Background.

The authors
describe how oral disease,
particularly periodontal
disease, may place certain
patients at increased risk
of developing cardiovas-
cular disease and stroke.
Results. Although the precise
mechanisms of interaction are not clear,
two biological mechanisms that may
explain the relationship are presented. In
addition, the authors describe the dental
management issues that need to be under-
stood in treating patients compromised by
cardiovascular disease.
Conclusions and Clinical
Implications. The patient with cardio-
vascular disease may present a challenge to
the dental health care provider, depending
on the degree of hemodynamic compromise
and the stability of his or her condition.
Oral care
for patients with
cardiovascular
disease and stroke
LOUIS F. ROSE, D.D.S., M.D.; BRIAN MEALEY,
D.D.S., M.S.; LAURA MINSK, D.M.D.; D. WALTER
COHEN, D.D.S.
I
n May 2000, the U.S. surgeon generals office pub-
lished its first report on oral health in America,
emphasizing that oral health means much more
than healthy teeth and that it is integral to general
health.
1
Included in the report is an extensive
review of the burden that oral health problems place on
vulnerable populations. The surgeon general confirmed
that many systemic diseases and conditions have oral
manifestations that may be the initial signs of clinical
disease. In addition, the mouth is a portal of entry as
well as the site of disease for microbial infections that
affect general health status. Its functions can be affected
adversely by many pharmaceuticals and other therapies
commonly used to treat systemic conditions.
Oral Health in America: A Report of the Surgeon
General concluded with the recognition
that the mouth is the center of vital tis-
sues and functions that are critical to
total health and well-being across the
life span. The mouth serves as a
mirror of health or disease, as a sentinel
or early warning system, as an acces-
sible model for the study of other tissues
and organs, and as a potential source of
pathology affecting other systems and
organs.
1
CARDIOVASCULAR DISEASE
Cardiovascular diseases make up the most prevalent
category of systemic disease in the United States and in
many other countries, and increase in prevalence with
age.
2
AB STRACT
JADA, Vol. 133, June 2002 37S
The patient
with
cardiovascular
disease may
present a
challenge to
the dental
health care
provider.
Atherosclerosis is a progressive dis-
ease process that involves the large- to
medium-sized muscular and large
elastic arteries. It can lead to ischemic
lesions of the brain, heart or extremi-
ties, and can result in thrombosis and
infarction of affected vessels, leading to
death. The impact of atherosclerosis on
overall health is staggering. World
Health Organization statistics indicate
that in 1995, cardiovascular diseases
were responsible for 20 percent of
deaths worldwide (14 million people). In
some developing countries, cardiovas-
cular disease accounts for about 50 per-
cent of deaths.
3
For years, dentists have noticed that
certain characteristics are common to
patients with periodontitis and patients
with cardiovascular disease (Figures 1
and 2). Both cardiovascular disease and
periodontal disease are more likely to
occur in people who are older, in men,
in people of lower educational status
with fewer financial resources, in those
who smoke, in people who have stress
and in those who are socially isolated.
The classical risk factors for cardiovas-
cular diseasehypertension, hyper-
J
A
D
A
C
O
N
T
I
N
U
I
N
G E
D
U
C
A
T
I
O
N

A
R
T
I CL
E
4
Copyright 2002 American Dental Association. All rights reserved.
cholesterolemia and cigarette smokingaccount
for only about one-half to two-thirds of all cases of
the disease. Research has shown that atheroscle-
rosis is more common in patients with periodon-
titis.
2
This suggests that periodontal disease and
cardiovascular disease may have similar
causative pathways.
Some scientific studies have shown a link
between infections of the mouth and coronary
artery disease. In one such study, Mattila and col-
leagues
4
compared patients who had experienced
a myocardial infarction, or MI, with healthy con-
trol subjects. They found that after adjusting for
age, socioeconomic status, smoking, serum lipid
levels and diabetes, dental health (as measured
by the Total Dental Index) was worse in subjects
who had experienced an MI. In another study by
Mattila and colleagues,
5
a statistically significant
association was found between dental infections
and atheromatosis.
In examining the effects of different oral infec-
tions on the incidence of strokes, Grau and col-
leagues
6
re-examined the Total Dental Index and
found that only the periodontal component of the
index was responsible for the association between
oral infection and cerebrovascular ischemia
(stroke).
