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Thesis, antithesis, and synthesis in periodontal and systemic interlink

Identifieur interne : 002058 ( Pmc/Corpus ); précédent : 002057; suivant : 002059

Thesis, antithesis, and synthesis in periodontal and systemic interlink

Auteurs : K. R. Akshata ; V. Ranganath ; Ashish S. Nichani

Source :

RBID : PMC:3459494

Abstract

The theory of focal infection, which was promulgated during the 19th and early 20th centuries, stated that "foci" of sepsis were responsible for the initiation and progression of a variety of inflammatory diseases such as arthritis, peptic ulcers, and appendicitis. In the oral cavity, therapeutic edentulation was common as a result of the popularity of the focal infection theory. Since many teeth were extracted without evidence of infection, thereby providing no relief of symptoms, the theory was discredited and largely ignored for many years. Recent progress in classification and identification of oral microorganisms and the realization that certain microorganisms are normally found only in the oral cavity have opened the way for a more realistic assessment of the importance of oral focal infection. It has become increasingly clear that the oral cavity can act as the site of origin for dissemination of pathogenic organisms to distant body sites, especially in immunocompromised hosts such as patients suffering from malignancies, diabetes, rheumatoid arthritis, or in patients undergoing other immunosuppressive treatment. A number of epidemiological studies have suggested that oral infection, especially periodontitis, may be a risk factor for systemic diseases.


Url:
DOI: 10.4103/0972-124X.99257
PubMed: 23055580
PubMed Central: 3459494

Links to Exploration step

PMC:3459494

Le document en format XML

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<p>The theory of focal infection, which was promulgated during the 19
<sup>th</sup>
and early 20
<sup>th</sup>
centuries, stated that "foci" of sepsis were responsible for the initiation and progression of a variety of inflammatory diseases such as arthritis, peptic ulcers, and appendicitis. In the oral cavity, therapeutic edentulation was common as a result of the popularity of the focal infection theory. Since many teeth were extracted without evidence of infection, thereby providing no relief of symptoms, the theory was discredited and largely ignored for many years. Recent progress in classification and identification of oral microorganisms and the realization that certain microorganisms are normally found only in the oral cavity have opened the way for a more realistic assessment of the importance of oral focal infection. It has become increasingly clear that the oral cavity can act as the site of origin for dissemination of pathogenic organisms to distant body sites, especially in immunocompromised hosts such as patients suffering from malignancies, diabetes, rheumatoid arthritis, or in patients undergoing other immunosuppressive treatment. A number of epidemiological studies have suggested that oral infection, especially periodontitis, may be a risk factor for systemic diseases.</p>
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<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">J Indian Soc Periodontol</journal-id>
<journal-id journal-id-type="iso-abbrev">J Indian Soc Periodontol</journal-id>
<journal-id journal-id-type="publisher-id">JISP</journal-id>
<journal-title-group>
<journal-title>Journal of Indian Society of Periodontology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0972-124X</issn>
<issn pub-type="epub">0975-1580</issn>
<publisher>
<publisher-name>Medknow Publications & Media Pvt Ltd</publisher-name>
<publisher-loc>India</publisher-loc>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">23055580</article-id>
<article-id pub-id-type="pmc">3459494</article-id>
<article-id pub-id-type="publisher-id">JISP-16-168</article-id>
<article-id pub-id-type="doi">10.4103/0972-124X.99257</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Prize Winning Essay</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Thesis, antithesis, and synthesis in periodontal and systemic interlink</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Akshata</surname>
<given-names>K. R.</given-names>
</name>
<xref ref-type="aff" rid="aff1"></xref>
<xref ref-type="corresp" rid="cor1"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Ranganath</surname>
