Recent research reveals a link between gum disease and an increased risk of blood clots, highlighting the potential health advantages of maintaining oral health for those liable to developing blood clots.
Test: The impact of periodontitis on thrombotic diseases: from the clinical aspect to future therapeutic approaches. Photo credit: Olga, Shefer/Shutterstok.com
Recent review in International Journal of Oral Science discusses the impact of periodontal diseases on thrombotic diseases.
Background
Periodontitis refers back to the chronic inflammation of the tooth-supporting tissues brought on by biofilm-forming bacteria. Immune imbalance mediates this condition. Uncontrolled periodontal disease is the leading reason behind tooth loss in individuals.
Thrombosis can restrict blood flow in blood vessels, causing ischemia, necrosis, local swelling, discomfort and vascular instability, which in extreme cases might be fatal.
Studies have shown that periodontitis may increase thrombosis because of systemic inflammation or bacterial transfer and affect platelet function and coagulation. Periodontal treatment can have a preventive effect in patients with thrombotic diseases.
Concerning the review
This review highlights the connection between periodontal disease and thrombotic diseases.
The connection between periodontitis and thrombosis
Pathogens corresponding to Porphyromonas gingivalis, Tannerella forsythia, T. denticola, A. actinomycetemcomitansAND F. nucleus cause periodontal infections and damage the periodontium, i.e. the tissue supporting and surrounding the teeth. Periodontal infections corresponding to P. gingivalis they enter the bloodstream from periodontal pockets and colonize distant organs.
These infections produce toxins that cause systemic inflammation and predispose to thrombotic diseases. Systemic inflammation can damage the endothelial barrier, causing hypercoagulability, slowed blood flow, and excessive pressure on immune cells involved in platelet activation. A number of causes of Virchow’s triad can directly cause arterial thrombosis and venous thromboembolism.
People affected by periodontitis have increased concentrations of circulating thrombotic aspects corresponding to fibrinogen and increased hemocyte reactivity, indicating that this will contribute to the event of thrombotic disease.
Moreover, periodontitis causes a microbial imbalance within the stomach. Intestinal dysbiosis increases the extent of trimethylamine-N-oxide (TMAO), which causes atherosclerosis. Studies have linked periodontitis with atherosclerosis, endothelial dysfunction, and migration of leukocytes, which can harbor bacteria.
Studies have shown the presence of deoxyribonucleic acid (DNA) of periodontal bacteria in atherosclerotic plaques of the carotid arteries and thrombotic material in patients treated with percutaneous coronary intervention (PCI). Patients with vasculitis obliterans (TAO) are characterised by a high incidence of periodontitis and better titers of antibodies within the blood against periodontal pathogens.
Individuals with severe periodontal disease can have features of heart problems corresponding to arterial stiffness, impaired flow-mediated dilation (FMD), and greater carotid intima-media thickness (cIMT).
Thrombosis is a crucial consequence of heart problems (CVD) and plays a big role in various cardiovascular diseases, including ischemic heart disease, ischemic stroke, and venous thromboembolism.
Periodontitis increases the chance of carotid plaque rupture, peripheral arterial disease (PAD), atrial fibrillation (AF), arterial dissection, and major hostile cardiovascular events (MACE) during coronary artery bypass grafting (CABG).
Patients with venous thrombosis have periodontal microorganisms corresponding to Dialister pneumosints, Eikenella corrodes, Parvimonas micraAND Provetella orally occur in patients with venous thrombosis.
Periodontitis, thrombosis and autoimmune disease
Periodontitis is related to the onset, severity, and prognosis of thrombotic disease. Periodontitis increases the chance of heart problems and thrombosis by overactivating platelets and promoting blood clotting through platelet dysregulation.
Periodontitis worsens the clinical course of thrombotic events. Nonetheless, periodontal treatment improves endothelial cell function and prognosis. P. gingivalis stimulates platelet activation through Toll-like receptor 2 (TLR2) and TLR4 signaling.
Overactivated platelets overexpress P-selectin and cluster of differentiation ligands 40 (CD40L), while they don’t express prostaglandin E1 and endothelial nitric oxide synthase (peNOS) in blood vessels. Data suggest that periodontal disease causes the circulatory system to turn out to be prothrombotic.
Periodontitis can increase circulating levels of neutrophil extracellular traps (NETs) and high mobility group protein B1 (HMGB1), indicating that platelet-neutrophil interactions will be the immunological mechanism underlying the periodontitis-thrombosis association.
In periodontitis, inflammatory mediators corresponding to 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 characterised 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). ).
The D-dimer biomarker of pulmonary embolism (PE) and deep vein thrombosis (DVT) is higher in individuals with periodontal disease.
Periodontitis exacerbates thrombotic disorders related to autoimmune diseases, as indicated by higher levels of anticardiolipin (aCL), antineutrophil cytoplasmic antibodies (ANCA), and antibodies in patients with periodontitis.
Periodontal procedures corresponding to scaling and root planning reduce blood levels of anticardiolipin, indicating that periodontal care may prevent thrombosis in individuals with autoimmune diseases.
Application
The findings show that periodontitis causes bacterial-induced thrombosis and inflammation, and periodontal treatment may help improve the prognosis. Nonetheless, existing clinical recommendations don’t cover the treatment of oral diseases.
Health care providers must consider monitoring periodontal health in individuals in danger for thrombosis, and periodontal therapies could also be effective in each prevention and treatment. Nonetheless, more multicenter, randomized, controlled trials are required to substantiate the outcomes.