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Interleukin-17 (also known as interleukin-17A) is a key cytokine that links T-cell activation to neutrophil mobilization and activation. As such, interleukin-17 can mediate protective innate immunity to pathogens or contribute to the pathogenesis of inflammatory diseases, such as psoriasis and rheumatoid arthritis. This review summarizes the basic biology of interleukin-17 and discusses its emerging role in periodontal disease. The current burden of evidence from human and animal model studies suggests that the net effect of interleukin-17 signaling promotes disease development. In addition to promoting neutrophilic inflammation, interleukin-17 has potent pro-osteoclastogenic effects that are likely to contribute to the pathogenesis of periodontitis, rheumatoid arthritis and other diseases involving bone immunopathology. Systemic treatments with anti-interleukin-17 biologics have shown promising results in clinical trials for psoriasis and rheumatoid arthritis; however, their impact on the highly prevalent periodontal disease has not been investigated or reported. Future clinical trials, preferably using locally administered interleukin-17 blockers, are required to implicate conclusivelyinterleukin-17 in periodontitis and, more importantly, to establish an effective adjunctive treatment for this oral inflammatory disease.
Zenobia et al. (Fri,) studied this question.