scholarly journals Fibroblasts from the inner granulation tissue of the pseudocapsule in hips at revision arthroplasty induce osteoclast differentiation, as do stromal cells

2002 ◽  
Vol 61 (2) ◽  
pp. 103-109 ◽  
Author(s):  
H Sakai
Bone ◽  
1995 ◽  
Vol 17 (6) ◽  
pp. 578 ◽  
Author(s):  
R.A. Dodd ◽  
I.E. James ◽  
D.L. Olivera ◽  
E. Lee-Rykaczewski ◽  
A. Gohlke ◽  
...  

2012 ◽  
Vol 92 (4) ◽  
pp. 600-605 ◽  
Author(s):  
Richard MI Taylor ◽  
Takeshi G Kashima ◽  
Francesca K E Hemingway ◽  
Arundhati Dongre ◽  
Helen J Knowles ◽  
...  

2005 ◽  
Vol 129 (3) ◽  
pp. 360-365
Author(s):  
Rolando Y. Ramos ◽  
Helen M. Haupt ◽  
Peter A. Kanetsky ◽  
Rakesh Donthineni-Rao ◽  
Carmen Arenas-Elliott ◽  
...  

Abstract Context.—Osteoclast-like giant cells (GCs) in giant cell tumors (GCTs) are thought to derive from a monocyte-macrophage lineage. Microphthalmia transcription factor (MITF) is necessary for osteoclast gene expression and tartrate-resistant acid phosphatase (TRAP) activation; c-Kit plays a role in regulation of MITF. Objective.—To gain insight into the differentiation of GCTs of bone (GCTBs) and GCTs tendon sheath (GCTTSs) by investigating immunohistochemical staining for c-Kit, MITF, TRAP, and HAM-56 in the GCs and stroma. Design.—Immunoreactivity for CD117 (c-Kit), MITF, TRAP, and HAM-56 was studied in 35 GCTBs, 15 GCTTSs, and 5 foreign-body GC controls. Results.—Across tumors, MITF and TRAP but not c-Kit were generally expressed in GCs; TRAP was variably expressed in stromal cells. The MITF was expressed more consistently in stromal cells of GCTTSs than GCTBs (P < .001). The GCTBs showed more intense MITF stromal (P < .001) and TRAP GC staining (P = .04) than GCTTSs. HAM-56 staining by stromal cells was associated with MITF stromal staining (r2 = 0.6, P < .001). Conclusions.—Results suggest that MITF and TRAP are expressed during osteoclast differentiation and that a proportion of mononuclear cells in GCTs express the macrophage marker HAM-56. Both GCTBs and GCTTSs show similar patterns of immunohistochemical expression.


Bone Reports ◽  
2020 ◽  
Vol 13 ◽  
pp. 100421
Author(s):  
Valérie Trichet ◽  
Louis-Romée Le Nail ◽  
Régis Brion ◽  
Françoise Rédini ◽  
François Vallette ◽  
...  

Blood ◽  
2002 ◽  
Vol 100 (6) ◽  
pp. 2195-2202 ◽  
Author(s):  
Masahiro Abe ◽  
Kenji Hiura ◽  
Javier Wilde ◽  
Keiji Moriyama ◽  
Toshihiro Hashimoto ◽  
...  

Abstract Multiple myeloma (MM) cells cause devastating bone destruction by activating osteoclasts in the bone marrow milieu. However, the mechanism of enhanced bone resorption in patients with myeloma is poorly understood. In the present study, we investigated a role of C-C chemokines, macrophage inflammatory protein (MIP)–1α and MIP-1β, in MM cell-induced osteolysis. These chemokines were produced and secreted by a majority of MM cell lines as well as primary MM cells from patients. Secretion of MIP-1α and MIP-1β correlated well with the ability of myeloma cells to enhance osteoclastic bone resorption both in vitro and in vivo as well as in MM patients. In osteoclastogenic cultures of rabbit bone cells, cocultures with myeloma cells as well as addition of myeloma cell-conditioned media enhanced both formation of osteoclastlike cells and resorption pits to an extent comparable to the effect of recombinant MIP-1α and MIP-1β. Importantly, these effects were mostly reversed by neutralizing antibodies against MIP-1α and MIP-1β, or their cognate receptor, CCR5, suggesting critical roles of these chemokines. We also demonstrated that stromal cells express CCR5 and that recombinant MIP-1α and MIP-1β induce expression of receptor activator of nuclear factor-κB (RANK) ligand by stromal cells, thereby stimulating osteoclast differentiation of preosteoclastic cells. These results suggest that MIP-1α and MIP-1β may be major osteoclast-activating factors produced by MM cells.


1998 ◽  
Vol 141 (6) ◽  
pp. 1467-1476 ◽  
Author(s):  
Gabriel Mbalaviele ◽  
Riko Nishimura ◽  
Akira Myoi ◽  
Maria Niewolna ◽  
Sakamuri V. Reddy ◽  
...  

