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3 CEUs
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and assistants.
The Significance of
Periodontal Infection
in Cardiology
A Peer-Reviewed Publication
Written by Stanley Shanies, MD, FACP and Casey Hein, BSDH, MBA
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Reprinted from Grand Rounds, May 2006, Vol. 1, No. 2. This course has been made possible through an unrestricted educational grant. The cost of this CE course is $59.00 for 3 CEUs.
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2. Educational Objectives eromas which result in myocardial infarction (MI) and stroke.1,2
Upon completion of this course, the clinician will be able to do It is the atherosclerotic lesion that amplifies the risk for CVD.
the following: Is human atherosclerosis an inevitability of aging? The
1. Understand the risk factors associated with hypothesis that human atherosclerosis is not an absolute conse-
cardiovascular disease quence of aging and can be reversed was put forth in the 1980s
2. Understand the role of infection in the developing by Malinow’s pioneering work aimed at halting the progression
atherosclerotic lesion and understand the evolution of of atherosclerosis and promoting its regression.3,4 Mounting
these lesions evidence appears to strengthen Malinow’s hypothesis that old
3. Understand the association of periodontal disease with age may not necessarily equate to atherosclerosis. A recent
cardiovascular disease study of more than 1,000 participants with a mean age of 73
4. Understand the role of dental professionals in screening found that for older adults, periodontal disease, which is one of
patients for cardiovascular disease the infections implicated as a cause of endothelial injury leading
to atherosclerosis, is a modifiable risk indicator for elevated lev-
Abstract els of systemic inflammatory markers, including interleukin-6
Molecular and cellular biology and the physiologic mechanisms (IL-6), tumor necrosis factor (TNF- ), and hsCRP.5 All
of disease constitute the basis of treatment in both cardiology three of these markers are widely recognized as being associated
and periodontics. Recognizing inflammation as the common with periodontal infection.6–8 The question becomes, “Could
denominator in the pathobiology of cardiovascular and peri- treatment of periodontal disease in patients both at an earlier
odontal disease provides an excellent opportunity for dental stage and age translate into greater longevity?”
and medical professionals to collaborate on decreasing patients’
risk for cardiovascular disease (CVD), or its progression. This Challenges in Decreasing the
article focuses on empowering dental and medical professionals Incidence and Severity of CVD
to incorporate the latest evidence on the relationship of peri- More than 20 years have passed since Malinow tackled CVD.
odontal and cardiovascular disease by presenting an in-depth With an array of therapeutic strategies at hand, many health-
view of the inflammatory process involved with atherosclerosis. care providers hoped that CVD would be eliminated by the end
Further, this article will discuss the significance of infections of the 20th century. At the beginning of the 21st century, despite
such as periodontal disease in increasing the systemic inflamma- cardiologists’ recommendations to patients for therapeutic
tory burden and risk for atherosclerosis and, thereby, increasing lifestyle changes targeting classic risk factors — a diet restricted
the risk for CVD. In addition, a rationale for why periodontal in calories to reach a body mass index of <25 kg/m2; a waist
disease should be considered a risk correlate of CVD is pre- circumference <105 cm in men and <90 cm in women; physical
sented. Also discussed is the use of the Framingham CVD exercise, smoking cessation, and blood pressure control; and
risk assessment instrument and high-sensitivity C-reactive the widespread use of statins in treating hypercholesterolemia
protein (hsCRP) testing in dental practices and screening for — CVD still accounts for 38% of all deaths in North America.2
periodontal disease in medical practices. This article concludes Largely because of its rapidly increasing prevalence in Eastern
by challenging readers to realize the undeniable therapeutic Europe and developing countries, and the obesity trends and
opportunity of medical-dental collaboration in reversing the rising incidence of diabetes in the West, coronary heart disease
rather somber trends in CVD. (CHD) is expected to be the main cause of death globally.9
Citation: Shanies, S. Hein, C. The significance of peri- However, about half of patients presenting with MI do not have
odontal infection in cardiology. Grand Rounds Oral-Sys Med. classic risk factors for CVD.10 CVD was once thought of as a
2006;1:24– 33. disease primarily induced by accumulation of lipid-laden cells.
(A complimentary copy of this article may be downloaded at What we now know is that high cholesterol is important in only
www.thesystemiclink.com.) 50% of patients with coronary artery disease (CAD).1 “Even
Key words: Periodontitis, cardiovascular disease, bacteria, with intensive statin therapy, the best current evidence-based
inflammation, risk factors treatment available, many patients will still have recurrent
cardiovascular events.”11 Although statin therapies have been
Introduction successful for a large segment of the population, it appears that
Most of us have heard the refrain from an old song, “The ankle the medical community may need to pursue approaches beyond
bone is connected to the leg bone.” Can we now sing, “The statins to modify the course of vascular diseases.11
gums are connected to the heart?” As unlikely as this may Hardly daunted by the most progressive disease-manage-
sound, researchers and clinicians may have ample evidence ment strategies, the prediction, prevention, and treatment of
to support this claim. Pilot intervention studies are now un- CVD represents one of the greatest challenges facing all of
derway, but should we wait for those final answers before we us in the health-care arena. This dismal revelation begs an
consider periodontal disease as a risk correlate for CVD? And, important question: “If we are to implement the recommen-
if we move ahead now, how do health-care providers implement dations made by the Surgeon General in the Oral Health in
the current evidence? America report,12 already five years old, and achieve the target
Cardiologists and dental professionals appear to have a goals set by the Centers for Disease Control and Prevention,13
common enemy — chronic inflammation and its potential to should we include in risk assessments for CVD those factors
accelerate the process of atherosclerosis, a widely recognized associated but that, at present, are not proven to be causative,
prelude to cardiovascular diseases. Science is beginning to re- independent, or quantitative?
