The Effect of Melatonin on Periodontitis.

BACKGROUND: Periodontitis is a chronic disease with a complex etiology that includes bacterial colonization, excessive inflammation, and oxidative stress. The hormone melatonin has antioxidant properties and might contribute to alleviating chronic conditions by reducing oxidative stress. The aim of this study was to analyze the effect of exogenous melatonin on periodontitis in an animal model of the disease as well as in patients with periodontitis. METHODS: In rats with ligature-induced periodontitis, melatonin was administered in drinking water for two weeks. In the human study, patients with treatment-resistant periodontitis were asked to rinse their mouths with a solution containing melatonin or placebo every evening for two weeks. Periodontal status as well as salivary markers of oxidative stress were assessed at the end of the study. RESULTS: Neither radiography nor µCT revealed any significant effects of melatonin on alveolar bone loss. Gum recession was the only improved macroscopic measure in rats (p < 0.05). Analysis of salivary markers of oxidative stress revealed no effects of treatment in rats or humans despite clearly elevated melatonin concentrations in melatonin treated groups. CONCLUSION: Our results do not support the use of melatonin for the treatment of periodontitis. However, the negative outcome is limited by the short duration of the study and the chosen route of application as well as the dose of melatonin.

Blood Contamination in Saliva: Impact on the Measurement of Salivary Oxidative Stress Markers.

Salivary oxidative stress markers represent a promising tool for monitoring of oral diseases. Saliva can often be contaminated by blood, especially in patients with periodontitis. The aim of our study was to examine the impact of blood contamination on the measurement of salivary oxidative stress markers. Saliva samples were collected from 10 healthy volunteers and were artificially contaminated with blood (final concentration 0.001-10%). Next, saliva was collected from 12 gingivitis and 10 control patients before and after dental hygiene treatment. Markers of oxidative stress were measured in all collected saliva samples. Advanced oxidation protein products (AOPP), advanced glycation end products (AGEs), and antioxidant status were changed in 1% blood-contaminated saliva. Salivary AOPP were increased in control and patients after dental treatment (by 45.7% and 34.1%, p < 0.01). Salivary AGEs were decreased in patients after microinjury (by 69.3%, p < 0.001). Salivary antioxidant status markers were decreased in both control and patients after dental treatment (p < 0.05 and p < 0.01). One % blood contamination biased concentrations of salivary oxidative stress markers. Saliva samples with 1% blood contamination are visibly discolored and can be excluded from analyses without any specific biochemic detection of blood constituents. Salivary markers of oxidative stress were significantly altered in blood-contaminated saliva in control and patients with gingivitis after dental hygiene treatment.

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

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.

Salivary markers of oxidative stress in patients with oral premalignant lesions.

The aetiology of oral premalignant lesions is unknown. Oxidative stress is associated with inflammation and cancerogenesis. The aim of our study was to compare salivary markers of oxidative and carbonyl stress in patients with oral premalignant lesions and age-matched healthy controls. Unstimulated saliva samples were collected from 16 patients with oral premalignant lesions (leukoplakia, lichen planus, erythroplakia) and 16 age-matched healthy controls. Biochemical analysis included measurement of thiobarbituric acid reacting substances (TBARS), advanced oxidation protein products (AOPP), advanced glycation endproducts (AGEs) and total antioxidant capacity (TAC). Salivary RNA was analyzed using real time PCR. Salivary TBARS and AGEs were significantly higher in patients than in controls. No differences were found in AOPP. TAC and expression of superoxide dismutase were lower in patients than in age-matched controls. Other analyzed transcripts (vascular endothelial growth factor, sialotransferase, neuraminidase) did not differ between patients and the control group. Markers of lipoperoxidation and carbonyl stress were increased in patients with oral premalignant lesions. Decreased antioxidant status potentially due to decreased expression of antioxidant enzymes might be responsible for these findings. Our results might point to the aetiology or pathogenesis of oral premalignant lesions as well as to the mechanism of transition to oral carcinoma.