Osteoclast Differentiation Factor (ODF) Induces Osteoclast-like Cell Formation in Human Peripheral Blood Mononuclear Cell Cultures

Matsuzaki, Kei; Udagawa, Nobuyuki; Takahashi, Naoyuki; Yamaguchi, Kyoji; Yasuda, Hisataka; Shima, Nobuyuki; Morinaga, Tsutomu; Toyama, Yoshiaki; Yabe, Yutaka; Higashio, Kanji; Suda, Toshio

doi:10.1006/bbrc.1998.8586

Cited by 324 publications

(222 citation statements)

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“…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. Therefore, bone remodeling during orthodontic tooth movement is thought to be regulated by OPG, RANK, and RANKL to maintain well-balanced alveolar bone structure and bone mass.…”

Section: Discussionmentioning

confidence: 75%

“…OPG appears to locally and/or systemically inhibit the differentiation of osteoclast precursors into mature osteoclasts, by interrupting the osteoblast-osteoclast precursor interaction (Simonet et al, 1997;Akatsu et al, 1998;Yasuda et al, 1998a, b). OPG also inhibits in vitro osteoclastogenesis elicited through distinct signaling pathways stimulated by 1,25(OH)2D3, PTH, or IL-11 (Simonet et al, 1997;Tsuda et al, 1997;Matsuzaki et al, 1998;Yasuda et al, 1998a). Therefore, OPG inhibits ovariectomy-induced bone loss in rats (Bateman et al, 2000).…”

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confidence: 97%

“…Another osteoblast-derived factor, the receptor activator of the NFkB ligand (RANKL), has been identified as a member of the membrane-associated TNF ligand family and an important regulatory molecule of osteoclastogenesis Yasuda et al, 1998b;Matsuzaki et al, 1998;Tsukii et al, 1998;Fuller et al, 1998;Jimi et al, 1999;Takami et al, 1999;Udagawa et al, 1999). RANKL was found to induce osteoclast differentiation from hemopoietic precursors and stimulate their bone resorptive activity Matsuzaki et al, 1998;Yasuda et al, 1998b;Tsukii et al, 1998;Fuller et al, 1998;Takami et al, 1999;Udagawa et al, 1999).…”

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confidence: 99%

“…RANKL was found to induce osteoclast differentiation from hemopoietic precursors and stimulate their bone resorptive activity Matsuzaki et al, 1998;Yasuda et al, 1998b;Tsukii et al, 1998;Fuller et al, 1998;Takami et al, 1999;Udagawa et al, 1999). RANKL is a ligand of OPG and is expressed on the plasma membrane of osteoblasts/stromal cells Tsukii et al, 1998;Yasuda et al, 1998a, b).…”

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confidence: 99%

“…RANKL is a ligand of OPG and is expressed on the plasma membrane of osteoblasts/stromal cells Tsukii et al, 1998;Yasuda et al, 1998a, b). OPG is a soluble decoy receptor for RANKL, and its inhibition of osteoclast differentiation is due to direct binding to a ligand for OPG expressed on osteoblasts/stromal cells (Matsuzaki et al, 1998;Yasuda et al, 1998a, b;Udagawa et al, 1999Udagawa et al, , 2000. The resorptive activity of osteoclasts induced by soluble RANKL or osteoblasts is completely inhibited by the simultaneous addition of soluble OPG .…”

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confidence: 99%

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

et al. 2002

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Osteoprotegerin (OPG) is a novel secreted member of the tumor necrosis factor (TNF) receptor superfamily that negatively regulates osteoclastogenesis. The receptor activator of the NFKB ligand (RANKL) is one of the key regulatory molecules in osteoclast formation and binds to OPG. In this study, it was suggested that OPG and RANKL are involved in alveolar bone remodeling during orthodontic tooth movement. We examined RANKL localization and osteoclast induction in periodontal tissues during experimental movement of incisors in OPG-deficient mice. To produce orthodontic force, an elastic band was inserted between the upper right and left incisors for 2 or 5 days, and the dissected maxillae were examined for cytochemical and immunocytochemical localization of tartrate-resistant acid phosphatase (TRAP), vacuolar-type H ϩ -ATPase, and RANKL. Compared to wild-type OPG (ϩ/ϩ) littermates, TRAP-positive multinucleated cells were markedly induced in the periodontal ligament (PDL) on the compressed side and in the adjacent alveolar bone of OPG-deficient mice. These multinucleated cells exhibited intense vacuolar-type H ϩ -ATPase along the ruffled border membranes. Because of accelerated osteoclastic resorption in OPG-deficient mice, alveolar bone was severely destroyed and partially perforated at 2 and 5 days after force application. In both wild-type and OPG-deficient mice, RANKL expression became stronger at 2 and 5 days after force application than before force application. There was no apparent difference in intensity of RANKL expression between OPG (ϩ/ϩ) littermates and OPGdeficient mice. In both wild-type and OPG-deficient mice, expression of RANKL protein was detected in osteoblasts, fibroblasts, and osteoclasts mostly located in resorption lacunae. These results suggest that during orthodontic tooth movement, RANKL and OPG in the periodontal tissues are important determinants regulating balanced alveolar bone resorption. Anat Rec 266:218 -225, 2002.

