Focal Infection Theory and Buteyko Breathing Practice
Content of this web page
1. Western medical
1.1 Historical roots of the focal infections theory
1.2 Modern focal infections research
1.3 Cavities as a common focal infection
1.4 Effects of dead tonsils on health
1.5 Athlete's feet as a focal infection
1.6 Helminthes or large parasites living in humans
1.7 Non-surgical (or traditional) treatment of root canals
2. Buteyko focal infections and clinical experience
2.1 How dead tonsils prevent high CPs
2.2 How cavities in teeth block the CP growth
2.3 Effects of breathing training on feet mycosis (athlete's feet)
2.4 Intestinal parasites prevent CP increase
2.5 Effects of root canals on health and CP
3. Practical actions in relation to focal infections
3.2 Cavities in teeth
3.3 Feet mycosis
3.4 Intestinal parasites
3.5 Root canals
4. Mercury amalgams
5. Visiting a chiropractor
Dr. Frank Billings (MD) was the most visible Western proponent of the theory of focal infections. He was quite an unusual President of the AMA (American Medical Association) by stating, I place NO confidence in drugs. Drugs are valueless as cures. Dr. Billings suggested in 1898 that microorganisms could contribute to numerous systemic diseases. Among his more recent publications was the article "Systemic Diseases of Focal Origin." Forchheimer'i Therapeusis, 1914, V, 169. 10.
His theory was at first very popular among medical professionals, causing widespread surgeries of tonsils (even after the slightest provocation) and extraction of dead teeth. Such an over-zealous practice naturally resulted in reasonable criticism from other doctors. As a result, later his theory was largely forgotten. (For a historical review of his theory one can consult the recent paper, Germs, Dr. Billings, and the theory of focal infection by R.V. Gibbons published in 1998 in Clinical Infectious Diseases).
However, recent works and studies confirmed the connection between certain local pathological processes (especially in teeth and tonsils) and various systemic diseases. In particular, there is impressive modern research collected by Japanese (Mizutani et al, 1997; Hattori, 1998; Okuda & Ebihara, 1998; Kataura, 2002), Norwegian (Debelian et al,1994; Li et al, 2000), American (Meyer & Fives-Taylor, 1998; Lockhart & Durack, 1999; Joshipura et al, 2000), and other medical professionals (e.g., Meurman, 1997; Gendron et al, 2000) in relation to oral focal infections.
The connection between the focal infections and various health problems is now a fact that is proven by detailed biochemical investigations, which show the mechanism of pathological interactions. For example, Japanese researchers summarized, It is known that primary lesions of these chronic [oral] bacterial infections secondarily cause nephritis, rheumatoid arthritis, and dermatitis. Further, it has been demonstrated in recent years that bacteria inhabiting the oral cavity can cause bacterial pneumonia and endocarditis and that the periodontal-disease-associated bacteria become causative agents for pregnancy troubles and are involved in blood circulation problem and coronary heart disease (Okuda & Ebihara, 1998). That is the reason why, for example, in Japan certain blood tests and troubles with skin, heart, blood vessels, kidneys and pregnancies can be the indications for tonsillectomy and other steps of oral sanitation.
Serious health complications are expected in cases of periodontal
problems as American authors of the article Periodontal disease and its
association with systemic disease revealed:
Currently, there is increasing evidence that the relationship between these entities may be bidirectional. Recent case-control and cross-sectional studies indicate that periodontitis may confer a 7-fold increase in risk for preterm low birth weight infants and a 2-fold increase in risk for cardiovascular disease. These early reports indicate the potential association between systemic and oral health. Additionally, these studies support the central hypothesis that periodontal disease involves both a local and a systemic host inflammatory response. This knowledge of disease interrelationships may prove vital in intervention strategies to reduce patient risks and prevent systemic disease outcomes (Fowler et al , 2001).
A recent review by Dr. Shay from the University of Michigan School of Dentistry suggested that Dental caries occurs when acidic metabolites of oral streptococci dissolve enamel and dentin. Dissolution progresses to cavitation and, if untreated, to bacterial invasion of dental pulp, whereby oral bacteria access the bloodstream. Oral organisms have been linked to infections of the endocardium, meninges, mediastinum, vertebrae, hepatobiliary system, and prosthetic joints. Periodontitis is a pathogen-specific, lytic inflammatory reaction to dental plaque that degrades the tooth attachment. Periodontal disease is more severe and less readily controlled in people with diabetes; impaired glycemic control may exacerbate host response. Aspiration of oropharyngeal (including periodontal) pathogens is the dominant cause of nursing home-acquired pneumonia; factors reflecting poor oral health strongly correlate with increased risk of developing aspiration pneumonia. Bloodborne periodontopathic organisms may play a role in atherosclerosis. Daily oral hygiene practice and receipt of regular dental care are cost-effective means for minimizing morbidity of oral infections and their nonoral sequelae (Shay, 2002).
Is there any Western data supporting the increased sensitivity of the immune system, for example, in case of caries or cavities, when the organism is healthier? That was the subject of part 3 of the review paper Dental caries: a dent on dogma written by Dr. John Gabrovsek (Gabrovsek, 1997). The subtitle of part 3 is Stronger host response to dental caries infection. Result: More dental caries development! There he starts with, Is this an outrageous statement? Just think what a little pollen can do to you? If you are allergic to the pollen your body defenses can kill you. The fact that the host defense response may harm the host itself is recognized in pathology for quite some time. This fact is certainly not taken into account, or recognized in dental caries research (Gabrovsek, 1997).
