Focal infection theory

Source: Wikipedia, the free encyclopedia.
For the epidemiology concept, see Focus of infection.

Focal infection theory is the historical concept that many chronic diseases, including systemic and common ones, are caused by focal infections. In present medical consensus, a focal infection is a localized infection, often asymptomatic, that causes disease elsewhere in the host, but focal infections are fairly infrequent and limited to fairly uncommon diseases.[1] (Distant injury is focal infection's key principle, whereas in ordinary infectious disease, the infection itself is systemic, as in measles, or the initially infected site is readily identifiable and invasion progresses contiguously, as in gangrene.)[2][3] Focal infection theory, rather, so explained virtually all diseases, including arthritis, atherosclerosis, cancer, and mental illnesses.[4][5][6][7]

An ancient concept that took modern form around 1900, focal infection theory was widely accepted in medicine by the 1920s.

endodontically treated teeth were blamed as foci.[3][7] The putative oral sepsis was countered by tonsillectomies and tooth extractions, including of endodontically treated teeth and even of apparently healthy teeth, newly popular approaches—sometimes leaving individuals toothless—to treat or prevent diverse diseases.[7]

Drawing severe criticism in the 1930s, focal infection theory—whose popularity zealously exceeded consensus evidence—was discredited in the 1940s by research attacks that drew overwhelming consensus of this sweeping theory's falsity. Thereupon, dental restorations and endodontic therapy became again favored.

enter blood and infect the heart, perhaps its valves.[2]

Entering the 21st century, scientific evidence supporting general relevance of focal infections remained slim, yet evolved

immunologic injury—that might occur simultaneously and even interact.[2][13] Meanwhile, focal infection theory has gained renewed attention, as dental infections apparently are widespread and significant contributors to systemic diseases, although mainstream attention is on ordinary periodontal disease, not on hypotheses of stealth infections via dental treatment.[14][15][16] Despite some doubts renewed in the 1990s by conventional dentistry's critics, dentistry scholars maintain that endodontic therapy can be performed without creating focal infections.[3][7]

Rise and popularity (1890s–1930s)

Roots and dawn

Germ theory

William Henry Welch, tasked to design the medical department at the newly forming Johns Hopkins University, imported the German model, "scientific medince", to America.[20]

As progressively more diseases drew an infectious hypothesis that led to a pathogen discovery, conjectures grew that virtually all diseases are infectious.

humoral medicine, found new outlet in medical bacteriology, a pillar of the new "scientific medicine".[27] Around 1900, British surgeons, still knife-happy, were urging "surgical bacteriology".[27]

Autointoxication

In 1877, French chemist

autointoxication.[27][29][31] Metchnikoff reasoned that the colon functions as a "vesitigal cesspool" that stores waste but is unneeded.[32]

Abdominal surgery's pioneer,

Sir Arbuthnot Lane, based in London, drew from Metchnikoff and clinical observation to identify "chronic intestinal stasis"—in lay terms, intractable constipation—presumably, "flooding of the circulation with filthy material".[27] Reporting surgical treatment in 1908, Lane eventually offered total colon removal, but later favored simply surgical release of colonic "kinks", and in 1925, abandoning surgery, began promoting prevention and intervention by diet and lifestyle, how Lane secured his contemporary reputation as a crank.[27][31] Since 1875, in the American state Michigan, physician John Harvey Kellogg had targeted "bowel sepsis"—an allegedly prime cause of degeneration and disease—at his health resort, Battle Creek Sanitarium.[27] Having, in fact, coined the term sanitarium, Kellogg yearly received several thousand patients, including US Presidents and celebrities, at his huge resort, advertised as the "University of Health".[27] But in the 1910s, as North American medical schools emulated the German model—that is, "scientific medicine"[33]—medical doctors who recognized "focal infection" were hinting a scientific basis versus the older, alleged "health faddists" like medical doctor Kellogg and like minister Sylvester Graham.[27]

Medical popularity

Hunter on "oral sepsis"

In 1900, British surgeon

partial dentures.[36][37]