Several longitudinal studies have followed a
population of otherwise healthy people to deter-
mine what factors increase the risk of developing
heart disease. The first National Health and
Nutrition Examination Survey followed up 9,760
subjects for 14 years; DeStefano and colleagues
studied these data and found that people with
periodontitis at baseline had a 25 percent
increased risk of having coronary artery disease.
7
After adjusting for age, sex, race, education,
poverty index, marital status, systolic blood pres-
sure, total cholesterol level, diabetes, body mass
index, physical activity, alcohol consumption and
cigarette smoking, the researchers found that
men with periodontitis had a 1.72 relative risk
compared with men without periodontitis. The
authors concluded that dental disease was associ-
ated with an increased risk of cardiovascular dis-
ease, particularly in men younger than age 50
years.
7
Potential biological mechanisms. Most of
these studies
4-7
have shown that there is an asso-
ciation between periodontal disease and cardio-
vascular disease. These associations have been
demonstrated across diverse populations and
appear to be independent of traditional risk fac-
tors, but do not provide for a biological rationale
for the association.
Two biological mechanisms that may explain
the relationship between cardiovascular disease
and periodontal disease are discussed in this
article:
dBacteria from periodontal disease may enter
the circulation and contribute directly to the
atheromatous or thrombotic processes.
dSystemic factors alter the immunoinflamma-
tory process involved in both periodontal and car-
diovascular diseases.
Role of infections in atherosclerosis. Since
1908, when Sir William Osler proposed that car-
diovascular disease itself was an infection, the
role of infection in cardiovascular disease has
been discussed.
8
Infection is now recognized as a
risk factor for atherogenesis and thromboembolic
events.
5-7
38S JADA, Vol. 133, June 2002
Figure 1. A 45-year-old man with coronary artery disease
who smokes two packs of cigarettes per day. He has not
responded well to periodontal treatment and does not
practice good oral hygiene.
Figure 2. Histologic section of a coronary artery demon-
strating atherosclerosis and thrombus formation.
Copyright 2002 American Dental Association. All rights reserved.
Infectious agents may cause injury directly to
the epithelium and partially activate the inflam-
matory response seen with atherosclerosis. There
is evidence that infection with certain bacteria,
such as Chlamydia pneumonae, Helicobacter
pylori, cytomegalovirus and other periodonto-
pathic bacteria are associated with heart disease.
Haraszthy and colleagues
9
studied 50 carotid
atheromas via polymerase chain reaction.
Seventy-two percent of the surgical specimens
indicated bacterial content and 44 percent of the
atheromas contained at least one of the peri-
odontal microorganisms studied (Porphyromonas
gingivalis, Prevotella intermedia, Bacteroides
forsythus and Actinobacillus actinomycetemcomi-
tans) (Figure 3
10
).
People with severe periodontitis have the
strongest link to cardiovascular disease. These
people also have the greatest amounts of
pathogenic bacteria and systemic factors that
may contribute to an altered immunoinflamma-
tory response.
Common systemic factors involved in
periodontal and cardiovascular diseases.
Considerable evidence has identified atheroscle-
rosis as an inflammatory disease. This hypoth-
esis, which is also known as the Ross Response-
to-Injury Hypothesis,
11,12
explains how
inflammation relates to atherosclerosis. Ross
hypothesis suggests that injury to the epithelium
causes the initial lesion, leading to a chronic arte-
rial inflammatory process. During this inflamma-
tory process, monocytes migrate through the
endothelium into the underlying tissue, where
there is a proliferation of smooth muscle cells.
Hydrolytic enzymes, cytokines, chemokines
and growth factors are released as a result of acti-
vation of the monocytes (macrophages) into the
blood vessel, resulting in further damage and
focal necrosis. A major feature of this process is
lipid accumulation, and the atheromatous plaque
can become covered with a fibrous cap over the
focal necrotic area in the later stages of this pro-
cess. This fibrous cap also may erode and rupture,
leading to thrombus formation, arterial occlusion
and infarction.
Certain people may be genetically predisposed
to experience a hyperinflammatory response
when stimulated by a bacterial challenge such as
periodontal disease. These people may produce
higher levels of proinflammatory cytokines, par-
ticularly interleukin-1, prostaglandins (in partic-
ular, prostaglandin E
2
) and tumor necrosis factor
(in particular, tumor necrosis factor-). These bio-
logical mediators can have a direct effect on the
periodontal pocket, as well as on the vascular
endothelium and smooth muscle. In the peri-
odontal pocket, these mediators cause vasodila-
tion and increased vascular permeability.