Is there a known biochemical mechanism that causes such an adverse reaction? As Dr. Gabrovsek explains, For those who are not familiar with what inflammatory cells can do, I quote a short paragraph from Baer and Benjamin: These cells are attracted to the site by the presence of bacteria and bacterial by-products, and conjugates of antigen-complement- antibody may not only act beneficially by phagocytizing these elements, with subsequent intracellular digestion, but may also liberate their cellular compliments of acid hydrolases, as lysosomal membrane dissolved. These enzymes are multiphasic in their effects, and serve to invoke collagen resorption, matrix dissolution, vascular dilation, and permeability - the destructive facet of the inflammatory state. The inflammatory cells with the greatest propensity for tissue destruction are neutrophil, and monocyte (p.21, Baer & Benjamin, 1974).
The most successful practical Western methods for the treatment of, for example, cancer are also based on due attention to focal infections. Dr. Josef Issels, in his famous book "Cancer: a second opinion", wrote, "The emphasis I place on removal of devitalized teeth and chronically-diseased tonsils is one of the better-known aspects of my work, but also one of the most criticized and misunderstood. I do not, for instance, recommend that healthy tonsils and teeth be removed from a healthy person. But I believe if they are diseased, they cause the body's natural resistance to be lowered, thus acting as an important contributory factor to tumor development. In these cases, I insist on their removal" (p. 117, Issels, 1975).
Interestingly, his chart with the title "Hypothesis of pathogenesis of cancer" lists the following causal (or primary) factors for cancer development: foci, teeth, tonsils, fields of natural disturbance, abnormal intestinal flora, faulty diet, chemical factors, physical factors, and psychic factors (p. 53, Issels, 1975).
The influence of tonsils on psoriasis was investigated by Japanese dermatologists who found, using a tonsillar provocation test, certain negative biochemical changes in the blood contributing to psoriasis (Mizutani et al, 1997).
Moreover, fever and other complications can be successfully treated by
tonsillectomy (of course, if tonsils are dead), as another group of Japanese
Thirty patients (above 18 years) who had complained of low grade fever were diagnosed as having tonsillar focal infection. We performed tonsillectomies on all the patients. A total of 24 were cured and 6 patients improved after the operation. These results indicate that tonsillectomy is often an effective treatment for tonsillar focal infection. However, the provocation test did not always give a good result (Takeuchi et al, 1996). Thus, all 30 patients in this study benefited from the operation.
About 15% of the population have fungal infections of the feet (tinea
pedis or athlete's foot) (Bell-Syer et al, 2002), as US researchers report.
These infections also seriously affect the immune system.
Patients with mycoses of the soles with involvement of the nail plates, as well as those suffering from eczemas combined with mycoses developed a most marked reduction of the activity of the leukocyte migration inhibition factor (LMIF) and of the T lymphocyte mediator activity in the presence of the fungal antigen. The studies have detected the pattern of the leukocyte phagocytic reaction disturbances in the patients with mycoses and eczemas of the soles (abstract, Iutskovskii, 1989).
According to Dr. P. J. Brindley and his colleagues from the Department of Microbiology, Immunology, and Tropical Medicine (George Washington University Medical Center, Washington, D. C., USA), "More than two billion people (one-third of humanity) are infected with parasitic roundworms or flatworms, collectively known as helminthic parasites. These infections cause diseases that are responsible for enormous levels of morbidity and mortality, delays in the physical development of children, loss of productivity among the workforce, and maintenance of poverty" (Brindley et al, 2009).
Among the most common helminth species that affect humans are roundworms, tapeworms, pinworms, trichina spiralis, and flukes. Generally, only mature worms produce symptoms and these symptoms depend on the type of the parasite and personal parameters.
Since the official mainstream medicine does not know the cause and methods of treatment of chronic diseases, there are no published studies that explain interactions between large parasites and chronic diseases.
It is obvious that mainstream dentists, endodontists (dentists specializing in diseases of the dental pulp and nerve), and periodontists (dentists specializing in diseases of the gums and other structure surrounding the teeth) do not routinely deal with people who recover from chronic diseases and improve their health using breathing techniques. They simply do not have any clinical experience in relation to the dynamic and interactions between endodontic infections and host defense response during breathing retraining. Therefore, while the information presented in their research is probably accurate, it cannot be applied directly for breathing retraining since most of their conclusions relate to the nearly static situations common for ordinary sick and relatively healthy people.
What are the findings?
1. All root canals contain anaerobic bacteria regardless of the methods and techniques used by dental professionals these days (Weiger et al, 1995; Debelian et al, 1998; Peters et al, 2002). Anaerobes, which produce most powerful toxins, as in the case of cavities, usually represent more than half of the different types of bacteria found in extracted root canals or root canals removed from human cadavers. It was also found that bacteria from the sinus cavities are usually identical to those found in root canals.
2. While the main concerns of holistically-oriented people relate to toxins and inflammation produced by these anaerobes and other pathogens, the main danger of the root canal conventional operation is due to the apical part of the treated tooth. Up to 50-90% of root canals develop periodontitis (inflammation) in the apical part of root canals according to (Wu et al, 2006). The 2-part review study "Outcome of primary root canal treatment: systematic review of the literature" (Ng et al, 2008-2008) has found that the average short-term success rate of modern root canals treatments ranges between 68% and 85%. The same review discovered 4 factors that can improve the success rate: pre-operative absence of periapical radiolucency, root filling with no voids (this is often impossible due to the complex shape of many root canals), root filling extending to 2 mm within the radiographic apex and satisfactory coronal restoration.
3. The most common cause of the failure of the root canal treatment operation is the incomplete blockage of the entire root canal system (Chevigny et al, 2008).
