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Discussion
Cross-sectional
studies performed with convenience samples, such as
this study, cannot be generalized to the entire population.
However, they can identify as risk indicators those
parameters that are significantly associated with the
condition being investigated (in this case, CHD). Whether
these risk indicators prove to be risk factors (that
is, causally related) remains to be demonstrated in
prospective studies performed with a more representative
population.
The results of this cross-sectional study confirmed
those of previous studies conducted with younger subjects
that showed a significant association between dental
disease and CHD.1-6
We found that the subjects with one to 14 teeth were
most likely to have CHD, and observed this association
in subjects in both independent living and dependent
living circumstances. Chronic
infection hypothesis. The importance of having
only a few teeth in these subjects seems to be related
to the greater periodontal morbidity of their teeth�that
is, a higher percentage of teeth with attachment loss�to
poorer oral hygiene as assessed by higher plaque scores,
and to less-frequent visits to the dentist (Table
3). In the multivariate analysis, a high BANA test
score was positively associated with CHD in both the
all-subjects dentate model (Table
4) and the independent living dentate model (Table
5).
The BANA test detects the presence of an enzyme(s) that
hydrolyzes the synthetic trypsinlike substrate benzoyl-DL-arginine-naphthylamide,
or BANA, in plaque samples.16
Of more than 60 plaque bacterial species that have been
tested, only P. gingivalis, Treponema denticola and
Bacteroides forsythus always exhibit strong BANA activity,
although some species, like the Capnocytophaga species,
occasionally exhibit weak BANA activity.16
The three strongly BANA-positive species are invariably
elevated in plaque samples removed from teeth with periodontal
pathology.17-20
Thus, a higher plaque BANA score would indirectly indicate
that these periodontopathic species are elevated on
the tooth surfaces of subjects with CHD. This implies
some degree of periodontal pathology, which was documented
by the significantly higher PBS in the multivariate
model of independent living dentate subjects (Table
5).
These BANA-positive species are gram-negative anaerobes,
so that their elevation in the dental plaque would support
the various hypotheses linking chronic bacterial infection
to CHD via effects mediated by endotoxins or lipopolysaccharides,
or LPS.21-23
The confrontation of the varied host-defense mechanisms
with these LPS-containing invaders may lead to the supplementation
of serum cytokine levels with inflammatory mediators
derived from this confrontation,24
which could contribute to the chronic inflammatory process
that leads to increased levels of C-reactive proteins
in the serum.8
LPS has long been known to promote atherosclerosis and
thrombus formation.25
An additional factor in this process could be an exaggerated
host response to LPS, mediated by the presence of hyperresponsive
monocytic cells.6
Certain patients with early-onset perio-dontitis, refractory
periodontitis or insulin-dependent diabetes have peripheral
blood monocytes that secrete threefold to 10-fold greater
amounts of PGE2, IL-1b and TNFa when exposed to LPS
in vitro. These people would react to the penetration
of gram-negative bacteria, such as the BANA-positive
species, from the subgingival plaque into the periodontium
by the overproduction of cytokines that could leak from
the gingival tissue into the general circulation and
have an effect on distant organs.
Other studies have proposed a chronic infection hypothesis
involving dental disease as a possible risk factor for
the development of a cardiovascular event.21,22
In their prospective study, Mattila and colleagues3
were able only to associate dental infections as measured
by the TDI and a history of myocardial infarction with
a subsequent acute myocardial infarction. They then
showed that there are elevated levels of von Willebrand
factor antigen in subjects with an elevated TDI,26
which could reflect increased endothelial cell damage
induced by the LPS derived from the gram-negative dental
plaque flora. Grau and colleagues7
have shown that the TDI may be associated with an increased
risk of cerebral vascular ischemia. Missing
teeth. The number of missing teeth was independently
associated with CHD in the two epidemiologic surveys
that randomly selected their study populations,4,5
but these studies did not distinguish between edentulous
subjects and dentate subjects with many missing teeth.
Our results indicate that in these elderly subjects,
it is the presence of only a few teeth that is associated
with CHD. When we divided our subjects into groups with
one to 14 teeth and 15 to 28 teeth, the presence of
one to 14 teeth was significantly associated with CHD
in both the all-subjects and dentate subjects models
(Table 4).
An indirect confirmation of the importance of having
15 to 28 teeth in protecting against CHD was the relationship
between the salivary levels of S. sanguis and CHD status.
