Inhibition of CCL2 by bindarit alleviates diabetes-associated periodontitis by suppressing inflammatory monocyte infiltration and altering macrophage properties

Cell Mol Immunol. 2021 Sep;18(9):2224-2235. doi: 10.1038/s41423-020-0500-1. Epub 2020 Jul 16.


Diabetes-associated periodontitis (DP) aggravates diabetic complications and increases mortality from diabetes. DP is caused by diabetes-enhanced host immune-inflammatory responses to bacterial insult. In this study, we found that persistently elevated CCL2 levels in combination with proinflammatory monocyte infiltration of periodontal tissues were closely related to DP. Moreover, inhibition of CCL2 by oral administration of bindarit reduced alveolar bone loss and increased periodontal epithelial thickness by suppressing periodontal inflammation. Furthermore, bindarit suppressed the infiltration of proinflammatory monocytes and altered the inflammatory properties of macrophages in the diabetic periodontium. This finding provides a basis for the development of an effective therapeutic approach for treating DP.

Keywords: Diabetes-associated periodontitis; bindarit; macrophages; proinflammatory monocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chemokine CCL2 / antagonists & inhibitors*
  • Diabetes Mellitus*
  • Humans
  • Indazoles / pharmacology
  • Macrophages
  • Monocytes
  • Periodontitis* / complications
  • Periodontitis* / drug therapy
  • Propionates / pharmacology


  • CCL2 protein, human
  • Chemokine CCL2
  • Indazoles
  • Propionates
  • bindarit