It is only through considering the breathing retraining process that the full picture of the relationship between the focal infection and chronic disease can be provided. Dr. Buteyko and his colleagues clinically observed, tested and developed their theory of focal infections. They suggested that the ideal situation for the clinical remission from chronic disease is to have holistically oriented dentists and otolaryngologists who are familiar with breathing training, know about the effects of focal infections on the health of Buteyko students, and treat the focal infections with the goal of breathing normalization. Let us consider some of these effects.
The presence of focal infections interferes with the ability of patients to increase their CPs, normalize breathing, or even to recover from relapses of the main disease (if present). The focal infections cannot be eliminated using the Buteyko breathing exercises and lifestyle changes. Moreover, due to the "rebound effect", the health of patients who have focal infections may get even worse when the breathing exercises are practiced and higher CPs are temporarily achieved.
The effect of dead or degenerated tonsils on one's health and CP is easy to understand using a practical example. Imagine an asthmatic, who starts with about a 10 second CP and raises it up to 20-25 s. His asthma is then under control (no attacks at all) when his CP gets up to 20-23 s, but if this patient has, for example, dead tonsils, further progress (beyond 25 s CP) would cause a high-grade fever and throat pain with coughing, angina, and copious mucosal discharges, all due to the severe reaction of the immune system which tries to fight the bacteria and toxins generated in the dead tonsils.
The problem is that the degenerated tonsils have no normal blood supply and the immune cells in the blood cannot reach the pathogens hiding in his tonsils. As a result, the immune system creates inflammation in the surrounding tissues and the pathogens use this inflamed area to their advance as a new breeding ground. That leads to fever and infection with heavier breathing and sudden CP drop down to about 10-15 s. As a result, this student may again get his asthma attacks due to the fact that the focal infection in the dead tonsils became worse due to the higher CP achieved (25-30 s) and this made the CP drop back down due to the rebound effect caused by his dead tonsils. This vicious circle (Breath work and better health → Higher CP → Tonsillar infection and fever → Low CP and recovery from the infection → Breath work and better health → Higher CP → Tonsillar infection and fever → Low CP ) can go on forever due to the rebound effect, even with application of other therapies (medication and antibiotics, throat gargling with best natural remedies, and many others), if these techniques do not kill the pathogens in the tonsils.
These adverse reactions cause the students with focal infections to lose their enthusiasm for practicing the Buteyko method, as Russian MDs reported, and resulted in their quitting therapy (e.g., Souliagin, 1991). Indeed, why should one continue to do something that causes strong adverse effects?
As another example, imagine that a student has cavities in her teeth. This person can improve her breathing, and thus recover from a chronic health condition. When her CP rises up to about 30-40 s, her immune system can turn its attention to cavity-causing pathogens, but cannot defeat them since these pathogens reside on the surface of the teeth with no blood access. More breath work leads to an even stronger immune response, but this enemy (cavities) is beyond the immune abilities. Therefore, no further progress is possible although here there is no noticeable rebound effect if the student maintains good or normal dental hygiene. (Poor hygiene with higher CP will favor the advance of cavities in other teeth.)
If a student has low CP (e.g., below 20 s), his athlete's feet infection usually remains dormant. While there could be an affected area between the smallest fingers/toes and light skin peeling, there is no redness, bleeding or feeling hot. This status quo can be present for years. However, when his CP rises up to 25-40 s, mycosis of the feet advances to neighboring areas causing intense skin peeling, redness, deep lesions, bleeding and a sensation of heat in the foot. The higher the CP achieved, the worse the spread of this fungal infection due to the same rebound effect.
The toxins produced by mature intestinal parasites intensify breathing regardless of the CP (immature parasites do not affect breathing to the same extent). Their negative effects depend mostly on their types and load, as well as their feeding cycles and food availability. Generally, depending on these factors, the presence of intestinal parasites restricts the CP to the range between 20 and 40 s CP.
This is the most unpredictable focal infection. It can be deadly for some patients or hardly noticeable at medium CP levels depending on the quality of periodontal work done. Properly done root canal treatment, with the right disinfection and correct sealing procedures, would probably not cause any big problems for a person with a moderate CP (about 25-30 s). In this case, the immune system is strong enough to prevent the interaction of bacteria from dead teeth with other organs, while the toxins can be safely eliminated by the immune system of the organism.
If one's tonsils have been infected for several years, it is impossible to restore their functional abilities. In this case, tonsillectomy is necessary for breathing normalization and going beyond 25-30 s CP. Children who have had infected tonsils for only 1-2 years can sometimes restore their tonsils using special conservative and prophylactic measures.
Regular visits to dentist are important for general health. However, sometimes caries can develop in the tiny cracks of treated teeth (between the filling and tooth) so that they are invisible even during dental examination, but still a very small amount of toxins are able to leak out. When the Buteyko student gets a daily CP of over 40-50 CPs, while following the Level 3 course, he may notice that something prevents his further CP progress, while the morning CP remains below 40 s.
Gargling the mouth with a strong antiseptic solution for several minutes 3-4 times per day can suppress the pathogens and that can allow him to temporary achieve much higher CP numbers (e.g., 10 s more with the application of this method) and maybe even temporary break through 40 s. If the use of this method does not yield any CP improvements, there are no cavities present.
The application of over-counter creams and the disinfection of all shoes and socks are necessary to deal with this fungus causing athlete's feet. There are new creams available on the market that have a double action. The cream is to be applied exactly as instructed: usually twice per day using a very thin layer, but for the whole affected area. The therapy should continue for some 5-7 days after all signs of the infections have disappeared. Natural remedies (including essential oils, garlic, hydrogen peroxide, alcohol, urine, and many others) have notoriously poor success rate against athlete's feet.
