Title: Oral Pathogens, Immunity, and Periodontal Diseases
Volume: 7
Issue: 1
Author(s): Francisco Mesa, Jose Liebana, Pablo Galindo-Moreno and Francisco J. O'Valle
Affiliation:
Keywords:
Periodontitis, immunity, periodontopathogen, Pathogens, Periodontal Diseases, macrophages, fibroblasts, cytokines, monocytes, B-cells, plasma cells, T-cell, Adaptive immunity, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Lipopolysaccharides, toll-like receptor-2, interleukin-1, interleukin-8, prostaglandin E2, tumor necrosis factor-, gingivitis, diabetes, matrix metalloproteinases, arachidonic acid, lipoxins, Osteoprotegerin, osteoimmunology, homeostasis, Langerhans cells, lamina propria, immunoglobulin, Tannerella forsythensis, Staphylococus aureus, pathogen-associated molecular patterns, CD207, Porphyiromona gingivalis, Tannerella forsytensis, Treponema dentícola, reverse-transcription PCR, RT-PCR
Abstract: The pathogenesis of periodontal disease is not fully understood. Subgingival bacterial pathogens are essential for the initiation and development of the disease, but it is the resulting host reaction that primarily mediates tissue damage. Complex inflammatory and immune responses are involved in the progression of periodontitis. Activated monocytes, macrophages, and fibroblasts all produce cytokines that orchestrate the cascade of destructive events in periodontal tissues. Cells from individuals with immune-mediated diseases exhibit different cytokine profiles, which may be due to genetic differences among individuals, causing hyper-responsiveness in some patients. Adaptive immunity, involving Bcells and subsets (B1, B2), plasma cells, and T-cell subsets, can be estimated by their cytokine profiles (Th1, Th2, Th17). Based on these data, it may be feasible to distinguish a protective from a destructive host response in periodontitis. Gene polymorphisms of inflammatory markers are also associated with the presence of viable periodontopathogenic bacteria. Lipopolysaccharides of Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans are considered key factors in the development of chronic periodontitis. Lipopolysaccharides utilize toll-like receptor-2 and increase osteoblastic expression of RANKL, interleukin-1, interleukin-8, prostaglandin E2, and tumor necrosis factor-α, which are all known to induce osteoclastic activity. The aforementioned findings support the hypothesis that complex interactions among microbiota, immune system, and host genome may underlie susceptibility to aggressive periodontitis. This article reviews research on periodontopathogens and provides an update on immunity paradigms in the pathogenesis of periodontal diseases.
