done

1

INTRODUCTION

Background. This article is a critical review of disassociating oral conditions with
stroke. We evaluated the oral conditions of periodontal disease or tooth

loss as risk factors for
arterial disease and stroke.
1

Results. Seven of nine studies evaluating tooth loss and periodontal

disease as risk
factors for stroke or PVD showed some significant

associations. The studies varied in the
exposures and outcomes

evaluated; therefore, the associations were not consistently

replicated. It is unclear whether the associations found between

these oral conditions and
cardiovascular disease had any causal

component. In the absence of any causal relationship,
the associations

may be explained by common risk factors. Alternatively, there

may be a
causal relationship that may be explained by one or

more potential causal pathways. Further
epidemiologic studies

are needed, and the role of nutrition and other inflammatory

mediators
needs to be explored further in this context.









2

DENTAL CARIES

Dental Caries is a tooth disease caused by the complex interaction of food, especially
starches and sugars, with the bacteria that form dental plaque. The term also refers to the
tooth cavities that result from the disease. Two groups of bacteria are responsible for
initiating caries: Streptococcus mutans and Lactobacillus.
6

The presentation of caries is highly variable; however, the risk factors and stages of
development are similar. Initially, it may appear as a small chalky area that may eventually
develop into a large cavitation. Sometimes caries may be directly visible, however other
methods of detection such as radiographs are used for less visible areas of teeth and to judge
the extent of destruction.
Patofisiology

Dental Caries begin asymptomatically as a destructive process of the hard surface of
tooth. Streptococcus mutans, principally, along with other bacteria colonize the organic
buffering film on the tooth surface to produce plaque. If not removed by brushing or the
natural cleaning action of saliva and oral soft tissue, bacterial acids demineralize the enamel.
Plaque bacteria produce acids that cause demineralization of enamel and enzymes that attack
the protein component of the tooth. Tooth decay is caused by specific types of acid-producing
bacteria that cause damage in the presence of fermentable carbohydrates such as sucrose,
fructose, and glucose.
2



3

The mineral content of teeth is sensitive to increases in acidity from the production of
lactic acid. Specifically, a tooth (which is primarily mineral in content) is in a constant state
of back-and-forth demineralization and remineralization between the tooth and surrounding
saliva. . When the pH at the surface of the tooth drops below 5.5, demineralization proceeds
faster than remineralization (meaning that there is a net loss of mineral structure on the
tooth's surface). This results in the ensuing decay. Fissures and pits on the occlusion surfaces
are the most frequent sites of decay.
2

This process, if untreated, ultimately leads to the formation of deep cavities and
bacterial infection of the pulp chamber, which contains blood vessels and nerves. Surfaces
adjacent to tooth restorations and exposed roots are also vulnerable, particularly as teeth are
retained in an aging population. Overtime, dental caries extend to the underlying dentin,
leading to cavitation of the enamel and ultimately penetration to the tooth pulp, producing
acute pulpitis.
At this early stage, when the pulp infection is limited, the tooth become sensitive to
percussion and hot or cold, and pain resolves immediately when the irritating stimulus is
removed. Should the infection spread throughout the pulp, irreversible pulpitis occurs,
leading to pulp necrosis. At this late stage pain is severe and has a sharp or throbbing visceral
quality that may be worse when the patient lies down. Once pulp necrosis is complete, pain
may be constant or intermittent, but cold sensitivity is lost.
The development of dental caries in a debilitated patient is a concern because of the
danger that infections of the teeth or gingival tissues may spread to the rest of the body. In
addition, teeth that are decayed or painful inhibit mastication and can lead to dietary changes,
which may in turn cause nutritional and digestive disorders.

