The intriguing commonality of NETosis between COVID-19 &amp; Periodontal disease

Gupta, Shipra; Sahni, Vaibhav

doi:10.1016/j.mehy.2020.109968

Cited by 44 publications

(58 citation statements)

References 2 publications

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“…Also, it was suggested that periodontopathic bacteria might enhance SARS‐CoV‐2 virulence by cleaving its S glycoproteins (Madapusi Balaji et al, 2020; Takahashi et al, 2020) and that the oral cavity, and specially periodontal pockets could act as a viral reservoir (Badran et al, 2020; Bao et al, 2020; Botros et al, 2020; Herrera et al, 2020; Kheur et al, 2020). Gupta et al indicated that Neutrophil Extracellular Trap production is involved in the pathogenesis of both diseases (Gupta & Sahni, 2020), and Sahni et al suggested that the strong Th17 response in severe periodontitis could exacerbate the cytokine storm in COVID‐19 (Sahni & Gupta, 2020). All these hypothetical pathways could also foresee an increased incidence of periodontal lesions, especially necrotizing periodontal disease (NPD) during this pandemic (Patel & Woolley, 2020).…”

Section: Discussionmentioning

confidence: 99%

Association between periodontitis and severity of COVID‐19 infection: A case–control study

Marouf

Cai

Said

et al. 2021

J Clinic Periodontology

296

330

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Aim COVID‐19 is associated with an exacerbated inflammatory response that can result in fatal outcomes. Systemic inflammation is also a main characteristic of periodontitis. Therefore, we investigated the association of periodontitis with COVID‐19 complications. Materials and Methods A case–control study was performed using the national electronic health records of the State of Qatar between February and July 2020. Cases were defined as patients who suffered COVID‐19 complications (death, ICU admissions or assisted ventilation), and controls were COVID‐19 patients discharged without major complications. Periodontal conditions were assessed using dental radiographs from the same database. Associations between periodontitis and COVID 19 complications were analysed using logistic regression models adjusted for demographic, medical and behaviour factors. Results In total, 568 patients were included. After adjusting for potential confounders, periodontitis was associated with COVID‐19 complication including death (OR = 8.81, 95% CI 1.00–77.7), ICU admission (OR = 3.54, 95% CI 1.39–9.05) and need for assisted ventilation (OR = 4.57, 95% CI 1.19–17.4). Similarly, blood levels of white blood cells, D‐dimer and C Reactive Protein were significantly higher in COVID‐19 patients with periodontitis. Conclusion Periodontitis was associated with higher risk of ICU admission, need for assisted ventilation and death of COVID‐19 patients, and with increased blood levels of biomarkers linked to worse disease outcomes.

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Section: Discussionmentioning

confidence: 99%

Association between periodontitis and severity of COVID‐19 infection: A case–control study

Marouf

Cai

Said

et al. 2021

J Clinic Periodontology

296

330

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“…По данным ряда авторов, среди пациентов с COVID-19, страдающих ОРДС и нуждающихся в проведении инвазивной ИВЛ, смертность составляет от 24 до 53% [16,20,21]. Тяжесть состояния усугубляется частично из-за дистального слизисто-гнойного секрета, препятствующего свободной вентиляции легких.…”

Section: Discussionunclassified

“…Тяжесть состояния усугубляется частично из-за дистального слизисто-гнойного секрета, препятствующего свободной вентиляции легких. Исследования сыворотки крови и жидкости бронхоальвеолярного лаважа у этих больных выявили высокое содержание НВЛ, которые, в свою очередь, способствуют увеличению вязкости слизисто-гнойной мокроты [16,20,21], что полностью согласуется с полученными нами результатами.…”

