Effect of photodynamic therapy, diode laser, and deep scaling on cytokine and acute-phase protein levels in gingival crevicular fluid of residual periodontal pockets.

BACKGROUND: There is an ongoing controversy on the benefits of treatment protocols, including dental lasers and photodynamic therapy (PDT). The purpose of this study is to compare the local biologic effects of PDT, diode soft laser (DSL) therapy, and conventional deep scaling and root planing (SRP) in residual pockets. METHODS: Thirty-two individuals were included based on a history of previous treatment for periodontitis and the persistence of sites with probing depths >4 mm and bleeding on probing. Residual pockets were debrided with an ultrasonic device and then randomly assigned either to PDT, DSL, or SRP. Gingival crevicular fluid was collected before treatment, after 14 days, and at 2 and 6 months. Levels of 13 cytokines and nine acute-phase proteins were measured using a bead-based multiplexing analysis system. RESULTS: Treatment with PDT, DSL, or SRP led to significant changes in several cytokines and acute-phase proteins: Compared with baseline, levels of interleukin-17, basic fibroblast growth factor, granulocyte colony-stimulating factor, granulocyte macrophage colony-stimulating factor, and macrophage inflammatory protein 1-α were lower 14 days and 2 months after treatment. Except for granulocyte colony-stimulating factor, these differences remained significant throughout the observation period. The levels of five acute-phase proteins (α-2 macroglobulin, haptoglobin, serum amyloid P, procalcitonin, and tissue plasminogen activator) were significantly higher at 6 months than at baseline. No significant differences were observed among the three treatment modalities at any time point for any biochemical parameter. CONCLUSIONS: Levels of several cytokines and acute-phase proteins significantly changed after treatment regardless of treatment modality. There was no evidence for a specific DSL- or PDT-enhanced expression of inflammatory mediators.

Treatment of residual pockets with photodynamic therapy, diode laser, or deep scaling. A randomized, split-mouth controlled clinical trial.

The objective of this work was to compare the effects of antimicrobial photodynamic therapy (PDT), diode soft laser therapy (DSL), and thorough deep scaling and root planing (SRP) for treatment of residual pockets. Thirty-two subjects with a history of non-surgical treatment for chronic periodontitis were included. Residual pockets >4 mm and bleeding upon probing were debrided with an ultrasonic device and then subjected to either PDT, DSL, or SRP. Pocket probing depth (PPD), bleeding on probing (BOP), and gingival recession were monitored over 6 months. Counts of four microorganisms were determined by direct hybridization with RNA probes. PPD decreased from 5.6 ± 1.0 to 3.8 ± 1.1 in 6 months (p < 0.001), and BOP decreased from 100% to 52% (p < 0.01). The risk for a site to remain >4 mm with BOP depended on initial PPD (p = 0.036) and was higher if treated with DSL (p = 0.034). Frequencies of three microorganisms were significantly lower in PDT- and SRP-treated than in DSL-treated quadrants (p = 0.02) after 14 days, but not at months 2 and 6. All three treatments resulted in a significant clinical improvement. PDT and SRP suppressed Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola stronger, and resulted in fewer persisting pockets after 6 months, than DSL application.

Effect of smoking on gingival crevicular fluid cytokine profile during experimental gingivitis.

BACKGROUND: Cigarette smoking is a significant risk factor in the pathogenesis of periodontal disease, able to influence both the subgingival microbiota and host responses. AIM: The aim of the present study was to determine the influence of smoking on the amount of IL-1beta, IL-4 and IL-8 in gingival crevicular fluid (GCF) during experimental gingivitis in humans. MATERIAL AND METHODS: Twenty-two healthy subjects, 10 smokers and 12 non-smokers, participated in the study. After professional cleaning, they performed optimal hygiene to reach perfect clinical gingival health. Oral hygiene measures were ceased for a period of 10 days. Clinical indices, including plaque index (PI), gingival index (GI), probing pocket depth (PPD) and bleeding on probing (BOP), were assessed 2 days before (day -2), at the beginning (day 0) and at the end of the experimental gingivitis period (day 10). At the same time, GCF was collected from 12 sites in each patient, by means of durapore filter membranes. Total amounts of IL-1beta, IL-4 and IL-8 were determined by enzyme-linked immunoadsorbent assay. RESULTS: Clinical data revealed that both smokers and non-smokers showed an increase in PI, GI and BOP scores during the experiment. Although no differences were noted with regard to PI at day 10, the GI and BOP were significantly less pronounced in smokers than non-smokers (p < 0.005). Non-smokers showed higher total amounts of IL-4 but lower amounts of IL-8 than smokers, throughout the experiment. Total amounts of IL-1beta and IL-8 increased significantly during plaque accumulation in both groups. IL-4 remained stable for the smoker group and decreased for the non-smoker group. CONCLUSIONS: The present results indicate that smoking interferes with cytokine production. When performing studies regarding the pathogenesis of periodontitis, the smoking status of the participants needs to be taken into consideration.