Periodontal Disease and Rheumatoid Arthritis

The Evidence Accumulates for Complex Pathobiologic Interactions

Clifton O. Bingham III; Malini Moni


Curr Opin Rheumatol. 2013;25(3):345-353. 

In This Article

Moving From Clinical Associations to Mechanism

Rheumatoid arthritis and periodontal disease share a number of pathobiologic processes that have been previously reviewed.[21,38,39,40,41,42,43,44] These include similar cellular participation at the inflammatory focus, microenvironmental and serum cytokine, matrix metalloproteinase and other mediator profiles, and osteoclast-mediated bone destruction. Studies[45] have shown the presence of periopathogenic bacteria in the synovium of patients with rheumatoid arthritis indicating that joint seeding and localized inflammatory amplification may be operative. Others[46,47] have shown common genetic risk factors including the Human Leukocyte Antigen (HLA)-DR shared epitope and polymorphisms and epigenetic modifications in cytokine genes, including a recent report showing similar interleukin-6 promoter methylation in rheumatoid arthritis and periodontal disease.[48]

A foundational event in the establishment of periodontal disease is the orderly development of a biofilm composed of an array of oral bacteria. In the initial colonization stages, a localized inflammatory response may be seen, but not tissue destruction. The later colonization with a group of specific bacteria appears to be necessary for progression. This group of predominantly anaerobic bacteria, recently referred to as 'keystone pathogens', have unique properties promoting their survival through a number of virulence factors, mechanisms for host defense evasion, tissue penetration, and activation of inflammatory and tissue destructive pathways.[49] As recently reviewed, modern methods of bacterial identification and taxonomic classification are providing a growing appreciation for the complex interactions between bacterial species and their combinatorial interactions with host defenses.[50]