<given-names>V.</given-names>
</name>
<xref ref-type="aff" rid="aff1"></xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Nichani</surname>
<given-names>Ashish S.</given-names>
</name>
<xref ref-type="aff" rid="aff1"></xref>
</contrib>
</contrib-group>
<aff id="aff1">
<italic>Department of Periodontology, AECS Maaruti College of Dental Sciences and Research Centre, Bangalore, Karnataka, India</italic>
</aff>
<author-notes>
<corresp id="cor1">
<bold>Address for correspondence:</bold>
Dr. K. R. Akshata, Department of Periodontology, AECS Maaruti College of Dental Sciences and Research Centre, BTM 6
<sup>th</sup>
stage, 1
<sup>st</sup>
phase, Hulimavu Tank Band Road, Kammanahalli, Bangalore, Karnataka, India. E-mail:
<email xlink:href="dr.akshatakr@gmail.com">dr.akshatakr@gmail.com</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub">
<season>Apr-Jun</season>
<year>2012</year>
</pub-date>
<volume>16</volume>
<issue>2</issue>
<fpage>168</fpage>
<lpage>173</lpage>
<history>
<date date-type="received">
<day>16</day>
<month>10</month>
<year>2011</year>
</date>
<date date-type="accepted">
<day>17</day>
<month>6</month>
<year>2012</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright: © Journal of Indian Society of Periodontology</copyright-statement>
<copyright-year>2012</copyright-year>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc-sa/3.0">
<license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p>
</license>
</permissions>
<abstract>
<p>The theory of focal infection, which was promulgated during the 19
<sup>th</sup>
and early 20
<sup>th</sup>
centuries, stated that "foci" of sepsis were responsible for the initiation and progression of a variety of inflammatory diseases such as arthritis, peptic ulcers, and appendicitis. In the oral cavity, therapeutic edentulation was common as a result of the popularity of the focal infection theory. Since many teeth were extracted without evidence of infection, thereby providing no relief of symptoms, the theory was discredited and largely ignored for many years. Recent progress in classification and identification of oral microorganisms and the realization that certain microorganisms are normally found only in the oral cavity have opened the way for a more realistic assessment of the importance of oral focal infection. It has become increasingly clear that the oral cavity can act as the site of origin for dissemination of pathogenic organisms to distant body sites, especially in immunocompromised hosts such as patients suffering from malignancies, diabetes, rheumatoid arthritis, or in patients undergoing other immunosuppressive treatment. A number of epidemiological studies have suggested that oral infection, especially periodontitis, may be a risk factor for systemic diseases.</p>
</abstract>
<kwd-group>
<kwd>Focal infection theory</kwd>
<kwd>periodontal disease</kwd>
<kwd>periodontal medicine</kwd>
<kwd>systemic disease</kwd>
</kwd-group>
</article-meta>
</front>
<body>
<sec id="sec1-1">
<title>INTRODUCTION</title>
<p>It is estimated that 10
<sup>14</sup>
normal or commensal microbes reside on the surfaces of teeth, prosthetic implants, dentures, dental restorations, and the mucosal epithelia lining the oral cavity, respiratory tract, gastrointestinal tract, and urinary tract. The oral cavity contains almost half the commensal bacteria in the human body – approximately 6 billion microbes representing 300–500 species In certain conditions, some of these microorganisms may become opportunistic species that contribute to local and/or systemic infections. It is known that the oral microbial ecosystem is highly dynamic and the oral cavity faces a constant challenge of opportunistic infections and various oral complications of systemic diseases and disorders.[
<xref ref-type="bibr" rid="ref1">1</xref>
]</p>
<p>In some ways, periodontal diseases are among the most unusual human infections. The major reason for this uniqueness is the unusual anatomic feature that the tooth passes through the integument, so that part of it is exposed to the external environment while part is solidly rooted in the connective tissues. In contrast to the outer surface of most parts of the body, the outer layers of the tooth do not shed and thus provide a relatively stable surface for microbial colonization.[
<xref ref-type="bibr" rid="ref2">2</xref>
