Welcome to Life Guard Your Health Website

William D. Nordquist DMD MS
1901 4th Avenue Suite 300
San Diego, California 92101
619-236-7959
wnordquist@yahoo.com

Life guard your health: Diagnosing and treating periodontal disease website is dedicated to education concerning the relationship between periodontal disease (“gum”) and a wide diversity and probable cause of chronic inflammatory diseases. The relationship between diseases including; periodontal disease, heart disease, atherosclerosis, diabetes, psychological diseases, arthritis, osteoporosis, and many others are being strongly linked to the bacteria, especially spirochetes, that cause periodontal disease. This website will include the theory, diagnosis, and new treatments to help mitigate and/or possibly cure these chronic diseases that renders people miserable during the last two decades of life.

The website will also discuss root canal treatment of teeth and the infection that is associated with these teeth that cause adjacent dental implants to failure. If infection associated with root canals, then what other infections in the body are being caused by these pathogens. A new Actual Tooth Replacement technique will be discussed describing a new alternative method replacing the root canal treatment  therapy.

Women are 80% more vulnerable to chronic disease than men. The theory will be detailed. Typically these older women suffer from multiple missing teeth, periodontal disease, thyroid problems, osteoporosis, and many other chronic inflammatory diseases. These diseases are more and more being related to the bacteria that cause periodontal disease. These bacteria are especially active during pregnancy and several days during the menstrual cycle.

Dental implant design is also important in the life guard program. A concept called micro-leakage or micro-gap allows bacteria to thrive around leaking implant-abutment junctions causing periodontal disease next to the bone eventually resulting in bone loss and eventual loss of the implant itself.

The Lifeguard program is designed to train patients in cleaning their teeth in a way to eliminate most if not all pathogenic bacteria that causes periodontal disease.

By. William d. Nordquist

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The Problems with Root Canal Treatment William D. Nordquist DMD MS

The Problems with Root Canal Treatment

William D. Nordquist DMD MS*

David J. Krutchkoff DMD MS**

When a tooth decays or periodontal disease occurs to the extent that infection enters the pulp chamber of a tooth, the traditional treatment involves the mechanical removal of infected pulpal tissue and replacement with an inert root canal filling. If done properly, this form of treatment is usually quite effective from a clinical standpoint in that the area in question usually becomes asymptomatic, and all clinical means of assessment available to the treating dentist usually reveal local osseous regeneration and healing in addition to restoration of function. In spite of the apparent success of this form of treatment, there is recent suspicion that this might represent an over-simplification of this common clinical situation. In fact, if one examines the situation from strictly a biologic point of view, there is little question that, in spite of the many forms of clinical measurement to the contrary, traditional root canal treatment (RCT) is far from ideal. We  know this to be the case since even when root canal debridement is accomplished in the best manner possible, subsequent analysis of treated teeth reveals small foci of bacterial debris that are nonetheless left behind within tiny irregularities of the root canal or apical surface of the tooth.[1] [2] These foci, even though clinically innocuous in most cases, can and sometimes do represent the source of infection of adjacent contiguous bone that later causes subsequently placed adjacent implants to fail[3] [4] [5] [6]. If such infection is capable of causing a nearby implant to fail, it begs a larger and much more important question: that is, can these apparently innocent but persistent dental foci of infection at the apices of teeth also represent the source of distant infection or chronic inflammatory processes elsewhere in the body that occur via blood-borne spread? If so, this would represent a potentially serious problem.

It is generally accepted fact that once being diagnosed, infections that occur elsewhere in the body (e.g., the appendix or the skin etc.) are ordinarily treated aggressively in order to prevent further damage to adjacent tissues and spread of infection to vital organs. Yet low grade, chronic dental infection, because it is usually clinically silent and apparently innocuous, is commonly tolerated by the dental profession and is usually passed over lightly or is basically ignored. It has been common practice for dentists to assume this practice since, in reality, there has been no real impetus to pursue any therapeutic solution since the presence of a few bacteria surrounding RCT-treated teeth was generally assumed to be less than clinically significant and thus, for all practical purposes, a non-problem. In any case, there was certainly not enough rationale to consider more aggressive treatment (such as the sacrifice an otherwise good tooth), and further still, there were no good alternatives to root canal therapy short of apical surgery or extraction. In spite of the fact that clinically silent root canal fillings are usually deemed clinically acceptable, the assumption of innocence with regard to apparently normal, apical tissues following RCT has not always been the case.

Looking back into history, we note that the efficacy of root canal treatment has, at times, been called into question, but the politics of practice were usually sufficient to silence such critics. One prominent example of such is the case of Weston A. Price, DDS (1870–1948), a prominent dentist and also a nutritionist. Price was the chairman of the Research Section of the American Dental Association from 1914–1923 but was later marginalized by the ADA for his outspoken views on what he considered the detrimental aspects of  root-canal therapy. In our opinion, however, after a thorough reading and review of Price’s work, it is clear that he practiced and understood the concept of infection associated with root canal treatment therapy far better than we do today.  One only has to examine his research to make this point. For example, in one experiment performed nearly 100 years ago, Price[7] took infected teeth or extracts of such from patients suffering from a wide range of serious “medical” problems, and implanted these samples under the skin of laboratory animals. Subsequent examination revealed that the laboratory animals quickly came down with infections in distant parts of their bodies. Expected results from such an experiment would be that an infection from the implanted infected tooth material might go anywhere in the body of the experimental animal to cause disease in more or less a random distribution pattern. However, that was not the effect that Price observed. What was observed was that if the donor patient had infected kidneys and his infected dental material was implanted into several lab animals, essentially all the animals developed infected kidneys, and did so with rapidity[8]. As a result of his experiments, Price claimed that as many as 95% of focal infections in distant tissues started in the teeth and tonsils[9]! Price theorized that ordinarily harmless bacteria normally found in the mouth get trapped in the dentinal tubules or root surfaces of infected teeth or tonsils and somehow mutated into a more dangerous form. The new mutated bacteria and /or the toxic poisons they produced would travel through the blood stream and lymphatic system to remote body parts and cause disease elsewhere. Price went on to show that even when root canal treatment was done according to what at the time was accepted modern principles and standards, and even when follow-up radiographs showed  evidence of adequate healing, such treatment did not prevent or preclude the presence and subsequent spread of infection in laboratory animals.

In addition, Price also proved that infection in the area of a treated tooth can spread contiguously to infect adjacent bone in that biopsy specimens of bone adjacent to RCT-treated teeth revealed bacteria within the first millimeter or two from the apical surface.[10] Clearly, there is abundant evidence from Price’s work alone that even clinically adequate, root-canal-treated teeth can and do harbor residual bacteria that, at least potentially, can cause problems for implant dentists when subsequently placing dental implants in bone adjacent to root-canal-treated teeth.

Research done much later adds additional evidence in support of Price’s earlier conclusions. In his classic 1967 study, Brynolf[11], used cadavers as source material to study root canal treated teeth. These cadaver teeth, all previously treated by RCT, were radiographed and evaluated for evidence of apical radiolucent lesions and subsequently divided into those with and without periapical lucenceis. The teeth and surrounding bone were then cut from the jaws in block sections and later treated, prepared and sectioned for microscopic examination. As a result of his investigation, Brynolf’s concluded that the lack of radiographic evidence of pathologic change at the base of a root canal–treated tooth did not preclude the presence of small foci of inflammation or infection at the apex of the tooth in question. He went onto say that 93 percent of root canal–treated teeth examined in his cadaver study had microscopic signs of inflammation (infection), presumably caused by bacteria in the area. Later,  Green et al[12] performed additional cadaver studies and characterized Brynolf’s previous results as somewhat questionable due primarily to differences both in treatment techniques and methods of radiographic and histological analysis that were being used at the time. Green reported that out of the 29 teeth examined, 15, and (52 percent of his cases) exhibited histologic evidence of inflammation, presumably due to causative infective bacteria that remained in the periapical area after root canal treatment was performed.

 

The question as to which specific bacteria are involved in apparent residual low-grade periapical infection (related to prior root-canal-treated teeth) has not been addressed until relatively recently when  techniques became available that enabled identification of small amounts of DNA material unique to a specific bacterial genus or species. With specific regard to the oral spirochetes, Ôças [13] and his group used a nested PCR assay in an effort to determine the presence or absence of four distinct Treponema species associated with primary root canal infections. Samples from 32 cases of infected root canals were obtained, twenty-two of which exhibited chronic, asymptomatic peri-radicular lesions whereas 10 were symptomatic cases diagnosed as acute apical periodontitis. Small traces of DNA extracted from all samples were amplified using universal 16S rDNA primers to detect a specific fragment of the 16S rDNA from each of the following Treponema species: Treponema denticola, T. socranskii, T. vincentii and T. pectinovorum. Results showed that in asymptomatic cases, T. denticola, the most common oral spirochete, was detected in 77.3% of the samples; T. socranskii was seen in 40.9%, T. vincentii in 18.2% and T. pectinovorum in 13.6%, whereas in the acute apical periodontitis cases, T. denticola was detected in 80%, whilst T. socranskii and T. vincentii were detected in 40% and 10% of cases, respectively. Based on these data, it is clear that, in addition to a number of other bacteria (tests for such were not run); the various oral spirochetes must be considered as potential infectious microbial sources with regard to their likely role as putative pathogens for endodontically-related periapical disease as well as for other oral infections.