The significant negative association seen in all models
(Table 4)
can be explained by the fact that this organism is associated
with teeth, and is among the best microbial colonizers
on the tooth surface.27
This
organism is dominant in early plaque formation, so that
people with good oral hygiene would have higher proportions
of S. sanguis in the mouth. The more teeth in the mouth,
the more likely that the salivary levels of S. sanguis
would be higher.
S. sanguis has been studied for its role in endocarditis,28,29
and a platelet-aggregation-associated protein has been
identified as a virulence factor because it interacts
with platelets, promoting coagulation, or it may behave
as a heat-shock protein, which, by causing an autoimmune
response, could initiate the early atherosclerotic lesion.30
Our findings do not support a role for S. sanguis in
CHD in these older subjects, but it is possible that
such interactions could have occurred earlier in their
lives.
Evidence in the literature suggests that edentulous
people with and without dentures and dentate people
with missing teeth change their eating habits after
they lose their teeth.31,32
They may avoid certain nutritious foods because of difficulty
in chewing, and select high-calorie, high-fat foods
whose consumption is recognized as a risk factor for
cardiovascular disease.33
But an additional feature of this dietary change that
could be particularly relevant in those dentate subjects
with one to 14 teeth is that dietary-induced elevation
of serum low-density lipoprotein levels has been shown
to increase monocytic responses to LPS.34
These subjects would have both the dietary-induced sensitization
of the monocytes and the plaque-laden teeth and gingivitis
that could provide the LPS challenge to these cells.
The advanced age of our subjects might explain the absence
of an association between edentulism and CHD in the
logistic regression models, since people most susceptible
to the linkage between edentulism and CHD may already
be dead. This would be consistent with the National
Health and Nutrition Examination Survey, or NHANES,
data that showed that in males younger than 50 years
of age, edentulism was 2.6 times more likely to be associated
with death resulting from any cause.4
However, this explanation, as well as the chronic infection
hypothesis involving dental infections, would not seem
to explain why 53 percent of our edentulous subjects
had CHD, unless these patients experienced their first
heart attack while they had teeth. It is possible that
by having had their teeth extracted, these people coincidentally
had the tooth-related microbial challenge removed that
had been a major contributor to the events leading to
their heart attack. Edentulism in this sense would be
protective, although in the younger subjects in the
NHANES study, edentulism might have been a marker for
rampant dental disease that could have predisposed them
to CHD by the mechanisms described above. Other
significant findings. The possible protective
role of daily alcohol consumption noted in the all-subjects
model in this study has been observed by others.35
The greater use of all types of medications was significantly
associated with CHD in both the all-subjects and dentate
subjects models. This was expected, as our subjects
were taking many types of medications associated with
old age and a diagnosis of cardiovascular and other
diseases.36
It is not clear how a complaint of xerostomia could
be such a powerful risk indicator for CHD. Xerostomia
is a common complaint of older people,37
and it has been associated with poor oral hygiene, the
inability to chew and involuntary weight loss among
both institutionalized38,39
and independent older adults.38
We have found that people with complaints of xero-stomia
avoid crunchy (carrots), dry (bread) and sticky (peanut
butter) foods, but not crumbly (cake) or chewy (red
meat) foods.40
This choice of foods could lead to the selection of
the high-calorie, high-fat foods that are associated
with obesity and CHD.33
The use of a convenience sample of older subjects for
our analysis may explain why recognized risk factors,
such as serum cholesterol levels, BMI, smoking status
and diabetes, were not more prominent in the modeling
procedure. The use of medications to control blood pressure
or cholesterol levels was not included in our analysis;
as these subjects were actively receiving treatment
for CHD, this could explain why these risk factors were
not associated with CHD.
In other studies performed with convenience samples,
the dental variables were significantly associated with
CHD, whereas the classical risk factors such as cholesterol
levels, alcohol consumption, BMI and hypertension were
not.1-3,7
Thus, our investigation, like others performed with
convenience samples, cannot be generalized to the entire
population, and because of the cross-sectional nature
of our study, the oral health variables can at best
be considered risk indicators. Despite these limitations,
for this group of older veterans, our findings suggest
that the oral health parameters may play an important
role in the occurrence of CHD. We are following up these
subjects to determine whether any of these dental parameters
can be shown to be risk factors. |
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Results |
Conclusion
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