Abstract

Background/purposeWe 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 methodsThirty-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. ResultsMany 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. ConclusionT cells and the periosteum are closely involved in osteoclastogenesis in inflammatory bone resorption in vivo.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call