Host responses in periodontal diseases.
Great progress has been made in our understanding of the pathogenesis of periodontal disease, the primary role of bacteria as etiologic agents, and the critical modifying role of host responses. It is useful to consider several stages in the pathogenesis of periodontal disease - (a) colonization, (b) invasion, (c) destruction, and (d) healing - and to place into perspective the various host responses as they may affect each of these four stages (Table 5). With respect to colonization, although very little direct evidence is available, it is reasonable to suggest that antibodies, either secretory or serum-derived, acting by virtue of their ability to block attachment, could inhibit colonization by immune reduction of adherence mechanisms. With respect to invasion of the tissue, it appears that phagocytes, particularly the neutrophils, are important, acting in concert with opsonic antibody and complement in ingesting and killing the periodontal microflora before or during the early invasive process. A major advance in our understanding of the pathogenesis of periodontal diseases is the realization that the virulence of periodontopathic bacteria relates to their leukaggressive properties, allowing them to evade neutrophil protective mechanisms. Invasion of the periodontal tissues by bacterial products may be inhibited by the complexing of these products with antibody with the formation of antigen-antibody complexes that are phagocytosed and digested, particularly by scavenger phagocytes such as the macrophage. With respect to the destructive phase of periodontal disease, it is clear that the direct effect of lymphocytes mediated either through direct cytotoxic activity, or through biologically-active destructive lymphokines (such as alpha-lymphotoxin and osteoclast activating factor), can lead to tissue destruction. Macrophages, through the production of monokines, collagenase, and reactive oxygen species, can also lead to tissue destruction. The direct effects of bacterial toxins or enzymes which can lead to tissue destruction can be inhibited by complexing with antitoxic or enzyme-neutralizing antibodies. With respect to healing and fibrosis, very little direct information is available; however, it is possible that the lymphocytes and macrophages affect fibrosis by the production of chemotactic factors for fibroblasts which would be expected to bring them to the area of periodontal inflammation and also by production of fibroblast-activating factors, which then cause the fibroblasts to proliferate and produce collagen which replaces lost collagen or results in fibrosis.(ABSTRACT TRUNCATED AT 400 WORDS)
D010520:Aggressive Periodontitis / Q000276:immunology; D000907:Antibodies, Bacterial / Q000502:physiology; D001419:Bacteria / Q000166:cytology / Q000276:immunology; D001439:Bacteroides / Q000276:immunology; D002634:Chemotaxis, Leukocyte; D003165:Complement System Proteins / Q000276:immunology; D005347:Fibroblasts / Q000502:physiology; D005883:Gingival Crevicular Fluid / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D007962:Leukocytes / Q000276:immunology; D008222:Lymphokines / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008407:Mast Cells / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D010510:Periodontal Diseases / Q000276:immunology* / Q000382:microbiology; D010518:Periodontitis / Q000276:immunology / Q000382:microbiology; D010586:Phagocytes / Q000276:immunology
D000907:Antibodies, Bacterial; D008222:Lymphokines; D003165:Complement System Proteins