 

In a later investigation involving spirochetes, Montagner[14] designed a study to detect the presence of Treponema species in infected root canals (RCs) and exudates related to acute apical abscesses (AAAs) as well as to determine positive association between targeted species and clinical signs/symptoms. Paired samples of infected RCs and AAAs were collected from 20 subjects. Nested polymerase chain reaction assay with species-specific primers for 16S rDNA and downstream intergenic spacer region was used for microbial detection. The frequency of species and statistical associations between species and signs/symptoms of endodontic origin as well as their simultaneous detection in both milieus were probed.

 

The most frequently detected species were T. socranskii (RC, 17/20; AAA, 15/20), T. denticola (RC, 8/20; AAA, 11/20); T. medium (RC, 6/20; AAA, 9/20); and T. amylovorum (RC, 5/20; AAA, 9/20). Positive correlation was found for simultaneous presence of T. denticola in both RCs and AAAs (p = 0.01). Positive association was observed between T. medium and T. vincentii (p = .037). No positive statistical association was observed between the targeted species and signs/symptoms. The high prevalence of Treponema species in RC and AAA samples from the same tooth indicated that these organisms are important pathogens in acute endodontic infections.

 

Other more recent research perhaps gives us more cause to be concerned about potential dangers of oral spirochetes. In his excellent article published in the Journal of Dental Research, Foschi[15] showed that Treponema denticola, the most commonly implicated oral spirochete associated with periodontal disease can disseminate into a variety of distant body tissues subsequent to being artificially introduced into the pulp chambers of healthy mouse teeth by surgical means. Within a short period of time following surgical implantation, spirochetes produced abscesses that drained through the “gums” adjacent to the roots of the infected teeth. He later sacrificed the mice and studied a variety of tissues to determine the anatomic location where the spirochetes were able to migrate and later infect. He found that the spirochetes were able to spread to virtually all vital tissues of the mice including the brain. Although spirochetes may have been present in far greater numbers in Foschi’s experiment than in actual human periapical disease, this is nonetheless powerful evidence that implicates spirochetes as possible, if not likely, candidates for causing or initiating chronic inflammatory diseases in remote tissues distant from their site of origin.

 

Nordquist[16] [17] [18] [19] [20]has discussed the potential role of infected teeth (including root canal treated teeth) in the complex labyrinth of systemic chronic inflammatory diseases. He showed that undiagnosed, clinically silent, infected teeth adjacent to a subsequently placed dental implant can be the source of the infection that ultimately causes the adjacent implant to fail.

 

Reports of a disproportionate number of dental implant failures (when the latter are placed adjacent to RCT-treated teeth) along with the large percentage of periapical infections associated with root canal teeth in cadavers gives both the dental and medical professions real cause for concern. How do we know with certainty which root canal teeth, if any, will later surface as problematic sources of infection prior to the time that implants are placed? Can dentists afford to ignore adjacent root-canal-treated teeth when contemplating the placement of an implant? The risks to patients regarding local contiguous spread of infection to adjacent bone and implant failure are obvious. However, there would seem to be a much more serious potential risk to those involved in various fields of dental practice, and these involve potential liability issues that may arise for dental clinicians. That is, if a causative link between dental infection and systemic disease becomes more firmly established, dentists could potentially be held liable for failing to deal with asymptomatic periapical infection should that infection lead to more serious consequences down the road. Clearly, an acceptable therapeutic alternative to RCT, i.e., dental implants, that diminishes such risks both to the patient and the dentist would not only be beneficial but also desirable.

 

*Private practice

Implant Dentistry of San Diego

2304 6th Avenue San Diego, California 92101 wnordquist@yahoo.com

**Professor Emeritus, Department of Oral Pathology, University of Connecticut School of Dental Medicine, Farmington, Connecticut

 


[2] Price WA. Dental Infections Oral and Systemic. Volume I. Price-Pottenger Nutrition Foundation La Mesa California 2008.

[8] Price: Ibid:155-171.

[9] Price WA. Ibid;407.

[10] Meinig GE. Ibid. Pg.31.

[12] Green T, Walton R, Merrell P. Radiographic and histologic periapical findings of root canal treated teeth in cadaver. Oral surg Oral Med Oral Pathol Radiol Endol 1997;83:707-11.

[13] IN ôças, JF Siqueira, AF Andrade, M Uzeda. Oral treponemes in primary root canal infections as detected by nested PCR. Int Endod J 2003;36:20-6.

[14] Montagner F, Jacinto RC, Signoretti FG, Gomes BP. Treponema species detected in infected root canals and acute apical abscess exudates. J Endod. 2010 Nov; 36 (11):1796-9.

[15] Foschi F. Treponema denticola in disseminating endodontic infections. J Dent Res 2006; 85(8):761-765.

[16] Nordquist W. Ibid. 2009.

[17] Nordquist W. Oral spirochetosis associated with dental implants: Important clues to systemic disease. Int’n J of Clin Impl Dent 2009 Jan-Apr;1(1):32-39.

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The Mystery of Diminished Cognition, Dementia and Alzheimer’s disease Unraveled

The Mystery of Diminished Cognition, Dementia and Alzheimer’s disease Unraveled

William D. Nordquist DMD MS

The author wondered why patients with many missing teeth have health histories with one or multiple chronic inflammatory diseases such as heart disease, dementia and Alzheimer’s disease[1] [2]. What is it about fabrication of dentures cause the vast majority of dentists to be wary of providing this service? Why would a famous lecturer make a statement like this, “I’ve noticed that patients’ brains must be located in their teeth; the more missing teeth they have, the (more mentally challenged) they seem to be.[3] The author and Krutchkoff’s recently published book, The Silent Saboteurs[4], describes the relationship between  the specific pathogen, oral spirochetes, found in periodontal (gum) disease and the possible causation of heart disease[5], as well as, with other systemic chronic inflammatory diseases[6] [7] [8] [9] [10] [11], including Alzheimer’s and other plaque-forming neurological diseases, diabetes, premature birth, autoimmune diseases, and cancer. Recent research[12] has collaborated this theory and pointed a conclusive accusing finger specifically stating that any spirochetal disease, such as, syphilis, Lyme disease and now the very common disease, periodontitis, can cause neurological damage.

The relationship between dental and heart disease has been reported in scientific literature and national news for several years. The relationship between periodontal disease and cognitive ability has only recently surfaced with university studies. A study done in West Virginia showed that patients among community-dwelling older adults have diminished health, as well as, decreased cognitive ability[13]. Tooth loss and tooth decay was studied in very old Swedish people. The conclusions surmised that an association between the cognitive and functional status of these individuals and aspects of oral health were correlated. Further studies were recommended to determine better the oral health status of these individual leading to the deterioration of overall health in older adults[14].  A London study showed that there is a correction between poor oral health and worse cognitive function throughout adult life[15]. Crout, in a report to the WVU Health News Letter reported finding that “keeping the mouth free of infection could cut down on cases of dementia”[16].

A Japanese group headed by Okamoto[17], investigated a very large group of elderly population in a cross-sectional study in the relationship between the number of remaining teeth (a proxy to periodontal disease) to mild memory impairment, which is a preclinical stage of dementia, and to cognitive impairment. The subjects were aged 65 years or older and were grouped according to their score for the Mini-Mental State Examination, the three-word delayed recall test, and the Geriatric Depression Scale into the control group (n = 3,696), the mild memory impairment group. They collected data on the number of remaining teeth, the length of the edentulous (missing teeth) period, health-related lifestyle, medical history, blood pressure, height, and body weight. Fasting venous blood samples were also obtained.

The results reported include: The test were adjusted for depressive symptoms, age, sex, length of education, and other explanatory variables. The results revealed a significant relationship between the length of the edentulous period and the risk of a low Mini-Mental State Examination strongly suggest that tooth loss is associated with cognitive function.

Judith Miklossy[18], a Swiss researcher, published the most authoritative paper to date on the subject, categorically states that oral spirochetes, as well as, the spirochetes that cause Lyme disease and syphilis all cause dementia and Alzheimer’s disease. She reports that the “accumulated knowledge, the various views, and hypotheses proposed to explain the pathogenesis of Alzheimer’s disease form together a comprehensive entity when observed in the light of a persisting chronic inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection. As suggested by Hill, once the probability of a causal relationship is established prompt action is needed. Similarly to syphilis, one may prevent and eradicate dementia in Alzheimer’s disease. The impact on healthcare costs and on the suffering of the patients would be substantial.”

