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Introduction: Antioxidant agents such as cocoa could have some benefits in treatment of inflammation including periodontitis. The aim of this study was to investigate the effects of cocoa consumption on moderate chronic periodontitis. Materials &Methods: This single-blind randomized clinical trial study was performed on 40 subjects who were randomly divided into two groups. Treatment group received 30 gr dark chocolate (78% cocoa) and control group received 22.5 gr white chocolate three times a day for 4 weeks. Saliva samples were collected from patients at baseline and t wenty-eight days after eating chocolate. Probing pocket depth (PPD), Gingival index (GI, Silness and Loe), Modified papillary bleeding index (MPBI, Barnett), Clinical attachment loss (CAL) were recorded at baseline and 2nd, 4th, 6th, 8th weeks later in ramfjord teeth. Total antioxidant capacity (TAC) and lipid peroxidation of saliva were estimated by Ferric reducing antioxidant power (FRAP) and Tiuborbituric acid reactive substances ( TBARS ) methods. Data of clinical parameters were analyzed using t-test and repeated measures test. Biochemical parameters were analyzed using t-test. Results: Intra-group comparison of clinical parameters demonstrated significant decrease in both groups (p

Background: Cyclosporine A (CsA) is a potent immunosuppressant drug with therapeutic and toxic actions. The use of CsA is limited by its toxicity. Several researchers had proposed that oxidative stress could play an important role in CsA-induced toxicity. Arbutin has recently been shown to possess antioxidative and free radical scavenging abilities. The present study was designed to investigate the in vivo effects of arbutin on lipid peroxidation and antioxidant capacity in the serum of cyclosporine treated rats. Methods: Adult male Wistar rats were divided into six groups (n=8/group): (I) control (no CsA and arbutin administration), (II and III) were treated subcutaneously (Sc) with arbutin (50,100 mg/kg/bw), respectively, (IV) administered CsA (25 mg/kg/bw) intraperitoneally (IP), (V and VI) received the combination of CsA (25 mg/kg/bw) i.p and arbutin (50,100 mg/kg/bw) Sc daily, respectively. At the end of the treatment (after3 weeks), serum lipid peroxidation was measured by thiobarbituric acid-reacting substances (TBARS) and serum total antioxidant capacity (ferric reducing ability of plasma [FRAP]) was assayed based on spectrophotometric method. Results: TBARS had been significantly increased by CsA administration compared with control rats. Arbutin (50mg/kg/bw) completely prevented this effect, but arbutin (100 mg/kg/bw) alone or in combination with CsA significantly increased lipid peroxidation compared with controls. Conclusion: Our data indicate that arbutin (50mg/kg/bw) had protective effect in the CsA-induced toxicity but high concentration of arbutin (100mg/kg/bw) showed meaningful oxidative and lipoperoxidative effects.