These findings suggest that the antioxidant capacity of GCF is both qualitatively and quantitatively distinct from that of saliva, plasma and serum. Whether changes in the GCF compartment in periodontitis reflect predisposition to or the results of ROS-mediated damage remains unclear. Reduced plasma total antioxidant defence could result from low-grade systemic inflammation induced by the host response to periodontal bacteria, or may be an innate feature of periodontitis patients.

Local total antioxidant capacity in CP appears to reflect increased oxygen radical activity during periodontal inflammation and can be restored to control subject levels by successful non-surgical therapy.

No abstract

These data demonstrate high concentrations of GSH within GCF, which are compromised in chronic periodontitis. While therapy does not appear to fully restore GSH concentrations in GCF, it does restore the redox balance (GSH:GSSG ratio), suggesting that the abnormal redox balance arises secondary to oxidative stress resulting from periodontal inflammation.

Levels of substance P, cathepsin G, interleukin-1β and neutrophil elastase act as objective biomarkers of gingival inflammation induction and resolution that typically precede phenotypical changes.