Interleukin-6 receptor inhibitor tocilizumab ameliorates periodontal inflammation in patients with rheumatoid arthritis and periodontitis as well as tumor necrosis factor inhibitors.

Interleukin-6 (IL-6) may play a pathological role in rheumatoid arthritis (RA) and periodontitis. Although the efficacy of medication with IL-6 receptor inhibitor, tocilizumab (TCZ), has been demonstrated in the treatment of RA, very little is known about whether TCZ therapy affects periodontitis. The aim of the present study is to compare periodontal condition in patients with RA and periodontitis before and after TCZ therapy. The study participants consisted of 20 patients with RA and periodontitis who were treated with TCZ and 40 patients with RA and periodontitis who received medication with tumor necrosis factor inhibitor (TNFI). Clinical periodontal and rheumatologic assessments and serum biochemical measurements using enzyme-linked immunosorbent assays were performed at baseline and 3 and 6 months later. TCZ and TNFI therapies significantly reduced periodontal inflammation that was determined by gingival index, bleeding on probing, and probing depth (p < 0.017), although plaque levels were comparable before and after the therapies. Both therapies also significantly decreased disease activity score including 28 joints using C-reactive protein (CRP), number of tender and swollen joints, and serum levels of anti-cyclic citrullinated peptide antibodies, rheumatoid factor, CRP, and matrix metalloproteinase-3 (p < 0.017). Additionally, a significant decrease was observed in periodontal clinical attachment level after TCZ therapy (p < 0.017), but not after TNFI therapy. TCZ therapy significantly decreased serum levels of TNF-α, total immunoglobulin G, and serum amyloid A (p < 0.017), although serum levels of IL-6 and soluble IL-6R were significantly increased (p < 0.017). These results suggest a beneficial effect of TCZ therapy on levels of periodontal inflammation in patients with RA and periodontitis, which might be related to decrease in serum inflammatory mediators.