Anti-Tumor Necrosis Factor Alpha Therapy and Periodontal Inflammation in Rheumatoid Arthritis. A clinical and biochemical approach

Although the relationship between periodontal disease and rheumatoid arthritis (RA) is widely documented, centered by common pathobiologic pathways, the effect of various tumor necrosis factor alpha (TNF) antagonists in modulating not only inflammatory and immune articular damage, but also periodontal microenvironment remain debatable. We aimed to evaluate the periodontal status with and without TNF inhibitors in RA patients and to identify potential relation among these entities. We performed a prospective longitudinal 6-months analysis on 96 RA initiating their first biological therapy. Standard assessments included a dual rheumatologic (RA activity, disability, serological, inflammatory prolife) and dental evaluation such as plaque index (PI), gingival index (GI), bleeding on probing (BOP), pocket depth (PD), clinical attachment level (CAL). More than half of RA presented at baseline with chronic periodontitis, as suggested by high prevalence of sites with dental plaque, abnormal BOP, PD and CAL. Advanced inflammatory (CRP, ESR) and immune (anti-cyclic citrullinated peptide antibodies, ACPA) markers were described in RA subsets presenting with aggressive periodontal diseases, while significant correlations between dental pathology, RA activity and ACPA levels were also reported (p[0.05). Furthermore, we revealed significant improvement in both RA-related characteristics and periodontal status after 6 months of anti-TNF therapy (p[0.05). RA, particularly active severe, ACPA positive disease, is essentially accompanied by comorbid periodontal disease. TNF blockade is efficient in patients with active RA and potentially able to modulate the inflammatory process in the periodontal tissue.