This is followed by inflammatory cell recruit-
ment, connective-tissue degradation and bone
destruction. The result of recruitment of inflam-
matory cells into the major blood vessels is the
proliferation of vascular smooth muscles, vascular
fatty degeneration and intravascular coagulation.
People who are genetically predisposed to this
proinflammatory response may be at a higher
risk of developing periodontal disease and cardio-
vascular disease.
Prospective interventional studies are needed
to determine the exact link between periodontal
disease and cardiovascular disease, as well as to
evaluate whether periodontal treatment may
reduce the risk of developing cardiovascular
disease.
DENTAL MANAGEMENT OF PATIENTS
WITH CARDIOVASCULAR DISEASE
The primary management goal for the patient
with cardiovascular disease during dental
therapy is to ensure that any hemodynamic
change produced by dental treatment does not
exceed the cardiovascular reserve of the patient.
This is best achieved by minimizing any hemody-
namic alterations during treatment (that is, by
maintaining the patients optimum blood pres-
sure, heart rate, heart rhythm, cardiac output
and myocardial oxygen demand).
13,14
Psychological and physiological stress during
periodontal treatment has the potential to signifi-
cantly alter hemodynamic stability.
13,15,16
Conse-
quently, a stress-reduction protocol is frequently
JADA, Vol. 133, June 2002 39S
Figure 3. Carotid artery atheroma. (Reprinted with
permission of the publisher from Genco and colleagues.
10
)
Copyright 2002 American Dental Association. All rights reserved.
suggested for patients with significant cardiovas-
cular compromise, which includes the following:
dshorter appointments, preferably in the
morning when the patient is well-rested and has
a greater physical reserve;
duse of profound local anesthesia to minimize
discomfort;
dpreoperative or intraoperative conscious seda-
tion or both;
dexcellent postoperative analgesia.
17,18
We should note that almost all references sug-
gesting a stress-reduction protocol do so on the
assumption that such a protocol will minimize
adverse hemodynamic alterations. There is little
objective evidence, however, that such a protocol
is required for the majority of patients with car-
diovascular disease, or that it produces a better
outcome in regard to cardiovascular complications
associated with periodontal therapy.
Anesthetic agents. The use of
local anesthetic agents with vaso-
constrictors in patients with cardio-
vascular disease remains contro-
versial. The two most commonly
used vasoconstrictors are
epinephrine and levonordefrin.
Levonordefrin is only 20 percent as
potent as epinephrine; therefore, its
concentration in dental anesthetics
is fivefold greater (that is, 1:20,000)
than the most common concentration of
epinephrine (1:100,000).
Normal epinephrine release from the adrenal
medulla can increase 20- to 40-fold during
stress.
19
Such stress may be induced by pain
during dental treatment. Patients receiving local
anesthetic without vasoconstrictor often have sig-
nificantly impaired pain control compared with
those receiving local anesthetic with
epinephrine.
20
For this reason, patients with car-
diovascular disease may be at greater risk of
experiencing massive endogenous epinephrine
release secondary to poor local anesthesia than
they are from the small amount of vasoconstrictor
used in local anesthetics.
Most human studies examining hemodynamic
variables after dental injection of 1.8 to 5.4
milliliters of 2 percent lidocaine with 1:100,000
epinephrine have found no significant changes in
mean arterial pressure, blood pressure or heart
rate in healthy patients or in those with mild-to-
moderate cardiovascular disease.
16,19,21,22
So it is
recommended that patients with mild-to-
moderate cardiovascular disease receive the
smallest amount of local anesthetic needed to pro-
vide profound anesthesia, with aspiration per-
formed to prevent intravascular injection.
Researchers have suggested that the use of con-
scious sedation to decrease stress and therefore
minimize endogenous release of epinephrine may
be a more important factor in ensuring hemody-
namic stability in patients with cardiovascular
disease than are attempts to avoid the small
amount of epinephrine used in local anesthetic
injections.
Although small amounts of vasoconstrictor pro-
duce little risk for the average patient with car-
diovascular disease, exogenous vasoconstrictors
may be contraindicated in patients with severe
cardiovascular compromise, including unstable
angina, recent myocardial infarction or coronary
artery bypass surgery, uncontrolled dysrhyth-
mias, severe hypertension and
severe congestive heart failure.