Billings & Rosenow

Focal infection theory's modern era really began with physician Frank Billings,[21] based in Chicago, and his case reports of tonsillectomies and tooth extractions that apparently cured infections of distant organs.[36] Replacing Hunter's term oral sepsis with focal infection,[7] Billings in November 1911 lectured at the Chicago Medical Society, and published it in 1912 as an article for the American medical community.[38] In 1916, Billings lectured in California at Stanford University Medical School, this time printed in book format.[39] Billings thus popularized intervention by tonsillectomy and tooth extraction.[6] A pupil of Billings, Edward Rosenow held that extraction alone was often insufficient, and urged teamwork by dentistry and medicine.[22] Rosenow developed the principle elective localization, whereby microorganisms have affinities for particular organs, and also espoused extreme pleomorphism, whereby a bacterium can drastically change form and perhaps evade conventional detection methods.[36][40][41]

Preeminent recognition

Since 1889, in the American state Minnesota, brothers William Mayo and Charles Mayo had built an international reputation for surgical skill at their Mayo Clinic, by 1906 performing some 5,000 surgeries a year, over 50% intra-abdominal, a tremendous number at the time, with unusually low mortality and morbidity.[27][42] Though originally distancing themselves from routine medicine and skeptical of laboratory data, they later recruited Edward Rosenow from Chicago to help improve Mayo Clinic's diagnosis and care and to enter basic research via experimental bacteriology.[27][42] Rosenow influenced Charles Mayo,[27] who by 1914 published to support focal infection theory alongside Rosenow.[43][44][45]

At

Sir William Osler was succeeded as professor of medicine by Llewellys Barker,[46] who became a prominent proponent of focal infection theory.[27] Although many of the Hopkins medical faculty remained skeptics, Barker's colleague William Thayer[47] cast support.[27] As Hopkins' chief physician, Barker was a pivotal convert propelling the theory to the center of American routine medical practice.[27] Russell Cecil,[48] famed author of Cecil's Essentials of Medicine, too, lent support.[36] In 1921, British surgeon William Hunter announced that oral sepsis was "coming of age".[8]

Although physicians had already interpreted pus within a bodily compartment as a systemic threat, pus from infected tooth roots often drained into the mouth and thereby was viewed as systemically inconsequential.

neurological, could result.[49] By 1930, excision of focal infections was considered a "rational form of therapy" undoubtedly resolving many cases of chronic diseases.[5] Its inconsistent effectiveness was attributed to unrecognized foci—perhaps inside internal organs—that the clinicians had missed.[5]

Dental reception

In 1923, upon some 25 years of researches, dentist

root canal therapy, teeth routinely host bacteria producing potent toxins.[3] Transplanting the teeth into healthy rabbits, Price and his researchers duplicated heart and arthritic diseases.[3] Although Price noted often seeing patients "suffering more from the inconvenience and difficulties of mastication and nourishment than they did from the lesions from which their physician or dentist had sought to give them relief",[52] his 1925 debate with John P Buckley was decided in favor of Price's position: "practically all infected pulpless teeth should be extracted".[53] As chairman of the American Dental Association's research division, Price was a leading influence on the dentistry profession's opinion.[54] Into the late 1930s, textbook authors relied on Price's 1923 treatise.[55]

In 1911, the year that Frank Billings lectured on focal infection to the Chicago Medical Society, unsuspected

hard labor.[7]

Psychiatric promulgation

Near the turn of the 20th century, psychiatry's predominant explanations of schizophrenia's causation, besides heredity, were focal infection and autointoxication.

nasal sinuses and to extract the tonsils and the teeth, but also to remove the appendix, gall bladder, spleen, stomach, colon, cervix, ovaries, and testicles, while Cotton claimed up to 85% cure rate.[61]

Despite Cotton's death rate of some 30%, his fame rapidly spread through America and Europe, and the asylum drew influx of patients.[61] The New York Times heralded "high hope".[61] Cotton made a European lecture tour,[61] and Princeton University Press and Oxford University Press simultaneously published his book in 1922.[62] Despite skepticism in the profession, psychiatrists sustained pressure to match Cotton's treatments, as patients would ask why they were being denied curative treatment.[61] Other patients were pressured or compelled into the treatment without their own consent.[63] Cotton had his two sons' teeth extracted as preventive healthcare—although each later committed suicide.[61] In the 1930s, however, focal infection fell from psychiatry as an explanation,[60] Cotton having died in 1933.[61]

Criticism and decline (1930s–1950s)

