cavitated'' lesions on intra-oral radiographs. Usually housed within the cancellous bone, the cortical plates and their different x-ray absorption qualities obscure and alter the true picture lying deep within the jaw bone.

In reality, this is not the case as certain radiographic landmarks are quiate visible and will readily confirm the presence of these lesions. With continued x-ray evaluation along with curettage of a suspected lesion, they will become obvious.
The above mentioned as been well documented by Jerry Bouquot, D.D.S., M.S.D., in his numerous articles on NICO (Neuralgia Industing Cavitational Osteonecrosis) lesions describing ``laminar rain,'' the x-ray visible, boney changes resemblung the rungs of a ladder. This results when the bone of the extraction site refuses to heal properly, literally leaving the root outlined. Micro calcification within the confines of the original extraction site, further confirms the presence of an inflammatory bone lesion, often referred to as a cavitation.''.
In surgerizing mandibular lesions, involvement of the inferior alveolar nerve (IAN) by the obstructive process creates a characteristic appearance on the x-ray. The superior aspect of the mandibular canal, the ``roof,'' is usually eliminated and the fine, dense superior white line is seen to disappear as the IAN courses through the lesion site. Absolute certainty of course only occurs with biopsy confirmation of curettaged tissue from these lesions. With little practice and suspicion, near one hundred percent accuracy is possible when performing the surgical debridements.
Perhaps our subject matter has been ignored for decades because of a failure to biopsy on the part of dentistry as a whole. Do endodontists rely on the biopsy for verification of tissue? Hardly, for my dental training down-played the role. Do oral surgeons send their extracted teeth in for biopsy along with any abnormal bone that may be removed along with those teeth? It is my policy to biopsy every tissue fragment I remove from the mouth. My judgement in determining pathology has been incorrect less than .5% of the time. Once you begin to recognize the disease, the diagnosis becomes much easier.
When curetted, the contents of these intraosseous lesions may present varying types of diseased tissue. Commonly, when surgically opened, the lesion site is void of caancellous bone; thus the derivation of the term ``cavitation,'' a hollow cavity exists. Other presentations include hemorrhagic bone with easily curettaged spicules of both viable and non-viable bone. Multiple globules of adipose tissue representing degenerated bone can commonly be curettaged; in fact, **************opening up one of these lesions with a fissure burr causes an exudate not unlike bloody chicken soup with countless micelles of fat floating on the surface of the serium***************.
If an area of condensing osteomyelitis/osteitis is evident on an x-ray associated with a suspected cavitational area, surgically speaking the alveolar bone will usually possess a consistency of pearl-like hardness implying condensed bone that has been made devital by ischemia. This is extremely difficult bone to surgically eliminate especially in the presence of the inferior alveolar nerve. These patients will often develop facial pain syndrome and can be difficult to treat.
Microscopically most biopsy reports will demonstrate marrow fibrosis as the body attempts to regenerate itself, fibrotic material heals easier than bone. Multiple fragments of bone shard appear as the impaired blood supply cannot provide adequate flow to new bone attempting to replace diseased bone. When your patients come to you months after a difficult extraction, showing a small bone fragment that has worked its way through the gingiva, you didn't forget to irrigate it out; the body refused to nourish it and it sloughed. Lymphocytes may or may not be encountered depending on the chronicity of the infection, the immunity of the patient, nutritional status, and other factors. Neurophils, most commonly seen with acute inflammatory processes, are seen infrequently with cavitations. What is seen primarily is necrotic bone flake often intermingled with viable bone. Remarkably, very few osteoblasts or osteoclasts are observed in specimens.
Most articles covering facial pain are written dealing with trigeminal neuralgia, atypical facial pain (AFP) and TMJ, with the latter two being the most common. Most of these reading this article are well-versed in the treatment of TMJ disorders. However, what treatments do you prescribe to the patient who has had 5 or 6 bite splints from other practitioners and his facial pain persists without alleviation? You must always be suspicious of a ``NICO'' process smoldering in the patient's alveolus when consulted by such a patient.
********************Their orruccurrence is of epidemic proportions; if the patient has had any third molars removed, it's a safe bet to conclude that cavitations are present. Why do they cause pain in some and not others Multiple theories have been proposed as to what mechanisms exist allowing NICO's to generate pain
A general consensus agrees upon the initial development of an intra-alveolar infection from a devital tooth, root-canaled tooth, ir extraction site. This infection persists within the alveolus and can ``tunnel'' or remain localized. In the mandible, the bascula system is an end-organ type or terminal vessel allowing basically one-way flow of blood. Chronic infectious agents harboed in these cavities, namely bacteria and their endotoxins along with what appear to be viral agents causes a vasculitis in the arterial side eventually compromising the flow of blood.
With the onset of ischemia other changes occur. Antibiotics are not as effectivce for they rely on a blood supply to reach their target zone. Infectious agents often will die off or become rapidly attentuated and be rarely seen in biopsy. Bone necrosis develops, the affected alveolus cannot heal properly, and a pathologice entity arises called ``NICO.'' What caused the pain?

The physiology of the trigeminal nerval is extremely complex. Peripherally, the dentin contains 30,000 to 70,000 microtubules per square millimeter! Free sensory nerve endings and dentinoblasts course through these tubules and communicate with each other and pulped nerve fibers, The pulp itself contains at best 600 t 700 nerve fibers with a majority consisting of the myelinated type. This concentration of fibers is higher than the corney making human pulp an extremely pain sensitive structure. Sensory distribution of the trigeminal nerve is extensive as it supplies the ``central computer'' with information on pain, temperature and touch impulses from most of the head, skin, face, oral and nasal mucosa and dura mater.

*******************The axonal transport mechanism is capable of antegrade and retrograde flow, nourishing the periupheral branches with antegrade flow. Retrograde flow brings bacteria, viruses, endotoxins, and other degenerated compounds that are generated by devital teeth, N's, etc., to the central nervous system (CNS) and ultimately the main sensory trigeminal nucleus and spinal trigeminal nucleus. At some point, the CNS perceives a threat based on this feedback mechanism and goes on alert.

The multiplicy and overlapping peripheral innervation (dentinoblasts, pulpal fibers, periodevital ligament fibers) further complicates the picutre by converging as it approaches the CNS. An inflamed pulp from a hot tooth could be causing impulses that are below the threshold of pain perception of the patient. Add to this, a root canal and two NICO leasions from old third molar sites and the CNS, via cranbial nerve #5, is aroused it lets the patient know there is something wrong causing pain. The pain can be intermittend and excruciating like that of trigeminal neuralgia or vague and heavy, disguised as a headache, ear pain, sinus pain or non-specific jaw pain, troublesome enough to cause suicide.**********************

Localization of these pathological ``foci'' of pain-causing disease is best accomplished by anesthetic confirmation of ``neural therapy''. This technique utilizes local anesthetic, both vasoconstrictor and preservative free, that is injected into and about the periapical mucosal area of suspect N leasions or teeth in order to ascertain their effect on the patient's perception of pain. Approximately 1/2 cc of anesthetic solution is delivered to the suspected site via 30 gauge needle. If the pain is abolished, it is with high certainty that you have found the primary lesion. If only some of the pain has been attenuated, then continued testing in other regions both ipsilaterally and contralaterally in the arches is necessary. Be suspicious of any edentulous regions.

******************* You will discover every third molar area is usually associated with a NICO lesion prior to extraction. W I S D O M T E E T H are misnamed; they are teeth of misfortune.**********************

References in my files /I think I typed enough for now/gg

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