veal that destructive inflammatory periodontal diseases release The answer may be “yes,” but this level of comprehensive
substances that are involved in arterial wall inflammation, care will require medical and dental professionals who are
development of atherosclerosis, and rupture of established ath- willing to champion this message and initiate models of collab-
2 www.ineedce.com

3. Once coronary atherosclerosis is clinically manifested, the risk
Table 1
Factors Associated With Increased Risk for CVD. 15 for future coronary events is much higher than that for patients
(Correlated to the Framingham Heart Study.) without CVD, regardless of other risk factors.15 Therefore, the
Framingham scores no longer apply.15
Should periodontal disease be added to this list? When considering the various risk factors for CHD (Table
1), it is important to understand that major risk factors are ad-
Major Independent Risk Factors ditive in predictive power in that total risk can be estimated by
• Advancing age the summation of the individual risks related to each factor.15
• Cigarette smoking However, the major risk factors for CVD as identified in Table
• Diabetes 1 do not account for all the variations in the incidence and se-
verity of CVD. Accordingly, it is important to point out that
• Elevated blood pressure
other, less well documented risk factors for CVD may play a
• Elevated serum total (and LDL) cholesterol
significant role.16
• Low serum HDL cholesterol A strong argument may be made that periodontal disease
Predisposing Risk Factors
should be considered both a predisposing and a conditional
risk factor for CVD. Predisposing risk factors are agents that
• Abdominal obesity§
worsen independent risk factors.15 The bidirectional relation-
• Ethnic characteristics
Periodontal ship between periodontal disease and diabetes would seem to
• Family history of premature qualify periodontal disease as a predisposing risk factor for
coronary heart disease disease?
diabetic complications.17–21 Conditional risk factors are associ-
• Obesity†§ ated with an increased risk for CVD, although their causative
• Physical inactivity† contributions to CVD have not been well documented.15 Such
• Psychosocial risk factors is the case for the correlation between periodontal disease and
increased risk for atherosclerosis. The presence of predisposing
Conditional risk factors and conditional risk factors in the assessment of risk for CVD
• Elevated serum homocysteine may confer greater risk than revealed from the summation of
• Elevated serum lipoprotein (a) the major risk factors.15 Although their contribution has not
• Elevated serum triglycerides been quantified, this does not mean that they do not make an
• Inflammatory markers (e.g. C-reactive protein) independent contribution to risk when they are present.15 Ac-
• Prothrombotic factors (e.g. fibrinogen) cordingly, what may be left off this list of risk factors in Table
• Small LDL particles 1 is the contribution of periodontal infection in accelerating
atherosclerosis eventuating in CVD.
† These risk factors are defined as major risk factors by the American Heart Association During the last 20 years there has been significant progress
§ Body weights are currently defined according to BMI as follows: normal weight 18.5 in understanding the link between periodontal infections and
kg/m 2 to 24.9 kg/m 2; overweight 25 kg/m 2 to 29 kg/m 2; obesity >30.0 kg/m 2; (obesity
class I 30.0 kg/m 2 to 34.9 kg/m 2; class II 35.9 kg/m 2 to 39.9 kg/m 2, class III ≥50 kg/m 2). risk for CVD such as heart disease22, stroke, and peripheral vas-
Abdominal obesity is defined according to waist circumference: men >102 cm (>40") culature disease, all of which share atherosclerosis as a common
and women >88 cm (>35").
feature.16,23 Recent research found bacterial levels were elevated
in only those patients with a history of myocardial infarction,
orative care. The intervention trials necessary to prove a cause- suggesting that increased loads of subgingival bacteria present
and-effect relationship between periodontal disease and CVD a danger for systemic health.24
are currently underway or about to be funded. Accumulation of The growing research to support the contribution of peri-
that evidence will take years. In the meantime, do we not have odontal infection to the inflammatory burden is theorized to
enough evidence to support periodontal disease at least as a risk be through both a direct action on blood vessel walls, and by
correlate for CVD? indirectly inducing the liver to produce acute phase proteins
The prevalence of both periodontitis and atherosclerosis is (e.g., CRP) (Figure 1).25 Until recently, DNA footprints com-
rampant. Periodontal disease is a “preventable [and treatable] prised the bulk of evidence suggesting that periodontal bacteria
contributor to the burden of cardiovascular disease,”14 and as were directly involved in atherosclerosis. However, research at
such, is a modifiable risk factor — a fact that may be escaping the University of Florida has demonstrated that Porphyromonas
the attention of both medical and dental professionals. If only gingivalis (P. gingivalis) and Actinobacillus actinomycetemcomi-
a marginal association between these two diseases is found, tans (A. actinomycetemcomitans) are capable of adapting to the
prevention and treatment of periodontal disease may have an vasculature to live in human atherosclerotic lesions.26 On the
impact on the prevalence of CVD. It is not premature to include medical side, a study recently reported in the American Heart
periodontal disease as a risk correlate for CVD, and failure to do Journal found that periodontal disease is common in patients
so may forfeit an important therapeutic opportunity to reduce with MI and associated with elevated hsCRP levels typical
or eliminate a modifiable risk factor for CVD. of an enhanced systemic inflammatory response.27 These as-
sociations were found to be independent of other contributing
Quantifying Risk for CVD factors.27 Other studies indicate an association between peri-
Table 1 classifies various risk factors according to their quanti- odontal disease and elevated hsCRP and IL-6, and, conversely,
tative association with CVD as elucidated by the Framingham that periodontal treatment lowered hsCRP and IL-6 with a si-
Heart Study, which estimates risk for people without clinical multaneous improvement in endothelial function.28 As compel-
manifestations of CVD. Scores derived from the Framingham ling as this research may be, the truth is that the evidence only
risk assessment only apply to the primary prevention of CVD.15 supports, but does not prove, a causal association between peri-
www.ineedce.com 3

4. There are many studies to support the specific correlation
Figure 1 ¥ of periodontal infection and atherosclerosis, and a few more
Model for systemic spread of periodontal recent pieces of evidence merit mention. Various studies have
infection and effects on the vasculature
implicated P. gingivalis, a virulent periodontal pathogen, as
part of a transient bacteremia that can lead to the direct inva-
Periodontal sion of blood vessels.30 In addition, P. gingivalis is implicated
