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Inter-Individual Variation in Saliva Antioxidant Status in Relation to Periodontal Disease

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posted on 06.05.2011, 12:06 by Dean Vincent Sculley
Free radicals have been implicated in the aetiology of many human disease states, including periodontal disease (PD). Saliva contains an array of antioxidants that neutralise the harmful effects of free radical formation within the oral cavity. Increased salivary antioxidant capacity may limit oxidative tissue damage and improve the health of the gingival tissues. In this thesis, the antioxidant profile of saliva was assessed in relation to PD severity. Salivary protein carbonyl concentration was assessed as a biomarker of oxidative tissue damage. Urate, ascorbate and albumin contributed 85% of the total scavenging antioxidant capacity (TAA) which followed a diurnal rhythm (peak 5.00pm, nadir 3.00am). Salivary antioxidant flow rate was significantly lower in individuals with severe PD (TAA 0.210 f 0.02 μM/ml/min) than those with healthy gingivae (TAA 0.270 ± 0.02 PM/ml/min) (p<0.05). Oxidative injury was greater in the group with severe PD (protein carbonyls = 25.43 ± 11.09 fmoles/g protein) compared to the healthy group (7.77 ± 2.38 fmoles/g protein) (p<0.05). Individuals with low salivary TAA were 4.5 times more likely to suffer severe PD. TAA in males (654 ± 25 gWral/min) was significantly higher than in females (545 ± 23 pWml/min) (p=0.002), but no relationship was noted between sex and periodontal health. TAA and urate flow rates followed the same monthly cyclical pattern as progesterone and ß-estradiol in women. Nutritional antioxidant supplementation was found to have little effect on salivary antioxidant status with only a transient increase in ascorbate evident. These data suggest that severe PD is associated with a decreased salivary antioxidant flow rate and increased oxidative injury. In addition, dietary antioxidant supplementation does not appear to increase salivary antioxidant status as it does in plasma. Toothpastes and mouthrinses containing antioxidants may reduce the extent of oxidative injury in vivo, with more research required in this area.



Langley-Evans, Simon

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University of Leicester

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