Rheumatoid arthritis ( RA) is among the most prevalent autoimmune diseases (1-3 % worldwide). RA is a prototypic inflammatory disease, characterized by a changed homeostasis state in which immunological stimulation and unwanted inflammation take precedence. The disordered inflammation has painful and deteriorating immediate effects while causing accumulated tissue damage that could contribute to symmetric polyarthritis leading to lifelong discomfort, impairment and shorter life expectancy. RA is affected by genetic and environmental influences, smoking, diet, obesity, microbiota, and infections were suggested induced illness in individuals genetically prone. The clinical representation of RA is the product of a cascade of responses and close interactions between immune and non-immune cells (e.g., endothelial and fibroblast-like synoviocytes), autoantibodies, soluble mediators such as cytokines and chemokines, and signal transduction pathways of the innate and adaptive immune system. Different immune system players include neutrophils, macrophages, B cells, natural killer ( NK ) cells, and T cells migrate to the synovial membrane and accumulate in the synovial fluid, resulting in the release of mediators such as cytokines, chemokines, adhesion molecules, matrix metalloproteinases ( MMPs) and reactive oxidative species ( ROS) which result in joint destruction.