Here, we show that CRP regulates the differentiation of osteoclasts, a central mediator of joint inflammation and bone erosion in RA, in a conformation- and receptor activator of NF-κB ligand (RANKL)-dependent manner.
We investigated the role of IRAK1 single-nucleotide polymorphism (SNP) rs3027898 (IRAK1 rs3027898) and miR-146a SNP rs2910164 (miR-146a rs2910164) in Tunisian patients with RA and their association with C reactive protein (CRP), rheumatoid factor (RF), anticyclic citrullinated peptide (anti-CCP) antibodies, and erosion.
Also, our results points to a synergism between TGF-β1 TT genotype and elevated serum RF or elevated CRP that lead to the development of osteoporosis and bone erosion in patients with rheumatoid arthritis.
However, we did not find any association between the three tested SNPs and RA patients according to clinical features, including erythrocyte sedimentation rate, C-reactive protein level, rheumatoid factor (+ and -) and bone erosion (+ and -).
When the patients were divided into two groups according to the parameters of disease activity, including C-reactive protein (CRP) level (> or = 0.5 or < 0.5 mg/dL), the erythrocyte sedimentation rate (ESR) (> or = 30 or < 30 mm/h), and parameters of severity, including rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP), and bone erosion (positive or not), we found significant associations between the parameters, including CRP, ESR, and bone erosion, and SNPs of the IL-1 family genes in RA.