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ISRCTN: 01982076 Rheumatoid arthritis (RA) is a long-term inflammatory disease affecting about 1% of the population and is characterised by joint inflammation, progressive joint destruction and increasing functional disability [ 1].
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Consistently, the expansion of Tregs in vivo by a CD28 super antibody suppressed local and systemic bone destruction and increased bone density in healthy mice.
Hence, the crosstalk between breast cancer cells and the bone microenvironment results in a vicious cycle of bone destruction and increased tumor growth in bone.
Consequently, an effective strategy for RA treatment is the removal of synovial hyperplasia to prevent cartilage destruction and increase the quality of life (QOL) of patients [ 1, 2].
For instance, a prospective two-year trial of 88 postmenopausal women with RA found that estrogen-containing HRT ameliorated clinical disease, retarded joint destruction, and increased bone mineral density (BMD) [ 6].
In rheumatoid arthritis (RA), chemokine upregulation is associated with tissue and joint destruction and increased levels of CCR5 receptor ligands (Regulated on Activation, Normal T-cell Expressed, and Secreted [RANTES], macrophage inflammatory protein [MIP]-1α, and MIP-1β) in the synovial fluid [ 8- 11].
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