19
Intraligamentary injection of local
anesthetics with vasoconstrictor
generally is contraindicated in
patients with significant cardiovas-
cular disease,
19
since the hemody-
namic effects are similar to those
observed after intravenous
epinephrine injection.
23
Ischemic heart disease.
Ischemic heart disease, most commonly mani-
fested as angina or myocardial infarction, is the
major cause of sudden death in the United
States.
16,22,24
It usually is caused by decreased
coronary blood flow, increased myocardial oxygen
demand or both. There are three types of angina:
stable, unstable and variant (Prinzmetals
angina). It is clear from the literature that psy-
chological or physiological stress may exacerbate
ischemic symptoms. Therefore, use of a stress-
reduction protocol and profound anesthesia is an
integral part of periodontal therapy for these
patients.
13,15,17,18
Stable angina generally is caused by
atherosclerotic narrowing of coronary vessels and
presents with infrequent episodes of pain, usually
precipitated by physical exertion or emotional
stress. The medications most commonly used to
treat patients with stable angina include nitrates
such as nitroglycerin, -andrenergic blocking
agents and calcium channel blockers.
15
Periodontal treatment planning may be altered
in these patients by the need for shorter appoint-
40S JADA, Vol. 133, June 2002
The use of local
anesthetic agents
with vasoconstrictors
in patients with
cardiovascular disease
remains controversial.
Copyright 2002 American Dental Association. All rights reserved.
ments, use of only small amounts of vasocon-
strictor in local anesthetics and possible indica-
tions for preoperative or intraoperative conscious
sedation. Supplemental oxygen delivered via a
nasal canal may help prevent intraoperative
anginal attacks.
17
The drugs of choice for treating
an acute anginal attack are 100 percent oxygen
and sublingual nitroglycerin.
15,18
The patient may
be instructed to bring his or her own nitroglycerin
tablets to each appointment, and the health care
provider also may place nitroglycerin tablets in
the emergency medical kit.
Unstable angina occurs when there is a dra-
matic increase in the frequency or severity of
anginal attacks or when angina appears while the
patient is at rest.
15,24
Patients with unstable
angina generally are not candidates for elective
dental therapy, and consultation with the
patients physician usually is indicated. If emer-
gency dental care is needed, preoperative anxi-
olytic agents may be indicated for stress reduction
and to minimize endogenous epinephrine release.
The dentist should closely monitor
the patients hemodynamic status
and oxygen saturation before and
during treatment.
Variant angina (that is,
Prinzmetals angina) usually occurs
at rest and probably is caused by
coronary artery spasm.
15,25
The other major category of
ischemic heart disease frequently
encountered by oral health care providers is
myocardial infarction. Researchers and clinicians
commonly recommend that patients not receive
routine dental care for at least six months after
experiencing a myocardial infarction.
18,19,24
This
recommendation is based on the fact that the
peak mortality rate following myocardial infarc-
tion occurs during the first year,
26
primarily
resulting from the increased electrical instability
of the myocardium after the infarction.
27
During this six-month period, dental treatment
generally is limited to managing acute dental
needs, and consultation with the patients physi-
cian may be needed.
28
Acute dental needs usually
are addressed definitively, since continued pain
may potentiate hemodynamic alterations or dan-
gerous cardiac dysrhythmias.
17,24
A protocol sim-
ilar to that described above for unstable angina
may provide the best means of managing acute
dental needs.
16,17
After the six-month postmyocar-
dial infarction period, most patients may be
treated with techniques similar to those used for
the patient with stable angina, including rela-
tively short appointments and a stress-reduction
protocol where indicated.
Dysrhythmias. Patients with cardiac dys-
rhythmias may require special precautions
during dental therapy. Antidysrhythmic drugs
commonly are used, many of which have side
effects such as gingival overgrowth or xerostomia
that may impact the dentition or periodontium.
The use of local anesthetics with vasoconstrictors
may be contraindicated in patients with refrac-
tory dysrhythmias
19
; dental treatment may best
be accomplished in a controlled medical setting
with careful cardiac monitoring.
24
Some dysrhythmias are treated with
implantable pacemakers or automatic defibrilla-
tors in addition to drug therapy. Pacemakers and
automatic defibrillators present a low risk of
infective endocarditis and do not require prophy-
lactic antibiotic coverage before dental therapy.