An understanding of, or probable theories of cognitive disorders have here to now been veiled in mystery. However, a mounting body of evidence points to a viable prevention of mental disorders, if oral health is maintained in healthy individuals and periodontal disease is intercepted and treated in periodontal disease individuals. Also, understanding the cause can lead to curing this devastating disease.


[1] Nordquist W. The Stealth Killer: Is oral spirochetosis the missing link in the dental-heart disease labyrinth? BioMed Publishing Group.

http://www.lymebook.com/stealth-killer-nordquist.

[2] Nordquist W. Oral spirochetosis associated with dental implants: Important clues to systemic disease. Int’n J of Clin Impl Dent 2009 Jan-Apr;1(1):32-39.

[3] Nordquist WD, Is Oral Spirochetosis the Missing Link in the Spectrum of Chronic Inflammatory Disease? Western district American Academy of Implant Dentistry, Annual Meeting, San Antonio, Texas, 2008.

[4] Nordquist WD and Krutchkoff DJ: The Silent Saboteur. BioMedical Publishing Group. Lake Tahoe, California 2011.

[5] Beck JD et al. Periodontitis: a risk factor for coronary heart disease? Ann Periodontol. 1998;3(1):127-41.

[7] Jodhpur K et al. Strength of evidence linking oral conditions and systemic diseases. Commend Cetin Educe Dent Supply. 2000;( 30):12-23.

[9] Loesche WJ. Et al. Periodontal disease as a risk factor for heart disease Compendium. 1994 Aug;15(8):976, 978-82, 985-6.

[10] Behle JH, Papapanou PN. Periodontal infections and atherosclerotic vascular disease: an update. 2006;56(4 Suppl 1):256-62.

[13] Wu S et al. Cognitive function and oral health among community-dwelling older adults. J Gerontal A Biol Sci Med Sci. 2008 May;63(5):495-500.

[14] Avlund K. Tooth loss and caries prevalence in very old Swedish people: the relationship to cognitive and functionsl ability. Gerodontology. 2004;21(1)17-26.

[15] Stewart R. Oral health and cognitive function in the Third national health and Nutrition Examination Survey (NHANES III). Psychosom Med. 2008 Oct;70(8)936-41.

[16] Crout R. WVU School of Dentistry studies link between oral health and memory. WVU Health News, www. Health.wvu.edu/newsrelease/news-details.aspx?ID=1211.

[17] Okamoto N, Morikawa M, Okamoto K, Habu N, Iwamoto J, Tomioka K, et al. Relationship of tooth loss to mild memory impairment and cognitive impairment: findings from the Fujiwara-kyo study. Behavioral and Brain Functions 2010, 6:77

[18] Miklossy J. 22.

Posted in Alzheimer's disase, Cognition, Dementia, Life Guard Your Health, Periodontal Disease-Systemic Disease, Womens issues | Comments Off on The Mystery of Diminished Cognition, Dementia and Alzheimer’s disease Unraveled

Spirochete Plait-form transition within a Polymorphic Nucleocytes (PMN) Immune Cell

Possible Recognition of a Spirochete Plait-form transition within a Polymorphic Nucleocytes (PMN) Immune Cell

In recent literature, Wolf[i] working in the Robert Koch-Institut des Bundesgesundheitsamtes, reported quasi-multi-cellular-bodies of Treponema denticola, the most common oral spirochete. They analyzed its forms using electron microscopic methods and found a total of four forms: normal helical, twisted spirochetes that formed plaits, twisted spirochetes that formed club-like structures, and spherical bodies of different sizes. The researchers theorized that such forms were better able to resist adverse conditions such as antibiotics and toxins.

Even though these forms have been identified using scanning Electron Microscopy (SEM), little is known concerning their role in disease and “live” microscopic morphological appearance in the gingival sulcus plaque or their role in the immune response. Wolf identified these in pure culture by freezing them, fracturing the frozen samples, coating them with metal plasma spray, dissolving the organic substrate, and performing (SEM) on the metal replicas. They were summarized in a diagram (figure 1).

 

 

 

 

 

Figure 1

The one or more spirochetes under certain conditions can weave themselves into a hollow tube called a “plait-form” (figure 2 top shows two spirochetes beginning the weave, bottom shows the “plait-form” in the making and figure 3 show the completed “plait-from”).

 

The video (using a phase contrast oil immersion at 1000X amplified using a Canon Rebel T2i HD camera with an optical focusing attachment mounted in the lens housing of the camera. The camera magnified the image by 5X to 5000X) was taken of exudate draining from a fistulas tract located on the buccal gingival tissue adjacent to tooth #31. This tooth has complete lost bone from the distal root.

 

 

 

A torpedo rod-like microbe is observed with spirochete-like movement vigorously propelling itself in all confined spaces of a (PMN) immune cell. This is best described as furious movement to free itself from the cell confinement. At one point in this escape attempt of the unidentified microbe, it is successful. However, a bizarre transformation occurs and as the microbe is successful in penetrating the immune cell’s outer membrane. It increases its length by a factor of 10 and appears as a typical helical form spirochete. Not completely successful in extirpating itself from the immune cell, it converts back to the shorter torpedo form and then is successful in escaping from the cell. A fleeing spirochete can be seen exiting to the 12 o’clock position above the PMN.

These torpedo tube forms (plait-form) are quite numerous microbes observed when examining plaque samples taken from the disease gingival sulcus of periodontal diseased patients. These forms are best describes as hollow tubes that have a opalescent appearing fluid in its center when observing them oriented perpendicular to the microscopic slide or parallel to the light source. More research and observation is necessary to confirm these observations. If collaborated by other investigators, this “plait” form could be routinely identified as spirochetal and diagnosed as yet one more identifiable oral spirochete form of spirochetosis and treated appropriately.


[i] Wolf V, Lange R. Weeks J. (1993) Development of quasi-multicellular bodies of Treponema denticola. Arch Microbiol 160:206-213.

 

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Spirochete producing “granular forms” live within a polymorphic nucleocyte (PMN) Immune Cell

Live-microscopic video (5000X) of spirochete producing “granular forms” within a polymorphic nucleocyte (PMN) Immune Cell

 

Dental clinicians are well aware that spirochetes are present in large numbers particularly in samples taken from advanced stages of human periodontal disease and also found associated with necrotic teeth requiring endodontic procedures[1] [2] [3] [4] yet most are unaware of either their virulence or the precise role(s) played by these organisms in the pathogenesis of disease. A thorough literature review has produced an astonishing story concerning “spore-like” bodies, bud-like extensions of helical spirochetes that separate off to eventually populate adjacent fluid, in this case, an  immune cell taken from a draining abscess(See previous post for literature concerning granular, cell-wall deficient and spherical bodies). It is proposed that with death of these immune cells, the same “granular forms” become liberated and then serve to re-populate the gingival un-cleansed crevice to increase their populations and lead to more advanced disease. A review of the literature will be presented along with data which support this novel concept. Also, in this example, the immune system is operating normally thus performing phagocytosis and draining the resultant exudate from a periapical infection of tooth #31 to the oral cavity.

Early studies with the light microscope have shown aberrant forms of spirochetes with external granules, buds, round bodies, etc., attached to the spirochete. Further, granules have been observed lying free within the surrounding medium. These “granular” structures were first reported over 100 years ago, around the time that the spirochetal organism was first discovered[5] [6] [7].

In the early stages of preparing his previous first book, Nordquist[8] initially researched this idea of “spore-like” structures through the Internet and found only one text book reference to this form of transmission mode for oral spirochetes in the earlier literature, and this was published in the year 1960[9]. The author of the latter-cited chapter stated the following: “External granules may become free from the cell and in old cultures, containing granular forms when examined by dark-field microscopy, have been shown to give rise to typical spirochetes on subculture to fresh mediumthe granules may therefore be a stage in the lifecycle of the organism.” These granules apparently appeared on the surface of the spirochetes just prior to their death. The bacteriologist who reported this finding also observed that these spores were biologically active and reportedly developed later into multiple replicated spirochetes.

A patient recently ( August 2011) presented to Nordquist’s office with an abscessed tooth #31 with a draining fistula. Microscopic samples were taken of this pus and studied under phased contrast oil emersion microscopy at 1000X power amplified 5X with a Canon Rebel T2i camera in high definition. In the vast microscopic field of active spirochete activity, a single spirochete was observed in the upper portion of a polymorphic nucleocytes (PMN) immune cell. The spirochete clearly has an outer membrane, however, its movement is sluggish and appears to be at the end of its active helical lifecycle. As the spirochete breaks down, small black internal granules form pseudo-pods and then become free from the outer membrane thus exiting the spirochete floating freely into the intra-cellar fluid. Within seconds, the entire spirochete loses its outer membrane and releases the remaining granular bodies.


