Advances in Dental Research, Vol 8, 320-328, Copyright © 1994 by International & American Associations for Dental Research
Pathogenic mechanisms in periodontal disease
J. W. Smalley
Department of Clinical Dental Sciences, The University of Liverpool, UK.
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.
