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Article ; Online: TGFβ priming promotes TNF-induced bone erosion: a promising new target in RA?

Yao, Zhenqiang / Boyce, Brendan F

2022 Volume 18, Issue 11, Page(s) 617–618

MeSH term(s)	Humans ; Transforming Growth Factor beta ; Arthritis, Rheumatoid/drug therapy ; Osteoclasts
Chemical Substances	Transforming Growth Factor beta
Language	English
Publishing date	2022-09-16
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2491532-4
ISSN	1759-4804 ; 1759-4790
ISSN (online)	1759-4804
ISSN	1759-4790
DOI	10.1038/s41584-022-00843-y
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Article ; Online: Nuclear Factor-Kappa B Regulation of Osteoclastogenesis and Osteoblastogenesis.

Boyce, Brendan F / Li, Jinbo / Yao, Zhenqiang / Xing, Lianping

Endocrinology and metabolism (Seoul, Korea)

2023 Volume 38, Issue 5, Page(s) 504–521

Abstract: Maintenance of skeletal integrity requires the coordinated activity of multinucleated bone-resorbing osteoclasts and bone-forming osteoblasts. Osteoclasts form resorption lacunae on bone surfaces in response to cytokines by fusion of precursor cells. ... ...

Abstract	Maintenance of skeletal integrity requires the coordinated activity of multinucleated bone-resorbing osteoclasts and bone-forming osteoblasts. Osteoclasts form resorption lacunae on bone surfaces in response to cytokines by fusion of precursor cells. Osteoblasts are derived from mesenchymal precursors and lay down new bone in resorption lacunae during bone remodeling. Nuclear factorkappa B (NF-κB) signaling regulates osteoclast and osteoblast formation and is activated in osteoclast precursors in response to the essential osteoclastogenic cytokine, receptor activator of NF-κB ligand (RANKL), which can also control osteoblast formation through RANK-RANKL reverse signaling in osteoblast precursors. RANKL and some pro-inflammatory cytokines, including tumor necrosis factor (TNF), activate NF-κB signaling to positively regulate osteoclast formation and functions. However, these cytokines also limit osteoclast and osteoblast formation through NF-κB signaling molecules, including TNF receptor-associated factors (TRAFs). TRAF6 mediates RANKL-induced osteoclast formation through canonical NF-κB signaling. In contrast, TRAF3 limits RANKL- and TNF-induced osteoclast formation, and it restricts transforming growth factor β (TGFβ)-induced inhibition of osteoblast formation in young and adult mice. During aging, neutrophils expressing TGFβ and C-C chemokine receptor type 5 (CCR5) increase in bone marrow of mice in response to increased NF-κB-induced CC motif chemokine ligand 5 (CCL5) expression by mesenchymal progenitor cells and injection of these neutrophils into young mice decreased bone mass. TGFβ causes degradation of TRAF3, resulting in decreased glycogen synthase kinase-3β/β-catenin-mediated osteoblast formation and age-related osteoporosis in mice. The CCR5 inhibitor, maraviroc, prevented accumulation of TGFβ+/CCR5+ neutrophils in bone marrow and increased bone mass by inhibiting bone resorption and increasing bone formation in aged mice. This paper updates current understanding of how NF-κB signaling is involved in the positive and negative regulation of cytokine-mediated osteoclast and osteoblast formation and activation with a focus on the role of TRAF3 signaling, which can be targeted therapeutically to enhance bone mass.
MeSH term(s)	Mice ; Animals ; NF-kappa B/metabolism ; Osteogenesis ; TNF Receptor-Associated Factor 3/metabolism ; Ligands ; Osteoclasts/metabolism ; Osteoclasts/pathology ; Transforming Growth Factor beta/metabolism
Chemical Substances	NF-kappa B ; TNF Receptor-Associated Factor 3 ; Ligands ; Transforming Growth Factor beta
Language	English
Publishing date	2023-09-26
Publishing country	Korea (South)
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2802452-7
ISSN	2093-5978 ; 2093-5978
ISSN (online)	2093-5978
ISSN	2093-5978
DOI	10.3803/EnM.2023.501
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Article: RANKL inhibition reduces lesional cellularity and Gα

de Castro, Luis F / Whitlock, Jarred M / Michel, Zachary / Pan, Kristen / Taylor, Jocelyn / Szymczuk, Vivian / Boyce, Brendan / Martin, Daniel / Kram, Vardit / Galisteo, Rebeca / Melikov, Kamran / Chernomordik, Leonid V / Collins, Michael T / Boyce, Alison M

Bone research

2024 Volume 12, Issue 1, Page(s) 10

Abstract: Fibrous dysplasia (FD) is a rare, disabling skeletal disease for which there are no established treatments. Growing evidence supports inhibiting the osteoclastogenic factor receptor activator of nuclear kappa-B ligand (RANKL) as a potential treatment ... ...

