Abstract

Calprotectin, a heterodimer of S100A8 and S100A9 subunits, is associated with inflammatory disorders such as rheumatoid arthritis and cystic fibrosis. Although calprotectin levels are increased significantly in the gingival crevicular fluid (GCF) of periodontitis patients, its effects on periodontal ligament cells (PDLCs) remain largely unknown. The aim of this study was to evaluate calprotectin levels in the GCF of generalized aggressive periodontitis (AgP) patients and to investigate the effects of recombinant human calprotectin (rhS100A8/A9) and its subunits (rhS100A8 and rhS100A9) in PDLCs. Both the concentration and amount of crevicular calprotectin were significantly higher in the AgP group compared with healthy controls. In addition, the GCF calprotectin levels were correlated positively with clinical periodontal parameters including bleeding index, probing depth, and clinical attachment loss. rhS100A8/A9 promoted cell apoptosis, whereas rhS100A8 and rhS100A9 individually exerted little effect on apoptosis in PDLCs. rhS100A9 and rhS100A8/A9 increased the activation of nuclear factor-κB (NF-κB) by promoting the nuclear translocation of p65 in PDLCs, subsequently inducing expression of the pro-inflammatory cytokines IL-6, IL-8, TNFα, and COX2. Treatment with an NF-κB inhibitor partially reversed the rhS100A9- and rhS100A8/A9-induced upregulation of the pro-inflammatory cytokines. rhS100A9, and not rhS100A8, was mainly responsible for the pro-inflammatory role of calprotectin. Collectively, our results suggest that calprotectin promotes apoptosis and the inflammatory response in PDLCs via rhS100A9. These findings might help identify novel treatments for periodontitis.

Highlights

  • Periodontitis is an infectious disease that affects the tissues supporting the teeth and leads to eventual tooth loss [1]

  • The present study revealed that calprotectin levels were significantly higher in the gingival crevicular fluid (GCF) of aggressive periodontitis (AgP) patients compared with the control group, which is consistent with the previous studies [15,29,30]

  • The biological function of calprotectin in periodontal ligament cells (PDLCs) and the mechanism by which calprotectin contributes to the pathogenesis of periodontitis remain unclear

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Summary

Introduction

Periodontitis is an infectious disease that affects the tissues supporting the teeth and leads to eventual tooth loss [1]. Current knowledge regarding the pathogenesis of periodontal disease suggests that its central cause is an imbalance in the host-parasite relationship. The host inflammatory response plays a role. A large number of cytokines and other effector molecules released by resident and migrating cells contribute to the destruction of soft and hard tissues seen in periodontitis [2]. Calprotectin is a heterodimeric calcium-binding protein consisting of S100A8 and S100A9 subunits [3]. It is expressed constitutively in neutrophils [4], monocytes [4], keratinocytes [5]

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