During an inflammatory status such as rheumatoid arthritis and periodontitis, the memory B cells (e.g., CD27+CD38− memory B cells) tend to improve RANKL expression and osteoclastogenesis and support osteoclast differentiation in vitro in a RANKL-dependent manner (51–54), which probably supported the findings from our mediation analyses that the potential associations of several memory B cells expressing CD25 or CD27 with BMD can be mediated by CD40 on monocytes. This evidence concerns the gene TNFSF11 and rheumatoid arthritis.