Joint inflammation, generically described as Arthritis (RA), affects the body's synovial joints. It is typically characterized by the presence of local painful inflammation, swelling, and stiffness, causing limitation or loss of function of the site involved. The incidence of RA increases with age, reaching 85% of the population up to the age of 64, and this fact results in an important social impact and degree of disability. The etiology of RA types, where there is no associated autoimmune factor, is still unknown, but it is known that, in pathophysiological parameters, a lymphocytic infiltrate and neoangiogenesis lead to the formation of the pannus, which reaches the subchondral bone and joint cartilage, cartilage involvement being the biggest problem in RA. Preliminary studies by our group showed that 30 days after the induction of monoarthritis there is an intense tissue degeneration, showing characteristics of osteoarthritic cartilage. Therefore, knowing that the treatment for RA needs to start earlier and earlier, in order to preserve the osteocartilaginous structure, and even though the drugs currently used have high cost and often side effects that limit their use, we postulate that knowledge of the degree of cartilage impairment and its relationship with the evolution of the synovial inflammatory process would be of great help for the targeting and association of therapies in RA.
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