Enhanced osteolytic potential of monocytes/macrophages derived from bone marrow after particle stimulation

Tamaki, Yasuhiro; Sasaki, Kan; Sasaki, Akira; Takakubo, Yuya; Hasegawa, Hiroshi; Ogino, Toshihiko; Konttinen, Yrjö T.; Salo, Jari; Takagi, Michiaki

doi:10.1002/jbm.b.30861

Cited by 33 publications

(42 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This probably reflects interactions between multiple types of cells. Specifically, cathepsin K is expressed in monocytes and macrophages as well as in osteoclasts [52], and in human osteoblasts [53,54]. We assayed cathepsin K mRNA and did immune labeling in human CD14-positive cells and osteoblasts and results (not shown) were in accord with these reports.…”

Section: Discussionmentioning

confidence: 58%

Estrogen inhibits RANKL-stimulated osteoclastic differentiation of human monocytes through estrogen and RANKL-regulated interaction of estrogen receptor-α with BCAR1 and Traf6

Robinson

Yaroslavskiy

Griswold

et al. 2009

Experimental Cell Research

View full text Add to dashboard Cite

The effects of estrogen on osteoclast survival and differentiation were studied using CD14-selected mononuclear osteoclast precursors from peripheral blood. Estradiol at ~1 nM reduced RANKLdependent osteoclast differentiation by 40-50%. Osteoclast differentiation was suppressed 14 days after addition of RANKL even when estradiol was withdrawn after 18 hours. In CD14+ cells apoptosis was rare and was not augmented by RANKL or by 17-β-estradiol. Estrogen receptor-α (ERα) expression was strongly down-regulated by RANKL, whether or not estradiol was present. Mature human osteoclasts thus cannot respond to estrogen via ERα. However, ERα was present in CD14+ osteoclast progenitors, and a scaffolding protein, BCAR1, which binds ERα in the presence of estrogen, was abundant. Immunoprecipitation showed rapid (~5 minute) estrogen-dependent formation of ERα-BCAR1 complexes, which were increased by RANKL co-treatment. The RANKLsignaling intermediate Traf6, which regulates NF-κB activity, precipitated with this complex. Reduction of NF-κB nuclear localization occurred within 30 minutes of RANKL stimulation, and estradiol inhibited the phosphorylation of IκB in response to RANKL. Inhibition by estradiol was abolished by siRNA knockdown of BCAR1. We conclude that estrogen directly, but only partially, curtails human osteoclast formation. This effect requires BCAR1 and involves a non-genomic interaction with ERα. KeywordsEstrogen receptor-α; Breast cancer antiestrogen resistance-1; p130Cas; Nuclear factor-κB; TNFreceptor associated factorsOsteoclasts are multinucleated bone-degrading cells that differentiate from monocytic precursors. They are critical to bone modeling and maintenance, and mediate the release of skeletal mineral for calcium and pH homeostasis. Consequently, osteoclast differentiation and activity are regulated by several systems. Because bone loss occurs when estrogen declines at the menopause, the modulation of osteoclast formation and activity by estrogen is an important issue. The mechanisms by which estrogen regulates bone turnover remain unclear [1]. *Corresponding author: Lisa J. Robinson, 707 Scaife Hall, University of Pittsburgh, Pittsburgh, PA 15261, Tel: +1 412 647-0365, Fax: +1 412 647-4008, robinsonlj@msx.upmc.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptUnresolved issues include whether estrogen causes apoptosis of osteoclasts or osteoclast precursors, and whether estrogen suppresses osteoclast formation directly or whether effects are mediated via oth...

show abstract

Section: Discussionmentioning

confidence: 58%

Estrogen inhibits RANKL-stimulated osteoclastic differentiation of human monocytes through estrogen and RANKL-regulated interaction of estrogen receptor-α with BCAR1 and Traf6

Robinson

Yaroslavskiy

Griswold

et al. 2009

Experimental Cell Research

View full text Add to dashboard Cite

show abstract

“…However, monocytes that were differentiated on HDI or MDI had a significantly lower expression of CD68 that did not increase during differentiation (Fig. Recently, adherent MDM derived from bone marrow, although able to resorb dentine disks, did not express osteoclastic markers and were CD68 positive (Tamaki et al, 2007). Monocytes typically display the differentiation marker CD14 and as these cells mature into macrophages, the expression of CD14 has been shown to decrease (Ziegler-Heitbrock and Ulevitch, 1993;Kruger et al, 1996).…”

