Periodontal Disease and Overall Health: A Clinician's Guide

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CHAPTER 3 Infection and Inflammation 25directed at mechanisms of inflammationresolution that may be used in treating in -flammatory diseases.PART I: INFLAMMATIONAT THE GINGIVAL LEVELPeriodontal disease is an inflammatorydisorder of the gingiva initiated by bacteriathat leads to the destruction of the supportingtissues of the teeth in a susceptible host. Bacteriain the oral cavity colonize the teeth, thegingival sulcus, and eventually the perio -dontal pocket, forming an organized biofilm.Depending upon the stage of maturation, thebiofilm may consist of several hundred differentbacterial species, many of which haveyet to be identified. 6 Some of these speciesare associated with health, whereas othersare associated with pathology. 7 However,which organisms actually initiate disease remainsunknown.Bacterial ComponentsThe formation of organized biofilmsenhances the ability of bacteria to survive.Bacteria have also evolved a variety of virulencefactors to further enhance their survival,such as toxins, proteases, and glyco -sidases. Virulence factors are presumablyintended to hide the bacteria from host detectionas well as to provide essential moleculesfor nourishment. Conversely, the hosthas evolved mechanisms for detection ofbacteria through the recognition of structuralcomponents of the bacterial surface, such aslipopolysaccharide (LPS), peptidoglycan(PGN), and other cell surface componentssuch as fimbriae that perform essential physiologicfunctions for the bacteria. Variationsof these bacterial components may be seenbetween various species, or even betweendifferent strains of the same species. Despitetheir structural heterogeneity, most of thesemolecules have conserved motifs known aspathogen-associated molecular patterns(PAMPs) that are recognized by host cellreceptors called pattern recognition receptors(PRRs). These highly conserved innate immunereceptors evolved for detection of invadingbacteria. Binding of PAMPs by PRRsactivates specific signaling pathways in hostcells that are important for the initiation of aninflammatory response. Although this responseis intended to eliminate the microbialchallenge, the inflammatory mediators thatare secreted may lead to further tissue damageif bacterial clearance is not achieved.Today, the most studied bacterial factorsinclude LPS, PGN, lipoteichoic acids (LTAs),fimbriae, proteases, heat-shock proteins(HSPs), formyl-methionyl-leucyl-phenyl -alanine (fMLP) and toxins. Host PRRs includethe Toll-like receptors (TLRs) and theG-protein-coupled receptors (GPCRs). Table1 presents a summary of the results by actionsof various bacterial factors after inter -action with specific host cells. 8Bacteria and GI EquilibriumThe oral cavity, as part of the gastro -intestinal tract, is naturally colonized by awide variety of bacteria. This is a physiologicsituation that does not always result inpathology. The tooth-gingival interface is thesite of a variety of natural, innate host defensemechanisms, including the regular sheddingof epithelial cells, the washing effect of thesaliva and the gingival crevicular fluid (GCF),and most importantly, the phagocytic actionof neutrophils that migrate continuouslythrough the junctional epithelium into thegingival sulcus. However, if this equilibriumis disturbed, pathogenic bacteria may overgrow,initiating the pathogenesis of gingivitisand possibly periodontitis. Current under -standing of the steps leading to overgrowthof pathogens includes periodontal bacteriaattaching to epithelial cells using their fimbriaeand PRR recognition of PAMPs, inducingepithelial cell secretion of pro-inflammatorycytokines (TNF-, IL-1, IL-6)and the chemokine IL-8 in the connective
26 Periodontal Disease and Overall Health: A Clinician's GuideTable 1. Summary of Main Effects of Bacterial Virulence Factors on Host CellsResponses of Host CellsBacterial Epithelial Monocytes/ Endothelial FibroblastFactor Cells Macrophages Cells Cells Mast CellsIL-1βTNF-αIFN-γIL-6IL-1βIL-12 MCP-1 TNF-αIP-10 IL-1β IFN-γLPS IL-8MCP-5 E-, P-selectin IL-6 IL-6IL-8 MCP-1 IL-8 IL-12MIP-1α, MIP-2 ICAM-1 IP-10PGE 2NOL-selectinCD11α/CD18,CD11β/CD18IL-1βHistamineTNF-αTNF-αPGN IL-8IL-6ICAM-1ProstaglandinsIL-8IL-8 IL-8 IL-4MIP-1αIL-5NOIL-10IL-1βTNF-αIFN-γIL-6LTA IL-8 IL-6 IL-8IL-8E-selectinIL-10NOIL-1β IL-1β MCP-1FimbriaeTNF-α TNF-α IL-8 IL-1βIL-6 IL-6 ICAM-1, TNF-αIL-8 VCAM-1 IL-6P-, E-selectinProteasesHSPfMLPToxinsIL-6β-defensinsIL-6TNF-αCD11α/CD18CD11β/CD18IL-1βIFN-γIL-6IL-8IL-10Adapted from J Clin Periodontol 2005;32(Suppl 6):57–71. 8IL-6IL-8
Page 5: ivCONTRIBUTORSSrividya Kidambi, MDA
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