Early skepticism

Addressing the Eastern Medical Society in December 1918, New York City physician Robert Morris had explained that focal infection theory had drawn much interest but that understanding was incomplete, while the theory was earning disrepute through overzealousness of some advocates.[64] Morris called for facts and explanation from scientists before physicians continued investing so steeply in it, already triggering vigorous disputes and embittering divisions among clinicians as well as uncertainty among patients.[64]

In 1919, the American Dental Association's forerunner, the National Dental Association, held in New Orleans its annual meeting, where C Edmund Kells, the originator and pioneer of dental X-ray,[56] delivered a lecture, published in 1920 in the association's journal,[65] largely discussing focal infection theory, which Kells condemned as a "crime".[57] Kells stressed that X-ray technology is to improve dentistry, not to enhance the "mania of extracting devitalized teeth".[57] Kells urged dentists to reject physicians' prescriptions of tooth extractions.[66]

Focal infection theory's elegance suggested simple application, but the surgical removals brought meager "cure" rate, occasional disease worsening, and inconsistent experimental results.

Ward's Island.[67] As colleagues of Kirby, two researchers—bacteriologist Nicolas Kopeloff and psychiatrist Clarence Cheney—ventured from Ward's Island to Trenton, New Jersey, to investigate Cotton's practice.[61]

Research attacks

In two

Cotton's psychiatric surgeries ineffective: those who improved were already so prognosed, and others improved without surgery.[61][68] Publishing two papers, the team presented the findings at the American Psychiatric Association's 1922 and 1923 annual meetings.[61][69] At Johns Hopkins University, Phyllis Greenacre questioned most of Cotton's data, and later helped steer American psychiatry into psychoanalysis.[61] Antipsychotic colectomy vanished except in Trenton until Cotton—who used publicity and word of mouth, kept the 30% death rate unpublicized, and passed a 1925 investigation by New Jersey Senate—died by heart attack in 1933.[61]

By 1927,

endontically treated teeth during extraction.[3] In 1938, Russell Cecil and D Murray Angevine reported 200 cases of rheumatoid arthritis, but no consistent cures by tonsillectomies or tooth extractions.[3][71] They commented, "Focal infection is a splendid example of a plausible medical theory which is in danger of being converted by its enthusiastic supporters into the status of an accepted fact."[6] Newly a critic, Cecil alleged that foci were "anything readily accessible to surgery".[36]

In 1939, E W Fish published landmark findings that would revive endodontics.[3] Fish implanted bacteria into guinea pigs' jaws, and reported that four zones of reaction consequently developed.[3][72] Fish reported that the first zone was the zone of infection, whereas the other three zones—surrounding the zone of infection—revealed immune cells or other host cells but no bacteria.[3] Fish theorized that by removing the infectious nidus, dentists would permit recovery from the infection[3] This reasoning and conclusion by Fish became the basis for successful root-canal treatment.[3] Still, endodontic therapy of the era indeed posed substantial risk of failure, and fear of focal infection crucially motivated endontologists to develop new and improved technology and techniques.[7]

End of the focal era

The review and "critical appraisal" by

antibiotics, a backlash to the "orgy" of tooth extractions and tonsillectomies ensued.[6]

K A Easlick's 1951 review in the

Journal of the American Medical Association tolled the era's end by stating that "many patients with diseases presumably caused by foci of infection have not been relieved of their symptoms by removal of the foci", that "many patients with these same systemic diseases have no evident focus of infection", and that "foci of infection are as common in apparently healthy persons as in those with disease".[75][76] Although some support extended into the late 1950s,[77][78] focal infection vanished as the primary explanation of chronic, systemic diseases,[15] and the theory was generally abandoned in the 1950s.[79]

Revival and evolution (1990s–2010s)

Despite the general theory's demise, focal infection remained a formal, if rare, diagnosis, as in

case-control study, as the species usually involved is present throughout the human body.[82]

Stealth pathogens

With the 1950s introduction of antibiotics, attempts to explain unexplained diseases via bacterial etiology seemed all the more unlikely.

viruses—became the entities expected in the theory of focal infection.[83][84] Yet until the 1980s, such researchers were scarce, largely due to scarce funding for such investigations.[83]

