Periodontal Disease and Overall Health: A Clinician's Guide

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.