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Effects of B-cell depletion on bone turnover in Rheumatoid Arthritis

Rheumatoid arthritis is associated not only with joint damage, but generalised bone loss which ultimately can result in osteoporosis and an increased risk of fractures. This bone loss is driven by a variety of factors, including loss of mobility and inflammation which activate bone cells to break down (resorption) more bone than they form. There is also growing evidence that there is close interaction between immune cells and bone cells. Many immune cells produce molecules which stimulate both the inflammation underlying rheumatoid arthritis and bone breakdown. One such cell is a white cell known as the B-cell. Recently, a new and successful treatment for rheumatoid arthritis called Rituximab has been developed which destroys B-cells.

The Foundation funded a recent study to see if the removal of B-cells would also improve bone quality which was led by Roger Francis and Stephen Tuck. Preliminary evidence was sought by measuring markers of bone cell activity using stored blood from a previous study of 46 patients who had been given Rituximab every 6 months. Bone cell activity could be measured in blood prior to being given Rituximab and the effects 6 and 12 months after starting Rituximab. We found that B-cell depletion by Rituximab increased bone formation and decreased bone resorption. This suggests that there may be an improvement in bone density over time, which could help to prevent osteoporosis and fractures. The study has just been published in Osteoporosis International (Osteoporosis Int. 2011; 22:3067-3072). The success of this study has enabled us to obtain a further £150,000 in funding from the Pharmaceutical Company Roche to undertake a prospective study to measure bone density and confirm these findings.

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