Despite the limited funding, research established that L forms can adhere to

endodontically treated teeth were L forms,[88] thought nonexistent by bacteriologists of his time and widely overlooked into the 21st century.[89] Apparently, dental infections, including by uncultured or cryptic microorganisms, contribute to systemic diseases.[90][91][92][93][88][87]

Periodontal medicine

At the 1990s' emergence of

epidemiological associations between dental infections and systemic diseases, American dentistry scholars have been cautious,[79] some seeking successful intervention to confirm causality.[3][94] Some American sources emphasized epidemiology's inability to determine causality, categorized the phenomena as progressive invasion of local tissues, and distinguished that from focal infection theory—which they assert was evaluated and disproved by the 1940s.[3] Others have found focal infection theory's scientific evidence still slim, but have conceded that evolving science might establish it.[2] Yet select American authors affirm the return of a modest theory of focal infection.[95][96]

European sources find it more certain that dental infections drive systemic diseases, at least by driving systemic inflammation, and probably, among other immunologic mechanisms, by

antigenic crossreaction with host biomolecules,[16][97][98] while some seemingly find progressive invasion of local tissues compatible with focal infection theory.[98] Acknowledging that beyond epidemiological associations, successful intervention is needed to establish causality, they emphasize that biological explanation is needed atop both, and the biological aspect is thoroughly established already, such that general healthcare, as for cardiovascular disease, must address prevalent periodontal disease,[97][99] a stance matched in Indian literature.[100] Thus, there has emerged the concept periodontal medicine.[16][79]

Dental controversies

During the 1980s, dentist

cavitation seeping infectious and toxic material.[12] Sometimes forming elsewhere in bones after injury or ischemia,[17] jawbone cavitations are recognized as foci also in osteopathy[17] and in alternative medicine,[101] but conventional dentists generally conclude them nonexistent.[17] Although the International Academy of Oral Medicine & Toxicology claims that the scientific evidence establishing existence of jawbone cavitations is overwhelming and even published in textbooks, the diagnosis and related treatment remain controversial,[102] and allegations of quackery persist.[103]

Huggins and many biological dentists also espouse

George Meinig's 1994 book, Root Canal Cover-Up, discussing researches of Rosenow and of Price, some dentistry scholars reasserted that the claims were evaluated and disproved by the 1940s.[108][109] Yet Meinig was but one of at least three authors who in the early 1990s independently renewed the concern.[59]

asplenic, elderly, rheumatoid arthritic, or using steroid drugs—there remained a lack of carefully controlled studies definitely establishing adverse systemic effects.[59] Conversely, some if few studies have investigated effects of systemic disease on root-canal therapy's outcomes, which tend to worsen with poor glycemic control, perhaps via impaired immune response, a factor largely ignored until recently, but now recognized as important.[59] Still, even by 2010, "the potential association between systemic health and root canal therapy has been strongly disputed by dental governing bodies and there remains little evidence to substantiate the claims".[59]

The traditional root-filling material is

bacteremia traced to asymptomatic endodontic infection.[7] In any event, the predominant view is that shunning endodonthic therapy or routinely extracting endodontically treated teeth to treat or prevent systemic diseases remains unscientific and misguided.[3][109][115]

