The peridontal anaerobe Porphyromonas gingivalis induced platelet activation and increased aggregation in whole blood by rat model

Yu, Kaijiang; Inoue, Yasuhiro; Umeda, Makoto; Terasaki, Hiroaki; Chen, Zhiyong; Iwai, Takehisa

doi:10.1016/j.thromres.2010.12.004

Cited by 23 publications

(20 citation statements)

References 31 publications

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“…Activated platelets release antibacterial peptides [37], but some evidence also indicates that certain pathogens may have developed a way to exploit activated platelets by binding to their surfaces to establish or propagate infection [38]. This is in agreement with the results of several studies reporting that periodontitis and periodontal pathogens may be associated with platelet activation and with a prothrombotic state [14,33,[39][40][41][42][43]. An alternative explanation for the higher MPV levels among cases in our study can be found in the reported association between changes in the levels of MPV and various non-infectious inflammatory processes [44][45][46][47], which may suggest that MPV changes reflect disease activity in inflammation [45,46].…”

Section: Discussionsupporting

confidence: 82%

Hematological features in adolescents with periodontitis

2011

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The aim of this study was to assess whether adolescent cases of periodontitis present with different hemogram findings than control subjects. This case-control study comprised 87 adolescent cases presenting with clinical attachment loss ≥3 mm in at least two teeth and 73 control subjects. Blood samples were obtained by venipuncture and analyzed in an Abbott Cell-Dyn 3,500 hematology analyzer for values of white blood cells and red blood cells, hemoglobin, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, red-cell distribution width, platelets, and mean platelet volume. Hematocrit values were obtained using volume fractions read from capillary tubes. The associations between log-transformed hemogram variables with each of the three exposure variables "case status" (yes/no), a "high percent sites with PD ≥4 mm" (yes/no), and a "high percent sites with BOP" (yes/no) were investigated using multivariate linear regression analyses. Periodontitis cases presented with 5% higher values for the mean platelet volume than did controls. Subjects with a high percent sites with probing depth ≥4 mm had eosinophil counts that were on average 27% lower than among subjects with fewer deepened pockets. They also had 7% higher values for the mean platelet volume than did persons with less pocketing. Eosinophil counts and mean platelet volumes may be associated with the parameters of periodontitis in adolescents. While standard hematological testing did not show abnormalities in adolescents with periodontitis compared to healthy controls, eosinophil counts and mean platelet volumes may reflect periodontal inflammation.

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Section: Discussionsupporting

confidence: 82%

Hematological features in adolescents with periodontitis

2011

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“…One tube of each donor's blood was assigned for PPP preparation only. Baseline whole blood PLT aggregation studies were performed as per manufacturer's instructions on a whole blood lumi aggregometer (560VS, Chrono‐Log Corp.) and as previously described 20,21 . Aggregation was induced by 20 µmol/L ADP, and the change in impedance was recorded at 10 minutes.…”

Section: Methodsmentioning

confidence: 99%

Alterations of platelet function and clot formation kinetics after in vitro exposure to anti‐A and ‐B

et al. 2012

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Background ABO mismatched platelets are commonly transfused despite reported complications. We hypothesized that because platelets possess A and B antigens on their surface, ABO mismatched transfused or recipient platelets could become activated and/or dysfunctional after exposure to anti-A or -B antibodies in the transfused or recipient plasma. We present here in vitro modeling data on the functional effects of exposure of platelets to ABO antibodies. Methods Platelet functions of normal platelets of all ABO types were assessed before and after incubation with normal saline, ABO identical plasmas, or O plasmas with varying titers of anti-A and anti-B (anti-A/B) antibodies. Assays used for this assessment include: platelet aggregation, clot kinetics, thrombin generation, platelet cytoskeletal function, and mediator release. Results Exposure of antigen bearing platelets to O plasma with moderate to high titers of anti-A/B antibodies significantly inhibits aggregation, prolongs PFA-100 epinephrine closure time, disrupts clot formation kinetics, accelerates thrombin generation, reduces total thrombin production, alters platelet cytoskeletal function, and influences pro-inflammatory and pro-thrombotic mediator release. Conclusions Our findings demonstrate a wide range of effects that anti-A/B antibodies have on platelet function, clot formation, thrombin generation, platelet cytoskeletal function, and mediator release. These data provide potential explanations for clinical observations of increased red cell utilization in trauma and surgical patients receiving ABO non-identical blood products. Impaired hemostasis caused by anti-A/B antibodies interacting with A and B antigens on platelets, soluble proteins, and perhaps even endothelial cells is a potential contributing factor to hemorrhage in patients receiving larger volumes of ABO non-identical transfusions.

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“…As the thrombotic and thrombolytic systems are closely related to the pathogenesis of cardiovascular diseases, many studies on bacteria-induced platelet activation have been performed78910. Most reports describe the induction of platelet activation and aggregation by various bacteria such as Staphylococcus aureus and Porphyromonas gingivalis , and their mechanisms are well investigated78910. In contrast, there is a possibility that some bacteria may inhibit platelet aggregation.…”

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confidence: 99%

The collagen-binding protein of Streptococcus mutans is involved in haemorrhagic stroke

et al. 2011

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Although several risk factors for stroke have been identified, one-third remain unexplained. Here we show that infection with Streptococcus mutans expressing collagen-binding protein (CBP) is a potential risk factor for haemorrhagic stroke. Infection with serotype k S. mutans, but not a standard strain, aggravates cerebral haemorrhage in mice. Serotype k S. mutans accumulates in the damaged, but not the contralateral hemisphere, indicating an interaction of bacteria with injured blood vessels. The most important factor for high-virulence is expression of CBP, which is a common property of most serotype k strains. The detection frequency of CBP-expressing S. mutans in haemorrhagic stroke patients is significantly higher than in control subjects. Strains isolated from haemorrhagic stroke patients aggravate haemorrhage in a mouse model, indicating that they are haemorrhagic stroke-associated. Administration of recombinant CBP causes aggravation of haemorrhage. Our data suggest that CBP of S. mutans is directly involved in haemorrhagic stroke.

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The peridontal anaerobe Porphyromonas gingivalis induced platelet activation and increased aggregation in whole blood by rat model

Cited by 23 publications

References 31 publications

Hematological features in adolescents with periodontitis

Hematological features in adolescents with periodontitis

Alterations of platelet function and clot formation kinetics after in vitro exposure to anti‐A and ‐B

The collagen-binding protein of Streptococcus mutans is involved in haemorrhagic stroke

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