29
Older pacemaker models were unipolar and could
be disrupted by equipment that
generates an electromagnetic field,
such as ultrasonic instruments
and electrocautery units. Most
pacemakers placed within the last
30 years are bipolar and generally
are not affected by the small elec-
tromagnetic fields created by
dental equipment.
Automatic defibrillators often
activated without warning, which may cause
sudden movement and endanger the patient in
the dental setting. The dental health care
provider must be aware of this potential during
treatment, and may need to stabilize the oper-
ating field through use of a bite-block or other
such devices.
Cerebrovascular accident. Although stroke
is a cerebrovascular disorder or cerebrovascular
accident, or CVA, it is discussed in the above sec-
tion entitled Cardiovascular Disease, because
CVAs occur most frequently in patients with
existing cardiovascular disease, especially hyper-
tension. A stroke results from sudden interrup-
tion of blood flow to the brain, which deprives it of
oxygen. The survival rate and severity of the
ensuing functional deficit depend on the type of
stroke and the extent of the lesion.
30
Patients with
stroke frequently are treated with oral anticoagu-
lants and may, in consultation with their physi-
cians, need alteration of the drug regimen before
JADA, Vol. 133, June 2002 41S
Patients with cardiac
dysrhythmias may
require special
precautions during
dental therapy.
Copyright 2002 American Dental Association. All rights reserved.
undergoing periodontal therapy.
To prevent a subsequent stroke, clinicians
must treat active infections aggressively, since
even minor infection may alter blood coagulation
and trigger thrombus formation and ensuing cere-
bral infarction.
31
Dysphasia may be present in the
patient with stroke and can cause changes in diet,
mastication, nutrition and body weight. Inability
to completely clear the mouth of food particles
may result in halitosis, caries and increased risk
of infection. The dental health care provider
should counsel the patient about the importance
of thorough oral hygiene. Weakness of the facial
area or paralysis of extremities may make oral
hygiene procedures extremely difficult,
30
and the
dental health care provider may
need to modify oral hygiene instru-
ments for ease of use, perhaps in
consultation with an occupational
therapist.
The dentist may initiate a long-
term regimen of chlorhexidine
rinses to aid in plaque control.
30
The
gag reflex may be diminished after
a CVA as well, which may require
particular attention during dental
therapy. The patients head position
can be adjusted if needed, while
thorough and constant evacuation
will help prevent aspiration of foreign matter.
30
Valvular heart disease. The most important
goal of dental therapy in patients with valvular
heart disease is the need to prevent infective
endocarditis. Dental procedures often cause a
transient bacteremia that rarely lasts longer than
15 minutes,
32
but the bacteria may lodge on
abnormal or damaged cardiac tissue, especially
valves, which may result in endocarditis. The per-
centage of patients with endocarditis who have
had recent dental treatment varies widely in the
literature from 3 to 40 percent.
32-35
Most cases of infective endocarditis involving
oral microorganisms probably are caused not by
dental treatment, but by dental disease, mastica-
tion and oral hygiene procedures.
32
Guntheroth
34
found that while dental extractions induced bac-
teremia in 40 percent of patients, normal masti-
cation and tooth brushing induced bacteremias in
38 percent and 25 percent of patients, respec-
tively.
34
He concluded that the exposure time to
bacteremias during a one-month period was 1,000
times greater from routine chewing and tooth
brushing than it was from a dental extraction.
Periodontal disease may predispose patients to
an increased incidence of bacteremia, a fact
implicit in the American Heart Association, or
AHA, recommendations in regard to the preven-
tion of bacterial endocarditis. These recommenda-
tions stress the importance of establishing and
maintaining the best possible oral health to
reduce potential sources of bacterial seeding.
32
The recommendations further emphasize the role
of the dentist in reducing periodontal inflamma-
tion through professional therapy and oral
hygiene instruction. Because dental procedures
that involve bleeding may induce a transient bac-
teremia, the AHA recommends antibiotic prophy-
laxis prior to dental procedures known to induce
gingival or mucosal bleeding,
including professional cleaning.
32
Patients at risk of developing
infective endocarditis may undergo
multiple courses of antibiotic
therapy, increasing the risk of
establishing resistant strains;
alternatively, numerous procedures
may be accomplished at the same
appointment, if possible. It may be
prudent to allow at least seven
days to elapse between appoint-
ments or to select an alternate
antibiotic regimen for appoint-
ments within this one-week period.
