1. Capstone Research Journal Article
(This manuscript fulfills the requirements for the North Carolina Agricultural and
Technical State University Department of Biology Senior Project BIOL 496)
Miquise Carlton
North Carolina Agricultural & Technical State University
Biology 496
Fall 2015
Drs. White & Lang
Signature of Author: Miquise D. Carlton Date: 11-30-2015
CHRONIC PERIODONTITIS
A relationship to the Heart

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CHRONIC PERIODONTITIS
A relationship to the Heart
Student Demographic:
Greetings! My name is Miquise D. Carlton and I am a Biology student here at North
Carolina Agriculture and Technical State University. I was born into a single parent
household and raised by my beautiful mother, Mildred N. Johnson, in Hickory, North
Carolina. I am one of three on my mother’s side of the family spectrum and one of nine
on my father’s side of the family spectrum. We roll deep!!!! While living in an area, in
which was highly known for crime, my mother was very determined to introduce myself
and along with my brother and sister to a healthier life style. At the beginning of the
transformation, my brother, sister and I was extremely heartbroken from the new
transformation into a different neighborhood and a better life-style because the change
caused for us to loose old friends. However, from my understanding, in order for a
change to be extremely beneficial for a family, the family will have to disconnect from
other families and/or individuals who they are not equally yoked with and who does not
have the aspiration to enhance their way of living.
With the painful yet awesome change in effect, I was able to enhance my critical thinking
skills, mathematical skills, reading and writing skills, and etcetera. I was able to graduate
within the top 15% of my high school, consisting of approximately 250 graduates. This
was an extremely great accomplishment, considering some, if not all, African American
males from my home town do not necessarily graduate from their local high school but
instead become a high school dropout.

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After graduation, I had the opportunity to enroll into North Carolina Agriculture and
Technical State University, in which I am currently attending as I previously stated
before, and from there I decided to major in biology. I decided to become a biology
student because I have always dreamed of becoming a doctor, more specifically a dentist.
In addition of knowing dentistry was the profession I wanted to pursue as a professional
career, I eagerly decided to design a literature research review on the subject matter,
chronic periodontitis and its relationship to the heart.
Furthermore, I would like to personally thank each professor who contributed to
providing me with the necessary tools and information I needed to enhance my education.
In addition, I would also like to thank Dr. White for her dedication and inspiration
towards me because it allowed me to develop endurance and push myself beyond
measure. In addition, I would personally like to thank my friend, Crystal Hill, for being a
phone call away to assist with sentence structure and grammatical errors. Lastly, I would
personally like to thank my family, for keeping me grounded during my last three years
of college. They were always a text message and a phone call away to allow for me to
vent about my college life, when I began to become overwhelmed by my studies.

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Table of Contents:
Description: Page Number:
I. Title Page
II. Student Demographics-----------------------------------------------------1-2
III. Table of Contents ------------------------------------------------------3
IV. Abstract ----------------------------------------------------------------------4
V. Body of Paper
a. Introduction --------------------------------------------------------
b. Understanding Chronic Periodontitis----------------------------5-6
c. Understanding Coronary Heart Disease-------------------------6
d. Literature Review--------------------------------------------------6-13
i. Mechanical Linkage of Periodontitis to Cardiovascular/Coronary
Disease------------------------------------------------------6-11
ii. Statistical Linkage of Chronic Periodontitis to Cardiovascular
Disease------------------------------------------------------12-13
e. Conclusion/Discussion---------------------------------------------13-15
f. References------------------------------------------------------------16
VI. Appendix A.-------------------------------------------------------------------17-20

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Abstract:
Chronic Periodontitis…….. A relationship to the Heart
Miquise D. Carlton
Coronary heart disease is the leading cause of death amongst men and women. As the
population of victims of CHD increases, it becomes more imperative that causes of CHD
be defined and prevented. The traditional factors of CHD have been outlined by the
American Health Association; yet, the AHA’s prescribed factors only accurate describe
one-third of those who suffer from CHD. The presence oral periodontitis in
atherosclerotic plaque and the chronic periodontitis evident in those who suffer from
acute myocardial infarction, provides substantial evidence that periodontitis is linked to
CHD. In proving that such a linkage is statistically significant and mechanically
plausible, the underlying cause for CHD morbidity will be revealed, for chronic
periodontitis can be a more accurate predictor and descriptor of those at risk for heart
disease. Whereas, the tradition factors prescribed by AHA are merely symptoms of the
symbiosis between chronic periodontitis and CHD.
Representative Article:
http://www.jisponline.com/article.asp?issn=0972124X;year=2012;volume=16;issue=4;sp
age=487;epage=491;aulast=Arigbede#ft12

