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Rheumatoid arthritis (RA) linkage has been observed on the 18q chromosome in the white population.1 The 18q locus has also shown evidence of linkage with type I insulin-dependent diabetes mellitus, systemic lupus erythematosus and Grave’s disease.2 A candidate gene on chromosome 18q, the TNFRSF11A (RANK) gene, which encodes the receptor activator of nuclear factor kappa B, has been shown to be involved in the osteoclast differentiation playing a pivotal role in bone resorption.3 A single RANK haplotype was reported to be associated with RA in a case–control association study.4 Furthermore, activating mutations in the RANK gene cause bone disorders such as early-onset Paget’s disease,5 expansile skeletal hyperphosphatasia6 and familial expansile osteolysis.7 The aim of this …
Competing interests: None.
Funding: This work was supported by Association Française des Polyarthritiques, Société Française de Rhumatologie, Association Rhumatisme et Travail, European Union for AutoCure, Association Polyarctique, Groupe Taitbout, Genopole. The work of VHT was supported by the Foundation for Science and Technology, Portugal (grant SFRH/BD/23304/2005).
ECRAF, The European Consortium on Rheumatoid Arthritis Families initiated with funding from the European Commission (BIOMED2) is coordinated by FC. The first two authors contributed equally to the study.
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