] This facilitates microorganisms maintaining continuous immediate proximity to the periodontal tissues. Furthermore, the tooth surface and the attached microorganisms are immersed in an aqueous environment, where any bacterial infection is less able to be controlled by the potent mechanisms of host defenses and antimicrobial therapy.[
<xref ref-type="bibr" rid="ref1">1</xref>
]</p>
<p>In advanced stages of periodontitis, the gums markedly separate from the teeth. Continuing destruction of the periodontal attachment and deep periodontal pockets may develop with significant loss of tooth-supporting tissues and alveolar bone. Under these conditions, the thin, highly permeable, and frequently ulcerated pocket epithelium is the only barrier between the bacterial biofilms and the underlying connective tissues. It is apparent that in the presence of uncontrolled advanced periodontitis, microbial-induced infection presents a substantial infectious burden for the entire body by releasing bacteria, bacterial toxins, and other inflammatory mediators into the bloodstream that then affect the other parts of the body. This notion represents a paradigm shift in thinking about the directionality of oral and systemic associations.[
<xref ref-type="bibr" rid="ref3">3</xref>
]</p>
</sec>
<sec id="sec1-2">
<title>THESIS, ANTITHESIS, AND SYNTHESIS</title>
<p>The triad
<italic>thesis, antithesis</italic>
, and
<italic>synthesis</italic>
is often used to describe the thought of German philosopher Georg Wilhelm Friedrich Hegel. Hegel never used the term himself, and almost all of his biographers have been eager to discredit it.</p>
<p>The triad is usually described in the following way:</p>
<p>
<list list-type="bullet">
<list-item>
<p>The thesis is an intellectual proposition</p>
</list-item>
<list-item>
<p>The antithesis is simply the negation of the thesis, a reaction to the proposition</p>
</list-item>
<list-item>
<p>The synthesis solves the conflict between the thesis and antithesis by reconciling their common truths and forming a new proposition.</p>
</list-item>
</list>
</p>
<p>“
<italic>Oral health is not an independent entity cut off from the rest of the body. Rather, it is woven deeply into the fabric of overall health</italic>
.”</p>
<p>What researchers are trying to determine is whether oral health is woven into that fabric with paper or steel threads.[
<xref ref-type="bibr" rid="ref4">4</xref>
] The foundation of our knowledge of periodontal disease(s) is not the product of a linear chronology of events, but rather a bringing together of theories, discoveries, and advances that have occurred in parallel.</p>
<p>Specifically, what is the relationship between periodontal disease and systemic diseases?</p>
<p>There are three possibilities: 1)
<italic>Thesis/association</italic>
: Periodontitis is a cause for systemic disease – along with many others – showing the patient is at an increased risk, but with no causation, 2)
<italic>antithesis/no relationship</italic>
: periodontal disease and systemic disease are random concomitant occurrence/happen stances or coincidences, and 3)
<italic>synthesis</italic>
: a causal relationship requiring intervention; periodontitis is a contributing cause that initiates or aggravates systemic diseases [
<xref ref-type="fig" rid="F1">Figure 1</xref>
].</p>
<fig id="F1" position="float">
<label>Figure 1</label>
<caption>
<p>Relationship between periodontal disease and systemic disease: thesis, antithesis, and synthesis</p>
</caption>
<graphic xlink:href="JISP-16-168-g001"></graphic>
</fig>
</sec>
<sec id="sec1-3">
<title>THESIS/ASSOCIATION</title>
<p>A careful review of the medical literature indicates the belief that conditions affecting the mouth could have implications on peripheral tissues and organs [Tables
<xref ref-type="table" rid="T1">1</xref>
–
<xref ref-type="table" rid="T3">3</xref>
].[
<xref ref-type="bibr" rid="ref5">5</xref>
–
<xref ref-type="bibr" rid="ref9">9</xref>
]</p>
<table-wrap id="T1" position="float">
<label>Table 1</label>
<caption>
<p>Relationship of mouth to body during the ancient civilization</p>
</caption>
<graphic xlink:href="JISP-16-168-g002"></graphic>
</table-wrap>
<table-wrap id="T2" position="float">
<label>Table 2</label>
<caption>
<p>Relationship of mouth to body during the middle ages</p>
</caption>
<graphic xlink:href="JISP-16-168-g003"></graphic>
</table-wrap>
<table-wrap id="T3" position="float">
<label>Table 3</label>
<caption>
<p>Relationship of mouth to body during the modern times</p>
</caption>
<graphic xlink:href="JISP-16-168-g004"></graphic>
</table-wrap>
