Surgical management of gingival recession using autogenous soft tissue grafts

One of the chief goals of periodontal plastic surgery is establishment of ideal pink esthetics through the reconstruction of gingival recessions. A gold standard treatment approach for coverage of gingival recession with predictable esthetic outcomes is the transplantation of autogenous soft tissue grafts. Various surgical techniques can be used in combination with autogenous soft tissue grafts for gingival recession coverage

Immediate versus delayed implant placement after anterior single tooth extraction: the timing randomized controlled clinical trial

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Immediate vs. Delayed Implant Placement after Anterior Single Tooth Extraction: The Timing Randomised Controlled Clinical Trial.

to compare need for bone augmentation, surgical complications, periodontal, radiographic, aesthetic and patient reported outcomes in subjects receiving implant placement at the time of extraction (IMI) or 12 weeks thereafter. METHODS: Subjects requiring single tooth extraction in the anterior and premolar areas were recruited in 7 private practices. Implant position and choice of platform were restoratively driven. Measurements were performed by calibrated and masked examiners. RESULTS: IMI was unfeasible in 7.5% of cases. 124 subjects were randomized. One implant was lost in the IMI group. IMI required bone augmentation in 72% of cases compared with 43.9% for delayed (P=0.01), while wound failure occurred in 26.1% and 5.3% of cases, respectively (P=0.02). At 1 year, IMI had deeper probing depths (4.1±1.2 mm vs. 3.3±1.1 mm, P<0.01). A trend for greater radiographic bone loss was observed at IMI over the initial 3-year period (Ptrend<0.01). Inadequate pink aesthetic scores were obtained in 19% of delayed and in 42% of IMI implant cases (P=0.03). No differences in patient reported outcomes were observed. CONCLUSIONS: Immediate implant placement should not be recommended when aesthetics are important, IMI should be limited to selected cases. Longer follow-up is needed to assess differences in complication rates. This article is protected by copyright. All rights reserved

Circulating extracellular particles from severe COVID-19 patients show altered profiling and innate lymphoid cell-modulating ability

Introduction: Extracellular vesicles (EVs) and particles (EPs) represent reliable biomarkers for disease detection. Their role in the inflammatory microenvironment of severe COVID-19 patients is not well determined. Here, we characterized the immunophenotype, the lipidomic cargo and the functional activity of circulating EPs from severe COVID-19 patients (Co-19-EPs) and healthy controls (HC-EPs) correlating the data with the clinical parameters including the partial pressure of oxygen to fraction of inspired oxygen ratio (PaO2/FiO2) and the sequential organ failure assessment (SOFA) score. Methods: Peripheral blood (PB) was collected from COVID-19 patients (n=10) and HC (n=10). EPs were purified from platelet-poor plasma by size exclusion chromatography (SEC) and ultrafiltration. Plasma cytokines and EPs were characterized by multiplex bead-based assay. Quantitative lipidomic profiling of EPs was performed by liquid chromatography/mass spectrometry combined with quadrupole time-of-flight (LC/MS Q-TOF). Innate lymphoid cells (ILC) were characterized by flow cytometry after co-cultures with HC-EPs or Co-19-EPs. Results: We observed that EPs from severe COVID-19 patients: 1) display an altered surface signature as assessed by multiplex protein analysis; 2) are characterized by distinct lipidomic profiling; 3) show correlations between lipidomic profiling and disease aggressiveness scores; 4) fail to dampen type 2 innate lymphoid cells (ILC2) cytokine secretion. As a consequence, ILC2 from severe COVID-19 patients show a more activated phenotype due to the presence of Co-19-EPs. Discussion: In summary, these data highlight that abnormal circulating EPs promote ILC2-driven inflammatory signals in severe COVID-19 patients and support further exploration to unravel the role of EPs (and EVs) in COVID-19 pathogenesis

Expression of caspase-3, p53 and Bcl-2 in generalized aggressive periodontitis

BACKGROUND: Apoptosis, or programmed cell death is a form of physiological cell death. It is increased or decreased in the presence of infection, inflammation or tissue remodelling. Previous studies suggest that apoptosis is involved in the pathogenesis of inflammatory periodontal disease. The aim of the present study was to investigate the clinical features and known indicators of apoptosis (p53, Bcl-2, Caspase-3) in patients with generalized aggressive periodontitis (GAP) METHODS: Eight patients with GAP, who had sites with probing depths (PD) > 5 mm, and 10 periodontally-healthy persons were included in the study. Clinical examinations and PD were performed, and the plaque index and gingival index were recorded. Gingival tissues biopsies were obtained from active site of each patient and from healthy individuals. The expression of caspase-3, Bcl-2, and p53 was evaluated by immunohistochemistry RESULTS: There were no significant differences between GAP and control group with respect to levels of caspase-3 and p53 expression (P > 0.05). Contrary, the frequency of grade 3 expression of Bcl-2 was higher in GAP group than the control group. CONCLUSION: The higher frequency of Bcl-2 expression in GAP group indicates and delayed apoptosis can lead to increasing resident inflammatory cells in periodontal tissues and resulting in progressive periodontal destruction