Abstract
Introduction The essential role of RANKL/RANK/OPG axis in osteoclast differentiation/activation in inflammatory bone diseases, including periodontal disease is widely acknowledged [1]. In the inflamed periodontal microenvironment, various cell types are capable of expressing RANKL, including periodontal ligament fibroblasts, leading to tissue destruction through activation of RANK on pre-osteoclasts [2]. In fact,
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