CHAPTER
Potential Impact of Periodontal Infections
20   on Overall General Health
C O M P E T E NCIES
1. Discuss the connection between periodontal infections
and overall general health, including why the presence
of bleeding upon periodontal probing means that the
“door is open” for a wide range of adverse effects on
the overall health of the individual.
2. Explain the potential connection between periodontal
diseases and coronary heart disease (atherosclerosis,
myocardial infarction), cerebrovascular disease
(stroke), pregnancy complications and adverse
outcomes, diabetes mellitus, pulmonary diseases,
neurologic diseases, gastrointestinal diseases, and
cancer of the stomach and pancreas.
Background
Emerging evidence implicates periodontal infections as one
of several important factors that exert negative effects on
overall general health. The potential impact of oral infections
on general health has had extensive coverage in the lay press.
Accordingly, dental hygienists and other oral healthcare pro-
fessionals often are asked to explain the potential connection
between gum disease and serious medical problems such as
atherosclerosis (hardening of the arteries), myocardial infarc-
tion (heart attack), cerebrovascular disease (stroke), diabetes
mellitus, and adverse pregnancy outcomes. This chapter
reviews how periodontal infections may affect overall general
or systemic health and provides information needed to
answer questions about this important topic.
Box 20-1 lists associations supported by scientific evidence
between periodontal infections and adverse systemic out-
comes. For most of these associated conditions, the connec-
tion begins with the entry of bacteria into the bloodstream
from infected periodontal tissues. Bacteria in the bloodstream
(bacteremia) is a common occurrence in patients with peri-
odontitis because the epithelial lining of the soft tissue wall
of the pocket is ulcerated (i.e., the pocket wall is disrupted
and has holes in it) (Figure 20-1). Bacteria infecting periodon-
tal pockets easily enter the bloodstream at these ulcerated
sites. “Bleeding gums,” a commonly reported symptom of
gum disease, often is noticed by the individual after routine
daily activities such as eating or toothbrushing. In contrast,
healthy gum tissues do not bleed under these normal mechan-
ical stimuli. The presence of bleeding gums strongly suggests
sufficient gingival inflammation to cause pocket wall ulcer-
ations that lead to repeated episodes of bacteremia through-
out the day. In addition, an important clinical sign of
inflammation is the presence of bleeding when the site is
354
Gary C. Armitage
examined gently with a periodontal probe (Figure 20-2). Such
sites bleed when probed because the epithelial lining of the
pocket wall is thin and ulcerated. Therefore the presence of
bleeding means that the “door is open” and bacteria from
periodontal pockets can enter the bloodstream readily. If bac-
teremias occur on a chronic basis, the blood-borne bacteria
can contribute to a wide range of adverse effects on the
overall health of the individual.
Periodontal Diseases and Common
Medical Conditions
Coronary Heart Disease (Atherosclerosis)
In coronary heart disease (CHD) the walls of key arteries to
the heart (coronary arteries) thicken. Thickening of the arte-
rial walls is not the simple accumulation of fats and lipids.
Research clearly indicates that CHD is an inflammatory
disease in which the blood vessel walls thicken in response
to chronic injury.1,2 This thickening may become so extensive
that the artery becomes completely occluded, thereby block-
ing the flow of blood to a portion of the heart. When this
happens, a myocardial infarction (heart attack) occurs, which
may lead to death or disability.
The potential connection of periodontal disease to this
process starts with chronic bacteremias. Some blood-borne
bacteria attach to, invade, and injure the single layer of endo-
thelial cells that line the circulatory system. Injured endothe-
lial cells trigger inflammation of the blood vessel wall that
subsequently leads to the development of an atheroma
or intimal thickening of the vessel wall. Well-developed
atheromas contain lipids such as cholesterol covered with a
fibrous cap surrounding a necrotic core laden with scaveng-
ing macrophages. Periodontal bacteria are not the only source
of chronic injury to endothelial cells. Other factors can injure
endothelial cells and contribute to atheroma formation,
including certain viruses, environmental toxins, components
of cigarette smoke, hypertension, and diets leading to hyper-
lipidemia. Therefore CHD is a multifactorial disease in which
many risk factors play a role. A common event leading to
a heart attack is the disruption of a well-developed atheroma
by vascular inflammation induced by one or more of these
risk factors. Disruption of the atheroma can lead to the
formation of a blood clot that occludes or blocks the vessel
(Figure 20-3).
Evidence suggesting that periodontal infections contribute
to CHD include the following:
• Epidemiologic studies3,4
• Presence of DNA and other components of periodontal
pathogens in thrombi5 and atheromas6
 CHAPTER 20  n  Potential Impact of Periodontal Infections on Overall General Health 355

