Could periodontal disease be killing your patients? This seems, taken literally, an
absurd statement. However evidence has been mounting that points to a link between chronic
periodontal disease and an increased risk for coronary artery disease as well as stroke.
And the risk level is not so small that it can be considered inconsequential. While
smoking, hypertension, excessive lipids in the bloodstream and diabetes remain major
determinants of risk for cardiovascular incidents, periodontal disease may rank above
stress, sedentary lifestyle and obesity as a contributor to heart disease. During the past
ten years at least 12 papers have appeared in the worldwide literature relating
periodontal disease to heart disease. Some indicate periodontal disease to nearly double
the risk of a coronary incident in those with other major risk factors. Since the major
risk factors account for only 50% to 60% of the incidence of cardiovascular disease
chronic periodontal infection may be a source of frequent bacterial challenge to heart and
brain vessel walls, accelerating the disease process. Your patients with periodontal
disease should be made aware of
the interactions between periodontal disease, heart disease and stroke.They may have
several questions regarding the relationship between periodontal disease and heart disease
and the steps which should be taken tor educe their risk. This newsletter provides youwith
the latest background information on the development of vascular disease and the
influence periodontal disease may have on its progression.
of
the interactions between periodontal disease, heart disease and stroke.They may have
several questions regarding the relationship between periodontal disease and heart disease
and the steps which should be taken toreduce their risk. This newsletter provides youwith
the latest background inforrnation on the development of vascular disease and the
influence periodontal disease may have on its progression.
To begin this review let's examine the anatomy of the arterial wall shown tothe right.
(Figure 1) The intima is theinner endothelial layer of the vessel wall. |
Adventitia
Media
Intima
Endothelium
vessel lumen
Figure 1
|
 |
 The second
layer is termed the media. It has anexternal and internal elastic lamina with
smooth muscle between. The adventitia is
the layer furthest from the endothelium and
consists of fibroblasts, collagen and vessels
termed "vasa vasorem" because they supply
nutrition to the blood vessel components. In
certain individuals with a genetic predisposition
fatty streaks form immediately below the endothe-
lial layer. (Figure 2) These are called fatty streaks
because they are made of foam cells filled with lipids.
Foam cells come from macrophages and, to a lesser extent, smooth muscle cells. Fatty
streaks are often found by age 20 and may have a hereditary tendency. In some individuals
they recede with age. Bulging or stretching of the intima from the formation of fatty
streaks may increase the likelihood of the endothelium being injured by irregular blood
flow. Vascular disease is initiated through injury to the endothelium of the intimal layer
which may have been made susceptible by
the formation of a so called "fatty streak" in the medial layer of the
vessel.
|
vessel
lumen
Figure
2 |
Media Smooth Muscle
fatty streak "bulges"
endothelium into lumen |
When the endothelial layer becomes injured, the damaged endothelial cells develop wider
inter-endothelial spaces. Injury can occur from smoking (reduced oxygen carrying by red
blood cells produces endothelial cell hypoxia), hypertension (increased blood pressure on
endothelial cells) and hyperlipidemia (primary mechanism related to lipid release into
endothelial cells by lowdensity lipoproteins [LDL] circulating in bloodstream). These are
identified primary factors. But bacteremias from chronic periodontal disease may serve as
repeated sources of infection to the endothelium which has been conditioned by prior
trauma. Dom and Progulske-Fox have demonstrated that two periodontal pathogens, P.
Gingivalis and P. Intermedia, do invade endothelium in a laboratory setting. In addition,
Herzberg and Meyer found the otherwise innocuous bacteria Streptococcus Sanguis to induce
the aggregation of platelets. When introduced in experimental animals with hyperlipidemia
the resulting red blood cell aggregations triggered signs of myocardial infarction.
Once endothelial cells have been injured monocytes in the blood stream migrate to the
area of injury and proceed into the intimal layer of the transient bacteremias of vessel,
between endothelial cells. They, along with smooth muscle cells from the medial layer of
the blood vessel, transform into foam cells. Cellular debris and cholesterol crystals fill
the foam cells. This "core" of foam cells becomes surrounded by connective
tissue,
forming the fibrous plaque we hear about in much medical literature.
These fibrous plaques displaced smooth muscle cells are most common in the aorta,
coronary arteries, internal carotids and circle of Willis in the cranium. Lilly, in his
text on the pathophysiology of heart disease, lists the five complications of the fibrous
plaque.
The chronic nature of periodontal infection makes it a particularly significant factor
in the process of plaque formation. In moderate periodontal disease with pockets of 4-5mm
depth throughout the mouth the surface area of infection in the pockets added together
would be equivalent to creating an ulcer the size of your palm with fingers extended on
the side of your face. When this condition exists bacteremias occur over 40% of the times
the teeth are brushed. It is the repeated introduction to the bloodstream of these
bacteria which may increase periodontitis as a risk factor for myocardial infarction or
stroke.
Repetitive challenges to the vascular endothelium from the periodontal bacteremias
initiate the inflammatory cycle in the vascular endothelium already involved with plaque
formation. Observations of myocardial infarction cases indicate that rupture of the
atherosclerotic plaque (the fibrous plaque mentioned earlier) with superimposed thrombosis
is the primary mechanism in myocardial infarction rather than a progressive, gradual
enlargement of the fibrous plaque. The repetitive challenge produced by oral bacteremias
may cause the production of more foam cells (in the presence of too many circulating low
density lipoproteins [LDL]) and, at the same time, inhibit collagen synthesis increasing
the likelihood of rupture of the fibrous plaque. As noted earlier some oral pathogens also
cause alterations in the inflammatory process resulting in more sticking of platelet cells
to the damaged endothelium.
Just as we attempt to treat hyperlipidemia to reduce the risk of atherlerosclerotic
heart disease periodontal bacteremias need to be reduced in the coronary high risk
patient. Patients who have high blood pressure, hyperlipidemia, diabetes or smoke are at
greater risk for myocardial infarction and stroke when periodontal pockets are of moderate
depth. In these cases good oral hygiene, pocket reduction and short interval maintenance
may be the best method of reducing periodontal risk factors. In several of the studies the
impact of periodontitis as a risk factor was greatest in males under 50. Since many of the
studies were on male populations the impact on females may be similar but less well
documented.
Our office welcomes the opportunity to assist you in assessing the periodontal status
of those patients at risk for significant cardiac disease. Your patients who smoke, have
high cholesterol, hypertension or diabetes should be closely scrutinized for periodontal
disease and aggressively treated. Together we can improve not only the dental health
status of patients but their overall health as well.