Section: Discussionmentioning

confidence: 94%

Influence of biodegradable and non-biodegradable material surfaces on the differentiation of human monocyte-derived macrophages

2008

View full text Add to dashboard Cite

“…A wealth of preclinical and clinical data showed that wear particle‐activated macrophages play an essential role in the pathogenesis of bone loss by producing multiple pro‐inflammatory cytokines and chemokines . Furthermore, macrophages may resorb bone directly by themselves or differentiate into osteoclasts . It was observed that significantly more macrophages infiltrated into the peri‐implant soft tissue with obvious crestal bone loss in the Ti + PBS group compared with Control group, whereas macrophage depletion by clodronate liposome treatment significantly attenuated the severity of Ti particles‐induced inflammation and bone resorption.…”

Section: Discussionmentioning

confidence: 99%

Macrophage polarization in aseptic bone resorption around dental implants induced by Ti particles in a murine model

Wang

Liu

Feng

et al. 2019

J of Periodontal Research

View full text Add to dashboard Cite

Background and Objectives Titanium particles/ions detected in peri‐implant tissues have been considered as a potential etiologic factor for crestal bone loss around oral implants. However, the definite impact of titanium wear particles on the health of surrounding structures remains undetermined. The purpose of this study was to investigate the effects of titanium particles‐induced foreign body reaction on peri‐implant bone level and the related mechanism by using clodronate liposomes to deplete macrophages. Material and Methods Sprague Dawley rats with custom‐made titanium screw implanted in bilateral maxillary first molar area for 4 weeks to obtain osseointegration were randomly divided into four groups. Twenty microgram titanium particles were introduced into the peri‐implant tissue to induce aseptic foreign body reaction, and macrophages were depleted by the local injection of 100 μL clodronate liposome immediately and re‐injection every 3 days until the sacrifice of the rats (Ti + LipClod group). Titanium‐injected rats also treated with phosphate buffer solution (Ti + PBS) or empty liposome (Ti + Lip) as well as rats injected with PBS alone (Control) were included as controls. Eight weeks later, animals were sacrificed and samples containing implants were collected. Half of the samples were analyzed radiologically to measure bone level change, and macrophage markers (CD68, CCR7, CD163) was also characterized by immunofluorescence to evaluate macrophage number, density, and phenotype distribution (CCR7+M1/CD163+M2). The rest of the samples were used to determine the relative mRNA expression levels of TNF‐α, IL‐1β, IL‐6, and RANKL with real‐time PCR analysis. Results No obvious bacterial contamination was found in all titanium‐injected areas, and the implant survival rate was 100% with no implant loss. Compared with Ti + PBS and Ti + Lip group, macrophage density (1.64 ± 0.86%) infiltrated into peri‐implant tissue and bone loss (0.17 ± 0.03 mm) around implant decreased significantly in the Ti + LipClod group. Immunofluorescence analysis showed that more macrophage infiltrated into peri‐implant tissue in the Ti + PBS and Ti + Lip groups, predominantly with M1 phenotype. In contrast, the macrophage density was lower and M2 phenotype was dominant in the Control group, while macrophages density was significantly reduced and the M1 type macrophages were slightly more than M2 type in the Ti + LipClod group. Accordingly, TNF‐α, IL‐1β, IL6, and RANKL mRNA expression increased significantly in the Ti + PBS and Ti + Lip groups compared with Control and Ti + LipClod groups. Conclusions Titanium particles had a negative effect on peri‐implant tissue by activating macrophages which induced an M1 macrophage phenotype promoting local secretion of inflammatory cytokines. It was found that clodronate liposome treatment attenuated the severity of inflammation and bone loss by depletion of macrophages. Therefore, the present study revealed the marked impact of macrophage polarization with respect to peri‐implant bone loss caused...

show abstract

Enhanced osteolytic potential of monocytes/macrophages derived from bone marrow after particle stimulation

Cited by 33 publications

References 67 publications

Estrogen inhibits RANKL-stimulated osteoclastic differentiation of human monocytes through estrogen and RANKL-regulated interaction of estrogen receptor-α with BCAR1 and Traf6

Estrogen inhibits RANKL-stimulated osteoclastic differentiation of human monocytes through estrogen and RANKL-regulated interaction of estrogen receptor-α with BCAR1 and Traf6

Influence of biodegradable and non-biodegradable material surfaces on the differentiation of human monocyte-derived macrophages

Macrophage polarization in aseptic bone resorption around dental implants induced by Ti particles in a murine model

Contact Info

Product

Resources

About