Bone stromal cells in pagetic bone and Paget's sarcoma express RANKL and support human osteoclast formation

2006 ◽  
Vol 209 (1) ◽  
pp. 114-120 ◽  
Author(s):  
SG Sun ◽  
YS Lau ◽  
I Itonaga ◽  
A Sabokbar ◽  
NA Athanasou
Keyword(s):  
Stromal Cells ◽  
Osteoclast Formation ◽  
Pagetic Bone ◽  
Human Osteoclast ◽  
Paget's Sarcoma ◽  
Paget’S Sarcoma

CALCITONIN THERAPY IN PAGET'S SARCOMA

1979 ◽  
Vol 1 (3) ◽  
pp. 99-100 ◽  
Author(s):  
Paul C. Bartley ◽  
A. Chotai ◽  
G. Ward ◽  
H. M. Lloyd
Keyword(s):  
Paget's Sarcoma ◽  
Paget’S Sarcoma

scholarly journals Immunological Reaction in TNF-α-Mediated Osteoclast Formation and Bone ResorptionIn VitroandIn Vivo

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Hideki Kitaura ◽  
Keisuke Kimura ◽  
Masahiko Ishida ◽  
Haruka Kohara ◽  
Masako Yoshimatsu ◽  
...  
Keyword(s):  
T Cells ◽  
Bone Metabolism ◽  
Stromal Cells ◽  
Fas Ligand ◽  
Bone Marrow Cells ◽  
Bone Destruction ◽  
Osteoclast Formation ◽  
Bone Diseases

Tumor necrosis factor-α(TNF-α) is a cytokine produced by monocytes, macrophages, and T cells and is induced by pathogens, endotoxins, or related substances. TNF-αmay play a key role in bone metabolism and is important in inflammatory bone diseases such as rheumatoid arthritis. Cells directly involved in osteoclastogenesis include macrophages, which are osteoclast precursor cells, osteoblasts, or stromal cells. These cells express receptor activator of NF-κB ligand (RANKL) to induce osteoclastogenesis, and T cells, which secrete RANKL, promote osteoclastogenesis during inflammation. Elucidating the detailed effects of TNF-αon bone metabolism may enable the identification of therapeutic targets that can efficiently suppress bone destruction in inflammatory bone diseases. TNF-αis considered to act by directly increasing RANK expression in macrophages and by increasing RANKL in stromal cells. Inflammatory cytokines such as interleukin- (IL-) 12, IL-18, and interferon-γ(IFN-γ) strongly inhibit osteoclast formation. IL-12, IL-18, and IFN-γinduce apoptosis in bone marrow cells treated with TNF-α  in vitro, and osteoclastogenesis is inhibited by the interactions of TNF-α-induced Fas and Fas ligand induced by IL-12, IL-18, and IFN-γ. This review describes and discusses the role of cells concerned with osteoclast formation and immunological reactions in TNF-α-mediated osteoclastogenesisin vitroandin vivo.

PAGET'S SARCOMA OF BONE

1969 ◽  
Vol 51-B (2) ◽  
pp. 205-224 ◽  
Author(s):  
C. H. G. Price ◽  
W. Goldie
Keyword(s):  
Paget's Sarcoma ◽  
Paget’S Sarcoma

scholarly journals Peri-Implant Crestal Bone Loss: A Putative Mechanism

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Yuko Ujiie ◽  
Reynaldo Todescan ◽  
John E. Davies
Keyword(s):  
Bone Loss ◽  
Stromal Cells ◽  
Cell Types ◽  
Osteoclast Formation ◽  
Rt Pcr ◽  
Crestal Bone Loss ◽  
Bacterial Endotoxins ◽  
Immunological Mechanisms ◽  
Study Support ◽  
Putative Mechanism

Purpose. The immunological mechanisms of peri-implant crestal bone loss have, hitherto, not been elucidated. We hypothesized that bacterial products from the microgap cause upregulation of cytokines in otherwise healthy peri-implant cells, which results in osteoclast formation and, ultimately, in bone resorption.Materials and Methods. We used RT-PCR and ELISA to assay mediators of osteoclastogenesis in rat and human macrophages (r-and hMO); bone marrow derived stromal cells (r-and hBMCs); and human gingival fibroblasts (hGF)—with or without stimulation by LPS. TRAP positive multinucleate cells were assessed for their resorptive ability.Results. We show that IL-1α, IL-1β, and IL-6 were expressed by all examined cell types, and TNF-αwas upregulated in hGF. Secretion of IL-1αand IL-1βproteins was stimulated in hMO by LPS, and IL-6 protein secretion was highly stimulated in hBMCs and hGF. Both LPS and RANKL stimulated macrophages to form osteoclast-like TRAP positive cells, which resorbed calcium phosphate substrates.Conclusion. Taken together, the results of our study support the hypothesis that bacterial endotoxins upregulate enhanced mediators of osteoclastogenesis in resident cells found in the healthy peri-implant compartment and that the local synergistic action of cytokines secreted by such cells results in the genesis of resorptively active osteoclasts.

MIP-1α utilizes both CCR1 and CCR5 to induce osteoclast formation and increase adhesion of myeloma cells to marrow stromal cells

2005 ◽  
Vol 33 (3) ◽  
pp. 272-278 ◽  
Author(s):  
Yasuo Oba ◽  
Jun Won Lee ◽  
Lori A. Ehrlich ◽  
Ho Yeon Chung ◽  
Diane F. Jelinek ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Osteoclast Formation ◽  
Marrow Stromal Cells ◽  
Myeloma Cells
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