Abstract	Fibrous dysplasia (FD) is a rare, disabling skeletal disease for which there are no established treatments. Growing evidence supports inhibiting the osteoclastogenic factor receptor activator of nuclear kappa-B ligand (RANKL) as a potential treatment strategy. In this study, we investigated the mechanisms underlying RANKL inhibition in FD tissue and its likely indirect effects on osteoprogenitors by evaluating human FD tissue pre- and post-treatment in a phase 2 clinical trial of denosumab (NCT03571191) and in murine in vivo and ex vivo preclinical models. Histological analysis of human and mouse tissue demonstrated increased osteogenic maturation, reduced cellularity, and reduced expression of the pathogenic Gα
MeSH term(s)	Animals ; Humans ; Mice ; Denosumab/pharmacology ; Fibrous Dysplasia of Bone/drug therapy ; Ligands ; Osteoblasts/metabolism ; Osteogenesis/genetics
Chemical Substances	Denosumab (4EQZ6YO2HI) ; Ligands
Language	English
Publishing date	2024-02-20
Publishing country	China
Document type	Clinical Trial, Phase II ; Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2803313-9
ISSN	2095-6231 ; 2095-4700
ISSN (online)	2095-6231
ISSN	2095-4700
DOI	10.1038/s41413-023-00311-7
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Article ; Online: Intraligamentous synovial osteochondroma of the ligamentum teres: a series of 14 cases.

Ajabnoor, Rana M / Quinzi, David A / Carmody, Emily / Boyce, Brendan F

International journal of clinical and experimental pathology

2022 Volume 15, Issue 7, Page(s) 282–288

Abstract: Background: The ligamentum teres (LT) is covered by synovium. It acts as a stabilizer of the hip and as such it has been compared to the ACL of the knee joint. Pathologic changes occur in the LT with aging and osteoarthritis (OA), including degeneration, ...

Abstract	Background: The ligamentum teres (LT) is covered by synovium. It acts as a stabilizer of the hip and as such it has been compared to the ACL of the knee joint. Pathologic changes occur in the LT with aging and osteoarthritis (OA), including degeneration, occasional chondroid metaplasia, and synovial chondromatosis are well-recognized in the literature. However, there are no reports of intraligamentous synovial osteochondroma occuring in the LT. Methods: We reviewed the pathology reports of 542 osteoarthritic femoral arthroplasty specimens between January 2016 and December 2018. The LT was examined histologically in 55 cases because it was abnormal on gross examination. Results: A single synovial osteochondroma, ranging in size from 0.4-1.7 cm in diameter, was present in the body of the LT in 14 cases (9 males; 5 females, aged 34 to 81 years), representing 2.6% of 542 arthroplasty cases. Ten of the osteochondromas had bone marrow fat without hematopoietic elements, 1 had hematopoietic elements, and 3 had no marrow among the bony trabeculae. Radiographically, all cases had moderate to severe osteoarthritis with no mention of an abnormality of LT. Conclusion: To our knowledge, this is the first report of intraligamentous synovial osteochondroma in the LT in osteoarthritis patients undergoing hip arthroplasty. It provides further support for microscopic examination of arthroplasty specimens for histologic abnormalities. Further prospective study is needed to determine if this lesion contributes adversely to the development or progression of osteoarthritis and if it is a reactive or neoplastic process.
Language	English
Publishing date	2022-07-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2418306-4
ISSN	1936-2625 ; 1936-2625
ISSN (online)	1936-2625
ISSN	1936-2625
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Article: Molecular signatures distinguish senescent cells from inflammatory cells in aged mouse callus stromal cells.