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Introduction:
The purpose of this study is to explore chronic periodontitis as it relates to patients that
suffer from coronary heart disease. More specifically focusing on the question is there a
linkage between chronic periodontitis and coronary heart disease. This study will analyze
a verity of different clinical research linking chronic periodontitis to chronic heart diseases.
If chronic periodontitis is linked to coronary heart disease-statistically and mechanically,
then a significant factor responsible for cardiovascular morbidity will be evinced.
Furthermore, chronic periodontitis may prove to be a more accurate predictor and
descriptor of those at risk for heart disease, when compared to traditional risk factors
prescribed by the American Heart Association.
Understanding Chronic Periodontitis
Chronic periodontitis, a severe case of inflammation around an individuals’ tooth, begins
with a bacterial growth within the oral region of a human. During the process of chronic
periodontitis, the gums begins to loosen and creating spaces, better known as pockets,
between the tooth and the gum that will however become infected. An individuals’ immune
system will begin to attack the invading bacteria as the plaque spreads and develops below
the gum line. The bacterial toxins and an individuals’ natural response to invading bacteria
will begin to break down the bone and connective tissue associated with holding the tooth
in place. Scientist and other physicians across the nation has stated if chronic periodontitis
id not treated in a timely fashion, the bones, gums, and the connective tissue will be
destroyed and could lead to the removal of many teeth due to the destruction. Periodontitis
is primarily caused by plaque, bacteria, but there are serval other factors contributing to

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periodontal disease, such as hormonal changes, illnesses, smoking, medications, bad
habits, poor oral hygiene habits, and family history of dental disease.(1) Researchers across
the world have uncovered potential links between chronic periodontitis and other serious
health conditions. It has been stated, in humans with healthy immune systems the bacteria
within the oral region could enter the bloodstream and effect other areas within the body.
Understanding Coronary Heart Disease:
Coronary heart disease (CHD), also known as coronary artery disease, is the leading cause
of death amongst men and women in the United States of America. CHD is a narrowing of
the small blood vessels that supply oxygen-rich blood to the heart. Researchers have stated
and proven that CDH is caused by the buildup of plaque in the arties of the human heart.
The buildup of plaque within the arteries will allow them to become narrow and as a result,
the blood flow, in which is flowing to the heart, could travel at a much slower rate or could
eventually stop (2).
Literature Review:
Mechanical Linkage of Periodontitis to Cardiovascular/Coronary Disease:
Atherosclerotic coronary artery disease, the main underlying disease responsible for
cardiovascular and cerebrovascular morbidity-which includes thrombosis and myocardial
infarction- is a contributing factor in 50% of United States’ deaths. Yet more than one-third
of patients dying from atherosclerotic coronary vascular disease do not possess any of the
traditional risk factors such as: obesity, hyperlipidemia, diabetes, hypertension, and

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cigarette smoking (3,4). It has been long since known that there are associations of
atherosclerotic risk with infectious agents and several pathogens. This association is a
rational one, for the process of development of atherosclerosis involves chronic
inflammation (3). To make the involvement of pathogens more concrete, it is also
understood that chlamydia phneumonia, herpes simplex virus, streptococcus sanguis, and
porphyromonas gingivalis have been detected in human atheromas (4). Though
porphyromonas gingivalis is mentioned, it is necessary to further define the role of the oral
cavity/teeth in the pathogenesis of atherosclerotic vascular disease.
It has become increasingly clear that the oral cavity possesses the ability to function as the
site of origin for dissemination of pathogenic organisms to distant body sites, especially in
immunocompromised hosts-including patients suffering from diabetes (a traditional factor
of CHD). This is possible, due to the fact that the teeth are the only non-shedding surfaces
in the body, and bacteria levels can reach more than 1011
microorganisms per milligram of
dental plague (4). Human periodontal infections are associated with complex microfloras
in which approximately 200 species in apical periodontitis and more than 500 species in
marginal periodontitis have been encountered (4). These pathogenic infections are
predominantly anaerobic and gram-negative (4). The mere anatomic proximity of these
complex microfloras to the blood stream can easily facilitate bacteria and the systematic
spread of bacterial products, components, and immunocomplexes (4).
Porphyromonas gingivalis (Pg) is the most common form of adult periodontitis and is
estimated to affect 116 million Americans (5). The consequences of Pg are local
inflammations characterized by gingival ulceration and vascular changes, both of which
increase the incidence and severity of transient oral bacterias (5). Also, various studies have