When the parasitic load is high, the student can easily notice that while she eats more food, she does not gain weight, but may possibly even lose it. If this is the case, a family physician can take fecal samples (2-3 times may be required since many worms have cycles of laying eggs). Then either the standard medication or some natural remedies (papaya diet and/or water fasting and certain herbs) can be used. It is much more difficult to identify the presence of intestinal parasites, when there are only a few worms, which are not large in size. Paying attention to symptoms is useful in such cases: for example, activities of hook worms usually cause anal itching (since these worms lay their eggs at night near the anus), roundworms cause cold feet even at high CPs, etc.
There are people who achieved up to 2-3 min CPs. However, any student with a serious chronic health problem (cancer, COPD, ephysema, diabetes, arthritis, combinations of 2 or more chronic conditions, and some other cases) should not have root canals present.
The root canal not only generates toxins due to anaerobes and other pathogens living inside about 20 km tiny tubules (former blood vessels of the live teeth), but in addition there is a film formed around the dead tooth and, when the CP is below 20 s, even temporarily, the tissues of the dead-end artery leading to this tooth and the vein leaving the same tooth often become the source of infection and toxicity. Indeed, when the artery leading to the healthy live tooth is cut, the stagnated blood cannot offer resistance to pathogens at low CPs. Furthermore, these dead blood vessels, since they become available to pathogens often cause the appearance of cardiovascular problems due to activities of the same pathogens in other parts of the human body causing the spread of this systemic disease. These processes and blood bacteremia are very active when the CP drops below 10 s (e.g., during early morning hours), since the immune system does not offer its resistance to bacteria, viruses and fungi in the blood for the last 2 stages of the disease (see the Buteyko Table of Health Zones for other parameters of the last 2 terminal stages). Even when the CP is between 10 and 20 s, the immune processes are severely suppressed by hyperventilation and cell hypoxia.
If the CP remains low (less than 20 s) for weeks after the root canal operation, these dysfunctional tissues putrefy and become the source of spreading infection and inflammation that, at a certain stage, is even visible on X-Rays (see the picture at the top of this web page).
The presence of long-standing health problems often results in the situation when bacteria from the teeth start to interact with the pathogens existing in other diseased organs (that can probably happen due to their mutations since a long time is available for these enemies to unite against the immune system). As a result, the treatment of other health problems becomes impossible (the teeth bacteria, which are inaccessible, provide a support for other pathogens) unless the dead teeth are extracted. Therefore, in cases of poor health, long-standing serious health problems or the weakened immune system, it is advisable to extract the dead teeth as soon as possible even without cardiovascular-problem manifestations.
Several published studies found a link between root canals and an increased incidence of the heart diseases (Mattila, 1993; Mattila et al, 2000; Dorn et al, 2002; Willershausen et al, 2009). In my view, the existence or appearance of any cardiovascular problem is the definite indication of the necessity of removing one's root canals. Only then progress with breathing training and higher CP is more certain.
References: Root canals and cardiovascular disease
Conclusions. The student may do the best breathing exercises, follow the best dietary suggestions and the optimum plan for physical activity, but if he or she has any of these focal problems, he/she will be forever stuck at the level of about 25-40 s CP or even less.
If somebody cannot eliminate any of these focal infections (e.g., an old person with severe periodontal disease does not want all his teeth to be extracted), it is not advisable and is even dangerous to increase the CP beyond 30-40 s (Souliagin, 1991).
This is not the classical Buteyko focal infection, but the biochemical and physiological effects of silver amalgam fillings, which are more than 50% mercury and which are often associated with chronic fatigue syndrome, digestive problems, and nerve diseases, are similar, in many ways, to cavities and root canals. There were separate cases when some Buteyko students, with no serious chronic health problems, were able to achieve very high CPs (up to 1-2 min) even with mercury amalgams present. However, with the presence of chronic diseases, mercury amalgams can become and often do become the main factor that prevents personal recovery.
When mercury amalgams are present, consider using Selenium-antioxidant supplementation (about 200 mcg per day). Selenium forms an insoluble and absolutely harmless salt with mercury SeHg even in blood plasma (e.g., Yoneda & Suzuki, 1997; Cherdwongcharoensuk et al, 2010). Furthermore, if one chews the Se tablet and keep it in the mouth for some 2-3 minutes, the selenium should even react with the mercury present on the surface of the amalgam and form the same salt SeHg as a ceramic coating that prevents mercury leaking. Mercury leaking takes place 24/7 at a rate of about 1-10 mcg/day (depending on the total area of the mercury amalgams) and especially during chewing or having chemically active substances in the mouth (e.g., acids). Adding seaweeds to one's diet will also help to chelate Hg from the body, since seaweeds, especially when they are eaten in a raw form, are the best natural absorbents of heavy and radioactive metals.
When the disks of the spine are not correctly aligned, various pains can appear, including chest pain, angina pain, stomach pain, appendix pain, etc. However all these organs may be healthy, and in such cases the student and his doctors cannot find the cause of pain since all tests would be negative. If the spine is poorly aligned, only manual correction can help. Moreover, pathological processes in the spine due to displacement of its disks can lead to inflammation, infections, bone overgrowth, intensive wear, and other negative effects. For these reasons Doctor Buteyko and his wife, Ludmila Buteyko learned professional chiropractic techniques to help their patients. If a student suspects that the spine requires manual adjustment, a visit to a good chiropractor would be as important, in relation to his or her health normalization and CP growth, as fixing dental cavities or removing intestinal worms.
