A. Amano1,* C. Chen2 K. Honma3 C. Li3,4 ...

1. Genetic Characteristics and Pathogenic Mechanisms of
Periodontal Pathogens
A. Amano1,* C. Chen2 K. Honma3 C. Li3,4 R.P. Settem3 A. Sharma3, 1Department of Preventive
Dentistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita-Osaka 565-0871,
Japan 2Division of Periodontology, Diagnostic Sciences and Dental Hygiene, Herman Ostrow School
of Dentistry of the University of Southern California, Los Angeles, CA, USA 3Department of Oral
Biology, School of Dental Medicine, the State University of New York at Buffalo, NY 14214, USA
4Department of Microbiology and Immunology, the State University of New York at Buffalo, NY
14214, USA * amanoaatdent.osaka-u.ac.jp All authors contributed equally to this paper
Abstract Periodontal disease is caused by a group of bacteria that utilize a variety of strategies and
molecular mechanisms to evade or overcome host defenses. Recent research has uncovered new
evidence illuminating interesting aspects of the virulence of these bacteria and their genomic
variability. This paper summarizes some of the strategies utilized by the major species
Aggregatibacter actinomycetemcomitans, Tannerella forsythia, Treponema denticola, and
Porphyromonas gingivalis implicated in the pathogenesis of periodontal disease. Whole-genome
sequencing of 14 diverse A. actinomycetemcomitans strains has revealed variations in their genetic
content (ranging between 0.4% and 19.5%) and organization. Strikingly, isolates from human
periodontal sites showed no genomic changes during persistent colonization. T. forsythia
manipulates the cytokine responses of macrophages and monocytes through its surface
glycosylation. Studies have revealed that bacterial surface-expressed O-linked glycans modulate T-
cell responses during periodontal inflammation. Periodontal pathogens belonging to the red complex
consortium express neuraminidases, which enables them to scavenge sialic acid from host
glycoconjugates. Analysis of recent data Congress dental has demonstrated that the cleaved sialic
acid acts as an important nutrient for bacterial growth and a molecule for the decoration of bacteria
surfaces to help evade the host immune attack. In addition, bacterial entry into host cells is also an
important prerequisite for the lifestyle of periodontal pathogens such as P. gingivalis. Studies have
shown that, after its entry into the cell, this bacterium uses multiple sorting pathways destined for
autophagy, lysosomes, or recycling pathways. In addition, P. gingivalis releases outer membrane
vesicles which enter cells via endocytosis and cause cellular functional impairment.
Article Notes CC was supported by National Institute of Dental and Craniofacial Research (NIDCR)
grant R01 DE12212. AS thanks http://www.ada.org/ Dr. Graham P. Stafford, University of Sheffield,
UK, for the TEM micrographs and acknowledges support from U.S. Public Health R01 grants
DE14749 and DE019424. CL was supported by National Institutes of Health (NIH) grant, NIDCR,
DE019667. AA received grants-in-aid for Fundamental Research (B23390477), Exploratory Research
(24659933) and Scientific Research in Priority Areas (23113715) from the Ministry of Education,
Culture, Sports, Science and Technology of Japan.
The authors declare no potential conflicts of interest with respect to the authorship and/or
publication of this article.
This article summarizes information presented during a session of the 50th Anniversary of the
University at Buffalo Oral Biology Graduate Program, which took place June 12-14, 2013, in Buffalo,
New York. Sponsored by Sunstar Americas Inc.
International & American Associations for Dental Research

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