<p>Frank Billings defined a focus of infection as a “circumscribed area of tissue infected with pathogenic organisms.” He said that the term focal infection implied: 1) that such a focus or lesion of infection existed; 2) that the infection was bacterial in nature; and 3) that as such it was capable of dissemination, resulting in systemic infection of other contiguous or noncontiguous parts.[
<xref ref-type="bibr" rid="ref10">10</xref>
]</p>
<p>William Hunter stated that the degree of systemic effect produced by oral sepsis depended on the virulence of the infection and individual's resistance, and also that oral organisms had specific action on different tissues and that these microbes acted by producing toxins, resulting in low-grade “subinfection,” which produced systemic effects for prolonged periods [
<xref ref-type="table" rid="T4">Table 4</xref>
]. Finally, Hunter believed that the connection between oral sepsis and the resulting systemic conditions could be shown by removal of the causative sepsis through extraction and observation of improvement systemically.[
<xref ref-type="bibr" rid="ref11">11</xref>
] This theory was widely accepted in Britain and USA. Many patients became edentulous as a result of the (unnecessary) removal of teeth [
<xref ref-type="fig" rid="F2">Figure 2</xref>
].[
<xref ref-type="bibr" rid="ref6">6</xref>
]</p>
<table-wrap id="T4" position="float">
<label>Table 4</label>
<caption>
<p>Focal infections leading to acute systemic disease noted by Dr. Billings in 1912</p>
</caption>
<graphic xlink:href="JISP-16-168-g005"></graphic>
</table-wrap>
<fig id="F2" position="float">
<label>Figure 2</label>
<caption>
<p>Advertisement for treatment of focal infection during the 1920s</p>
</caption>
<graphic xlink:href="JISP-16-168-g006"></graphic>
</fig>
</sec>
<sec id="sec1-4">
<title>ANTITHESIS/NO ASSOCIATION</title>
<p>There is no good scientific evidence to support the theory that removal of infected teeth would relieve or cure arthritis, rheumatic heart disease, and kidney, eye, skin, or other disorders [
<xref ref-type="table" rid="T5">Table 5</xref>
].</p>
<table-wrap id="T5" position="float">
<label>Table 5</label>
<caption>
<p>Theories/evidence against focal infection theory</p>
</caption>
<graphic xlink:href="JISP-16-168-g007"></graphic>
</table-wrap>
<p>An editorial in
<italic>The Dental Cosmos</italic>
in 1930 suggested that the concept of the mouth causing all or most human illness was irrational. It called for a return to
<italic>constructive rather than destructive treatment</italic>
.[
<xref ref-type="bibr" rid="ref12">12</xref>
]</p>
<p>By 1950s, an issue of the
<italic>Journal of the American Dental Association</italic>
stated: “Many authorities who formally felt that focal infection was an important etiologic factor in systemic disease have become skeptical and now recommend less radical procedures in the treatment of such disorders.”[
<xref ref-type="bibr" rid="ref12">12</xref>
]</p>
<p>The application of the focal infection theory eventually fell from scientific favor for many reasons including the following:</p>
<p>
<list list-type="bullet">
<list-item>
<p>Improvement in dental care</p>
</list-item>
<list-item>
<p>Advent of antibiotics</p>
</list-item>
<list-item>
<p>Small percent of “cures”</p>
</list-item>
<list-item>
<p>Inability of science to prove the value of the theory</p>
</list-item>
<list-item>
<p>Eventual unfavorable reaction to the “orgy” of dental extractions and tonsillectomies</p>
</list-item>
<list-item>
<p>Inability to replicate the experiments of its advocates</p>
</list-item>
<list-item>
<p>Occasional exacerbation of the disease by the removal of the focus</p>
</list-item>
<list-item>
<p>Lack of controlled clinical trials</p>
</list-item>
</list>
</p>
<p>By the middle of the 20
<sup>th</sup>
century, medicine and dentistry concluded that medical surgery and tooth extraction had no effect on ending the ills.</p>
</sec>
<sec id="sec1-5">
<title>SYNTHESIS</title>
<p>It was not until the last decade of the 20
<sup>th</sup>
century that dentistry and medicine again began to consider the role of oral diseases, such as periodontal disease, as a contributor to the risk for certain systemic diseases.</p>
<p>This link between periodontal and systemic disease came to the forefront in the late 1980s, when preliminary research in dental journals identified systemic diseases also seen in those with periodontal disease.[
<xref ref-type="bibr" rid="ref13">13</xref>
