Can sulforaphane prevent the onset or slow the progression of osteoarthritis?. Issue 2 (June 2016)

• Record Type: Journal Article
• Authors: Davidson, R. K.; Jupp, O.; Bao, Y.; MacGregor, A. J.; Donell, S. T.; Cassidy, A.; Clark, I. M.
• Is Part Of: Nutrition bulletin. Volume 41:Issue 2(2016:Jun.)
• Page Start: 175
• Page End: 179
• Publication Date: 2016-06
• Subjects: cartilage -- dietary bioactive -- osteoarthritis -- sulforaphane; Nutrition -- Periodicals; 613.2
• DOI: 10.1111/nbu.12207
• Languages: English
• ISSNs: 1471-9827

Abstract

Abstract: Osteoarthritis (OA) is a degenerative joint disease characterised in part by destruction of articular cartilage. There are currently no disease‐modifying drugs to treat OA, with joint replacement the only treatment offered to patients at end‐stage disease. With age the major risk factor for OA, the number of patients is predicted to double by 2030. An understanding of the role of bioactive molecules from the habitual diet on joint health offers a novel way in which to prevent the onset or slow the progression of OA. Our research has indicated that sulforaphane (SFN), gained from the consumption of cruciferous vegetables, particularly broccoli, could impact upon articular cartilage in laboratory models of OA because (1) it decreased the cytokine‐induced expression of cartilage‐degrading proteinases from chondrocytes (cartilage cells); (2) it prevented the cytokine‐induced degradation of cartilage explants; and (3) it attenuated cartilage destruction in a murine model of OA. The major mechanism of action for SFN in human articular chondrocytes was inhibition of NFκB, not activation of Nrf2 nor inhibition of histone deacetylases. A proof‐of‐principle human trial was performed to measure uptake of SFN, or its metabolites, in the human knee joint following a broccoli‐rich diet, and the expression or levels of several genes and proteins in cartilage, fat and synovial fluid were also measured. Data from this trial are about to be published. Overall, these findings support the utility of SFN in the prevention or treatment of OA. The proof of this requires an appropriately designed clinical trial of pain and function which we are currently pursuing.