
pmid: 17391995
handle: 2066/52274
OBJECTIVE: Cartilage damage is a major problem in osteoarthritis (OA). Growth factors like transforming growth factor-beta (TGF-beta) have great potential in cartilage repair. In this review, we will focus on the potential therapeutic intervention in OA with TGF-beta, application of the growth factor TGF-beta in cartilage repair and on the side effects of TGF-beta treatment that could occur. METHODS: This review summarizes peer-reviewed articles published in the PubMed database before November 2006. In addition, this review is supplemented with recent data of our own group on the use of TGF-beta as a cartilage reparative factor in OA. RESULTS: TGF-beta is crucial for cartilage maintenance and lack there of results in OA-like changes. Moreover, TGF-beta supplementation can enhance cartilage repair and is therefore a potential therapeutic tool. However, application of TGF-beta supplementation provides problems in other tissues of the joint and results in fibrosis and osteophyte formation. This can potentially be overcome by local inhibition of TGF-beta at sites of unwanted side-effects or by blocking downstream mediators of TGF-beta that are important for the induction of fibrosis or osteophyte formation. CONCLUSION: Current understanding of TGF-beta suggests that it essential for cartilage integrity and that it is a powerful tool to prevent or repair cartilage damage. The side-effects that occur with TGF-beta supplementation can be overcome by local inhibition of TGF-beta itself or downstream mediators.
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Cartilage, Articular, Male, UMCN 4.2: Chronic inflammation and autoimmunity, NCMLS 1: Infection and autoimmunity, NCMLS 1: Immunity, infection and tissue repair, NCMLS 3: Tissue engineering and pathology, N4i 1: Pathogenesis and modulation of inflammation, Mice, N4i 4: Auto-immunity, transplantation and immunotherapy, Transforming Growth Factor beta, Osteoarthritis, Animals, Humans, Female
Cartilage, Articular, Male, UMCN 4.2: Chronic inflammation and autoimmunity, NCMLS 1: Infection and autoimmunity, NCMLS 1: Immunity, infection and tissue repair, NCMLS 3: Tissue engineering and pathology, N4i 1: Pathogenesis and modulation of inflammation, Mice, N4i 4: Auto-immunity, transplantation and immunotherapy, Transforming Growth Factor beta, Osteoarthritis, Animals, Humans, Female
| selected citations These citations are derived from selected sources. This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 339 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 1% | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 1% | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 1% |
