Gum Bacteria Escape Into Bloodstream And Increase Risk Of Cl

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  • #9612
    Anonymous
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    Gum Bacteria Escape Into Bloodstream And Increase Risk Of Clots And Heart Attack

    UK researchers have found another reason for us to keep brushing and flossing our teeth: the same gum bacteria that cause dental plaque can escape from the mouth into the bloodstream and trigger clots that increase risk of heart attack and heart disease.

    The study that led to this finding was the work of University of Bristol researchers, in collaboration with scientists at the Royal College of Surgeons in Dublin, Ireland (also called the RCSI) and was presented Monday at the Society for General Microbiology’s autumn meeting that is running from 6-9 September at the University of Nottingham, UK.

    Dr Howard Jenkinson, professor of Oral Microbiology at Bristol’s School of Oral and Dental Science, presented the findings at the meeting. He said in a press statement that:

    “Poor dental hygiene can lead to bleeding gums, providing bacteria with an escape route into the bloodstream, where they can initiate blood clots leading to heart disease.”

    He said we all need to be aware that it’s not only diet, exercise, cholesterol and blood pressure that we should keep an eye on, but it’s also important to have good dental hygiene to reduce our risk of heart problems.

    Tooth plaque and gum disease are what happens when Streptococcus bacteria build up in our mouths when we don’t brush and floss regularly. Gum disease makes gums sore and they bleed, allowing the bacteria to get into the bloodstream.

    In their study, Jenkinson and colleagues found that once Streptococcus bacteria get into the bloodstream, they use a protein called PadA which sits on their outer surface, to hijack blood platelets and force them to clump together and make blood clots.

    Jenkinson described this as a “selfish trick” on the part of the bacteria, which completely encase themselves in a clump of platelets, enabling them to avoid detection by the host immune system, and also, to hide from antibiotics.

    “Unfortunately, as well as helping out the bacteria”, explained Jenkinson, “platelet clumping can cause small blood clots, growths on the heart valves (endocarditis) or inflammation of blood vessels that can block the blood supply to the heart and brain”.

    The team are now investigating how PadA makes blood platelets clump together so they can find a way to block it. They are doing it with the help of a new blood flow model that mimics the human circulatory system. The model was developed by Dr Steve Kerrigan of RCSI’s School of Pharmacy.
    “This could eventually lead to new treatments for cardiovascular disease which is the biggest killer in the developed world,” said Jenkinson.

    Dr Damian Walmsley, professor of Restorative Dentistry, in the School of Dentistry at the University of Birmingham, who is also scientific adviser to the British Dental Association, told the BBC that this kind of research is very welcome because it increases understanding of the relationship between gum disease and heart disease.

    Walmsley said it also underlines “the high importance of brushing twice a day with fluoride toothpaste, restricting your intake of sugary foods and drinks and visiting the dentist regularly in order to maintain good oral health”.

    There are over 100 species and strains of bacteria in the Streptococcus genus, some so diverse they are considered species in their own right.

    It wasn’t until advances in genetics, such as genome sequencing, arrived in the lab that scientists were able to see the links among strains in the genus. As more links emerge, the more collaboration ensues between microbiologists who until then had no idea that others in apparently unrelated fields were actually working on the same problems.

    Jenkinson is also the organizer of the Streptococcus session of the Society for General Microbiology’s Autumn Meeting, and in his notes about the symposium he wrote that it should not only provide an overview of “this important research field”, but hopefully it will also “re-engage microbiologists working on streptococci and related areas into a UK Streptococcus grouping (UKSTREP) for future benefit”.

    “Oral streptococci behaving badly.”
    Presented by Howard Jenkinson.
    Autumn Meeting of the Society for General Microbiology, 6 September 2010, Nottingham.

    Sources: Bristol University, BBC News.

    #14251
    tirath
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    sub acute bacterial endo carditis is a common problem

    #14252
    divyanshee
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    What is the latest antibiotics prophylaxis regimen for the prevention of SABE?

    #14253
    tirath
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    Dental/Oral/Upper Respiratory Tract Procedures

    I. Standard Regimen in Patients at Risk (including those with prosthetic heart valves and other high risk patients):

    For Penicillin/Ampicillin/Amoxicillin allergic patients:
    Erythromycin ethylsuccinate 800 mg or erythromycin stearate 1.0 gm orally 2 hours before a procedure, then one-half the original dose 6 hours after the initial administration…OR…
    Clindamycin 300 mg orally 1 hour before a procedure and 150 mg 6 hours after the initial dose.

    For Non-Allergic patients:
    Amoxicillin 3.0 gm orally one hour before procedure, then 1.5 gm six hours after initial dose.
    II. Alternate Prophylactic Regimens in Patients at Risk

    For Patients who cannot take oral medications
    For Penicillin/Ampicillin/Amoxicillin allergic patients:
    Clindamycin 300 mg IV 30 minutes before a procedure and 150 mg IV (or orally) 6 hours after the initial dose.
    For Non-Allergic patients:
    Ampicillin 2.0 gm IV (or IM) 30 minutes before a procedure, then ampicillin 1.0 gm IV (or IM) OR amoxicillin 1.5 gm orally 6 hours after the initial dose.
    For high risk patients who are not candidates for the standard regimen:
    For Penicillin/Ampicillin/Amoxicillin allergic patients:
    Vancomycin 1.0 gm IV administered over 1 hour, starting one hour before the procedure. No repeat dose is necessary.
    For Non-Allergic patients:
    Ampicillin 2.0 gm IV (or IM) plus gentamicin 1.5 mg/kg IV (or IM) (not to exceed 80 mg) 30 minutes before the procedure, followed by amoxicillin 1.5 gm orally 6 hours after the initial dose. Alternatively, the parenteral regimen my be repeated 8 hours after the initial dose.

    #14254
    tirath
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    Pediatric Drug Doses

    For Children, the doses are:
    Amoxicillin: 50 mg/kg initial then 25 mg/kg subsequently
    Ampicillin 50 mg/kg initially then 25 mg/kg subsequently
    Clindamycin: 10mg/kg initially and 5 mg/kg subsequently
    Erythromycin ethylsuccinate and stearate: 20 mg/kg initially then 10 mg/kg subsequently
    Gentamicin 2.0 mg/kg initially then 1.0 mg/kg subsequently
    Vancomycin 20 mg/kg initially and 10 mg/kg subsequently
    The following weight ranges may also be used for the initial pediatric dose of Amoxicillin
    <15 kg (33 lbs) ... 750 mg of Amoxicillin orally
    15-30 kg (33-66 lbs) … 1.5 gm of Amoxicillin orally
    >30 kg (66 lbs) … 3.0 gms (full adult dose)

    #14255
    gaurang_thanvi2003
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    Can we substitue Amoxicillin because it cause harmful effect on children.

    #14256
    sushantpatel_doc
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    Gingival microflora has since long been implicated in predisposing to a lot of cardiac problems..

    #14257
    tirath
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    yes obviously genta mycin vancomycin and erythromycin are the substitutes

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