Abstract

BackgroundThe pathobiology of rheumatoid arthritis (RA) is similar to that of periodontitis in that proinflammatory cytokines play an important pathologic role. There is evidence to suggest that inhibitors of tumor necrosis factor (TNF) and interleukin-6 (IL-6) receptor for the treatment of RA ameliorated periodontal inflammation. However, no study has evaluated the effect of tofacitinib, an oral Janus kinase inhibitor for the treatment of RA, on periodontitis.Case presentationThe present report cases are 51- and 43-year-old non-smoking women with RA who demonstrated localized moderate chronic periodontitis. Both cases showed improvement in the periodontal inflammatory condition after 3 months of tofacitinib therapy, although the teeth count and supragingival bacterial plaque level were relatively unchanged. Improvements were also observed in the serum levels of IL-6 in both cases as well as in the serum levels of TNF-α and anti-cyclic citrullinated peptide immunoglobulin G in one case and of rheumatoid factor and matrix metalloproteinase-3 in the other case. Patients who received tofacitinib exhibited an inconsistent clinical response, likely due to the low disease activity of RA at the start of the administration.ConclusionsThese are the first reported cases in which tofacitinib may have a beneficial effect on periodontitis. However, more research is required to understand the relationship between periodontitis and tofacitinib therapy.

Highlights

  • The pathobiology of rheumatoid arthritis (RA) is similar to that of periodontitis in that proinflammatory cytokines play an important pathologic role

  • These are the first reported cases in which tofacitinib may have a beneficial effect on periodontitis

  • More research is required to understand the relationship between periodontitis and tofacitinib therapy

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Summary

Introduction

The pathobiology of rheumatoid arthritis (RA) is similar to that of periodontitis in that proinflammatory cytokines play an important pathologic role. Evidence suggests that RA has an epidemiological, serological, and clinical interrelationship with periodontitis, a chronic inflammatory disease that is characterized by the destruction of the tooth-supporting tissues and is a major cause of tooth loss in adults, through common pathogenic mechanisms [1,2,3,4] One of these mechanisms includes the constitutive overproduction of proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin-6. Tofacitinib, an oral small-molecule inhibitor for Janus kinase (JAK) that integrates signals from many cytokines, has been shown to be effective in the treatment of RA [11, 12] These observations have led to the hypothesis that tofacitinib may be effective in reducing periodontal inflammation in patients with RA. No study has yet documented the effect of tofacitinib on periodontitis

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