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Porphyromonas gingivalis-Epithelial Cell Interactions in Periodontitis

Groupe de Recherche en Écologie Buccale, Faculté de médecine dentaire, Université Laval, Quebec City, Quebec, Canada, G1K 7P4

View larger version (77K): [in this window] [in a new window]   Figure 1. P. gingivalis invasion of a three-dimensional (3-D) engineered human oral mucoasa model. (A) Structural modifications to the 3-D engineered human oral mucosa model following a P. gingivalis ATCC 33277 infection. (a) Uninfected control model; (b) P. gingivalis ATCC 33277-infected model. Scale bars, 50 µm. (B) Transmission electron micrograph of P. gingivalis in a multilayer of epithelial cells and in the underlying connective tissue of a 3-D engineered human oral mucosa model. These Figs. are from Andrian et al.(2004), and are reprinted with permission.

View larger version (31K): [in this window] [in a new window]   Figure 2. Current model of P. gingivalis interactions with gingival epithelial cells. Interactions between P. gingivalis fimbriae, gingipains, and other potential adhesins with various epithelial cell-surface receptors (PAR-1/2, TLR2, integrins) lead to the activation of epithelial cell signaling pathways and the modulation of gene expression. The entry of P. gingivalis into epithelial cells is associated with the phosphorylation/dephosphorylation of signaling molecules such as MAP kinases, the modulation of calcium influx, and the re-arrangement of the cell cytoskeleton. Interactions of fimbriae with integrins initiate down-stream signaling events, including the formation of focal adhesion molecules such as FAK/paxillin. The intracellular localization of gingipains can interfere with the pathways of the focal adhesion molecules FAK/paxillin and MAP kinase. This model has been adapted from a model proposed by Lamont and Jenkinson (1998). See text for references. Abbreviations: Ca++, calcium; ERK, extracellular signal-regulated kinase; GTP, guanosine triphosphate; IkB, inhibitory factor; ILβ, interleukin; JNK, c-Jun N-terminal; MAPKKK, mitogen-activated protein kinase kinase kinase; MEK, extracellular signal-regulated kinase activator kinase; NF-B, nuclear transcriptional factor; PAR, protease-activated receptor; RAS, small-GTPase; and TLR, Toll-like receptor.

Journal of Dental Research, Vol. 85, No. 5, 392-403 (2006)
DOI: 10.1177/154405910608500502


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