Inflammatory and immune pathways in the pathogenesis of periodontal disease

Abstract

The pathogenesis of periodontitis involves a complex immune/inflammatory cascade that is initiated by the bacteria of the oral biofilm that forms naturally on the teeth. The susceptibility to periodontitis appears to be determined by the host response; specifically, the magnitude of the inflammatory response and the differential activation of immune pathways. The purpose of this review was to delineate our current knowledge of the host response in periodontitis. The role of innate immunity, the failure of acute inflammation to resolve (thus becoming chronic), the cytokine pathways that regulate the activation of acquired immunity and the cells and products of the immune system are considered. New information relating to regulation of both inflammation and the immune response will be reviewed in the context of susceptibility to, and perhaps control of, periodontitis.

Fig. 1

The immune inflammatory response in periodontitis is complex and involves both innate and acquired immunity. This diagram presents an overview of the effector molecules and effector cells in the pathogenesis of periodontitis based on our current understanding of disease pathways. BCA-1, B cell-attracting chemokine 1; CGRP, calcitonin gene-related peptide; CTLA-4, cytotoxic T-lymphocyte-associated antigen 4; GM-CSF, granulocyte– macrophage colony-stimulating factor; IFN-γ, interferon gamma; Ig-A, immunglobulin A; Ig-G, immunglobulin G; Ig-M, immunglobulin M; IL-1β, interleukin-1beta; IL-2, interleukin-2; IL-3, interleukin-3; IL-4, interleukin-4; IL-5, interleukin-5; IL-6, interleukin-6; IL-8, interleukin-8; IL- 13, interleukin-13; IL-17, interleukin-17; IL-22, interleukin-22; LPS, lipopolysaccharide; M-CSF, macrophage colony-stimulating factor; MAC, membrane attack complex; MCP-1, macrophage chemotactic protein-1; MDC, macrophage-derived chemokine; MMPs, matrix metalloproteinases; OPG, osteoprotegerin; PGE₂, prostaglandin E₂; RANTES, regulated and normal T cell expressed and secreted; SDF-1a, stromal cell-derived factor-1alpha; TARC, thymus and activation-regulated chemokine; TGF-β, transforming growth factor beta; Th1, T-helper 1 cell; Th2, T-helper 2 cell; Th17, T-helper 17 cell; TIMP, tissue inhibitor of matrix metalloproteinases; TNF-α, tumor necrosis factor alpha; Treg T-regulatory cell.