Literature DB >> 24677171

Salivary DNA and markers of oxidative stress in patients with chronic periodontitis.

Lenka Baňasová1, Natália Kamodyová, Katarína Janšáková, Ľubomíra Tóthová, Peter Stanko, Ján Turňa, Peter Celec.   

Abstract

OBJECTIVES: Previous observational studies have shown that periodontal status is associated with salivary markers of oxidative damage. A direct comparison of periodontitis patients and controls using a wide palette of salivary markers of oxidative stress is lacking. Characteristics of salivary DNA in periodontitis are unknown. The aim of this study was to compare the salivary markers of oxidative stress and characteristics of salivary DNA between patients with chronic periodontitis and periodontitis-free controls.
MATERIALS AND METHODS: Saliva was collected from 23 patients with chronic periodontitis and 19 periodontitis-free controls. All participants underwent a clinical periodontal examination. Markers of oxidative and carbonyl stress were measured in saliva. Human and bacterial DNA was quantified, and human DNA integrity was assessed.
RESULTS: Salivary thiobarbituric acid-reacting substances were higher in patients than in controls; at least in men, the difference was significant (p < 0.01). In women, patients had significantly lower salivary antioxidant status (p < 0.001). No quantitative differences were found regarding salivary DNA. Tendencies towards reduced DNA integrity were found in periodontitis patients.
CONCLUSIONS: The results confirmed the association of salivary thiobarbituric acid-reacting substances with periodontitis. Lipid peroxidation in periodontitis seems to be caused by increased production of reactive oxygen species in men and by decreased antioxidant status in women. Whether lower salivary DNA integrity is involved in the pathogenesis of periodontitis remains to be elucidated. CLINICAL RELEVANCE: Salivary thiobarbituric acid-reacting substances are associated with periodontitis at least on a population level. Sex-specific causes of lipid peroxidation might point towards different pathogenic mechanisms.

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Year:  2014        PMID: 24677171     DOI: 10.1007/s00784-014-1236-z

Source DB:  PubMed          Journal:  Clin Oral Investig        ISSN: 1432-6981            Impact factor:   3.573


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