Vanessa Tubero Euzebio Alves

Efficacy of high intensity diode laser as an adjunct to non-surgical periodontal treatment: a randomized controlled trial.

The high intensity diode laser has been studied in periodontics for the reduction of subgingival bacteria in non-surgical treatment. Our study evaluated the bacterial effect as well as changes in periodontal clinical parameters promoted by root scaling and planing associated with this wavelength. Twenty-seven patients randomly assigned in two groups underwent root scaling and planing on the tested sites, and only the experimental group received the diode laser irradiation. Among the clinical parameters studied, the clinical probing depth (CPD) and the clinical attachment level (CAL) resulted in significant enhancement in the control group when compared with the experimental group (P = 0.014 and P = 0.039, respectively). The results were similar for both groups regarding the plaque index (PI) and bleeding on probing (BP). No significant difference in the microbiological parameters was observed between the control and experimental groups. It was possible to conclude that the high power diode laser adjunct to the non-surgical periodontal treatment did not promote additional effects to the conventional periodontal treatment.

Porphyromonas Gingivalis is Associated With Protease-Activated Receptor-2 Upregulation in Chronic Periodontitis

BACKGROUND We previously reported a higher expression of protease-activated receptor-2 (PAR(2)) together with higher interleukin (IL)-1α, IL-6, IL-8, and tumor necrosis factor-α levels, total proteolytic activity, Porphyromonas gingivalis (Pg) prevalence, and neutrophil-protease 3 messenger RNA (mRNA) expression in patients with chronic periodontitis compared to healthy control patients. The aim of the present study is to expand this observation by considering the site level according to the presence of Pg. METHODS Microbiologic and gingival crevicular fluid samples were collected from patients with chronic periodontitis. Pg presence was evaluated by polymerase chain reaction and PAR(2) mRNA expression was evaluated by reverse-transcription polymerase chain reaction. Total proteolytic activity in the crevicular fluid was analyzed by using a specific substrate benzoylarginine nitroanilide, and the proinflammatory mediators IL-1α, IL-6, IL-8, and tumor necrosis factor-α were analyzed by enzyme-linked immunosorbent assay. RESULTS In Pg-positive periodontal sites, the mean probing depth and clinical attachment level, the prevalence of bleeding on probing sites, and crevicular fluid volume were higher (P <0.05) compared to Pg-negative sites. In addition, with the exception of IL-8, all other inflammatory mediators were positively (P <0.05) associated with Pg presence. Pg presence was also positively associated with a higher proteolytic activity (P = 0.0037) and higher PAR(2) mRNA expression (P = 0.0271). CONCLUSIONS We conclude that in chronic periodontitis, periodontal pockets presenting Pg show an upregulation of PAR(2) gene expression, and higher proinflammatory profile associated with advanced clinical destruction, therefore suggesting that Pg plays a pivotal role on PAR(2)-mediated periodontal inflammation in humans.

Periodontal Treatment Downregulates Protease-Activated Receptor 2 in Human Gingival Crevicular Fluid Cells

ABSTRACT Protease-activated receptor 2 (PAR2) is implicated in the pathogenesis of chronic inflammatory diseases, including periodontitis; it can be activated by gingipain and produced by Porphyromonas gingivalis and by neutrophil protease 3 (P3). PAR2 activation plays a relevant role in inflammatory processes by inducing the release of important inflammatory mediators associated with periodontal breakdown. The effects of periodontal treatment on PAR2 expression and its association with levels of proinflammatory mediators and activating proteases were investigated in chronic periodontitis patients. Positive staining for PAR2 was observed in gingival crevicular fluid cells and was reflective of tissue destruction. Overexpression of PAR2 was positively associated with inflammatory clinical parameters and with the levels of interleukin-6 (IL-6), IL-8, tumor necrosis factor alpha, matrix metalloprotease 2 (MMP-2), MMP-8, hepatocyte growth factor, and vascular endothelial growth factor. Elevated levels of gingipain and P3 and decreased levels of dentilisin and the protease inhibitors secretory leukocyte protease inhibitor and elafin were also associated with PAR2 overexpression. Healthy periodontal sites from individuals with chronic periodontitis showed diminished expression of PAR2 mRNA and the PAR2 protein (P < 0.05). Furthermore, periodontal treatment resulted in decreased PAR2 expression and correlated with decreased expression of inflammatory mediators and activating proteases. We concluded that periodontal treatment resulted in decreased levels of proteases and that proinflammatory mediators are associated with decreased PAR2 expression, suggesting that PAR2 expression is influenced by the presence of periodontal infection and is not a constitutive characteristic favoring periodontal inflammation.

Expression of Protease Activated Receptor-1 in Chronic Periodontitis

BACKGROUND Protease activated receptor-1 (PAR1) activation by thrombin may play a role in repair and homeostasis of periodontal tissues. The main objective of this study is to investigate PAR1 expression in patients with periodontitis, before and after non-surgical periodontal treatment, and to associate its expression with the presence of inflammatory biomarkers and PAR2 expression. METHODS Gingival crevicular fluid (GCF) samples and clinical parameters, including probing depth, clinical attachment level, bleeding on probing, and gingival and plaque indices, were collected from periodontally healthy individuals and patients with moderate chronic periodontitis (CP) before and 6 weeks after periodontal non-surgical treatment. PAR1 and PAR2 messenger RNA (mRNA) at the GCF were evaluated by quantitative polymerase chain reaction (qPCR). Flow cytometry analysis identified the GCF PAR1-expressing cells. GCF inflammatory biomarkers were also determined. RESULTS Clinical parameters were significantly improved after therapy (P <0.01). The qPCR analysis showed that, before therapy, PAR1 mRNA levels in CP were similar to controls. Periodontal treatment led to increased PAR1 expression in CP (P <0.05). PAR1 expression was inversely correlated to PAR2 expression and with interleukins 6 and 8, tumor necrosis factor-α, interferon-γ, and matrix metalloproteinase-2 levels. CONCLUSIONS Periodontal treatment results in PAR1 overexpression in the GCF, and PAR1 expression is associated with decreased expression of inflammatory biomarkers and inversely correlated to PAR2 expression in the GCF. Therefore, the data suggest the importance of PAR1 mediating the known anabolic actions of thrombin in the periodontium.

Influence of Parstatin on Experimental Periodontal Disease and Repair in Rats

BACKGROUND Parstatin is a 41-amino acid peptide, formed by proteolytic cleavage on activation of the protease activated receptor-1, with antiangiogenic properties. The purpose of this study is to evaluate the influence of synthetic parstatin on experimental periodontal disease and repair in rats. METHODS Ligature-induced periodontitis was established in rats and the influence of parstatin administration was assessed after 8 and 15 days for periodontal disease and 24 hours and 8 days after repair after ligature removal. RESULTS Parstatin administration significantly inhibited gingival myeloperoxidase activity, interleukin (IL)-1β, tumor necrosis factor-α, and IL-6 levels and led to suppression of macrophages and collagen degradation. At periodontal tissues under repair, parstatin increased the gingival levels of endostatin and decreased vascular endothelial growth factor expression and blood vessel number but did not influence histologic healing. In addition, the tomographic linear bone loss was significantly reduced at 15 days of periodontitis when the rats were treated with parstatin compared to their respective phosphate-buffered saline-treated controls. CONCLUSIONS Parstatin suppresses the periodontal tissue breakdown followed by experimental periodontitis in rats and did not impair periodontal tissue repair, despite its antiangiogenic effect. Parstatin may represent a novel approach to modulate host response in chronic periodontal disease.