 

 

If, this is the case, where all spirochetes undergo phagocytosis by PMNs in this type of periapical tooth infection, then the immune cells within the pus are draining through the discharge fistula harmlessly from the body through a drain in the “gums” into the mouth. This is the normal immune reaction and the body rids itself of these pathogens. However, in other parts of the body where spirochetes are encountered by the immune system, i.e., in atherosclerotic lesions, this easy exit strategy is not possible, thus evidently the spirochete “granular form” loaded PMN immune cell breaks down releasing these “granular forms” without successfully eliminating them from the inter sanctuary of the body.

Once release from the breakdown of the phagocyte, these granular forms have two options; 1. Transform into the active forms and re-infect the area where they were originally attacked and/or 2 remain in the vicinity as an unaltered antigen thus could stimulate further inflammation and continuation of the inflammatory disease process in the area. This mechanism provides one more clue as to how spirochetes cause and perpetuate chronic disease utilizing the human body’s immune system.

[1] IN ôças, JF Siqueira, AF Andrade, M Uzeda. Oral treponemes in primary root canal infections as detected by nested PCR. Int Endod J 2003;36:20-6.

[2]Montagner F, Jacinto RC, Signoretti FG, Gomes BP. Treponema species detected in infected root canals and acute apical abscess exudates. J Endod. 2010 Nov; 36 (11):1796-9.

[3] Foschi F. Treponema denticola in disseminating endodontic infections. J Dent Res 2006; 85(8):761-765.

[4] Nordquist W. Oral spirochetosis associated with dental implants: Important clues to systemic disease. Int’n J of Clin Impl Dent 2009 Jan-Apr;1(1):32-39.

[5] Schaudinn, F. & Hoffmann, P. O0ber (1905) Spirochaeta pallida bei Syphilis und die Unterschiede dieser Form gegenuiber anderen Arten dieser Gattung. Ber. Klin. Wschr 42, 673-5.

 

[6] Jacquet L Sezary A. (1907) Des formes atypiquees et degeneratives du treponeme pale. Bull Soc Med HSP Paris 4:114-116.

 

[7] Hindle E. (1912) On the life-cycle of Spirochaeta gallinarum. Parasitology 4:463-477.

 

[8] Nordquist WD. The Stealth Killer. BioMed Publishing Group. Lake Tahoe, California 2009.

 

[9] Melville TH, Slack GL. (1960) Bacteriology for Dental Students. William Hienemann Medical Books:170.

 

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Spirochete Spore like Forms Found inside the Cells of the “GUMS” Around Teeth

 

“Spore-like” Forms Found inside the Cells of the “GUMS” Around Teeth: The reason why Periodontal Disease has been almost impossible to cure.

Source material primarily from The Silent Saboteur[1]

By: William D. Nordquist DMD MS

In the last one hundred years since Noguchi, a famous Japanese microbiologist whose picture is on the 1000 yen note, first discovered spirochetes as the cause of syphilis. These peculiar organisms have been studied intensively ever since. Noguchi also found these spirochetes in the brains of patients suffering the long-term consequences of syphilis. Many species of spirochetes in the brain has been shown to cause multiple neurologic problems, such as dementia and Alzheimer’s disease. During World War I it was discovered that a very near cousin of the syphilis spirochete causes Trench Mouth, a severe form of periodontal disease. Spirochetes in their role as major co-bacteria in periodontal disease have been studied for years.

When studying the old literature when microbiology was at its “hay-day” (pre-1920’s), it seems that these astute microbiology scientists understood the fact that spirochetes, unlike most other bacteria, have many forms better then we recognize today. Krutchkoff[2], when presenting the data and literature review from the book, The Silent Saboteur, he coauthored to his fellow professors, Deans of three dental schools, astute colleagues and longtime academic friends found a militant rejection of the basic principle of pleomorphism, “spore-like” forms and cell-wall deficient forms of spirochetes even though, as will be presented here, there are references to these facts that go back almost one hundred years proving that these forms exist. It’s hard to understand why dentistry doesn’t want to expose these facts to the public.

A thorough review of the literature detailing the way spirochetes interacts with their environment and how they are such a major player in chronic disease will be discussed in this article.

 

SPORE-LIKE FORMS

 

Wilcox [3] in a review paper of spirochetes discussed the extent of the pleomorphism of spirochetes and the arguments for and against a life-cycle was summarized as follows:

  1. Early studies with light microscope showed aberrant forms of spirochetes with external granules, buds, round bodies, etc., attached to the spirochete and with granules lying free, have been reported since the organism was first discovered by Schaudinn & Hoffmann (1905)[4], who themselves reported a granular phase.
  2. Other forms were discovered including buds or granules, spore-like spherical bodies-small structures attached either laterally or terminally, or occasionally separated by a stalk or delicate filament but apparently originating from the cell walls[5]
  3. The granules, however, minute and highly refractory, were found in cultures growing under unfavorable conditions when the spirochetes were few in number (Noguchi, 1912a)[6].
  4. Czekalowski[7], in the 1950’s reported with electron microscopy the “spore-like” forms of spirochetes (figure 1). When “free” the large granules are circular and well delineated by a cell membrane, with the central part consisting of spiral fragments embedded in a homogeneous substance. The authors were satisfied that these granules are not artifacts or products of degeneration or disintegration of spirochete, and that their constant and rhythmic appearance points to their playing some role in the life cycle of the spirochete are reproductive bodies of spirochete.
  5. Kersten[8] noticed that Borrelia spirochete (Lyme disease spirochete) can survive in the tissues in spite of seemingly adequate antibiotic therapy. According to experiences from studies with other spirochetes it is suggested that encysted Borrelia, granules, and the remaining blebs might be responsible for the ongoing antigenic stimulus leading to complaints of chronic Lyme spirochetosis.
  6. Nordquist[9], in the early stages of developing his book included the gathering of as many old textbooks on oral bacteriology as possible. Although Nordquist thought he might find some references to this “spore” transmission mode for oral spirochetes in the earlier literature, he found only one that mentioned the presence of oral spirochete “spores” or granules, and this was in a book published in the year 1960. The author stated the following: “External granules may become free from the cell and in old cultures, containing granular forms when examined by dark-field microscopy, have been shown to give rise to typical spirochetes on subculture to fresh mediumthe granules may therefore be a stage in the lifecycle of the organism.” These granules appeared on the surface of the spirochetes just prior to their death. The bacteriologist who reported this finding also observed that these spores developed into multiple replicated spirochetes.
  7. In more recent literature, Wolf[10] working in the Robert Koch-Institut des Bundesgesundheitsamtes reported quasi-multi-cellular-bodies of Treponema denticola, the most common oral spirochete. They analyzed its forms using electron microscopic methods and found it had four forms: normal helical, twisted spirochetes that formed plaits, twisted spirochetes that formed club-like structures, and spherical bodies of different sizes. The researchers theorized that such forms were better able to resist adverse conditions such as antibiotics and toxins (See drawings of the various forms in reference to (Figure 2).
  8. In 1999, De Ciccio[11] of McGill University reported finding various forms of the same oral spirochete, Treponema denticola, in the form of spherical bodies (figure 3). Up until this time in history, it was not known what influenced oral spirochetes to form these bodies. The authors of this report attributed the changes to environmental stress and related their findings to periodontal disease by stating that the “spherical bodies” represented resting forms of these organisms. Their presence corresponds with periods of disease quiescence or non-activity.
  1. In earlier studies, Nordquist[12] examined plaque samples and granulation tissue taken from patients with varying severity of periodontal disease using a microscope both before and after antibiotic treatment. He found an abundance of the classic, active helical form of spirochetes before treatment. When Nordquist treated severe cases of periodontal disease (exhibiting very active spirochetes) with antibiotics, he also routinely performed a microscopic examination during the second week of antibiotic treatment to verify the efficacy of the antibiotic. That is when he first observed granular bodies and/or cyst forms, all of which fit previous descriptions of so-called “spores” referenced in Figures 4.

 

These forms of spirochetes had been unknown to Nordquist for years; however, after finding literature references to these “spore” variations, Nordquist then went back and studied the microscopic videos of patients he had previously treated. As part of his examination procedure, he observed the microscopic appearance of plaque samples on all patients before and after antibiotic treatment and recorded such on DVD discs. Nordquist then found visual evidence of inactive “spore-like” forms in these patients within videos of all post-treatment stages. It was obvious to him that the antibiotic treatment was not effective in actually eliminating the spirochete organisms; it merely forced them into an altered, protective “spore” form. This is the all-too-clear explanation for why dentists, in most instances, cannot routinely treat periodontal disease effectively except for highly compliant patients who will accept aggressive forms of therapy. In essence, the “spore” form persists after antibiotics to give rise to a continuation of disease following treatment.