Reference pages: Breathing norms and the DIY body oxygen test:
- Breathing norms: Parameters, graph, and description of the normal breathing pattern
- Body-oxygen test (CP test) : How to measure your own breathing and body oxygenation (two in one) using a simple DIY test
References: pages about CO2 effect:
- Vasodilation: CO2 expands arteries and arterioles facilitating perfusion (or blood supply) to all vital organs
- The Bohr effect: How and why oxygen is released by red blood cells in body tissues
- Nerve stabilization: Carbon dioxide has powerful calmative and sedative effects on brain neurons and nerve cells
Baer PN & Benjamin SD, Periodontal Disease in Children and Adolescents,
Philadelphia, Toronto, 1974, Lippincott.
Bell-Syer SE, Hart R, Crawford F, Torgerson DJ, Tyrrell W, Russell I, Oral treatments for fungal infections of the skin of the foot, Cochrane Database Syst Rev 2002; (2): CD003584.
Cherdwongcharoensuk D, Oliveira MJ, Aguas AP, In vivo formation and binding of SeHg complexes to the erythrocyte surface, Biol Trace Elem Res. 2010 Aug;136(2):197-203.
Debelian GJ, Olsen I, Tronstad L, Anaerobic bacteremia and fungemia in patients undergoing endodontic therapy: an overview, Ann Periodontol. 1998 Jul; 3(1): 281-287.
Fowler EB, Breault LG, Cuenin MF, Periodontal disease and its association with systemic disease, Mil Med 2001 Jan; 166(1): 85-89.
Gabrovsek J, Dental caries: a dent on dogma, Apr 1997 (www.priory.com/den/caries04.htm).
Gendron R, Grenier D, Maheu-Robert L, The oral cavity as a reservoir of bacterial pathogens for focal infections, Microbes Infect 2000 Jul; 2(8): 897-906.
Gibbons RV, Germs, Dr. Billings, and the theory of focal infection, Clin Infect Dis 1998 Sep; 27(3): 627-633.
Hattori K, Therapeutic effects and prognostic factors of tonsillectomy for IgA nephropathy in long-term follow-up [Article in Japanese], Nippon Jibiinkoka Gakkai Kaiho 1998 Dec; 101(12): 1412-1422.
Issels J, Cancer: a second opinion, Hodder and Stoughton: London, 1975.
Iutskovskii AD, The immune status of patients with foot mycosis and eczema [in Russian], Vestn Dermatol Venerol 1989; (1): 52-57.
Joshipura K, Ritchie C, Douglass C, Strength of evidence linking oral conditions and systemic disease, Compend Contin Educ Dent Suppl 2000; (30): 12-23.
Kataura A, Tonsillar focal infection - Present clinical situation and prospects in the future of tonsillar focal infection, Practica Oto-Rhino-Laryngologica Aug 2002; 95 (8).
Li X, Kolltveit KM, Tronstad L, Olsen I, Systemic diseases caused by oral infection, Clin Microbiol Rev 2000 Oct; 13(4): 547-558.
Lockhart PB & Durack DT, Oral microflora as a cause of endocarditis and other distant site infections, Infect Dis Clin North Am 1999 Dec; 13(4): 833-850, vi.
Meurman JH, Dental infections and general health, Quintessence Int 1997 Dec; 28(12): 807-811.
Meyer DH & Fives-Taylor PM, Oral pathogens: from dental plaque to cardiac disease, Curr Opin Microbiol 1998 Feb; 1(1): 88-95.
Mizutani H, Ohmoto Y, Mizutani T, Murata M, Shimizu M, Role of increased production of monocytes TNF-alpha, IL-1beta and IL-6 in psoriasis: relation to focal infection, disease activity and responses to treatments, J Dermatol Sci 1997 Feb; 14(2): 145-153.
Okuda K & Ebihara Y, Relationships between chronic oral infectious diseases and systemic diseases, Bull Tokyo Dent Coll 1998 Aug; 39(3): 165-174.
Siqueira Junior JF, Aetiology of root canal treatment failure: why well-treated teeth can fail, Int Endod J, 2001 Jan; 34 (1): 1-10.
Souliagin SS, Treatment of patients with focal infections using VEDB method [in Russian], in Buteyko method. Its application in medical practice, ed. by K.P. Buteyko, 2nd ed., 1991, Titul, Odessa, p.56-63.
Takeuchi J, Yagisawa M, Nishimura T, Tonsillar focal infection: clinical observations of low grade fever, Acta Otolaryngol Suppl 1996; 523: 204-205.
Yoneda S, Suzuki KT, Detoxification of mercury by selenium by binding of equimolar Hg-Se complex to a specific plasma protein, Toxicol Appl Pharmacol. 1997 Apr;143(2):274-80, Faculty of Pharmaceutical Sciences, Chiba University, Japan.
Warren J, The head trip, Random House, 2007.
Int Endod J. 2002 Aug;35(8):698-702.
Combinations of bacterial species in endodontic infections.
Peters LB, Wesselink PR, van Winkelhoff AJ.
Department of Cariology Endodontology Pedodontology, Academic Center for Dentistry Amsterdam, the Netherlands.
AIM: This study was undertaken to investigate combinations of bacteria found in root-canal infections of teeth with periapical bone destruction without clinical signs and symptoms.
METHODOLOGY: Endodontic samples from 58 root canals were cultured anaerobically and microorganisms were counted and identified. Eighty-one combinations of microorganisms were found and tested for a symbiotic relationship using the Fisher's exact test and Odds ratio calculation.
RESULTS: All samples contained microorganisms with a median CFU mL(-1) of 8x10(4) per sample. Strict anaerobic species accounted for 87% of the microflora. The most prevalent bacteria were Prevotella intermedia, Peptostreptococcus micros and Actinomyces odontolyticus, present in 33, 29 and 19%, respectively, of the cultured canals. A significant relationship (P<0.05) and an Odds ratio >2 were found between P. intermedia and P. micros, P. intermedia and P. oralis, A. odontolyticus and P. micros, Bifidobacterium spp. and Veillonella spp. Conclusions: These results indicate that endodontic pathogens do not occur at random but are found in specific combinations.
