Pathogenic mechanisms in periodontal disease.
Periodontal diseases have been considered as "infections" in which micro-organisms initiate and maintain the destructive inflammatory response. Host-mediated tissue destruction occurs via complement activation and the release of lysosomal enzymes, and connective tissue matrix metalloproteinases. Microbial enzymes may damage connective tissues directly, and, together with toxic metabolites and structural materials, are thought to disrupt the reparative activities of fibroblasts and cells of the immune defenses. The significance and relative contributions of host and microbial factors to the disease process remain unresolved. Environmental changes in the gingival sulcus and periodontal pocket and tissues, the degree of the host response and nutrient availability, concomitant with disease progression, compromise tissue metabolism and repair, and allow for enhanced or de novo expression of microbial virulence factors, such as proteases, which alter microbial pathogenicity. Proteolytic destruction of specific antibodies and complement by both viable and non-viable bacterial cells may retard phagocytic killing and removal of pathogens, thus prolonging the inflammatory response. Bacterial products may indirectly mediate tissue destruction by stimulating release of matrix metalloproteinases or by proteolytically inactivating the specific inhibitors of these enzymes.
Smalley
J W
JW
Department of Clinical Dental Sciences, The University of Liverpool, UK.
D004731:Endotoxins; D006089:Gram-Negative Anaerobic Bacteria / Q000472:pathogenicity; D006801:Humans; D008666:Metalloendopeptidases / Q000378:metabolism; D010510:Periodontal Diseases / Q000201:enzymology / Q000209:etiology* / Q000276:immunology / Q000382:microbiology; D010518:Periodontitis / Q000209:etiology; D014774:Virulence
D004731:Endotoxins; D008666:Metalloendopeptidases