Direct Indirect in several steps involved in the formation of the atherosclerotic
Effect Infection Effect
lesion.31,32 In 2003, it was reported that subjects with advanced
Bacteria periodontal disease exhibited endothelial dysfunction and evi-
or LPS dence of systemic inflammation (elevated serum CRP levels),
Monocytes
Monophages Liver placing them at increased risk for CVD.33 More recently, there
is serological evidence that an infection caused by P. gingivalis
increases the risk for MI; high P. gingivalis antibody levels have
IL-1, IL-6 CRP, fibrinogen, been shown to predict MI independently of classical cardiovas-
TNF lipid abnormalities, cular risk factors,34 and infection caused by major periodontal
coagulation factors
pathogens may be associated with future stroke.35 Periodontal
Vascular disease was found to be a treatable, independent risk factor for
Lesion cerebral ischemia in male subjects (<60 years of age). Those
with severe periodontitis had a 4.3 times greater risk of cere-
¥ Reprinted from Periodontics: Medicine, Surgery, and Implants, Rose LF, Mealey BL, Genco bral ischemia than subjects with mild periodontitis or healthy
RJ, Cohen DW, pg 848, Copyright 2004, with permission from Elsevier. subjects.36 Gingivitis and severe radiological bone loss were
also independently associated with the risk of cerebral ischemia
odontal disease and atherosclerosis-related diseases. Until this while tooth decay was not.36
etiological mystery is decoded, we are faced with the dilemma A recent investigation demonstrated a direct relationship
of how to implement treatment strategies that are supported by between microorganisms from periodontal infection and sub-
the existing body of evidence. clinical (undetected) atherosclerosis.37 This relationship was
Although a combination of risk factors may contribute to the found to be independent of hsCRP.37 The same research found
progression of an atherosclerotic lesion, researchers now consider that bacteria causally related to periodontitis are related to in-
infection to be a significant inflammatory stimulus.28 Inflamma- creased carotid intima-media thickness (IMT),37 an important
tion is directly implicated in destabilization of atherosclerotic marker of early atherosclerosis. This was true even after adjust-
plaque in the carotid artery1 and may lead to aneurism and embo- ing for conventional risk factors (i.e., age, race/ethnicity, body
lism.1 Seeding of live periodontal bacteria from the oral cavity to mass index (BMI), smoking, diabetes, systolic blood pressure,
vessel walls,26 a hyperinflammatory response to those periodontal LDL, and high-density lipoprotein [HDL] cholesterol),37 pro-
pathogens,29 and activation of proinflammatory mediators are viding even more evidence of a direct role of certain infections in
three biological mechanisms implicated in the induction of a the pathogenesis of atherosclerosis. The same study found that
systemic inflammatory response.26 This chain of events may white blood cell values tend to rise with both increasing levels of
describe the link between periodontal disease and CVD. periodontopathic bacteria and increased carotid IMT.37 Similar
To fully understand the significance of periodontal dis- research findings continue to accumulate, strengthening the
ease in the cascade of events implicated in the formation of evidence that inflammation, either direct or from a distance (as
an atherosclerotic lesion, it is important that dental practi- in periodontal disease) is a primary etiology for affecting altera-
tioners understand that infection is a well-established risk tions in endothelial function which, left untreated, eventually
factor for atheroma formation and thromboembolic events.16 develops into an atherosclerotic lesion.
To that end, discussion and illustration of the role of infec- An atheroma forms in the arterial wall as a result of inflam-
tion in the developing atherosclerotic lesion may help read- mation.1 The atheroma is made up of smooth muscle prolif-
ers gain a more comprehensive understanding of this cascade eration in the media of the arterial wall.1 Other infl ammatory
of pathological events. changes in the media are seen distorting the anatomy of the
arterial wall.1 This is covered by a fibrous cap on the luminal
The Contribution of Infection in the surface narrowing the lumen to a greater or lesser extent,
Developing Atherosclerotic Lesion depending on the circumstances.38 Some feel that distortion
It is known that atherosclerosis is the main cause of CVD.1,2 Pos- is more dangerous than luminal stenosis.38 Over time, the
sible causes of the endothelial dysfunction that lead to athero- fibrous cap thins and ruptures with matrix metalloprotein-
sclerosis include elevated and modified low density lipoprotein ases (MMPs) playing a role in the degradation of the collagen
(LDL); free radicals caused by cigarette smoking; hypertension within the fibrous cap.38 This presents a rough surface to
and diabetes; genetic alterations; and elevated plasma homo- flowing blood in the lumen.38 Platelets adhere to this surface
cysteine concentrations.1 Most germane are the studies that under the influence of adhesion factor activity, causing a
have also linked infection to atherosclerotic-induced diseases. coagulation cascade leading to an occluding clot, cutting off
What has become apparent is that several types of microbial all blood flow.38 This results in stroke or MI, depending on
pathogens may contribute to atherosclerosis, making it highly the location.38
unlikely that a single microbe causes atherosclerosis.2 It is now Ross wrote a 1999 review article in the New England Jour-
thought that the cumulative burden of infection at various sites nal of Medicine titled “Atherosclerosis — An Inflammatory
is what affects the progression of atherosclerosis and its clinical Disease,” which is used in teaching institutions to provide a
manifestations of CVD.2 step-by-step description of the development of the atheroscle-
4 www.ineedce.com

5. Figures 2 –5: Evolution of the atherosclerotic lesion
Figure 2 — Endothelial dysfunction in atheroslerosis. 1 Figure 3 — Fatty-streak formation in atherosclerosis. 1
The earliest changes preceding the formation of atherosclerotic lesions Fatty streaks initially consist of lipid-laden monocytes and macrophages
involve the endothelial lining of the vessel lumen. The changes include (foam cells) together with T-lymphocytes. Later, they are joined by in-
increased endothelial permeability that leads to acculumation of lipo- creasing numbers of smooth muscle cells, some of which may also contain
proteins and development of the fatty streak; up-regulation of endo- varying amounts of lipid. The increasing population of smooth muscle
thelial adhesion molecules that facilitate the aggregation of monocytes, cells is promoted by various growth factors, such as Platelet-Derived
T-lymphocytes, and blood platelets; and endothelial/platelet interactions Growth Factor (PDGF), Fibroblast Growth Factor (FGF), and Transforming
resulting in the release of growth factors that, in turn, promote progres- Growth Factor-ß (TGF-ß).
sive development of the lesion.
