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. 2009:50:52-64.
doi: 10.1111/j.1600-0757.2008.00288.x.

Saliva as a diagnostic tool for periodontal disease: current state and future directions

William V Giannobile, Thomas Beikler, Janet S Kinney, Christoph A Ramseier, Thiago Morelli, David T Wong

Saliva as a diagnostic tool for periodontal disease: current state and future directions

William V Giannobile et al. Periodontol 2000. 2009.
No abstract available

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Figures

Fig. 1
Fig. 1
Schematic overview of the stimulation of CRP (C-reactive protein) in the liver by periodontal pathogens and its subsequent release into GCF (gingival crevice fluid) and whole saliva respectively. Reprinted with permission (62).
Fig. 2
Fig. 2
Schematic overview of the pathogenic processes in periodontal disease. Initial events are triggered by lipopolysaccharide (LPS) from gram-negative bacteria on the tooth root surfaces. As a first line of defense, polymorphonuclear leukocytes (PMNs) are recruited to the site. Monocytes and activated macrophages respond to endotoxin by releasing cytokines [tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β)] which stimulate further tissue destruction. Matrix metalloproteinases (MMPs), powerful collagen destroying enzymes, are produced by fibroblasts and PMNs. TNF-α, IL-1β and receptor activator of NF-kB ligand (RANKL) are elevated in active sites and mediate osteoclastogenesis and bone breakdown. Bone-specific markers such as pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP) are released into the surrounding area and transported by way of gingival crevice fluid (GCF) into the pocket and serve as potential biomarkers for periodontal disease detection. Reprinted with permission (62).
Fig. 3
Fig. 3
Genome-wide view of the distribution of the salivary proteome (parotid and submandibular / sublingual). Note there is no salivary protein expressed by the Y chromosome.
Fig. 4
Fig. 4
Strategy for oral fluid sampling and analysis with a rapid point-of-care or lab-on-a-chip device for the generation of a periodontal disease biomarker report. Reprinted with permission (62).
See this image and copyright information in PMC

References

    1. Airila-Mansson S, Soder B, Kari K, Meurman JH. Influence of combinations of bacteria on the levels of prostaglandin E2, interleukin-1beta, and granulocyte elastase in gingival crevicular fluid and on the severity of periodontal disease. J Periodontol. 2006;77:1025–1031. - PubMed
    1. Albandar JM, Brunelle JA, Kingman A. Destructive periodontal disease in adults 30 years of age and older in the United States, 1988–1994. J Periodontol. 1999;70:13–29. - PubMed
    1. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol. 1999;4:1–6. - PubMed
    1. Armitage GC. The complete periodontal examination. Periodontol 2000. 2004;34:22–33. - PubMed
    1. Azuma M. Fundamental mechanisms of host immune responses to infection. J Periodontal Res. 2006;41:361–373. - PubMed

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