Host–biofilm interface interactions lead to oral infectious diseases and contain promise for disease amelioration

Abstract

Host immune response has been demonstrated to be of considerable importance in oral infections, namely dental caries and periodontal diseases. The molecular pathogenesis of dental caries has been well recognized and evidence indicates that salivary antibodies can modify the course of infection caused by mutans streptococci. The use of specific antigens from mutans streptococci and passive antibody administration has been shown to result in protection from dental caries. Thus, dental caries can be considered a conventional bacterial infectious disease where the major causative organism is recognized. However, periodontal disease is a more specialized type of infectious disease, related to a constellation of oral biofilm microorganisms. These organisms initiate a host immune response and produce symptoms of periodontitis. Antibodies from gingival crevicular fluid have shown the potential to alter the nature of the pathogenic flora. Recent findings suggest that lymphocytes can be the key to bone resorption in the pathogenesis of periodontal disease. Activated lymphocytes that infiltrate the gingival/periodontal tissues upregulate receptor activator of NF-κB ligand (RANKL) and subsequently induce osteoclastogenesis. Interference with antigen-specific T and B cell activation should provide new approaches for amelioration of inflammatory bone resorption in periodontal diseases.