555 research outputs found

    Randomized controlled pilot study comparing small buccal defects around dental implants treated with a subepithelial connective tissue graft or with guided bone regeneration

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    AIM To compare subepithelial connective tissue grafts (SCTG) versus guided bone regeneration (GBR) for the treatment of small peri-implant dehiscence defects in terms of profilometric (primary outcome), clinical, and patient-reported outcome measures (PROMs). METHODS Sixteen patients who presented with small buccal bone dehiscences (≤3 mm) following single implant placement were recruited. Following implant placement, buccal bone defect sites were randomly treated either with a SCTG or GBR. Six patients who lacked bone dehiscences after implant placement were assigned to a negative control. Transmucosal healing was applied in all patients. Patients were examined prior (T1) and after (T2) implant placement, at suture removal (T3), at implant impression (T5), at crown delivery (T6), and 12 (T7) months after crown delivery. Measurements included profilometric outcomes, marginal bone levels, buccal bone and soft tissue thickness, PROMs, and clinical parameters. All data were analyzed descriptively. RESULTS The median changes in buccal contour as assessed by profilometric measures between T1 and T5 showed a decrease of 1.84 mm for the SCTG group and 1.06 mm for the GBR group. Between T2 and T7, the median change in the buccal contour amounted to 0.45 mm for SCTG and -0.94 mm (=loss) for GBR. Patients' pain perception tended to be higher in SCTG than in GBR. All peri-implant soft tissue parameters showed healthy oral tissues and no clinically relevant differences between groups. CONCLUSION Within the limitations of this pilot study, treating small peri-implant dehiscence defects with a SCTG might be a viable alternative to GBR. The use of a SCTG tended to result in more stable profilometric outcomes and comparable clinical outcomes to GBR. However, patient-reported outcome measures tended to favor GBR

    Effect of peri-implant mucosal thickness on esthetic outcomes and the efficacy of soft tissue augmentation procedures: Consensus report of group 2 of the SEPA/DGI/OF workshop

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    OBJECTIVES: The aim of this study was to comprehensively assess the literature in terms of the effect of peri‐implant mucosal thickness on esthetic outcomes and the efficacy of soft tissue augmentation procedures to increase the mucosal thickness with autogenous grafts or soft tissue substitutes. MATERIAL AND METHODS: Two systematic reviews (SR) were performed prior to the consensus meeting to assess the following questions. Review 1, focused question: In systemically healthy patients with an implant‐supported fixed prosthesis, what is the influence of thin as compared to thick peri‐implant mucosa on esthetic outcomes? Review 2, focused question 1: In systemically healthy humans with at least one dental implant (immediate or staged implant), what is the efficacy of connective tissue graft (CTG), as compared to absence of a soft tissue grafting procedure, in terms of gain in peri‐implant soft tissue thickness (STT) reported by randomized controlled clinical trials (RCTs) or controlled clinical trials (CCTs)? Review 2, focused question 2: In systemically healthy humans with at least one dental implant (immediate or staged implant), what is the efficacy of CTG, as compared to soft tissue substitutes, in terms of gain in peri‐implant STT reported by RCTs or CCTs? The outcomes of the two SRs, the consensus statements, the clinical implications, and the research recommendations were discussed and subsequently approved at the consensus meeting during the group and plenary sessions. CONCLUSIONS: There was a tendency of superior esthetic outcomes in the presence of a thick mucosa. The connective tissue graft remains the standard of care in terms of increasing mucosa thickness

    Boosting Wnt activity during colorectal cancer progression through selective hypermethylation of Wnt signaling antagonists.

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    BACKGROUND: There is emerging evidence that Wnt pathway activity may increase during the progression from colorectal adenoma to carcinoma and that this increase is potentially an important step towards the invasive stage. Here, we investigated whether epigenetic silencing of Wnt antagonists is the biological driver for this increased Wnt activity in human tissues and how these methylation changes correlate with MSI (Microsatelite Instability) and CIMP (CpG Island Methylator Phenotype) statuses as well as known mutations in genes driving colorectal neoplasia. METHODS: We conducted a systematic analysis by pyrosequencing, to determine the promoter methylation of CpG islands associated with 17 Wnt signaling component genes. Methylation levels were correlated with MSI and CIMP statuses and known mutations within the APC, BRAF and KRAS genes in 264 matched samples representing the progression from normal to pre-invasive adenoma to colorectal carcinoma. RESULTS: We discovered widespread hypermethylation of the Wnt antagonists SFRP1, SFRP2, SFRP5, DKK2, WIF1 and SOX17 in the transition from normal to adenoma with only the Wnt antagonists SFRP1, SFRP2, DKK2 and WIF1 showing further significant increase in methylation from adenoma to carcinoma. We show this to be accompanied by loss of expression of these Wnt antagonists, and by an increase in nuclear Wnt pathway activity. Mixed effects models revealed that mutations in APC, BRAF and KRAS occur at the transition from normal to adenoma stages whilst the hypermethylation of the Wnt antagonists continued to accumulate during the transitions from adenoma to carcinoma stages. CONCLUSION: Our study provides strong evidence for a correlation between progressive hypermethylation and silencing of several Wnt antagonists with stepping-up in Wnt pathway activity beyond the APC loss associated tumour-initiating Wnt signalling levels.A.L.S. was supported by the Fundacao para a Ciencia e Tecnologia (Portugal); A.I. by a Clinician Scientist Fellowship from Cancer Research UK (grant no C10112/A11388); M.B. by the Medical Research Council (U105192713) and by Cancer Research UK (grant no C7379/A8709).This is the final published version. It first appeared at http://www.biomedcentral.com/1471-2407/14/891
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