The effect of periodontal treatment on serum leptin, interleukin-6, and C-reactive protein.

BACKGROUND: Previous studies suggest that periodontitis is closely related to obesity and metabolic syndrome. Leptin, a pleiotrophic hormone produced by adipose tissue, has been reported to be related to periodontitis. This study investigates the effects of periodontal treatment on the serum levels of leptin and other cytokines in patients with chronic periodontitis (CP). METHODS: Serum samples were taken from 33 CP patients (22 non-smokers, 11 smokers) and 18 healthy subjects. The serum leptin, adiponectin, tumor necrosis factor-alpha, interleukin (IL)-6, and C-reactive protein (CRP) levels were measured before and after non-surgical periodontal treatment. RESULTS: Significant differences between healthy and CP patients were found in serum leptin, IL-6, and CRP levels (P = 0.0018, P = 0.0064, and P = 0.0095, respectively). The serum leptin level was associated with mean probing depth, mean clinical attachment level, mean alveolar bone loss, and body mass index. There were significant associations between serum leptin levels and IL-6 and CRP levels. After non-surgical periodontal treatment, serum leptin, IL-6, and CRP levels were significantly decreased (mean +/- SD before and after, P value, respectively: leptin, 8.02 +/- 5.5, 7.10 +/- 4.4, P = 0.015; IL-6, 1.73 +/- 1.02, 1.36 +/- 0.73, P = 0.048; and CRP, 802.0 +/- 1065, 491.2 +/- 479.3, P = 0.047). CONCLUSIONS: Periodontal treatment is effective in reducing serum leptin, IL-6, and CRP levels. The results suggest that leptin, IL-6, and CRP could be mediating factors that connect metabolic syndrome and periodontitis.

Effects of ascorbic acid on gingival melanin pigmentation in vitro and in vivo.

BACKGROUND: Gingival melanin pigmentation may cause esthetic concerns, even if no serious medical problem is present. As an inhibitor of melanin formation, ascorbic acid is often used to treat skin melanin pigmentation. Thus, the present study investigated the effects of ascorbic acid on gingival melanin pigmentation in vitro and in vivo. METHODS: The effects of ascorbic acid on melanin formation were evaluated in vitro in B16 mouse melanoma cells and three-dimensional human skin models. In addition, a clinical trial was performed to investigate the inhibitory effects of a gel containing ascorbic acid 2-glucoside (AS-G gel) on gingival melanin pigmentation. This study used a double-masked, split-mouth design on 73 subjects with symmetric gingival melanin pigmentation. AS-G gel was applied to one side of the gingiva for 12 weeks, whereas placebo gel was applied to the other side as a control. Luminance (L*)-value, which describes the lightness of gingiva, was determined by spectrophotometry to obtain an objective measure of melanin pigmentation every 4 weeks. RESULTS: Ascorbic acid significantly inhibited tyrosinase activity and melanin formation in B16 mouse melanoma cells (P <0.01 and P <0.05, respectively). The inhibitory effects of ascorbic acid on melanin formation were also significant in three-dimensional human skin models (P <0.01). Moreover, in the clinical trial, a significant relative change in pigmentation was seen after 4 weeks with the application of AS-G gel compared to placebo (L*-value ratio). CONCLUSION: Ascorbic acid (AS-G) has potential for the treatment of gingival melanin pigmentation.

Effects of treatment on soluble tumour necrosis factor receptor type 1 and 2 in chronic periodontitis.

AIM: We reported that soluble tumour necrosis factor receptor type 2 (sTNFR2)/type 1 (sTNFR1) ratios in gingival crevicular fluid (GCF) decreased as the severity of chronic periodontitis (CP) increased. This study investigated the effects of the periodontal treatment on TNF-alpha, sTNFR1 and R2 in GCF and serum of CP patients. MATERIAL AND METHODS: Thirty-five serum and 90 GCF samples were obtained from 35 CP patients (23 non-smokers and 12 smokers) at baseline and after treatment. The levels of TNF-alpha, sTNFR1 and R2 in serum and GCF were quantified by enzyme-linked immunosorbant assay. RESULTS: No significant differences were found in the serum levels of TNF-alpha, sTNFR1 and R2 and the ratio of sTNFR2/R1 between baseline and after treatment. After treatment, sTNFR1 and R2 levels in GCF of non-smokers and smokers were significantly decreased compared with baseline. However, the sTNFR2/R1 ratio was significantly increased (non-smoker: 0.56+/-0.03-0.84+/-0.03, p<0.0001; smoker: 0.59+/-0.06-0.85+/-0.04, p=0.0019). There were no significant differences between non-smoking and smoking CP groups in serum and GCF. CONCLUSION: The ratio of sTNFR2/R1 in GCF significantly increased after treatment, and could be related to the clinical state of CP.