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DOI

10.1016/j.jds.2018.03.001

First Page

226

Last Page

233

Abstract

Abstract Background/purpose We previously reported that injedctions of lipopolysaccharide (LPS) into the gingiva of mice induce inflammatory bone resorption that actively involved T cells. Receptor activator of NF-κB ligand (RANKL), which is an essential factor for osteoclastogenesis, was reportedly produced by osteoblasts, fibroblasts, and T cells in vitro; however, it has not been established which cells affect osteoclastogenesis in vivo. Here we determined the roles of T cells and the periosteum on osteoclastogenesis in LPS-induced inflammatory bone resorption. Materials and methods Thirty-five BALB/c (wild-type: WT) and 10 BALB/c-nu/nu (nude: Nu) mice congenitally lacking T cells were used. Using inbred WT mice, tibias were transplanted with and without the periostea [(+) and (−), respectively, n = 15 per group] into the dorsal subcutaneous connective tissue of WT or Nu mice. Each group received four injections around the transplanted site: experimental groups were injected with LPS, and control groups were injected with phosphate-buffered saline. Isolated tissues were prepared for histopathological observation of the transplanted bone surface. Results Many infiltrating inflammatory cells were present near the surface of the tibias in the LPS-injected groups. Only the WT (+) LPS group showed osteoclasts. The number of mononuclear preosteoclasts and RANKL-positive cells was highest in the WT (+) LPS group, and there were no significant differences among the other three groups. Conclusion T cells and the periosteum are closely involved in osteoclastogenesis in inflammatory bone resorption in vivo.

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