Host defence mechanisms against bacterial aggression in periodontal disease: basic mechanisms

Abstract

Periodontal diseases are complex bacteria-induced infections characterised by an inflammatory host response to plaque microbiota and their by-products. Most of these microorganisms have virulence factors capable of causing massive tissue destruction both directly, through tissue invasion and the production of harmful substances, or indirectly, by activation of host defense mechanisms, creating an inflammatory infiltrate of potent catabolic activity that can interfere with normal host defense mechanisms. In response to the aggression, host defense mechanisms activate innate and adaptive immune responses. Our aim is to offer a general overview of the main mechanisms involved in the host response to bacterial aggression in periodontitis, such as lipopolysaccharide receptor CD14, complement system, polymorphonuclear neutrophils, antibodies and immunoglobulins.

Human soluble receptor for advanced glycation end products and tumor necrosis factor-α as gingival crevicular fluid and serum markers of inflammation in chronic periodontitis and type 2 diabetes

“…Activation of the inflammatory-immune system by periodontal pathogens leads to chronic inflammation, causing progressive destruction of the connective tissues and resorption of the alveolar bone; if left untreated, it finally leads to tooth loss (2,3). The extent of inflammation and destruction of the periodontal tissues can be evaluated by analyzing the components of the gingival crevicular fluid (GCF) because several inflammatory and immune mediators implicated in periodontal destruction have been established in GCF (4,5).…”

Efficacy of subantimicrobial-dose doxycycline against nitrosative stress in chronic periodontitis

“…When stimulated with bacteria or bacterial components, human monocytes, endothelial cells, macrophages, and gingival fibroblasts produce inflammatory mediators that perpetuate and amplify chronic periodontal inflammation through numerous autocrine and paracrine loops [2] . Epidemiological and interventional studies have revealed close associations between periodontal disease and systemic diseases, such as cardiovascular disease, preterm delivery and low birthweight, diabetes mellitus, respiratory infections, osteoporosis, and cancer [3][4][5] . The main causes of periodontitis-related systemic diseases are thought to be the oral-hematogenous spread of bacteria and the excessive release of periodontal inflammatory mediators [3] .…”

“…Accordingly, therapeutic strategies for periodontal disease have been directed towards two different and complementary paths: antimicrobial therapy and host modulation. Three categories of host-modulating agents have been tested experimentally and clinically in periodontal therapy: antiproteinases (tetracyclines), anti-inflammatory drugs, and bone-sparing drugs (antiresorptive agents such as bisphosphonates) [2,4] . Tetracyclines are the most extensively investigated host-modulatory agents, and subantimicrobial-dose doxycycline (SDD) is widely used as an adjunct to scaling and root planing (SRP).…”

Impact of Dental Plaque Biofilms in Periodontal Disease: Management and Future Therapy

“…As the disease worsens, periodontal pockets deepen, the components of the extracellular matrix of the gingiva and periodontal ligament are destroyed, and alveolar bone is desorbed [88]. On the other hand, bacterial LPS can subsequently interact with macrophage or dendritic cell receptors, including CD14 and TLRs, to stimulate the production of inflammatory cytokines, especially IL1, and other proinflammatory mediators [89].…”