Periodontal Disease and Rheumatoid Arthritis
Periodontal Disease and Rheumatoid Arthritis
The gram-negative, anaerobic, oral coccobacillus Pg has received considerable attention for its role in the development of periodontal disease. This bacterial species is rarely present in periodontally healthy individuals, but colonization by Pg is one of the permissive steps in the propagation of the periodontal lesion. Pg has a number of characteristics that allow it to initially elude host defense mechanisms, promoting tissue ingress, with a resultant upregulation of a number of local inflammatory responses, further propagating tissue damage. The virulence factors and properties of Pg have been recently comprehensively reviewed. These include the gingipain family of arginine-specific and lysine-specific proteases, lipopolysaccharide, and fimbriae that have a number of deleterious effects on tissue. Among its features, Pg traverses the normally tight epithelial junctions through specific interactions with integrins and the cleavage of adhesion molecules, inactivates certain proinflammatory cytokines and chemokines, degrades components of the extracellular matrix, increases oxidative stress, can cause cell apoptosis including chondrocytes, and can activate coagulation pathways by cleaving fibrinogen and induce vascular permeability via the kinin cascade.
The recognition that Pg was unique among oral bacteria in having a PAD spurred considerable interest among the rheumatologic community, given the appreciation of ACPA in rheumatoid arthritis. This provided an additional potential mechanistic explanation for the relationship between periodontal disease and rheumatoid arthritis, a hypothesis that has been reviewed in depth by others.
Porphyromonas Gingivalis
The gram-negative, anaerobic, oral coccobacillus Pg has received considerable attention for its role in the development of periodontal disease. This bacterial species is rarely present in periodontally healthy individuals, but colonization by Pg is one of the permissive steps in the propagation of the periodontal lesion. Pg has a number of characteristics that allow it to initially elude host defense mechanisms, promoting tissue ingress, with a resultant upregulation of a number of local inflammatory responses, further propagating tissue damage. The virulence factors and properties of Pg have been recently comprehensively reviewed. These include the gingipain family of arginine-specific and lysine-specific proteases, lipopolysaccharide, and fimbriae that have a number of deleterious effects on tissue. Among its features, Pg traverses the normally tight epithelial junctions through specific interactions with integrins and the cleavage of adhesion molecules, inactivates certain proinflammatory cytokines and chemokines, degrades components of the extracellular matrix, increases oxidative stress, can cause cell apoptosis including chondrocytes, and can activate coagulation pathways by cleaving fibrinogen and induce vascular permeability via the kinin cascade.
The recognition that Pg was unique among oral bacteria in having a PAD spurred considerable interest among the rheumatologic community, given the appreciation of ACPA in rheumatoid arthritis. This provided an additional potential mechanistic explanation for the relationship between periodontal disease and rheumatoid arthritis, a hypothesis that has been reviewed in depth by others.
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