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RANKL related to joint destruction in patients with early RA
Receptor activator of nuclear factor kappa-B ligand, but not sclerostin or gene polymorphisms, were linked to joint destruction in patients with early rheumatoid arthritis in Northern Sweden, according to recently published data.
“[We] have shown that measurement of [receptor activator of nuclear factor kappa-B ligand] RANKL concentration, on its own, can be a valuable predictor for Larsen score at 24 months and long-term radiological progression irrespective of disease activity,” Solbritt Rantapää Dahlqvist, MD, PhD, professor of rheumatology at the University of Umeå, and colleagues wrote. They added, “Furthermore, we were unable to show that the polymorphisms of the RANKL [single nucleotide polymorphisms] SNPs were associated with the concentration of RANKL or with the radiological progression. Sclerostin was not related to the radiological findings during the first 24 months.”
Researchers radiologically examined and recorded disease activity score and C-reactive protein for 407 patients who had symptomatic rheumatoid arthritis (RA) for less than 1 year and for 71 age- and sex-matched controls. Researchers also examined sclerostin, RANKL and anti-CCP2 antibodies at baseline and extracted gene polymorphism data for each group.
Researchers found RANKL was significantly higher in patients with RA vs. controls (0.56 nmol/L vs. 0.20 nmol/L). Sclerostin was significantly higher in female patients with RA vs. those in the control group (0.59 ng/mL vs. 0.49 ng/mL). RANKL, but not sclerostin, was related to Larsen score at baseline and at 24 months and was related to radiological progression after 24 months. RANKL positivity and anti-CCP2 were associated with significant risk for progression with negativity. In addition, no single nucleotide polymorphism of TNFSF11 or SOST was associated with increased RANKL or anti-CCP2. – by Will Offit
Disclosure: The researchers report no relevant financial disclosures.