Periodontitis and Rheumatoid Arthritis: The Same Inflammatory Mediators?

• Published in: Mediators of inflammation Vol. 2019; no. 2019; pp. 1 - 8
• Main Authors: Polimeni, Antonella, Valesini, Guido, Pranno, Nicola, Pilloni, Andrea, Lucchetti, Ramona, Di Carlo, Gabriele, Saccucci, Matteo, Ceccarelli, Fulvia, Luzzi, Valeria
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2019; Hindawi; John Wiley & Sons, Inc; Wiley
• Subjects: Analysis; Animals; Antigens; Arthritis; Arthritis, Rheumatoid - blood; Arthritis, Rheumatoid - immunology; Autoantibodies; Autoantibodies - blood; Autoantibodies - immunology; Autoimmunity; B cells; Biomarkers; Biomarkers - blood; Citrulline; Cytokines; Drb1 protein; Genetic factors; Genetic polymorphisms; Gum disease; Histocompatibility antigen HLA; Histocompatibility antigens; HLA histocompatibility antigens; Humans; Immunoglobulins; Inflammation; Interleukin 6; Interleukin-6 - blood; Interleukin-6 - immunology; Neutrophils; Periodontitis; Periodontitis - blood; Periodontitis - immunology; Review; Rheumatic diseases; Rheumatoid arthritis; Rheumatoid factor; TNF inhibitors; Tumor necrosis factor; Tumor necrosis factor-TNF
• ISSN: 0962-9351; 1466-1861; 1466-1861
• DOI: 10.1155/2019/6034546

The strict link between periodontitis (PD) and rheumatoid arthritis (RA) has been widely demonstrated by several studies. PD is significantly more frequent in RA patients in comparison with healthy subjects: this prevalence is higher in individuals at the earliest stages of disease and in seropositive patients. This is probably related to the role of P. gingivalis in inducing citrullination and leading to the development of the new antigens. Despite the many studies conducted on this topic, there is very little data available concerning the possibility to use the same biomarkers to evaluate both RA and PD patients. The aim of the review is to summarize this issue. Starting from genetic factors, data from literature demonstrated the association between HLA-DRB1 alleles and PD susceptibility, similar to RA patients; moreover, SE-positive patients showed simultaneously structural damage to the wrist and periodontal sites. Contrasting results are available concerning other genetic polymorphisms. Moreover, the possible role of proinflammatory cytokines, such as TNF and IL6 and autoantibodies, specifically anticyclic citrullinated peptide antibodies, has been examined, suggesting the need to perform further studies to better define this issue.