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concluded that Pg can not only adhere but also invade and proliferate in artotic and heart
endothelial cells and coronary artery smooth muscle cells (5,3). In action this translates to
a host having efficient endocytic (endocytosis: form of active transport in which a cell
transports molecules into the cell by engulfing them, includes pinocytosis and
phagocytosis) uptake and Pg persisting within endothelial cells and altering the cells’
integrity (5). Consequently, the transience of such an infection into the systemic circulation
of frequent bacteria would cause chronic inflammatory damage to vasculature and further
the initiation and progression of atherosclerosis and/or atherosclerosis lesions (5).
Furthermore, Li Li and colleagues hypothesized and demonstrated: in vivo long-term
systemic circulatory challenge with Pg can promote and accelerate the development of
atherosclerotic lesions (5). To test such a hypothesis, apoliprotein E-deficient (apoliprotein
E is the official name of the APOE gene/its protein product apo E; it is essential for the
prevention of disorders that affect the heart and blood vessels, i.e-cardiovascular diseases)
heterozygous mice were challenged with Pg (5).
In the study, Pg A7436 was grown on anaerobic blood plates in and anaerobic chamber
with an environment composed of: 85% nitrogen, 5% hydrogen, and 10% carbon dioxide
for 3 to 5 days, and then the grown Pg was inoculated with Shaedler Broth for twenty-four
hours until the culture reached an optical density of 0.8 at 660nm, equivalent to 109
CFU/mL (5). As specified by Neogen Corporation, the manufacturer and distributor of
Schaedler Broth, the utilized broth is specified for the cultivation of anaerobic
microorganisms. Neogen Corporation also mentions that “Shaedler Broth in an atmosphere
of 5% carbon dioxide, 10% hydrogen, and 85% nitrogen exhibited the fastest and highest
growth response” (6). Though the 1%: 2% ratio of hydrogen: carbon in the study is the

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reciprocal of that specified by the manufacturer, given the period of time to grow Pg A7436
it is safe to assume that in the experiment the pathogen also exhibited an equally fast and
high growth rate.
Male Apo E homozygotes (ApoE -/-
) and the corresponding female wild-type hybrids were
obtained at eight weeks of age. Both groups were fed regular mouse food. To generate
apoliprotein E-deficient heterozygous (ApoE +/-
), ApoE -/-
mice were crossed with the
female wild type mice (5, Figure 1). At four weeks of age, the Male ApoE heterozygous
mice and wild-type mice were randomly assigned to either a high-fat diet (HFD)- the
experimental diet- or the regular mouse food - the control diet (5, Figure 1). At ten weeks
of age, ApoE +/-
or wild-type mice, HFD-fed or regular food-fed, were divided at random
into two groups: inoculated with live Pg (107
CFU/50 µL/mouse) or diluted medium (50
µL/mouse) (5). The inoculation was performed intravenously once per week for 10, 14, or
24 consecutive weeks (5, Figure 1).
For tissue harvesting, the mice underwent an overnight fast then, were sedated with
isoflurane, and exsanguinated as approved by The Institutional Animal Care and Use
Committee of Boston University (5). The aortic tree and proximal aorta were separated
close to the heat; after which, the aortic tree- including the arch and thoracic and abdominal
aorta- was processed for en face morphometric analysis. This type of analysis refers to the
quantitative analysis of form, which encompasses size and shape, the impact of mutations
on shape, developmental changes in form, etc.
The extent of atherosclerosis in the aortic tree was determined by en face quantification. In
which, the total aortic surface area and the atherosclerosis lesion area were measured with

