Activation of the inducible nitric oxide synthase pathway contributes to inflammation-induced osteoporosis by suppressing bone formation and causing osteoblast apoptosis

K J Armour; K E Armour; Rob van 't Hof; D M Reid; X Q Wei; F Y Liew; S H Ralston

Activation of the inducible nitric oxide synthase pathway contributes to inflammation-induced osteoporosis by suppressing bone formation and causing osteoblast apoptosis

K J Armour, K E Armour, Rob van 't Hof, D M Reid, X Q Wei, F Y Liew, S H Ralston

Research output: Contribution to journal › Article › peer-review

Abstract / Description of output

Osteoporosis is a major clinical problem in chronic inflammatory diseases such as rheumatoid arthritis. The mechanism of bone loss in this condition remains unclear, but previous studies have indicated that depressed bone formation plays a causal role. Since cytokine-induced nitric oxide (NO) production has been shown to inhibit osteoblast growth and differentiation in vitro, this study was undertaken to investigate the role of the inducible NO synthase (iNOS) pathway in the pathogenesis of inflammation-mediated osteoporosis (IMO) by studying mice with targeted inactivation of the iNOS gene (iNOS knockout [iNOS KO] mice).

Original language	English
Pages (from-to)	2790-6
Number of pages	7
Journal	Arthritis and rheumatism
Volume	44
Issue number	12
Publication status	Published - 2001

Cite this

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title = "Activation of the inducible nitric oxide synthase pathway contributes to inflammation-induced osteoporosis by suppressing bone formation and causing osteoblast apoptosis",

abstract = "Osteoporosis is a major clinical problem in chronic inflammatory diseases such as rheumatoid arthritis. The mechanism of bone loss in this condition remains unclear, but previous studies have indicated that depressed bone formation plays a causal role. Since cytokine-induced nitric oxide (NO) production has been shown to inhibit osteoblast growth and differentiation in vitro, this study was undertaken to investigate the role of the inducible NO synthase (iNOS) pathway in the pathogenesis of inflammation-mediated osteoporosis (IMO) by studying mice with targeted inactivation of the iNOS gene (iNOS knockout [iNOS KO] mice).",

author = "Armour, {K J} and Armour, {K E} and {van 't Hof}, Rob and Reid, {D M} and Wei, {X Q} and Liew, {F Y} and Ralston, {S H}",

year = "2001",

language = "English",

volume = "44",

pages = "2790--6",

journal = "Arthritis and rheumatism",

issn = "0004-3591",

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TY - JOUR

T1 - Activation of the inducible nitric oxide synthase pathway contributes to inflammation-induced osteoporosis by suppressing bone formation and causing osteoblast apoptosis

AU - Armour, K J

AU - Armour, K E

AU - van 't Hof, Rob

AU - Reid, D M

AU - Wei, X Q

AU - Liew, F Y

AU - Ralston, S H

PY - 2001

Y1 - 2001

N2 - Osteoporosis is a major clinical problem in chronic inflammatory diseases such as rheumatoid arthritis. The mechanism of bone loss in this condition remains unclear, but previous studies have indicated that depressed bone formation plays a causal role. Since cytokine-induced nitric oxide (NO) production has been shown to inhibit osteoblast growth and differentiation in vitro, this study was undertaken to investigate the role of the inducible NO synthase (iNOS) pathway in the pathogenesis of inflammation-mediated osteoporosis (IMO) by studying mice with targeted inactivation of the iNOS gene (iNOS knockout [iNOS KO] mice).

AB - Osteoporosis is a major clinical problem in chronic inflammatory diseases such as rheumatoid arthritis. The mechanism of bone loss in this condition remains unclear, but previous studies have indicated that depressed bone formation plays a causal role. Since cytokine-induced nitric oxide (NO) production has been shown to inhibit osteoblast growth and differentiation in vitro, this study was undertaken to investigate the role of the inducible NO synthase (iNOS) pathway in the pathogenesis of inflammation-mediated osteoporosis (IMO) by studying mice with targeted inactivation of the iNOS gene (iNOS knockout [iNOS KO] mice).

M3 - Article

C2 - 11762939

SN - 0004-3591

VL - 44

SP - 2790

EP - 2796

JO - Arthritis and rheumatism

JF - Arthritis and rheumatism

IS - 12

ER -

Activation of the inducible nitric oxide synthase pathway contributes to inflammation-induced osteoporosis by suppressing bone formation and causing osteoblast apoptosis

Abstract / Description of output

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