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Kanzaki H, Wada S, Narimiya T, et al. Pathways that Regulate ROS Scavenging Enzymes, and Their Role in Defense Against Tissue Destruction in Periodontitis. Front Physiol. 2017;8:351doi: 10.3389/fphys.2017.00351.
Kanzaki, H., Wada, S., Narimiya, T., Yamaguchi, Y., Katsumata, Y., Itohiya, K., Fukaya, S., Miyamoto, Y., & Nakamura, Y. (2017). Pathways that Regulate ROS Scavenging Enzymes, and Their Role in Defense Against Tissue Destruction in Periodontitis. Frontiers in physiology, 8351. https://doi.org/10.3389/fphys.2017.00351
Kanzaki, Hiroyuki, et al. "Pathways that Regulate ROS Scavenging Enzymes, and Their Role in Defense Against Tissue Destruction in Periodontitis." Frontiers in physiology vol. 8 (2017): 351. doi: https://doi.org/10.3389/fphys.2017.00351
Kanzaki H, Wada S, Narimiya T, Yamaguchi Y, Katsumata Y, Itohiya K, Fukaya S, Miyamoto Y, Nakamura Y. Pathways that Regulate ROS Scavenging Enzymes, and Their Role in Defense Against Tissue Destruction in Periodontitis. Front Physiol. 2017 May 30;8:351. doi: 10.3389/fphys.2017.00351. eCollection 2017. PMID: 28611683; PMCID: PMC5447763.
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Front Physiol. 2017 May 30;8:351. doi: 10.3389/fphys.2017.00351. eCollection 2017.

Pathways that Regulate ROS Scavenging Enzymes, and Their Role in Defense Against Tissue Destruction in Periodontitis.

Frontiers in physiology

Hiroyuki Kanzaki, Satoshi Wada, Tsuyoshi Narimiya, Yuuki Yamaguchi, Yuta Katsumata, Kanako Itohiya, Sari Fukaya, Yutaka Miyamoto, Yoshiki Nakamura

Affiliations

  1. Maxillo-Oral Disorders, Tohoku University HospitalSendai, Japan.
  2. Department of Orthodontics, School of Dental Medicine, Tsurumi UniversityYokohama, Japan.

PMID: 28611683 PMCID: PMC5447763 DOI: 10.3389/fphys.2017.00351

Abstract

Periodontitis, an inflammatory disease that affects the tissues surrounding the teeth, is a common disease worldwide. It is caused by a dysregulation of the host inflammatory response to bacterial infection, which leads to soft and hard tissue destruction. In particular, it is the excessive inflammation in response to bacterial plaque that leads to the release of reactive oxygen species (ROS) from neutrophils, which, then play a critical role in the destruction of periodontal tissue. Generally, ROS produced from immune cells exhibit an anti-bacterial effect and play a role in host defense and immune regulation. Excessive ROS, however, can exert cytotoxic effects, cause oxidative damage to proteins, and DNA, can interfere with cell growth and cell cycle progression, and induce apoptosis of gingival fibroblasts. Collectively, these effects enable ROS to directly induce periodontal tissue damage. Some ROS also act as intracellular signaling molecules during osteoclastogenesis, and can thus also play an indirect role in bone destruction. Cells have several protective mechanisms to manage such oxidative stress, most of which involve production of cytoprotective enzymes that scavenge ROS. These enzymes are transcriptionally regulated via NRF2, Sirtuin, and FOXO. Some reports indicate an association between periodontitis and these cytoprotective enzymes' regulatory axes, with superoxide dismutase (SOD) the most extensively investigated. In this review article, we discuss the role of oxidative stress in the tissue destruction manifest in periodontitis, and the mechanisms that protect against this oxidative stress.

Keywords: ROS; cytoprotective enzymes; osteoclast; oxidative stress; periodontitis

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