2012
DOI: 10.1002/art.33504
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Abstract: Objective Inflammation in the bone microenvironment stimulates osteoclast differentiation, resulting in uncoupling of resorption and formation. Mechanisms contributing to the inhibition of osteoblast function in inflammatory diseases, however, have not been elucidated. Rheumatoid arthritis (RA) is a prototype of an inflammatory arthritis that results in focal loss of articular bone. The paucity of bone repair in inflammatory diseases such as RA raises compelling questions regarding the impact of inflammation o… Show more

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Cited by 121 publications
(115 citation statements)
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“…A plausible explanation would be the presence of LPS-induced systemic inflammation and elevated circulating TNF-a, which has been reported to inhibit the differentiation of MSCs in bone-forming osteoblasts by suppressing Cbfa1 [19]. Moreover, resolution of the inflammatory phase of bone healing is proposed to be necessary for effective osteoblast function [33]. The concurrent expression of peak levels of ALP-positive osteogenic and CD34 vascular endothelial cells at 1 week postoperative in the condensing mesenchyme at the site of repair supports the hypothesis that there is crosstalk between the lineages destined to become bone and vascular tissue [4].…”
Section: Discussionmentioning
confidence: 99%
“…A plausible explanation would be the presence of LPS-induced systemic inflammation and elevated circulating TNF-a, which has been reported to inhibit the differentiation of MSCs in bone-forming osteoblasts by suppressing Cbfa1 [19]. Moreover, resolution of the inflammatory phase of bone healing is proposed to be necessary for effective osteoblast function [33]. The concurrent expression of peak levels of ALP-positive osteogenic and CD34 vascular endothelial cells at 1 week postoperative in the condensing mesenchyme at the site of repair supports the hypothesis that there is crosstalk between the lineages destined to become bone and vascular tissue [4].…”
Section: Discussionmentioning
confidence: 99%
“…Recent studies have focused on the impact of inflammation in osteoblasts, which exhibit important functions within the arthritic bone microenvironment and thus in RA pathogenesis (16, 34); whereas, during the past decade, RA studies had focused on the effects of inflammation on osteoclast-mediated bone resorption ( 35,36). These studies highlight that the influence of inflammation on bone is specific to the site of inflammation and dependent on the cytokines present within the local bone microenvironment.…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, Wnt10b seems to stimulate osteoblast functions through a positive autocrine loop [21]. Furthermore, it was recently suggested that resolution of inflammation may stimulate osteoblasts in part through Wnt10b [22]. Interestingly, TNF-a stimulates the expression of Wnt10b in preadipocytes, resulting in the activation of the canonical Wnt pathway characterized by b-catenin activity and inhibition of adipogenesis [23].…”
Section: Introductionmentioning
confidence: 99%