Cellular and molecular mechanisms of cartilage damage and repair
•Cartilage breakdown is the disabling outcome of rheumatic diseases.•Inflammation, chondrocyte phenotype and homeostatic mechanisms have recently been the focus of research.•This review forms part of a supplement on rheumatology. Cartilage breakdown is the disabling outcome of rheumatic diseases, wh...
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Published in | Drug discovery today Vol. 19; no. 8; pp. 1172 - 1177 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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Elsevier Ltd
01.08.2014
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Abstract | •Cartilage breakdown is the disabling outcome of rheumatic diseases.•Inflammation, chondrocyte phenotype and homeostatic mechanisms have recently been the focus of research.•This review forms part of a supplement on rheumatology.
Cartilage breakdown is the disabling outcome of rheumatic diseases, whether prevalently inflammatory such as rheumatoid arthritis or prevalently mechanical such as osteoarthritis (OA). Despite the differences between immune-mediated arthritides and OA, common mechanisms drive cartilage breakdown. Inflammation, chondrocyte phenotype and homeostatic mechanisms have recently been the focus of research and will be summarised in this review. |
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AbstractList | Cartilage breakdown is the disabling outcome of rheumatic diseases, whether prevalently inflammatory such as rheumatoid arthritis or prevalently mechanical such as osteoarthritis (OA). Despite the differences between immune-mediated arthritides and OA, common mechanisms drive cartilage breakdown. Inflammation, chondrocyte phenotype and homeostatic mechanisms have recently been the focus of research and will be summarised in this review. •Cartilage breakdown is the disabling outcome of rheumatic diseases.•Inflammation, chondrocyte phenotype and homeostatic mechanisms have recently been the focus of research.•This review forms part of a supplement on rheumatology. Cartilage breakdown is the disabling outcome of rheumatic diseases, whether prevalently inflammatory such as rheumatoid arthritis or prevalently mechanical such as osteoarthritis (OA). Despite the differences between immune-mediated arthritides and OA, common mechanisms drive cartilage breakdown. Inflammation, chondrocyte phenotype and homeostatic mechanisms have recently been the focus of research and will be summarised in this review. |
Author | Sherwood, Joanna C. Dell’Accio, Francesco Eldridge, Suzanne E. Bertrand, Jessica |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24880104$$D View this record in MEDLINE/PubMed |
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SubjectTerms | Animals Arthritis, Rheumatoid - pathology Arthritis, Rheumatoid - physiopathology Cartilage - pathology Cartilage - physiopathology Chondrocytes - pathology Chondrocytes - physiology Humans Inflammation - pathology Inflammation - physiopathology Osteoarthritis - pathology Osteoarthritis - physiopathology Wound Healing - physiology |
Title | Cellular and molecular mechanisms of cartilage damage and repair |
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