Footnotes

  1. ^ See, for example, David Schlossberg, ed, Clinical Infectious Disease, 2nd edn (Cambridge University Press, 2015), and Yomamoto T, "Triggering role of focal infection...", in Harabuchi Y et al, eds, Recent Advances in Tonsils and Mucosal Barriers of the Upper Airways (Karger, 2011).
  2. ^ a b c d Jed J Jacobson & Sol Silverman Jr, ch 17 "Bacterial infections", in Sol Silverman, Lewis R Eversole & Edmond L Truelove, eds, Essentials of Oral Medicine (Hamilton Ontario: BC Decker, 2002), pp 159–62.
  3. ^ a b c d e f g h i j k l m n o p q r s t u v w x y J Craig Baumgartner, José F Siqueira Jr, Christine M Sedgley & Anil Kishen, ch 7 "Microbiology of endodontic disease", in John I Ingle, Leif K Bakland & J Craig Baumgartner, eds, Ingle's Endodontics, 6th edn (Hamilton Ontario: BC Decker, 2008), p 221–24.
  4. ^ Paul R Stillman & John O McCall, A Textbook of Clinical Periodontia, (New York: Macmillan Co, 1922), "ch 18 Focal infection".
  5. ^
    PMID 20318466
    .
  6. ^
    S2CID 42277199
    .
  7. ^ a b c d e f g h i j k l m n o Nils Skaug & Vidar Bakken, ch 8 "4Systemic complications of endodontic infections", subchapter "Chronic periapical infections as the origin of metastatic infections", in Gunnar Bergenholtz, Preben Hørsted-Bindslev & Claes Reit, eds, Textbook of Endodontology, 2nd ed. (West Sussex: Wiley-Blackwell, 2010), pp 135–37.
  8. ^
    PMID 20770334
    .
  9. PMID 18739726
    .
  10. ^ a b James M Dunning, Principles of Dental Public Health, 4th edn (Cambridge MA: Harvard University Press, 1986), ch 13 "Dental needs and resources", § "Systemic infection of dental origin", p 272–73.
  11. ^ Gavett G, "Tragic results when dental care is out of reach"4, PBS Frontline website, 26 Jun 2012
  12. ^ a b c Hal A Huggins & Thomas E Levy, Uninformed Consent: The Hidden Dangers in Dental Care (Charlottesvi4lle VA: Hampton Roads Publishing, 1999), ch 12 "The cavitation" & ch 13 "Focal infection".
  13. PMID 22529571
    .
  14. PMID 15366304
    .
  15. ^ a b Shantipriya Reddy, Essentials of Clinical Periodontology and Periodontics, 2nd edn (New Delhi: Jaypee Brothers Medical Publishers, 2008), ch 13 "Periodontal medicine", esp pp 115–16.
  16. ^
    PMID 21111933
    .
  17. ^ a b c d Leon Chaitow, Cranial Manipulation: Theory and Practice, 2nd edn (Edinburgh, London, New York, etc.: Elsevier, 2005), pp 348–49 & 350–51.
  18. ^ In 1876, employing innovative bacteriology protocols more stringently reductionist than previous bacteriology techniques, Koch confirmed that a recurrently suspected bacterial species—later named Bacillus anthracis—causes anthrax, which thus became the first mammalian disease scientifically explained as infectious.
  19. PMID 9770165
    .
  20. ^ Barry D. Silverman, "William Henry Welch (1850–1934): The road to Johns Hopkins", Proc (Bayl Univ Med Cent), 2011 Jul;24(3):236–242.
  21. ^
    Clin Infect Dis
    , 1998 Sep;27(3):627–633.
  22. ^
    PMID 17012729
    .
  23. doi:10.1016/S0140-6736(02)01387-9
    .
  24. ^ Willoughby D Miller, The Micro-Organisms of the Human Mouth: The Local and General Diseases Which Are Caused by Them (Leipzig: Verlag von Georg Thieme, 1892).
  25. ^ Shanon Patel & Justin J Barnes, "Introduction: How has endodontics developed?", in Shanon Patel & Justin J Barnes, eds, The Principles of Endodontics, 2nd edn (Oxford: Oxford University Press, 2013), pp 4–5.
  26. ^ Miller WD (1894). "An introduction to the study of the bacteriopathology of the dental pulp". Dental Cosmos. 36: 505–28.
  27. ^ a b c d e f g h i j k l m n o Andrew Scull, Madhouse: A Tragic Tale of Megalomania and Modern Medicine (New Haven: Yale University Press, 2005), pp 33–37.
  28. ^ a b Caroline Barranco, "The first live attenuated vaccines", Nature Portfolio, Springer Nature Limited, 28 Sep 2020.
  29. ^ a b c Alfred I Tauber & Leon Chernyak, Metchnikoff and the Origins of Immunology: From Metaphor to Theory (New York: Oxford University Press, 1991), pp viii, 11.
