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Chapter 25 : Infection with Porphyromonas gingivalis, a Potential Risk Factor for Chronic Systemic Disease
Category: Clinical Microbiology
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In this chapter, periodontal disease will be used as an example of a polymicrobial disease that represents a potential risk factor for chronic systemic diseases. The chapter focuses on Porphyromonas gingivalis, a predominant periodontopathogenic bacterium that can leave the oral cavity, enter the circulatory system, and invade the vascular endothelium and cardiac tissues. Periodontal disease has a polymicrobial etiology. An extensive combination of bacteria, fungi, and even viruses has been reported to be present simultaneously within infected periodontal sites. Periodontal disease induces chronic inflammation in the oral cavity, and chronic inflammation from various sources is linked with increased cardiovascular risk. Cardiovascular diseases include atherosclerosis, coronary artery disease, cerebrovascular disease, and peripheral arterial disease. Periodontitis may exacerbate preexisting chronic conditions, like rheumatoid arthritis, renal disease, and diabetes mellitus. P. gingivalis can be actively transported across inflamed gingival tissues, and this may occur during infection. The most convincing evidence of P. gingivalis as a potential risk factor for chronic systemic diseases is its ability to invade vascular endothelial and coronary artery cells. P. gingivalis and its extracellular products induce the production of proinflammatory cytokines in epithelial cells and induce the production of proinflammatory cytokines, cell adhesion molecules, and inflammatory genes in endothelial cells. The variability of virulent properties among strains may reflect the extreme adaptability of P. gingivalis and the ability to specialize in the function of the tissue, thereby becoming a catalyst to the development of chronic systemic diseases.
Polymicrobial biofilm in the oral cavity showing microorganisms, inflammatory cells, and erythrocytes in human plaque. Bar, 5 μm. (Micrograph by Janet M. Guthmiller and John Laffoon, courtesy of ASM Press.)
Scanning electron micrograph of HCAE cells infected with P. gingivalis 381 for 30 minutes. Bar, 2.3 μm. (Micrograph by A. Progulske-Fox.)
Transmission electron micrograph of HCAE cells infected with P. gingivalis W83. After 3 hours of infection, P. gingivalis W83 was found in vacuoles that either contained (black arrow) or lacked (white arrow) acid phosphatase. Nascent autophagosomes (AP) that had not yet acquired acid phosphatase and mature autolysosomes (AL) that contained acid phosphatase were observed in infected cells. The presence of autophagic vacuoles and autolysosomes in the infected HCAE cells suggests that P. gingivalis is capable of promoting autophagy. P. gingivalis W83 is localized predominantly in vacuoles which contained multiple bacteria but lacked lysosomal acid phosphatase. Bar, 1 μm. (Micrograph by M. Bélanger, W. A. Dunn, Jr., and A. Progulske-Fox.)
Studies suggesting an association between periodontal disease and long-term chronic systemic disease
General virulence factors used by P. gingivalis to attach, infect, colonize, and activate cardiovascular tissues