 

Dr. Theodor Rosebury[13] [14] [15] [16], is a professor at Washington University of Dentistry during the late 1950’s and 60’s and is a world-recognized authority in spirochetal disease. When one reviews history in the light of present-day knowledge, it is now evident that Rosebury had considerable difficulty in explaining puzzling phenomena observed during his classic experiments published during the late 1930s. In these experiments, Rosebury, then at Colombia University, took exudate (pus) or gingival plaque from Vincent’s (Trench Mouth) infection patients and injected this material into the groin of guinea pigs. He then took the infected pus from these lesions of the first series of guinea pigs and infected a second set of guinea pigs. He repeated this procedure for many generations and was successful in infecting as many as 20 subsequent generations of guinea pigs.

 

However, when he isolated each individual bacterium from the initial pus and grew them individually in separate culture media and then later recombined them in the same numbers of bacteria originally found in the pus, he was unable to infect guinea pigs with this artificially produced mixture of the same bacteria. The missing ingredient in this artificial recombined mixture was apparently some other substance contained within the pus but absent in pure cultures. Could it be some unrecognized product of mixed infection that was somehow missing from a combination of pure culture? Could this unrecognized factor be the unknown (at the time), granular bodies and/or “cyst” forms (spores), only later to be described in subsequent research of early syphilis and Lyme disease? The missing ingredient in this artificial recombined mixture was apparently some other substance   contained within the pus but absent in pure cultures. Could it be some unrecognized product of mixed infection that was somehow missing from a combination of pure culture? Could this unrecognized factor be the unknown (at the time), granular bodies and/or “cyst” forms (spores), only later to be described in subsequent research of early syphilis and Lyme disease?

 

When present, spirochetes produce granules, cysts or “spores” which are detected within phase-contrast microscopic preparations. When studying the plaque harvested from the diseased gingival sulcus non-immune epithelial cells are frequently found that are loaded with “spore-like” bodies. It is inevitable to harvest these infected epithelial or “sulcus lining cells” when taking a plaque sample from around the teeth. These infected cells are thought by Nordquist to represent a powerful indicator that shows how relatively advanced the disease process has become. If the epithelial cells are loaded with “spores,” it is a certainty then that the disease process is advanced thus requiring more aggressive treatment to eliminate the infected cells within the gingival sulcus. If this tissue is not removed, the disease will eventually return since the source of the infection, albeit in an inactive form, remains behind as a contaminant that will ultimately lead to recurrence. Microscopically diagnosing the presence of these “spores” is important for determining the proper treatment plan for the periodontal-diseased patient.

 

Dashper[17], reported in his article, Virulence Factors of the Oral Spirochete Treponema denticola, supported Nordquist’s contention detailed above and is an important key to the treatment of periodontal disease. He states; “Invasion of, or internalization by, epithelial cells provides oral bacteria with a nutrient-rich environment that is partially protected from the host immune system. While not immediately contributing to disease, T. denticola may use the intracellular locale to persist safely and possibly replicate (Colombo et al., 2007[18]; Johnson et al., 2008[19]). During treatment of disease, intracellular bacteria are less likely to be physically removed by scaling and root planning and are more resistant to antibiotics. Furthermore, this intracellular population could constitute a reservoir of bacteria for the repopulation of treated subgingival sites in refractory periodontitis (Tribble and Lamont, 2010[20]).”

 

Nordquist routinely finds exfoliated gingival cells in gingival plaque samples loaded with the “spherical forms” of spirochetes (figure 5). Nordquist uses a Deka CO2 laser to help entirely remove the diseased gingival sulcus. It has been observed clinically that these patients have long-term success in their home care with little to no re-population of the gingival sulcus with spirochetes. Understanding the fact that spirochetes populate epithelial cells in the diseased gingival sulcus of periodontal disease patients is a major breakthrough in the understanding and treatment of periodontal disease. Presently, these invaded gingival cells can only be diagnosed with a phase contrast microscope.

 


[1] Nordquist & Krutchkoff DJ. The Silent Saboteur. BioMedi Publishing Group. Lake Tahoe, California 2010.

[2] Krutchkoff DJ. Personal conversation.

[3] Wilcox RR, Guthe T: Treponema pallidum. A bibliographical review of the morphology, culture,

and survival of T. pallidum. Bull WHO J 35:1-169, 1966

[4] Schaudinn, F. & Hoffmann, P. (1905) O0ber Spirochaeta pallida bei Syphilis und die Unterschiede dieser Form gegenuiber anderen Arten dieser Gattung. Ber. Klin. Wschr., 42, 673-5.

 

[5] Coutts, W. E. & Coutts, W. R. (1953) Treponemapallidum buds, granules and cysts as found in human syphilitic chancres and seen in fixed unstained smears observed underdark-ground illumination. Amer. J. Syph.,37,29-36.

[6] Noguchi, H. (1912a) Identification of Spirochaeta pallida in culture. J. Amer. med. Ass., 59, 1236

 

[7] Czekalowski W AND Eaves G. FORMATION OF GRANULAR.STRUCTURES BY LEPTOSPIRAE AS REVEALED

BY THE ELECTRON MICROSCOPE. J Bacteriol. 1954 June; 67(6): 619–627.

[8] KERSTEN, POITSCHEK AC, RAUCH S, AND ABERER E. Effects of Penicillin, Ceftriaxone, and Doxycycline on

Morphology of Borrelia burgdorferi. ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, May 1995, p. 1127–1133.

[9] Nordquist WD. The Stealth Killer. BioMed Publishing Group Lake Tahoe California 2009.

[10]Wolf V, Lange R. Weeks J. Development of quasi-multicellular bodies of Treponema denticola. Arch Microbiol;1993:160:206-213.

[11] De Ciccio A, McLaughlin R, Chan C. Factors affecting the formation of spherical bodies in the spirochete Treponema denticola. Oral Microbiol Immunol 1999:14(6);384-386.

[12] Nordquist W The Stealth Killer. BioMed Publishing Group. Lake Tahoe CA 2009.

 

[13] Rosebury T Foley MA. Experiemntal Vincent’s infection. 1939. JADA:vol26;1797-1811

[14] Rosebury T. Recent development in fusospirochtetal and related infections. 1946 J Perio. Vol 17:121-5.

[15] Rosebury T. The nature and significance in periodontal disease. 1947 Amer J Ortho and oral Sur. 1947:33(9) Sept;B658-65

[16] Rosebury T. Studies of fusospirochetal infection. 1950. J Infectious Dis:vol 87;234-248.

[17] S.G. Dashper SG, Seers CA,Tan KH, Reynolds EC. Virulence Factors of the Oral Spirochete Treponema denticola. JDR June 2011 vol. 90 no. 6 691-70.

[18] Colombo AP, Boches SK, Cotton SL, Goodson JM, Kent R, Haffajee AD, et al. (2009). Comparisons of subgingival microbial profiles of refractory periodontitis, severe periodontitis, and periodontal health using the human oral microbe identification microarray. J Periodontol 80:1421- 1432.

[19] Johnson J, Chen R, Lenton P, Zhang G, Hinrichs J, Rudney J (2008). Persistence of extracrevicular bacterial reservoirs after treatment of aggressive periodontitis. J Periodontol 79:2305-2312.

[20] Tribble GD, Lamont RJ (2010). Bacterial invasion of epithelial cells andspreading in periodontal tissue. Periodontol 2000 52:68-83.

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Gum Disease Tied to Worsening Rheumatoid Arthritis

Gum Disease Tied to Worsening Rheumatoid Arthritis

 

By: RICHARD M. KIRKNER, Internal Medicine News Digital Network

05/25/11

EXPERT ANALYSIS FROM THE ANNUAL EUROPEAN CONGRESS OF RHEUMATOLOGY

Recent laboratory findings from Australia have shown a strong correlation between gum disease and worsening signs and symptoms of rheumatoid arthritis, one of the lead investigators reported May 25.

During his presentation at the annual European Congress of Rheumatology, Mark Bartold, Ph.D., who is a periodontist and the director of the Colgate Dental Research Centre at the University of Adelaide (South Australia), discussed his group’s recently published study of laboratory mice with preexisting periodontitis and worsening RA. “Emerging evidence now suggests a strong relationship between the extent and severity of periodontal disease and rheumatoid arthritis,” Dr. Bartold said in an interview.

The experiments showed that mice with coexisting periodontitis and RA exhibited more severe joint inflammation than did the mice with just RA, he said. Also, mice with both periodontitis and RA were more likely to demonstrate signs of arthritis in their rear paws, compared with mice with arthritis only. The progress of RA in mice with both conditions followed a more rapid course than it did in mice with just RA or just periodontitis, he reported.

Gum disease and RA could be related through common underlying dysfunction of fundamental inflammatory mechanisms. The nature of the dysfunction remains unknown, but recent scientific studies have suggested a link between the two, he said.

Although this relationship is unlikely to be causal, it is clear that individuals with advanced RA are more likely to have significant periodontal problems, compared with their nonrheumatoid counterparts. Likewise, people with severe gingivitis are more likely to have severe RA. Data from earlier studies have shown that individuals with RA had a 3.6-fold greater risk of moderate to severe periodontitis, and those with gum disease had a 2.2-fold greater risk of RA than did the general population.