Section: Discussionunclassified

Neutrophil extracellular traps: diagnostic and prognostic value in COVID-19

et al. 2020

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Rationale: An important element of antiviral defense in the pathophysiology of COVID-19 is the innate cell immunity including polymorphonuclear neutrophils prone to netotic transformation. Neutrophils can be not only a marker of acute infection, but, being a source of neutrophil extracellular traps (NET), can play a key role in the development of thrombotic complications leading to acute respiratory insufficiency in COVID-19.Aim: To determine the diagnostic and prognostic value of NET levels in patients with COVID-19.Materials and methods: We monitored NET levels in peripheral blood of 34 patients with COVID-19 (mean age, 67 ± 15.8 years), admitted to MONIKI hospital. The control group consisted of 54 healthy volunteers (mean age, 52 ± 11.5 years). Whole blood samples of 2 μL each were used for the preparation of monolayer smears (Giemsa stain) and calculation of at least 200 cell structures including native intact and transformed neutrophils (MECOS-C2 microscope, Medical computer systems).Results: Patients with COVID-19 had higher NET levels, compared to those in healthy controls: 14.5% (2.9–28.6%) vs. 5.0% (1.8–11.9%, p < 0.0001). The patients who were on non-invasive respiratory support (23.5%) had a NET level of 12% (8.1– 22.3%), whereas those on invasive mechanical ventilation (17.6%) had a 1.5-fold higher NET level of 17.9% (12.3–28.2%) (p < 0.05). In the patients who died (11.8% of the cases), the NET level amounted to 19% (16.5–26%, p < 0.05). Monitoring of blood NET levels was performed in 9 patients from the day of admittance to the day of their transfer to the intensive care unit / discharge / death. It was shown that a decrease of NET levels mirrors an improvement of the patient’s clinical condition and efficacy of his/hers treatment. On the opposite, an increase of NET levels can indicate a deterioration and risk of unfavorable course.Conclusion: We have identified some pathophysiological mechanisms in COVID-19, related to the neutrophil compartment. Patients with coronavirus infection are characterized by high NET levels which is at least 3-fold higher than that in healthy volunteers. This indicates an abnormality in immune host defense and development of an inadequate inflammatory response. An increase of NET in whole blood smears of more than 16% can be a criterion of an unfavorable prognosis of the disease course and the risk of death.

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“…Cellular release of histones, major mediators of death in sepsis and neutrophil extracellular trap (NET) formation, has been implicated in COVID-19 coagulopathy [8][9][10][11][12]. Histones increase plasma thrombin generation directly through interactions with coagulation proteins [13,14], platelets, neutrophils, and endothelial cells [15,16].…”

Section: Introductionmentioning

confidence: 99%

Increased Histone-DNA Complexes and Endothelial-Dependent Thrombin Generation in Severe COVID-19

Bouchard

Colovos

Lawson

et al. 2021

Preprint

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Objective: Coagulopathy in severe COVID-19 is common but poorly understood. The purpose of this study was to determine how SARS-CoV-2 infection impacts histone levels, fibrin structure, and endogenous thrombin potential in the presence and absence of endothelial cells. Approach: We studied individuals with SARS-CoV-2 infection and acute respiratory distress syndrome at the time of initiation of mechanical ventilation compared to healthy controls. Blood samples were assayed for levels of histone-DNA complexes. Confocal microscopy was used to evaluate fibrin structure in clots formed from recalcified plasma samples using fluorescently-labeled fibrinogen. Endogenous thrombin potential was measured by calibrated automated thrombin assays in the presence of tissue factor and phospholipid (PCPS) or cultured human endothelial cells. Results: Circulating nucleosomes were elevated in the plasma of COVID-19 patients relative to healthy controls (n=6, each group). COVID-19 patient plasma thrombin generation was also altered. Despite having an increased endogenous thrombin potential, patient plasma samples exhibited prolonged lag times and times to peak thrombin in the presence of added tissue factor and PCPS. Strikingly different results were observed when endothelial cells were used in place of tissue factor and PCPS. Control plasma samples did not generate measurable thrombin (lag time >60 min); in contrast, plasma samples from COVID-19+ patients generated thrombin (mean lag time ~20 min). Consistent with the observed alterations in thrombin generation, clots from COVID-19 subjects exhibited a denser fibrin network, thinner fibers and lower fibrin resolvability. Conclusions: Elevated histones, aberrant fibrin formation, and increased endothelial-dependent thrombin generation in COVID-19 may contribute to coagulopathy.

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The intriguing commonality of NETosis between COVID-19 & Periodontal disease

Cited by 44 publications

References 2 publications

Association between periodontitis and severity of COVID‐19 infection: A case–control study

Association between periodontitis and severity of COVID‐19 infection: A case–control study

Neutrophil extracellular traps: diagnostic and prognostic value in COVID-19

Increased Histone-DNA Complexes and Endothelial-Dependent Thrombin Generation in Severe COVID-19

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