Receptor activator of NF-kappaB ligand (RANKL) and CD 31 expressions in chronic periodontitis patients before and after surgery.

AIM OF THE STUDY: The present study investigated the hypothesis that upregulation of receptor activator of NF-kappaB ligand (RANKL) expression may be associated with upregulation of endothelial cell activitiy, which is common for periods of periodontal bone loss in chronic periodontitis. MATERIAL AND METHODS: RANKL expression of activated cells in soft tissue biopsies with CD 31 activity and the presence of RANKL and osteoprotegerin (OPG) in gingival crevicular fluid (GCF) were assessed in chronic periodontitis patients. Biopsies from 17 patients and 10 healthy subjects were immunohistochemically analyzed. Clinical measurements [plaque index (PI), the gingival index (GI), probing pocket depth (PPD), clinical attachment level (CAL) and gingival bleeding index (GBI)] and GCF samples were obtained before and after periodontal therapy. RESULTS: CD31 staining did not support the assumption that endothelium-like cells were predominantly associated with RANKL expression. CONCLUSIONS: RANKL-positive cells were widely distributed in periodontitis patients giving only partial support to the hypothesis that RANKL expression is restricted to T- and B-cell activation.

Short term effects of non-surgical periodontal treatment on gingival crevicular fluid levels of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 2 (PAI-2) in patients with chronic and aggressive periodontitis.

OBJECTIVE: The purpose of this study was to evaluate the gingival crevicular fluid (GCF) levels of tissue type plasminogen activator (t-PA) and plasminogen activator inhibitor 2 (PAI-2) in aggressive periodontitis (AgP), chronic periodontitis (CP) and periodontally healthy control subjects, before (BT) and after (AT) the non-surgical periodontal treatment. DESIGN: Systemically healthy 12 CP and 13 AgP patients and 20 control subjects were included in this study. Plaque index, gingival index, probing depth and clinical attachment levels were recorded and GCF samples were collected BT and AT. Assays for GCF t-PA and PAI-2 levels were carried out by an enzyme linked immunosorbent assay (ELISA). The χ(2), Wilcoxon and Mann-Whitney U tests and Spearman correlation coefficient were used for data analyses. RESULTS: Statistically significant reductions in clinical index scores were noted in both periodontitis groups after treatment. No significant differences were detected in GCF levels of t-PA and PAI-2 between CP and AgP groups at either BT or AT. There was a statistically significant decrease in GCF PAI-2 levels in CP after therapy (p<0.01). GCF t-PA levels in CP and AgP groups exhibited significant correlations with PD and CAL measurements at both BT and AT (p<0.01). CONCLUSION: Significant decrease was detected for GCF PAI-2 levels in CP and clinical parameters in both CP and AgP by non-surgical periodontal treatment.

Lactoferrin in Gingival Crevicular Fluid and Peripheral Blood during Experimental Gingivitis.

OBJECTIVES: Lactoferrin (LF) is an iron binding protein and stored in the specific granules of granulocytes. It is released by degranulation following granulocyte activation. A positive correlation was previously reported between periodontitis and LF titers of gingival crevicular fluid (GCF) and blood. The purpose of this study was to examine alterations of GCF and blood levels of LF (LF-GCF and LF-BL, respectively), employing the experimental gingivitis model. METHODS: Twelve systemically healthy volunteers, aged 19-21, were selected. Pre-experimental phase of hygiene was followed by a 14-day experimental gingivitis phase in which subjects refrained from all oral hygiene procedures. After that subjects resumed optimal plaque control for 21 days of recovery period. At days 0 (baseline), 14 and 35 gingival crevicular fluid (GCF) and blood samples were collected and plaque index (PI), gingival index (GI), bleeding on probing (BOP) and probing pocket depth scores were recorded. LF levels were measured with commercial enzyme-linked immunosorbent assay (ELISA) kit. RESULTS: PI, GI, BOP and LF-GCF increased significantly after 14 days of experimental gingivitis period and decreased significantly after reinstitution of oral hygiene measures (P<.05). LF-BL appeared to follow the same pattern. Significant negative correlation was detected between the level of LF-BL and BOP at day 14 (P<.05), whereas significant positive correlation was noticed between LF-BL and clinical scores PI, GI and BOP at day 35 (P<.05). CONCLUSIONS: LF-BL followed the same pattern with LF-GCF and clinical scores during the experimental gingivitis and recovery periods, although alterations of the LF-BL appeared statistically insignificant.

Effects of phase I periodontal treatment on gingival crevicular fluid levels of matrix metalloproteinase-3 and tissue inhibitor of metalloproteinase-1.

OBJECTIVES: The aim of this study was to evaluate the effects of phase I periodontal treatment on gingival crevicular fluid (GCF) levels of matrix metalloproteinase (MMP)-3 and tissue inhibitors of metalloproteinase (TIMP)-1. METHODS: Plaque index, gingival index, pocket depth and clinical attachment loss were recorded and GCF samples were collected from 20 chronic periodontitis (CP) patients and 20 periodontally healthy controls (C) before treatment. CP patients received phase I periodontal treatment and all clinical parameters were recorded and GCF samples were collected once more after treatment. Assays were performed by an enzyme-linked immunosorbent assay. RESULTS: All of the clinical parameters improved significantly after the therapy (p<0.05). Baseline GCF levels of MMP-3 were significantly higher than C and that level was reduced significantly by treatment compared with baseline levels (p<0.05). Baseline GCF levels of TIMP-1 were lower than post-treatment levels and C (p<0.05). GCF levels of TIMP-1 increased significantly by treatment compared with baseline levels (p<0.05). CONCLUSION: This study shows that the clinical improvements after phase I periodontal therapy are accompanied by reduction in MMP-3 and increasing in TIMP-1 GCF levels.