Improved RANKL expression and osteoclastogenesis induction of CD27+CD38− memory B cells: A link between B cells and alveolar bone damage in periodontitis

Background and Objective Periodontitis is a bacteria‐induced disease that often leads to alveolar bone damage. Its mechanisms were considered to be complicated, involving an imbalance of the formation and resorption of bone. We sought to disclose the antibody‐independent function of B cells during periodontitis. Material and Methods Production of receptor activator for nuclear factor‐κB ligand (RANKL) by total lymphocytes or sorted B‐cell subsets in gingiva from healthy or experimental periodontitis animals was examined by flow cytometry, real‐time polymerase chain reaction, and enzyme‐linked immunosorbent assay. To define the effects of lymphocytes or B‐cell subsets on osteoclastogenesis induction, bone marrow mononuclear cells were culture in culture medium of lymphocytes or cocultured with B‐cell subsets. Osteoclasts were enumerated by tartrate‐resistant acid phosphatase staining. Constituent ratio of B‐cell subsets in healthy or experimental periodontitis was also detected by flow cytometry. Result Gingiva B cells produce more RANKL and support more osteoclastogenesis than T and other lymphocytes, and this potential improved in periodontitis. Memory B cells (CD27+CD38−) decreased their percentage in periodontitis. Memory B cells have the highest propensity for RANKL production. Remarkably, memory B cells from periodontitis animals expressed significantly more RANKL compared to healthy controls. Memory B cells supported osteoclast differentiation in vitro in a RANKL‐dependent manner, and the number of osteoclasts was higher in cultures with memory B cells from periodontitis animals than in those derived from healthy ones. Other B‐cell subsets have limited impact on osteoclast formation. Conclusion Findings of this study further disclose the roles of B cells engaged in periodontal immunomodulation and reveal the considerable importance of memory B cells in alveolar bone homeostasis and their likely contribution to alveolar bone destruction in periodontitis.