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Section: Discussionmentioning

confidence: 75%

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confidence: 97%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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

et al. 2002

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Multiple myeloma cells and cells of the human osteoclast lineage share morphological and cell surface markers

et al. 1998

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This study demonstrates that the multiple myeloma cell (MMC) in its plasma cell form is morphologically indistinguishable from human osteoclast-like cells that form in culture when peripheral blood mononuclear cells (PBMCs) are plated at high density in serum containing medium. MM has been described as a disease of B-cell lineage, monoclonal immunoglobulin (Ig) producing cells with unique properties: MM precursor cells lodge in bone, where they proliferate and differentiate into plasma cell tumors. Then, by some mechanism, presumably involving cytokines, these cells mediate an increase in neighboring osteoclast numbers and activity, leading to excessive bone erosion and hypercalcemia. Three days after plating PBMCs, tartrate resistant acid phosphatase- (TRAP-) blasts as well as TRAP+ cells, each with an eccentric nucleus, appear in culture. By day 10, TRAP+, vitronectin+ (VR+) cells, appear to be morphologically indistinguishable from multiple myeloma plasma cells (MMPCs) on cytocentrifuge preparations. These cells are CD19- and CD38++, as are MMCs reported by others. Other surface markers are also shared. Furthermore, Ig mRNA is demonstrated in the cytoplasm of cells at 8 days by in situ hybridization with the IgG FcA3 sequence. This novel finding is not unusual, in light of reports, demonstrating non-B-lineage Ig-producing cells. Thus, this study raises some serious questions about the true nature of MMCs.

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Osteoprotegerin and osteoprotegerin ligand effects on osteoclast formation from human peripheral blood mononuclear cell precursors

et al. 1999

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Osteoprotegerin (OPG) and its ligand (OPGL) negatively and positively regulate osteoclastogenesis in the mouse. OPG inhibits osteoclastogenesis by sequestering its ligand, OPGL, the osteoclast differentiation and activation factor. This study demonstrates the effects of soluble muOPGL and huOPG on the developing human osteoclast phenotype, on bone slices, using peripheral blood mononuclear cells (PBMCs), cultured for 2 weeks, without stromal cells. OPGL (2-50 ng/ml), in combination with CSF-1, hydrocortisone (HC), and 1,25(OH)2D3, increases the size of osteoclast-like cells on bone, as defined by the acquisition of osteoclast markers: vitronectin receptor (VR), tartrate-resistant acid phosphatase (TRAP), multinuclearity, and bone resorption. By 14 days, with 20 ng/ml OPGL, the largest cells/10x field have achieved an average diameter of 163+/-38 microm, but only approximately 10-20 microm in its absence and the number of osteoclast-like cells/mm2 bone surface is about 128. By scanning electron microscopy, OPGL-treated (20-ng/ml) cultures contain small osteoclast-like cells on bone with ruffled "apical" surfaces by day 7; by day 15, large osteoclast-like cells are spread over resorption lacunae. At 15 ng/ml OPGL, about 37% of the bone slice area is covered by resorption lacunae. OPG (5-250 ng/ml) antagonizes the effects of OPGL on the morphology of the osteoclast-like cells that form, as well as bone erosion. For cells grown on plastic, Cathepsin K mRNA levels, which are barely detectable at plating, are elevated 7-fold, by 5 days, in the presence, not the absence, of OPGL (20 ng/ml) + CSF-1 (25 ng/ml). Similar findings are observed in experiments performed in the absence of HC and 1,25(OH)2D3, indicating that HC and 1,25(OH)2D3 are not needed for OPGL-induced osteoclast differentiation. In conclusion, this study confirms a pivotal role for OPGL and OPG in the modulation of human osteoclast differentiation and function, suggesting a use for OPG for treating osteoclast-mediated bone disease in humans.

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Osteoclast Differentiation Factor (ODF) Induces Osteoclast-like Cell Formation in Human Peripheral Blood Mononuclear Cell Cultures

Cited by 324 publications

References 21 publications

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

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

Multiple myeloma cells and cells of the human osteoclast lineage share morphological and cell surface markers

Osteoprotegerin and osteoprotegerin ligand effects on osteoclast formation from human peripheral blood mononuclear cell precursors

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