Periodontal surgery using rhFGF-2 with deproteinized bovine bone mineral or rhFGF-2 alone: 2-year follow-up of a randomized controlled trial.

AIM: To compare outcomes of rhFGF-2 + DBBM therapy with rhFGF-2 alone in the treatment of intrabony defects. This study provides 2-year follow-up results from the previous randomized controlled trial. MATERIALS AND METHODS: Defects were randomly allocated to receive rhFGF-2 + DBBM (test) or rhFGF-2 (control). Treated sites were re-evaluated at 2 years postoperatively, using original clinical and patient-centred measures. RESULTS: Thirty-eight sites were available for re-evaluation. At 2 years, both groups showed a significant improvement in clinical attachment level (CAL) from baseline. A gain in CAL of 3.4 ± 1.3 mm in the test group and 3.1 ± 1.5 mm in the control group was found. No significant inter-group difference was noted. Both groups showed a progressive increase in radiographic bone fill (RBF). The test treatment yielded greater RBF (56%) compared with the control group (41%). The control treatment performed better in contained defects in terms of CAL and RBF. There was no significant difference in patient-reported outcomes between groups. CONCLUSIONS: At 2-year follow-up, the test and cotrol treatments were similarly effective in improving CAL, whereas the test treatment achieved a significantly greater RBF. In both treatments, favourable clinical, radiographic, and patient-reported outcomes can be sustained for at least 2 years. TRIAL REGISTRATION: The University Hospital Medical Information Network-Clinical Trials Registry (UMIN-CTR) 000025257.

Treatment of Gingival Fenestration with Connective Tissue Graft: A Case Report.

Here, we report a case of gingival fenestration requiring periodontal plastic surgery. The patient was a 32-year-old man presenting with the chief complaint of esthetic impairment and gingival twitching due to gingival fenestration. Baseline examination revealed localized periodontal breakdown, including gingival fenestration in the lower right central incisor (#41). Periodontal examination revealed 3% of sites with a probing depth of ≥4 mm and 8.9% with bleeding on probing. Radiographic examination revealed vertical bone loss in #15 and 36, together with buccal fenestration in #41. Based on a clinical diagnosis of chronic periodontitis with gingival fenestration, initial periodontal therapy comprised plaque control and scaling and root planing. Following suppression of inflammation, occlusal adjustment was performed in the anterior teeth. As plastic surgery, combined use of an elevated flap and a connective tissue graft was applied at #41. Following reevaluation, the patient was placed on maintenance care. The patient's periodontal condition has remained stable over a 6-month period.

In vitro Effect of Mouthrinse Containing Essential Oils on Proliferation and Migration of Gingival Epithelial Cells.

We aimed to investigate in vitro the effects of mouthrinses containing essential oils (EOs) on proliferation and migration of gingival epithelial cells. Human gingival epithelial cells were treated with predetermined dilutions of commercially available EO mouthrinses with or without ethanol and a mouthrinse containing cetyl pyridinium chloride (CPC) for 60 s. Cell proliferation was evaluated using WST-1 assay. Cell migration was assessed using a wound closure model. Within 10 s of exposure to EO mouthrinse without ethanol, the epithelial cells became aberrant and shrank. No statistically significant difference in cell migration or proliferation was observed among cells pretreated by the EO mouthrinse with ethanol, CPC mouthrinse and control (phosphate buffered saline). In contrast, the EO mouthrinse without ethanol significantly reduced cell proliferation (p < 0.001) to approximately 20% relative to control. As for the EO mouthrinse without ethanol, it was not possible to assess its effect on cell migration using this model, because treated cells could be easily detached from the culture plate upon scratch, possibly because of the surfactant ingredient in the formulation. Within the limitations of the study, the EO mouthrinse with ethanol exerted no inhibitory effect on proliferation and migration of the gingival epithelial cells. Copyright © 2016 John Wiley & Sons, Ltd.

Effect of a mouthrinse containing rice peptide CL(14-25) on early dental plaque regrowth: a randomized crossover pilot study.

BACKGROUND: We aimed to evaluate clinically the effect of mouthrinse containing a rice peptide on early dental plaque regrowth. METHODS: The study was designed as a double-masked, two-group crossover randomized pilot trial, involving 10 periodontally healthy volunteers. After receiving a professional tooth cleaning at baseline, over the next 3 days each participant refrained from all oral hygiene measures and had two daily rinses with 20 ml of the test mouthrinse containing 0.4 % rice peptide CL(14-25) or placebo rinse. At the end of each experimental period, plaque score was assessed using the modified Volpe's method, and the participants filled out a questionnaire. Each participant underwent a 7-day washout period followed by a second allocation. The plaque score was the primary outcome of the study and participant perception was the secondary outcome. RESULTS: No adverse effects were observed in the participants during the study. Clinically, the mean plaque score of the examined teeth was significantly lower in the test group (2.44 ± 0.74, CI: 1.91-2.96) than the placebo group (2.65 ± 0.63, CI: 2.20-3.10) (P < 0.05). When analyzed according to the type of teeth, a significantly lower score of the premolars/molars was observed in the test group (2.39 ± 0.68, CI: 2.08-2.71) than that in the placebo group (2.66 ± 0.58, CI: 2.39-2.93) (P < 0.05). CONCLUSIONS: The mouthrinse containing 0.4 % rice peptide CL(14-25) was effective in reducing the early regrowth of dental plaque. However, clinical relevance of this efficacy needs to be validated in a future large-scale study. TRIAL REGISTRATION: UMIN Clinical Trials Registry (UMIN-CTR) R000014000. Date of formal registration: November 1, 2013.

Porphyromonas gingivalis entry into gingival epithelial cells modulated by Fusobacterium nucleatum is dependent on lipid rafts.

Host cell invasion by a major periodontal pathogen, Porphyromonas gingivalis, has been proposed as an important mechanism involved in host-pathogen interactions in periodontal and cardiovascular diseases. The present study sought to gain insight into the underlying mechanism(s) involved in previously demonstrated fusobacterial modulation of host cell invasion by P. gingivalis. An immortalized human gingival cell line Ca9-22 was dually infected with P. gingivalis ATCC 33277 and Fusobacterium nucleatum TDC 100, and intracellular invasion was assessed by scanning electron microscopy (SEM) and confocal scanning laser microscopy (CSLM). SEM observation showed that P. gingivalis and F. nucleatum formed consortia and were in the process of penetrating into Ca9-22 by 30-60 min after infection. In CSLM, Ca9-22 cells that contained both P. gingivalis and F. nucleatum were frequently observed after 2 h, although cells that contained exclusively P. gingivalis were also found. Infection by P. gingivalis and/or F. nucleatum revealed evident colocalization with a lipid raft marker, GM1-containing membrane microdomains. In an antibiotic protection assay, depletion of epithelial plasma membrane cholesterol resulted in a significant reduction of recovered P. gingivalis or F. nucleatum (∼33% of untreated control; p < 0.001). This inhibition was also confirmed by CSLM. Sequential infection experiments showed that timing of infection by each species could critically influence the invasion profile. Co-infection with F. nucleatum significantly enhanced host cell invasion by P. gingivalis 33277, its serine phophatase SerB mutant and complemented strains, suggesting that the SerB does not play a major role in this fusobacterial enhancement of P. gingivalis invasion. Thus, the interaction between F. nucleatum and host cells may be important in the fusobacterial enhancement of P. gingivalis invasion. Collectively, these results suggest that lipid raft-mediated process is at least one of the potential mechanisms involved in fusobacterium-modulated host cell invasion by P. gingivalis.