Osteoarthritis is a common, degenerative, joint disease that increases in prevalence with age. During the disease, the matrix structure comprising cartilage in the joints is significantly diminished, inflicting severe frictional pain and restricting joint movement. One reason for this phenomenon is reduced matrix production and gene expression.
SirT1 is a nuclear enzyme that regulates the expression of many genes through alterations in chromatin structure. Chromatin is the combination of DNA and other proteins that make up the contents of the cell nucleus.
In laboratory work carried out at the Laboratory of Cartilage Biology at the Hebrew University of Jerusalem Faculty of Dental Medicine, researchers headed by Dr. Mona Dvir-Ginzberg showed that SirT1 positively regulates the expression of many cartilage-tissue components. Her work was carried out in cooperation with researchers at the US National Institutes of Health in Bethesda, MD.
This data, published in the Arthritis and Rheumatism journal, showed that when there is joint inflammation, SirT1 degenerates and is inactivated, thereby accelerating joint destruction through altered gene expression.
Understanding these events will enable the design of drug targets to serve as potential therapies that may retard or reverse OA through possibly boosting SirT1 production. Additionally, testing of SirT1 levels could serve as an early indicator for OA susceptibility and thus serve as a signal for beginning timely treatment.
"Developing a combined strategy for diagnosis and treatment, based on these data, could provide an efficient alternative for joint replacement surgery and enable susceptible individuals to experience a better quality of life for years to come," said Dr Dvir-Ginzberg.
Jerry Barach | Hebrew University of Jerusalem
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