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 journalArticlepeer-review

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).
Original languageEnglish
Pages (from-to)2790-6
Number of pages7
JournalArthritis and rheumatism
Volume44
Issue number12
Publication statusPublished - 2001

Fingerprint Dive into the research topics of 'Activation of the inducible nitric oxide synthase pathway contributes to inflammation-induced osteoporosis by suppressing bone formation and causing osteoblast apoptosis'. Together they form a unique fingerprint.

Cite this