Abstract
Periodontal disease (PD) is a common infectious and inflammatory disease characterised by inflammation of tissues surrounding and supporting the teeth and destruction of the associated alveolar bone, eventually resulting in tooth loss. This disease is caused by periodontopathic bacteria in plaque biofilm and resultant innate and adaptive immune responses in periodontal tissues. Calprotectin (CLP) is a calcium-binding protein of the S-100 protein family and is found to be induced by activated granulocytes, monocytes, and epithelial cells. CLP has been shown to play an important role in numerous inflammatory diseases and disorders. Increasing evidence indicates that CLP is involved in the progression of PD, and its levels may be associated with disease severity and outcome of periodontal treatments. This review will summarise recent studies regarding the presence, regulation, and function of CLP in PD. The findings indicate that CLP may be an effective biomarker for diagnosis and treatment for the PD.
Highlights
Periodontal disease (PD) is a chronic inflammatory disease caused by infection by oral microorganisms, leading to periodontal tissue damage and alveolar bone destruction and tooth loss
Serum levels of inducible protein 10 (IP-10) in patients with blunt trauma were positively correlated with CLP levels and were significantly higher in trauma survivors than in nonsurvivors. These results indicated that CLP might mediate IP-10 expression, which is involved in inflammation induced by injury, in monocytes/macrophages [46]
Hayashi et al observed that CLP production and expression of S100A8/S100A9 mRNAs were increased by stimulation with IL-1α and calcium through activation of C/EBPα DNA-binding complex in normal human gingival keratinocytes
Summary
Periodontal disease (PD) is a chronic inflammatory disease caused by infection by oral microorganisms, leading to periodontal tissue damage and alveolar bone destruction and tooth loss. By binging on the critical components of NADPH oxidase complex, p67phox and rac-2, CLP induces reactive oxygen species (ROS) production, which is essential for normal functioning of PMNs [33] In addition to these intracellular functions, CLP is released and acts as an alarm in different inflammatory diseases, showing proinflammatory activity in a wide range of cell types, such as lymphocytes, phagocytes, and endothelial and epithelial cells. Secreted CLP in turn triggered a TLR4-Rap1-GTPase-dependent pathway of rapid β2 integrin activation in neutrophils This extracellular activation cycle reduced rolling velocity of leukocytes and stimulated adhesion, which determined CLP as an important regulator of leukocyte recruitment cascade during inflammation [44]. These results indicated that CLP might mediate IP-10 expression, which is involved in inflammation induced by injury, in monocytes/macrophages [46]
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