4

When there is bleeding in the gums, these cans bacteria get into the blood vessels,
can cause blood vessel blockage. Obstruction of blood flow to the heart cans cause heart
attacks. Meanwhile, if it occurs in the brain, the obstruction will of cause a stroke.
3


Prevention
Instead, dental health organizations advocate preventive and prophylactic measures,
such as regular oral hygiene and dietary modifications, to avoid dental caries. Dental caries
may be prevented by a reduction in the frequency of sugar consumption, use of dental floss
between the teeth, regular brushing of the teeth with a fluoridated toothpaste, drinking of
fluoridated water, topical application of fluorides to the teeth, and removal of plaque and
calculus by a dental hygienist.
2

Treatment

Depending on the extent of tooth destruction, various treatments can be used to
restore teeth to proper form, function, and aesthetics, but there is no known method to
regenerate large amounts of tooth structure, though stem cell related research suggests one
possibility. Treatment of dental caries includes removal of the decayed material and
restoration of the surface of the affected tooth with a silver amalgam or other restorative
material. If the cavity has reached the pulp chamber, it may be necessary to remove the pulp
tissues to alleviate pain, prevent the spread of infection to the rest of the body, and allow the
continued use of the tooth. Alternatively, the entire tooth may be extracted.



5

STROKE

A stroke, previously known medically as a cerebrovascular accident (CVA), is the
rapidly developing loss of brain function due to disturbance in the blood supply to the brain.
This can be due to ischemia (lack of blood flow) caused by blockage (thrombosis, arterial
embolism), or a hemorrhage (leakage of blood).
4

Hemorrhagic stroke accounts for about 13 percent of stroke cases. It results from a
weakened vessel that ruptures and bleeds into the surrounding brain. The blood accumulates
and compresses the surrounding brain tissue. The two types of hemorrhagic strokes are
intracerebral hemorrhage or subarachnoid hemorrhage.
Hemorrhagic stroke occurs when a weakened blood vessel ruptures. Two types of
weakened blood vessels usually cause hemorrhagic stroke: aneurysms and arteriovenous
malformations (AVMs).
An aneurysm is a ballooning of a weakened region of a blood vessel. If left untreated,
the aneurysm continues to weaken until it ruptures and bleeds into the brain.
Nonischemic stroke—that is, hemorrhagic stroke—has

a different etiology, and is not
generally associated with dental

or other infections. The study that evaluated hemorrhagic
stroke

separately found null associations between it and any type of

infection.

Hence, it is
important to evaluate ischemic stroke

separately.
4




6

ISCHEMIC STROKE

Ischemic stroke accounts for about 87 percent of all cases. A Ischemic Stroke is a
sudden loss of function due to loss of blood supply to an area of the brain that controls that
function It is usually caused by partial or complete blockage of an artery that supplies the
brain. In this animation, atherosclerosis in the carotid artery of the neck reduces blood flow to
the brain. A rupture in the plaque can cause a blood clot to form. This clot may break loose
and travel to an artery in the brain where it becomes lodged and totally blocks blood flow,
causing permanent damage. Bleeding of an artery in the brain can also cause a stroke. Stroke
can cause loss of function (use of an arm, leg or drooping of the face).
Ischemic strokes occur as a result of an obstruction within a blood vessel supplying
blood to the brain. The underlying condition for this type of obstruction is the development of
fatty deposits lining the vessel walls. This condition is called atherosclerosis.
5
Cerebral thrombosis refers to a thrombus (blood clot) that develops at the clogged part
of the vessel.
Cerebral embolism refers generally to a blood clot that forms at another location in
the circulatory system, usually the heart and large arteries of the upper chest and neck. A
portion of the blood clot breaks loose, enters the bloodstream and travels through the brain's
blood vessels until it reaches vessels too small to let it pass. A second important cause of
embolism is an irregular heartbeat, known as atrial fibrillation. It creates conditions where
clots can form in the heart, dislodge and travel to the brain.