] By the 1990s, the term
<italic>periodontal medicine</italic>
was seen in the literature. It was observed that the periodontitis-plagued may also have cardiovascular disease (CVD), premature labor, and delivery (DeStefano
<italic>et al</italic>
., 1993; Offenbacher
<italic>et al</italic>
., 1996; Beck
<italic>et al</italic>
., 1996).[
<xref ref-type="bibr" rid="ref14">14</xref>
] In the early 2000s, dentists were being instructed to warn their patients that these systemic diseases may worsen when they have periodontal disease.</p>
</sec>
<sec id="sec1-6">
<title>CURRENT STATUS OF THE PERIODONTAL AND SYSTEMIC DISEASES CONNECTION</title>
<p>To date, findings from recent studies, mostly epidemiological studies, support an association between periodontal infection, with particular emphasis on chronic periodontitis, and a number of clinically important systemic diseases [
<xref ref-type="fig" rid="F3">Figure 3</xref>
].[
<xref ref-type="bibr" rid="ref15">15</xref>
–
<xref ref-type="bibr" rid="ref18">18</xref>
] These include CVD (Beck and Offenbacher, 2005), respiratory disease (Scannapieco and Ho, 2001), diabetes (Taylor
<italic>et al</italic>
., 1996), adverse pregnancy outcomes (Xiong
<italic>et al</italic>
., 2006), pancreatic cancer (Michaud
<italic>et al</italic>
., 2007), Alzheimer's disease (Kamer
<italic>et al</italic>
., 2008), and other systemic conditions, which continue to appear in the literature. However, to date, a direct causal role of periodontal infection in the development and or/progression of systemic diseases is not established (Hujoel
<italic>et al</italic>
. 2001; Friedewald
<italic>et al</italic>
. 2009).</p>
<fig id="F3" position="float">
<label>Figure 3</label>
<caption>
<p>Periodontal infection and systemic conditions – Potential linkage and possible pathogenic mechanisms</p>
</caption>
<graphic xlink:href="JISP-16-168-g008"></graphic>
</fig>
</sec>
<sec id="sec1-7">
<title>GENERAL MECHANISMS CONNECTING PERIODONTAL AND SYSTEMIC DISEASES</title>
<p>To better understand this association, a number of hypotheses have been proposed (Paquette, 2002; Seymour
<italic>et al</italic>
., 2007)[
<xref ref-type="bibr" rid="ref19">19</xref>
<xref ref-type="bibr" rid="ref20">20</xref>
]</p>
<p>
<list list-type="order">
<list-item>
<p>Common susceptibility to both oral infection and systemic diseases through shared risk factors: This common susceptibility can be mediated through genetic or environmental factors such as age, smoking, and socioeconomic status. According to this hypothesis, periodontal disease is associated with systemic diseases, but the relationship is not causal.</p>
</list-item>
<list-item>
<p>Systemic inflammation with heightened levels of circulating inflammatory biomediators in response to the local infection or circulating bacteria: According to this hypothesis, periodontal infection induces systemic inflammation and immune responses that may play a causal role in systemic disease.</p>
</list-item>
<list-item>
<p>Systemic dissemination of oral bacteria (i.e. bacteremia) and/or their products: According to this hypothesis, periodontal infection causes bacteremia and endotoxemias which may subsequently play a causal role in systemic diseases.</p>
</list-item>
<list-item>
<p>Cross-reactivity between bacterial and host heat-shock proteins: According to this hypothesis, the immune system does not discriminate between host and bacterial heat-shock proteins, and thus results in an autoimmune response that may contribute to the progression or development of systemic diseases.</p>
</list-item>
</list>
</p>
<sec id="sec2-1">
<title>Periodontal disease and coronary heart disease/atherosclerosis and stroke</title>
<p>CVDs are a group of diseases that include congestive heart failure, coronary artery disease (including atherosclerosis and myocardial infarction), valvular heart disease, and stroke. Among these, atherosclerosis, a major component of cardiovascular diseases, is characterized by the deposition of atherosclerotic plaques on the innermost layer of walls of large- and medium-sized arteries. End-stage outcomes associated with atherosclerosis include coronary thrombosis, myocardial infarction, and stroke. Several mechanisms that could explain this association have been investigated. The host response to the presence of periodontal pathogens may trigger the production of inflammatory mediators such as C-reactive protein, tumor necrosis factor (TNF)-α, prostaglandin E2 (PGE2), interleukin (IL)-1β, and IL-6, which can accelerate the progression of pre-existing atherosclerotic plaques and are related to an increased number of adverse cardiovascular events. Also, several studies demonstrated the ability of periodontal pathogens to induce platelet aggregation and the formation of atheroma.[
