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Inconsistency of the results regarding the genetic variability within genes coding for receptor activator of nuclear factor κB (RANK) and its ligand (RANKL) in rheumatoid arthritis (RA) prompted us to study the  RANK  and  RANKL  polymorphisms as potential biomarkers associated with disease predisposition and response to anti-TNF treatment in a group of Polish patients with RA. This study enrolled 318 RA patients and 163 controls.  RANK  (rs8086340, C > G; rs1805034, C > T) and  RANKL  (rs7325635, G > A; rs7988338 G > A) alleles were determined by real-time PCR with melting curve analysis and related with clinical parameters. In addition, RANKL serum levels were measured by ELISA. The  RANK  rs8086340- G  allele was overrepresented among patients as compared to controls (OD = 1.777,  p  = 0.038). C-reactive protein (CRP) levels were significantly ( p  < 0.05) associated with  RANK  rs8086340 polymorphism and were higher in the  CC -homozygotes at the baseline while lower in the  GG -carriers at the 12th week of the treatment. At the latter time point  RANKL  rs7325635- GG- positive patients also showed significantly lower CRP concentrations. Higher alkaline phosphatase levels before induction of anti-TNF therapy were observed in  RANK  rs8086340 and  RANK  rs1805034  CC  homozygotes ( p  = 0.057 and  p  = 0.035, respectively). The  GG  homozygosity of both  RANKL  single nucleotide polymorphisms was significantly associated with the number of swollen joints (rs7988338 and rs7325635, before and at the 12th week of therapy, respectively,  p  < 0.05 in both cases). These results imply that polymorphisms within the  RANK  and  RANKL  genes affect RA susceptibility and anti-TNF treatment outcome.

archivum immunologiae et therapiae experimentalis

Polymorphisms within the RANK and RANKL Encoding Genes in Patients with Rheumatoid Arthritis: Association with Disease Progression and Effectiveness of the Biological Treatment