The aetiopathogenesis of periodontal diseases is initiated by microbial biofilm which could lead to a hyperinflammatory status in aggressive forms of the disease; and cause an imbalance in the redox status, resulting in oxidative stress-induced damage. There is increasing documentation of the link between periodontal and other inflammatory diseases driven by a pro-oxidant profile. This could impose a significant systemic loading of reactive oxygen species relevant to metabolic, arthritic, age related and neoplastic diseases. They demonstrate similar markers of risk / oxidative stress induced injury during disease progression which abate in response to treatment. In certain aggressive forms of periodontal diseases resulting in a substantial systemic pro-oxidant profile, the co-existence of systemic diseases with a similar inflammatory pathogenesis could lead to progressive tissue / organ damage fuelled by the same process. Some of the common mechanisms involved are discussed, relevant to periodontal, metabolic and rheumatoid diseases, pregnancy and the foetus, age related changes and certain neoplasias which have been recently linked to periodontal disease progression. In view of a distinct pro-oxidant profile in severe cases there may a role for selective use of antioxidant adjuncts with suitable therapeutic targeting. It is relevant that periodontal diseases are associated with the above diseases and a small but significant overall cancer risk which persists in non-smokers. Periodontal disease may be a useful marker of a susceptible immune system, or directly affect the progression of systemic diseases due to inflammatory loading. Formulation of therapeutic agents shown to have efficacy in this context, with accurate targeting is a challenge.
Keywords: Periodontitis, systemic diseases, oxidative stress, lipid peroxidation, risk markers, antioxidants, therapeutic targets