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a stereomiscroscope with computer-assisted image analysis capabilities possessed by the
Image Pro Plus 40 (5). However in the regular mice food fed group, the sensitivity of this
procedure did not allow for the detection of any lesion at any time point. The percentage
of aortic surface area covered by lesions at all time points was greater in the Pg-challenged
mice, than in vehicle control animals, P<0.05 (5, Figure 2A). In the HFD-fed mice groups,
red-stained, lipid-rich lesions were first evident ten weeks after the onset of inoculation
with Pg. Furthermore, at 14- and 24-week time points, red-stained lesions were observed
in both Pg-inoculated and non-inoculated mice but to a greater extend in Pg-challenged
mice (5, Figure 2B).
For histomorphometric and histopathological analysis, the proximal aortic cross-sections
for quantitative and histopthalogical evaluation of atherosclerotic lesions were performed.
In which, the percentage of total aortic lumen occupied by lesions per section were
calculated. Also, the total lesion area and the percentage of total aortic lumen occupied by
lesions were averaged over four sections per animal to develop both the mean lesion area
and percentage of total lumen of the proximal aorta occupied by lesions per section within
each animal (5). In the groups of mice who were fed regular mouse food, lesions were not
evident after 10 weeks of inoculation. In Pg-challenged mice, foam cell lesions were
evident after 14 weeks of inoculation (P<0.01) (5, Figure 3A). After 24 weeks of
inoculation, the average lesion area of the Pg was 9 times greater than in the vehicle
controlled mice; instead, the average lesion area was similar in level to HFD-fed mice
injected with vehicle (5). Also in regards to the HFD groups, the mean lesion area was
greater in Pg- challenged mice than in the unchallenged control mice, as well as attaining
a significance level 2 times greater (P<0.001) after 24 weeks of inoculation, with the same

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persistent pattern for percentage of total lumen of the proximal aorta occupied by lesions
per section within each animal (5, Figure 3B).
Furthermore, two stages were observed to characterize the progression of lesions: stage 1
lesions were characterized by sudanophilic (stained by Sudan IV dye, lipid-rich) lesions;
stage 2 lesions were composed of a mixture of sudanophic cells, spindle-shaped cells,
acellular zones, and inflammation (5, Figure 4E, 5C, 5D, 5E, 5F). In relation to location,
lesions primarily occurred in the aortic valve attachments and the free aortic wall, in which
stained cells adhered to the surface of the endothelial lining.
Within 10 weeks, staining of macrophages was evident in HFD mice injected with saline
or Pg and thusly, intensified with the development of lesions until the conclusion of the
24-week period. However, staining was more pronounced in Pg- injected mice than in
saline-injected mice. Mice that were fed regular mouse food exhibited Mac-3 staining
[M3/84 monoclonal antibody reacts with mouse Mac-3. The Mac-3 antigen is upregulated
during macrophage differentiation. Peritoneal and tissue macrophages, dendritic cells, and
endothelial cells express this antigen on their surface (7).] only in Pg-injected mice,
beginning at the 14-week period (5). In wild-type mice that were fed regular mouse food
atherosclerotic lesions were not observed from the 10 to 24-week period, after Pg-
inoculation; while in HFD-fed wild-type mice, early stages of foam cell lesions were
observed at 24 weeks after Pg-inoculation- which is similar to the lesions observed in ApoE
heterozygous, regular food fed mice at 14 weeks after Pg-inoculation (5, Figure 5).
Statistical Linkage of Chronic Periodontitis to Cardiovascular Disease:

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In mid-2009, Willershausen et. al. sought to investigate whether a statistically significant
association between periodontal disease and coronary heart disease could be established.
This association was indeed proven in the discovery that dental chronic inflammatory
diseases correlate with the occurrence of acute myocardial infarction (AMI); thusly,
periodontal diseases can be viewed as possible risk factors for CHD (8).
To establish such a correlation, basic statistics-standard deviation, p-value, and the
implications of the normal curve- were combined with standard scientific procedures, i.e.-
control group and an experimental group. The experimental patient group consisted of one
hundred twenty-five of 568 AMI patients (all of which had been previously verified for
having AMI by hospitalization at the Department of Cardiology and Angiology of the
University of Mainz). The remaining 443 patients were excluded from the study on basis
of having previous dental examinations (including those whose most recent dental history
was already known would inhibit a random statistical study), lack of teeth, and death (8).
The experimental group possessed a mean age of 61.8 years, with a standard deviation of
10.7 years, and a distribution of 85% male and 15% female (8). The control group was
comprised of 125 of 352 healthy patients, who were selected along the same criteria of
being alive, possessed 5 or more teeth, and had not a recent dental examination. Also, no
statistical difference regarding age and gender was found between the AMI (experimental
group) and healthy control group, for the healthy group had a mean age of 63.4 years, with
a standard deviation of 10.7 years, and a distribution of 82% male and 18% female (8).
Once the groups were characterized by age and gender, the differences of the two groups
were then characterized via physical and clinical oral findings. These differences are listed