Other studies have demonstrated that OPG (osteoprotegerin) and RANKL (receptor-activated nuclear factor–kappaB ligand) are highly expressed in both RA synovium and periodontitis lesions. Dr. Bartold noted pilot studies that have confirmed the potential to identify periodontal pathogen DNA in synovial tissues and inflamed human periodontal tissues. “It remains to be established whether treatment of periodontal disease and reduction of periodontal inflammation in patients with chronic rheumatoid arthritis will reduce the disease activity of rheumatoid arthritis,” Dr. Bartold said.

Dr. Bartold’s research suggests that periodontitis and rheumatoid arthritis share a common development pathway within the RANK/RANKL/OPG axis, where a drop in OPG leads to reduced vascular protection. “Increases in RANKL levels within inflamed tissues may result in not only the development of vascular damage, but also activation of osteoclasts and subsequent bone resorption,” he said.

The role of bacteria in arthritis has also garnered considerable attention, noted Dr. Bartold. Animal studies have demonstrated that arthritis can develop in response to different stimuli and through different effector pathways, including exogenous infections or microbial antigens. “If these observations are also applicable to human rheumatoid arthritis, we might expect that different types of infections – as well as other environmental exposures with the capacity to induce excessive proinflammatory cytokines in genetically susceptible individuals – may contribute to disease,” he said.

Among the pathogens that have been implicated in rheumatoid arthritis patients are periodontopathic bacteria including Porphyromonas gingivalis, Prevotella intermedia, Prevotella melaninogenica, Bacteroides forsythus, and Aggregatibacter actinomycetemcomitans. Elevated antibodies to B. forsythus and P. intermedia have also been found in synovial fluid, he added.

The ultimate goal of emerging research is to determine whether the reduction of periodontal inflammation improves the disease activity of RA, he said. The clinical implications of these findings are that early intervention strategies to aid in the overall management of rheumatoid arthritis could include a periodontal assessment.

Dr. Bartold disclosed that he receives research support from the National Health and Medical Research Council of Australia, and acts as a consultant for Colgate and Nobel Biocare.

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The Co-relationship between Depression, Periodontal Disease, and Chronic Inflammatory Diseases

The Co-relationship between Depression, Periodontal Disease, and Chronic Inflammatory Diseases

By William D Nordquist DMD MS

Recently, Hauser[1] Klinikum Saarbrücken, Department of Internal Medicine, Saarbrücken, Germany, reported that anxiety and depression is related to patients with active inflammatory bowel disease (Crohn’s disease and ulcerative colitis). Mikocka-Walus[2] School of Psychology, University of Adelaide, Adelaide, SA, Australia also reports that anxiety/depression and inflammatory bowel disease frequently interact. Parker[3] reports that a strong interdependence between anxiety and depression in a sample of patients with an acute coronary syndrome. Stafford[4] Department of Psychology, University of Melbourne, Victoria, Australia reported that depressive symptoms significantly undermine health-related quality of life in patients with coronary artery disease despite successful medical and surgical management. Egede[5], (Department of Medicine, Medical University of South Carolina, Charleston, South Carolina) states that the odds of depression are higher in individuals with diabetes than in those without diabetes.

Krishnan[6] (Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, North Carolina) discusses the relationship between depression and the rapid increase in the prevalence of a number of medical disorders in the aged, including cancer, heart disease, Parkinson’s disease, Alzheimer’s disease, stroke, and arthritis. This list of chronic inflammatory diseases and their co-existence with depression has become more and more recognized.

Gotsman (Heart Institute, Hadassah-Hebrew University Medical Center, Jerusalem, Israel), reports periodontal destruction measures are significantly correlated with Coronary artery disease severity, whereas periodontal infectious measures are significantly associated with clinical cardiac status. Emrich[7] (Roswell Park Cancer Institute, Buffalo, NY) reported findings that demonstrate diabetes increases the risk of developing destructive periodontal disease about threefold. The proposed relationship between dental and heart disease has been reported in scientific literature[8] [9] [10] [11] [12] [13] [14] [15] [16]

This discussion of the co-relationship of chronic inflammatory diseases, periodontal disease and depression leads to an interesting article that tries to explain this relationship. The purpose of posting this on my Life Guard Your health Blog is to emphasize how all these diseases are interrelated to each other. The Silent Saboteur[17] explains how the source of all the bacteria that is proposed to cause all these diseases in the first place can be prevented with good oral hygiene practices. Also, by eliminating the periodontal infection around the teeth, the source of the chemicals that cause depression discussed below in Phyllida Broun’s article can be reduced and even eliminated.

The source is: New Scientist Date: 16 June 2001

A Mind Under Seige

 

By: Phyllida Brown

Could an overactive immune system be the trigger for some people’s life-threatening depression? If so, we might just be on the way to a cure, says Phyllida Brown

A FIFTY-year-old woman living in Japan is infected with a potentially fatal virus, hepatitis C. Doctors bombard her body with a powerful drug to boost her immune response. The drug beats back the virus, but has horrific side effects. She becomes inexplicably moody, rapidly sinking into a depression so savage that the woman douses herself in oil and sets herself alight.

Fortunately, her suicide attempt fails and she recovers fully. But the woman’s terrifying experience is not unique. Over the past few years, there’s been a steady trickle of bizarre reports of people becoming suicidal after taking alpha interferon and interleukin-2, two popular immune-boosting drugs. Hundreds of others have become seriously depressed.

But here’s the rub. Patients and doctors are not rounding on the makers of these drugs. Instead, everyone tends to think the psychological side effects are a price worth paying for drugs that can combat cancer, hepatitis and other life-threatening infections. Indeed even the terrible suicidal urges themselves are now turning out to have a silver lining. They are awakening interest in one of the most promising new avenues in depression research since Prozac left the labs.

Most of us associate depression with being run down and having poor immunity to infections. The startling side effects of the immune-boosting drugs turn that notion on its head. They suggest that some people who are depressed may actually be suffering from an over-heated immune system, and that damping down inflammation could offer a brand new way to treat routine clinical depression–while making billions for the pharmaceuticals industry into the bargain. It’s a theory that recasts depression–one of the great plagues of our time–as a chronic inflammatory disease like rheumatoid arthritis.

In an inflammatory attack, immune cells rev each other up by pumping out substances known as inflammatory cytokines. Drugs like interferon are simply artificial versions of these substances. That’s why they boost immunity so well–and why, according to the new “immune theory” of depression, they also induce such dark moods in some patients. If the body’s own supplies of cytokines stay too high for too long, maybe they too become toxic to mood and trigger depression.

The case is far from proven but evidence is mounting. “At the beginning I was very reluctant to get into this question because depression is such a can of worms,” says neurobiologist Robert Dantzer of France’s national medical research agency INSERM at the University of Bordeaux 2. “But when we saw the way these drugs affected patients, it made me sure that it was worth it.”

The first inkling of a connection between mood and inflammation came around 1990. Michael Maes, a psychiatrist now at the University of Maastricht in the Netherlands, was investigating claims that depressed people are unusually vulnerable to infections and cancer, a theory that could be explained by a lacklustre immune system. But when Maes looked at immune cells from depressed people such as natural-killer cells, monocytes and macrophages, he found instead that the cells were more active than normal, and spewed out more inflammatory cytokines. “We had expected to find just the opposite,” admits Maes.

The surprise results did fit in with some other vague hints that depression and inflammation are entwined. Depressed people tend to have slightly raised temperatures, which suggests that they are suffering from some chronic inflammation. They are also three times as likely to die of heart disease–often caused by arteriosclerosis, itself an inflammatory condition of the linings of arteries.

Still, Maes’s results languished in obscurity, being contradicted by other studies almost as often as they were confirmed–until, that is, Dantzer decided to take a second look at some old rat studies he had done in the late 1980s.

When you inject rats with parts of bacterial cell walls called lipopolysaccharides, their temperatures rise, their sleep patterns change, they become less sociable and stop eating. And it isn’t the bits of bacteria that trigger this so-called “sickness behaviour”, but the immune response to those bits. An injection of the cytokine interleukin-1 (IL-1), which marauding macrophages produce when they meet bacteria, makes the animals behave in exactly the same way. In other words, the rat studies showed that inflammatory cytokines directly influence behaviour.

“For the first time it became clear,” says Dantzer. “Sickness behaviour is like fear–it is a state that makes the animal reorganise its priorities.” Just as the sight of a predator makes animals release hormones that drive the “flight-or-fight” response, infection triggers the release of cytokines, which make the animal rest and conserve its resources to fight the infection. And of course, sickness behaviour is not exclusive to rats–think of the last time you got flu.

At first, researchers were puzzled at how the cytokines could affect behaviour. How could great big molecules like IL-1 get across the barrier that protects the brain from all the potentially dangerous chemicals sloshing around in the blood?