32
As a local
adjunct to systemic antibiotic prophylaxis, a
chlorhexidine mouthrinse has been recommended
before dental procedures.
Anticoagulant therapy. Patients with pros-
thetic heart valves; other valvular disorders; or a
history of myocardial infarction, CVA or throm-
boembolism frequently receive anticoagulant
therapy consisting of coumadin derivatives, such
as dicumarol and warfarin.
18,36
Most patients maintain a therapeutic level of
anticoagulation, resulting in a prothrombin time,
or PT, of 1.5 to 2.0 times that of the laboratory
control PT, although some patients may require
greater levels of anticoagulation (> 2.0 times the
control time).
Historically, the PT has been expressed as the
ratio of the patients actual PT (in seconds) to a
control value that varies between laboratories.
This PT ratio method of reporting PT is no longer
used in most countries, and is being replaced in
the United States by the International Normal-
ized Ratio, or INR, method.
37
The INR, also
known as the corrected PT ratio, is the PT value
42S JADA, Vol. 133, June 2002
Most cases of
infective endocarditis
involving oral
microorganisms
probably are caused
by dental disease,
mastication and oral
hygiene procedures.
Copyright 2002 American Dental Association. All rights reserved.
that would have been determined had the test
been done using the World Health Organizations
standard thromboplastin, an international refer-
ence thromboplastin.
38
The major source of vari-
ability in reporting (due to differences in calcu-
lating) is the PT ratio to the international
reference standard.
The dental health care provider may consult
with the patients physician before treatment
(which can induce bleeding) to determine whether
modification of anticoagulant therapy is indicated.
In addition, drug interactions with warfarin and
other similar agents are numerous, and these must
be considered. Aspirin and other nonsteroidal anti-
inflammatory drugs may dramatically increase the
risk of warfarin-associated bleeding.
37,39,40
Tetracy-
clines may decrease vitamin K production, inter-
fere with formation of prothrombin and increase
anticoagulation.
41,42
Metronidazole may inhibit
coumadins metabolism, potentiating its anticoagu-
lant effect, while penicillin may counteract
coumadins effect.
37
Clinicians should alter anticoagulant therapy
only in consultation with the patients physician,
since some people are more at risk of developing
thrombus formation or hemorrhage than are
others.
43
Aspirin, an inhibitor of platelet aggregation,
often is used to prevent thrombosis formation.
44
Because of its irreversible binding to platelets,
the effect of aspirin lasts at least four to seven
days. It generally is used in small doses of 325
milligrams or less and usually will not alter
bleeding time significantly at this dose. However,
higher doses may increase bleeding time and pre-
dispose the patient to develop postoperative
bleeding. For these patients, aspirin therapy may
be discontinued for several days before the dental
procedure if treatment is expected to induce sig-
nificant bleeding.
CONCLUSION
In May 2000, the public health community was
alerted to the need to promote oral health by the
first surgeon generals report on oral health.
Although the precise mechanisms of interaction
are not clear, sufficient evidence exists to conclude
that oral lesions, especially advanced periodontic
pathologies, place certain patients at increased
risk of developing cardiovascular disease and
stroke. These observations are leading dentists
and physicians to interact more closely in caring
for patients. In addition, a greater burden is being
placed on the dental community to become more
familiar with oral microbiology and the pharmaco-
logical approaches available to treat oral diseases
that may have systemic implications.
The patient with cardiovascular disease may
present a challenge to the dental health care
provider, depending on the degree of hemody-
namic compromise and the stability of his or her
condition. Many of the dental treatment
approaches used for these patients are based on
consensus opinion established through years of
experience and informed clinical judgment. Few
of the treatment approaches are founded on con-
trolled clinical trials that have assessed the effect
of different treatment modalities on well-defined
outcome criteria.
In many instances, such studies are limited by
ethical or medicolegal considerations involved
with placing patients at risk of developing sys-
temic complications. Research also may be lim-
ited by the difficulty in obtaining study popula-
tions of adequate size for relatively rare disorders
such as infective endocarditis. "
Dr. Rose is a professor of surgery and medicine, MCP Hahnemann
School of Medicine, Philadelphia, a clinical professor of periodontics,
University of Pennsylvania School of Dental Medicine, Philadelphia,
and in private practice in periodontics, 2020 Land Title Building, 100
S. Broad St., Philadelphia, Pa. 19110, e-mail dentalteam@speakeasy.
net. Address reprint requests to Dr. Rose.