BOX 20-1 
Potential Associations Between Periodontal
Infections and Adverse General Health Outcomes

Heart Diseases
• Infective endocarditis
• Coronary heart disease (atherosclerosis) A B
Arthritis and Failure of Artificial Joints
Neurologic Diseases Figure 20-2.  A, Clinical appearance of a 55-year-old female with chronic
• Nonhemorrhagic (ischemic) stroke periodontitis. Clinical signs of inflammation include redness and swelling
• Brain abscesses (edema) of the gingival papillae. B, Bleeding on probing in the same patient
• Alzheimer’s disease shown in A.
• Meningitis
Pregnancy Complications and Outcomes
• Preterm birth
• Low birthweight
• Preeclampsia • Periodontal pathogens, such as Porphyromonas gingiva-
• Fetal growth restriction lis, are capable of adhering to, invading, and replicating
Diabetes Mellitus within endothelial cells7,8
Pulmonary Diseases • Plausible mechanisms by which periodontal pathogens
• Aspiration and ventilator-associated pneumonias trigger inflammatory reactions that promote the forma-
• Chronic obstructive pulmonary disease tion and disruption of atheromas8
Gastrointestinal Diseases Including Cancer • Preliminary data suggesting that periodontal therapy
• Gastric ulcers promotes vascular health9,10
• Stomach cancer Although no conclusive data show an unequivocal cause-
• Pancreatic cancer and-effect relationship between periodontal infections and
cardiovascular disease,11,12 the association is strong enough
that prudent clinicians should include “improvement in
overall general health” as one of the possible benefits of treat-
ing periodontal disease.

Nonhemorrhagic (Ischemic) Stroke

A stroke is the sudden interruption of the blood supply to
Ulcerated periodontal part of the brain. There are two general types of strokes:
pocket wall Crown
hemorrhagic and nonhemorrhagic. The hemorrhagic type
accounts for about 20% of all strokes and occurs when there
is bleeding within or around the brain usually resulting from
the spontaneous rupture of an artery. The nonhemorrhagic
or ischemic type accounts for approximately 80% of all
Biofilm strokes and is caused by a clot or other blockage of one or
more of the arteries supplying blood to the brain (e.g., the
internal carotid arteries). The process of blocking the artery
usually involves the same atherosclerotic changes in blood
vessels that lead to coronary heart disease. Indeed, the risk
factors for nonhemorrhagic (ischemic) stroke are identical to
those for CHD. Atherosclerotic changes in the carotid arteries
are associated strongly with the amount of periodontal bone
loss.13 At the present time, however, no intervention data
show that treatment of periodontal infections lowers the risk
of developing an ischemic stroke. However, a strong circum-
Root stantial argument can be made that periodontal therapy may
decrease the development of atherosclerotic changes in blood
vessels and thereby decrease the risk of having a stroke.

Pregnancy Complications and Outcomes

Alveolar bone
Figure 20-1.  Drawing of the interface between the gingival and tooth in a
case of periodontal disease. The epithelium of the pocket wall is ulcerated.
These ulcerations allow subgingival bacteria in the adjacent periodontal
pocket access to the systemic circulation.
The presence of infection, particularly in the cervical area of
the uterus, increases the risk of delivering a preterm low
birth-weight baby (PTLBW). (See Chapter 54.)
Preterm birth is defined as a pregnancy of less than 37
weeks, and low birthweight is less than 5.5 pounds or 2400
grams. One suggested explanation is that endotoxin from
356 SECTION III  n  Assessments