It turned out they didn’t need to. The exact mechanism is still a mystery, but it seems that another set of far smaller signalling molecules, such as nitric oxide and prostaglandins, tell the brain that a part of the body is inflamed. Once in the inner sanctum, these molecules instruct the brain’s glial cells to make their own supplies of inflammatory cytokines. These cytokines act on receptors in areas of the brain such as the hippocampus, the cerebellum, and–crucially–the hypothalamus, which is involved in regulating both mood and temperature. “The brain builds a representation of the disease in the body,” says Dantzer.

By the mid-1990s, Dantzer was wondering whether sickness behaviour wasn’t in some way comparable with depression, and, if so, whether antidepressants could prevent sickness behaviour. After all, some of the symptoms are similar to depression– disturbed sleep, for instance, or a lack of interest in food or sex.

Dantzer’s results were dramatic. He injected rats repeatedly with the antidepressant tianeptine, before treating them with pieces of bacterial wall or IL-1 (Psychopharmacology, vol 24, p 50). The antidepressant sharply reduced the sickness behaviour created by the treatments. What’s more, the rats’ brains made much smaller amounts of their own IL-1, and much larger amounts of another cytokine, IL-10, which soothes inflammation. “It looks like some antidepressant drugs are working like some anti-inflammatory agents,” concludes Dantzer.

The next piece in the puzzle was to take a closer look at those people who get depressed while taking immune-boosting drugs. From about 1996 onwards, study after study showed that about one-third of patients taking cytokine drugs get depressed, sometimes seriously. The trouble is that they also have life-threatening illnesses such as cancer or hepatitis so it’s hardly surprising they should feel despair.

To get around that problem, Dantzer’s PhD student Lucile Capuron assessed the psychological state of patients with advanced skin or kidney cancers before and during treatment with interleukin-2 (IL-2) or alpha interferon. The results, which appeared last year in the Journal of Clinical Oncology, left Dantzer in no doubt.

Both drugs appeared to induce depression, but there were also some clear differences. The patients on alpha interferon developed symptoms after a few weeks, while people on IL-2 took only a few days. More subtly, the patients taking alpha interferon tended to have slower reaction times, while patients on IL-2 were more likely to have memory problems. To Danzter, such differences are a telling sign that the depression is a specific side effect of the drugs, rather than simply general despair at being ill.

Then, just this spring, Andrew Miller at Emory University in Atlanta announced in The New England Journal of Medicine that a Prozac-like drug called paroxetine actually protects people who take alpha interferon for skin cancer from depression brought on by the immune-boosting drug.

“It’s exciting, because in psychiatry we don’t do a whole lot of prevention,” says Miller. Miller even suspects that antidepressants could help a wider group of hospital patients who may be exposed to sudden surges in their own levels of inflammatory cytokines. For example, he says, inflammatory cytokines soar in people who have major heart surgery as their immune systems respond to their wounds. Up to 30 per cent get depressed soon after the operation. Treating them with antidepressants before surgery could spare them this extra mental suffering, says Miller.

Still, the bigger question remains: does inflammation also play a role in depression that is triggered by more familiar messy circumstances like bereavement, divorce, trauma and persistent stress?

To settle that question, neurobiologists will have to learn more about how inflammatory cytokines interact with mood-altering neurotransmitters and hormones. So far, there are tantalising hints that the cytokines could alter those chemicals enough to help tip vulnerable minds over the edge (see “How can the body’s immune system cause depression?” p 36). But the puzzle is complex and incomplete.

Another question is whether the link with inflammation is evidence of something more disturbing–namely, that clinical depression is really caused by some sort of mysterious infectious agent. To be fair, viruses can cause inflammation, and a few years ago German researchers thought they had found one that might trigger depression–a Borna virus that normally infects the nervous systems of horses and sheep (New Scientist, 27 July, 1996, p 14). But the excitement evaporated as others failed to repeat the German results, and today there is no evidence that you can “catch” depression.

Of course for people with depression, the most pressing issue is better treatments. One option is to try tackling depression with anti-inflammatory drugs. There is no evidence that familiar anti-inflammatories such as ibuprofen would help. But St John’s Wort, which many people take to combat symptoms of depression, is also an anti- inflammatory. And over in Bordeaux, Dantzer says there have been rumours that certain drugs that block inflammatory cytokines significantly lift people’s mood. For example, an antibody called infliximab, designed to ease joint pain in patients with rheumatoid arthritis, is rumoured to induce a feeling of well-being even before the inflammation has begun to subside.

At least one rheumatology expert emphatically endorses that claim. “I have been consistently struck by the comments of patients on an enhanced sense of well-being ever since we treated the first patients,” says Ravinder Maini, at the Kennedy Institute of Rheumatology in London. Anecdotes aside, at least one rheumatoid arthritis trial found patients scored higher on “vitality” and “social functioning” after taking this type of drug (The New England Journal of Medicine, vol 343, p 1594).

Drugs companies are understandably keen to find out whether these “anti-cytokine” drugs can help depressed patients too. One in five of us will get depressed at some point in our lives and, since older people are more vulnerable, the figures are destined to climb as populations age. Yet existing antidepressants are far from perfect and don’t work for everyone.

Even if anti-cytokines could help only some of the millions who get depressed every year, that would still be a dramatic health gain and a multibillion-dollar money spinner for the pharmaceuticals industry. And although researchers are keeping quiet about the details, at least two groups are gearing up to start trials within the year. “This will be the proof of the pudding,” says Miller. “The need for these trials is tremendous.”

A lot of people’s health–and a lot of dollars for the drugs companies–are resting on these results.


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[2] Mikocka-Walus AA, Turnbull DA, Moulding NT, Wilson IG, Andrews JM, Holtmann GJ. Controversies surrounding the comorbidity of depression and anxiety in inflammatory bowel disease patients: a literature review. Inflamm Bowel Dis. 2007 Feb;13(2):225-34.

[3] Parker G, Heruc G, Hilton T, Olley A, Brotchie H, Hadzi-Pavlovic D, Owen C, Friend C, Walsh WF. Explicating links between acute coronary syndrome and depression: study design and methods. Aust N Z J Psychiatry. 2006 Mar;40(3):245-52.

[4] Stafford L, Berk M, Reddy P, Jackson HJ. Comorbid depression and health-related quality of life in patients with coronary artery disease. J Psychosom Res. 2007 Apr;62(4):401-10.

[5]Egede L, Deyi ZhengD, Simpson K. Comorbid Depression is Associated With Increased Health Care Use and Expenditures in Individuals With Diabetes Diabetes Care March 2002 vol. 25 no. 3 464-470.

[6] Krishnan KR, Delong M, Kraemer H, Carney R, Spiegel D, Gordon C, et al. Comorbidity of depression with other medical diseases in the elderly. Biol Psychiatry. 2002 Sep 15;52(6):559-88.

[7] Emrich LJ, Shlossman M, Genco RJ. Periodontal disease in non-insulin-dependent diabetes mellitus. J Periodontol. 1991 Feb;62(2):123-31.

[8] Scannapieco FA Position paper of the American Academy of Periodontology: periodontal disease as a potential risk factor for systemic diseases. J Periodol 1998;69(7):841-50.

[9] Beck JD et al. Periodontitis: a risk factor for coronary heart disease? Ann Periodontol. 1998;3(1):127-41

[10] Jodhpur K et al. Strength of evidence linking oral conditions and systemic diseases.  Commend Cetin Educe Dent Supply. 2000;( 30):12-23.

[11] Jodhpur KJ et al. Possible explanations for the tooth loss and cardiovascular disease relationship. Ann Periodontol. 1998;3(1):175-83.

[12] DeStefano F et al. Dental disease and risk of Coronary heart disease and mortality. BMJ 1993;306:688-992.

[13] Loesche WJ. Et al. Periodontal disease as a risk factor for heart disease. 1994 Compend Contin Educ Dent;25(8):976-992

[14] Loesche WJ et al. Periodontal disease: link to cardiovascular disease. 2000;21(6):463-6, 468, 470 passim.

[15] Behle JH, Papapanou PN. Periodontal infections and atherosclerotic vascular disease: an update. 2006;56(4 Suppl 1):256-62.

[16] Geerts SO, et al. Further evidence of the association between periodontal conditions and coronary artery disease. J Periodol;75(9):1274-80.

[17] Nordquist WD & Krutchkoff DJ. The Silent Saboteur. BioMed Publishing Group. 2010.

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Periodontal Disease and Muliple Sclerosis?

Could Multiple Sclerosis (MS) have its Origin from Periodontal Disease?

