Bugs, gums, and blood vessels

June 25, 2015
New research is filling in more details regarding the mechanisms by which periodontal bugs destroy the gums and bone and participate in the development and progression of atherosclerosis.

Richard H. Nagelberg, DDS

New research is filling in more details regarding the mechanisms by which periodontal bugs destroy the gums and bone and participate in the development and progression of atherosclerosis. The periodontal pathogen Fusobacterium nucleatum has previously been shown to damage the arterial endothelium by creating gaps between the endothelial cells, allowing the bacteria and anything smaller (LDL, HDL, etc.) to migrate into the arterial wall and contribute to atherogenesis.

Recently published research1 focuses on the mechanism by which Porphyromonas gingivalis is involved in the onset of inflammation and tissue destruction in periodontal disease and the initiation and progression of atherosclerosis.

Biofilm accumulation in the gingival sulcus leads to the development of a periodontal pocket. The gingival crevicular fluid (GCF), an inflammatory exudate, is the source of nutrients essential for P. gingivalis growth. These nutrients are present in low levels in healthy individuals but drastically increase during gum inflammation. P. gingivalis invades the gingival epithelial cells by binding the bacterial fimbriae to the host cell surface. The bacteria then block epithelial cell apoptosis (programmed cell death), allowing bacterial proliferation inside the gingival epithelial cell.

Additionally, through inhibition of IL-8 expression, the bacteria induce a delay in neutrophil recruitment, further allowing bacterial proliferation. In short, the bacteria hijack the body's local defenses, prevent the infected cells from committing suicide, and ensure their proliferation by delaying bacterial killing by white blood cells.

Furthermore, P. gingivalis has developed strategies to evade the complement system, which is present in the GCF at about 70% of its serum concentration. There are several mechanisms of this bacterial evasion of the complement system. P. gingivalis produces two types of proteases, called gingipains. These proteases participate in destruction of the extracellular matrix and also cleave some complement components, leading to the inhibition of complement activation, which can allow colonization and proliferation of other bacterial strains. In short, the study's authors indicate that P. gingivalis manipulates the host complement components to escape immune clearance, colonize its new niche, and modify the local microbiota.

P. gingivalis has been observed at many sites other than the oral cavity. Pg has also been shown to survive intracellularly in macrophages, epithelial, endothelial, and smooth muscle cells. Smooth muscle cells are an integral component of arterial cell walls. In addition to surviving in these various cells, Pg spreads from one cell to another, potentially using these cells as means of transportation, travelling to peripheral tissues. Viable periodontal pathogens, including Pg, have been found in atherosclerotic plaques. Antimicrobial peptides and complement activation products are also present in the arterial plaques. The ability of P. gingivalis to manipulate complement and the antimicrobial systems could contribute to the progression of atherosclerosis. In animal models, Pg has been shown to accelerate arterial plaque formation.2

There are other mechanisms by which P. gingivalis plays a role in the initiation and progression of atherosclerosis. For example, modification of certain components of the complement system leads to the accumulation of complement proteins (C5a) that promote apoptosis in endothelial cells and induce the expression of proteases in macrophages in atherosclerotic plaques, which leads to the degradation of the extracellular matrix and arterial plaque rupture.

Current strategies to address periodontitis focus on bacterial reduction. Research on periodontal vaccines is underway and has shown promising results in animal models. Another avenue of research is looking at mediators produced by the body called resolvins. Evidence indicates that resolvins reduce cellular inflammation by inhibiting the production and transportation of inflammatory cells and chemicals to the sites of inflammation. Topical applications of resolvins were able to reduce and to some extent restore periodontitis-associated bone loss in a rabbit model.

It is worth noting that a significant portion of new research is being published in a wide variety of peer-reviewed medical journals. Hopefully, this type of exposure will help disseminate the information to medical professionals. Teasing out more details of the pathogenic activity of periodontal pathogens in the oral cavity and remotely will lead to new treatment modalities and novel ways to address the ravages of periodontal disease and atherosclerosis.

Richard H. Nagelberg, DDS, has practiced general dentistry in suburban Philadelphia for more than 30 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations. He lectures on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity.


1. Hussain M, Stover CM, Dupont A. P. gingivalis in periodontal disease and atherosclerosis - Sciences of action for antimicrobial peptides and complement. Front Immunol. 2015;10:45. doi: 10.3389.

2. Hayashi C, Viereck J, Hua N, et al. Porphyromonas gingivalis accelerates inflammatory atherosclerosis in the innominate artery of ApoE deficient mice. Atherosclerosis. 2011;215:52-9.

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