Endothelium Endothelial Response to Injury

Intima Fatty streak
Media
Adventia

Lymphocyte

1 Chronic endothelial “injury”:

4 Macrophages and smooth muscle cells engulf lipid
Hyperlipidemia Homocysteine Viruses
Hypertension Hemodynamic factors Immune reactions
Smoking Toxins Bacteria
Fibrofatty atheroma
Endothelial response to Injury

Monocyte
Platelets (macrophage line)

Collagen

Lymphocyte

Lipid debris

5 Smooth muscle proliferation, collagen and

other ECM deposition, extracellular lipid

2 Endothelial dysfunction (e.g., increased permeability,

Acute Coronary Syndromes
leukocyte adhesion)
Monocyte adhesion and emigration

Platelet
aggregate

Plaque disruption

Thrombus

3 Smooth muscle emigration from media to intima

Macrophage activation Mural thrombus with Occlusive thrombus
variable obstruction / possible emboli (Acute transmural myocardial
(Unstable angina or acute subendocardial infarction or sudden death)
myocardial infarction or sudden death)

Figure 20-3.  Drawing of the development and eventual disruption of an atherosclerotic plaque (atheroma) that can lead to heart attacks and nonhemorrhagic
strokes.

gram-negative bacteria enters the circulation at high enough
levels to stimulate production of inflammatory mediators,
such as prostaglandin E2 (PGE2), by the amnion. PGE2
and other inflammatory mediators are potent inducers of
labor.14 The connection between periodontal infections and
adverse pregnancy outcomes is supported by epidemiologic
studies.14,15 The association is even stronger in women whose
periodontal disease is progressing or getting worse.15
For blood-borne periodontal bacteria to trigger preterm
birth they must first reach the amnion and the fetus by cross-
ing the placental barrier. Evidence clearly demonstrates that
this does happen because umbilical cord blood from some
preterm infants contains antibodies (immunoglobulin M
[IgM]) of fetal origin directed against periodontal pathogens
such as Campylobacter rectus and Prevotella intermedia.16 Intra-
uterine access of bacteria to the developing baby also appears
 CHAPTER 20  n  Potential Impact of Periodontal Infections on Overall General Health 357