Liu, Jiatong / Lin, Xi / McDavid, Andrew / Yang, Yutiancheng / Zhang, Hengwei / Boyce, Brendan F / Xing, Lianping

Frontiers in endocrinology

2023 Volume 14, Page(s) 1090049

Abstract: Cellular senescence plays important roles in age-related diseases, including musculoskeletal disorders. Senescent cells (SCs) exert a senescence-associated secretory phenotype (SASP) by producing SASP factors, some of which overlap with factors produced ... ...

Abstract	Cellular senescence plays important roles in age-related diseases, including musculoskeletal disorders. Senescent cells (SCs) exert a senescence-associated secretory phenotype (SASP) by producing SASP factors, some of which overlap with factors produced by inflammatory cells (Inf-Cs). However, the differences between SCs and Inf-Cs and how they interact with each other during fracture repair have not been well studied. Here, we analyzed single cell RNA sequencing data of aged mouse fracture callus stromal cells. We defined Inf-Cs as cells that express NF-κB
MeSH term(s)	Animals ; Mice ; NF-kappa B ; Stromal Cells ; Fractures, Bone ; Osteogenesis ; Cellular Senescence
Chemical Substances	NF-kappa B
Language	English
Publishing date	2023-02-16
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1090049
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Article ; Online: Safety and Efficacy of Denosumab for Fibrous Dysplasia of Bone.

de Castro, Luis F / Michel, Zachary / Pan, Kristen / Taylor, Jocelyn / Szymczuk, Vivian / Paravastu, Sriram / Saboury, Babak / Papadakis, Georgios Z / Li, Xiaobai / Milligan, Kelly / Boyce, Brendan / Paul, Scott M / Collins, Michael T / Boyce, Alison M

The New England journal of medicine

2023 Volume 388, Issue 8, Page(s) 766–768

MeSH term(s)	Humans ; Bone Density Conservation Agents/therapeutic use ; Denosumab/therapeutic use ; Fibrous Dysplasia of Bone/drug therapy ; Treatment Outcome
Chemical Substances	Bone Density Conservation Agents ; Denosumab (4EQZ6YO2HI)
Language	English
Publishing date	2023-02-20
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMc2214862
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Article ; Online: RANKL-Based Osteoclastogenic Assay from Murine Bone Marrow Cells.

Yao, Zhenqiang / Xing, Lianping / Boyce, Brendan F

Methods in molecular biology (Clifton, N.J.)

2020 Volume 2230, Page(s) 457–465

Abstract: The osteoclast is the unique type of cell that resorbs bone in vivo and it is required for normal skeletal development and postnatal homeostasis. Osteoclast deficiency impairs skeletal development during embryogenesis and results in osteopetrosis and ... ...

Abstract	The osteoclast is the unique type of cell that resorbs bone in vivo and it is required for normal skeletal development and postnatal homeostasis. Osteoclast deficiency impairs skeletal development during embryogenesis and results in osteopetrosis and impaired tooth eruption. In contrast, excessive osteoclast formation in adults results in bone loss in a number of conditions, including osteoporosis, rheumatoid arthritis, and metastatic bone disease. Osteoclasts are derived from monocytes/macrophages; they can be generated in vitro by treatment of these precursor cells with macrophage colony stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL). This chapter describes procedures for generating osteoclasts from mouse bone marrow cells in vitro using M-CSF and RANKL and assessing their ability to form resorption lacunae on thin bone slices.
MeSH term(s)	Animals ; Bone Marrow Cells/drug effects ; Bone Marrow Cells/metabolism ; Cell Culture Techniques/methods ; Cell Differentiation/drug effects ; Macrophage Colony-Stimulating Factor/pharmacology ; Mice ; Osteoclasts/drug effects ; Osteoclasts/metabolism ; Osteogenesis/genetics ; RANK Ligand/pharmacology
Chemical Substances	RANK Ligand ; Tnfsf11 protein, mouse ; Macrophage Colony-Stimulating Factor (81627-83-0)
Language	English
Publishing date	2020-08-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1028-2_29
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Article ; Online: Age-associated callus senescent cells produce TGF-β1 that inhibits fracture healing in aged mice.

Liu, Jiatong / Zhang, Jun / Lin, Xi / Boyce, Brendan F / Zhang, Hengwei / Xing, Lianping

The Journal of clinical investigation

2022 Volume 132, Issue 8

Abstract: Cellular senescence plays an important role in human diseases, including osteoporosis and osteoarthritis. Senescent cells (SCs) produce the senescence-associated secretory phenotype to affect the function of neighboring cells and SCs themselves. Delayed ... ...