  30. helper T cells
    , bridge innate immunity and adaptive immunity.
  31. ^
    PMID 2668399
    .
  32. Front Public Health
    , 2013 Nov 13;1:52.
  33. J R Soc Med
    , 1992 Oct;85(10):598–602, especially pp 599–600.
  34. PMID 20759127
    .
  35. ^ William Hunter, Oral Sepsis as a Cause of Septic Gastritis, Toxic Neuritis, and Other Septic Conditions (London: Cassell & Co, 1901).
  36. ^ a b c d e f g John I Ingle, PDQ Endodontics, 2nd edn (Shelton CT: People's Medical Publishing House, 2009), p xiv.
  37. ^
    doi:10.1001/jama.1940.02810010003001
    .
  38. doi:10.1001/archinte.1912.00060160087007
    .
  39. ^ Frank Billings, Focal Infection: The Lane Lectures (New York & London: D Appleton & Co, 1918).
  40. JSTOR 30080461
    .
  41. ^ Edward C Rosenow, ch 43 "Elective localization of bacteria in the animal body", in Edwin O Jordan & I S Falk, eds The Newer Knowledge of Bacteriology and Immunology (Chicago IL: University of Chicago Press, 1928), pp 576–89.
  42. ^ a b "Mayo Clinic history", Mayo Clinic, Website access: 21 Sep 2013.
  43. doi:10.1001/jama.1914.02570230034010
    .
  44. doi:10.1001/jama.1914.02570230035011
    .
  45. S2CID 72457427
    .
  46. ^ "The Lewellys Franklin Barker Collection", Alan Mason Chesney Medical Archives, Johns Hopkins Medical Institutions, Website access: 23 Sep 2013.
  47. ^ "The William S Thayer Collection Archived 2013-09-22 at the Wayback Machine", Repository Guide to the Personal Papers Collections of Alan Mason Chesney Medical Archives, Johns Hopkins Medical Institutions, Website access: 21 Sep 2013.
  48. PMC 1031019
    .
  49. ^
    doi:10.1001/jama.1914.02570230037013
    .
  50. ^ Weston A Price, Dental Infections, Oral and Systemic, Vol 1 & Vol 2 (Cleveland: Penton Publishing, 1923).
  51. doi:10.1001/jama.1925.02660300012006
    .
  52. ^ Weston A Price, Dental Infections, Oral and Systemic, Vol 1 (Cleveland: Penton Publishing, 1923), p 488.
  53. doi:10.14219/jada.archive.1925.0307
    .
  54. ^ British Journal of Dental Science, 1928;72:101.
  55. ^ Examples: William H O McGehee, A Text-book of Operative Dentistry, 2nd edn (Philadelphia: Blackiston's Son & Co, 1936), pp 39 & 110; Louis V Hayes, Clinical Diagnosis of Diseases of the Mouth: A Guide for Students and Practitioners of Dentistry and Medicine (Brooklyn NY: Dental Items of Interest Publishing, 1935), p 389.
  56. ^
    PMID 11794365
    .
  57. ^ a b c ADA: "C Edmund Kells was a dental pioneer who championed the use of X-rays in dentistry during the late 19th century and early 20th century. 'The X-ray in dental practice' is a paper read by Dr Kells at a 1919 Association meeting in New Orleans. Much of the paper discusses focal infection theory, which Dr Kells argued was leading to the unnecessary extraction of teeth. He also made it clear that dental X-rays should be used to enhance dentistry, and not to encourage the 'mania for extracting devitalized teeth' " ["JADA Centennial: From the February 2013 issue of JADA", American Dental Association, Website access: 21 Sep 2013].
  58. ^ Journal of the Canadian Dental Association, 1935;1:451.
  59. ^ a b c d e f g C Murray, ch 48 "Endontology and general systemic health", §§ "The 'focal infection' era" & "Effects of general systemic health on endodontics", in Michael Baumann & Rudolf Beer, eds, Endodontology, 2nd edn (New York: Thieme, 2010).
  60. ^
    S2CID 41416327
    .
  61. ^
    PMID 19797603
    .
  62. ^ Henry A Cotton, The Defective, Delinquent, and Insane: The Relation of Focal Infections to their Causation, Treatment and Prevention (Princeton/London: Princeton University Press/Oxford University Press, 1922).
  63. ^ Phil Fennell, Treatment Without Consent: Law, Psychiatry and the Treatment of Mentally Disordered People since 1845 (London & New York: Routledge, 1996), p. 120.
