The aim of this study was to measure lipid peroxidation (as an end product of oxidative stress) and corresponding antioxidant activity in patients with periodontitis and assess the influence of smoking and periodontal treatment on these parameters. Thirty healthy subjects (including 15 smokers) were compared to periodontitis patients (n = 30, including 15 smokers). Malondialdehyde (MDA), glutathione peroxidase (GSHPx) and the total antioxidant capacity (TAOC) were recorded in saliva. The lowest level of lipid peroxidation (MDA) was measured in saliva in the non-smoking periodontally healthy subjects (0.065 +/- 0.05 micromol/l). MDA levels were significantly higher in periodontitis patients who smoked (0.123 +/- 0.08 micromol/l) compared to non-smoking controls (0.065 +/- 0.05 micromol/l; p < 0.05). The periodontally healthy subjects demonstrated significantly lower levels of GSHPx (antioxidative parameter) than the periodontitis group (p < 0.05). The TAOC flow rate (delivered antioxidant components within saliva) was significantly lower in patients with periodontitis (0.34 +/- 0.26 micromol/ml) in comparison to the controls (0.62 +/- 0.24 micromol/ml; p < 0.05). Patients with periodontitis demonstrate more lipid peroxidation than healthy subjects, and this effect is enhanced by smoking. Imbalance between oxidative stress and antioxidant capacity may play a role in the pathogenesis of periodontal disease. Non-surgical periodontal treatment leads to a reduction of MDA and GSHPx to levels comparable to healthy controls.

The present results show that metronidazole and clindamycin are effective antibiotics when used adjunctively in a 2-step nonsurgical procedure of scaling and root planing in RPP patients.

This study demonstrated that the photodynamic therapy using photosensitizer and a 662 nm laser light source is distinctly advantageous in reducing the periodontal signs of redness and bleeding on probing. The procedure also appears to significantly suppress P. gingivalis.

The data collected to date suggest that photodynamic therapy with chlorin e6 and BLC 1010 is advantageous for suppressing periodontopathogenic bacteria.

AIM The aim of this in vitro study was to study phagocytosis and killing of Porphyromonas gingivalis ATCC 33277 and Aggregatibacter actinomycetemcomitans Y4 by peripheral blood PMNs taken from aggressive and chronic periodontitis patients. Also, the release of reactive oxygen species (ROS) and human neutrophil elastase (HNE) upon the interaction of PMNs with bacteria was measured. METHODS Peripheral blood PMNs obtained from 12 chronic periodontitis patients, 6 aggressive periodontitis patients and 12 healthy controls were exposed to Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans following opsonisation of the bacteria using the patient’s own serum. Phagocytosis and killing of the bacteria as well as the extracellular HNE activity were quantified for up to 2 hours. The total amount and the extracellular release of ROS were measured by luminol and isoluminol dependent chemiluminescence. RESULTS PMNs from chronic (62.16 ± 19.39 %) and aggressive periodontitis (43.26 ± 26.63 %) patients phagocytosed more P. gingivalis than the healthy controls (24.43 ± 19.87 %) at 30 mins after exposure to the bacteria (p < 0.05). PMNs from subjects with chronic and aggressive periodontitis released significantly more ROS and demonstrated greater HNE activity in the absence of any stimulus than PMNs from healthy controls (p < 0.05). The total release of ROS increased in chronic periodontitis PMNs and in the control group PMNs after interaction with P. gingivalis. The interaction with A. actinomycetemcomitans resulted in greater total ROS release in chronic periodontitis PMNs and in the control group PMNs than P. gingivalis. CONCLUSION PMNs in aggressive and chronic periodontitis are hyperactive even without any particular stimulus. The extracellular release of ROS and neutrophil elastase by PMNs may not only affect bacterial virulence and/or viability, but also contribute to damage of the surrounding periodontal tissues.