martes, 18 de junio de 2013


Focal infection theory Willoughby D. Miller (1853–1907), whose work was
very much influenced by Robert Koch, is best known for his groundbreaking ideas on the etiology of caries.
He also postulated a role for bacteria in the etiology of alveolar pyorrhea , and concluded that, in the presence of predisposing factors, many bacteria found normally in the mouth can cause periodontal disease (e.g., non-specific plaque hypothesis). Miller advocated that such bacteria could also play a role in
the etiology of many other diseases in humans. He coined the expression focus of infection, but stopped short of promoting eradication of infected teeth to prevent or treat systemic illnesses. This step was made by Frank Billings (1854–1932), a highly respected American physician and academic leader. Billings and his student and colleague Edward C. Rosenow (1875–1966) promoted the theory of focal infection in the USA . Like Miller, Billings spent time in Europe, where the germ theory of disease, initiated by the groundbreaking discoveries of Koch, Lister, Pasteur and other luminaries, was heavily debated. According to Billings  theory, the germ carrier harbors pleiomorphic microorganisms that may cause disease at any time. Dissemination of such germs from a latent localized infection to a distant organ would occur through the blood and lymphatic systems. The focal infection paradigm was quickly adopted by many dentists and physicians, especially surgeons in the USA. Its clinical implementation, which was further promoted by substantial improvements in asepsis, led to uncountable unwarranted tooth extractions, tonsillectomies and other surgical procedures. In 1928, Holman publicly questioned the validity of the focal infection theory. Its importance started to decline in the 1930s as evidence accumulated indicating that surgical removal of suspected foci has no beneficial effect on the medical status of affected patients. It is tempting to speculate about apparent similarities between the focal infection theory and the so-called systemic link. However, a closer look at the basis of the two paradigms reveals fundamental discrepancies, especially with regard to bacterial pleiomorphism and tissue lesion latency.

A N D R E W D E N T I N O , S E O K W O O L E E , J A S O N M A I L H O T & A R T H U R F. H E F T I, Principles of periodontology, Periodontology 2000, Vol. 61, 2013, 16–53

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