  64. ^ a b Robert T Morris: "The matter of focal infections is one of the very new subjects of the day which men are taking up with a great deal of interest but are going ahead perhaps with incomplete knowledge and not comprehending the range and scope of the entire subject; consequently this subject is falling into disrepute in certain fields because of the over-enthusiasm of some of the advocates of focal infection theory in relation to distant demonstration—endocarditis, rheumatism, gastric ulcer, cholecystitis, various forms of neuritis, etc. The philosopher, taking all evidence judicially, will eventually give the medical profession the basic facts and what is valuable in the subject. Right now one might utter a warning to the general medical profession against taking too active an interest in the subject." ["Address on medicine and surgery", American Medicine, 1919 Jan;25(1):17–23, pp 18–19].
  65. ^ C Edmund Kells, "X-ray in dental practice", Journal of the National Dental Association, 1920 Mar;7(3):241–72 [JADA provides the article free in two parts (1 Archived 2013-09-27 at the Wayback Machine & 2 Archived 2013-09-27 at the Wayback Machine)].
  66. PMID 23372129
    .
  67. Facts on File, 2007), pp 170–170
    .
  68. PMID 21507275
    .
  69. doi:10.1176/ajp.80.2.149
    .
  70. ^ Henry W Crowe & Herbert G Franking, "Aetiology continued: Dental infections and degenerative diseases—a review and commentary", pp 23–32, Bacteriology and Surgery of Chronic Arthritis and Rheumatism with End-Results of Treatment (New York/London: Humphrey Milford/Oxford University Press, 1927), p 32.
  71. ^ Russell L Cecil & D Murray Angevine, "Clinical and experimental observations on focal infection, with an analysis of 200 cases of rheumatoid arthritis", Annals of Internal Medicine, 1938 Nov 1;12(5):577–584.
  72. doi:10.14219/jada.archive.1939.0156
    .
  73. ^ Louis I Grossman, Root Canal Therapy (Philadelphia: Lea & Febiger, 1940), ch 2, reprinted in Journal of Endodontics, 1982 Jan;8(Suppl):S18-S24, available at Robert Kaufmann's EndoExperience.com under "The endo file cabinet: Textbook excerpts: Grossman's Endodontics: Chapter on focal infection", Accessed online 17 Feb 2014.
  74. PMID 14831976
    .
  75. ^ Philip M Preshaw & John J Taylor, ch 21 "Periodontal pathogenesis", in Michael G Newman, Henry Takei, Perry R Klokkevold & Fermin A Carranza, Carranza's Clinical Periodontology, 11th edn (St Louis: Saunders/Elsevier, 2012).
  76. ^
    PMID 14955464
    .
  77. ^ Joseph M Dougherty & Anthony J Lamberti, Textbook of Bacteriology, 3rd edn (St Louis: Mosby, 1954), p 231
  78. PMID 13398294
    .
  79. ^ a b c d Nikos Donos & Francesco D'Aiuto, ch 3 "Periodontitis: A modern clinical perspective", in Brian Henderson, Michael Curtis, Robert Seymour & Nikolaos Donos, eds, Periodontal Medicine and Systems Biology (West Sussex: Wiley-Blackwell, 2009), pp 33–34.
  80. ^ Ronald T Lewis, ch 25 "Soft tissue infection and loss of abdominal wall substance", in Robert Bendavid, ed, Abdominal Wall Hernias: Principles and Management (New York, Berlin, Heidelberg: Springer, 2001), p 192.
  81. ^ Technical Manual #8-225: Dental Specialist (Washington DC: Department of the Army Headquarters, 20 Sep 1971), pp Glossary-7 & 5-14.
  82. ^ John I Ingle, PDQ Endodontics, 2nd edn (Shelton CT: People's Medical Publishing House, 2009), p xv.
  83. ^ a b c Michael Wilson, Rod McNab & Brian Henderson, Bacterial Disease Mechanisms: An Introduction to Cellular Microbiology (Cambridge: Cambridge University Press, 2002), p 597.
  84. ^
    PMID 269356
    .
  85. ^ Gerald J Domingue, Cell Wall-Deficient Bacteria: Basic Principles and Clinical Significance (Reading MA: Addison-Wesley Publishing, 1982), p 455.
  86. PMID 10962273.{{cite journal}}: CS1 maint: multiple names: authors list (link
    )
  87. ^
    PMID 25940667
    .
