World Journal of Pharmaceutical Research

Gayathri et al. SJIF Impact

World Journal of Pharmaceutical Factor 7.523
Research
Volume 6, Issue 7, 484-490. Review Article ISSN 2277– 7105

FOCAL INFECTION THEORY: A FOCUS ON CURRENT ASPECTS

1
*Dr. Gayathri S., 2Dr. Nandhini V., 3Dr. Sumathi H. Rao and 4Dr. P. B. Anand

1
Reader, Department of Periodontics, Sathyabama University Dental College and Hospital,
Rajiv Gandhi Salai OMR Road, Chennai 600119.
2
Senior Lecturer, Department of Periodontics, Sathyabama University of Dental College and
Hospital, Chennai.
3
Reader, Sathyabama University of Dental College and Hospital, Chennai.
4
Reader, Department of Periodontics, Sathyabama University of Dental College and Hospital,
Chennai.

ABSTRACT
Article Received on
24 April 2017, Systemic health is often closely linked to the state of the oral health.
Revised on 14 May 2017, Systemic diseases and conditions have oral manifestations and oral
Accepted on 04 June 2017
cavity reflects the signs of systemic diseases at its early stage. The
DOI: 10.20959/wjpr20177-8738
mouth –body connection or focal infection is proved through numerous
published researches. This article reviews pertinent literature detailing
*Corresponding Author
both the history of the focal infection theory and current focus on the
Dr. Gayathri S.
possible association between oral and systemic diseases.
Reader, Department of
Periodontics, Sathyabama
KEYWORDS: Focal infection, Systemic diseases, Periodontitis,
University Dental College
and Hospital, Rajiv Gandhi Periodontal medicine.
Salai OMR Road, Chennai
600119. INTRODUCTION
The relationship of our teeth and oral cavity to overall health is
undisputable. The mouth body connection or focal sepsis theory is proved through numerous
researches. A focal infection is a localized or generalized infection caused by the
dissemination of microorganisms or toxic products from a focus of infection.[1] Billings gave
the first definition of focal infection: A focus of infection may be described as a
circumscribed area of tissue infected with pathogenic microorganisms.[2,3]

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HISTORY
The first report of focal infection was reported by Hippocrates who attributed the cure of a
case of arthritis to a tooth extraction. In 1800s Benjamin Rush, an American physician also
related arthritis cure to tooth extraction.[1]

In 1890, the dentist and physician WD Miller published his treatise, The Microorganisms of
the Human Mouth. The local and general diseases which are caused by them. A year later in
Dental Cosmos first used the term “Focal infection”.[4] Miller did not advise extraction of
teeth as a focus of infection and also suggested „treating and filling root canals‟. In 1900, the
English physician, William Hunter, reported in the British Medical Journal on „Sepsis as a
Cause of Disease‟ listing poor oral health and the expanding use of „conservative dentistry‟ as
a cause of diseases attributed to focal infection. Miller promoted importance on sterilization
of instruments would prevent spread of infection.[5]

The era of focal infection in medicine began in 1912 when the physician, Frank Billings.[2,6]
introduced the concept of focal infection to American physicians through case reports that
tonsillectomies and dental extractions claim to remove various foci of infections at distant
organs.

In the 1920s, the theory of focal infection was the main cause taught as the cause of a wide
range of illnesses with infected teeth[7] All pulpless teeth were focus of infection and the
extraction of healthy teeth was justified to prevent focal infection.

In 1935, Cecil and Angevine[8] published an analysis of 200 cases of rheumatoid arthritis that
documented no benefit from tonsillectomy or dental extractions, but rather occasional
exacerbations of the arthritis and concluded that: „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,‟ and that „the time has arrived for a complete reevaluation
of the focal infection theory.‟

In 1939, Vaizey and ClarkKennedy[9] demonstrated that patients who were edentulous
developed subsequent arthritis and dyspepsia and that edentulism actually caused indigestion
rather than cured it.

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In 1940, Reimann and Havens published the most influential criticism of focal infection
theory and observed that: the theory of focal infection had not been proved due to the
following observations:
(1) Its infectious agents was not known
(2) Large groups of people whose tonsils are present are no worse than those whose tonsils
have been removed,
(3) Patients who had tonsillectemy continue to suffer from the disease, for which they were
removed,
(4) Any beneficial effects can seldom be ascribed to surgical procedures alone,
(5) Beneficial effects that occasionally occur after surgical measures are often lead by
harmful effects or no effects.
(6) Foci of infection would be cured after recovery from systemic disease or when general
health is improved with oral hygiene and nutritious diet. Only areas superficially
accessible to surgery were listed as foci of infection. While deeper structures were
conspicuously absent leaving one of its harshest critics to comment that a focus of
infection was: „anything readily accessible to surgery.[10]

During 1950s came an end of focal theory of infection era when authorities who felt that
focal infection was an important factor in systemic disease have become skeptical and
recommend less radical procedure in treatment of diseases.[4,11] There was a support for the
theory till late 1950s[12] and later focal infection vanished as the primary cause of chronic,
systemic diseases. In 1990s' emergence of epidemiological associations between dental
infections and systemic diseases, researches have been cautious, seeking association between
dental infections like periodontitis and systemic diseases which marked the beginning of
Periodontal medicine.[13]

MECHANISM OF SPREAD FROM ORAL INFECTION[14]

Three mechanisms oral infections to secondary systemic effects have been proposed. These
are: (a) metastatic spread of infection from the oral cavity due to transient bacteremia,
(b) metastatic injury from the effects of circulating oral microbial toxins, and (c) metastatic
inflammation caused by immunological injury by oral microflora.

