Localization of receptor activator of NFkappaB ligand, RANKL, in periodontal tissues during experimental movement of rat molars

Abstract

The receptor activator of NFkappaB ligand, RANKL, is one of the key regulatory molecules in osteoclast formation and function. We examined RANKL localization in the periodontal tissues during experimental movement of rat molars. To produce orthodontic force, an elastic band was inserted between the upper first and second molars for 4 days, and the dissected maxillae were subjected to light and electron microscopic immunocytochemical examination for RANKL. Expression of RANKL protein was detected in osteoblasts, osteocytes, fibroblasts, and osteoclasts mostly located in resorption lacunae. In osteoblasts, osteocytes, and fibroblasts, RANKL localization was mainly observed in the cytoplasm, the cisternae of rough endoplasmic reticulum and along plasma membranes. In osteoclasts, RANKL was expressed along the ruffled, border membranes and in the cytoplasm, including the clear zone. These results suggest that during tooth movement, osteoclast differentiation and activation are regulated, at least in part, by RANKL, possibly produced by osteoblasts/stromal cells and osteoclasts themselves in the periodontal tissues.

Osteoclast induction in periodontal tissue during experimental movement of incisors in osteoprotegerin‐deficient mice

“…We previously localized RANKL expression in PDL fibroblasts and osteoblasts on the compressed side of the PDL (Shiotani et al, 2001). Because cell-to-cell interaction between osteoblasts/stromal cells and osteoclast precursors is essential for osteoclast formation Matsuzaki et al, 1998;Tsukii et al, 1998), our observation suggests that these osteoblasts/stromal cells and fibroblasts in PDL are involved in supporting osteoclast differentiation during tooth movement.…”

“…We recently localized RANKL expression in PDL tissue during orthodontic tooth movement (Shiotani et al, 2001). However, the involvement of RANKL and OPG in PDL tissue during orthodontic tooth movement has not yet been examined.…”

Local delivery of osteoprotegerin inhibits mechanically mediated bone modeling in orthodontic tooth movement

“…Indeed, it has been shown that application of orthodontic forces results in the expression of RANKL protein in osteoblasts, osteocytes, fibroblasts, and osteoclasts [42]. In our studies, we utilized the knowledge of the basic biologic mechanisms of osteoclastogenesis and the important role played by the OPG-RANKL axis in osteoclast function to test the hypothesis that OPG participates in mechano-modulation of osteolysis to diminish orthodontic tooth movement and could therefore serve as a biologic mediator for enhancing orthodontic anchorage.…”

Prevention of root resorption in hypofunctional teeth by occlusal function recovery

“…A recent immunocytochemical study reported that RANKL/RANK and M-CSF/c-fms were also observed in osteoblasts, osteocytes, fibroblasts, osteoclasts, and odontoclasts during the application of orthodontic forces. 16,17 Furthermore, recent studies have recognized the role of inflammatory cytokines such as IL-8 in transmitting signals for osteoclastogenesis. 18 It is reported that RANKL/RANK, M-CSF/c-fms, and IL-8 are expressed in root resorption lacunae around rat molar by heavy orthodontic force.…”