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as age, body mass index (BMI), diabetes, number of missing teeth, number of treated teeth,
apical lesions, number of crowns, and the increasing severity of periodontitis (PSI).
In comparison to the control patients, the AMI patients had an unfavorable dental status- a
statistically higher number of missing teeth and a higher frequency of dental infection (8).
Furthermore, a significant relationship between increasing severity of periodontitis and
AMI could be observed, for a PSI degree of 4 was found in 42.3% of AMI patients, while
only 17.1% of the control patients (8, Figure 6). A high number of apical lesions was found
in 19.5% of the AMI patients, whereas only 2.3% of the healthy population had less than
the AMI patients; hence, apical lesions do not correlate to CHD (8, Figure 7).
Conclusion/Discussions:
The systematic intravascular challenge with Pg inoculation was shown to accelerate the
progression of atherosclerosis in an ApoE +/-
murine model. However, this acceleration
required genetic susceptibility and/or a dietary risk factor and/or an infectious agent. The
importance of genetic susceptibility was evident in the failure to produce atherosclerotic
lesions in regular food, wild type mice after 24 weeks of Pg- inoculation (5). The
importance of dietary risk factors is emphasized by the earlier, more extensive, and more
advanced progression of atherosclerotic lesions in ApoE +/-
mice that were fed HFD,
when compared to ApoE +/-
mice fed regular mouse food (5). The influence of the
infectious agent is illustrated by the fact that wild-type mice fed HFD had early foam cell
lesions after 24 weeks of Pg-inoculation, compared to those observed in regular food fed
ApoE +/-
mice at 14 weeks of inoculation (5). Also in the context of a genetic

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predisposition such as ApoE +/-
or an environmental risk factor, i.e.- HFD, Pg infection
importantly accelerates the progression of atherosclerosis: aortic atherosclerotic lesions in
Pg-inoculated ApoE +/-
mice developed earlier and were larger and more advanced than
in non-inoculated mice with the same genetics and diet (5). In context of short/long term
exposure to the Pg, long-term Pg inoculation contributed to more significantly than in
short-term acceleration of atherosclerosis: at 14 week Pg inoculation, there were mild
effects in mice that were fed regular mice food, whereas at 24 weeks of Pg inoculation
the lesions in regular food fed ApoE +/-
mice were similar to those of the HFD-fed vehicle
control group (5). Thusly showing, the mild effects of Pg could accumulate, resulting in a
remarkable acceleration of atherosclerosis. The murine model employed establishes
periodontal pathogens contribute to the development and progression of atherosclerosis.
Ergo mechanically speaking, periodontitis is a factor in CHD.
Though PSI and lack of teeth correlate dental disease to myocardial infarcation, This
association is more concretely illustrated, using blood glucose levels, C-reactive protein
(CRP) serum levels, and leukocyte numbers. These same factors point to patients with AMI
exhibiting an unfavorable dental state of health (8,9). Thusly, these variables are evidence
that patients with acute myocardial infarction also suffer from chronic dental infection (9)
. Hence one can conclude periodontal disease can be utilized as an established factor for
CHD, as individuals with periodontal disease have an approximately 24% -35% increase
in risk of developing CHD” (8).
The factors of CHD given by the American Heart Association: age, gender, BMI, diabetes,
and ethnicity were directly/in-directly included in each presented study. Willershausen et.
al. includes them directly, and Li et. al. includes them in an indirectly wholistic approach,

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for each of the AHA factors can be applied in the categories of genetic susceptibility and/or
dietary risk factor. The inclusion of these factors suggests that the classic AHA factors of
CHD are linked and emphasized, if not merely symptoms, of chronic periodontal pathogens
as they relate to CHD. From this symbiosis of factors, it is understood periodontitis may
be a more accurate descriptor of those at risk for heart disease than classic AHA factors.

