**1. Introduction**

Research on animal models is necessary to better understand the etiopathology of rheumatoid arthritis (RA) and has enabled successful new strategies for innovative drug research. Recently the discovery of novel biomarkers of presymptomatic and emerging stages of human RA focused the attention on interventions that underlie different disease variants. This development in the field underlying RA pathogenesis has also led to the increased need of new animal models. Integration of the knowledge on human and animal models will allow to create a comprehensive "pathogenesis map" to the subset of disease they mimic [1].

cause of bone erosion is the pannus that is found at the interface with the cartilage and bone. Angiogenesis is a key process in the formation and maintenance of pannus because invasion of cartilage and bone requires increased blood supply. In patients with RA, many pro-angiogenic factors are expressed in synovium, among them, VEGF plays the central role in new blood vessel development [17]. Cartilage degradation in RA occurs when TNF-α, IL-1, and IL-6 activate synoviocytes, resulting in the secretion of MMPs into the SF [6, 7]. Cytokines also activate chondrocytes (**Figure 1**), leading to the direct release of additional MMPs into the cartilage [7]. ROS have been produced mainly during oxidative phosphorylation and by activated phagocytic cells during oxidative burst. It has been known that ROS can function as a second messenger to activate nuclear factor kappa-B (NF-κB) which orchestrates the expression of a spectrum of genes involved in the inflammatory response. Several cytokines, including TNF-α and IL-1β, are known initiators of NF-κB activation cascade [18] and are under its transcriptional control.

*Impact of Oxidative Stress on Inflammation in Rheumatoid and Adjuvant Arthritis: Damage…*

*DOI: http://dx.doi.org/10.5772/intechopen.89480*

*Pathogenesis of cartilage and bone damage in rheumatoid arthritis. MHC, major histocompatibility complex; TCR,T-cell receptor; TACI, transmembrane activator and CAML interactor; BLyS, B-lymphocyte stimulator; RANK, receptor activator of nuclear factor κ B; RANKL, receptor activator of nuclear factor κ B ligand; TNF, tumor necrosis factor; INF, interferon; IL, interleukin; CR, complement receptor; RF, rheumatoid factor.*

**Figure 1.**

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Rheumatoid arthritis occurs due to the continuous deterioration of cells and tissues that ultimately affects major organs. Both oxidative stress (OS) and inflammation are considered major role players in the pathogenesis of RA [2]. Even if there is a lot of evidence from animal models of RA and human RA, about that OS plays an important role in tissue damage and also promotes cardiovascular diseases in patients with RA [3]; until now, a therapeutic strategy to reduce OS in RA has not yet been established. Thus, understanding how the OS is influencing the development of animal and human RA is of great importance.

In this chapter, we will discuss the importance of OS in the pathogenesis of human RA and its experimental model, rat adjuvant arthritis (AIA).
