Free radicals are widely recognized as overloaded atoms, molecules or compounds that become unstable when lacking an electron; they steal an electron from various macromolecules (eg DNA, RNA, proteins) to chemically stabilize, while preferred targets remains polyunsaturated fatty acids in their membranes. When electron theft produces a chain reaction, normal cell processes turn into a real chaos that ultimately degrades the normal functioning of the cell. Variance of free radicals existing or formed in nature as a result of many processes (ultraviolet radiation, gamma, action specific particles, etc.) makes extremely difficult their classification. A partof the oxygen molecules (O2) that have entered the body through breathing is divided and oxygen atoms become reactive (free radicals) damaging the cell wall by oxidation. Oxidative stress, a term widely used to characterise inflammatory disorders caused by destructive oxygen molecules called free radicals, may exacerbate inflammation and impair immune system response due to free radicals. Oxidative stress is defined as the imbalance between oxidants and antioxidants, in favour of oxidants, with destructive and pathogenic potential. Depending on intensity, oxidative stress can occur inside or outside the cell. Intracellular stress can lead to cell necrosis or a more or less marked disruption of the cell, and may be catastrophic in the case of a non-reproducible cell; the extracellular oxidative stress is cytotoxic. Although considered in the pathobiology of several inflammatory immune-mediated rheumatic conditions, the exact role of oxidative stress in ankylosing spondylitis is still debatable.