The role of local and peripheral antioxidants in the pathogenesis of chronic Periodontitis in smokers

Abstract

Chronic periodontitis is one of the most common chronic inflammatory diseases of man and accounts for 60% of tooth loss. It is initiated by the subgingival biofilm and in susceptible individuals an abnormal inflammatory-immune response fails to resolve the inflammation and leads to destruction of the supporting tissues and the teeth. Risk factors for periodontitis may be systemic or local and of the systemic risk factors the most significant is smoking. Periodontitis patients appear to express a hyper-inflammatory phenotype involving excess or prolonged production of enzymes and reactive oxygen species (ROS) from cells of the innate immune response (primarily neutrophils). Neutrophil hyper-reactivity and hyperactivity, with respect to ROS production, has been demonstrated by several authors. Consistent with the exaggerated ROS production is the depletion of antioxidant defences against ROS within the periodontal pockets. Cigarette smoke is also reported to increase the oxidative burden and deplete antioxidant defences, but no data are available on gingival crevicular (GCF) antioxidant levels in smokers compared to non-smokers. This thesis explores the total antioxidant capacity (TAOC) of GCF and plasma in smokers and non-smokers with periodontitis and analyses the impact of smoking on the outcomes of periodontal therapy and upon local and peripheral antioxidant status in both groups. The working hypothesis is that an important mechanism underpinning the increased prevalence of periodontitis in smokers involves reduction of antioxidant defences due to smoking and thus increased oxidative stress and tissue damage. The cross-sectional data presented here suggest that smokers with periodontitis have a further compromise in GCF TAOC compared to age-, gender- and disease-matched non-smokers with periodontitis. The longitudinal data presented within this thesis suggest that the compromised GCF TAOC concentration seen in periodontitis irrespective of smoking status is likely to result from the inflammatory lesion, rather than predisposing to it. Moreover, the impact of the periodontal inflammation upon TAOC compromise appears more dominant than the effects of smoking