Dr. Mealey is chief of periodontics and chief of Dental Professional
Services, U.S. Air Force Hospital, Eglin Air Force Base, Florida, and a
clinical assistant professor of periodontics, University of Texas Health
Science Center, San Antonio.
Dr. Minsk is an assistant professor of surgery and medicine, MCP
Hahnemann School of Medicine, Philadelphia, a clinical assistant pro-
fessor of periodontics, University of Pennsylvania School of Dental
Medicine, and in private practice in periodontics, Philadelphia.
Dr. Cohen is chancellor-emeritus, MCP Hahnemann School of
Medicine, Philadelphia, dean-emeritus, University of Pennsylvania
School of Dental Medicine, Philadelphia, and in private practice in
periodontics, Philadelphia.
1. Oral health in America: a report of the surgeon general: executive
summary. Rockville, Md.: National Institute of Dental and Craniofacial
Research; 2000.
2. World Health Organization. The World Health Report 1995:
bridging the gaps. Geneva: World Health Organization; 1995;16:377-85.
3. Umino M, Nagao M. Systemic diseases in elderly dental patients.
Int Dent J 1993;43:213-8.
4. Mattila KJ, Nieminen MS, Valtonen VV, et al. Association between
dental health and acute myocardial infarction. BMJ 1989;298:779-81.
5. Mattila KJ, Valle MS, Nieminen MS, Valtonen VV, Hietaniemi KL.
Dental infections and coronary atherosclerosis. Atherosclerosis
1993;103:205-11.
6. Grau AJ, Buggle F, Ziegler C, et al. Association between acute
cerebrovascular ischemia and chronic and recurrent infection. Stroke
1997;28:1724-9.
7. DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM.
Dental disease and risk of coronary heart disease and mortality. BMJ
1993;306:688-91.
8. Osler W. Diseases of the arteries. In: Osler W, ed. Modern medicine:
Its practice and theory. Philadelphia: Lea & Febiger; 1908:429-47.
9. Haraszthy VI, Zambon JJ, Trevisan M, Zeid M, Genco RJ. Identifi-
JADA, Vol. 133, June 2002 43S
Copyright 2002 American Dental Association. All rights reserved.
cation of pathogens in atheromatous plaques. J Periodontol
2000;71:1554-60.
10. Genco, RJ, Glurich I, Haraszthy V. Overview of risk factors for
periodontal disease and implications for diabetes and cardiovascular
disease. Compend Contin Educ Dent 1999;19(1 supplement):40-5.
11. Ross R, Glomset J. The pathogenesis of atherosclerosis (first of
two parts). N Engl J Med 1976;295:369-77.
12. Ross R, Glomset J. The pathogenesis of atherosclerosis (second of
two parts). N Engl J Med 1976;295:420-5.
13. Matsuura H. The systemic management of cardiovascular risk
patients in dentistry. Anesth Pain Control Dent 1993;2:49-57.
14. Council on Community Health, Hospital, Institutional, and Med-
ical Affairs. Hypertension update: a survey of the literature of interest
to dentists. 1989;118:645-6.
15. MacAfee KA 2nd, Chisdak B, Hersh EV Angina pectoris:
diagnosis and treatment in the outpatient setting. Compendium
1993;14:892-900.
16. Findler M, Galili D, Meidan Z, Yakirevitch V, Garfundel AA.
Dental treatment in very high risk patients with active ischemic heart
disease. Oral Surg Oral Med Oral Pathol 1993;76:298-300.
17. McCarthy FM. Safe treatment of the post-heart-attack patient.
Compendium 1989;10:598-604.
18. Shuman SK. A physicians guide to coordinating oral health and
primary care. Geriatrics 1990;45(8):47-57.
19. Perusse R, Goulet JP, Turcotte JY. Contraindications to vasocon-
strictors in dentistry, part I: cardiovascular diseases. Oral Surg Oral
Med Oral Pathol 1992;74:687-91.
20. Knoll-Kohler E, Fortsch G. Pulpal anesthesia dependent on
epinephrine dose in 2% lidocaine: a randomized controlled double-blind
crossover study. Oral Surg Oral Med Oral Pathol 1992;73:537-40.
