Periodontitis and Rheumatoid Arthritis

Author: Gum Specialist Dr Sajni

Rheumatoid arthritis is a chronic autoimmune disease that mostly affects joints.  Oral manifestations of the condition include Sjogren’s and xerostomia, TMD, methotrexate-induced ulcers, and an increased emphasis on periodontal disease. 

Most studies have shown positive associations with periodontal disease. Periodontal parameters such as bleeding and probing depths seem to be worse in rheumatoid arthritis patients. An important confounder has been smoking status, and although it is a shared risk factor for both rheumatoid arthritis and periodontal disease, associations have been reported in non-smoking rheumatoid arthritis patients.

Periodontal disease severity also seems to reflect rheumatoid arthritis activity and non-surgical treatment has shown to improve rheumatoid arthritis parameters. 

Potential biological mechanisms that may explain the relationship between the two conditions include those associated with common genetic factors, pathogens, inflammation and osteoclast-mediated bone resorption. 

Periodontal bacteria may translocate through the ulcerated epithelium of the periodontal pockets into the circulation. This can result in bacteraemia and systemic inflammation. Porphyromonas gingivalis (Pg) has shown to increase the serum levels of IL-6, which can then induce an increase in the population of osteoclast precursors in the bone marrow, which have and enhanced osteoclastogenic lineage bias. These precursors populate various bone resorption sites where they then can differentiate into mature osteoclasts in response to RANKL (receptor activator of NF-kB ligand). 

Peptide citrullination has been shown to potentially play a role in the aetiology of rheumatoid arthritis. Pg has a PAD (peptidylarginine deimase) enzyme capable of citrullination. Citrullination has shown to be more abundant in inflammatory periodontitis than in non-inflamed tissue.  

Periopathogenic bacteria have been shown to be present in the synovium of patients with rheumatoid arthritis. Potential common genetic risk factors include epigenetic modifications in cytokine genes.