A basic research on coupling factors between bone resorption and bone formation

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The involvement of RANKL and OPG in lipopolysaccharide-induced bone resorption is not well understood. So in the first study, we examined changes in the number of RANKL- and OPG-expressing cells when bone resorption was increased by repeated injections of LPS and decreased by additional injection of PBS. The number of RANKL-expressing inflammatory cells increased and OPG-expressing non-inflammatory cells decreased with enhancement of bone resorption. On the other hand, the number of OPG-expressing inflammatory cells increased with decrease of bone resorption. Of the inflammatory cells assay, RANKL-expressing T cells were detected in the lesions of mice with increased bone resorption and OPG-expressing polymorphonuclear leukocytes (PMN) were detected in the lesions of mice with decreased bone resorption. These results suggested that T cells and PMNs play important roles in the regulation of inflammatory bone resorption.The aim of the second study was to examine whether B cells truly influence inflammatory bone resorption in vivo. Alveolar bone resorption in normal mice, in SCID mice that lack both B and T cells, and in B cell-reconstituted SCID mice were compared histopathologically after repeated injections of lipopolysaccharide into mouse gingival. Furthermore, we examined whether the B cells that are stimulated by lipopolysaccharide are involved in osteoclastogenesis in vitro. As a result, the B cell-reconstituted SCID mice group showed stronger inflammatory bone resorption than the SCID mice group. Also, in vitro, lipopolysaccharide-stimulated B cells enhanced osteoclastogenesis and anti-TNF-α antibody completely blocked osteoclastogenesis induced by lipopolysaccharide-stimulated B cells. These results suggest that B cells promote inflammatory bone resorption through TNF-α.