Figure 4 — Formation of an advanced, complicated lesion Figure 5 — Unstable fibrous plaques in atherosclerosis. 1
of atherosclerosis. 1 Rupture or ulceration of the fibrous cap can lead to hemorrhage and
Intermediate and advanced atherosclerotic lesions are characterized by a thrombosis and usually occurs at sites where the connective tissue layer is
fatty streak covered by a fibrous connective tissue cap. The cap represents thin. Thinning of the fibrous cap is apparently because of the continuing
a healing response to injury and forms a barrier between the underlying influx and activation of macrophages, which release metalloproteinases
lesion and the vessel lumen. The fibrous connective tissue layer is infil- and other proteolytic enzymes. The enzymes degrade collagen and non-
trated by lipid-filled macrophages and smooth muscle cells, all of which collagenous matrix proteins, which then leads to hemorrhage, thrombus
cover a mixture of leukocytes, extracellular lipids, and debris that, in turn, formation, and occlusion of the vessel. In some cases, an embolus of
may form a necrotic core. clotted blood may be released and occlude a downstream vessel.
Medical illustrations used with permission from the New England Journal of Medicine

6. rotic lesion.1 In this review, Ross detailed the atherosclerotic dental practices has the potential to become a significant tool
process beginning with endothelial dysfunction, the formation for identification of patients at risk for CVD. This may be
of the fatty streak, and then the formation of the advanced especially valuable in primary prevention of CVD. Current
complicated atherosclerotic lesion, ending with how unstable research considers subclinical (undetected) inflammation to be
fibrous plaque can rapidly lead to thrombosis. Illustrations and an accelerant of vascular inflammation and markers of inflam-
accompanying explanations of the contribution of infection in mation (both systemic and local), which, in turn, appear to play
the atherosclerotic process are provided in Figures 2 to 5 to help a central role in the development and progression of atheroscle-
readers better understand the pathobiological cascade of events rosis.10 Indeed, many patients seen by health-care professionals
implicated in the formation of an atherosclerotic lesion. are at increased risk for MI or stroke because of undiagnosed
and asymptomatic atherosclerosis which may be accelerated by
Making the Case for hsCRP Testing chronic periodontal infection.
in Dental Practices In 2002, the Centers for Disease Control and Prevention
It is becoming increasingly clear that the variety of cardiovas- and the American Heart Association held a conference to
cular events cannot be explained by a single pathobiological examine (among other things) the selection and use of inflam-
pathway. The relationship between novel biological markers matory markers to predict CVD risk. Recommendations made
of inflammation and traditional risk factors, such as high blood at the conference which have specific relevance to the present
pressure, smoking, obesity, diabetes, low levels of physical discussion follow:42
activity, and use of hormone-replacement therapy, may be of
variable importance for individual patients.39 This has spawned 1) Of all the inflammatory markers identified, hsCRP, as an
a search for other factors that may be implicated and, when independent marker of risk, may be used at the discretion of
present, help to identify patients at greater risk for MI and other the physician as part of an office-based global risk assessment
cardiovascular events.10 Certain markers of inflammation (sys- (i.e., the Framingham Heart Study) in adults without
temic and local) appear to play a central role in the development known CVD. HsCRP may identify those patients for further
and progression of atherosclerosis.10 HsCRP, one of the acute- intervention or therapy in the primary prevention of CVD.42
phase proteins produced by the liver in response to infection, is
a specific systemic marker of vascular inflammation that appears Dental professionals also are well-positioned to assist pa-
to have a strong association with adverse vascular events.39 tients in assessing their global risk for CVD through use of an
Both hsCRP and LDL cholesterol levels are elevated in assessment such as the Framingham instrument.
people at risk for cardiovascular events. However, hsCRP
and LDL cholesterol measurements tend to identify different 2) Testing for hsCRP provides an additive element to global risk
high-risk groups.39 Researchers have found that independent assessment. As a result, patients without known CVD who
effects were observed for hsCRP in analyses adjusted for all were not previously considered to be at risk will be identified
components of the Framingham risk score39 (i.e., traditional and targets for more aggressive risk reduction interventions.
risk factors for CVD). Specifically, hsCRP and LDL choles- It was recommended that hsCRP be measured in patients who
terol levels are minimally correlated and hsCRP has been found are at intermediate risk of CHD per 10 years (as indicated
to be a stronger predictor of future cardiovascular events than in global risk assessment) to direct further evaluation and
LDL cholesterol.39 This advantage persisted after adjusting for therapy in the primary prevention of CVD.42
all traditional cardiovascular risk factors and included the effect
of hormone-replacement therapy at baseline.39 The researchers A good example of this would be a patient who has been
further concluded that the combined evaluation of both hsCRP identified by a dental professional as being at intermediate risk
and LDL cholesterol proved to be a superior method of detect- of CVD via global risk assessment such as the Framingham risk
ing risk for cardiovascular events than measurement of either assessment. For example, if a person’s cardiovascular risk score
biological marker alone.39 — judged by global risk assessment — is low (the possibility
What is the normal range of hsCRP level? 40 of developing CVD is <10% in 10 years), hsCRP testing is not
• If hsCRP level is lower than 1.0 mg/L, a person has a low immediately warranted.39 If the risk score is in the intermediate
risk of developing cardiovascular disease. range (10% to 20% in 10 years), such a test can help predict a
• If hsCRP is between 1.0 mg/L and 3.0 mg/L, a person has cardiovascular and stroke event and help direct further evalua-
an average risk. tion and therapy.39 However, the benefits of such therapy based
• If hsCRP is higher than 3.0 mg/L, a person is at high risk. on this strategy remain uncertain.39 If a dental professional
intercepts a person with a high risk score (>20% in 10 years)
Low-grade chronic inflammation as measured by hsCRP or established heart disease or stroke, this is an individual who
predicts future risk of acute coronary syndromes independent should receive intensive medical care regardless of hsCRP lev-
of traditional cardiovascular risk factors.41 Because periodontal els38 and should be triaged to the care of a cardiologist as soon
infection appears to be a source of low-grade chronic infec- as possible.
tion, the use of hsCRP testing in dental practices provides an
excellent opportunity for identifying patients at risk for acute 3) It was recommended that patients with persistently
coronary syndromes. unexplained marked elevation of hsCRP (>10 mg/L) after
repeated testing should be evaluated for noncardiovascular
The Role of Dental Professionals in causes, such as infection and inflammation.42
Screening Patients for CVD Risk —
Along with monitoring blood pressure, which has long been These are the types of patients cardiologists should refer to
routine in practice, the addition of chairside hsCRP testing in periodontists to be examined for periodontal disease.