Ann Periodontol. 1998 Jul;3(1):281-7.
Anaerobic bacteremia and fungemia in patients undergoing endodontic therapy: an overview.
Debelian GJ, Olsen I, Tronstad L.
Division of Endodontics, Dental Faculty, University of Oslo, Norway.
Oral focal infection, a concept neglected for several decades, is a subject of controversy. Recent progress in classification and identification of oral microorganisms has renewed interest in focal infection. The aim of this study was to use phenotypic and genetic methods to trace microorganisms released into the bloodstream during and after endodontic treatment back to their presumed source--the root canal. Microbiological samples were taken from the root canals of 26 patients with asymptomatic apical periodontitis of single-rooted teeth. The blood of the patients was drawn during and 10 minutes after endodontic therapy. Microorganisms in blood were collected after anaerobic lysis filtration and cultured anaerobically on blood agar plates. The phenotypic methods used for characterization and tracing of microorganisms in blood and root canals were: biochemical and antimicrobial susceptibility test, SDS-PAGE of whole-cell soluble proteins, and gas chromatography of cellular fatty acids. Phenotypic data were verified by DNA restriction patterns and corresponding ribotypes of the root canal and blood isolates by using a computer-assisted system fro gel analysis. All root canals contained anaerobic bacteria. The frequency of bacteremia varied from 31% to 54%. The microorganisms from the root canal and blood presented identical phenotype and genetic characteristics within the patients examined. These characteristics differed between patients. The present study demonstrated that endodontic treatment can be the cause of anaerobic bacteremia and fungemia. The phenotypic and genetic methods used appeared valuable for tracing microorganisms in the blood back to their origin.
Endod Dent Traumatol. 1995 Feb;11(1):15-9.
Microbial flora of sinus tracts and root canals of non-vital teeth.
Weiger R, Manncke B, Werner H, Löst C.
Department of Conservative Dentistry, University of Tübingen, Germany.
The occurrence of bacteria in 12 endodontically induced periodontal lesions associated with sinus tracts was examined. The microbial flora encountered in the sinus tract was compared with that of the root canal of the involved teeth which had not experienced any prior endodontic therapy. All microbiological samples taken from the sinus tract and from the root canal system contained bacteria. Seventy-one strains were detected in the extraradicular lesions. Of the anaerobic species, Fusobacterium nucleatum (7 strains), Prevotella intemedia (4 strains) and P. oralis (4 strains) were most frequently found. In the group of the facultative anaerobes Streptococcus spp. were predominant. Ninety-four strains were isolated from the root canal system of the 12 teeth. P. intermedia (6 strains), P. buccae (5 strains), F. nucleatum (5 strains) and Lactobacillus plantarum (5 strains) were most common. In 9 cases, species present in the root canal could be revealed in the extraradicular lesions. It was concluded that a variety of microorganisms were capable of colonizing endodontically induced, extraradicular lesions clinically characterized by sinus tracts.
Int Endod J. 2006 May;39(5):343-56.
Consequences of and strategies to deal with residual post-treatment root canal infection.
Wu MK, Dummer PM, Wesselink PR.
Department of Cariology Endodontology Pedodontology, Academic Centre for Dentistry Amsterdam (ACTA), Amsterdam, The Netherlands.
Bacterial sampling of prepared root canals is used to determine the presence and character of the remaining microbiota. However, it is likely that current sampling techniques only identify organisms in the main branches of the root canal system whereas it is unlikely that they can sample areas beyond the apical end-point of preparation and filling, or in lateral canals, canal extensions, apical ramifications, isthmuses and within dentinal tubules. Thus, it may be impossible by current techniques to identify residual post-treatment root canal infection. In histologic observations of root apices, bacteria have been found in inaccessible inter-canal isthmuses and accessory canals often in the form of biofilms. There is no in vivo evidence to support the assumption that these bacteria can be entombed effectively in the canal system by the root filling and thus be rendered harmless. As a consequence of this residual root infection, post-treatment apical periodontitis, which may be radiographically undetectable, may persist or develop as a defence mechanism to prevent the systemic spread of bacteria and/or their byproducts to other sites of the body. Histologic observation of root apices with surrounding bone removed from either patients or human cadavers has demonstrated that post-treatment apical periodontitis is associated with 50-90% of root filled human teeth. Thus, if the objective of root canal treatment is to eliminate apical periodontitis at a histological level, current treatment procedures are inadequate. It is essential that our knowledge of the local and systemic consequences of both residual post-treatment root infection and post-treatment apical periodontitis be improved. The continued development of treatments that can effectively eliminate root infection is therefore a priority in clinical endodontic research. Post-treatment disease following root canal treatment is most often associated with poor quality procedures that do not remove intra-canal infection; this scenario can be corrected via a nonsurgical approach. However, infection remaining in the inaccessible apical areas, extraradicular infection including apically extruded dentine debris with bacteria present in dentinal tubules, true radicular cysts, and foreign body reactions require a surgical intervention.
J Endod. 2008 Mar;34(3):258-63. Epub 2007 Dec 21.
Treatment outcome in endodontics: the Toronto study--phase 4: initial treatment.
de Chevigny C, Dao TT, Basrani BR, Marquis V, Farzaneh M, Abitbol S, Friedman S.
Discipline of Endodontics, Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada.
