Abstract
Osteoarthritis (OA) is a disease of the entire joint. Different treatment strategies for OA have been proposed and tested clinically without the desired efficacy. One reason for the scarcity of current chondroprotective agents may be the insufficient understanding of the patho-physiology of the joint and whether the joint damage is reversible or irreversible. In this review, we compile emerging data on cellular and pathological aspects of OA, and ask whether these data could give clue to when cartilage degradation is reversible and whether a point-of-no-return exists. We highlight different stages of OA, and speculate whether different intervention strategies (e.g. DMOAD vs. SMOADs) may only be efficacious at distinct stages of OA.
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Abbreviations
- ADAMTS:
-
A disintegrin and metalloproteinase with thrombospondin motifs
- BMP:
-
Bone morphogenetic protein
- CTX:
-
C-terminal telopeptide fragments
- DMOAD:
-
Disease modifying OA drug
- ECM:
-
Extracellular matrix
- FGF:
-
Fibroblast growth factor
- IGF-1:
-
Insulin growth factor
- JSW:
-
Joint space width
- MMP:
-
Matrix metalloproteinases
- OA:
-
Osteoarthritis
- OPG:
-
Osteoprotegerin
- PTH:
-
Parathyroid hormone
- RA:
-
Rheumatoid arthritis
- RANKL:
-
Receptor activator for nuclear factor κ B ligand
- SMOAD:
-
Structure modifying OA drug
- TGF:
-
Tissue growth factor
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Acknowledgments
We would like to thank our colleagues at Nordic Bioscience for their participation in inspirational discussions. We would also like to thank several of our fellow scientist, which we have continues discussion with at meetings and seminars.
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The authors are not aware of any conflict of interest pertaining to this manuscript.
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Bay-Jensen, AC., Hoegh-Madsen, S., Dam, E. et al. Which elements are involved in reversible and irreversible cartilage degradation in osteoarthritis?. Rheumatol Int 30, 435–442 (2010). https://doi.org/10.1007/s00296-009-1183-1
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DOI: https://doi.org/10.1007/s00296-009-1183-1