Periodontal Disease and Overall Health: A Clinician's Guide

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CHAPTER 2 Overview of Periodontal Disease:CHAPTER 2 Causes, Pathogenesis, and Characteristics 13the host immuno-inflammatory response toplaque bacteria produces destructive cytokinesand enzymes resulting in periodontaltissue destruction. The host response is essentiallyprotective by intent but can alsoresult in tissue damage, including the breakdownof connective tissue fibers in the periodontalligament and the resorption of alveolarbone. The host response to the plaquebiofilm is modified by genetic factors (helpingto explain why aggressive periodontitistends to have a familial aggregation), as wellas systemic and environmental factors (e.g.,diabetes, stress, smoking).To better treat and manage periodontaldiseases, we need a more detailed understandingof periodontal pathogenesis (Figure1). 35-37 The bacteria and their metabolic products(e.g., endotoxin) stimulate the junctionalepithelium to proliferate, and to produce tissue-destructiveproteinases. This infectionalso increases the permeability of the junctionalepithelium that allows microbes andtheir products to gain access to the subepithelialconnective tissue. Epithelial and connectivetissue cells are thus stimulated toproduce inflammatory mediators that resultin an inflammatory response within the tissues.Microbial products also chemotacticallyattract a constant flux of pro-inflamma -tory cells migrating from the circulation tothe gingival crevice. Neutrophils, or PMNLs,are predominant in the early stages of gingivalinflammation. Thus, an immune responseis generated in the periodontal tissues andpro-inflammatory cytokines such as IL-1β,TNF-α, and MMPs are produced by inflammatorycells recruited to the lesion site. Thefunctions of PMNLs include phagocytosisand destruction of bacteria. Initially the clinicalsigns of gingivitis are evident. This responseis essentially protective in nature toFigure 1. Schematic Illustration of the Pathogenesis of PeriodontitisGenetic risk factorsMicrobialchallengeAntibodyPMNsAntigensLPSOthervirulencefactorsHostimmuneinflammatoryresponseCytokinesProstanoidsMMPsConnectivetissue andbonemetabolismClinicalsigns ofdiseaseEnvironmental and acquiredrisk factorsTissue breakdown products and ecological changesCopyright 2006 by Saunders, an imprint of Elsevier Inc.Source: Carranza’s Clinical Periodontology, 10th Ed. WB Saunders Company; 2006:275–282. 36 Reproducedwith permission.
14 Periodontal Disease and Overall Health: A Clinician's Guidecontrol bacterial infection. In persons whoare not susceptible to periodontitis, the primarydefense mechanisms control the infection,and chronic inflammation (i.e., chronicgingivitis) may persist. However, in individualssusceptible to periodontitis, theabove inflammatory process will eventuallyextend apically and laterally to involvedeeper connective tissues and alveolar bone,recruiting monocytes and lymphocytes tothe site of infection at these later stages.These monocytes and macrophages areactivated by the bacterial endotoxins leadingto the production of high levels ofprostaglandins (e.g., PGE 2), interleukins(e.g., IL-1α, IL-1β, IL-6), TNF-α, and MMPsby the host cells. The MMPs break downcollagen fibers, disrupting the normalanatomy of the gingival tissues, resulting indestruction of the periodontal apparatus. Ifleft untreated, the inflammation continuesto extend apically, and osteoclasts are stimulatedto resorb alveolar bone triggered bythe high levels of PGs, ILs, and TNF-α in thetissues. The elevated levels of pro-inflammatorymediators and MMPs are counterbalancedby a protective response in the hostwith elevations in anti-inflammatory mediatorssuch as the cytokines IL-4 and IL-10, aswell as other mediators such as IL-1ra (receptorantagonist) and tissue inhibitors ofMMPs (TIMPs; Figure 2). 36,37 Under normal,healthy conditions, the anti-inflammatorymediators are balanced with inflammatorymediators, thereby controlling tissue destruc -tion. If an imbalance is seen, with excessivelevels of the pro-inflammatory mediators,upregulated MMP expression and activity,and insufficient levels of protective antiinflammatorymediators, loss of periodontalconnective tissue and bone will occur.Thus, plaque bacteria initiate an inflammatoryresponse by the host, resulting inexcessive levels of pro-inflammatory mediatorsand enzymes, leading to the destructionof periodontal tissues. If this inflammationFigure 2. The Periodontal BalanceRisk factors (e.g., genetics,smoking, diabetes)Overproduction of proinflammatory ordestructive mediators and enzymes (e.g.,IL-1, IL-6, PGE 2, TNF-, MMPsReduction ofrisk factorsExpression of host-derived antiinflammatoryor protective mediators(e.g., IL-4, IL-10, IL-1ra, TIMPs)Underactivity or overactivityof aspects of host responseHost modulatorytherapyResolution ofinflammationPoor compliancePoor plaque controlSubgingivalbioburdenOHI, SRP, surgery, antiseptics, antibioticsto reduce bacterial challengeDISEASEHEALTHCopyright 2006 by Saunders, an imprint of Elsevier Inc.Source: Carranza’s Clinical Periodontology, 10th Ed. WB Saunders Company; 2006:275–282. 36 Reproducedwith permission.
Page 5: ivCONTRIBUTORSSrividya Kidambi, MDA
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Periodontal Disease and Overall Health: A Clinician's Guide

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