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Aim: Periodontitis is a chronic inflammatory disease characterized by tissue destruction. Patients with diabetes mellitus are more susceptible to severe tissue destruction. Puerarin, a biological component derived from Pueraria lobate, has anti-inflammatory and anti-diabetic effects. The purpose of the study is to evaluate the protective role of puerarin on alveolar bone loss and connective tissue destruction in ligature induced diabetic and non-diabetic rats. Material and methods: Sixty rats were divided as non-diabetic control, non-diabetic-experimental periodontitis (EP)-systemic saline, non-diabetic-EP-systemic puerarin, diabetic control, diabetic-EP-systemic saline and diabetic-EP-systemic puerarin. Diabetes was induced by injection of streptozocin (200 mg/kg). EP was achieved by placing a sterile silk suture around the first molars into the gingival sulcus for 15 days. In puerarin treated groups, 200 mg/kg puerarin was applied daily for 15 days beginning one-day prior the placement of the ligature. The alveolar bone level of the first molar tooth, alveolar bone ratio in the furcation area and the attachment level were evaluated histologically. MMP-9, TIMP-1 levels and RANKL/OPG ratio were evaluated immunohistochemically. Results: Significantreduced alveolar bone and attachment losses were found in puerarin-treated groups comparing to in salineadministered groups (p<0.05). There was a significant reduction of RANKL/OPG ratio and MMP-9 levels and an increase in TIMP-1 levels in puerarin-treated groups compared with saline-administered groups during the induction of experimental periodontitis in both diabetic and non-diabetic condition (p<0.05). Conclusion: Puerarin might help to prevent alveolar bone loss and connective tissue destruction in periodontal disease in diabetic and non-diabetic condition. [ABSTRACT FROM AUTHOR]

Background: To investigate changes in the levels and relative ratios of sclerostin, osteoprotegerin (OPG), and receptor activator of nuclear factor-κB ligand (RANKL) in the gingival crevicular fluid (GCF) of patients with periodontitis after non-surgical periodontal treatment.Methods: Fifty-four individuals (27 healthy controls and 27 patients with chronic periodontitis [CP]) were enrolled in the study. Periodontitis patients received non-surgical periodontal therapy. GCF sampling and clinical periodontal parameters were assessed before and 6 weeks after therapy. Sclerostin, OPG, and RANKL levels were measured by enzyme-linked immunosorbent assay, and their relative ratios were calculated.Results: Total amounts and concentrations of sclerostin were significantly higher in patients with CP than in healthy individuals (P <0.025) and decreased after treatment (P <0.05). The RANKL/OPG ratio was significantly lower in healthy individuals than in patients with periodontitis before and after treatment (P <0.025), but no significant difference was observed in patients with periodontitis after treatment (P >0.05). The sclerostin/OPG and sclerostin/RANKL ratios were significantly lower in healthy individuals than in patients with periodontitis before and after treatment (P <0.025) and decreased in patients with periodontitis after treatment (P <0.05).Conclusions: The GCF sclerostin level may be more reliable than the RANKL/OPG ratio as a diagnostic and prognostic marker of periodontal disease and treatment outcome. Regulation of sclerostin levels may aid the development of new therapeutic strategies for the treatment of periodontal disease. [ABSTRACT FROM AUTHOR]

Background: The purpose of this study was to investigate gingival crevicular fluid (GCF) and serum folate-receptor 1 (FOLR1) levels in subjects with different periodontal status. Methods: The study consists of three groups: Healthy group (n = 15), gingivitis group (n = 15) and chronic periodontitis group (n = 15). Clinical periodontal parameters including probing pocket depth (PPD), clinical attachment level (CAL), gingival index (GI) and bleeding on probing (BOP) were assessed. GCF and serum samples were collected from each patient and were analyzed FOLR1 levels by enzyme-linked immunosorbent assay. Results: The values of FOLR1 in GCF were higher in gingivitis and periodontitis groups than among patient in control group (p < 0.016). Serum FOLR1 levels showed no significant difference between the groups. A significant correlation was observed between FOLR1 levels of GCF and BOP (p < 0.05). Conclusions: Our preliminary data suggest that FOLR1 is not useful in monitoring the periodontal disease. Further studies are necessary to clarify the role, regulation and function of folate and it's receptors in the pathogenesis of periodontal disease. [ABSTRACT FROM AUTHOR]