Micro-computed tomography analysis showed significant reduction of alveolar bone loss in the CCL2 MP treatment group when compared with a blank MP group and a no-treatment periodontitis group in both models.
Taken together, calprotectin induces IL-6 and MCP-1 production in HGFs via TLR4 signaling that involves MAPK and NF-κB, resulting in the progression of periodontitis..
Thus, in the present study, we tested the selective sEH inhibitor, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU), in a mouse model of periodontitis induced by infection with <i>Aggregatibacter actinomycetemcomitans</i> Oral treatment of wild-type mice with TPPU and sEH knockout (KO) animals showed reduced bone loss induced by <i>A. actinomycetemcomitans</i> This was associated with decreased expression of key osteoclastogenic molecules, receptor activator of nuclear factor-κB/RANK ligand/osteoprotegerin, and the chemokine monocyte chemotactic protein 1 in the gingival tissue without affecting bacterial counts.
Our results suggest that (1) DM may lead to enhanced MCP-1 production in periodontal tissues likewise for periodontitis and (2) there may be a positive correlation between the MCP-1 concentration and diseased nature of periodontium in both diseases.
These results suggest that T. denticola can evade host defense mechanisms by modulating production of IL-8 and MCP-1, and that this play a role in the development of chronic infections such as periodontitis.