Positive regulators of osteoclastogenesis and bone resorption in rheumatoid arthritis
Bone destruction is a frequent and clinically serious event in patients with rheumatoid arthritis (RA). Local joint destruction can cause joint instability and often necessitates reconstructive or replacement surgery. Moreover, inflammation-induced systemic bone loss is associated with an increased...
| Main Authors: | , |
|---|---|
| Format: | Online |
| Language: | English |
| Published: |
BioMed Central
2011
|
| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3239343/ |
| id |
pubmed-3239343 |
|---|---|
| recordtype |
oai_dc |
| spelling |
pubmed-32393432012-01-28 Positive regulators of osteoclastogenesis and bone resorption in rheumatoid arthritis Braun, Tobias Zwerina, Jochen Review Bone destruction is a frequent and clinically serious event in patients with rheumatoid arthritis (RA). Local joint destruction can cause joint instability and often necessitates reconstructive or replacement surgery. Moreover, inflammation-induced systemic bone loss is associated with an increased fracture risk. Bone resorption is a well-controlled process that is dependent on the differentiation of monocytes to bone-resorbing osteoclasts. Infiltrating as well as resident synovial cells, such as T cells, monocytes and synovial fibroblasts, have been identified as sources of osteoclast differentiation signals in RA patients. Pro-inflammatory cytokines are amongst the most important mechanisms driving this process. In particular, macrophage colony-stimulating factor, RANKL, TNF, IL-1 and IL-17 may play dominant roles in the pathogenesis of arthritis-associated bone loss. These cytokines activate different intracellular pathways to initiate osteoclast differentiation. Thus, over the past years several promising targets for the treatment of arthritic bone destruction have been defined. BioMed Central 2011 2011-07-28 /pmc/articles/PMC3239343/ /pubmed/21861862 http://dx.doi.org/10.1186/ar3380 Text en Copyright ©2011 BioMed Central Ltd |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Braun, Tobias Zwerina, Jochen |
| spellingShingle |
Braun, Tobias Zwerina, Jochen Positive regulators of osteoclastogenesis and bone resorption in rheumatoid arthritis |
| author_facet |
Braun, Tobias Zwerina, Jochen |
| author_sort |
Braun, Tobias |
| title |
Positive regulators of osteoclastogenesis and bone resorption in rheumatoid arthritis |
| title_short |
Positive regulators of osteoclastogenesis and bone resorption in rheumatoid arthritis |
| title_full |
Positive regulators of osteoclastogenesis and bone resorption in rheumatoid arthritis |
| title_fullStr |
Positive regulators of osteoclastogenesis and bone resorption in rheumatoid arthritis |
| title_full_unstemmed |
Positive regulators of osteoclastogenesis and bone resorption in rheumatoid arthritis |
| title_sort |
positive regulators of osteoclastogenesis and bone resorption in rheumatoid arthritis |
| description |
Bone destruction is a frequent and clinically serious event in patients with rheumatoid arthritis (RA). Local joint destruction can cause joint instability and often necessitates reconstructive or replacement surgery. Moreover, inflammation-induced systemic bone loss is associated with an increased fracture risk. Bone resorption is a well-controlled process that is dependent on the differentiation of monocytes to bone-resorbing osteoclasts. Infiltrating as well as resident synovial cells, such as T cells, monocytes and synovial fibroblasts, have been identified as sources of osteoclast differentiation signals in RA patients. Pro-inflammatory cytokines are amongst the most important mechanisms driving this process. In particular, macrophage colony-stimulating factor, RANKL, TNF, IL-1 and IL-17 may play dominant roles in the pathogenesis of arthritis-associated bone loss. These cytokines activate different intracellular pathways to initiate osteoclast differentiation. Thus, over the past years several promising targets for the treatment of arthritic bone destruction have been defined. |
| publisher |
BioMed Central |
| publishDate |
2011 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3239343/ |
| _version_ |
1611494638319828992 |