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Work Cited:
1. "Periodontal (Gum) Disease: Causes, Symptoms, and Treatments." Periodontal
(Gum) Disease: Causes, Symptoms, and Treatments. Web. 9 Oct. 2015.
2. "Dentists: Doctors of Oral Health." Dentists: Doctors of Oral Health. Web. 9
Oct. 2015.
3. Fong, Ignatius W. "Infections and their role in atherosclerotic vascular
disease." The Journal of the American Dental Association 133 (2002): 7S-13S.
4. Li, Xiaojing, et. al. “Systemis Diseases Caused by Oral Infection. Clinical
Microbiology Reviews.13.4 (2000): 547- 558. Web. 28 Oct. 2015.
5. Li, Li et. al. “ Poryphyromonas Gingivalis Infection Accelerates the Progression
of Atherosclerosis in a Hetereozygous Apoliprotein E-Deficient Murine
Model.” American Heart Association Journal 2002; 105:861-867. Web. 28 Oct.
2015.
6. "Schaedler Broth (7154)." Schaedler Broth Product Information Page 06
(2010): n. pag. Neogen.Com. Web. 28 Oct. 2015
7. "Anti-Mouse CD107b (Mac-3) Purified." Mouse CD107b (Mac-3) Antibody
Purified M3/84 RUO. Ebioscience, 2010. Web. 17 Nov. 2015.
8. Willershausen, Brita, et al. "Association between chronic dental infection and
acute myocardial infarction." Journal of endodontics 35.5 (2009): 626-630.
9. Demmer, Ryan T., and Moïse Desvarieux. "Periodontal Infections and
Cardiovascular Disease." The Journal of the American Dental Association.
Print.
10. Cobb, Charles M. "Clinical significance of non‐surgical periodontal therapy: an
evidence‐based perspective of scaling and root planing." Journal of Clinical
Periodontology 29.s2 (2002): 22-32.
11. Arigbede, Abiodun O., B. Osagbemiro Babatope, and M. Kolude Bamidele.
“Periodontitis and Systemic Diseases: A Literature Review.” Journal of Indian
Society of Periodontology 16.4 (2012): 487–491. PMC. Web. 9 Oct. 2015.
12. Chiu, Brian. "Multiple infections in carotid atherosclerotic plaques." American
heart journal 138.5 (1999): S534-S536.
13. Dietrich, Thomas et al. “Age-Dependent Associations between Chronic
Periodontitis/edentulism and Risk of Coronary Heart Disease: Dietrich,
Periodontitis and CHD.” Circulation 117.13 (2008): 1668–1674. PMC. Web. 9
Oct. 2015.
14. Persson, G. Rutger, et al. "Chronic periodontitis, a significant relationship with
acute myocardial infarction." European heart journal 24.23 (2003): 2108-2115.
15. "Coronary Heart Disease: MedlinePlus Medical Encyclopedia." U.S National
Library of Medicine. U.S. National Library of Medicine. Web. 9 Oct. 2015.
Appendix A:

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Figure 1: Time schedule of the experiment (12).
Figure 2: (A) Percentage of aortic surface area covered by lesions. (B)
Representative results of en face analysis in HFD group showing absence of
lessions at 10 weeks of vehicle injection (1) and severity of lesions after 14 weeks
(II) and after 24 weeks (III) of Pg inoculations (12).

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Figure 3: (A) Mean lesion area per section per animal. (B) A percentage of total lumen
of proximal aortas occupied by lesions (12).
Figure 4: Cross-sections of aortic lesions in chow-fed ApoE+/ mice challenged
with Pg or vehicle. Normal configuration of proximal aorta from a chow-fed wild-type
mice at 20 weeks of age (A). After 14 weeks of inoculation, no lesion is found in
control mice (B), whereas foam cell lesion (first stage) is present adjacent to valve-
attachment in Pg-inoculated mice (C). After 24-week inoculation, lesions in control
mice remain at foam cell lesion stage (D), whereas most of lesions in Pg-inoculated
mice progress to the second stage (E). *Foam cell. L indicates aortic lumen; I, intima;
M, media; and A, adventitia (12).

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Figure 5: Cross-sections of aortic lesions in HFD-fed ApoE/mice challenged with Pg or
vehicle. First-stage lesions (foam cells) adjacent to valve attachments (A and B) and in free
aortic wall (B) are found in 10-week postinoculation mice; secondstage lesions are observed
in 14- and 24-week postinoculation mice (C through F). Lesions in Pg-inoculated ApoE+/-
mice are larger and more advanced than in noninoculated mice at same time point. *Foam
cell. L indicates aortic lumen; M, media; and A, adventitia (12).
Table 1: Basic Group Characteristics (SD or in Percentages) and P values for
Differences between patients with AMI and the Healthy Control Patients (1).

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Figure 6: PSI (degree: 0 - 4) distribution in patients after AMI and healthy controls (1).
Figure 7: Frequency of apical lesions in patients after AMI and healthy control patients
(1).