  88. ^ a b c Lida H Mattman, Cell Wall Deficient Forms: Stealth Pathogens, 3rd edn (Boca Raton FL: CRC Press, 2000), pp 286 & 289, while p 291 lists for p 289 a citation of Haley B (1996). "Root canal teeth contain toxins according to new and old research". Dent Amalgam Merc Synd. 6 (4): 1–4.
  89. ^ L H Mattman, Stealth Pathogens, 3rd edn (CRC Press, 2000), ch 1 "History".
  90. PMID 23717756
    .
  91. PMID 11023956
    .
  92. ^ Peter Mullany, Philip Warburton & Elaine Allan, ch 9 "The human oral metagenome", Karen E Nelson, ed, Metagenomics of the Human Body (New York, Dordrecht, Heidelberg, London: Springer, 2011), p 166.
  93. PMID 23055580
    .
  94. PMID 23040337
    .
  95. PMID 25813714
    .
  96. PMID 17012729
    .
  97. ^
    PMID 17716290
    .
  98. ^
    PMID 21375141
    .
  99. S2CID 43371539
    .
  100. PMID 23493942
    .
  101. ^ Examples: Ellen Hodgson Brown, Healing Joint Pain Naturally: Safe and Effective Ways to Treat Arthritis, Fibromyalgia, and Other Joint Diseases (New York: Broadway Books, 2001); Shirley MacLaine, Sage-ing While Age-ing (New York: Atria Books, 2007).
  102. ^ IAOMT, "IAOMT position paper on jawbone osteonecrosis", International Academy of Oral Medicine & Toxicology, 27 Jul 2014.
  103. ^ Stephen Barrett, "A critical look at cavitational osteopathosis, NICO, and 'biological dentistry'", Quackwatch, 4 Apr 2010.
  104. ^ Stephen Barrett, "Stay away from 'holistic' and 'biological' dentists", Quackwatch, accessed online: 17 Sep 2013.
  105. ^ a b J Craig Baumgartner, José F Siqueira Jr, Christine M Sedgley & Anil Kishen, ch 7 "Microbiology of endodontic disease", in John I Ingle, Leif K Bakland & J Craig Baumgartner, eds, Ingle's Endodontics, 6th edn (Hamilton Ontario: BC Decker, 2008), p 257: "Microorganisms found in failed endodontically treated teeth have either remained in the root canal from previous treatment or have entered since treatment via leakage. ... Those remaining from the original microbiota would need to have maintained viability throughout treatment procedures, including exposure to disinfectants, and thereafter adapted to a root canal environment in which the availability of a variety of nutrients is more limited because of lack of pulp tissue. This might occur as a result of an inability of chemomechanical instrumentation procedures to completely debride the root canal system in a single visit and because of the inaccessible locations of bacteria in isthmuses, accessory canals, and apical regions of canals. While it is considered that many such remaining bacteria will be unable to cause harm once entombed by the obturation material, there is little evidence for this".
  106. PMID 1066607
    .
  107. PMID 269357
    .
  108. ^ J Craig Baumgartner, Leif K Bakland & Eugene I Sugita, ch 3 "Microbiology of endodontics and asepsis in endodontic practice" Archived 2011-08-16 at the Wayback Machine, in John Ide Ingle & Leif K Bakland, eds, Endodontics, 5th edn (Hamilton Ontario: BC Decker, 2002), p 64.
  109. ^
    S2CID 9643840
    .
  110. ^ Mark A Breiner, Whole-Body Dentistry: A Complete Guide to Understanding the Impact of Dentistry on Total Health (Fairfield CT: Quantum Health Press, 2011), pp 171–174.
  111. ^ Mark A Breiner, Whole-Body Dentistry: A Complete Guide to Understanding the Impact of Dentistry on Total Health (Fairfield CT: Quantum Health Press, 2011), pp 168–69, 174–175.
  112. ^ a b Breiner, Whole-Body Dentistry (Quantum Health, 2011), pp
  113. PMID 19323310
    .
  114. PMID 17931389
    .
  115. ^ Highlighting publications and findings by Price, by Meinig, and by Haley, holistic dentist Mark A Breiner advises not routine extraction of root-filled teeth, but routine monitoring, and extraction only when the tooth seems to especially impair health [Mark A Breiner, Whole-Body Dentistry: A Complete Guide to Understanding the Impact of Dentistry on Total Health (Fairfield CT: Quantum Health Press, 2011), pp 164, 168 & 175].
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