What can the periodontal community learn from the pathophysiology of rheumatoid arthritis?

AIM

The aim of this paper is to provide a narrative review of the aetiopathogeneis and treatments of rheumatoid arthritis (RA), focusing on aspects that may share commonality with periodontitis.

RESULTS

A myriad of cell types, cytokines and pathways have been investigated in both periodontitis and RA. Chronic inflammatory diseases, including RA, psoriatic arthritis, ankylosing spondylitis and periodontitis are likely to share pathogenic mechanisms of inflammation-mediated solid tissue destruction. The aetiopathogenesis of these diseases has been extensively researched over the last several decades and advances in understanding have revolutionized arthritis therapeutics.

CONCLUSION

The rational, targeted inhibition of mediators in RA has provided clinically useful therapeutics and shed light on mechanisms underpinning disease pathogenesis. RA should be considered a prototypic disease revealing how understanding disease pathogenesis may transform therapeutic options and patient outcomes.