7

Pathophysiology
Acute occlusion of an intracranial vessel causes reduction in blood flow to the brain
region it supplies. The magnitude of flow reduction is a function of collateral blood flow and
this depends on individual vascular anatomy and the site of occlusion. A fall in cerebral blood
flow to zero causes death of brain tissue within 4 – 10 min; values < 16 – 18 mL/100g tissue
per min cause infarction within an hour; and values <20 mL/100 g tissue per min cause
ischemia without infarction unless prolonged for several hours or days. If blood flow is
restored prior to a significant amount of cell death, the patient may experience only transient
symptoms, i.e., a TIA. Tissue surrounding the core region of infarction is ischemic but
reversibly dysfunctional and is referred to as the ischemic penumbra. The penumbra may be
imaged by using perfusion-diffusion imaging with MRI. The ischemic penumbra will
eventually infarct if no change in flow occurs, and hence saving the ischemic penumbra is the
goal of revascularization therapies.
Focal cerebral infarction occurs via two distinct pathways (1) a necrotic pathway in
which cellular cytoskeletal breakdown is rapid, due principally to energy failure of the cell;
(2) an apoptotic pathway which cells become programmed to die. Ischemia produces necrosis
by starving neurons of glucose, which in turn results in failure of mitochondria to produce
ATP. Without ATP, membrane ion pumps stop functioning and neuron depolarize, allowing
intracellular calcium to rise. Cellular depolarization also causes glutamate release from
synaptic terminals; excess extracellular glutamate produces neurotoxicity by activating
postsynaptic glutamate receptors that increase neuronal calcium influx. Free radicals are
produced by membrane lipid degradation and mitochondrial dysfunction. Free radicals cause
catalytic destruction of membranes and likely damage other vital function of cells. Lesser
degrees of ischemia, as are seen within the ischemic penumbra, favor apoptotic cellular death
causing cells to die days to weeks later.

8

Fever dramatically worsens ischemia, as does hyperglycemia, so it is reasonable to
suppress fever and prevent hyperglycemia as much as possible. Include moderate
hypothermia to mitigate stroke is the subject of continuing clinical research.
Treatment
The first goal is to prevent or reverse brain injury. Attend to the patient’s airway,
breathing, circulation, and treat hypoglycemia or hyperglycemia if identified. Perform an
emergency noncontrast head CT scan in order to differentiate between ischemic stroke and
hemorrhagic stroke; there are no reliable clinical finding that conclusively separate ischemia
from hemorrhage, although a more depressed level of consciousness, higher initial blood
pressure, of worsening of symptoms after onset favor hemorrhage, and a deficit that remits
suggest ischemia.
Treatment designed to reverse or lessen the amount of tissue infarction and improve
clinical outcome fall within six categories :
1. Medical support
2. Intravenous thrombolysis
3. Endovascular techniques
4. Antithrombotic treatment
5. Neuroprotection
6. Stroke centers and rehabilitation




9

CORRELATION BETWEEEN DENTAL CARIES AND
ISCHEMIC STROKE

Streptococcus mutans, the type of bacteria that also causes inflammation of the gums
and tooth decay. When there is bleeding in the gums, these bacteria can get into the blood
vessels. In the blood, the bacteria Streptococcus has a defense mechanism against the human
immune system and antibiotics attack. How, bacteria use to bind several proteins in blood
cells that form the sheath. For the bacterial envelope was very useful, but instead is deadly to
humans. At a certain size, the veil is like blood clots that obstruct blood flow to the heart
vessels.
1











10

TABLE SUMMARY OF STUDIES EVALUATING
THE POTENTIAL RELATIONSHIP BETWEEN ORAL
CONDITIONS AND STROKE


11


The involvement of oral bacteria in the pathogenesis of cardiovascular

disease has
been studied, with Streptococcus mutans, a pathogen

of dental caries, detected in
cardiovascular lesions at a high

frequency. However, no information is available regarding
the

properties of S. mutans detected in those lesions. Heart valve

specimens were collected
from 52 patients and atheromatous plaque

specimens from 50 patients, all of whom
underwent cardiovascular

operations, and dental plaque specimens were taken from 41 of

those subjects prior to surgery. Furthermore, saliva samples

were taken from 73 sets of
healthy mothers (n=73) and their

healthy children (n=78). Bacterial DNA was extracted from
all

specimens, then analysed by PCR with S. mutans-specific and

serotype-specific primer
sets.
1



12

The detection rates of S. mutans

in the heart valve and atheromatous plaque specimens
were 63 and

64 %, respectively. Non-c serotypes were identified with a significantly

higher
frequency in both cardiovascular and dental plaque samples

from the subjects who underwent
surgery as compared to serotype

c, which was detected in 70–75 % of the samples from the

healthy subjects. The serotype distribution in cardiovascular

patients was significantly
different from that in healthy subjects,

suggesting that S. mutans serotype may be related to
cardiovascular

disease.
Streptococcus mutans, a major pathogen of dental caries, has

been detected in heart
valves and isolated from the blood of

patients with infective endocarditis (IE), suggesting its
close

relationship with S. mutans is classified

into four serotypes (c/e/f/k) based on the
chemical composition

of its cell surface serotype-specific rhamnose–glucose

polymers
(RGPs), which form a backbone of rhamnose polymers

with side chains of glucose polymers .
Serotype c is reported to be the most

prevalent in oral isolates at approximately 70–80 %,
followed

by e, f and k. In our previous

study, four S. mutans strains isolated from the blood of
patients

with bacteraemia after tooth extraction or IE were characterized;

