Periodontitis, also known as gum disease, is an infection of the soft tissues around the teeth. Untreated periodontitis can destroy the bone that supports the teeth and cause tooth loss. Neutrophils, a type of white blood cell, often appear in periodontitis gum lesions where they release neutrophil extracellular traps (NETs), mesh-like structures that are made of strings of DNA. This study demonstrated that neutrophil extracellular traps trigger an inflammatory response that leads to bone destruction during periodontitis through the recruitment of Th17 cells.

What is exciting about this article?

Neutrophil recruitment has been documented in blood samples of patients with periodontitis. However, the mechanisms by which neutrophils contribute to the disease process are not fully understood. The findings of this study demonstrated a causal relationship between NETs and bone destruction during gum disease. The researchers also demonstrated that extracellular histones, a major component of NETs, are involved in the initial triggering of IL-17/Th17 responses, which results in bone destruction in periodontitis lesions. In addition, this work reveals new insights and therapeutic avenues that could be used to treat the disease.

How does this fit into the larger NIAMS portfolio?

In line with the mission of NIAMS, Dr. Kaplan’s research focuses on finding abnormalities in neutrophils and understanding the role of NETs in systemic autoimmune disorders. This collaborative study discovered a novel role of NETs in the pathogenesis of periodontitis.

Grant support


Research Areas:

Autoimmunity Cell Biology Clinical Research Immunology Molecular Biology and Biochemistry Systems Biology


Neutrophil extracellular traps and extracellular histones potentiate IL-17 inflammation in periodontitis.

Kim TS, Silva LM, Theofilou VI, Greenwell-Wild T, Li L, Williams DW, Ikeuchi T, Brenchley L, NIDCD/NIDCR Genomics and Computational Biology Core, Bugge TH, Diaz PI, Kaplan MJ, Carmona-Rivera C, Moutsopoulos NM
J Exp Med.
2023 Sep 4;
doi: 10.1084/jem.20221751
PMID: 37261457

Research reported in this publication was supported by the Intramural Research Program of the NIHʼs National Institute of Arthritis and Musculoskeletal and Skin Diseases.