Recent studies reveal a connection between gum disease and an increased risk of blood clots, highlighting the potential life-saving benefits of oral health management for those at risk of thrombosis.
Study: Periodontitis impacts on thrombotic diseases: from clinical aspect to future therapeutic approaches. Image Credit: Olga by Shefer/Shutterstok.com
A recent review in the International Journal of Oral Science discusses the impact of periodontitis on thrombotic diseases.
Background
Periodontitis refers to chronic inflammation of teeth-supporting tissues caused by biofilm bacteria. Immune imbalances mediate the condition. Uncontrolled periodontal diseases are the primary reason for tooth loss among individuals.
Thrombosis can restrict blood flow within circulatory vessels, causing ischemia, necrosis, local edema, discomfort, and vasculature instability, which can be fatal in extreme cases.
Studies have shown that periodontitis may increase thrombosis through systemic inflammation or bacterial transmission and influence platelet function and coagulation. Periodontal treatment may have a preventive impact on thrombotic disease patients.
About the review
The present review highlights the relationship between periodontal and thrombotic disorders.
The link between periodontitis and thrombosis
Pathogens such as Porphyromonas gingivalis, Tannerella forsythia, T. denticola, A. actinomycetemcomitans, and F. nucleatum cause periodontal infections and damage the periodontium, which is the tissue that supports and surrounds teeth. Periodontal infections such as P. gingivalis enter the bloodstream from periodontal pockets to colonize distant organs.
These infections create toxins that cause systemic inflammation and predispose to thrombotic illness. Systemic inflammation can harm the endothelium barrier, resulting in hypercoagulability, slow blood flow, and undue stress on immune cells involved in platelet activation. One or more of Virchow's triad causes can directly induce arterial thrombosis and venous thromboembolism.
Individuals with periodontitis have enhanced circulating thrombotic factors such as fibrinogen and increased hemocyte reactivity, indicating that it may contribute to thrombotic disease development.
In addition, periodontal inflammation causes a microbial imbalance in the stomach. Intestinal dysbiosis raises trimethylamine N-oxide (TMAO), which causes atherosclerosis. Studies have linked periodontitis to atherosclerosis, endothelial dysfunction, and the migration of leukocytes that may house bacteria.
Studies have found deoxyribonucleic acid (DNA) from periodontal bacteria in carotid atherosclerotic plaques and thrombotic material in patients treated with percutaneous coronary intervention (PCI). Thromboangiitis obliterans (TAO) patients have a high frequency of periodontitis and higher blood antibody titers against periodontal pathogens.
Individuals with severe periodontal disease may exhibit cardiovascular illness characteristics like arterial stiffness, flow-mediated dilatation (FMD) impairment, and higher carotid intima-media thickness (cIMT).
Thrombosis is a prominent consequence of cardiovascular disease (CVD), and it plays a vital role in various cardiovascular diseases, including ischemic heart disease, ischemic stroke, and venous thromboembolism.
Periodontitis raises the possibility of carotid plaque rupture, peripheral arterial disease (PAD), atrial fibrillation (AF), arterial dissection, and major adverse cardiovascular events (MACE) during coronary artery bypass grafting (CABG).
Venous thrombosis patients exhibit periodontal microbes such as Dialister pneumosintes, Eikenella corrodens, Parvimonas micra, and Provetella oralis are present in venous thrombosis patients.
Periodontitis, thrombosis, and autoimmune disease
Periodontitis is related to thrombotic disease onset, severity, and prognosis. Periodontitis increases the risk of cardiovascular disease and thrombosis by hyperactivating platelets and promoting blood coagulation through platelet dysregulation.
Periodontitis exacerbates clinical outcomes in thrombosis incidents. However, periodontal treatment enhances endothelial cell function and prognosis. P. gingivalis stimulates platelet activation via toll-like receptor 2 (TLR2) and TLR4 signaling.
Hyperactivated platelets overexpress P-selectin and the cluster of differentiation 40 ligands (CD40L) while underexpressing prostaglandin E1 and endothelial nitric oxide synthases (peNOS) in blood vessels. The data suggest that periodontal diseases cause the circulatory system to become prothrombotic.
Periodontitis can increase the circulation levels of neutrophil extracellular traps (NETs) and high mobility group protein B1 (HMGB1), indicating that platelet-neutrophil interactions may be an immunological mechanism underlying the periodontitis-thrombosis link.
In periodontitis, inflammatory mediators like cell-free nucleic acid (cfNA) and inorganic polyphosphate (polyP) mediate systemic inflammation and procoagulant processes. Plasma cfNA levels increase in individuals with arterial and venous thrombosis.
Periodontitis is characterized by high levels of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and IL-6, in addition to fibrinogen and C-reactive protein (CRP).
The D-dimer biomarker for pulmonary embolism (PE) and deep vein thrombosis (DVT) is higher in people with periodontal disease.
Periodontitis exacerbates autoimmune disease-associated thrombotic disorders, as indicated by higher levels of anticardiolipin (aCL), antineutrophil cytoplasmic antibodies (ANCA), and antibodies in patients with periodontitis.
Periodontal treatments like scaling and root planning lower blood anticardiolipin concentrations, indicating that periodontal care may prevent thrombosis in individuals with autoimmune disorders.
Conclusion
Based on the findings, periodontitis causes thrombosis through bacteria and inflammation, and periodontal treatment can help improve the prognosis. However, the existing clinical recommendations do not include oral health treatment.
Health professionals must consider periodontal health surveillance for those at risk of thrombosis, and periodontal therapies may be effective for both prevention and treatment. However, more multicenter randomized controlled studies are required to validate the findings.
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