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Open AccessJournal ArticleDOI

Mobile Microbiome: Oral Bacteria in Extra-oral Infections and Inflammation

Yiping W. Han, +1 more
- 01 Jun 2013 - 
- Vol. 92, Iss: 6, pp 485-491
TLDR
The most recent findings on systemic infections and inflammation complicated by oral bacteria, including cardiovascular disease, adverse pregnancy outcomes, rheumatoid arthritis, inflammatory bowel disease and colorectal cancer, respiratory tract infections, and organ inflammations and abscesses are reviewed.
Abstract
The link between oral infections and adverse systemic conditions has attracted much attention in the research community. Several mechanisms have been proposed, including spread of the oral infection due to transient bacteremia resulting in bacterial colonization in extra-oral sites, systemic injury by free toxins of oral pathogens, and systemic inflammation caused by soluble antigens of oral pathogens. Mounting evidence supports a major role of the systemic spread of oral commensals and pathogens to distant body sites causing extra-oral infections and inflammation. We review here the most recent findings on systemic infections and inflammation complicated by oral bacteria, including cardiovascular disease, adverse pregnancy outcomes, rheumatoid arthritis, inflammatory bowel disease and colorectal cancer, respiratory tract infections, and organ inflammations and abscesses. The recently identified virulence mechanisms of oral species Fusobacterium nucleatum, Porphyromonas gingivalis, Streptococcus mutans, and Campylobacter rectus are also reviewed. A pattern emerges indicating that only select subtype(s) of a given species, e.g., F. nucleatum subspecies animalis and polymorphum and S. mutans non-c serotypes, are prone to extra-oral translocation. These findings advocate the importance of identification and quantification of potential pathogens at the subtype levels for accurate prediction of disease potential.

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Citations
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Journal ArticleDOI

The Placenta Harbors a Unique Microbiome

TL;DR: A unique placental microbiome niche was characterized, composed of nonpathogenic commensal microbiota from the Firmicutes, Tenericute, Proteobacteria, Bacteroidetes, and Fusobacteria phyla, which was consistently different from those reported in other parts of the body, including the skin and urogenital tract.
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Periodontitis: from microbial immune subversion to systemic inflammation

TL;DR: The mechanisms of microbial immune subversion that tip the balance from homeostasis to disease in oral or extra-oral sites are discussed.
Journal ArticleDOI

The oral microbiota: dynamic communities and host interactions.

TL;DR: Current knowledge and emerging mechanisms governing oral polymicrobial synergy and dysbiosis that have both enhanced the understanding of pathogenic mechanisms and aided the design of innovative therapeutic approaches for oral diseases are discussed.
Journal ArticleDOI

Immunomicrobial pathogenesis of periodontitis: keystones, pathobionts, and host response.

TL;DR: New paradigms in the understanding of periodontitis are discussed, which may shed light into other polymicrobial inflammatory disorders and highlight gaps in knowledge required for an integrated picture of the interplay between microbes and innate and adaptive immune elements that initiate and propagate chronic periodontal inflammation.
References
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Infective endocarditis

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Fusobacterium nucleatum infection is prevalent in human colorectal carcinoma

TL;DR: Overabundance of Fusobacterium sequences in tumor versus matched normal control tissue is verified by quantitative PCR analysis from a total of 99 subjects, and a positive association with lymph node metastasis is observed.
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Identification of periodontal pathogens in atheromatous plaques.

TL;DR: periodontal pathogens are present in atherosclerotic plaques where, like other infectious microorganisms such as C. pneumoniae, they may play a role in the development and progression of atherosclerosis leading to coronary vascular disease and other clinical sequelae.
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Low-Abundance Biofilm Species Orchestrates Inflammatory Periodontal Disease through the Commensal Microbiota and Complement

TL;DR: It is shown that P. gingivalis, at very low colonization levels, triggers changes to the amount and composition of the oral commensal microbiota leading to inflammatory periodontal bone loss, demonstrating that a single, low-abundance species can disrupt host-microbial homeostasis to cause inflammatory disease.
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