By: William D. Nordquist DMD MS

Multiple Sclerosis is a very serious disease attacking the nervous system, and many theories have been proposed to divulge the origin of the disease. The causative agent responsible for the development of Multiple Sclerosis has not yet been revealed, but Multiple Sclerosis has been suggested to be activated by various viral infections, e.g. human herpes virus, rubella, measles, and by Chlamydia pneumoniae[1] [2] [3]. Autoimmune disorders have also been proposed as the cause of the disease[4], but no definite corroboration is specified.  From 1909 until the 1950s many researchers considered Multiple Sclerosis to have a spirochetal origin because of its similarity to other spirochetal diseases[5] . Steiner [6] observed Spirochaeta myelophthora in brain lesions from autopsied Multiple Sclerosis patients in the 1950s. When Adams et al. [7] inoculated rhesus monkeys with material from cases of disseminated sclerosis, spirochetes were observed in the ventricular fluid after some months. Multiple Sclerosis has also been proposed to be caused by an oral spirochete[8] [9].

Spirochetes in general are known to produce large cyst-like bodies which have been documented numerous times with electron micrographs[10] [11]. These are the same bodies identified by Nordquist and related to oral spirochetes[12]. Brorson[13] reported a significant association of cerebral spinal fluid (CSF) cysts and Multiple Sclerosis was identified in this small study among residents in a coastal area of southern Norway. The cysts could be of spirochetal origin. Since spirochetes have multiple forms, it is imperative that these forms be understood and identified when examining microscopically in the dental plaque of patients with chronic inflammatory diseases, especially now with the mounting evidence that this MS could have its origin in mouths of periodontal disease patients.


[1] Reiber H. Ungefehr S. Jacobi C: The intrathecal, polyspeciflc and oligoclonal immune response in multiple sclerosis. Mult Scler 1998; 4: 111-117.

[2] Sriram 5. Stratton CW. Yao 5Y, Tharp A, Ding l, Bannan JD, Michell WM: Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis. Ann Neurol 1999; 46: 6-14.

[3] Challoner PB, Smith KT; Parker JD, MacLeod DL. Coulter SN, Rose TM, Schultz ER: Plaque associated expression of human herpesvirus 6 in multiple sclerosis. Proc Natl Acad Sci 1995; 92: 7440-7444

[4] Weiner HL.: A 21 point unifying hypothesis on the etiology and treatment of multiple sclerosis. Can J Neuro15ci 1998; 25: 93-101.

[5] Marshall v: Multiple sclerosis is a chronic central nervous system infection by a spirochetal agent. Med Hypoth 1988; 25: 89-92.

[6] Steiner G: Morphology of Spirochaeta myelophthora in M5. J Neuropathol Exp NeuroI19S4; 13: 221-229.

[7] Adams DK. Blacklock W5. M’Ouskie JAW: 5piroch~tes in ventricular fluid of monkeys inoculated from cases of disseminated sclerosis. J Path Bacteriol1925; 28:7-118.

[8] Gay D, Dick G, Upton G: Multiple scleroSis associated with sinusitis: case-controlled study in general practice. Lancet 1986; 12: 815-819.

[9] Matyszak MK: Inflammation in the balance between immunological privilege  and immune responses. Prog Neurobiol 1998;  56: 19-35.

[10] Mattman L. Cell Wall Deficient Forms. CRC Press Boca Raton,2001:241.

[11] CZEKALOWSKI J AND EAVES G. FORMATION OF GRANULAR.STRUCTURES BY LEPTOSPIRAE AS REVEALED

BY THE ELECTRON MICROSCOPE. J Bacteriol. 1954 June; 67(6): 619–627.

[12] Nordquist W. The Stealth Killer. BioMed Publishing Group. 2009:68-78..

[13] Brorson O, Brorson SH, Henriksen TH, Skogen PR, Schoyen R. Association between multiple sclerosis and cystic structures in cerebrospinal fluid. Infection 2001 Dec;29(6):315-9.

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Crohn’s Disease: Is it related to Periodontal Disease?

Crohn’s Disease: Is it related to Periodontal Disease?

By William D Nordquist DMD MS

Inflammatory bowel diseases have become a significant public health problem because of the increase in the incidence of inflammatory bowel diseases, particularly Crohn’s disease, in the U.S. population[1]. Ulcerative colitis and Crohn’s disease are chronic intestinal disorders of unknown cause. Crohn’s disease is characterized by tissue wall penetration and infiltration by inflammation of immune cells; i.e., lymphocytes, macrophages, and plasma cells. In 70% of the cases, granulomas (a roughly spherical mass of immune cells that forms when the immune system attempts to wall off substances; especially infectious microbes) are found. Despite the intense interest in transmissible agents, abnormal changes in cell lines, and the role of cell-wall deficient pseudomonads (L forms of amoebas) investigated at the time Van dyke[2] (1986) reported his findings there was still no evidence for an infective etiology for Inflammatory bowel diseases.

Van dyke when on to report in his study a total of 20 patients with inflammatory bowel disease (Crohn’s disease, ulcerative colitis) were evaluated with regard to the role of infectious agents and host response. Patients were selected based upon oral manifestations of their disease, 10 with periodontal disease and 10 without. Microbiologic studies of the periodontal flora of inflammatory bowel disease-affected patients revealed a unique microflora composed predominantly of small, motile, gram-negative rods, which were most consistent with the genus Wolinella. Further studies of the host response of these patients revealed a serum-mediated defect in neutrophil chemotaxis (movement of immune cells toward infectious bacteria) in all 10 patients with periodontal disease. Neutrophil phagocytosis (ability of immune cells to “eat” invading bacteria) was normal. Test tube studies of neutrophil immune cell function in response to Wolinella extracts and culture concentrates revealed inhibition of neutrophil chemotaxis in a dose-response fashion. The organism was “eaten” by neutrophils but not attached to them close enough to be “eaten”. In other words, the immune system was suppressed by the bacteria. The data suggest that unusual microorganisms colonizing the oral cavity of Crohn’s disease patients potentially play a role in the pathogenesis of the disease as infectious agents or modifiers of the host response or both.

Areas affected far away from the intestinal tract include manifestations of mouth ulcers, severe periodontal disease, and involvement of heart and lungs, skin, joints, liver, and urine tracts[3] [4] [5] [6] [7] [8]. More recent studies have shown the Vitamin D dysfunction and elevated 1,25-D levels in Crohn’s disease patients indicates cell-wall deficient bacteria within macrophages may play a role in the immune suppression aspect of the disease process[9]. If this is the case, then Crohn’s disease has a bacterial cause and could very well be instigated by bacteria that come from the mouth. Nordquist and Krutchkoff further discuss the Vitamin D dysfunction and its cause related to bacteria that get into the body through bleeding diseased “gums” resulting from periodontal disease[10]. If you have Crohn’s disease, it wouldn’t hurt to get your “gums” checked for periodontal disease.

 


[1] Sleisenger, M. H. 1981. Pathophysiology of the gastrointestinal tract, p. 1506-1689. In L. H. Smith and S. 0. Thie (ed.), Pathophysiology: the biologic principles of disease. The W. B. Saunders Co., Philadelphia.

[2] Van Dyde T, Dowell V, Offendbacker S, Snyder W and Hersh T. Potential Role of Microorganisms Isolated from Periodontal Lesions in the Pathogenesis of Inflammatory Bowel Disease. Infection and immunity. Sept 1986: 671-677.

[3] Bartlett, J. G., and S. M. Finegold. 1972. Anaerobic pleuropulmonary infections. Medicine (Baltimore) 51:413-450.

[4] Bartlett, J. G., S. L. Gorbach, F. P. Tally, and S. M. Finegold. 1974. Bacteriology and treatment of primary lung abscess. Am. Rev. Respir. Dis. 109:510-518.

[5] Frederick, J., and A. I. Braude. 1974. Anaerobic infection of the paranasal sinuses. N. Engi. J. Med. 209:135-137.

[6] Hodgson, H. J. E., B. J. Potter, and D. P. Jewell. 1977. Immune complexes in ulcerative colitis and Crohn’s disease. Clin. Exp. Immunol. 29:187-196.

[7] Nastro, L. J., and S. M. Finegold. 1973. Endocarditis due to anaerobic gram-negative bacilli. Am. J. Med. 54:482-496.

[8] Nielsen, H., V. Binder, H. Daughtarty, and S. E. Svehag. 1978. Circulating immune complexes in ulcerative colitis. I. Correlation to disease activity. Clin. Exp. Immunol. 31:72-80.

[9] Waterhouse JC Marshall TG Fender B et al. High levels of active 1,25-Dihydroxyvitamin D despite low levels of 25-Hydroxyvitamin D Precursor-Implications of dysregulated vitamin D for diagnosis and treatment of chronic disease. In: Vitamin D New Research, Stolt, 2006 Nova Science Publications, Inc.

[10] Nordquist W & Krutchkoff D. The Silent Saboteur. 2010. Bio-Med Publishing Group.

* spelled without hyphen for search engine that doesn’t recognize them

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Dr John Lin and Dr. Bill Nordquist are treating oral spirochetes with a NdYag laser

Dr John Lin and Dr. Bill Nordquist are treating oral spirochetes with a NdYag laser. they came up with some unusual results.

By William D Nordquist

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