Rheumatoid arthritis (RA) is a symmetrical polyarticular disease of unknown 
aetiology that affects primarily the articular cartilage and bone. 
Characteristic features of RA pathogenesis are persistent inflammation, synovium 
hyperplasia and cartilage erosion accompanied by joint swelling and joint 
destruction. Several lines of evidence have showed a crucial role of activated 
fibroblast-like synoviocytes (FLS) in the pathogenesis of RA. MicroRNAs (miRNAs) 
are endogenous, single-stranded, non-coding RNAs with about 21 nucleotides in 
length and have been detected in a variety of sources, including tissues, serum, 
and other body fluids, such as saliva. In light of key roles of miRNAs in the 
regulation of gene expression, miRNAs influence a wide range of physiological 
and pathological processes. For example, miRNAs are evident in various malignant 
and nonmalignant diseases, and accumulating evidence also shows that miRNAs have 
important roles in the pathogenesis of RA. It has been demonstrated that miRNAs 
can be aberrantly expressed even in the different stages of RA progression, 
allowing miRNAs to help understand the pathogenesis of the disease, to act as 
important biomarkers, and to monitor the disease severity and the effects of 
drug treatment. In addition, miRNAs are emerging as potential targets for new 
therapeutic strategies of this kind of autoimmune disorders. The ultimate goal 
is the identification of miRNA targets that could be manipulated through 
specific therapies, aiming at activation or inhibition of specific miRNAs 
responsible for the RA development. In this review, the importance of miRNAs in 
the pathogenesis of RA is discussed systematically, with particular emphasis on 
the role of the crosstalk between DNA methylation and the microRNA machinery.