We have recently demonstrated that treatment of gingival fibroblasts with the pan-HDACi suberoylanilide hydroxamic acid (SAHA) and ITF2357 (givinostat) can suppress P. gingivalis-induced expression of a broad range of inflammatory mediators involved in periodontitis pathogenesis, including chemokines (CCL2, CCL5, and CXCL10), matrix metalloproteinases (MMP1, MMP3), and components of the prostaglandin E2 synthesis pathway (PTGS2) [53]. Here, CCL2 is linked to periodontitis.