Double-application of platelet-rich plasma on bone healing in rabbits.

OBJECTIVE: Platelet-rich plasma (PRP) is considered to enhance bone formation especially at early stages of wound healing, depending on the limited and short life-span of platelets and growth factors. The aim of this study was to evaluate efficacy of double-application of PRP (DA-PRP) on bone healing in a rabbit calvarial defect model. STUDY DESIGN: Twenty-eight rabbits, each had two surgically prepared calvarial bone defects (10mm diameter), were included in this study and randomly divided into six groups. Defects (n=56) were treated with single-application of PRP (SA-PRP)(n=10), SA-PRP and beta-tricalciumphosphate (SA-PRP+TCP)(n=10), DA-PRP (n=8), DA-PRP and beta-tricalciumphosphate (DA-PRP+TCP)(n=8), beta-tricalciumphosphate (TCP)(n=10) or left empty (Control)(n=10). Animals were sacrificed at 30 days postoperatively. RESULTS: The new bone (NB%) and defect fill (DF%) percentages were calculated from histological slides by image-analyzer software and statistically analysed. All test groups showed higher NB% than control, but differences among all groups were insignificant. The TCP treated groups had significantly higher DF% than groups treated without TCP, however the DF% differences between control, SA-PRP and DA-PRP or TCP, SA-PRP+TCP or DA-PRP+TCP were insignificant. CONCLUSION: Although new bone formation was histomorphologically remarkable at double-application PRP groups, statistical analyses of the histomorphometric data revealed no significant difference.

GCF MMP-8 levels in smokers and non-smokers with chronic periodontitis following scaling and root planing accompanied by systemic use of flurbiprofen.

BACKGROUND: Cigarette smoking has been identified as an important risk factor for the initiation and progression of chronic periodontitis (CP). The aim of this study was to investigate the effects of phase I periodontal therapy and adjunctive flurbiprofen administration on matrix metalloproteinase (MMP)-8 levels in gingival crevicular fluid (GCF) samples from smoking and non-smoking patients with CP. METHODS: Twenty-nine non-smoking and 29 smoking patients with CP were divided into four groups according to periodontal treatment modalities. Group 1 (non-smokers with CP) and group 3 (smokers with CP) patients received daily 100-mg flurbiprofen tablets in a 2 x 1 regimen for 10 days together with scaling and root planing (SRP). Patients in group 2 (non-smokers with CP) and group 4 (smokers with CP) received placebo tablets in a 2 x 1 regimen for 10 days together with SRP. Plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) measurements were recorded; GCF samples were collected from each sampling area at baseline and after the 10-day period of drug intake by a single examiner who was unaware of the treatment modality. Assays for GCF MMP-8 were carried out by an enzyme-linked immunosorbent assay. RESULTS: All groups showed statistically significant reductions in PI and GI scores following the phase I periodontal treatment (P < 0.05), but no statistical differences were observed in PD and CAL scores after therapy. In all groups, the reduction of GCF MMP-8 levels after therapy was statistically significant compared to baseline levels (P < 0.001). When groups 1 and 3 and 2 and 4 were compared according to GCF MMP-8 levels after the therapy, no statistically significant differences were observed (P = 0.117 and P = 0.485, respectively). CONCLUSION: Flurbiprofen administration had no additional inhibitory effect over SRP alone on GCF levels of MMP-8 in smokers compared to non-smokers with CP.

Gingival crevicular fluid prostaglandin E(2) and thiobarbituric acid reactive substance levels in smokers and non-smokers with chronic periodontitis following phase I periodontal therapy and adjunctive use of flurbiprofen.