Abstract	Cellular senescence plays an important role in human diseases, including osteoporosis and osteoarthritis. Senescent cells (SCs) produce the senescence-associated secretory phenotype to affect the function of neighboring cells and SCs themselves. Delayed fracture healing is common in the elderly and is accompanied by reduced mesenchymal progenitor cells (MPCs). However, the contribution of cellular senescence to fracture healing in the aged has not to our knowledge been studied. Here, we used C57BL/6J 4-month-old young and 20-month-old aged mice and demonstrated a rapid increase in SCs in the fracture callus of aged mice. The senolytic drugs dasatinib plus quercetin enhanced fracture healing in aged mice. Aged callus SCs inhibited the growth and proliferation of callus-derived MPCs (CaMPCs) and expressed high levels of TGF-β1. TGF-β-neutralizing Ab prevented the inhibitory effects of aged callus SCs on CaMPCs and promoted fracture healing in aged mice, which was associated with increased CaMPCs and proliferating cells. Thus, fracture triggered a significant cellular senescence in the callus cells of aged mice, which inhibited MPCs by expressing TGF-β1. Short-term administration of dasatinib plus quercetin depleted callus SCs and accelerated fracture healing in aged mice. Senolytic drugs represent a promising therapy, while TGF-β1 signaling is a molecular mechanism for fractures in the elderly via SCs.
MeSH term(s)	Animals ; Cellular Senescence ; Dasatinib/pharmacology ; Fracture Healing ; Fractures, Bone/drug therapy ; Fractures, Bone/genetics ; Mice ; Mice, Inbred C57BL ; Quercetin/pharmacology ; Transforming Growth Factor beta1/genetics
Chemical Substances	Transforming Growth Factor beta1 ; Quercetin (9IKM0I5T1E) ; Dasatinib (RBZ1571X5H)
Language	English
Publishing date	2022-04-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI148073
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Article ; Online: Optimizing the use and applications of special stains: clinical and experimental approaches.

Boyce, Brendan F

Biotechnic & histochemistry : official publication of the Biological Stain Commission

2012 Volume 87, Issue 1, Page(s) 1–2

MeSH term(s)	Guidelines as Topic ; Humans ; Staining and Labeling/standards
Language	English
Publishing date	2012-01
Publishing country	England
Document type	Introductory Journal Article
ZDB-ID	1069349-x
ISSN	1473-7760 ; 1052-0295
ISSN (online)	1473-7760
ISSN	1052-0295
DOI	10.3109/10520295.2011.591839
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Article ; Online: Advances in osteoclast biology reveal potential new drug targets and new roles for osteoclasts.

Boyce, Brendan F

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2013 Volume 28, Issue 4, Page(s) 711–722

Abstract: Osteoclasts are multinucleated myeloid lineage cells formed in response to macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL) by fusion of bone marrow-derived precursors that circulate in the blood and are ... ...

Abstract	Osteoclasts are multinucleated myeloid lineage cells formed in response to macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL) by fusion of bone marrow-derived precursors that circulate in the blood and are attracted to sites of bone resorption in response to factors, such as sphingosine-1 phosphate signaling. Major advances in understanding of the molecular mechanisms regulating osteoclast functions have been made in the past 20 years, mainly from mouse and human genetic studies. These have revealed that osteoclasts express and respond to proinflammatory and anti-inflammatory cytokines. Some of these cytokines activate NF-κB and nuclear factor of activated T cells, cytoplasmic 1 (NFATc1) signaling to induce osteoclast formation and activity and also regulate communication with neighboring cells through signaling proteins, including ephrins and semaphorins. Osteoclasts also positively and negatively regulate immune responses and osteoblastic bone formation. These advances have led to development of new inhibitors of bone resorption that are in clinical use or in clinical trials; and more should follow, based on these advances. This article reviews current understanding of how bone resorption is regulated both positively and negatively in normal and pathologic states.
MeSH term(s)	Animals ; Bone Remodeling ; Bone Resorption/drug therapy ; Bone Resorption/pathology ; Humans ; Molecular Targeted Therapy ; Osteoclasts/metabolism ; Osteogenesis
Language	English
Publishing date	2013-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.1885
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