Osteoclasts are multinucleated cells of hemopoietic origin that are responsible for bone resorption during physiological bone remodeling and in a variety of bone diseases. Osteoclast development requires direct heterotypic cell–cell interactions of the hemopoietic osteoclast precursors with the neighboring osteoblast/stromal cells. However, the molecular mechanisms underlying these heterotypic interactions are poorly understood. We isolated cadherin-6 isoform, denoted cadherin-6/2 from a cDNA library of human osteoclast-like cells. The isolated cadherin-6/2 is 3,423 bp in size consisting of an open reading frame of 2,115 bp, which encodes 705 amino acids. This isoform lacks 85 amino acids between positions 333 and 418 and contains 9 different amino acids in the extracellular domain compared with the previously described cadherin-6. The human osteoclast-like cells also expressed another isoform denoted cadherin-6/1 together with the cadherin-6. Introduction of cadherin-6/2 into L-cells that showed no cell–cell contact caused evident morphological changes accompanied with tight cell–cell association, indicating the cadherin-6/2 we isolated here is functional. Moreover, expression of dominant-negative or antisense cadherin-6/2 construct in bone marrow–derived mouse stromal ST2 cells, which express only cadherin-6/2, markedly impaired their ability to support osteoclast formation in a mouse coculture model of osteoclastogenesis. Our results suggest that cadherin-6 may be a contributory molecule to the heterotypic interactions between the hemopoietic osteoclast cell lineage and osteoblast/bone marrow stromal cells required for the osteoclast differentiation. Since both osteoclasts and osteoblasts/bone marrow stromal cells are the primary cells controlling physiological bone remodeling, expression of cadherin-6 isoforms in these two cell types of different origin suggests a critical role of these molecules in the relationship of osteoclast precursors and cells of osteoblastic lineage within the bone microenvironment.


2017 ◽  
Vol 5 (1) ◽  
pp. 14-22 ◽  
Author(s):  
O. Tykhvynskaya ◽  
O. Rogulska ◽  
N. Volkova ◽  
E. Revenko ◽  
S. Mazur ◽  
...  

Prospects for the widespread use of multipotent mesenchymal stromal cells (MSCs) in regenerative medicine determine the relevance of studying their abilities to affect the reparative process in experimental systems in vivo.Materials and methods. The effect of human adipose-derived MSCs on the healing rate and completeness of damaged skin site reconstitution was examined using full-thickness excision wound model in mice. The reparative activity of MSCs was revealed in planimetric and histological studies. Human blood plasma-derived fibrin gel was used as a scaffold for MSCs delivery.Results and conclusions. Compared to the spontaneous healing process, application of fibrin gel on the excisional skin wounds promotes earlier maturation of granulation tissue and further formation of loose scar tissue with skin derivates. MSCs in the fibrin gel contribute to the improve of wound epithelialization, the decrease of the inflammatory response, faster maturation of the granulation tissue, including marks of angiogenesis, as well as promotes complete recovery of the dermal and epidermal layers of the damaged site of skin.


2000 ◽  
Vol 15 (8) ◽  
pp. 1459-1466 ◽  
Author(s):  
Julian M. W. Quinn ◽  
Nicole J. Horwood ◽  
Jan Elliott ◽  
Matthew T. Gillespie ◽  
T. John Martin

Endocrinology ◽  
1997 ◽  
Vol 138 (11) ◽  
pp. 4852-4857 ◽  
Author(s):  
Diane M. Biskobing ◽  
Dongjie Fan ◽  
Xian Fan ◽  
Janet Rubin

Abstract Carbonic anhydrase II (CA II) expression is vital to normal osteoclast function. We and others have previously reported induction of CA II messenger RNA (mRNA) expression by 1,25(OH)2D3 in myelomonocytic cells and marrow culture. However, since 1,25(OH)2D3 stimulates osteoclast differentiation as well, we wished to separate direct effects of 1,25(OH)2D3 on the CA II gene from the differentiating effects of the hormone. Using primary murine mixed marrow cultures, we measured CA II mRNA expression by RT-PCR. 10 nm 1,25(OH)2D3 dose dependently induced expression of CA II mRNA (4.12 ± 0.68-fold) at day 4 in culture compared with control with an ED50 of 0.25 nm. When nonadherent marrow cells containing osteoclast progenitors were depleted of stromal cells and exposed to 10 nm 1,25(OH)2D3, CA II mRNA expression was decreased by more than 60%. Coculture of progenitors with ST-2 stromal cells for 3 days with 10 nm 1,25(OH)2D3 stimulated CA II expression by 22 ± 3.6-fold. 1,25(OH)2D3 stimulated CA II mRNA expression in progenitors separated from ST-2 cells by transwells was insignificant demonstrating that the two cell types must be in physical contact. PTH also stimulated CA II mRNA expression (4.91 ± 0.01-fold) to a similar degree as seen with 1,25(OH)2D3 treatment. These results demonstrate that induction of CA II in osteoclast progenitors requires their physical communication with stromal cells and is inseparable from the osteoclast differentiation process.


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