Volume 84, Issue 4S p. S30-S50
Article

Periodontal bacterial invasion and infection: contribution to atherosclerotic pathology

Leticia Reyes

Leticia Reyes

Department of Oral Biology, College of Dentistry and Center for Molecular Microbiology, University of Florida, Gainesville, FL, USA

Contributed equally to this study.

Search for more papers by this author
David Herrera

David Herrera

ETEP (Etiology and Therapy of Periodontal Disease) Research Group, University Complutense, Madrid, Spain;

Contributed equally to this study.

Search for more papers by this author
Emil Kozarov

Emil Kozarov

Institute for Cardiovascular Science (CSIC-ICCC), St. Paul Hospital, Barcelona, Spain

Section of Oral and Diagnostic Sciences, Columbia University Medical Center, New York, NY, USA

Search for more papers by this author
Silvia Roldá

Silvia Roldá

ETEP (Etiology and Therapy of Periodontal Disease) Research Group, University Complutense, Madrid, Spain;

Search for more papers by this author
Ann Progulske-Fox

Corresponding Author

Ann Progulske-Fox

Department of Oral Biology, College of Dentistry and Center for Molecular Microbiology, University of Florida, Gainesville, FL, USA

Address:

Ann Progulske-Fox, Department of Oral

Biology, Center for Molecular Microbiology,

PO Box 100424 JHMHSC, University of

Florida, Gainesville, FL 32610-0424, USA

E-mail: [email protected].

Search for more papers by this author
First published: 01 April 2013
Citations: 58

The proceedings of the workshop were jointly and simultaneously published in the Journal of Clinical Periodontology and Journal of Periodontology. www.joponline.org/doi/abs/10.1902/jop.2013.1340012 http://onlinelibrary.wiley.com/doi/10.1111/jcpe.12079/abstract

Abstract

Objective: The objective of this review was to perform a systematic evaluation of the literature reporting current scientific evidence for periodontal bacteria as contributors to atherosclerosis.

Methods: Literature from epidemiological, clinical and experimental studies concerning periodontal bacteria and atherosclerosis were reviewed. Gathered data were categorized into seven “proofs” of evidence that periodontal bacteria: 1) disseminate from the oral cavity and reach systemic vascular tissues; 2) can be found in the affected tissues; 3) live within the affected site; 4) invade affected cell types in vitro; 5) induce atherosclerosis in animal models of disease; 6) non-invasive mutants of periodontal bacteria cause significantly reduced pathology in vitro and in vivo; and 7) periodontal isolates from human atheromas can cause disease in animal models of infection. Results: Substantial evidence for proofs 1 to 6 was found. However, proof 7 has not yet been fulfilled.

Conclusions: Despite the lack of evidence that periodontal bacteria obtained from human atheromas can cause atherosclerosis in animal models of infection, attainment proofs 1 to 6 provides support that periodontal pathogens can contribute to atherosclerosis.