BACKGROUND: It has been established that smoking is an important risk factor for the initiation and progression of chronic periodontitis (CP). This study investigates the effects of phase I periodontal therapy and adjunctive flurbiprofen administration on prostaglandin E(2) (PGE(2)) and thiobarbituric acid reactive substance (TBARS) levels in gingival crevicular fluid (GCF) samples from smoker and non-smoker patients with CP. METHODS: Twenty-one non-smoker and 21 smoker patients with CP were divided into four groups according to treatment modalities. Group 1 (non-smokers with CP) and group 3 (smokers with CP) patients received daily 100-mg flurbiprofen tablets in a 2 x 1 regimen for 10 days together with scaling and root planing (SRP). Patients in group 2 (non-smokers with CP) and group 4 (smokers with CP) received placebo tablets in a 2 x 1 regimen for 10 days together with SRP. Plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) measurements were recorded and GCF samples were collected at baseline and on day 10 of drug intake from each sampling area by a single examiner who was unaware of the treatment modality. Assays for GCF PGE(2) and TBARS were carried out by an enzyme-linked immunosorbent assay and fluorometric method, respectively. RESULTS: All groups showed statistically significant reductions in PI and GI scores following the phase I periodontal treatment on day 10 (P <0.05), but no statistical differences were observed in PD and CAL scores after the therapy. In groups 1 and 2, the reduction of GCF PGE(2) and TBARS levels were not significant after the therapy compared to baseline levels. In group 3, GCF PGE(2) and TBARS levels exhibited a statistically significant decrease (P <0.05) after the therapy. Group 4 showed significant reductions (P <0.05) in GCF PGE(2) levels after the therapy. No statistically significant reductions were observed in group 4 with regard to GCF TBARS levels. When groups 1 and 3 were compared according to GCF TBARS levels after the therapy, a more statistically significant reduction was observed in group 3 (P = 0.001). CONCLUSION: These results suggest that additional flurbiprofen administration may have more inhibitory effects on GCF levels of PGE(2) and TBARS in the groups of smokers compared to non-smokers with CP.

Gingival Crevicular Fluid Prostaglandin E2 and Thiobarbituric Acid Reactive Substance Levels in Smokers and Non-Smokers With Chronic Periodontitis Following Phase I Periodontal Therapy and Adjunctive Use of Flurbiprofen.

BACKGROUND: It has been established that smoking is an important risk factor for the initiation and progression of chronic periodontitis (CP). This study investigates the effects of phase I periodontal therapy and adjunctive flurbiprofen administration on prostaglandin E2 (PGE2 ) and thiobarbituric acid reactive substance (TBARS) levels in gingival crevicular fluid (GCF) samples from smoker and non-smoker patients with CP. METHODS: Twenty-one non-smoker and 21 smoker patients with CP were divided into four groups according to treatment modalities. Group 1 (non-smokers with CP) and group 3 (smokers with CP) patients received daily 100-mg flurbiprofen tablets in a 2 × 1 regimen for 10 days together with scaling and root planing (SRP). Patients in group 2 (non-smokers with CP) and group 4 (smokers with CP) received placebo tablets in a 2 × 1 regimen for 10 days together with SRP. Plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL) measurements were recorded and GCF samples were collected at baseline and on day 10 of drug intake from each sampling area by a single examiner who was unaware of the treatment modality. Assays for GCF PGE2 and TBARS were carried out by an enzyme-linked immunosorbent assay and fluorometric method, respectively. RESULTS: All groups showed statistically significant reductions in PI and GI scores following the phase I periodontal treatment on day 10 (P <0.05), but no statistical differences were observed in PD and CAL scores after the therapy. In groups 1 and 2, the reduction of GCF PGE2 and TBARS levels were not significant after the therapy compared to baseline levels. In group 3, GCF PGE2 and TBARS levels exhibited a statistically significant decrease (P <0.05) after the therapy. Group 4 showed significant reductions (P <0.05) in GCF PGE2 levels after the therapy. No statistically significant reductions were observed in group 4 with regard to GCF TBARS levels. When groups 1 and 3 were compared according to GCF TBARS levels after the therapy, a more statistically significant reduction was observed in group 3 (P = 0.001). CONCLUSION: These results suggest that additional flurbiprofen administration may have more inhibitory effects on GCF levels of PGE2 and TBARS in the groups of smokers compared to non-smokers with CP.