to retard fetal growth because mothers with moderate to be at high risk of adverse pregnancy outcomes27 or in those
severe periodontitis tend to deliver babies who are small for in whom “successful” responses to periodontal therapy are
their gestational age.17 obtained.28 Periodontal therapy may have positive effects on
A serious complication of pregnancy linked to periodontal birth outcomes if the treatment occurs before pregnancy.29
infections is preeclampsia.18 This complication is character- Future studies are needed to examine these possibilities.
ized by hypertension, edema or swelling of the ankles, and
proteinuria (protein in the urine). Failure to control these Diabetes Mellitus
physiologic abnormalities can lead to eclampsia, which may Diabetes mellitus (DM) is a group of diseases that results
lead to convulsions, coma, and death of the mother. in high levels of glucose in the blood because of either an
In spite of a strong relationship between periodontal infec- insufficient supply of insulin or the impaired availability
tions and several adverse pregnancy outcomes, large ran- of this pancreatic hormone that regulates carbohydrate
domized controlled clinical trials (RCTs) have not shown that metabolism. (See Chapter 44.) In type 1 DM, a severe defi-
routine periodontal therapy decreases the incidence of these ciency of insulin exists usually because of the destruction of
outcomes.19-22 These studies clearly show that the application the insulin-producing pancreatic beta cells. The disease rep-
of standard-of-care periodontal therapy as a public health resents only about 10% to 20% of all cases of DM and occurs
intervention (i.e., all pregnant individuals with periodontal with the highest frequency in people of Northern European
disease receive oral hygiene instructions + mechanical descent (e.g., those from Sweden and Finland). In type 2 DM,
removal of plaque and calculus) does not alter significantly which accounts for 80% to 90% of all cases, there is a chronic
the rates of preterm birth, low birthweight, or fetal develop- hyperglycemia (elevated blood sugar) that causes the exhaus-
ment. However, one positive aspect of these studies was the tion of pancreatic beta cells. In early stages of the disease there
finding that nonsurgical periodontal therapy during the is enough insulin, but it is not able to regulate glucose levels
second trimester is safe.19-22 in the peripheral tissues. This condition is known as insulin
One of the interesting findings from the RCTs dealing with resistance. Obesity is an extremely important environmental
the effects of periodontal therapy on birth outcomes is that risk factor that is linked to the onset of type 2 DM. In many
standard periodontal therapy is often less effective compared
with therapeutic results obtained in nonpregnant individu-
als.19,20 For example, data from the Obstetrics and Periodontal
Therapy (OPT) study revealed that the treated population Comparison of Baseline and Post-
treatment Bleeding on Probing (BOP) in
experienced a decrease in the percentage of sites with bleed- the Obstetrics and Periodontal Therapy
ing on probing (BOP) from a pretreatment baseline of 69.6% (OPT) Study
80
to a less-than-expected post-treatment value of 45.9% (P < 70
69% 66.9% 69.6%
0.001) (Figure 20-4).19 In a typical nonpregnant population the 60 N = 410 N = 413
45.9%
expected post-treatment percentage of sites with residual 50
BOP% 40
BOP should be approximately 10% (Figure 20-5).23 One of the NO TREATMENT
30 PERIODONTAL
probable reasons for the less-than-expected response to peri- 20 TREATMENT
odontal treatment is the profound changes that occur in a 10
woman’s immune system during pregnancy.24-26 The high per- 0
BASELINE CONTROL BASELINE EXPERIMENTAL
centage of sites with BOP after treatment means that the (CONTROL) (After Delivery) (EXPERIMENTAL) (After Delivery)
patients still were infected at the end of the study. This finding Figure 20-4.  Comparison of baseline and post-treatment bleeding on
may mean that pregnant women need more intensive peri- probing (BOP) in the Obstetrics & Periodontal Therapy (OPT) Study.19 Com-
odontal maintenance care than nonpregnant women. pared with controls, there is a statistically significant reduction (P < 0.001)
The effect of periodontal therapy on birth outcomes may in the percentage of sites with BOP in the women who received nonsurgical
be different in subpopulations of women who are known to therapy during pregnancy.

Should the Peridontal Therapy in the

OPT Study Have Been More Rigorous?
[Change in % Sites with Bleeding on Probing versus Baseline]
80
69.6% 68%
70
60 N = 413 N = 20
45.9%
50 TYPICAL
BOP% 40 (EXPECTED)
RESULTS OF RESULTS OF
30 PERIODONTAL SCALING AND
20 TREATMENT IN ROOT PLANING
OPT STUDY 10%
10
0
BASELINE 6 MONTHS BASELINE 6 MONTHS

