Recent studies reveal a link 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 blood clots.
Study: Impact of periodontitis on thrombotic diseases: from clinical perspective to future therapeutic approaches. Image Credit: Olga by Shefer/Shutterstok.com
A recent review on International Journal of Oral Science discusses the effect of periodontitis on thrombotic diseases.
Background
Periodontitis refers to the chronic inflammation of the tissues that support the teeth caused by biofilm bacteria. Immune imbalances mediate the condition. Uncontrolled periodontal diseases are the leading cause of tooth loss among individuals.
Thrombosis can restrict blood flow within circulatory vessels, causing ischemia, necrosis, local edema, discomfort, and vascular instability, which can be fatal in extreme cases.
Studies have shown that periodontitis can increase thrombosis through systemic inflammation or bacterial transmission and affect platelet function and coagulation. Periodontal treatment can have a preventive impact in patients with thrombotic disease.
About the review
This review highlights the relationship between periodontal and thrombotic disorders.
The relationship between periodontitis and thrombosis
Pathogens such as Porphyromonas gingivalis, Tannerella forsythia, T. denticola, A. actinomycetemcomitansand F. nucleatum they cause periodontal infections and damage the periodontium, which is the tissue that supports and surrounds the 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 disease. Systemic inflammation can damage the endothelial barrier, resulting in hypercoagulability, slow blood flow, and undue stress on immune cells involved in platelet activation. One or more of Virchow’s triad of causes can directly cause arterial thrombosis and venous thromboembolism.
Individuals with periodontitis have enhanced circulating thrombotic factors such as fibrinogen and increased hemocyte reactivity, suggesting that it may contribute to the development of thrombotic disease.
In addition, periodontal inflammation causes a microbial imbalance in the stomach. Intestinal dysbiosis increases trimethylamine N-oxide (TMAO), which causes atherosclerosis. Studies have linked periodontitis to atherosclerosis, endothelial dysfunction, and migration of leukocytes that may harbor bacteria.
Studies have found deoxyribonucleic acid (DNA) from periodontal bacteria in carotid atheromatous plaques and thrombotic material in patients treated with percutaneous coronary intervention (PCI). Patients with thromboangiitis obliterans (TAO) have a high incidence of periodontitis and higher blood antibody titers against periodontal pathogens.
Individuals with severe periodontal disease may exhibit features of cardiovascular disease such as arterial stiffness, flow-mediated dilation disorder (FMD), and higher carotid intima media thickness (cIMT).
Thrombosis is a prominent consequence of cardiovascular disease (CVD) and plays a vital role in various cardiovascular diseases, such as ischemic heart disease, ischemic stroke, and venous thromboembolism.
Periodontitis increases the likelihood of carotid plaque rupture, peripheral artery disease (PAD), atrial fibrillation (AF), arterial clearance, and major adverse cardiovascular events (MACE) during coronary artery bypass grafting (CABG).
Patients with venous thrombosis show periodontal microbes such as e.g Dialister pneumosyntes, Eikenella erodes, Parvimonas micraand Provetella oralis present in patients with venous thrombosis.
Periodontitis, thrombosis and autoimmune disease
Periodontitis is associated with the onset, severity and prognosis of thrombotic disease. Periodontitis increases the risk of cardiovascular disease and thrombosis by hyperactivating platelets and promoting blood clotting through platelet dysregulation.
Periodontitis worsens clinical outcomes in cases of thrombosis. However, periodontal therapy enhances endothelial cell function and prognosis. P. gingivalis stimulates platelet activation through toll-like receptor 2 (TLR2) and TLR4 signaling.
Hyperactivated platelets overexpress P-selectin and complex of differentiation 40 ligand (CD40L) while underexpressing prostaglandin E1 and endothelial nitric oxide synthases (peNOS) in blood vessels. Data suggest that periodontal disease causes the circulatory system to become prothrombotic.
Periodontitis can increase circulating levels of neutrophil extracellular traps (NETs) and high mobility group B1 (HMGB1) protein, indicating that platelet-neutrophil interactions may be an immunological mechanism underlying the periodontitis-thrombosis link.
In periodontitis, inflammatory mediators such as cell-free nucleic acid (cfNA) and inorganic polyphosphate (polyP) mediate systemic inflammation and procoagulant processes. Plasma cfNA levels are increased in subjects with arterial and venous thrombosis.
Periodontitis is characterized by high levels of proinflammatory 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). . ).
D-dimer biomarker for pulmonary embolism (PE) and deep vein thrombosis (DVT) is higher in people with periodontal disease.
Periodontitis exacerbates thrombotic disorders associated with autoimmune diseases, as indicated by higher levels of anticardiolipin (aCL), antineutrophil cytoplasmic antibodies (ANCA), and antibodies in patients with periodontitis.
Periodontal treatments such as scaling and root planning reduce anticardiolipin blood concentrations, suggesting that periodontal care may prevent thrombosis in people with autoimmune disorders.
Conclusion
Based on the findings, periodontitis causes thrombosis through bacteria and inflammation, and periodontal treatment can help improve the prognosis. However, existing clinical recommendations do not include oral health treatment.
Health professionals should consider periodontal health monitoring for those at risk of thrombosis, and periodontal treatments can be effective for both prevention and treatment. However, more multicenter randomized controlled studies are needed to validate the findings.