6 www.ineedce.com

7. 4) It was suggested that detection of an elevated hsCRP plaque), which ultimately leads to rupture, in-situ thrombo-
might serve to motivate patients to adhere to better sis, and subsequent vascular events.46 Although larger studies
preventive therapies.42 are needed to investigate its potential to reduce the risk of
rupture of atherosclerotic plaque, it appears that subantimi-
This might be the case for a prediabetic patient whose crobial doses of doxycycline, approved by the U.S. Food and
hsCRP is tested by a dental hygienist chairside and discovered Drug Administration for suppression of collagen-destroying
to be edging toward “high normal” (2 mg/L to 10 mg/L), which enzymes in the treatment of periodontal disease, may also
is predictive of heart disease. In this situation, a dental hygienist have cardioprotective benefits.46
has a valuable role to play in motivating that patient to adhere to
proper diet, physical fitness programs, compliance to medica- Conclusion
tion regimens, or, possibly, smoking cessation counseling. Despite the fact that the formation of the atherosclerotic le-
sion and its impending threat to cardiovascular health has a
Testing for hsCRP in Dental Practices very complex etiology, dental screening to identify patients
Is it time for dental professionals to screen patients for risk of at risk for CVD and those patients with diagnosed CVD who
future cardiovascular events by performing chairside testing are at greater risk for recurrent cardiovascular events offers
for hsCRP? Yes, and those technologies are now entering the an undeniable intervention opportunity. Likewise, physi-
health-care market. cians have an enormous part to play by screening patients
The cardiologist who co-authored this article frequently for periodontal disease.
asks new patients who have heart disease or who are at high For patients at intermediate risk (10% to 20% risk of
risk for heart disease when they last saw their dentists, and CHD per 10 years) as defined by the Framingham risk score,
whether they were examined for periodontal disease. He also testing for hsCRP may help direct further evaluation and
visually examines the gingival tissue and general conditions of therapy in primary prevention for CVD.47 For patients with
the teeth. An example of collaborative care involves a young, stable coronary disease and acute coronary syndromes, in-
non-obese female patient with an elevated hsCRP, but normal office testing in dental practices for hsCRP may prove to be
serum lipids and blood pressure, who presented with severe invaluable in identifying those patients who require signifi-
gingival inflammation. The cardiologist referred this patient cantly more aggressive therapies provided by cardiologists.
to a periodontist. Four months later, following periodontal Although the cardioprotective benefits of periodontal
therapy, her hsCRP was normal. treatment remain speculative at present, awareness of the re-
The cardioprotective benefits of periodontal treatment lationship between the increased burden of infectious agents
may represent an efficacious modification to contemporary and systemic inflammation may have a significant effect
therapies for vascular diseases. Several pilot studies have on the prevention and treatment of chronic inflammatory
shown that periodontal therapy consisting of scaling and root diseases and conditions. Transition toward interdisciplinary
planing and application of antimicrobial agents were effective health-care management must increase to better target those
in reducing levels of serum inflammatory markers, specifically at high risk and to devise a multidisciplinary integrated
hsCRP, IL-6, and TNF- .43,44 However, larger scale, random- care pathway for CVD. Those physicians and dentists who
ized interventional clinical trials are needed to investigate the collaborate on this integrated care pathway will be ahead of
potential cardiovascular benefits of periodontal therapy.7 If the curve.
future research provides evidence that treatment of periodon- It is not unusual to hear from physicians that they have
titis reduces hsCRP and/or decreases the incidence of CVD, seen patients with hyperparathyroidism, diabetes, osteopo-
this would provide a strong rationale for a change in health- rosis, and various other diseases that were first diagnosed in
care policy that would position periodontal care as medically the dental office. Indeed, astute dentists and dental hygien-
necessary for the prevention and management of CVD.7 In ists are often the first to note an undesirable side effect of
the meantime, it is time for physicians and other nondental calcium channel blockers (i.e. drug-induced gingival over-
health-care providers to begin to identify those patients who growth). Many within the medical profession also recognize
are at greater risk for periodontal disease because of their indi- the significant contributions of many dental professionals in
vidual risk profiles. Specifically, patients who smoke are at 3 to monitoring patients’ blood pressure. It is important to real-
7 times greater risk and patients with diabetes are at 2 to 5 times ize that we are now in an unprecedented era of explosion of
greater risk for developing periodontal disease.45 Patients who research related to periodontal medicine. For the well-being
report that a sibling or parent lost their teeth at an early age of our patients, the time has come for physicians, dentists,
may be genetically predisposed to periodontal disease with an nurses, and dental hygienists to work together to identify
odds ratio that confers 3 to 5 times greater risk for developing those at risk, both for atherosclerosis and periodontal dis-
periodontal disease.45 Those patients who both smoke and ease. Indeed, we are all treating “a patient,” not just one part
who are genotype positive have an 8 to 10 times greater risk or one organ.
for periodontal disease.45 These scenarios represent excellent It is interesting that the oldest medical school in the
opportunities for the medical community to screen for peri- world, the University of Bologna in Bologna, Italy (founded
odontal disease and triage patients to dental professionals for in 1088), still requires all medical students to take a one-year
evaluation and treatment of periodontal disease. course in oral medicine and dentistry. Nine hundred seven-
Discussion of the significance of periodontal infection teen years later, all physicians and dentists must realize that
in cardiology would be incomplete without mentioning the we treat an organism. The mouth is attached to the body and
potential role subantimicrobial doses of doxycycline may each may have an effect on the health of the other. We must
play in inhibiting MMPs. MMPs participate in degradation remember the ankle bone is connected to the leg bone and,
of the fibrous cap of an atherosclerotic lesion (the vulnerable indeed, the oral cavity is connected to the body.
www.ineedce.com 7

8. References levels. Am Heart J. 2004;147(6):1005–1009.
1. Ross R. Atherosclerosis — an inflammatory disease. N Engl J Med. 1999;340(2): 28. Offenbacher S, Beck J. A perspective on the potential cardioprotective benefits of
115–126. periodontal therapy. Am Heart J. 2005;149(6):950–954.
2. Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 29. Genco RJ, Offenbacher S, Beck J, et al. Cardiovascular disease and oral infections. In:
2005;352(16):1685–1695. Rose LF, Mealey BL, Genco RJ, et al (eds). Periodontal Medicine. Hamilton, Ontario,
3. Malinow MR. Atherosclerosis. Regression in nonhuman primates. Circ Res. Canada: BC Decker, Inc; 2000:71–74.
1980;46(3):311–320. 30. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation. 2002;105(9):
4. Malinow MR. Atherosclerosis. Progression, regression, and resolution. Am Heart J. 1135–1143.
1984;108(6):1523–1537. 31. Kuramitsu HK, Kang IC, Qi M. Interactions of Porphyromonas gingivalis with host cells:
5. Bretz WA, Weyant RJ, Corby PM, et al. Systemic inflammatory markers, periodontal implications for cardiovascular diseases. J Periodontol. 2003;74(1):85–89.
diseases, and periodontal infections in an elderly population. J Am Geriatr Soc. 2005 32. Miyakawa H, Honma K, Qi M, et al. Interaction of Porphyromonas gingivalis with
Sep;53(9):1532–1537. low-density lipoproteins: implications for a role for periodontitis in atherosclerosis. J
6. The Research, Science, and Therapy Committee of the American Academy Periodontol Res. 2004;39(1);1–9.
of Periodontology. The pathogenesis of periodontal diseases. J Periodontol. 33. Amar S, Gokce N, Morgan S, et al. Periodontal disease is associated with brachial artery
1999;70(4);457–470. endothelial dysfunction and systemic inflammation. Arterioscler Thromb Vasc Biol.
7. American Academy of Periodontology coordination meeting on oral health 2003;23(7):1245–1249.
and systemic health. Periodontal medicine: health policy implications. Geneva, 34. Pussinen PJ, Alfthan G, Tuomilehto J, et al. High serum antibody levels to
Switzerland, December 5 and 6, 2002. J Periodontol. 2003;74(7):1080–1095. Porphyromonas gingivalis predict myocardial infarction. Eur J Cardiovasc Prev Rehabil.
8. Noack B, Genco RL, Trevisan M, et al. Periodontal infections contribute to elevated 2004;11(5):408–411.
systemic C-reactive protein level. J Periodontol. 2001;72(9):1221–1227. 35. Pussinen PJ, Alfthan G, Rissanen H, et al. Antibodies to periodontal pathogens and
9. World Health Organization. The Atlas of Heart Disease and Stroke. 2005. Available stroke risk. Stroke. 2004:35(9):2020.
at: http://www.who.int/cardiovascular_diseases/resources/atlas/en/. Accessed 36. Grau AJ, Becher H, Ziegler CM, et al. Periodontal disease as a risk factor for ischemic
Dec 11, 2005. stroke. Stroke. 2004;35(2):496–501.
10. Koenig W. C-reactive protein: risk assessment in the primary prevention of 37. Desvarieux M, Demmer RT, Rundek T. Periodontal microbiota and carotid intima-media
atherosclerotic disease. Has the time come for including it in the risk profile? Ital Heart thickness; the oral infections and vascular disease epidemiology study (INVEST).
J. 2001;2(3):157–163. Circulation. 2005;111(5):576–582.
11. Cannon CP. The ideal cholesterol. JAMA. 2005;294(19):2492–2494. 38. Fuster V, Moreno PR, Fayad ZA, et al. Atherothrombosis and high risk plaque. Part I:
12. Satcher D. US Department of Health and Human Services. Oral Health in America: A Evolving Concepts. J Am Coll Cardiol. 2005;46(6):937–954.
Report of the Surgeon General. May 2000. Available at: http://www.surgeongeneral. 39. Ridker PM, Rifai N, Rose L, et al. Comparison of C-reactive protein and low-density
gov/library/oralhealth. Accessed Nov 18, 2005. lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J
13. US Department of Health and Human Services, Public Health Service. Healthy People Med. 2002;347(20):1557–1565.
2010 Progress Review-Heart Disease and Stroke. Available at: www.healthypeople. 40. American Heart Association. Inflammation, Heart Disease and Stroke: The Role of C-
gov/data/2010prog/focus12. Accessed April 15, 2005. Reactive Protein. Nov 2005. Available at: http://www.americanheart.org/presenter.
14. Beck JD, Elter JR, Heiss G, et al. Relationship of periodontal disease to carotid jhtml?identifier=4648. Accessed Nov 18, 2005.
artery intima-media wall thickness: The atherosclerosis risk in communities study. 41. Shishehbor MH, Bhatt DL. Inflammation and atherosclerosis. Curr Atheroscler Rep.
Atheroscler, Thromb, and Vasc Biology. 2001;21(11):1816–1822. 2004;6(2):131–139.
15. Grundy SM, Pasternak R, Greenland P, et al. AHA/ACC scientific statement: Assessment 42. Smith SC Jr, Anderson JL, Cannon RO, et al. CDC/AHA Workshop on Markers of
of cardiovascular risk by use of multiple-risk-factor assessment equations: a statement Inflammation and Cardiovascular Disease: Application to Clinical and Public Health
for health-care professionals from the American Heart Association and the American Practice: report from the clinical practice discussion group. Circulation. 2004;110(25):
College of Cardiology. J Am Coll Cardiol. 1999;34(4):1348–1359. E550–E553.
16. Jin LJ, Chiu GK, Corbet EF. Are periodontal diseases risk factors for certain systemic 43. D’Aiuto FD, Parkar M, Andreou G. Periodontitis and systemic inflammation: Control of
disorders—what matters to medical practitioners? Hong Kong Med J. 2003;9(1): the local infection is associated with a reduction in serum inflammatory markers. J
31–37. Dent Res. 2004;83(2):156–160.
