Many diseases share a common link to the inflammatory mechanisms that are at the heart of the inflammatory response to infections and traumas. The development and evolution of many illnesses may be affected by the intensity, the nature of the network of pro- and anti-inflammatory substances, and the direction of the inflammatory response. Current methods of treating inflammatory diseases may be unproductive because they focus on alleviating symptoms rather than addressing underlying causes. Since controlling when inflammation begins and ends is critical for preventing tissue damage, evolution has produced a number of mechanisms, including negative and positive feedback loops, to control the process. MicroRNAs (miRNAs) have recently been recognised as important gene regulators in the regulation of inflammation; their role in facilitating the orderly resolution and halting the out-of-control development of inflammatory responses is hypothesized. The potential of microRNAs as novel anti-inflammatory medicines in the treatment of inflammatory illnesses is discussed, along with other recent findings regarding the important functions miRNAs play in immune regulation. MiR-146a has been shown to play an important role in the negative regulation of inflammatory innate immune responses, and to be differentially expressed in a number of human diseases including rheumatoid arthritis (RA). However, evidence for the potential therapeutic use of miR-146a in human disease has been lacking. The current paper demonstrates the potential therapeutic application of miR-146a for RA by demonstrating the inhibitory effect of miR-146a on osteoclastogenesis in vitro. Moreover, using a collagen-induced arthritis mouse model, they were able to demonstrate that intravenous administration of double stranded miR-146a resulted in the suppression of cartilage and bone destruction, despite relatively unaffected immune cell infiltration of the synovium and inflammatory cytokine expression.