however, none of
those strains were classified as serotype c

.
1

The serotype-specific RGPs of S. mutans were demonstrated to

play important roles in
streptococcal adherence to human monocytic

and fibroblastic cells, and speculated to be its
most efficient

cytokine-stimulating components.

In addition, the hydrophilic nature of RGPs
is known to be associated

with the resistance to phagocytosis by human polymorphonuclear

leukocytes. Further, RGPs were shown to

possess properties allowing them to bind directly to
human platelets

and trigger their aggregation in a dose-dependent manner.

In our previous
study, serotype k strains featured a drastic

reduction in the amount of glucose side chains and
were shown

to be less susceptible to phagocytosis by human polymorphonuclear

leukocytes

13

than the parent strain. However,

the virulence of each serotype of S. mutans in blood remains

to be elucidated.


Recently, the association of cardiovascular diseases and periodontitis

has received
attention because of results showing that periodontopathic

bacterial DNA could be detected in
the diseased cardiovascular

tissues. We previously reported that

not only periodontopathic
bacterial species, but also several

streptococcal species, were detected in cardiovascular
specimens,

such as heart valve and atheromatous plaque, and S. mutans was

the most
frequently detected. In the

present study, detection of S. mutans in additional specimens,

as
well as serotype determination of S. mutans-positive specimens,

was carried out.


Fifty-two heart valve and fifty atheromatous plaque samples

were obtained from
subjects with cardiovascular diseases who

visited Osaka Rosai Hospital. Of these, 41 subjects
were referred

to the Department of Dentistry and Oral Surgery for a dental

examination prior
to cardiovascular surgery, and from whom dental

plaque specimens were obtained. All of the
specimens were collected

from December 2004 to August 2006 according to a protocol
approved

by the ethics committee of Osaka Rosai Hospital. The heart valve

tissue specimens
were excised during a valve replacement procedure,

following diagnosis of aortic
regurgitation, aortic stenosis,

mitral regurgitation, mitral stenosis or tricuspid regurgitation,

while the atheromatous plaque specimens were collected during

treatment for a thoracic or
abdominal aortic aneurysm. The specimens

were aseptically cut into small pieces, and
bacterial DNA was

extracted as described previously



14

The minimum amounts of genomic DNA required for S. mutans detection

and
serotype determination by PCR methods used in the present

study were evaluated using serial
dilution of known concentrations

of genomic DNA extracted from the reference strains
(Fig. 1 ).

The PCR results with gtfD- and gtfB-based primer sets showed

that the minimum
amount of template DNA for S. mutans detection

was 1–10 pg, which was also the detection
limit for the

template DNA for serotype c/e/f/k.















15

CONCLUSION

Dental caries, initiated by Streptococcus mutans, When there is bleeding in the gums,
these bacteria can get into the blood vessels. In the blood, the bacteria Streptococcus has a
defense mechanism against the human immune system and antibiotics attack. How, bacteria
use to bind several proteins in blood cells that form the sheath. For the bacterial envelope was
very useful, but instead is deadly to humans. At a certain size, the veil is like blood clots that
obstruct blood flow to the heart vessels.
Therefore very important to maintain oral hygiene to prevent dental caries and prevent
Obstruction of blood flow to the heart can cause heart attacks. Meanwhile, if it occurs in the
brain, the obstruction will cause a stroke.











16

REFERENCES

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JL, editors. Harrison’s Internal Medicine. 17th ed. New York: The McGraw-Hill
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http://www.mayoclinic.org/stroke/
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http://www.strokeassociation.org/STROKEORG/AboutStroke/TypesofStroke/Types-
of-Stroke_UCM_308531_SubHomePage.jsp
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