Diseases of the periodontium occurs in the childhood, adolescence and early adulthood, but the prevalence of periodontal diseases and tissue destruction increases with age. The increase may be caused by the cumulative effect of the number of bursts of periodontal destruction, deterioration in plaque removal efficiency, or an increase in the number of teeth retained in old age and therefore affected by plaque-indltced disease. But with appropriate periodontal therapy and self-performed plaque control, older patients can be expected to have as favorable treatment outcomes as young patients.

The human inflammatory periodontal diseases are amongst the most common of chronic diseases. The predominant inflammatory cell (96%) within the healthy connective tissue and epithelium of the gingiva is polymorphonuclear leucocyte (PMNL). Periodontopathic bacteria in the gingivomucosal tissue may functionally activate PMNLs leading to an increased production of reactive oxygen species (ROS). Chronic inflammation subjects the nearby cells to elevated levels of free radicals (ROS) due to extracellular release from phagocytic cells. Antioxidants block the process of oxidation by neutralizing free radicals. In doing so, the antioxidant themselves become oxidized. Because of this, there is a constant need to replenish our antioxidant resources.

In the late 1950's free radicals and antioxidants were almost unheard of in the clinical and biological sciences but chemists had known about them for years in the context of radiation, polymer and combustion technology. Daniel Gilbert, Rebeca Gerschman and their colleagues related the toxic effects of elevated oxygen levels on aerobes to those of ionizing radiation, and proposed that oxygen toxicity is due to free radical formation.