<xref ref-type="bibr" rid="ref21">21</xref>
<xref ref-type="bibr" rid="ref22">22</xref>
]</p>
<p>Myocardial infarction (MI) has been associated with acute systemic bacterial and viral infections.[
<xref ref-type="bibr" rid="ref23">23</xref>
] A systematic review published in 2003 (Scannapieco
<italic>et al</italic>
., 2003) studied the evidence supporting the association between periodontal disease (PD) and CVD. Thirty-one human studies were selected. The authors concluded that periodontal disease may be modestly associated with atherosclerosis, MI, and cardiovascular events. In cross-sectional studies of patients with acute MI or confirmed CHD compared with control patients, MI patients had significantly worse dental health (periodontitis) than the controls ( Janket
<italic>et al</italic>
., 2003, Mattila
<italic>et al</italic>
., 1989, 1993). This association between poor oral health and MI was independent of known risk factors for heart disease such as age, cholesterol levels, hypertension, diabetes, and smoking. Cross-sectional studies thus suggest a possible link between periodontal disease and CHD.</p>
<p>The established risk factors do not fully account for the risk of stroke. Periodontitis is associated with elevated markers of inflammation that are themselves indicators of stroke risk. Armin
<italic>et al</italic>
., 2004, Joshipura
<italic>et al</italic>
., 2003, Morrison
<italic>et al</italic>
., 1999, and Wu
<italic>et al</italic>
., 2000, found significant associations between stroke and periodontal disease.</p>
</sec>
<sec id="sec2-2">
<title>Periodontal disease and diabetes mellitus</title>
<p>Diabetes is a group of metabolic diseases characterized by hyperglycemia and results from either a deficiency in the secretion of insulin and/or reduced insulin action.[
<xref ref-type="bibr" rid="ref21">21</xref>
] The interrelationship between diabetes and periodontal disease is established through a number of pathways and is bidirectional. One of the mechanisms to explain the relationship between diabetes mellitus and periodontal disease suggests that the presence of periodontal disease may induce or perpetuate a state of chronic systemic inflammation, as demonstrated by the increase in the C-reactive protein, IL-6, IL-1, and fibrinogen levels found in individuals with periodontitis. Periodontal infection may elevate the state of systemic inflammation and exacerbate the resistance to insulin, as the inflammatory process induces this resistance. Furthermore, it may induce increased levels of IL-6 and TNF-α, which is similar to obesity inducing or exacerbating the resistance to insulin.[
<xref ref-type="bibr" rid="ref24">24</xref>
]</p>
<p>Diabetes increases the risk for and severity of periodontal diseases and periodontal disease is considered as the
<italic>sixth complication</italic>
of diabetes.[
<xref ref-type="bibr" rid="ref25">25</xref>
] The synergism between diabetes and periodontal disease has been demonstrated in a number of studies. It has been made clear that effective periodontal treatment can improve some complications of diabetes, especially hyperglycemia, and that severe periodontitis is associated with poor blood sugar control. Periodontal treatment improves blood sugar control, especially in individuals with type 2 diabetes, and its association with low glycated hemoglobin levels has been demonstrated. In a longitudinal study (Taylor
<italic>et al</italic>
. 1996) of patients with type 2 (non–insulin-dependent) diabetes, severe periodontitis was associated with significant worsening of glycemic control over time. Periodontal treatment designed to decrease the bacterial insult and reduce inflammation might restore insulin sensitivity over time, resulting in improved metabolic control (Mealey 1996, 1999).</p>
</sec>
<sec id="sec2-3">
<title>Periodontal disease and pregnancy outcome</title>
<p>It has been observed that oral infections may increase the risk of low birth weight (LBW). LBW is defined, according to the international definition established by the World Health Organisation in 1976, as a birth weight lower than 2500 g.</p>
