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Review
, 11 (7), e1004952
eCollection

Periodontal Diseases: Bug Induced, Host Promoted

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Review

Periodontal Diseases: Bug Induced, Host Promoted

Shariq A Khan et al. PLoS Pathog.

Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Images of patients demonstrating the clinical progression of periodontal disease from gingivitis to advanced periodontitis.
(A) If not treated, mild gingivitis leads to (B) severe gingival inflammation and (C) periodontitis characterized by separation of gingival tissue from the tooth, followed by (D) severe periodontitis, which eventually results in loss of teeth. Images taken are of patients attending the Oral Medicine Clinic at the University of Maryland School of Dentistry.
Fig 2
Fig 2. A schematic of the human tooth illustrating the process of periodontal disease development.
Accumulation of dental plaque leads to formation of tartar and inflammation of gingival tissue. Separation of the gum from the tooth creates a periodontal pocket and loss of bone support. Measuring disease progression is carried out by measuring pocket depth around the teeth, using a periodontal probe; pockets greater than 3 mm in depth are considered to be unhealthy, and 7 mm or deeper pockets indicate significant loss of attachment and carry risk of eventual tooth loss.
Fig 3
Fig 3. An overview schematic of the microbial and host-associated pathologies of periodontal disease.
Disease is initiated via dysregulation between the polymicrobial microbiota and the host immune barriers. Detection of microbial PAMPs by host immune PRRs evokes rapid induction of immune response and production of pro-inflammatory cytokines, which along with certain components of complement, results in recruitment of host immune cells. Degranulation of polymorphonuclear cells (PMNs) releases proteases and other lytic enzymes; localization of these inflammatory reactions results in tissue breakdown, providing nutrients for bacteria, in turn, inducing a feed-forward loop of disease progression. Therefore, although the initial trigger of gingival inflammation is microbial (green), the damage to tissue is largely host associated (blue).

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References

    1. Pihlstrom BL, Michalowicz BS, Johnson NW. Periodontal diseases. Lancet 2005; 366: 1809–20. - PubMed
    1. Calsina G, Ramon JM, Echeverría JJ. Effects of smoking on periodontal tissues. J Clin Periodontol. 2002; 29(8): 771–6. - PubMed
    1. Haffajee AD and Socransky SS. Microbial etiological agents of destructive periodontal diseases. Periodontol 2000. 2005; 5: 78–111. - PubMed
    1. Darveau RP. Periodontitis: a polymicrobial disruption of host homeostasis. Nat Rev Microbiol. 2010; 7: 481–490. - PubMed
    1. Dewhirst FE, Chen T, Izard J, Paster BJ, Tanner AC, Yu WH et al. The human oral microbiome. J Bacteriol. 2010; JB.00542-10. - PMC - PubMed

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