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Cardiovascular disease has been
predicted to be the most common cause of death worldwide by the year
2020. Fifty percent of heart disease patients lack established risk
factors. However, previous and more recent studies point to a linkage
between infections with bacteria and heart disease in the other fifty
percent of observed incidences. Pathogenesis of the disease, induced
by infectious agents, is described by three different mechanisms of
action. They are:
-
Induction of
inflammation
-
Release of toxins or
superantigens
-
Molecular mimicry or
cross-reactivity
Through the years, many
reports have incriminated various infectious agents in the
pathogenesis of autoimmune disease. Very recently, the American
College of Cardiology issued a list of harmful pathogens as possible
links to heart disease.
In addition, evidence
suggests that chronic dental infection may be another factor in the
development of atherosclerotic heart disease. Patients with poor
dentition, especially those with periodontal disease are noted to have
frequent recurrent episodes of bacteremia. Bacteria in dental plaque
may cause blood clots. This plausible cause was described in a study
published in The Journal of Periodontology (October 1996). A
separate study was presented at the 150th annual meeting of the
American Association of Advancement in Science, held in 1998, as
reported in an article published in USA Today.
Traditionally, it is
assumed that infectious agents induce disease by means of direct
tissue damage, via the secretion of toxins or different
antigens-particularly myosin. These toxins may either directly or
indirectly induce tissue damage and cause the release of tissue
antigens.
An infectious agent from
diseased gums or from the lungs can be taken up by macrophages and
transferred to the bloodstream and arteries. When a macrophage burrows
into the wall of a blood vessel to gobble up irritants, such as LDL
and oxidized LDL, it transfers the infectious agent into the
neighboring arterial cells. Infected arterial cells then attract more
macrophages and other inflammatory responses, such as platelets, and
subsequently die. If this vicious cycle of inflammation continues, it
may result in fibrous lesions or plaque formation. When pieces of the
plaque break loose, they can start blood clots and pave the way for a
heart attack.
Another mechanism by which
infectious agents cause autoimmune disease is molecular mimicry.
Molecular mimicry is defined as the structural similarity between
antigens coded by different genes. The best-known example of molecular
mimicry and autoimmunity is rheumatic fever, in which antigen
cross-reactivity between cardiac tissue and streptococcal
polysaccharides is believed to induce an autoimmune reaction targeted
at the heart valves.
Immunological
cross-reactivity can be found in proteins from a multitude of viruses,
bacteria, fungi, protozoa, and different human tissues (as is listed
on the succeeding page.)
Early intervention and
eradication of these microorganisms from the oral cavity,
gastrointestinal tract, lungs and blood with the use antibiotics or
probiotics may improve the clinical condition, as well as the overall
quality of life of patients suffering from cardiovascular and
autoimmune diseases.
Figure 25- The role
of oral, gastrointestinal and pulmonary pathogens in the induction of
atherosclerosis, showing how a bacteria or a virus could set the stage
for a heart attack.
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