Clinicians should have a sound understanding of the potential effects of endodontic diseases and their treatment on the systemic health of their patients, and an awareness of previous clinical studies. Miller originally implicated microorganisms in root canal infections in the early 1890s. However, it was not until Hunter (1900) theorized that oral-derived bacteria could disseminate throughout the body, thereby inducing disease, that the medical profession took significant interest in infections of the dental pulp and oral tissues. From 1910 to the 1940s, numerous studies reported the adverse effects that diseased tissue sites, particularly infected oral tissues, had on the host (Murray and Saunders, 2000). Billings et al. (1912), Mayo (1914), and Rosenow (1917) were instrumental in establishing acceptance within the medical profession that localized low-grade chronic infections were capable of inducing disease elsewhere in the body. These early studies established the “focal infection theory,” introducing the concept that systemic dissemination of microorganisms and associated toxins from a focus of circumscribed infection established or exacerbated systemic disease (Hunter, 1921). Indeed, Rosenow proposed that enclosed lesions capable of draining only into the circulation, such as infected root canals, were the most dangerous foci of infection.
The focal infection theory was fiercely debated, with root canal infections or infections of the surrounding periodontal attachment apparatus implicated as culprits in numerous diseases (Holman, 1928). Consequently, evidence from clinical research recommended wholesale dental extractions and tonsillectomies as the panacea for several systemic ailments. Rhoads and Dick (1932) purported all pulpless teeth as likely foci of infection, advising dental extractions as prerequisite in medically compromised patients to improve their health and well-being. Moreover, Rhein et al. (1926) even advocated extraction of healthy teeth for the prevention of focal infection! In the United States, opposition to root canal treatment (RCT) became so powerful that the majority of institutions ceased clinical endodontic teaching in favor of dental extractions (Grossman, 1971). As a result, progress in RCT procedures, still very much in their infancy, was curtailed for over 40 years.
However, by the 1930s the research community began to raise doubts about the quality of evidence endorsing the focal infection theory (Bernhardt and Hench, 1931). Indeed, Cecil and Angevine (1938) disputed the validity of results from previous work (Cecil and Archer, 1927), which had recommended prompt removal of infectious dental foci at an early stage to cure rheumatoid arthritis (RA). Furthermore, it proved difficult to reproduce results from earlier studies that had implicated Streptococcus sp-induced RA (Dawson et al., 1932). Reimann and Havens (1940) suggested that Hunter’s views, expressed 30 years previously, had been misinterpreted, concluding “the removal of local infections in the hope of influencing remote or general symptoms and disease must still be regarded as an experimental procedure not devoid of hazard.” Although a minority continued to uphold the general concept of focal infection (Ensign, 1945), it became accepted that a more logical and scientific approach to focal infection had to be adopted. In a critical review appraising the relationship between focal infection and rheumatoid disease, Freyberg (1946) postulated that removal of foci of infection should only be considered as part of a broad spectrum of treatment. Agreement was reached that removal of infected foci would be of little benefit in chronic diseases.
Importantly, researchers and clinicians began to acknowledge that not every “focus of infection” was responsible for a “focal infection” and that anemia, emotional strain, exposure, malnutrition, endocrine imbalance, fatigue, senility, trauma, age, and infectious disease all contributed to lowering patients’ resistance to disease (Arnett and Ennis, 1933; Shuster, 1941). Those refuting the focal infection theory claimed that generally no foci of infection could be located within afflicted individuals enrolled in the research studies (Easlick, 1951). Furthermore, following removal of infected foci, no discernible improvements were observed in the patients’ medical conditions. Indeed, Mitchell and Helman (1953) ascertained that perfectly healthy individuals had as many septic foci as those with diseases such as arthritis. Critically, early focal infection research was crude, with an absence of control cohorts and reliance on flawed bacteriologic culture techniques that biased findings. These substantial methodologic flaws led to the demise of the focal infection theory.
However, the focal infection theory has resurfaced in modern times, with publication of review papers (Hughes, 1994; Newman, 1996) and a popular book (Meinig, 1986), which contests that the dental profession has chosen to ignore a significantly researched concept related to the general health of the population. Once again, the role of RCT and its impact on long-term general health has been questioned. Nevertheless, the potential association between systemic health and RCT has been strongly disputed by dental governing bodies and there remains little evidence to substantiate the claims (Murray and Saunders, 2000).
Following the concept of focal infection, considerable research activity has attempted to analyze the relationship of oral diseases, in particular periodontal disease (reviewed in Dietrich and Garcia, 2005), with general systemic disease. In contrast, investigations detailing the relationship of PRD or root canal therapy to systemic health have been limited. However, antigen delivery through the root canals of primates and rabbits has been shown to induce b/>