17. Grossi SG, Genco RJ. Periodontal disease and diabetes mellitus: a two-way relationship. 44. Iwamoto Y, Nishimura F, Soga Y, et al. Antimicrobial periodontal treatment decreases
Ann Periodontol. 1998;3(1):51–61. serum C-reactive protein, tumor necrosis factor-α, but not adiponectin a levels in
18. Nishimura F, Takahashi K, Kurihara M, et al. Periodontal disease as a complication of patients with chronic periodontitis. J Periodontol. 2003;74(8):1231–1236.
diabetes mellitus. Ann Periodontol. 1998;3(1):20–29. 45. Cobb CM, Callan DP. Flashpoint in periodontics: patient referral. Triage. 2005;1(2):
19. Schmidt AM, Weidman E, Lalla E, et al. Advanced glycation endproducts (AGEs) 12–16.
induce oxidant stress in the gingiva: a potential mechanism underlying accelerated 46. Brown DL, Desai KK, Vakili BA, et al. Clinical and biochemical results of the
periodontal disease associated with diabetes. J Periodontol Res. 1996;31(7): metalloproteinase inhibition with subantimicrobial doses of doxycycline to prevent
508–515. acute coronary syndromes (MIDAS) pilot trial. Arterioscler Thromb Vasc Biol.
20. Ryan ME, Ramamurthy NS, Golub LM. Tetracyclines inhibit protein glycation in 2004;24(4):733–738.
experimental diabetes. Adv Dent Res. 1998;12(2):152–158. 47. Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and
21. Brownlee M. Glycation products and the pathogenesis of diabetic complications. cardiovascular disease: application to clinical and public health practice: a statement
Diabetes Care. 1992;15(12):1835–1843. for health-care professionals from the Centers for Disease Control and Prevention and
22. Dorfer CE, Becher H, Ziegler CM, et al. The association of gingivitis and periodontitis the American Heart Association. Circulation. 2003;107(3):499–511.
with ischemic stroke. J Clin Periodontol. 2004;31(5):396–401.
23. Fiehn NE, Larsen T, Christiansen N, et al. Identification of periodontal pathogens in Disclaimer
atherosclerotic vessels. J Periodontol. 2005;76(5):731–736. The authors of this course have no commercial ties with the
24. Dögan B, Buduneli E, Emingil G, et al. Characteristics of periodontal microflora in acute sponsors or the providers of the unrestricted educational grant
myocardial infarction. J Periodontol. 2005;76(5):740–748.
for this course.
25. Rose LF, Mealey BL, Genco RJ, et al (eds). Periodontics: Medicine, Surgery, and
Implants. St Louis, Mo: CV Mosby; 2004:848.
26. Kozarov EV, Dom BR, Shelburne CE, et al. Human atherosclerotic plaque contains Reader Feedback
viable invasive Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. We encourage your comments on this or any PennWell course.
Arterioscler Thromb Vasc Biol. 2005;25(3):E17–E18. For your convenience, an online feedback form is available at
27. Deliargyris EN, Madianos PN, Kadoma W, et al. Periodontal disease in patients with www.ineedce.com.
acute myocardial infarction: prevalence and contribution to elevated C-reactive protein
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9. Questions
1. About half of patients presenting 8. All the following statements are 14. If a person’s cardiovascular risk
with myocardial infarction, MI, true EXCEPT: score — judged by global risk
do not have “classic” risk factors a. If hsCRP level is lower than 2.0 mg/L, a person assessment — is in the intermediate
has a low risk of developing cardiovascular
for cardiovascular disease, CVD. disease within the next 10 years. range (10% to 20% in 10 years), what
One risk factor for MI that is not b. If hsCRP is between 1.0 and 3.0 mg/L, a person test/measurement can help predict
has an average risk of developing cardiovascular a cardiovascular and/or stroke event
currently considered a “classic” or
disease within the next 10 years.
major risk factor for CVD is: c. If hsCRP is higher than 3.0 mg/L, a person is and help direct further evaluation
a. Diabetes at high risk of developing cardiovascular disease and therapy?
b. Periodontal disease within the next 10 years. a. HbA1c
d. If hsCRP level is lower than 1.0 mg/L, a person b. HDL
c. Low serum HDL cholesterol
has a low risk of developing cardiovascular
d. Elevated LDL cholesterol c. hsCRP
disease within the next 10 years.
d. Blood pressure
2. CVD accounts for ___________ of 9. All the following are implicated in
15. ______________ play a role in the
all deaths in North America. the theorized relationship between
periodontal disease and a systemic degradation of collagen within the
a. 20%
b. 33% response EXCEPT: fibrous cap on the luminal surface
c. 38% a. A genetically programmed viral response that leads to rupture and thrombosis
d. 47% b. Activation of proinflammatory mediators of an atherosclerotic lesion.
c. A hyperinflammatory response to
a. MMPs
3. The intervention trials necessary to periodontal pathogens
d. Seeding of live periodontal bacteria from the oral b. Blood platelets
prove a cause-and-effect relation- cavity to vessel walls c. Fibroblast growth factor
ship between periodontal disease d. None of the above
10. Which of the following combina-
and CVD: 16. It has been recommended that
tions of bacteria did University of
a. Were completed in 1999 hsCRP be measured in patients
Florida researchers recently demon-
b. Will be completed at the end of 2006
strate are capable of adapting to the at intermediate risk of CHD per
c. Have not been contemplated at this time
vasculature and living within human ________ years.
d. Are currently underway or about to be funded
atherosclerotic lesions? a. Two
4. The earliest change preceding a. Streptococcus intermedius and Actinobacillus b. Five
actinomycetemcomitans c. Ten
the formation of atherosclerotic b. Porphyromonas gingivalis and Actinobacillus d. Twenty
lesions is: actinomycetemcomitans
a. Activation by macrophages c. Tannerella forsythia and Campylobacter rectus 17. Patients with diabetes are at
d. Prevotella intermedia and Treponema denticola
b. Increased endothelial permeability ___________ greater risk for
c. Infiltration by lipid-filled macrophages 11. One study found that individuals developing periodontal disease than
d. Increasing numbers of smooth muscle cells with severe periodontitis had a ____ non-diabetics.
times greater risk of ischemic stroke a. 1 to 3
5. The marker of vascular inflamma-
than subjects with mild periodontitis b. 3 to 7
tion that appears to be most closely
or healthy subjects. c. 2 to 5
associated with greater risk for a. 1.3 d. 2 to 7
myocardial infarction is: b. 2.3
a. TNF- c. 4.3 18. Subantimicrobial doses of
d. 4.5 ____________ may have cardio-
b. hsCRP
c. Cholesterol levels 12. White blood cell values tend to protective benefits.