Outcome 4-6 years after initial treatment was assessed for Phase 4 (2000-2001) of the Toronto Study. Of 582 teeth treated, 430 were lost to follow-up (99 discontinuers, 331 dropouts), 15 were extracted, and 137 (32% recall minus 15 extracted teeth) were examined for outcome: healed (no apical periodontitis, signs, symptoms) or diseased. When pooled with Phases 1-3, 439 of 510 teeth (86%) were healed. Logistic regression identified 2 significant (P < or = .05) preoperative outcome predictors: radiolucency (odds ratio [OR], 2.86; confidence interval [CI], 1.56-5.24; healed: absent, 93%; present, 82%) and number of roots (OR, 2.53; CI, 1.25-5.13; healed: single, 93%; multiple, 84%). In teeth with radiolucency, intraoperative complications (OR, 2.27; CI, 1.05-4.89; healed: absent, 84%; present, 69%) and root-filling technique (OR, 1.89; CI, 1.01-3.53; healed: lateral, 77%; vertical, 87%) were additional outcome predictors. A better outcome was suggested for teeth without radiolucency, with single roots, and without mid-treatment complications. The predictive value of root-filling technique in teeth with radiolucency requires validation from randomized controlled trials.
Int Endod J. 2007 Dec;40(12):921-39. Epub 2007 Oct 10.
Outcome of primary root canal treatment: systematic review of the literature - part 1. Effects of study characteristics on probability of success.
Ng YL, Mann V, Rahbaran S, Lewsey J, Gulabivala K.
Unit of Endodontology, UCL Eastman Dental Institute, University College London, London, UK.
AIMS: The aims of this study were (i) to conduct a comprehensive systematic review of the literature on the outcome of primary (initial or first time) root canal treatment; (ii) to investigate the influence of some study characteristics on the estimated pooled success rates.
METHODOLOGY: Longitudinal clinical studies investigating outcome of primary root canal treatment, published up to the end of 2002, were identified electronically (MEDLINE and Cochrane database 1966-2002 December, week 4). Four journals (International Endodontic Journal, Journal of Endodontics, Oral Surgery Oral Medicine Oral Pathology Endodontics Radiology and Dental Traumatology & Endodontics), bibliographies of all relevant papers and review articles were hand-searched. Three reviewers (Y-LN, SR and KG) independently assessed, selected the studies based on specified inclusion criteria, and extracted the data onto a pre-designed proforma. The study inclusion criteria were: longitudinal clinical studies investigating root canal treatment outcome; only primary root canal treatment carried out on the teeth studied; sample size given; at least 6-month postoperative review; success based on clinical and/or radiographic criteria (strict, absence of apical radiolucency; loose, reduction in size of radiolucency); overall success rate given or could be calculated from the raw data. The findings by individual study were summarized and the pooled success rates by each potential influencing factor were calculated for this part of the study.
RESULTS: Of the 119 articles identified, 63 studies published from 1922 to 2002, fulfilling the inclusion criteria were selected for the review: six were randomized trials, seven were cohort studies and 48 were retrospective studies. The reported mean success rates ranged from 31% to 96% based on strict criteria or from 60% to 100% based on loose criteria, with substantial heterogeneity in the estimates of pooled success rates. Apart from the radiographic criteria of success, none of the other study characteristics could explain this heterogeneity. Twenty-four factors (patient and operative) had been investigated in various combinations in the studies reviewed. The influence of preoperative pulpal and periapical status of the teeth on treatment outcome were most frequently explored, but the influence of treatment technique was poorly investigated.
CONCLUSIONS: The estimated weighted pooled success rates of treatments completed at least 1 year prior to review, ranged between 68% and 85% when strict criteria were used. The reported success rates had not improved over the last four (or five) decades. The quality of evidence for treatment factors affecting primary root canal treatment outcome is sub-optimal; there was substantial variation in the study-designs. It would be desirable to standardize aspects of study-design, data recording and presentation format of outcome data in the much needed future outcome studies.
Int Endod J. 2008 Jan;41(1):6-31. Epub 2007 Oct 10.
Outcome of primary root canal treatment: systematic review of the literature -- Part 2. Influence of clinical factors.
Ng YL, Mann V, Rahbaran S, Lewsey J, Gulabivala K.
Unit of Endodontology, UCL Eastman Dental Institute, University College London, London, UK
AIMS: (i) To carry out meta-analyses to quantify the influence of the clinical factors on the efficacy of primary root canal treatment and (ii) to identify the best treatment protocol based on the current evidence.
METHODOLOGY: The evidence for the effect of each clinical factor on the success rate (SR) of primary root canal treatment was gathered in three different ways: (i) intuitive synthesis of reported findings from individual studies; (ii) weighted pooled SR by each factor under investigation was estimated using random-effect meta-analysis; (iii) weighted effect of the factor under investigation on SR were estimated and expressed as odds ratio for the dichotomous outcomes (success or failure) using fixed- and random-effects meta-analysis. Statistical heterogeneity amongst the studies was assessed by Cochran's (Q) test. Potential sources of statistical heterogeneity were investigated by exploring clinical heterogeneity using meta-regression models which included study characteristics in the regression models.
RESULTS: Out of the clinical factors investigated, pre-operative pulpal and periapical status were most frequently investigated, whilst the intra-operative factors were poorly studied in the 63 studies. Four factors were found to have a significant effect on the primary root canal treatment outcome, although the data heterogeneity was substantial, some of which could be explained by some of the study characteristics.
CONCLUSIONS: Four conditions (pre-operative absence of periapical radiolucency, root filling with no voids, root filling extending to 2 mm within the radiographic apex and satisfactory coronal restoration) were found to improve the outcome of primary root canal treatment significantly. Root canal treatment should therefore aim at achieving and maintaining access to apical anatomy during chemo-mechanical debridement, obturating the canal with densely compacted material to the apical terminus without extrusion into the apical tissues and preventing re-infection with a good quality coronal restoration.
