Bone as a Target Organ in Rheumatic Disease: Impact on Osteoclasts and Osteoblasts
UMass Chan Affiliations
Department of Medicine, Division of RheumatologyDocument Type
Journal ArticlePublication Date
2015-09-28Keywords
Ankylosing spondylitisBone erosions
Bone formation
Bone remodeling
DKK1
Entheses
IL-23
Inflammation
Osteoblast
Osteoclast
Rheumatoid arthritis
Sclerostin
Wnt
microRNAs
Allergy and Immunology
Cell Biology
Musculoskeletal Diseases
Rheumatology
Skin and Connective Tissue Diseases
Metadata
Show full item recordAbstract
Dysregulated bone remodeling occurs when there is an imbalance between bone resorption and bone formation. In rheumatic diseases, including rheumatoid arthritis (RA) and seronegative spondyloarthritis, systemic and local factors disrupt the process of physiologic bone remodeling. Depending upon the local microenvironment, cell types, and local mechanical forces, inflammation results in very different effects on bone, promoting bone loss in the joints and in periarticular and systemic bone in RA and driving bone formation at enthesial and periosteal sites in diseases such as ankylosing spondylitis (AS), included within the classification of axial spondyloarthritis. There has been a great deal of interest in the role of osteoclasts in these processes and much has been learned over the past decade about osteoclast differentiation and function. It is now appreciated that osteoblast-mediated bone formation is also inhibited in the RA joint, limiting the repair of erosions. In contrast, osteoblasts function to produce new bone in AS. The Wnt and BMP signaling pathways have emerged as critical in the regulation of osteoblast function and the outcome for bone in rheumatic diseases, and these pathways have been implicated in both bone loss in RA and bone formation in AS. These pathways provide potential novel approaches for therapeutic intervention in diseases in which inflammation impacts bone.Source
Clin Rev Allergy Immunol. 2015 Sep 28. Link to article on publisher's siteDOI
10.1007/s12016-015-8515-6Permanent Link to this Item
http://hdl.handle.net/20.500.14038/30647PubMed ID
26411424Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1007/s12016-015-8515-6