21. Meyer FU. Haemodynamic changes under emotional stress fol-
lowing a minor surgical procedure under local anesthesia. Int J Oral
Maxillofac Surg 1987;16:688-94.
22. Levine E, Tzukert AA, Mosseri M, et al. Perioperative hemody-
namic changes in ischemic heart disease patients undergoing dental
treatment. Spec Care Dentist 1992;12(2):84-8.
23. Smith GN, Pashley DH. Periodontal ligament injection: evalua-
tion of systemic effects. Oral Surg Oral Med Oral Pathol 1983;56:571-4.
24. Findler M, Garfunkel AA, Galili D. Review of very high-risk car-
diac patients in the dental setting. Compendium 1994;15(1):58-66.
25. Farkas JA, Goebel WM. Assessing the risk of angina for dental
therapy. Oral Surg Oral Med Oral Pathol 1984;58:253-6.
26. Luria MH, Debanne SM, Osman MI. Long-term follow-up after
recovery from acute myocardial infarction: observations on survival,
ventricular arrhythmias, and sudden death. Arch Intern Med
1985;145:1592-5.
27. Ruberman W, Weinblatt E, Frank CW, Goldberg JD, Shapiro S.
Repeated 1-hour electrocardiographic monitoring of survivors of
myocardial infarction at six-month intervals: arrhythmia detection and
relation to prognosis. Am J Cardiol 1981;47:1197-204.
28. Cintron G, Medina R, Reyes AA, Lyman G. Cardiovascular effects
and safety of dental anesthesia and dental interventions in patients
with recent uncomplicated myocardial infarction. Arch Intern Med
1986;146:2203-4.
29. Gilbert GH, Minaker KL. Principles of surgical risk assessment of
the elderly patient. J Oral Maxillofac Surg 1990;48:972-9.
30. Ostuni E. Stroke and the dental patient. JADA 1994;125:721-7.
31. Syrjanen J, Peltola J, Valtonen V, Iivanainen M, Kaste M, Hut-
tunen JK. Dental infections in association with cerebral infarction in
young and middle-aged men. J Intern Med 1989;225(3):179-84.
32. Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial
endocarditis: recommendations by the American Heart Association.
JAMA 1997;277:1794-801.
33. Genco RJ, Grossi SG, Zambon JJ, Reynolds H, Ho A, Garrett S.
Frequency of bacteremia following different modalities of periodontal
treatment (abstract 842). J Dent Res 2001;80:141.
34. Guntheroth WG. How important are dental procedures as a cause
of infective endocarditis? Am J Cardiol 1984;54:797-801.
35. Creighton JM. Dental care for the pediatric cardiac patient. J Can
Dent Assoc 1992;58:201-7.
36. Martinowitz U, Mazar AL, Taicher S, et al. Dental extraction for
patients on oral anticoagulant therapy. Oral Surg Oral Med Oral
Pathol 1990;70:274-7.
37. Hirsh J, Dalen JE, Deykin D, Poller L. Oral anticoagulants:
mechanism of action, clinical effectiveness, and optimal therapeutic
range. Chest 1992;102:312S-26S.
38. Bussey HI. How to monitor the dosage of warfarin. Heart Dis
Stroke 1993;2:388-92.
39. Wynn RL. Dental nonsteroidal anti-inflammatory drugs and
prostaglandin-based drug interactions, part one. Gen Dent
1992;40(1):18-20.
40. Carr MM, Mason RB. Dental management of anticoagulated
patients. J Can Dent Assoc 1992;58:838-44.
41. Fay JT, ONeal R. Dental responsibility for the medically compro-
mised patient. J Oral Med 1984;39:218-45.
42. Felder RS, Miller SB. Dental care of the polymedication patient.
Dent Clin North Am 1994;38:525-36.
43. Scheitler LE, Hart N, Phillips G, Weinber JB. Hematologic and
surgical management of the dental patient with plasminogen activator
deficiency. Oral Surg Oral Med Oral Pathol 1988;66:680-2.
44. Kasco G, Terzhalmy GT. Acetylsalicylic acid and acetominophen.
Dent Clin North Am 1994;38:633-44.
44S JADA, Vol. 133, June 2002
Copyright 2002 American Dental Association. All rights reserved.