Osteoarthritis (OA) is the most common disease of the musculoskeletal system. Protein complex, the NLRP3 inflammasome plays the key role in the pathogenesis of OA. It consists of three components: the sensor – NLRP3, the adaptor – ASC and the effector – caspase. Activation of the NLRP3 inflammasome promotes the synthesis of pro-inflammatory cytokines, interleukin (IL) 1 β and IL18, and the formation of gasdermin pores, which – combined – leads to cell death, pyroptosis. Despite successes in understanding the processes of OA development, there are no therapeutic methods that can completely stop or slow the progression of the disease. In addition, the use of some medications, particularly nonsteroidal anti-inflammatory drugs (NSAIDs), is associated with a clinically significant increase in the risk of NSAID-induced pathology by 50– 100%.

Due to increased life expectancy and the frequency of concomitant diseases, the treatment strategy for OA had to be changed, leading to the emergence of phenotypes of the disease characterized by low-intensity systemic inflammation.

We present a review of modern data reflecting the involvement of components of innate immunity in the development and progression of OA, as well as possible ways to correct disturbances taking these aspects into consideration.