CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 8, September 2013
AFRICA
311
(2.4%) in group I showed progression of carotid artery intima–
media thickness. On the other hand, 47 patients (11%) in group
II showed progression of carotid artery intima–media thickness.
Patients with progressive atherosclerosis had significantly higher
DMFT and SLI indices than patients with stable disease.
Further analysing the sub-categories of DMFT, six-month
follow-up measurements revealed that the number of missing
teeth was strongly associated with disease progression (
p
=
0.001). However the significance of the number of decayed
teeth (
p
=
0.02) and filled teeth (
p
=
0.09) were not significantly
associated with disease progression.
Discussion
Cardiovascular disease is a major cause of morbidity and
mortality worldwide. In the last 10 years, a rising number
of epidemiological investigations have studied the possible
association between inflammatory diseases or chronic infections
(i.e. periodontal infections) and cardiovascular diseases.
8-10
According to these studies, atherosclerosis is considered a
process closely related to inflammation.
We know that infectious or inflammatory diseases elevate
levels of inflammatory markers, and autoimmune processes can
contribute to the development of atherosclerosis.
8
In addition,
several studies published during the last two decades indicate
that oral diseases, periodontal inflammation, and especially
poor oral hygiene may act as risk factors for the development of
atherosclerosis via chronic inflammation.
11-13
In particular, chronic microbial infection, including several
periodontal pathogens, may play an important role in the
development of atherosclerotic disease.
6,14,15
It is unclear how
periodontal disease causes thickening of the arterial intima–media
wall, which is a predictor of sub-clinical atherosclerosis.
16,17
It is
uncertain whether an immune response to the pathogens or the
pathogen itself triggers progression of atherosclerotic disease.
4,18
We could confirm that missing and decayed teeth were
significantly associated with progression of atherosclerosis rather
than filled teeth. Treated caries, where the hsCRP level was low,
did not seem to play a major role in promoting atherosclerosis.
Infectious, poor oral hygiene, a trigger for systemic inflammation,
was previously suggested to correlate with carotid intima–media
thickness, which is a surrogate marker of atherosclerosis.
2
Elter
et al
.
19
proposed a potential mechanism responsible for
vascular dysfunction in the presence of periodontal disease. A
study by Tonetti
et al
.
20
concluded that intensive periodontal
infection resulted in acute, short-term systemic inflammation
and endothelial dysfunction. In addition, periodontal disease has
been shown to be a strong predictor of mortality from ischaemic
heart disease and diabetic nephropathy in Pima Indians with type
2 diabetes.
21
Another study postulated that poor oral hygiene
may be an insidious cause of endothelial dysfunction and future
cardiovascular events.
22
Conclusion
The present study has clearly demonstrated a significant
relationship between dental diseases, especially tooth loss, and
sub-clinical atherosclerosis. We concluded that high DMFT
index is associated with increased carotid intima–media wall
thickness, and is a marker of early initiation of atherosclerotic
lesions. Clinical implications derived from our study are that
once a dentist diagnoses advanced dental disease or signs
of poor oral hygiene, the patient should be referred to an
internist for further screening and, if necessary, the treatment of
cardiovascular risk factors.
To demonstrate an association between inflammation, dental
indices, poor oral hygiene and disease progression however,
longer-term studies are needed. The mean six-month follow-up
period was a limitation in this study. Therefore, we will continue
to follow the investigation for two years to observe disease
progression.
There were other limitations to our study. Pathogen levels
or immune responses to the pathogens were not available in
our patient population. We could not determine the individual’s
propensity to develop inflammatory reaction. Microbial aspects,
which have been shown to be more specific than clinical signs of
poor oral hygiene, were not evaluated in our study. In addition,
the periodontal long-term status was not known. We only
investigated clinical measures of dental and periodontal disease.
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