Metastatic infection
Oral infections and dental procedures can cause transient bacteremia. The microorganisms
that enter systemic circulation are eliminated by the reticuloendothelial system within

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minutes and does not lead to clinical symptoms or it will lead to increase in body
temperature. If the microorganisms have favorable conditions, they multiply.

Metastatic injury
Bacteria have the ability to produce diffusible proteins, or exotoxins, which include cytolytic
enzymes and dimeric toxins. The exotoxins have pharmacological actions and are powerful
and lethal poisons.

Metastatic inflammation
Antigens enter the systemic circulation and react with specific antibody to cause
immunocomplexes that give rise to acute and chronic inflammatory lesions and conditions.

Periodontitis and Systemic diseases

To discuss all the systemic diseases associated with periodontitis is beyond the scope of this
review. However well documented possible associations between periodontitis and systemic
diseases are discussed below.

Periodontitis and Pre term low birth infants[15]

The etiology of pre term low birth weight is multifactorial. There is onging debate regarding
relationships between periodontitis during pregnancy and adverse pregnancy outcomes.
Periodontal inflammation produce significant amounts of proinflammatory cytokines, like
interleukin 1-beta (IL-1β), IL-6, prostaglandin E2, and tumor necrosis factor-alpha (TNF-α),
which may have systemic effects. Low birth weight, defined as birth weight less than 2,500 g,
which is a significant public health issue in both developed and developing countries.
Research suggests that the bacteria bloodstream from the inflamed periodontal tissues and
target the fetus, leading to premature labor and low-birth-weight (PLBW) babies. One
mechanism begins with deleterious effects of endotoxins released from Gram-negative
bacteria responsible for periodontal disease. periodontal disease appears to be an independent
risk factor for PLBW and there is a need to expand preventive measures for pregnant women
16
in harmonization with the gynecological and dental professions. Systemic review in 2013
suggested that, maternal periodontitis is modestly but significantly associated with LBW (low
birth weight) and preterm birth. Data from prospective studies followed a similar pattern, but
associations were generally weaker. It was found that Maternal periodontitis was significantly
associated with pre-eclampsia. Maternal periodontitis is modestly but independently
associated with adverse pregnancy outcomes.

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Periodontitis and Diabetes mellitus

Epidemiological data confirm that diabetes is a major risk factor for periodontitis; there is a
three fold increase in susceptibility to periodontitis in diabetics. There is a clear relationship
between degree of hyperglycemia and severity of periodontitis. The mechanisms that
underpin the links between these two conditions are not completely understood, but involve
immune functioning, neutrophil activity, and cytokine biology. There is emerging evidence to
support the existence of a two-way relationship between diabetes and periodontitis, with
diabetes increasing the risk for periodontitis, and periodontal inflammation negatively
affecting glycaemic control.[17] Several meta-analyses have confirmed that effective
periodontal therapy can result in reduced Glycated haemoglobin (Hb A1c) [18 ,19]

Periodontitis and cardiovascular diseases

Evidence continues to support the association between periodontal infections, atherosclerosis
and vascular disease. Recommending periodontal treatment for the prevention of
atherosclerotic cardio vascular disease (CVD) is not warranted based on scientific evidence.
Periodontal treatment must be recommended on the basis of the value of its benefits for the
oral health of patients, recognizing that patients are not healthy without good oral hygiene.
However, the emergence of periodontal infections as a potential risk factor for CVD is
leading to a convergence in oral and medical care that can only benefit the patients and public
health.[20] A systematic review concluded in 2008 Periodontal disease is a risk factor or
marker for CHD (Coronary heart diseases) that is independent of traditional CHD risk
factors, including socioeconomic status. Further research in this important area of public
health is warranted.[21]

CONCLUSION
In this era of Periodontal medicine, researches have been cautiously exploring to establish
definitive conclusions on the nature of associations between periodontitis and systemic
diseases. Oral health has a direct and or indirect impact on the overall general health. In
susceptible individuals, however periodontal infection may act as risk factor or may be
involved in pathogenic mechanisms. Dentists must improve their knowledge and clinical
exposure of relevant systemic conditions in order to interact and relate meaningfully with
their medical colleagues. Regular dental checkup is strongly advocated in the light of current
knowledge.

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