<p>The etiology of preterm birth (PB) is multifactorial, but inflammation is the common pathway that leads to uterine contractions and cervical changes with or without premature rupture of membranes. Inflammation associated with PB can be mainly attributable to intrauterine infection and bacterial vaginosis, and the latter accounts for up to 40% of the cases of spontaneous preterm labor and PB. There is also a causal relationship between bacterial vaginosis and PB and the presence of significantly higher levels of proinflammatory cytokines and prostaglandins in the amniotic fluid.[
<xref ref-type="bibr" rid="ref26">26</xref>
] Biological plausibility of the link between both conditions, periodontal disease and PB, does exist and can be summarized in three potential pathways. One of them refers to the hematogenous dissemination of inflammatory products from a periodontal infection, while the second potential pathway involves the fetomaternal immune response to oral pathogens. The third pathway proposed to explain the theoretical causal relationship between periodontal disease and PB involves bacteremia from an oral infection.</p>
<p>In 2007, Vergnes and Sixou published a systematic review where they concluded that PD may be an independent risk factor of PB or LBW. Association does not imply causation, and it seems important to consider the possibility that there is some underlying mechanism causing both PD and adverse pregnancy outcomes.[
<xref ref-type="bibr" rid="ref27">27</xref>
]</p>
</sec>
<sec id="sec2-4">
<title>Periodontal disease and respiratory infections</title>
<p>Respiratory diseases is the term for diseases of the respiratory system, including lung, pleural cavity, bronchial tubes, trachea, and upper respiratory tract. They range from a common cold to life-threatening conditions such as bacterial pneumonia or chronic obstructive pulmonary disease (COPD), which are important causes of death worldwide.[
<xref ref-type="bibr" rid="ref21">21</xref>
] There is increasing evidence that a poor oral health can predispose to respiratory diseases, especially in high-risk patients (nursing home residents, older subjects, intensive care unit patients, and hospitalized individuals requiring mechanical ventilation). The oral cavity is contiguous with the trachea and may be a portal for respiratory pathogen colonization. Dental plaque can be colonized by respiratory pathogens, which may be aspirated from the oropharynx into the upper airway and then reach the lower airway and adhere to bronchial or alveolar epithelium.</p>
<p>In 2003, Scannapieco
<italic>et al</italic>
. conducted a systematic literature review to examine whether the rate of pneumonia in high-risk populations is reduced by interventions that improve oral hygiene. They found an association between periodontal disease and pneumonia and a potential association between periodontal disease and COPD in several studies.[
<xref ref-type="bibr" rid="ref28">28</xref>
]</p>
</sec>
</sec>
<sec id="sec1-8">
<title>INTEGRATION OF PERIODONTAL MEDICINE IN CLINICAL PRACTICE</title>
<p>The concept of periodontal diseases as localized entities affecting only the teeth and supporting structures is oversimplified and in need of revision. Rather than being confined to the periodontium, periodontal diseases may have wide-ranging systemic effects. In most persons, these effects may be relatively inconsequential or at least not clinically evident. In susceptible individuals, however, periodontal infection may act as a risk factor or may be involved in the basic pathogenic mechanisms of these conditions. Furthermore, periodontal disease may exacerbate existing systemic disorders. Patient education is a priority. In the realm of periodontal medicine, patient education must emphasize the nature of periodontal infections, the increased risk for systemic disease associated, and the biologically plausible role periodontal infection may play in systemic disease. Most reliable origin of information should be the dental and medical professionals through daily contact with patients. Increased appreciation of the potential effects of periodontal infection on systemic health may result in increased patient demand for periodontal evaluation.</p>
</sec>
</body>
<back>
<fn-group>
<fn fn-type="supported-by">
<p>
<bold>Source of Support:</bold>
Nil</p>
</fn>
<fn fn-type="conflict">
<p>
<bold>Conflict of Interest:</bold>
None declared</p>
</fn>
</fn-group>
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