d. Matrix metalloproteinases rise with: a. Penicillin
a. Increasing levels of periodontopathic bacteria b. Doxycycline
6. Biological mechanisms implicated in and increased carotid IMT c. Chlorhexidine gluconate
the induction of a systemic inflam- b. Increasing levels of periodontopathic bacteria d. Metronidazole
matory response include: and decreased carotid IMT
c. Decreasing levels of periodontopathic bacteria 19. The Framingham risk assessment
a. Activation of pro-inflammatory mediators and increased carotid IMT scores apply to:
b. Seeding of live periodontal bacteria from the oral d. None of the above
cavity to vessel walls a. Primary prevention of CVD
c. Seeding of live cariogenic bacteria to vessel walls 13. All the following are thought b. Secondary prevention of CVD
to play roles in endothelial c. Primary and secondary prevention of CVD
d. a and b
dysfunction that leads to d. None of the above
7. Periodontal infection is a atherosclerosis EXCEPT:
20. Elevated serum triglycerides are a:
well-established risk factor for a. Osteoporosis
b. Genetic alterations a. Predisposing risk factor
thromboembolic events. b. Conditional risk factor
c. Elevated plasma homocysteine concentrations
a. True d. Elevated and modified low density lipoprotein, c. Major risk factor
b. False LDL, cholesterol d. Dominant risk factor
www.ineedce.com 9

10. ANSWER SHEET
The Significance of Periodontal Infection in Cardiology
Name: Title: Specialty:
Address: E-mail:
City: State: ZIP:
Telephone: Home ( ) Office ( )
Requirements for successful completion of the course and to obtain dental continuing education credits: 1) Read the entire course. 2) Complete all
information above. 3) Complete answer sheets in either pen or pencil. 4) Mark only one answer for each question. 5) A score of 70% on this test will earn
you 3 CE credits. 6) Complete the Course Evaluation below. 7) Make check payable to PennWell Corp.
Mail completed answer sheet to
Educational Objectives Academy of Dental Therapeutics and Stomatology,
1. Understand the risk factors associated with cardiovascular disease A Division of PennWell Corp.
P.O. Box 116, Chesterland, OH 44026
2. Understand the role of infection in the developing atherosclerotic lesion and understand the evolution of these lesions
or fax to: (440) 845-3447
3. Understand the association of periodontal disease with cardiovascular disease
4. Understand the role of dental professionals in screening patients for cardiovascular disease
For immEdiatE results, go to www.ineedce.com
Course Evaluation and click on the button “take tests Online.” answer
sheets can be faxed with credit card payment to
Please evaluate this course by responding to the following statements, using a scale of Excellent = 5 to Poor = 0. (440) 845-3447, (216) 398-7922, or (216) 255-6619.
1. Were the individual course objectives met? Objective #1: Yes No Objective #3: Yes No P
ayment of $49.00 is enclosed.
(Checks and credit cards are accepted.)
Objective #2: Yes No Objective #4: Yes No
If paying by credit card, please complete the
2. To what extent were the course objectives accomplished overall? 5 4 3 2 1 0 following: MC Visa AmEx Discover
Acct. Number: _______________________________
3. Please rate your personal mastery of the course objectives. 5 4 3 2 1 0
Exp. Date: _____________________
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5. How do you rate the author’s grasp of the topic? 5 4 3 2 1 0
6. Please rate the instructor’s effectiveness. 5 4 3 2 1 0
7. Was the overall administration of the course effective? 5 4 3 2 1 0
8. Do you feel that the references were adequate? Yes No
9. Would you participate in a similar program on a different topic? Yes No
10. If any of the continuing education questions were unclear or ambiguous, please list them.
___________________________________________________________________
11. Was there any subject matter you found confusing? Please describe.
___________________________________________________________________
___________________________________________________________________
12. What additional continuing dental education topics would you like to see?
___________________________________________________________________
___________________________________________________________________ AGD Code 490
PLEASE PHOTOCOPY ANSWER SHEET FOR ADDITIONAL PARTICIPANTS.
AUTHOR DISCLAIMER INSTRUCTIONS COURSE CREDITS/COST RECORD KEEPING
The authors of this course have no commercial ties with the sponsors or the providers of All questions should have only one answer. Grading of this examination is done All participants scoring at least 70% (answering 14 or more questions correctly) on the PennWell maintains records of your successful completion of any exam. Please contact our
the unrestricted educational grant for this course. manually. Participants will receive confirmation of passing by receipt of a verification examination will receive a verification form verifying 3 CE credits. The formal continuing offices for a copy of your continuing education credits report. This report, which will list
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SPONSOR/PROVIDER credit. Please contact PennWell for current term of acceptance. Participants are urged to of receipt.
This course was made possible through an unrestricted educational grant. No EDUCATIONAL DISCLAIMER contact their state dental boards for continuing education requirements. PennWell is a
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All content has been derived from references listed, and or the opinions of clinicians. in this course and expressed herein are those of the author(s) of the course and do not from $49.00 to $110.00. Any participant who is not 100% satisfied with this course can request a full refund by
Please direct all questions pertaining to PennWell or the administration of this course to necessarily reflect those of PennWell. contacting PennWell in writing.
Machele Galloway, 1421 S. Sheridan Rd., Tulsa, OK 74112 or macheleg@pennwell.com. Many PennWell self-study courses have been approved by the Dental Assisting National
Completing a single continuing education course does not provide enough information Board, Inc. (DANB) and can be used by dental assistants who are DANB Certified to meet © 2008 by the Academy of Dental Therapeutics and Stomatology, a division
COURSE EVALUATION and PARTICIPANT FEEDBACK to give the participant the feeling that s/he is an expert in the field related to the course DANB’s annual continuing education requirements. To find out if this course or any other of PennWell
We encourage participant feedback pertaining to all courses. Please be sure to complete the topic. It is a combination of many educational courses and clinical experience that PennWell course has been approved by DANB, please contact DANB’s Recertification
survey included with the course. Please e-mail all questions to: macheleg@pennwell.com. allows the participant to develop skills and expertise. Department at 1-800-FOR-DANB, ext. 445.
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