Eur Heart J. 1993 Dec;14 Suppl K:51-3.
Dental infections as a risk factor for acute myocardial infarction.
First Department of Medicine, Helsinki University Central Hospital, Finland.
The so-called classic risk factors of coronary heart disease (CHD) do not explain all its clinical and epidemiological features. Recent evidence suggests that certain infections, among them dental infections, are involved in the pathogenesis of CHD. Case-control studies have revealed an association between dental infections and acute myocardial infarction and chronic coronary heart disease. A large epidemiological survey revealed an association between missing teeth and CHD and a recent 14-year follow-up of 9760 individuals showed that periodontitis is associated with an increased risk of coronary heart disease. Preliminary results suggest that the severity of dental infections correlates with the extent of coronary atheromatosis. Individuals with severe dental infections also have higher level of von Willebrand factor antigen, leukocytes and fibrinogen. Streptococcus sanguis has been shown to aggregate human platelets in vitro. The mechanism behind the association between dental infections and CHD could be the effect of bacteria on the cells taking part in the pathogenesis of atherosclerosis and arterial thrombosis.
J Dent Res. 2000 Feb;79(2):756-60.
Age, dental infections, and coronary heart disease.
Mattila KJ, Asikainen S, Wolf J, Jousimies-Somer H, Valtonen V, Nieminen M.
Dept of Medicine, Helsinki University Central Hospital, Finland.
Epidemiological and intervention studies have suggested that infections are risk factors for coronary heart disease (CHD). Dental infections have appeared as cardiovascular risk factors in cross-sectional and in follow-up studies, and the association has been independent of the "classic" coronary risk factors. This case-control study aimed at detailed assessment of the dental pathology found in various CHD categories (including elderly patients). Altogether, 85 patients with proven coronary heart disease and 53 random controls, matched for sex, age, geographic area, and socio-economic status, were compared with regard to dental status, assessed blindly with four separate scores, and to the "classic" coronary risk factors (seven of the controls had CHD, and they were not included in the analyses). The dental indices were higher among CHD patients than in the controls, but, contrary to previous studies, the differences were not significant (between the CHD patients and their matched controls or among the different CHD categories). This result could not be explained by potential confounding factors. The participants in the present study were older and had more often undergone recent dental treatment in comparison with subjects in our earlier studies. Age correlated with the severity of dental infections only in the random controls but not in the coronary patients who, although young, already had high dental scores. We believe that the higher age of the participants in the present study is the most likely reason for the results. Other possible explanations include an age-related selection bias among older CHD patients, and the fact that those participating in studies like this may have better general health and thus also less severe dental infections. Thus, the role of dental infections as a coronary risk factor varies according to the characteristics of the population studied.
J Endod. 2009 May;35(5):626-30.
Association between chronic dental infection and acute myocardial infarction.
Willershausen B, Kasaj A, Willershausen I, Zahorka D, Briseño B, Blettner M, Genth-Zotz S, Münzel T.
Department of Operative Dentistry, Johannes Gutenberg University Mainz, Mainz, Germany.
INTRODUCTION: In patients with cardiovascular diseases several risk factors such as high blood pressure, diabetes, smoking and drinking habits, genetic disposition, and chronic inflammation must be considered. The aim of this study was to investigate whether there is a correlation between dental origin infections and the presence of an acute myocardial infarction (AMI). METHODS: A total of 125 patients who had experienced a myocardial infarction and 125 healthy individuals were included in this study. The oral examination was carried out following the consent of the ethics committee and the National Board for Radiation Protection and included the number of teeth, endodontically treated teeth, periodontal screening index (PSI), clinical attachment level, and radiographic apical lesions (radiograph examination). The medical examination included, among others, blood glucose level, C-reactive protein (CRP) serum levels, and leukocyte number. RESULTS: The study demonstrated that patients with AMI exhibited an unfavorable dental state of health. After statistical adjustment for age, gender, and smoking, they exhibited a significantly higher number of missing teeth (P = .001), less teeth with root canal fillings (P = .0015), a higher number of radiologic apical lesions (P = .001), and a higher PSI value (P = .001) compared with individuals without myocardial infarction. The medical data showed a nonsignificant correlation between CRP and the number of radiologic apical lesions. CONCLUSIONS: This study presents evidence that patients who have experienced myocardial infarction also exhibit an unfavorable dental state of health in comparison to healthy patients and suggests an association between chronic oral infections and myocardial infarction.
Int Endod J. 2002 Apr;35(4):366-71.
Invasion of vascular cells in vitro by Porphyromonas endodontalis.
Dorn BR, Harris LJ, Wujick CT, Vertucci FJ, Progulske-Fox A.
Center for Molecular Microbiology, Department of Oral Biology, College of Dentistry, University of Florida, Gainesville, FL 32610, USA.
AIM: The objective of this study was to determine whether laboratory strains and clinical isolates of microorganisms associated with root canal infections can invade primary cultures of cardiovascular cells. METHODOLOGY: Quantitative levels of bacterial invasion of human coronary artery endothelial cells (HCAEC) and coronary artery smooth muscle cells (CASMC) were measured using a standard antibiotic protection assay. Transmission electron microscopy was used to confirm and visualize internalization within the vascular cells. RESULTS: Of the laboratory and clinical strains tested, only P. endodontalis ATCC 35406 was invasive in an antibiotic protection assay using HCAEC and CASMC. Invasion of P. endodontalis ATCC 35406 was confirmed by transmission electron microscopy. DISCUSSION: Certain microorganisms associated with endodontic infections are invasive. If bacterial invasion of the vasculature contributes to the pathogenesis of cardiovascular disease, then microorganisms in the pulp chamber represent potential pathogens.
You can leave your feedback and comments below. Thanks.