Abstract
BACKGROUND: Superoxide dismutase (SOD), an antioxidant acting against superoxide (oxygen radical, O2.-), it is released in inflammatory pathways and causes connective tissue breakdown. Increased SOD activity in inflamed gingiva may indicate increased O2.-radical generation by neutrophils and other inflammatory cells at the diseased site. The aim of the study was to evaluate the effects of non-surgical periodontal therapy (NSPT) on SOD levels in gingival tissues of chronic periodontitis patients.METHODS: Forty subjects: 20 periodontally healthy (Control) and 20 chronic periodontitis (Test); age range 24–55 years were recruited. Gingival tissue samples were collected by excising the inner lining of the periodontal pocket at baseline (prior to non-surgical periodontal therapy) and 2 months post therapy. In controls, tissue samples were obtained immediately after tooth extraction scheduled for orthodontic reasons. Clinical parameters included probing depth, clinical attachment level, gingival index, bleeding index, plaque index. SOD activities were assessed spectrophotometrically at baseline and 2 months post NSPT, results were analysed statistically.RESULTS: At baseline, patients with chronic periodontitis had higher mean SOD activity (2.73 ± 1.36) than the control subjects (1.12 ± 1.13) withp= 0.00003 (p< 0.05). At 2 months post NSPT median SOD level (1.00) had come close to median SOD value of control group (0.85);p= 0.99 (p> 0.05). The resolution of inflammation with successful NSPT resulted in decreased SOD levels as in control group. Clinical parameters in patients with chronic periodontitis showed a significant improvement 2 months post NSPT (p< 0.05).CONCLUSION: Non-surgical periodontal therapy significantly improves the clinical parameters and restores previously increased SOD levels to normal in chronic periodontitis patients.
Highlights
Chronic periodontitis (CP) is initiated by sub-gingival biofilm
The present study evaluated the effect of non-surgical periodontal therapy (NSPT) on clinical parameters and gingival Superoxide dismutase (SOD) activity in chronic periodontitis patients compared with systemically healthy individuals
There was a significant reduction in clinical parameters (PI, Gingival Index (GI), Gingival bleeding Index (GBI), pocket depth (PD) and clinical attachment level (CAL)) after 2 months post NSPT
Summary
Chronic periodontitis (CP) is initiated by sub-gingival biofilm. the progression of destructive disease appears to be dependent upon abnormal host response to the biofilm organisms [1]. The aim of the study was to evaluate the effects of non-surgical periodontal therapy (NSPT) on SOD levels in gingival tissues of chronic periodontitis patients. Gingival tissue samples were collected by excising the inner lining of the periodontal pocket at baseline (prior to non-surgical periodontal therapy) and 2 months post therapy. SOD activities were assessed spectrophotometrically at baseline and 2 months post NSPT, results were analysed statistically. RESULTS: At baseline, patients with chronic periodontitis had higher mean SOD activity (2.73 ± 1.36) than the control subjects (1.12 ± 1.13) with p = 0.00003 (p < 0.05). Clinical parameters in patients with chronic periodontitis showed a significant improvement 2 months post NSPT (p < 0.05). CONCLUSION: Non-surgical periodontal therapy significantly improves the clinical parameters and restores previously increased SOD levels to normal in chronic periodontitis patients
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
