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.

Endocan and TNF-α levels, both in GCF and serum, increased from health to periodontitis and decreased with non-surgical periodontal treatment. Within the limits of the study, endocan may be considered as a potential inflammatory marker for periodontal disease.

The purpose of this study was to evaluate visfatin levels at different stages of periodontal disease and in healthy tissues. In addition, the effect of non-surgical periodontal therapy on visfatin levels in gingival crevicular fluid and serum was investigated. Forty-five patients were divided into three groups based on clinical and radiographical findings. Group 1 comprised periodontally healthy individuals (n = 15); group 2 comprised patients with gingivitis (n = 15); and group 3 was composed of patients with generalized chronic periodontitis (n = 15). Gingival crevicular fluid and serum samples were collected before treatment and at 1, 3, and 6 months after treatment. Visfatin levels were measured by enzymelinked immunosorbent assays. Gingival crevicular fluid and serum visfatin levels were higher in patients with chronic periodontitis than those with gingivitis or healthy controls (P < 0.016). In addition, visfatin levels were higher in the gingivitis group than in healthy controls (P < 0.016). Non-surgical periodontal treatment resulted in a significant reduction in gingival crevicular fluid and serum visfatin levels.

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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.