PERIODONTITIS AND THE ATHEROSCLEROTIC CORONARY CARDIOVASCULAR DISEASE. COMPARATIVE STUDY OF SYSTEMIC INFLAMMATION - PERIODONTITIS - IN CARDIOVASCULAR DISEASE ON A STUDY GROUP OF 916 PATIENTS
Abstract:
Recent parodontology studies claim that
periodontal disease causes predisposition to
atherosclerotic cardiovascular disease on account of
some derived pro-inflammatory local and systemic
reactions similar to atherosclerosis and consisting of
cytokines produced by monocytes and other inflammatory
intermediaries induced by periodontal pathogens and by
their endotoxin, lipopolysaccharide. This mechanism may
initiate vascular endothelial dysfunction with its
implications in atherosclerosis and in atheromatous
plaque inflammation. Inflammation is the
physiopathological link between periodontitis –
atherosclerosis – cardiovascular disease and it all links
obsessively starting with hygiene, more specifically oral
hygiene, chronic bacterial infection, gingivitis –
periodontitis – local and systemic inflammation.
Following the potential risk and the inflammatory
connections between the periodontal disease and the
complications of cardiovascular coronary disease we may
draw a few conclusions based on our investigations. The
inflammatory connections between the two affections are
made through common pro-inflammatory markers such as
C-reactive protein, different cytokines secreted both at
local inflammation level as well as at systemic
inflammation level, different cytokines present at the level
of atherosclerotic plaque or clinically deduced at the level
of endoarterial epithelium. A series of studies claim the
predictive value of C-reactive protein taken at admission
of the coronary patient and its dynamic monitoring
during hospitalization, correlated as maximum value at
CK-MB enzyme and LDH peak level. Out of the numerous
inflammatory markers studied for their potential risk
factor role, C-reactive protein has the best laboratory test
performance and presents the strongest association with
cardiovascular events. Plasmatic C-reactive protein is
produced by hepatocytes under transcriptional control of
pro-inflammatory cytokine (IL-6, IL-1, alpha TNF). The
plasmatic level of C-reactive protein may be highlighted
at 4 hours after tissues injury, since it increases 1000
times in 24-27 hours. Serum level of C-reactive protein
directly reflects the intensity of the pathological process
that stimulated its production. C-reactive protein is also
known as the “pro-inflammatory protein” due to its
ability to stimulate complement activity in defence of the
host and to mediate fagocitosis. C-reactive protein
induces monocyte production of tissue factor, a procoagulant
playing a key role in arterial thrombosis.
Examination results at all four groups of patients in our
study support the mechanisms of the local and systemic
pro-inflammatory reactions, derived from the host,
similar to atherosclerosis and consisting of cytokines
produced by monocytes and other inflammatory
intermediaries induced by periodontal pathogens and by
their endotoxins. These mechanisms may be the start of
vascular endothelial dysfunction and ulterior sequelae
leading to atherosclerosis with its complications. Clinical
evidence expressed through umoral markers show the
determination between the local and the systemic
inflammation as a result of localized chronic infection.
Alteration of the levels of inflammatory intermediaries
has a significant impact on the atherosclerotic processes
associated with the inflammation.
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