Medical Hypotheses
Volume 74, Issue 2 , Pages 374-376, February 2010

Mechanism of increased mortality in hemodialysed patients with periodontitis

  • Jiří Šedý

      Affiliations

    • Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Vídeňská 1083, Prague 4 142 20, Czech Republic
    • Institute of Dental Research, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
    • Corresponding Author InformationCorresponding author. Address: Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Vídeňská 1083, Prague 4 142 20, Czech Republic. Tel.: +420 241062717; fax: +420 241062783.
  • ,
  • Edita Horká

      Affiliations

    • Institute of Dental Research, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
  • ,
  • René Foltán

      Affiliations

    • Division of Oral and Maxillofacial Surgery, Department of Stomatology, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
  • ,
  • Jana Špačková

      Affiliations

    • Department of Pathology, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
  • ,
  • Jana Dušková

      Affiliations

    • Institute of Dental Research, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic

Received 14 April 2009; accepted 18 April 2009. published online 25 June 2009.

Summary 

Periodontitis significantly decreases survival in hemodialysed patients with end stage renal disease (ESRD). Periodontitis-related microorganisms spreading into the bloodstream are thought to impair blood rheological parameters – for example, increasing whole blood viscosity, aggregating blood elements, and decreasing blood flow – and thereby significantly accelerate systemic or local diseases, impairing survival. We discuss the ability of a prototypical pathogenic anaerobic polybacterial consortium to modulate and interfere with host immune responses and to enzymatically degrade host proteins, to bind to and cleave extracellular matrix proteins, to invade intercellularly as well as intracellularly, to promote vascular permeability, to disrupt polymorphonuclear leukocyte function, to cleave complement, and to degrade IgG heavy chains. To further elucidate these phenomena, studies involving detecting microorganism byproducts and monitoring blood rheological parameters are necessary.

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PII: S0306-9877(09)00374-0

doi:10.1016/j.mehy.2009.04.053

Medical Hypotheses
Volume 74, Issue 2 , Pages 374-376, February 2010