Figure 20-5.  Comparison of the percentage reduction in bleeding on probing (BOP) in the treated population in the Obstetrics & Periodontal Therapy (OPT)
Study19 versus what typically would be expected after nonsurgical treatment in a nonpregnant population.23 The high percentage of sites with residual BOP in
the OPT Study (45.9%) versus that expected (10%) in a typical population suggests that pregnant individuals may require more frequent periodontal care than
nonpregnant patients.
358 SECTION III  n  Assessments
people with long-standing type 2 DM, supplemental insulin
injections are needed because the exhausted pancreatic beta
cells eventually die.
People with uncontrolled or poorly controlled DM are
more susceptible to infections, including periodontal dis-
eases. This susceptibility to infections is due partly to impaired
antibacterial functions of neutrophils and wound healing
problems associated with vascular and connective tissue
abnormalities. People with diabetes whose disease is under
poor metabolic control have more severe periodontitis com-
pared with those who are medically well controlled.30
Depending on the severity of the DM, the metabolic control
of the disease sometimes can be achieved by a carefully
planned dietary program. In other people, ingestion of hypo-
glycemia agents (e.g., tolbutamide [Orinase]) or daily insulin
injections are necessary to achieve metabolic control of the
disease. Medical regulation of blood sugar levels is hampered
by the presence of infections such as untreated periodontitis.
Through a number of mechanisms, infections can increase
insulin resistance in peripheral tissues and make diabetic
control difficult. In some, but not all patients, nonsurgical
treatment of periodontitis makes the metabolic control of DM
easier.31 Indeed, physicians sometimes request that oral
healthcare professionals treat periodontitis in their DM
patients to facilitate metabolic control of the disease.
Pulmonary Diseases
Periodontal infections have been implicated as important in
the development of a number of pulmonary diseases, includ-
ing aspiration pneumonias, ventilator-associated pneumo-
nias (VAP), and chronic obstructive pulmonary disease
(COPD). (See Chapter 50.) In all of these conditions, members
of the oral microbiota gain access to and infect tissues of the
pulmonary tree.
Aspiration pneumonias occur most often in patients who
have impaired gag and swallowing reflexes. It is a common
occurrence in nursing home residents and sometimes is called
nursing home–associated pneumonia.32 People at the highest
risk are those who have dysphagia (difficulty in swallowing)
from a stroke, Parkinson’s disease, or other neurologic prob-
lems (see Chapter 47). The disease develops when oral fluids
containing large numbers of microorganisms are aspirated
into the bronchial tree and lungs. Some data suggest that
periodontal infections alter the local intraoral environment in
such a way that the mouth becomes colonized with elevated
numbers of respiratory pathogens.32
Ventilator-associated pneumonias (VAP) occur most
often in patients who need prolonged hospital care in an
intensive care unit (ICU). The risk of acquiring VAP dramati-
cally increases in patients who are intubated for longer than
4 or 5 days. In such cases, the breathing tube passes through
the mouth and oropharynx and becomes colonized by the
microbiota from these sites. Strong evidence from random-
ized controlled clinical trials indicates that oral hygiene pro-
cedures performed on ICU patients by hospital personnel
reduce the risk of developing VAP.32-34
Chronic obstructive pulmonary disease (COPD), a
common respiratory illness characterized by chronic bronchi-
tis and emphysema, is especially prevalent in cigarette
smokers. A statistically significant association between COPD
and periodontal infections has been demonstrated in a
number of epidemiologic studies in which loss of teeth, deep
probing depths, and clinical attachment loss were used as
surrogate markers for the presence of periodontal disease.33,35
No studies show that the presence of periodontal infections
influences the pathophysiology of COPD. However, a recent
pilot study found that periodontal treatment reduced the fre-
quency of occurrence of exacerbations of COPD (i.e., reduced
the episodes of difficulty in breathing).36 Periodontal disease
may promote the colonization of the mouth by respiratory
pathogens that subsequently lead to chronic bronchitis. It is
also possible that there is no causal link between periodontal
infections and COPD because smoking is a risk factor shared
by the two conditions and the association may be
coincidental.
Lung cancer also is linked to periodontal infections. A
statistically significant association was demonstrated in a ret-
rospective large national epidemiologic study, even when the
data were adjusted for history of smoking. However, prob-
lems in accurately measuring smoking history may explain
the apparent connection. Perhaps the two conditions have no
causal relationship and the association is spurious.37,38
Neurologic Diseases
Hematogenous spread of oral infections to the central nervous
system (CNS) is a rare occurrence. (See Chapter 47.) CNS
infections of oral origin include unusual brain abscesses and
extremely rare cases of meningitis. The rarity of these condi-
tions probably is related to the presence of the blood-brain
barrier, which consists of continuous tight junctions between
epithelial cells of the choroid plexus and capillary endothelial
