Mast Cells Are Critical Regulators of Bone Fracture-Induced Inflammation and Osteoclast Formation and Activity

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Mast Cells Are Critical Regulators of Bone Fracture-Induced Inflammation and Osteoclast Formation and Activity. / Kroner, Jochen; Kovtun, Anna; Kemmler, Julia; Messmann, Joanna J; Strauss, Gudrun; Seitz, Sebastian; Schinke, Thorsten; Amling, Michael; Kotrba, Johanna; Froebel, Julia; Dudeck, Jan; Dudeck, Anne; Ignatius, Anita.

In: J BONE MINER RES, Vol. 32, No. 12, 12.2017, p. 2431-2444.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Kroner, J, Kovtun, A, Kemmler, J, Messmann, JJ, Strauss, G, Seitz, S, Schinke, T, Amling, M, Kotrba, J, Froebel, J, Dudeck, J, Dudeck, A & Ignatius, A 2017, 'Mast Cells Are Critical Regulators of Bone Fracture-Induced Inflammation and Osteoclast Formation and Activity', J BONE MINER RES, vol. 32, no. 12, pp. 2431-2444. https://doi.org/10.1002/jbmr.3234

APA

Kroner, J., Kovtun, A., Kemmler, J., Messmann, J. J., Strauss, G., Seitz, S., Schinke, T., Amling, M., Kotrba, J., Froebel, J., Dudeck, J., Dudeck, A., & Ignatius, A. (2017). Mast Cells Are Critical Regulators of Bone Fracture-Induced Inflammation and Osteoclast Formation and Activity. J BONE MINER RES, 32(12), 2431-2444. https://doi.org/10.1002/jbmr.3234

Vancouver

Bibtex

@article{aef45f74577148b889ef84e4f5d2f68b,
title = "Mast Cells Are Critical Regulators of Bone Fracture-Induced Inflammation and Osteoclast Formation and Activity",
abstract = "Mast cells, important sensor and effector cells of the immune system, may influence bone metabolism as their number is increased in osteoporotic patients. They are also present during bone fracture healing with currently unknown functions. Using a novel c-Kit-independent mouse model of mast cell deficiency, we demonstrated that mast cells did not affect physiological bone turnover. However, they triggered local and systemic inflammation after fracture by inducing release of inflammatory mediators and the recruitment of innate immune cells. In later healing stages, mast cells accumulated and regulated osteoclast activity to remodel the bony fracture callus. Furthermore, they were essential to induce osteoclast formation after ovariectomy. Additional in vitro studies revealed that they promote osteoclastogenesis via granular mediators, mainly histamine. In conclusion, mast cells are redundant in physiologic bone turnover but exert crucial functions after challenging the system, implicating mast cells as a potential target for treating inflammatory bone disorders. {\textcopyright} 2017 American Society for Bone and Mineral Research.",
keywords = "Journal Article",
author = "Jochen Kroner and Anna Kovtun and Julia Kemmler and Messmann, {Joanna J} and Gudrun Strauss and Sebastian Seitz and Thorsten Schinke and Michael Amling and Johanna Kotrba and Julia Froebel and Jan Dudeck and Anne Dudeck and Anita Ignatius",
note = "{\textcopyright} 2017 American Society for Bone and Mineral Research.",
year = "2017",
month = dec,
doi = "10.1002/jbmr.3234",
language = "English",
volume = "32",
pages = "2431--2444",
journal = "J BONE MINER RES",
issn = "0884-0431",
publisher = "Wiley-Blackwell",
number = "12",

}

RIS

TY - JOUR

T1 - Mast Cells Are Critical Regulators of Bone Fracture-Induced Inflammation and Osteoclast Formation and Activity

AU - Kroner, Jochen

AU - Kovtun, Anna

AU - Kemmler, Julia

AU - Messmann, Joanna J

AU - Strauss, Gudrun

AU - Seitz, Sebastian

AU - Schinke, Thorsten

AU - Amling, Michael

AU - Kotrba, Johanna

AU - Froebel, Julia

AU - Dudeck, Jan

AU - Dudeck, Anne

AU - Ignatius, Anita

N1 - © 2017 American Society for Bone and Mineral Research.

PY - 2017/12

Y1 - 2017/12

N2 - Mast cells, important sensor and effector cells of the immune system, may influence bone metabolism as their number is increased in osteoporotic patients. They are also present during bone fracture healing with currently unknown functions. Using a novel c-Kit-independent mouse model of mast cell deficiency, we demonstrated that mast cells did not affect physiological bone turnover. However, they triggered local and systemic inflammation after fracture by inducing release of inflammatory mediators and the recruitment of innate immune cells. In later healing stages, mast cells accumulated and regulated osteoclast activity to remodel the bony fracture callus. Furthermore, they were essential to induce osteoclast formation after ovariectomy. Additional in vitro studies revealed that they promote osteoclastogenesis via granular mediators, mainly histamine. In conclusion, mast cells are redundant in physiologic bone turnover but exert crucial functions after challenging the system, implicating mast cells as a potential target for treating inflammatory bone disorders. © 2017 American Society for Bone and Mineral Research.

AB - Mast cells, important sensor and effector cells of the immune system, may influence bone metabolism as their number is increased in osteoporotic patients. They are also present during bone fracture healing with currently unknown functions. Using a novel c-Kit-independent mouse model of mast cell deficiency, we demonstrated that mast cells did not affect physiological bone turnover. However, they triggered local and systemic inflammation after fracture by inducing release of inflammatory mediators and the recruitment of innate immune cells. In later healing stages, mast cells accumulated and regulated osteoclast activity to remodel the bony fracture callus. Furthermore, they were essential to induce osteoclast formation after ovariectomy. Additional in vitro studies revealed that they promote osteoclastogenesis via granular mediators, mainly histamine. In conclusion, mast cells are redundant in physiologic bone turnover but exert crucial functions after challenging the system, implicating mast cells as a potential target for treating inflammatory bone disorders. © 2017 American Society for Bone and Mineral Research.

KW - Journal Article

U2 - 10.1002/jbmr.3234

DO - 10.1002/jbmr.3234

M3 - SCORING: Journal article

C2 - 28777474

VL - 32

SP - 2431

EP - 2444

JO - J BONE MINER RES

JF - J BONE MINER RES

SN - 0884-0431

IS - 12

ER -