How Is Cardiac Health Linked to Oral Health?
Coronary artery disease and atherosclerotic cardiovascular disease are one of the leading causes of death globally. Although research has been elusive on establishing the direct link between periodontitis, gingival disease, and cardiac health, there is evidential documentation that periodontal disease has pathogenesis associated with increased risk for coronary heart disease (CHD).
As per holistic model reviews, oral health pathogenesis and CHD pathogenesis are interlinked, measured by the level of serum biomarkers that indicate if an individual has an increased incidence of being prone to developing CHD. Due to the prevalence of more than 700 microbes populating the oral cavity, the dental plaque seen as a tooth biofilm is adapted to the changes in the environmental flora. When this plaque extends to the surrounding gingival structure, the immune response is triggered, and the resulting inflammation is termed gingivitis (inflammation of the gingiva).
If left untreated by the dental surgeon, gingivitis eventually progresses to periodontitis or periodontal disease, characterized by irreversible destruction of the connective tissue fibers to which teeth are bound. This leads to attachment loss in the long-term, causing tooth mobility due to the underlying alveolar bone resorption and eventually if left untreated again, leads to tooth loss.
What Are the Risk Factors of Periodontal Diseases?
The risk factors for developing periodontal disease are:
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Smoking.
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Diabetes, both type 1 and type 2.
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Certain therapeutic drugs.
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Genetic factors.
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Defective fillings.
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Ill-fitting bridges.
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Hormonal changes in pregnancy or use of oral contraceptives in females.
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Compromised immune functions in immunosuppressive patients.
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Medications that cause xerostomia or dry mouth.
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Obesity (associated with chronic inflammatory diseases).
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Poor oral hygiene.
What Does the Phenomenon of Dysbiosis and Bacteremia Mean?
Dysbiosis is a phenomenon that occurs due to periodontal disease because of an imbalance in the oral microbiota that triggers bacteremia (bacterial proliferation in the bloodstream). This bacteremia leads to local and, eventually, systemic immune-mediated responses associated with local or systemic inflammation in the host. This is because the bacteria are now systemically disseminated that compromises the normal host immune response.
The proposed mechanisms that link periodontal disease to the development of atherosclerotic cardiovascular disease (ASCVD) are associated with the presence of Interleukins, CRP (C-reactive protein), matrix metalloproteinases, TNF (tumor necrosis factor), intercellular adhesion molecules, and P-selectin. They have been implicated in triggering the inflammatory response that might cause the development of atherosclerotic disease (by the initiation and progression of ASCVD).
The biological mechanism widely elucidated is bacterial translocation. Though the exact picture may be unclear on how the bacteria or its byproducts translocate systemically, the identification of periodontal pathogens, as seen in aortic plaques in patients suffering from cardiovascular disease or in the thrombi of patients with acute myocardial infarction, suggest the direct effect of encroaching oral bacteria on these distant systemic sites.
As per research, the identified pathogens, Aggregatibacter actinomycetemcomitans or Porphyromonas Gingivalis (P. gingivalis, the keystone pathogen of periodontal disease), are known to cause a dysfunction of the vascular endothelium by the mechanism of LPS (lipopolysaccharide) mediated effect.
The pathways studied for P. gingivalis show how it can affect the oxidized LDL cholesterol levels (ox-LDL) due to periodontal infection and inflammation. This may happen or is attributed to the formation of ROS (reactive oxygen species) that oxidizes the LDL cholesterol. Similar pathways have been shown to induce an effect by these reactive oxygen species upon systemic inflammation by activating certain growth factors, inflammatory cytokines, and nuclear factors. These inflammatory factors may be capable o producing rampant, systemic inflammation that is unregulated by the presence of circulating periodontal pathogens (by the mechanism of bacteremia).
Studies have indicated a ride in the serum evaluation levels of C reactive protein, fibrinogen, tumor necrosis factor-alpha, and interleukins. These cardiac markers can be assessed by a blood test showing serum evaluation of markers if the dental surgeon suspects chronic or rampant periodontal disease, especially in elderly individuals. Also, the other detrimental effect of these pathogens, apart from causing systemic inflammation, is increased insulin resistance. High insulin resistance will cause vasodilatory changes because insulin is a potent vasodilator.
Another hypothesis elaborated for the potential link of cardiovascular diseases is periodontal pathogens in platelet activation associated with periodontal disease that contributes to thrombosis and plaque instability. In the documentation of animal models, there is a definitive link between the presence of periodontal pathogens and the formation of atheromas.
Thus, proatherogenic changes in lipoprotein metabolism are due to increased cholesterol, triglycerides, and non-esterified fatty acids in the circulation. Data collected from angiography studies also suggest a direct relationship between the degree of periodontal disease and cardiovascular disease in patients who have atherosclerosis. Though not causally linked with CHD, the research data is suggestive of the periodontal status of an individual playing a pivotal role while evaluating the cardiac health markers that are also affected by the presence of other risk factors like smoking, alcoholism, diabetes, diet, and socioeconomic factors.
Conclusion:
To conclude, systemic inflammation due to elevated cardiac risk markers, inflammatory cytokines, reactive oxygen species, increased insulin resistance, hypercoagulability, and vascular endothelium impairment is an indirectly proven yet definitive detrimental effect of periodontal disease. Maintaining periodontal and gingival health, regular visits to the dentist, and maintenance of oral hygiene can be crucial for stopping or altering the pathogenesis linked with the potential development of cardiovascular disease in all individuals.
Improved dental screening for periodontal disease and regular oral prophylaxis and hygiene are significant contributors to a healthy system. An interdisciplinary approach between the cardiologist and dentist can significantly benefit the patient suffering from cardiac disease. Dental surgeons should hence focus on the plausible ways or risk factors in individuals who can develop heart disease and vice versa with cardiologists.