cells in the brain. Spread of oral infections to the CNS also
can occur locally by a variety of anatomic routes such as the
infratemporal fossa through the greater wing of the sphenoid
bone near the foramen ovale. Spread of infection by either
route is rare and the literature addressing these conditions
usually consists of case reports.39
Alzheimer’s disease (AD) is characterized by a progres-
sive atrophy of the cerebral cortex with a gradual loss of
short-term and long-term memory. Characteristic brain
lesions contain abnormal proteins that take the form of senile
plaques with an amyloid core surrounded by dystrophic neu-
rites and neurofibrillary “tangles” composed of cytoskeletal
intermediate filaments. Components of some microorganisms
such as Chlamydia pneumoniae and spirochetes (the genus
Treponema) have been found in brain tissues of persons with
AD. In addition, antigens from oral spirochetes have been
detected in brain tissues at a higher rate in AD patients
(87.5%) compared with non-AD controls (22.2%).40 Elevated
serum antibodies to other oral bacteria also have been dem-
onstrated years before the onset of cognitive impairment
associated with Alzheimer’s disease.41 However, a cause-and-
effect relationship has not been shown because the microbial
material may have been deposited secondarily in previously
damaged tissue. Nevertheless, one should not rule out a role
for oral infections in AD because a recent long-term epide-
miologic study suggests that the development of dementia is
associated significantly with tooth loss.42 (See Chapter 47.)
Gastrointestinal Diseases and Cancer
It is well established that certain gastrointestinal diseases
such as chronic gastritis and peptic ulcers can be caused by
the overgrowth of Helicobacter pylori, a gram-negative micro-
aerophilic, motile, commensal bacterium of the stomach
 CHAPTER 20  n  Potential Impact of Periodontal Infections on Overall General Health 359
microbiota. (See Chapter 45.) The main suggested connection
between these gastrointestinal diseases and oral infections is
that the oral cavity can be a reservoir for this opportunistic
pathogen.43,44 In addition, a strong association exists between
chronic infection of gastric tissues with H. pylori and the
development of stomach cancer.45,46 Data from some epide-
miologic studies also suggest an association between peri-
odontal infections, tooth loss, and the development of
pancreatic cancer37,45-48 and even lung cancer.37 Although a
cause-and-effect relationship between periodontal infections
and these conditions has not been shown, the epidemiologic
associations are a good justification for more research in this
area.
CLIENT EDUCATION TIPS
Explain the potential connection between gum disease and
• Atherosclerosis (hardening of the arteries)
• Myocardial infarctions (heart attacks)
• Cerebrovascular disease (stroke)
• Diabetes mellitus
• Pulmonary diseases
• Adverse pregnancy outcomes
LEGAL, ETHICAL, AND SAFETY ISSUES
• Periodontal assessment findings must be communicated
to clients so that they have an understanding of their
current periodontal disease status and potential risk for
serious medical problems.
• All assessment findings must be documented, evaluated,
and monitored.
• Referrals are made to other health professionals when care
required is beyond the scope of dental hygiene practice
and skills of the practitioner.
KEY CONCEPTS
• Strong evidence supports that periodontal disease is one
of several important risk factors for the development of
CHD (atherosclerosis) and nonhemorrhagic (ischemic)
stroke. Because these diseases are chronic and multifacto-
rial, it is difficult to prove a cause-and-effect relationship
between the development of these diseases and any single
risk factor. In addition, it is unlikely that periodontal
therapy alone prevents heart attacks and strokes. However,
periodontal therapy should be part of a multidisciplinary
program of risk reduction that may include smoking ces-
sation, dietary counseling, weight reduction, and treat-
ment of other chronic infections (e.g., chronic bronchitis
caused by C. pneumoniae and peptic ulcers caused by H.
pylori). (See Chapters 45 and 50.)
• Convincing data suggest that the presence of moderate to
severe periodontitis during pregnancy adversely affects
birth outcomes, increases the risk of preeclampsia, and has
negative effects on fetal development. Because nonsurgical
periodontal therapy during pregnancy has been shown to
be safe, it is highly recommended that treatment of peri-
odontal infections should be part of prenatal care
programs.
• A two-way relationship exists between periodontitis and
diabetes mellitus (DM). Persons with poorly controlled
DM are at an elevated risk for developing periodontitis
because of a number of DM-associated factors that increase
susceptibility to infections. The presence of untreated
infections, including periodontitis, makes the metabolic
control of DM more difficult. Treatment of periodontitis in
persons with DM positively affects oral and systemic
health.
• Data from several randomized controlled clinical trials
clearly demonstrate that oral hygiene procedures per-
formed by nurses on hospitalized patients in ICUs signifi-
cantly reduce the risk of developing VAP and certain other
nosocomial infections.
• Preliminary data suggest that periodontal diseases have
adverse effects on systemic health. The old belief that peri-
odontal infections only have local effects on tissues sup-
porting the teeth is clearly false.
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